Islets of langerhans transplantation. Medical search

The transference of pancreatic islets within an individual, between individuals of the same species, or between individuals of different species.

Recirculating, dendritic, antigen-presenting cells containing characteristic racket-shaped granules (Birbeck granules). They are found principally in the stratum spinosum of the EPIDERMIS and are rich in Class II MAJOR HISTOCOMPATIBILITY COMPLEX molecules. Langerhans cells were the first dendritic cell to be described and have been a model of study for other dendritic cells (DCs), especially other migrating DCs such as dermal DCs and INTERSTITIAL DENDRITIC CELLS.

Irregular microscopic structures consisting of cords of endocrine cells that are scattered throughout the PANCREAS among the exocrine acini. Each islet is surrounded by connective tissue fibers and penetrated by a network of capillaries. There are four major cell types. The most abundant beta cells (50-80%) secrete INSULIN. Alpha cells (5-20%) secrete GLUCAGON. PP cells (10-35%) secrete PANCREATIC POLYPEPTIDE. Delta cells (~5%) secrete SOMATOSTATIN.

The transference of a part of or an entire liver from one human or animal to another.

Transplantation between individuals of the same species. Usually refers to genetically disparate individuals in contradistinction to isogeneic transplantation for genetically identical individuals.

The transference of a kidney from one human or animal to another.

A group of disorders resulting from the abnormal proliferation of and tissue infiltration by LANGERHANS CELLS which can be detected by their characteristic Birbeck granules (X bodies), or by monoclonal antibody staining for their surface CD1 ANTIGENS. Langerhans-cell granulomatosis can involve a single organ, or can be a systemic disorder.

The transference of BONE MARROW from one human or animal to another for a variety of purposes including HEMATOPOIETIC STEM CELL TRANSPLANTATION or MESENCHYMAL STEM CELL TRANSPLANTATION.

Transfer of HEMATOPOIETIC STEM CELLS from BONE MARROW or BLOOD between individuals within the same species (TRANSPLANTATION, HOMOLOGOUS) or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS). Hematopoietic stem cell transplantation has been used as an alternative to BONE MARROW TRANSPLANTATION in the treatment of a variety of neoplasms.

The transference of a heart from one human or animal to another.

Transplantation of an individual's own tissue from one site to another site.

The transference of either one or both of the lungs from one human or animal to another.

The survival of a graft in a host, the factors responsible for the survival and the changes occurring within the graft during growth in the host.

The transfer of STEM CELLS from one individual to another within the same species (TRANSPLANTATION, HOMOLOGOUS) or between species (XENOTRANSPLANTATION), or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS). The source and location of the stem cells determines their potency or pluripotency to differentiate into various cell types.

Preparative treatment of transplant recipient with various conditioning regimens including radiation, immune sera, chemotherapy, and/or immunosuppressive agents, prior to transplantation. Transplantation conditioning is very common before bone marrow transplantation.

Transference of an organ between individuals of the same species or between individuals of different species.

An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient.

The transference of a pancreas from one human or animal to another.

Individuals supplying living tissue, organs, cells, blood or blood components for transfer or transplantation to histocompatible recipients.

Transference of a tissue or organ from either an alive or deceased donor, within an individual, between individuals of the same species, or between individuals of different species.

A general term for the complex phenomena involved in allo- and xenograft rejection by a host and graft vs host reaction. Although the reactions involved in transplantation immunology are primarily thymus-dependent phenomena of cellular immunity, humoral factors also play a part in late rejection.

Transference of cells within an individual, between individuals of the same species, or between individuals of different species.

An organism that, as a result of transplantation of donor tissue or cells, consists of two or more cell lines descended from at least two zygotes. This state may result in the induction of donor-specific TRANSPLANTATION TOLERANCE.

Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.

Transplantation between genetically identical individuals, i.e., members of the same species with identical histocompatibility antigens, such as monozygotic twins, members of the same inbred strain, or members of a hybrid population produced by crossing certain inbred strains.

A pancreatic beta-cell hormone that is co-secreted with INSULIN. It displays an anorectic effect on nutrient metabolism by inhibiting gastric acid secretion, gastric emptying and postprandial GLUCAGON secretion. Islet amyloid polypeptide can fold into AMYLOID FIBRILS that have been found as a major constituent of pancreatic AMYLOID DEPOSITS.

Transplantation of tissue typical of one area to a different recipient site. The tissue may be autologous, heterologous, or homologous.

A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).

The clinical entity characterized by anorexia, diarrhea, loss of hair, leukopenia, thrombocytopenia, growth retardation, and eventual death brought about by the GRAFT VS HOST REACTION.

The external, nonvascular layer of the skin. It is made up, from within outward, of five layers of EPITHELIUM: (1) basal layer (stratum basale epidermidis); (2) spinous layer (stratum spinosum epidermidis); (3) granular layer (stratum granulosum epidermidis); (4) clear layer (stratum lucidum epidermidis); and (5) horny layer (stratum corneum epidermidis).

Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

Non-cadaveric providers of organs for transplant to related or non-related recipients.

Transplantation of STEM CELLS collected from the fetal blood remaining in the UMBILICAL CORD and the PLACENTA after delivery. Included are the HEMATOPOIETIC STEM CELLS.

The simultaneous, or near simultaneous, transference of heart and lungs from one human or animal to another.

A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.

Elements of limited time intervals, contributing to particular results or situations.

Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs.

A subclass of lectins that are specific for CARBOHYDRATES that contain MANNOSE.

An induced state of non-reactivity to grafted tissue from a donor organism that would ordinarily trigger a cell-mediated or humoral immune response.

Rare malignant neoplasm of dendritic LANGERHANS CELLS exhibiting atypical cytology, frequent mitoses, and aggressive clinical behavior. They can be distinguished from other histiocytic and dendritic proliferations by immunohistochemical and ultrastructure studies. Cytologically benign proliferations of Langerhans cells are called LANGERHANS CELL HISTIOCYTOSIS.

The administrative procedures involved with acquiring TISSUES or organs for TRANSPLANTATION through various programs, systems, or organizations. These procedures include obtaining consent from TISSUE DONORS and arranging for transportation of donated tissues and organs, after TISSUE HARVESTING, to HOSPITALS for processing and transplantation.

The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.

The grafting of skin in humans or animals from one site to another to replace a lost portion of the body surface skin.

A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.

Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.

Transplantation of stem cells collected from the peripheral blood. It is a less invasive alternative to direct marrow harvesting of hematopoietic stem cells. Enrichment of stem cells in peripheral blood can be achieved by inducing mobilization of stem cells from the BONE MARROW.

Transplantation between animals of different species.

Transference of fetal tissue between individuals of the same species or between individuals of different species.

Identification of the major histocompatibility antigens of transplant DONORS and potential recipients, usually by serological tests. Donor and recipient pairs should be of identical ABO blood group, and in addition should be matched as closely as possible for HISTOCOMPATIBILITY ANTIGENS in order to minimize the likelihood of allograft rejection. (King, Dictionary of Genetics, 4th ed)

Severe inability of the LIVER to perform its normal metabolic functions, as evidenced by severe JAUNDICE and abnormal serum levels of AMMONIA; BILIRUBIN; ALKALINE PHOSPHATASE; ASPARTATE AMINOTRANSFERASE; LACTATE DEHYDROGENASES; and albumin/globulin ratio. (Blakiston's Gould Medical Dictionary, 4th ed)

A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.

Partial or total replacement of the CORNEA from one human or animal to another.

Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.

A type of acute or chronic skin reaction in which sensitivity is manifested by reactivity to materials or substances coming in contact with the skin. It may involve allergic or non-allergic mechanisms.

Glycoproteins expressed on cortical thymocytes and on some dendritic cells and B-cells. Their structure is similar to that of MHC Class I and their function has been postulated as similar also. CD1 antigens are highly specific markers for human LANGERHANS CELLS.

A type of pancreatic cell representing about 5-20% of the islet cells. Alpha cells secrete GLUCAGON.

Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.

A nodular organ in the ABDOMEN that contains a mixture of ENDOCRINE GLANDS and EXOCRINE GLANDS. The small endocrine portion consists of the ISLETS OF LANGERHANS secreting a number of hormones into the blood stream. The large exocrine portion (EXOCRINE PANCREAS) is a compound acinar gland that secretes several digestive enzymes into the pancreatic ductal system that empties into the DUODENUM.

Prospective patient listings for appointments or treatments.

The return of a sign, symptom, or disease after a remission.

Transfer of MESENCHYMAL STEM CELLS between individuals within the same species (TRANSPLANTATION, HOMOLOGOUS) or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS).

Diabetes mellitus induced experimentally by administration of various diabetogenic agents or by PANCREATECTOMY.

A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro.

The degree of antigenic similarity between the tissues of different individuals, which determines the acceptance or rejection of allografts.

Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.

A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).

Neoplasms located in the blood and blood-forming tissue (the bone marrow and lymphatic tissue). The commonest forms are the various types of LEUKEMIA, of LYMPHOMA, and of the progressive, life-threatening forms of the MYELODYSPLASTIC SYNDROMES.

Transference of tissue within an individual, between individuals of the same species, or between individuals of different species.

A dead body, usually a human body.

The process by which organs are kept viable outside of the organism from which they were removed (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism).

Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.

Irradiation of the whole body with ionizing or non-ionizing radiation. It is applicable to humans or animals but not to microorganisms.

A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511)

Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).

Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.

A benign tumor of the PANCREATIC BETA CELLS. Insulinoma secretes excess INSULIN resulting in HYPOGLYCEMIA.

A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.

The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods.

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.

A strain of non-obese diabetic mice developed in Japan that has been widely studied as a model for T-cell-dependent autoimmune insulin-dependent diabetes mellitus in which insulitis is a major histopathologic feature, and in which genetic susceptibility is strongly MHC-linked.

Transference of brain tissue, either from a fetus or from a born individual, between individuals of the same species or between individuals of different species.

A class of animal lectins that bind to carbohydrate in a calcium-dependent manner. They share a common carbohydrate-binding domain that is structurally distinct from other classes of lectins.

The number of CELLS of a specific kind, usually measured per unit volume or area of sample.

The procedure established to evaluate the health status and risk factors of the potential DONORS of biological materials. Donors are selected based on the principles that their health will not be compromised in the process, and the donated materials, such as TISSUES or organs, are safe for reuse in the recipients.

Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.

The most benign and common form of Langerhans-cell histiocytosis which involves localized nodular lesions predominantly of the bones but also of the gastric mucosa, small intestine, lungs, or skin, with infiltration by EOSINOPHILS.

The transference between individuals of the entire face or major facial structures. In addition to the skin and cartilaginous tissue (CARTILAGE), it may include muscle and bone as well.

Antigens determined by leukocyte loci found on chromosome 6, the major histocompatibility loci in humans. They are polypeptides or glycoproteins found on most nucleated cells and platelets, determine tissue types for transplantation, and are associated with certain diseases.

The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.

Pathological processes of the LIVER.

Endocrine cells found throughout the GASTROINTESTINAL TRACT and in islets of the PANCREAS. D cells secrete SOMATOSTATIN that acts in both an endocrine and paracrine manner. Somatostatin acts on a variety of tissues including the PITUITARY GLAND; gastrointestinal tract; pancreas; and KIDNEY by inhibiting the release of hormones, such as GROWTH HORMONE; GASTRIN; INSULIN; and RENIN.

A pancreatic polypeptide of about 110 amino acids, depending on the species, that is the precursor of insulin. Proinsulin, produced by the PANCREATIC BETA CELLS, is comprised sequentially of the N-terminal B-chain, the proteolytically removable connecting C-peptide, and the C-terminal A-chain. It also contains three disulfide bonds, two between A-chain and B-chain. After cleavage at two locations, insulin and C-peptide are the secreted products. Intact proinsulin with low bioactivity also is secreted in small amounts.

A layer of vascularized connective tissue underneath the EPIDERMIS. The surface of the dermis contains innervated papillae. Embedded in or beneath the dermis are SWEAT GLANDS; HAIR FOLLICLES; and SEBACEOUS GLANDS.

An alkylating agent having a selective immunosuppressive effect on BONE MARROW. It has been used in the palliative treatment of chronic myeloid leukemia (MYELOID LEUKEMIA, CHRONIC), but although symptomatic relief is provided, no permanent remission is brought about. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), busulfan is listed as a known carcinogen.

Organs, tissues, or cells taken from the body for grafting into another area of the same body or into another individual.

Progenitor cells from which all blood cells derive.

The procedure of removing TISSUES, organs, or specimens from DONORS for reuse, such as TRANSPLANTATION.

Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.

The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.

Glycoproteins found on immature hematopoietic cells and endothelial cells. They are the only molecules to date whose expression within the blood system is restricted to a small number of progenitor cells in the bone marrow.

A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.

A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)

Glucose in blood.

Serum containing GAMMA-GLOBULINS which are antibodies for lymphocyte ANTIGENS. It is used both as a test for HISTOCOMPATIBILITY and therapeutically in TRANSPLANTATION.

The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.

Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.

Antibodies produced by a single clone of cells.

Inflammation of the BRONCHIOLES leading to an obstructive lung disease. Bronchioles are characterized by fibrous granulation tissue with bronchial exudates in the lumens. Clinical features include a nonproductive cough and DYSPNEA.

An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.

An antibiotic substance derived from Penicillium stoloniferum, and related species. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase. Mycophenolic acid is important because of its selective effects on the immune system. It prevents the proliferation of T-cells, lymphocytes, and the formation of antibodies from B-cells. It also may inhibit recruitment of leukocytes to inflammatory sites. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1301)

The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc.

An antibiotic that is produced by Stretomyces achromogenes. It is used as an antineoplastic agent and to induce diabetes in experimental animals.

The period following a surgical operation.

A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.

Therapeutic act or process that initiates a response to a complete or partial remission level.

The transference of a complete HAND, as a composite of many tissue types, from one individual to another.

A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.

Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.

Antigens on surfaces of cells, including infectious or foreign cells or viruses. They are usually protein-containing groups on cell membranes or walls and may be isolated.

An antigenic mismatch between donor and recipient blood. Antibodies present in the recipient's serum may be directed against antigens in the donor product. Such a mismatch may result in a transfusion reaction in which, for example, donor blood is hemolyzed. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984).

Disease having a short and relatively severe course.

Infection with CYTOMEGALOVIRUS, characterized by enlarged cells bearing intranuclear inclusions. Infection may be in almost any organ, but the salivary glands are the most common site in children, as are the lungs in adults.

Agents that destroy bone marrow activity. They are used to prepare patients for BONE MARROW TRANSPLANTATION or STEM CELL TRANSPLANTATION.

Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.

Large, transmembrane, non-covalently linked glycoproteins (alpha and beta). Both chains can be polymorphic although there is more structural variation in the beta chains. The class II antigens in humans are called HLA-D ANTIGENS and are coded by a gene on chromosome 6. In mice, two genes named IA and IE on chromosome 17 code for the H-2 antigens. The antigens are found on B-lymphocytes, macrophages, epidermal cells, and sperm and are thought to mediate the competence of and cellular cooperation in the immune response. The term IA antigens used to refer only to the proteins encoded by the IA genes in the mouse, but is now used as a generic term for any class II histocompatibility antigen.

RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

Cells contained in the bone marrow including fat cells (see ADIPOCYTES); STROMAL CELLS; MEGAKARYOCYTES; and the immediate precursors of most blood cells.

Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.

A state of prolonged irreversible cessation of all brain activity, including lower brain stem function with the complete absence of voluntary movements, responses to stimuli, brain stem reflexes, and spontaneous respirations. Reversible conditions which mimic this clinical state (e.g., sedative overdose, hypothermia, etc.) are excluded prior to making the determination of brain death. (From Adams et al., Principles of Neurology, 6th ed, pp348-9)

Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.

Final stage of a liver disease when the liver failure is irreversible and LIVER TRANSPLANTATION is needed.

They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system.

Criteria and standards used for the determination of the appropriateness of the inclusion of patients with specific conditions in proposed treatment plans and the criteria used for the inclusion of subjects in various clinical trials and other research protocols.

Experimental transplantation of neoplasms in laboratory animals for research purposes.

The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.

A short thick vein formed by union of the superior mesenteric vein and the splenic vein.

Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.

Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.

General term for the abnormal appearance of histiocytes in the blood. Based on the pathological features of the cells involved rather than on clinical findings, the histiocytic diseases are subdivided into three groups: HISTIOCYTOSIS, LANGERHANS CELL; HISTIOCYTOSIS, NON-LANGERHANS-CELL; and HISTIOCYTIC DISORDERS, MALIGNANT.

Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort T-lymphocytes into subsets based on CD antigens by the technique of flow cytometry.

Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.

Mice homozygous for the mutant autosomal recessive gene "scid" which is located on the centromeric end of chromosome 16. These mice lack mature, functional lymphocytes and are thus highly susceptible to lethal opportunistic infections if not chronically treated with antibiotics. The lack of B- and T-cell immunity resembles severe combined immunodeficiency (SCID) syndrome in human infants. SCID mice are useful as animal models since they are receptive to implantation of a human immune system producing SCID-human (SCID-hu) hematochimeric mice.

The transfer of lymphocytes from a donor to a recipient or reinfusion to the donor.

The middle segment of proinsulin that is between the N-terminal B-chain and the C-terminal A-chain. It is a pancreatic peptide of about 31 residues, depending on the species. Upon proteolytic cleavage of proinsulin, equimolar INSULIN and C-peptide are released. C-peptide immunoassay has been used to assess pancreatic beta cell function in diabetic patients with circulating insulin antibodies or exogenous insulin. Half-life of C-peptide is 30 min, almost 8 times that of insulin.

An encapsulated lymphatic organ through which venous blood filters.

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.

Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.

An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.

A form of rapid-onset LIVER FAILURE, also known as fulminant hepatic failure, caused by severe liver injury or massive loss of HEPATOCYTES. It is characterized by sudden development of liver dysfunction and JAUNDICE. Acute liver failure may progress to exhibit cerebral dysfunction even HEPATIC COMA depending on the etiology that includes hepatic ISCHEMIA, drug toxicity, malignant infiltration, and viral hepatitis such as post-transfusion HEPATITIS B and HEPATITIS C.

The major human blood type system which depends on the presence or absence of two antigens A and B. Type O occurs when neither A nor B is present and AB when both are present. A and B are genetic factors that determine the presence of enzymes for the synthesis of certain glycoproteins mainly in the red cell membrane.

A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.

Ducts that collect PANCREATIC JUICE from the PANCREAS and supply it to the DUODENUM.

Methods for maintaining or growing CELLS in vitro.

The occurrence in an individual of two or more cell populations of different chromosomal constitutions, derived from different individuals. This contrasts with MOSAICISM in which the different cell populations are derived from a single individual.

Blood of the fetus. Exchange of nutrients and waste between the fetal and maternal blood occurs via the PLACENTA. The cord blood is blood contained in the umbilical vessels (UMBILICAL CORD) at the time of delivery.

A malignancy of mature PLASMA CELLS engaging in monoclonal immunoglobulin production. It is characterized by hyperglobulinemia, excess Bence-Jones proteins (free monoclonal IMMUNOGLOBULIN LIGHT CHAINS) in the urine, skeletal destruction, bone pain, and fractures. Other features include ANEMIA; HYPERCALCEMIA; and RENAL INSUFFICIENCY.

A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.

A form of ischemia-reperfusion injury occurring in the early period following transplantation. Significant pathophysiological changes in MITOCHONDRIA are the main cause of the dysfunction. It is most often seen in the transplanted lung, liver, or kidney and can lead to GRAFT REJECTION.

A fibrous protein complex that consists of proteins folded into a specific cross beta-pleated sheet structure. This fibrillar structure has been found as an alternative folding pattern for a variety of functional proteins. Deposits of amyloid in the form of AMYLOID PLAQUES are associated with a variety of degenerative diseases. The amyloid structure has also been found in a number of functional proteins that are unrelated to disease.

The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.

Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.

A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.

Irritants and reagents for labeling terminal amino acid groups.

General dysfunction of an organ occurring immediately following its transplantation. The term most frequently refers to renal dysfunction following KIDNEY TRANSPLANTATION.

An individual that contains cell populations derived from different zygotes.

Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell.

Immunological rejection of leukemia cells following bone marrow transplantation.

Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.

Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation.

The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.

Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.

The process by which antigen is presented to lymphocytes in a form they can recognize. This is performed by antigen presenting cells (APCs). Some antigens require processing before they can be recognized. Antigen processing consists of ingestion and partial digestion of the antigen by the APC, followed by presentation of fragments on the cell surface. (From Rosen et al., Dictionary of Immunology, 1989)

Antibodies from an individual that react with ISOANTIGENS of another individual of the same species.

The chilling of a tissue or organ during decreased BLOOD perfusion or in the absence of blood supply. Cold ischemia time during ORGAN TRANSPLANTATION begins when the organ is cooled with a cold perfusion solution after ORGAN PROCUREMENT surgery, and ends after the tissue reaches physiological temperature during implantation procedures.

The process by which a tissue or aggregate of cells is kept alive outside of the organism from which it was derived (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism).

Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.

The application of probability and statistical methods to calculate the risk of occurrence of any event, such as onset of illness, recurrent disease, hospitalization, disability, or death. It may include calculation of the anticipated money costs of such events and of the premiums necessary to provide for payment of such costs.

The release of stem cells from the bone marrow into the peripheral blood circulation for the purpose of leukapheresis, prior to stem cell transplantation. Hematopoietic growth factors or chemotherapeutic agents often are used to stimulate the mobilization.

Progressive destruction or the absence of all or part of the extrahepatic BILE DUCTS, resulting in the complete obstruction of BILE flow. Usually, biliary atresia is found in infants and accounts for one third of the neonatal cholestatic JAUNDICE.

A primary malignant neoplasm of the pancreatic ISLET CELLS. Usually it involves the non-INSULIN-producing cell types, the PANCREATIC ALPHA CELLS and the pancreatic delta cells (SOMATOSTATIN-SECRETING CELLS) in GLUCAGONOMA and SOMATOSTATINOMA, respectively.

A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.

Measure of histocompatibility at the HL-A locus. Peripheral blood lymphocytes from two individuals are mixed together in tissue culture for several days. Lymphocytes from incompatible individuals will stimulate each other to proliferate significantly (measured by tritiated thymidine uptake) whereas those from compatible individuals will not. In the one-way MLC test, the lymphocytes from one of the individuals are inactivated (usually by treatment with MITOMYCIN or radiation) thereby allowing only the untreated remaining population of cells to proliferate in response to foreign histocompatibility antigens.

The induction of prolonged survival and growth of allografts of either tumors or normal tissues which would ordinarily be rejected. It may be induced passively by introducing graft-specific antibodies from previously immunized donors, which bind to the graft's surface antigens, masking them from recognition by T-cells; or actively by prior immunization of the recipient with graft antigens which evoke specific antibodies and form antigen-antibody complexes which bind to the antigen receptor sites of the T-cells and block their cytotoxic activity.

Invasion of the host organism by microorganisms that can cause pathological conditions or diseases.

Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.

Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.

All of the processes involved in increasing CELL NUMBER including CELL DIVISION.

The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.

Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response.

A contact dermatitis due to allergic sensitization to various substances. These substances subsequently produce inflammatory reactions in the skin of those who have acquired hypersensitivity to them as a result of prior exposure.

A delayed hypersensitivity involving the reaction between sunlight or other radiant energy source and a chemical substance to which the individual has been previously exposed and sensitized. It manifests as a papulovesicular, eczematous, or exudative dermatitis occurring chiefly on the light-exposed areas of the skin.

Any of a group of malignant tumors of lymphoid tissue that differ from HODGKIN DISEASE, being more heterogeneous with respect to malignant cell lineage, clinical course, prognosis, and therapy. The only common feature among these tumors is the absence of giant REED-STERNBERG CELLS, a characteristic of Hodgkin's disease.

One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.

Tolerance to antigen-presenting cell-depleted islet allografts is CD4 T cell dependent. (1/1138)

Pretreatment of pancreatic islets in 95% oxygen culture depletes graft-associated APCs and leads to indefinite allograft acceptance in immunocompetent recipients. As such, the APC-depleted allograft represents a model of peripheral alloantigen presentation in the absence of donor-derived costimulation. Over time, a state of donor-specific tolerance develops in which recipients are resistant to donor APC-induced graft rejection. Thus, persistence of the graft is sufficient to induce tolerance independent of other immune interventions. Donor-specific tolerance could be adoptively transferred to immune-deficient SCID recipient mice transplanted with fresh immunogenic islet allografts, indicating that the original recipient was not simply "ignorant" of donor antigens. Interestingly, despite the fact that the original islet allograft presented only MHC class I alloantigens, CD8+ T cells obtained from tolerant animals readily collaborated with naive CD4+ T cells to reject donor-type islet grafts. Conversely, tolerant CD4+ T cells failed to collaborate effectively with naive CD8+ T cells for the rejection of donor-type grafts. In conclusion, the MHC class I+, II- islet allograft paradoxically leads to a change in the donor-reactive CD4 T cell subset and not in the CD8 subset. We hypothesize that the tolerant state is not due to direct class I alloantigen presentation to CD8 T cells but, rather, occurs via the indirect pathway of donor Ag presentation to CD4 T cells in the context of host MHC class II molecules. (+info)

Auto- and alloimmune reactivity to human islet allografts transplanted into type 1 diabetic patients. (2/1138)

Allogeneic islet transplantation can restore an insulin-independent state in C-peptide-negative type 1 diabetic patients. We recently reported three cases of surviving islet allografts that were implanted in type 1 diabetic patients under maintenance immune suppression for a previous kidney graft. The present study compares islet graft-specific cellular auto- and alloreactivity in peripheral blood from those three recipients and from four patients with failing islet allografts measured over a period of 6 months after portal islet implantation. The three cases that remained C-peptide-positive for >1 year exhibited no signs of alloreactivity, and their autoreactivity to islet autoantigens was only marginally increased. In contrast, rapid failure (<3 weeks) in three other cases was accompanied by increases in precursor frequencies of graft-specific alloreactive T-cells; in one of them, the alloreactivity was preceded by a sharply increased autoreactivity to several islet autoantigens. One recipient had a delayed loss of islet graft function (33 weeks); he did not exhibit signs of graft-specific alloimmunity, but developed a delayed increase in autoreactivity. The parallel between metabolic outcome of human beta-cell allografts and cellular auto- and alloreactivity in peripheral blood suggests a causal relationship. The present study therefore demonstrates that T-cell reactivities in peripheral blood can be used to monitor immune mechanisms, which influence survival of beta-cell allografts in diabetic patients. (+info)

Islet transplantation restores normal levels of insulin receptor and substrate tyrosine phosphorylation and phosphatidylinositol 3-kinase activity in skeletal muscle and myocardium of streptozocin-induced diabetic rats. (3/1138)

Insulin-dependent diabetes in rats is characterized by abnormalities of post-binding insulin signaling reactions that are not fully corrected by exogenous insulin therapy. The aim of this study was to investigate the effects of islet transplantation on insulin signaling in skeletal muscle and myocardium of streptozocin (STZ)-induced diabetic rats. Control rats, untreated diabetic rats, and diabetic rats transplanted with syngeneic islets under the kidney capsule were studied. Compared with controls, diabetic rats were characterized by multiple insulin signaling abnormalities in skeletal muscle, which included 1) increased insulin-stimulated tyrosine phosphorylation of the insulin receptor beta-subunit and insulin receptor substrates IRS-1 and IRS-2, 2) increased substrate tyrosine phosphorylation in the basal state, 3) a decreased amount of IRS-1 protein, 4) markedly elevated basal and insulin-stimulated phosphatidylinositol (PI) 3-kinase activity in anti-IRS-1 immunoprecipitates from total tissue extracts, and 5) increased PI 3-kinase activity in low-density microsomes. A similar augmentation of insulin receptor and substrate tyrosine phosphorylation in response to STZ-diabetes was also found in myocardium, although with lower magnitude than that found in skeletal muscle. In addition, STZ-diabetes resulted in decreased IRS-1 and increased IRS-2 protein levels in myocardium. Islet transplantation fully corrected the diabetes-induced changes in protein tyrosine phosphorylation and PI 3-kinase activity and normalized IRS-1 and IRS-2 protein content in both skeletal muscle and myocardium. Thus, insulin delivered into the systemic circulation by pancreatic islets transplanted under the kidney capsule can adequately correct altered insulin signaling mechanisms in insulinopenic diabetes. (+info)

In autoimmune diabetes the transition from benign to pernicious insulitis requires an islet cell response to tumor necrosis factor alpha. (4/1138)

The islet-infiltrating and disease-causing leukocytes that are a hallmark of insulin-dependent diabetes mellitus produce and respond to a set of cytokine molecules. Of these, interleukin 1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma are perhaps the most important. However, as pleiotropic molecules, they can impact the path leading to beta cell apoptosis and diabetes at multiple points. To understand how these cytokines influence both the formative and effector phases of insulitis, it is critical to determine their effects on the assorted cell types comprising the lesion: the effector T cells, antigen-presenting cells, vascular endothelium, and target islet tissue. Here, we report using nonobese diabetic chimeric mice harboring islets deficient in specific cytokine receptors or cytokine-induced effector molecules to assess how these compartmentalized loss-of-function mutations alter the events leading to diabetes. We found that islets deficient in Fas, IFN-gamma receptor, or inducible nitric oxide synthase had normal diabetes development; however, the specific lack of TNF- alpha receptor 1 (p55) afforded islets a profound protection from disease by altering the ability of islet-reactive, CD4(+) T cells to establish insulitis and subsequently destroy islet beta cells. These results argue that islet cells play a TNF-alpha-dependent role in their own demise. (+info)

CTLA4 signals are required to optimally induce allograft tolerance with combined donor-specific transfusion and anti-CD154 monoclonal antibody treatment. (5/1138)

Sensitization to donor Ags is an enormous problem in clinical transplantation. In an islet allograft model, presensitization of recipients through donor-specific transfusion (DST) 4 wk before transplantation results in accelerated rejection. We demonstrate that combined DST with anti-CD154 (CD40L) therapy not only prevents the deleterious presensitization produced by pretransplant DST in the islet allograft model, it also induces broad alloantigen-specific tolerance and permits subsequent engraftment of donor islet or cardiac grafts without further treatment. In addition, our data strongly indicate that CTLA4-negative T cell signals are required to achieve prolonged engraftment of skin allograft or tolerance to islet allograft in recipients treated with a combination of pretransplant DST and anti-CD154 mAb. We provide direct evidence that a CD28-independent CTLA4 signal delivers a strong negative signal to CD4+ T cells that can block alloimmune MLR responses. In this study immune deviation into a Th2 (IL-4) response was associated with, but did not insure, graft tolerance, as the inopportune timing of B7 blockade with CTLA4/Ig therapy prevented uniform tolerance but did not prevent Th2-type immune deviation. While CTLA4-negative signals are necessary for tolerance induction, Th1 to Th2 immune deviation cannot be sufficient for tolerance induction. Combined pretransplant DST with anti-CD154 mAb treatment may be attractive for clinical deployment, and strategies aimed to selectively block CD28 without interrupting CTLA4/B7 interaction might prove highly effective in the induction of tolerance. (+info)

Control of autoimmune diabetes in NOD mice by GAD expression or suppression in beta cells. (6/1138)

Glutamic acid decarboxylase (GAD) is a pancreatic beta cell autoantigen in humans and nonobese diabetic (NOD) mice. beta Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the beta cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of beta cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, beta cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes. (+info)

Prior streptozotocin treatment does not inhibit pancreas regeneration after 90% pancreatectomy in rats. (7/1138)

The effects of residual beta-cell mass and glycemia on regeneration of endocrine pancreas after 90% pancreatectomy were investigated. Streptozotocin or buffer alone was injected into 4-wk-old male Lewis rats (day 0). On day 7, varying numbers of syngeneic islets were transplanted under the kidney capsule to achieve varying degrees of glucose normalization. On day 14, a 90% pancreatectomy or sham pancreatectomy was performed. On day 19, rats were killed and the pancreas was fixed for quantitative morphometric determination of beta-cell mass. Focal areas of regenerating pancreas were observed in all animals that underwent partial pancreatectomy. The percentage of remnant pancreas classified as foci was unaffected by streptozotocin treatment or by plasma glucose. Moderate to severe hyperglycemia did not promote regeneration of the pancreatic beta-cell mass; rather the total endocrine cell mass was inversely related to the plasma glucose level (r = -0.5, P < 0.01). These data suggest that the precursor population for both endocrine and exocrine tissue is not susceptible to damage by streptozotocin and that local effects of residual beta-cell mass are not important to regeneration after a 90% pancreatectomy. (+info)

NOD mice have a generalized defect in their response to transplantation tolerance induction. (8/1138)

A protocol consisting of a single donor-specific transfusion (DST) plus a brief course of anti-CD154 monoclonal antibody (anti-CD40 ligand mAb) induces permanent islet allograft survival in chemically diabetic mice, but its efficacy in mice with autoimmune diabetes is unknown. Confirming a previous report, we first observed that treatment of young female NOD mice with anti-CD154 mAb reduced the frequency of diabetes through 1 year of age to 43%, compared with 73% in untreated controls. We also confirmed that spontaneously diabetic NOD mice transplanted with syngeneic (NOD-Prkdc(scid)/Prkdc(scid)) or allogeneic (BALB/c) islets rapidly reject their grafts. Graft survival was not prolonged, however, by pretreatment with either anti-CD154 mAb alone or anti-CD154 mAb plus DST. In addition, allograft rejection in NOD mice was not restricted to islet grafts. Anti-CD154 mAb plus DST treatment failed to prolong skin allograft survival in nondiabetic male NOD mice. The inability to induce transplantation tolerance in NOD (H2g7) mice was associated with non-major histocompatibility complex (MHC) genes. Treatment with DST and anti-CD154 mAb prolonged skin allograft survival in both C57BL/6 (H2b) and C57BL/6.NOD-H2g7 mice, but it was ineffective in NOD, NOD.SWR-H2q, and NOR (H2g7) mice. Mitogen-stimulated interleukin-1beta production by antigen-presenting cells was greater in strains susceptible to tolerance induction than in the strains resistant to tolerance induction. The results suggest the existence of a general defect in tolerance mechanisms in NOD mice. This genetic defect involves defective antigen-presenting cell maturation, leads to spontaneous autoimmune diabetes in the presence of the H2g7 MHC, and precludes the induction of transplantation tolerance irrespective of MHC haplotype. Promising islet transplantation methods based on overcoming the alloimmune response by interference with costimulation may require modification or amplification for use in the setting of autoimmune diabetes. (+info)

The exact cause of LCH is not known, but it is believed to be related to genetic mutations and environmental factors. The disorder can affect people of all ages, but it most commonly occurs in children under the age of 10.

Symptoms of LCH can vary depending on the location of the affected tissue and can include:

* Skin rashes or lesions
* Bone pain
* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss

LCH can affect many different parts of the body, including the skin, bones, liver, spleen, and lungs. In some cases, the disorder can spread to the brain and spinal cord, which can be serious and potentially life-threatening.

Diagnosis of LCH typically involves a combination of physical examination, medical history, and diagnostic tests such as imaging studies (e.g., X-rays, CT scans) and biopsies. Treatment options for LCH depend on the severity and location of the disorder and can include:

* Observation and monitoring
* Medications to suppress the immune system (e.g., corticosteroids)
* Surgery to remove affected tissue
* Radiation therapy
* Chemotherapy

The prognosis for LCH varies depending on the severity of the disorder and the location of the affected tissue. With appropriate treatment, many people with LCH can experience long-term remission and a good quality of life. However, in some cases, the disorder can be severe and potentially life-threatening, especially if it affects the brain and spinal cord.

The diagnosis of GVHD is based on a combination of clinical findings, laboratory tests, and biopsies. Treatment options include immunosuppressive drugs, corticosteroids, and in severe cases, stem cell transplantation reversal or donor lymphocyte infusion.

Prevention of GVHD includes selecting the right donor, using conditioning regimens that minimize damage to the recipient's bone marrow, and providing appropriate immunosuppression after transplantation. Early detection and management of GVHD are critical to prevent long-term complications and improve survival rates.

The symptoms of Langerhans cell sarcoma can vary depending on the location and size of the tumor, but may include:

* A firm, painless lump or nodule on the skin
* Redness, swelling, or inflammation around the affected area
* Itching or tenderness in the affected area
* Bleeding or crusting of the affected area

If you suspect that you or someone you know may have Langerhans cell sarcoma, it is important to seek medical attention as soon as possible. A doctor will typically perform a physical examination and may also use diagnostic tests such as imaging studies (e.g., X-rays, CT scans) or biopsies to confirm the diagnosis.

Treatment for Langerhans cell sarcoma usually involves a combination of surgery, radiation therapy, and chemotherapy. The specific treatment plan will depend on the size, location, and stage of the cancer, as well as the patient's overall health and medical history. In some cases, clinical trials may also be an option.

Overall, Langerhans cell sarcoma is a rare and aggressive form of skin cancer that requires prompt medical attention for effective treatment and optimal outcomes.

There are several causes of liver failure, including:

1. Alcohol-related liver disease: Prolonged and excessive alcohol consumption can damage liver cells, leading to inflammation, scarring, and eventually liver failure.
2. Viral hepatitis: Hepatitis A, B, and C are viral infections that can cause inflammation and damage to the liver, leading to liver failure.
3. Non-alcoholic fatty liver disease (NAFLD): A condition where there is an accumulation of fat in the liver, leading to inflammation and scarring.
4. Drug-induced liver injury: Certain medications can cause liver damage and failure, especially when taken in high doses or for extended periods.
5. Genetic disorders: Certain inherited conditions, such as hemochromatosis and Wilson's disease, can cause liver damage and failure.
6. Acute liver failure: This is a sudden and severe loss of liver function, often caused by medication overdose or other toxins.
7. Chronic liver failure: A gradual decline in liver function over time, often caused by cirrhosis or NAFLD.

Symptoms of liver failure can include:

1. Jaundice (yellowing of the skin and eyes)
2. Fatigue
3. Loss of appetite
4. Nausea and vomiting
5. Abdominal pain
6. Confusion and altered mental state
7. Easy bruising and bleeding

Diagnosis of liver failure is typically made through a combination of physical examination, medical history, and laboratory tests, such as blood tests to check for liver enzymes and bilirubin levels. Imaging tests, such as ultrasound and CT scans, may also be used to evaluate the liver.

Treatment of liver failure depends on the underlying cause and severity of the condition. In some cases, a liver transplant may be necessary. Other treatments may include medications to manage symptoms, such as nausea and pain, and supportive care to maintain nutrition and hydration. In severe cases, hospitalization may be required to monitor and treat complications.

Prevention of liver failure is important, and this can be achieved by:

1. Avoiding alcohol or drinking in moderation
2. Maintaining a healthy weight and diet
3. Managing underlying medical conditions, such as diabetes and high blood pressure
4. Avoiding exposure to toxins, such as certain medications and environmental chemicals
5. Getting vaccinated against hepatitis A and B
6. Practicing safe sex to prevent the spread of hepatitis B and C.

Symptoms of type 1 diabetes can include increased thirst and urination, blurred vision, fatigue, weight loss, and skin infections. If left untreated, type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, and blindness.

Type 1 diabetes is diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood glucose measurements and autoantibody tests. Treatment typically involves insulin therapy, which can be administered via injections or an insulin pump, as well as regular monitoring of blood glucose levels and appropriate lifestyle modifications such as a healthy diet and regular exercise.

1. Infection: Bacterial or viral infections can develop after surgery, potentially leading to sepsis or organ failure.
2. Adhesions: Scar tissue can form during the healing process, which can cause bowel obstruction, chronic pain, or other complications.
3. Wound complications: Incisional hernias, wound dehiscence (separation of the wound edges), and wound infections can occur.
4. Respiratory problems: Pneumonia, respiratory failure, and atelectasis (collapsed lung) can develop after surgery, particularly in older adults or those with pre-existing respiratory conditions.
5. Cardiovascular complications: Myocardial infarction (heart attack), cardiac arrhythmias, and cardiac failure can occur after surgery, especially in high-risk patients.
6. Renal (kidney) problems: Acute kidney injury or chronic kidney disease can develop postoperatively, particularly in patients with pre-existing renal impairment.
7. Neurological complications: Stroke, seizures, and neuropraxia (nerve damage) can occur after surgery, especially in patients with pre-existing neurological conditions.
8. Pulmonary embolism: Blood clots can form in the legs or lungs after surgery, potentially causing pulmonary embolism.
9. Anesthesia-related complications: Respiratory and cardiac complications can occur during anesthesia, including respiratory and cardiac arrest.
10. delayed healing: Wound healing may be delayed or impaired after surgery, particularly in patients with pre-existing medical conditions.

It is important for patients to be aware of these potential complications and to discuss any concerns with their surgeon and healthcare team before undergoing surgery.

Dermatitis, contact can be acute or chronic, depending on the severity and duration of the exposure. In acute cases, the symptoms may resolve within a few days after removing the offending substance. Chronic dermatitis, on the other hand, can persist for weeks or even months, and may require ongoing treatment to manage the symptoms.

The symptoms of contact dermatitis can vary depending on the individual and the severity of the exposure. Common symptoms include:

* Redness and inflammation of the skin
* Itching and burning sensations
* Swelling and blistering
* Cracks or fissures in the skin
* Difficulty healing or recurring infections

In severe cases, contact dermatitis can lead to complications such as:

* Infection with bacteria or fungi
* Scarring and disfigurement
* Emotional distress and anxiety

Diagnosis of contact dermatitis is typically made based on the patient's medical history and physical examination. Allergic patch testing may also be performed to identify specific allergens that are causing the condition.

Treatment for contact dermatitis usually involves avoiding the offending substance and using topical or oral medications to manage symptoms. In severe cases, systemic corticosteroids or immunosuppressants may be prescribed. Phototherapy and alternative therapies such as herbal remedies or acupuncture may also be considered.

Prevention of contact dermatitis involves identifying and avoiding substances that cause an allergic reaction or skin irritation. Individuals with a history of contact dermatitis should take precautions when handling new substances, and should be aware of the potential for cross-reactivity between different allergens.

Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.

In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.

Types of Experimental Diabetes Mellitus include:

1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.

Experimental Diabetes Mellitus has several applications in research, including:

1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.

In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.

Hematologic neoplasms refer to abnormal growths or tumors that affect the blood, bone marrow, or lymphatic system. These types of cancer can originate from various cell types, including red blood cells, white blood cells, platelets, and lymphoid cells.

There are several subtypes of hematologic neoplasms, including:

1. Leukemias: Cancers of the blood-forming cells in the bone marrow, which can lead to an overproduction of immature or abnormal white blood cells, red blood cells, or platelets. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
2. Lymphomas: Cancers of the immune system, which can affect the lymph nodes, spleen, liver, or other organs. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
3. Multiple myeloma: A cancer of the plasma cells in the bone marrow that can lead to an overproduction of abnormal plasma cells.
4. Myeloproliferative neoplasms: Cancers that affect the blood-forming cells in the bone marrow, leading to an overproduction of red blood cells, white blood cells, or platelets. Examples include polycythemia vera and essential thrombocythemia.
5. Myelodysplastic syndromes: Cancers that affect the blood-forming cells in the bone marrow, leading to an underproduction of normal blood cells.

The diagnosis of hematologic neoplasms typically involves a combination of physical examination, medical history, laboratory tests (such as complete blood counts and bone marrow biopsies), and imaging studies (such as CT scans or PET scans). Treatment options for hematologic neoplasms depend on the specific type of cancer, the severity of the disease, and the overall health of the patient. These may include chemotherapy, radiation therapy, stem cell transplantation, or targeted therapy with drugs that specifically target cancer cells.

In medicine, cadavers are used for a variety of purposes, such as:

1. Anatomy education: Medical students and residents learn about the human body by studying and dissecting cadavers. This helps them develop a deeper understanding of human anatomy and improves their surgical skills.
2. Research: Cadavers are used in scientific research to study the effects of diseases, injuries, and treatments on the human body. This helps scientists develop new medical techniques and therapies.
3. Forensic analysis: Cadavers can be used to aid in the investigation of crimes and accidents. By examining the body and its injuries, forensic experts can determine cause of death, identify suspects, and reconstruct events.
4. Organ donation: After death, cadavers can be used to harvest organs and tissues for transplantation into living patients. This can improve the quality of life for those with organ failure or other medical conditions.
5. Medical training simulations: Cadavers can be used to simulate real-life medical scenarios, allowing healthcare professionals to practice their skills in a controlled environment.

In summary, the term "cadaver" refers to the body of a deceased person and is used in the medical field for various purposes, including anatomy education, research, forensic analysis, organ donation, and medical training simulations.

Insulinoma is a rare type of pancreatic tumor that produces excess insulin, leading to low blood sugar levels. These tumors are typically benign and can be treated with surgery or medication.

Insulinomas account for only about 5% of all pancreatic neuroendocrine tumors. They usually occur in the head of the pancreas and can cause a variety of symptoms, including:

1. Hypoglycemia (low blood sugar): The excess insulin produced by the tumor can cause blood sugar levels to drop too low, leading to symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Hyperinsulinism (elevated insulin levels): In addition to hypoglycemia, insulinomas can also cause elevated insulin levels in the blood.
3. Abdominal pain: Insulinomas can cause abdominal pain and discomfort.
4. Weight loss: Patients with insulinomas may experience unexplained weight loss.
5. Nausea and vomiting: Some patients may experience nausea and vomiting due to the hypoglycemia or other symptoms caused by the tumor.

Insulinomas are usually diagnosed through a combination of imaging tests such as CT scans, MRI scans, and PET scans, and by measuring insulin and C-peptide levels in the blood. Treatment options for insulinomas include surgery to remove the tumor, medications to control hypoglycemia and hyperinsulinism, and somatostatin analogs to reduce hormone secretion.

Insulinoma is a rare and complex condition that requires careful management by a multidisciplinary team of healthcare professionals, including endocrinologists, surgeons, and radiologists. With appropriate treatment, most patients with insulinomas can experience long-term remission and improved quality of life.

The symptoms of eosinophilic granuloma can vary depending on the location of the affected tissue. Common symptoms include skin lesions, fatigue, fever, and joint pain. In severe cases, the disorder can affect the lungs, liver, or gastrointestinal tract, leading to respiratory failure, liver damage, or gastrointestinal bleeding.

The diagnosis of eosinophilic granuloma is based on a combination of clinical findings, laboratory tests, and biopsy results. Laboratory tests may include blood counts, imaging studies, and other tests to rule out other potential causes of the symptoms. Biopsy samples of the affected tissue can be examined under a microscope to confirm the presence of eosinophils and other characteristics of the disorder.

Treatment for eosinophilic granuloma usually involves medications to reduce inflammation and suppress the immune system. Corticosteroids, such as prednisone, are often used to treat the disorder, along with other medications such as hydroxychloroquine or azathioprine. In severe cases, hospitalization may be necessary to manage complications such as respiratory failure or gastrointestinal bleeding.

While there is no cure for eosinophilic granuloma, the disorder can often be managed with medication and other treatments. With appropriate treatment, many people with eosinophilic granuloma can experience significant improvement in their symptoms and quality of life. However, in some cases, the disorder may persist or recur, requiring ongoing management and monitoring.

There are many different types of liver diseases, including:

1. Alcoholic liver disease (ALD): A condition caused by excessive alcohol consumption that can lead to inflammation, scarring, and cirrhosis.
2. Viral hepatitis: Hepatitis A, B, and C are viral infections that can cause inflammation and damage to the liver.
3. Non-alcoholic fatty liver disease (NAFLD): A condition where there is an accumulation of fat in the liver, which can lead to inflammation and scarring.
4. Cirrhosis: A condition where the liver becomes scarred and cannot function properly.
5. Hemochromatosis: A genetic disorder that causes the body to absorb too much iron, which can damage the liver and other organs.
6. Wilson's disease: A rare genetic disorder that causes copper to accumulate in the liver and brain, leading to damage and scarring.
7. Liver cancer (hepatocellular carcinoma): Cancer that develops in the liver, often as a result of cirrhosis or viral hepatitis.

Symptoms of liver disease can include fatigue, loss of appetite, nausea, abdominal pain, dark urine, pale stools, and swelling in the legs. Treatment options for liver disease depend on the underlying cause and may include lifestyle changes, medication, or surgery. In severe cases, a liver transplant may be necessary.

Prevention of liver disease includes maintaining a healthy diet and lifestyle, avoiding excessive alcohol consumption, getting vaccinated against hepatitis A and B, and managing underlying medical conditions such as obesity and diabetes. Early detection and treatment of liver disease can help to prevent long-term damage and improve outcomes for patients.

A condition in which the kidneys gradually lose their function over time, leading to the accumulation of waste products in the body. Also known as chronic kidney disease (CKD).

Prevalence:

Chronic kidney failure affects approximately 20 million people worldwide and is a major public health concern. In the United States, it is estimated that 1 in 5 adults has CKD, with African Americans being disproportionately affected.

Causes:

The causes of chronic kidney failure are numerous and include:

1. Diabetes: High blood sugar levels can damage the kidneys over time.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the blood vessels in the kidneys.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood.
4. Interstitial nephritis: Inflammation of the tissue between the kidney tubules.
5. Pyelonephritis: Infection of the kidneys, usually caused by bacteria or viruses.
6. Polycystic kidney disease: A genetic disorder that causes cysts to grow on the kidneys.
7. Obesity: Excess weight can increase blood pressure and strain on the kidneys.
8. Family history: A family history of kidney disease increases the risk of developing chronic kidney failure.

Symptoms:

Early stages of chronic kidney failure may not cause any symptoms, but as the disease progresses, symptoms can include:

1. Fatigue: Feeling tired or weak.
2. Swelling: In the legs, ankles, and feet.
3. Nausea and vomiting: Due to the buildup of waste products in the body.
4. Poor appetite: Loss of interest in food.
5. Difficulty concentrating: Cognitive impairment due to the buildup of waste products in the brain.
6. Shortness of breath: Due to fluid buildup in the lungs.
7. Pain: In the back, flank, or abdomen.
8. Urination changes: Decreased urine production, dark-colored urine, or blood in the urine.
9. Heart problems: Chronic kidney failure can increase the risk of heart disease and heart attack.

Diagnosis:

Chronic kidney failure is typically diagnosed based on a combination of physical examination findings, medical history, laboratory tests, and imaging studies. Laboratory tests may include:

1. Blood urea nitrogen (BUN) and creatinine: Waste products in the blood that increase with decreased kidney function.
2. Electrolyte levels: Imbalances in electrolytes such as sodium, potassium, and phosphorus can indicate kidney dysfunction.
3. Kidney function tests: Measurement of glomerular filtration rate (GFR) to determine the level of kidney function.
4. Urinalysis: Examination of urine for protein, blood, or white blood cells.

Imaging studies may include:

1. Ultrasound: To assess the size and shape of the kidneys, detect any blockages, and identify any other abnormalities.
2. Computed tomography (CT) scan: To provide detailed images of the kidneys and detect any obstructions or abscesses.
3. Magnetic resonance imaging (MRI): To evaluate the kidneys and detect any damage or scarring.

Treatment:

Treatment for chronic kidney failure depends on the underlying cause and the severity of the disease. The goals of treatment are to slow progression of the disease, manage symptoms, and improve quality of life. Treatment may include:

1. Medications: To control high blood pressure, lower cholesterol levels, reduce proteinuria, and manage anemia.
2. Diet: A healthy diet that limits protein intake, controls salt and water intake, and emphasizes low-fat dairy products, fruits, and vegetables.
3. Fluid management: Monitoring and control of fluid intake to prevent fluid buildup in the body.
4. Dialysis: A machine that filters waste products from the blood when the kidneys are no longer able to do so.
5. Transplantation: A kidney transplant may be considered for some patients with advanced chronic kidney failure.

Complications:

Chronic kidney failure can lead to several complications, including:

1. Heart disease: High blood pressure and anemia can increase the risk of heart disease.
2. Anemia: A decrease in red blood cells can cause fatigue, weakness, and shortness of breath.
3. Bone disease: A disorder that can lead to bone pain, weakness, and an increased risk of fractures.
4. Electrolyte imbalance: Imbalances of electrolytes such as potassium, phosphorus, and sodium can cause muscle weakness, heart arrhythmias, and other complications.
5. Infections: A decrease in immune function can increase the risk of infections.
6. Nutritional deficiencies: Poor appetite, nausea, and vomiting can lead to malnutrition and nutrient deficiencies.
7. Cardiovascular disease: High blood pressure, anemia, and other complications can increase the risk of cardiovascular disease.
8. Pain: Chronic kidney failure can cause pain, particularly in the back, flank, and abdomen.
9. Sleep disorders: Insomnia, sleep apnea, and restless leg syndrome are common complications.
10. Depression and anxiety: The emotional burden of chronic kidney failure can lead to depression and anxiety.

There are several different types of leukemia, including:

1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.

Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.

The exact cause of Bronchiolitis Obliterans is not fully understood, but it is believed to be due to a combination of genetic and environmental factors. The condition is often associated with allergies and asthma, and viral infections such as respiratory syncytial virus (RSV) can trigger the onset of symptoms.

Symptoms of Bronchiolitis Obliterans include:

* Persistent coughing, which may be worse at night
* Shortness of breath or wheezing
* Chest tightness or discomfort
* Fatigue and poor appetite
* Recurrent respiratory infections

BO is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or pulmonary function tests. There is no cure for Bronchiolitis Obliterans, but treatment options are available to manage symptoms and slow the progression of the disease. These may include:

* Medications such as bronchodilators and corticosteroids to reduce inflammation and improve lung function
* Pulmonary rehabilitation programs to improve breathing and overall health
* Oxygen therapy to help increase oxygen levels in the blood
* In severe cases, lung transplantation may be considered.

While Bronchiolitis Obliterans can significantly impact quality of life, with proper management and care, many individuals with the condition are able to lead active and productive lives.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Symptoms of aplastic anemia may include fatigue, weakness, shortness of breath, pale skin, and increased risk of bleeding or infection. Treatment options for aplastic anemia typically involve blood transfusions and immunosuppressive drugs to stimulate the bone marrow to produce new blood cells. In severe cases, a bone marrow transplant may be necessary.

Overall, aplastic anemia is a rare and serious condition that requires careful management by a healthcare provider to prevent complications and improve quality of life.

Blood group incompatibility can occur in various ways, including:

1. ABO incompatibility: This is the most common type of blood group incompatibility and occurs when the patient's blood type (A or B) is different from the donor's blood type.
2. Rh incompatibility: This occurs when the patient's Rh factor is different from the donor's Rh factor.
3. Other antigens: In addition to ABO and Rh, there are other antigens on red blood cells that can cause incompatibility, such as Kell, Duffy, and Xg.

Blood group incompatibility can be diagnosed through blood typing and cross-matching tests. These tests determine the patient's and donor's blood types and identify any incompatible antigens that may cause an immune response.

Treatment of blood group incompatibility usually involves finding a compatible donor or using specialized medications to reduce the risk of a negative reaction. In some cases, plasmapheresis, also known as plasma exchange, may be used to remove the incompatible antibodies from the patient's blood.

Prevention of blood group incompatibility is important, and this can be achieved by ensuring that patients receive only compatible blood products during transfusions. Blood banks maintain a database of donor blood types and perform thorough testing before releasing blood for transfusion to ensure compatibility. Additionally, healthcare providers should carefully review the patient's medical history and current medications to identify any potential allergies or sensitivities that may affect blood compatibility.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

CMV infections are more common in people with weakened immune systems, such as those with HIV/AIDS, cancer, or taking immunosuppressive drugs after an organ transplant. In these individuals, CMV can cause severe and life-threatening complications, such as pneumonia, retinitis (inflammation of the retina), and gastrointestinal disease.

In healthy individuals, CMV infections are usually mild and may not cause any symptoms at all. However, in some cases, CMV can cause a mononucleosis-like illness with fever, fatigue, and swollen lymph nodes.

CMV infections are diagnosed through a combination of physical examination, blood tests, and imaging studies such as CT scans or MRI. Treatment is generally not necessary for mild cases, but may include antiviral medications for more severe infections. Prevention strategies include avoiding close contact with individuals who have CMV, practicing good hygiene, and considering immunoprophylaxis (prevention of infection through the use of immune globulin) for high-risk individuals.

Overall, while CMV infections can be serious and life-threatening, they are relatively rare in healthy individuals and can often be treated effectively with supportive care and antiviral medications.

The committee defined "brain death" as follows:

* The absence of any clinical or electrophysiological signs of consciousness, including the lack of response to pain, light, sound, or other stimuli.
* The absence of brainstem reflexes, such as pupillary reactivity, oculocephalic reflex, and gag reflex.
* The failure of all brain waves, including alpha, beta, theta, delta, and epsilon waves, as detected by electroencephalography (EEG).
* The absence of any other clinical or laboratory signs of life, such as heartbeat, breathing, or blood circulation.

The definition of brain death is important because it provides a clear and consistent criteria for determining death in medical settings. It helps to ensure that patients who are clinically dead are not inappropriately kept on life support, and that organ donation can be performed in a timely and ethical manner.

ESLD is a critical stage of liver disease where the liver has failed to regenerate and recover from injury or damage, leading to severe impairment of liver function. This condition can arise due to various causes such as viral hepatitis, alcohol-related liver disease, non-alcoholic fatty liver disease (NAFLD), and other forms of liver cirrhosis.

The diagnosis of ESLD is based on a combination of clinical findings, laboratory tests, and imaging studies such as ultrasound, computed tomography (CT) or magnetic resonance imaging (MRI). Treatment options for ESLD are limited and may include liver transplantation, palliative care, and supportive therapies to manage complications.

The prognosis for patients with ESLD is generally poor, with a high mortality rate due to the advanced stage of the disease and the lack of effective treatment options. However, with advances in medical technology and the availability of liver transplantation, some patients with ESLD may have a chance of survival and improved quality of life.

There are several different types of histiocytosis, each with distinct clinical features and underlying genetic defects. The most common form of histiocytosis is called histiocytosis X, also known as Langerhans cell histiocytosis, which affects the skin, bone, and lymph nodes. Other forms of histiocytosis can affect the spleen, liver, and other organs.

The symptoms of histiocytosis vary depending on the specific type and severity of the disorder. Common symptoms include fever, fatigue, weight loss, and pain in the affected area. In severe cases, histiocytosis can lead to life-threatening complications such as infections, organ failure, and cancer.

The diagnosis of histiocytosis is based on a combination of clinical findings, laboratory tests, and imaging studies. Treatment options for histiocytosis include surgery, chemotherapy, and immunosuppressive therapy, depending on the severity and location of the disease.

In summary, histiocytosis is a group of rare genetic disorders characterized by an overproduction and accumulation of histiocytes, which can lead to a wide range of symptoms and complications. Early diagnosis and appropriate treatment are crucial for improving outcomes in patients with histiocytosis.

Causes:

1. Viral hepatitis (hepatitis A, B, or C)
2. Overdose of medications or supplements
3. Toxic substances (e.g., alcohol, drugs, or chemicals)
4. Sepsis or other infections that spread to the liver
5. Certain autoimmune disorders (e.g., hemochromatosis, Wilson's disease)
6. Cancer that has metastasized to the liver
7. Blood vessel blockage or clotting in the liver
8. Lack of blood flow to the liver

Symptoms:

1. Jaundice (yellowing of skin and eyes)
2. Nausea and vomiting
3. Abdominal swelling and discomfort
4. Fatigue, weakness, and loss of appetite
5. Confusion or altered mental state
6. Seizures or coma
7. Pale or clay-colored stools
8. Dark urine

Diagnosis:

1. Physical examination and medical history
2. Laboratory tests (e.g., liver function tests, blood tests, imaging studies)
3. Biopsy of the liver tissue (to rule out other liver diseases)

Treatment:

1. Supportive care (fluids, nutrition, and medication to manage symptoms)
2. Addressing underlying causes (e.g., stopping alcohol or drug use, treating infections)
3. Transjugular intrahepatic portosystemic shunt (TIPS), a procedure that creates a new pathway for blood to flow through the liver
4. Liver transplantation (in severe cases where other treatments have failed)

Prognosis:
The prognosis for acute liver failure depends on the underlying cause of the condition and the severity of the liver damage. In general, the earlier the diagnosis and treatment, the better the outcome. However, acute liver failure can be a life-threatening condition, and the mortality rate is high, especially in cases where there is severe liver damage or no available donor liver for transplantation.

Multiple myeloma is the second most common type of hematologic cancer after non-Hodgkin's lymphoma, accounting for approximately 1% of all cancer deaths worldwide. It is more common in older adults, with most patients being diagnosed over the age of 65.

The exact cause of multiple myeloma is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. There are several risk factors that have been associated with an increased risk of developing multiple myeloma, including:

1. Family history: Having a family history of multiple myeloma or other plasma cell disorders increases the risk of developing the disease.
2. Age: The risk of developing multiple myeloma increases with age, with most patients being diagnosed over the age of 65.
3. Race: African Americans are at higher risk of developing multiple myeloma than other races.
4. Obesity: Being overweight or obese may increase the risk of developing multiple myeloma.
5. Exposure to certain chemicals: Exposure to certain chemicals such as pesticides, solvents, and heavy metals has been linked to an increased risk of developing multiple myeloma.

The symptoms of multiple myeloma can vary depending on the severity of the disease and the organs affected. Common symptoms include:

1. Bone pain: Pain in the bones, particularly in the spine, ribs, or long bones, is a common symptom of multiple myeloma.
2. Fatigue: Feeling tired or weak is another common symptom of the disease.
3. Infections: Patients with multiple myeloma may be more susceptible to infections due to the impaired functioning of their immune system.
4. Bone fractures: Weakened bones can lead to an increased risk of fractures, particularly in the spine, hips, or ribs.
5. Kidney problems: Multiple myeloma can cause damage to the kidneys, leading to problems such as kidney failure or proteinuria (excess protein in the urine).
6. Anemia: A low red blood cell count can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
7. Increased calcium levels: High levels of calcium in the blood can cause symptoms such as nausea, vomiting, constipation, and confusion.
8. Neurological problems: Multiple myeloma can cause neurological problems such as headaches, numbness or tingling in the arms and legs, and difficulty with coordination and balance.

The diagnosis of multiple myeloma typically involves a combination of physical examination, medical history, and laboratory tests. These may include:

1. Complete blood count (CBC): A CBC can help identify abnormalities in the numbers and characteristics of different types of blood cells, including red blood cells, white blood cells, and platelets.
2. Serum protein electrophoresis (SPEP): This test measures the levels of different proteins in the blood, including immunoglobulins (antibodies) and abnormal proteins produced by myeloma cells.
3. Urine protein electrophoresis (UPEP): This test measures the levels of different proteins in the urine.
4. Immunofixation: This test is used to identify the type of antibody produced by myeloma cells and to rule out other conditions that may cause similar symptoms.
5. Bone marrow biopsy: A bone marrow biopsy involves removing a sample of tissue from the bone marrow for examination under a microscope. This can help confirm the diagnosis of multiple myeloma and determine the extent of the disease.
6. Imaging tests: Imaging tests such as X-rays, CT scans, or MRI scans may be used to assess the extent of bone damage or other complications of multiple myeloma.
7. Genetic testing: Genetic testing may be used to identify specific genetic abnormalities that are associated with multiple myeloma and to monitor the response of the disease to treatment.

It's important to note that not all patients with MGUS or smoldering myeloma will develop multiple myeloma, and some patients with multiple myeloma may not have any symptoms at all. However, if you are experiencing any of the symptoms listed above or have a family history of multiple myeloma, it's important to talk to your doctor about your risk and any tests that may be appropriate for you.

The primary graft dysfunction syndrome is a complex clinical entity characterized by severe respiratory and cardiovascular dysfunction, which develops within the first week after transplantation. PGD is associated with high morbidity and mortality rates, and it is one of the leading causes of graft failure after solid organ transplantation.

There are several risk factors for primary graft dysfunction, including:

1. Recipient age and comorbidities
2. Donor age and comorbidities
3. Cold ischemic time (CIT)
4. Hypoxic injury during procurement
5. Delayed recipient surgery
6. Inadequate immunosuppression
7. Sepsis
8. Pulmonary infection
9. Hemodynamic instability
10. Pulmonary edema

The diagnosis of primary graft dysfunction is based on a combination of clinical, radiologic, and pathologic findings. The condition can be classified into three categories:

1. Mild PGD: characterized by mild respiratory and cardiovascular dysfunction, with no evidence of severe inflammation or fibrosis.
2. Moderate PGD: characterized by moderate respiratory and cardiovascular dysfunction, with evidence of severe inflammation and/or fibrosis.
3. Severe PGD: characterized by severe respiratory and cardiovascular dysfunction, with extensive inflammation and/or fibrosis.

The treatment of primary graft dysfunction is aimed at addressing the underlying cause of the condition. This may include administration of immunosuppressive drugs, management of infections, and correction of any anatomical or functional abnormalities. In severe cases, lung transplantation may be necessary.

Prevention of primary graft dysfunction is crucial to minimize the risk of complications after lung transplantation. This can be achieved by careful donor selection, optimization of recipient condition before transplantation, and meticulous surgical technique during the procedure. Additionally, prompt recognition and management of early signs of PGD are essential to prevent progression to more severe forms of the condition.

In conclusion, primary graft dysfunction is a complex and multifactorial complication after lung transplantation that can lead to significant morbidity and mortality. Understanding the causes, clinical presentation, diagnosis, and treatment of PGD is essential for optimal management of patients undergoing lung transplantation.

The condition can be caused by a variety of factors, including excessive alcohol consumption, viral hepatitis, non-alcoholic fatty liver disease, and certain medications. It can also be a complication of other diseases such as hemochromatosis and Wilson's disease.

The symptoms of liver cirrhosis can vary depending on the severity of the disease, but may include fatigue, loss of appetite, nausea, abdominal swelling, and pain in the upper right side of the abdomen. As the disease progresses, it can lead to complications such as esophageal varices, ascites, and liver failure, which can be life-threatening.

There is no cure for liver cirrhosis, but treatment options are available to manage the symptoms and slow the progression of the disease. These may include medications to control swelling and pain, dietary changes, and in severe cases, liver transplantation. In some cases, a liver transplant may be necessary if the disease has caused significant damage and there is no other option to save the patient's life.

In conclusion, liver cirrhosis is a serious and potentially life-threatening condition that can cause significant damage to the liver and lead to complications such as liver failure. It is important for individuals to be aware of the risk factors and symptoms of the disease in order to seek medical attention if they suspect they may have liver cirrhosis. With proper treatment and management, it is possible to slow the progression of the disease and improve the patient's quality of life.

DGF can occur in various types of transplantations, including kidney, liver, heart, and lung transplants. The symptoms of DGF may include decreased urine production, decreased respiratory function, and abnormal liver enzymes. Treatment for DGF typically involves supportive care such as fluid and electrolyte replacement, management of infections, and immunosuppressive medications to prevent rejection. In some cases, additional surgical interventions may be necessary.

The diagnosis of DGF is based on clinical evaluation and laboratory tests such as blood chemistry, urinalysis, and biopsy findings. The prognosis for DGF varies depending on the underlying cause and the severity of the condition. In general, prompt recognition and treatment of DGF can improve outcomes and reduce the risk of complications.

In summary, delayed graft function is a common complication in transplantation that can result from various factors. Prompt diagnosis and treatment are essential to prevent long-term damage and improve outcomes for the transplanted organ or tissue.

AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.

There are several subtypes of AML, including:

1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.

The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:

* Fatigue
* Weakness
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Headache
* Confusion or seizures

AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:

1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.

Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:

1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.

It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.

The exact cause of Biliary Atresia is unknown, but it is thought to be related to genetic mutations or environmental factors during fetal development. Symptoms include jaundice (yellowing of the skin and eyes), poor feeding, and a large liver size. If left untreated, Biliary Atresia can lead to long-term complications such as liver cirrhosis, liver failure, and an increased risk of liver cancer.

Treatment for Biliary Atresia usually involves a surgical procedure called the Kasai procedure, where the damaged bile ducts are removed and replaced with a section of the small intestine. In some cases, a liver transplant may be necessary if the disease is advanced or if there are complications such as liver cirrhosis.

Overall, Biliary Atresia is a rare and complex condition that requires early diagnosis and treatment to prevent long-term complications and improve outcomes for affected individuals.

Types of Infection:

1. Bacterial Infections: These are caused by the presence of harmful bacteria in the body. Examples include pneumonia, urinary tract infections, and skin infections.
2. Viral Infections: These are caused by the presence of harmful viruses in the body. Examples include the common cold, flu, and HIV/AIDS.
3. Fungal Infections: These are caused by the presence of fungi in the body. Examples include athlete's foot, ringworm, and candidiasis.
4. Parasitic Infections: These are caused by the presence of parasites in the body. Examples include malaria, giardiasis, and toxoplasmosis.

Symptoms of Infection:

1. Fever
2. Fatigue
3. Headache
4. Muscle aches
5. Skin rashes or lesions
6. Swollen lymph nodes
7. Sore throat
8. Coughing
9. Diarrhea
10. Vomiting

Treatment of Infection:

1. Antibiotics: These are used to treat bacterial infections and work by killing or stopping the growth of bacteria.
2. Antiviral medications: These are used to treat viral infections and work by interfering with the replication of viruses.
3. Fungicides: These are used to treat fungal infections and work by killing or stopping the growth of fungi.
4. Anti-parasitic medications: These are used to treat parasitic infections and work by killing or stopping the growth of parasites.
5. Supportive care: This includes fluids, nutritional supplements, and pain management to help the body recover from the infection.

Prevention of Infection:

1. Hand washing: Regular hand washing is one of the most effective ways to prevent the spread of infection.
2. Vaccination: Getting vaccinated against specific infections can help prevent them.
3. Safe sex practices: Using condoms and other safe sex practices can help prevent the spread of sexually transmitted infections.
4. Food safety: Properly storing and preparing food can help prevent the spread of foodborne illnesses.
5. Infection control measures: Healthcare providers use infection control measures such as wearing gloves, masks, and gowns to prevent the spread of infections in healthcare settings.

The symptoms of dermatitis, allergic contact can vary depending on the severity of the reaction, but may include:

* Redness and swelling of the affected area
* Itching, burning, or stinging sensations
* Small blisters or hives
* Thickening or scaling of the skin
* Crusting or oozing of fluid

Dermatitis, allergic contact can be caused by a variety of substances, including:

* Metals, such as nickel, chrome, and mercury
* Plastics, such as latex and polyethylene
* Certain chemicals, such as perfumes, dyes, and preservatives
* Plant extracts, such as poison ivy or poison oak
* Insect bites or stings

The diagnosis of dermatitis, allergic contact is typically made through a combination of physical examination, medical history, and patch testing. Patch testing involves applying small amounts of potential allergens to the skin and observing for any signs of an allergic reaction over a period of time.

Treatment for dermatitis, allergic contact typically focuses on removing the allergen from the affected area and providing relief from symptoms. This may include:

* Avoiding exposure to the allergen
* Applying topical creams or ointments to reduce inflammation and itching
* Taking oral medications, such as antihistamines or corticosteroids, to reduce symptoms
* In severe cases, hospitalization may be necessary to manage the reaction.

Preventative measures for dermatitis, allergic contact include:

* Avoiding exposure to potential allergens
* Wearing protective clothing or gloves when handling suspected allergens
* Using hypoallergenic products and avoiding fragrances and dyes
* Performing patch testing before introducing new substances into the environment.

It is important to seek medical attention if symptoms persist or worsen over time, as dermatitis, allergic contact can lead to complications such as infection or scarring. Early diagnosis and treatment can help prevent these complications and improve outcomes for patients with this condition.

A type of skin reaction that occurs when certain substances in plants or substances in topical medications react with sunlight to cause an allergic response on the skin. This condition is also known as photocontact dermatitis.

Symptoms and Signs:

* Redness, itching, and burning of the affected area
* Blisters or hives
* Swelling and dry peeling of the skin

Causes and Risk Factors:

* Exposure to certain plants or substances that cause an allergic reaction when exposed to sunlight
* Use of topical medications that contain ingredients that cause photoallergic reactions
* Prolonged exposure to sunlight, particularly in areas with intense sunlight

Diagnosis:

* Physical examination of the affected area
* Allergy testing, such as patch testing or prick testing
* Blood tests to rule out other conditions that may cause similar symptoms

Treatment and Prevention:

* Avoidance of the substances that cause the photoallergic reaction
* Use of topical corticosteroids or antihistamines to reduce inflammation and itching
* Oral antibiotics or anti-itch medications if the condition is severe
* Protective clothing and sunscreen to prevent further exposure to sunlight

Prognosis:

* Most cases of photoallergic dermatitis resolve on their own within a few days to weeks, but some may persist for longer periods of time.
* In severe cases, the condition can lead to scarring and permanent disfigurement if left untreated.

There are several subtypes of NHL, including:

1. B-cell lymphomas (such as diffuse large B-cell lymphoma and follicular lymphoma)
2. T-cell lymphomas (such as peripheral T-cell lymphoma and mycosis fungoides)
3. Natural killer cell lymphomas (such as nasal NK/T-cell lymphoma)
4. Histiocyte-rich B-cell lymphoma
5. Primary mediastinal B-cell lymphoma
6. Mantle cell lymphoma
7. Waldenström macroglobulinemia
8. Lymphoplasmacytoid lymphoma
9. Myelodysplastic syndrome/myeloproliferative neoplasms (MDS/MPN) related lymphoma

These subtypes can be further divided into other categories based on the specific characteristics of the cancer cells.

Symptoms of NHL can vary depending on the location and size of the tumor, but may include:

* Swollen lymph nodes in the neck, underarm, or groin
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching
* Abdominal pain
* Swollen spleen

Treatment for NHL typically involves a combination of chemotherapy, radiation therapy, and in some cases, targeted therapy or immunotherapy. The specific treatment plan will depend on the subtype of NHL, the stage of the cancer, and other individual factors.

Overall, NHL is a complex and diverse group of cancers that require specialized care from a team of medical professionals, including hematologists, oncologists, radiation therapists, and other support staff. With advances in technology and treatment options, many people with NHL can achieve long-term remission or a cure.

VOD is most commonly seen in patients who have undergone hematopoietic stem cell transplantation (HSCT) or solid organ transplantation, as well as those with certain inherited genetic disorders. It is caused by a combination of factors, including immune system dysfunction, infection, and exposure to certain drugs or toxins.

Symptoms of VOD can include nausea, vomiting, abdominal pain, fatigue, and jaundice (yellowing of the skin and eyes). In severe cases, VOD can lead to liver failure, sepsis, and death.

Treatment for VOD typically involves supportive care, such as fluids and medications to manage symptoms, as well as therapies aimed at addressing any underlying causes of the condition. In severe cases, a liver transplant may be necessary. Prognosis for VOD varies depending on the severity of the condition and the presence of any underlying medical conditions.

Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.

There are several types of liver neoplasms, including:

1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.

The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.

Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.

Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.

Pre-B ALL is characterized by the abnormal growth of immature white blood cells called B lymphocytes. These cells are produced in the bone marrow and are normally present in the blood. In Pre-B ALL, the abnormal B cells accumulate in the bone marrow, blood, and other organs, crowding out normal cells and causing a variety of symptoms.

The symptoms of Pre-B ALL can vary depending on the individual patient, but may include:

* Fatigue
* Easy bruising or bleeding
* Frequent infections
* Swollen lymph nodes
* Enlarged liver or spleen
* Bone pain
* Headaches
* Confusion or seizures (in severe cases)

Pre-B ALL is most commonly diagnosed in children, but it can also occur in adults. Treatment typically involves a combination of chemotherapy and sometimes bone marrow transplantation. The prognosis for Pre-B ALL is generally good, especially in children, with a high survival rate if treated promptly and effectively. However, the cancer can be more difficult to treat in adults, and the prognosis may be less favorable.

Overall, Pre-B ALL is a rare and aggressive form of leukemia that requires prompt and specialized treatment to improve outcomes for patients.

There are several types of lymphoproliferative disorders, including:

1. Lymphoma: This is a type of cancer that affects the immune system and can arise from either B cells or T cells. There are several subtypes of lymphoma, including Hodgkin lymphoma and non-Hodgkin lymphoma.
2. Leukemia: This is a type of cancer that affects the blood and bone marrow. It occurs when there is an abnormal proliferation of white blood cells, which can lead to an overproduction of immature or malignant cells.
3. Myelodysplastic syndrome (MDS): This is a group of disorders that affect the bone marrow and can lead to an abnormal production of blood cells. MDS can progress to acute myeloid leukemia (AML).
4. Chronic lymphocytic leukemia (CLL): This is a type of cancer that affects the blood and bone marrow, characterized by the accumulation of mature-looking but dysfunctional B cells in the blood.
5. Marginal zone lymphoma: This is a type of cancer that arises from the marginal zone of the spleen, which is the area where the white pulp and red pulp of the spleen meet.
6. Mantle cell lymphoma: This is a type of cancer that affects the lymph nodes and other lymphoid tissues, characterized by the accumulation of malignant B cells in the mantle zone of the lymph node.
7. Primary central nervous system lymphoma (PCNSL): This is a rare type of cancer that affects the brain and spinal cord, characterized by the accumulation of malignant B cells in the central nervous system.
8. Hairy cell leukemia: This is a rare type of cancer that affects the blood and bone marrow, characterized by the accumulation of abnormal B cells with a "hairy" appearance in the blood and bone marrow.
9. Lymphoplasmacytic lymphoma: This is a type of cancer that affects the lymph nodes and other lymphoid tissues, characterized by the accumulation of malignant B cells in the lymph nodes and other lymphoid tissues.
10. AIDS-related lymphoma: This is a type of cancer that affects people with HIV/AIDS, characterized by the accumulation of malignant B cells in the lymph nodes and other lymphoid tissues.

It's important to note that these are just some examples of B-cell non-Hodgkin lymphomas, and there are many other subtypes and variants of this disease. Each type of lymphoma has its own unique characteristics and may require different treatment approaches.

The BCR-ABL gene is a fusion gene that is present in the majority of cases of CML. It is created by the translocation of two genes, called BCR and ABL, which leads to the production of a constitutively active tyrosine kinase protein that promotes the growth and proliferation of abnormal white blood cells.

There are three main phases of CML, each with distinct clinical and laboratory features:

1. Chronic phase: This is the earliest phase of CML, where patients may be asymptomatic or have mild symptoms such as fatigue, night sweats, and splenomegaly (enlargement of the spleen). The peripheral blood count typically shows a high number of blasts in the blood, but the bone marrow is still functional.
2. Accelerated phase: In this phase, the disease progresses to a higher number of blasts in the blood and bone marrow, with evidence of more aggressive disease. Patients may experience symptoms such as fever, weight loss, and pain in the joints or abdomen.
3. Blast phase: This is the most advanced phase of CML, where there is a high number of blasts in the blood and bone marrow, with significant loss of function of the bone marrow. Patients are often symptomatic and may have evidence of spread of the disease to other organs, such as the liver or spleen.

Treatment for CML typically involves targeted therapy with drugs that inhibit the activity of the BCR-ABL protein, such as imatinib (Gleevec), dasatinib (Sprycel), or nilotinib (Tasigna). These drugs can slow or stop the progression of the disease, and may also produce a complete cytogenetic response, which is defined as the absence of all Ph+ metaphases in the bone marrow. However, these drugs are not curative and may have significant side effects. Allogenic hematopoietic stem cell transplantation (HSCT) is also a potential treatment option for CML, but it carries significant risks and is usually reserved for patients who are in the blast phase of the disease or have failed other treatments.

In summary, the clinical course of CML can be divided into three phases based on the number of blasts in the blood and bone marrow, and treatment options vary depending on the phase of the disease. It is important for patients with CML to receive regular monitoring and follow-up care to assess their response to treatment and detect any signs of disease progression.

There are several subtypes of MDS, each with distinct clinical features and prognosis. The most common subtype is refractory anemia with excess blasts (RAEB), followed by chronic myelomonocytic leukemia (CMMoL) and acute myeloid leukemia (AML).

The exact cause of MDS is not fully understood, but it is believed to result from a combination of genetic mutations and environmental factors. Risk factors for developing MDS include exposure to certain chemicals or radiation, age over 60, and a history of previous cancer treatment.

Symptoms of MDS can vary depending on the specific subtype and severity of the disorder, but may include fatigue, weakness, shortness of breath, infection, bleeding, and easy bruising. Diagnosis is typically made through a combination of physical examination, medical history, blood tests, and bone marrow biopsy.

Treatment for MDS depends on the specific subtype and severity of the disorder, as well as the patient's overall health and preferences. Options may include supportive care, such as blood transfusions and antibiotics, or more intensive therapies like chemotherapy, bone marrow transplantation, or gene therapy.

Overall, myelodysplastic syndromes are a complex and heterogeneous group of disorders that can have a significant impact on quality of life and survival. Ongoing research is focused on improving diagnostic accuracy, developing more effective treatments, and exploring novel therapeutic approaches to improve outcomes for patients with MDS.

Examples of hematologic diseases include:

1. Anemia - a condition where there are not enough red blood cells or hemoglobin in the body.
2. Leukemia - a type of cancer that affects the bone marrow and blood, causing an overproduction of immature white blood cells.
3. Lymphoma - a type of cancer that affects the lymphatic system, including the bone marrow, spleen, and lymph nodes.
4. Thalassemia - a genetic disorder that affects the production of hemoglobin, leading to anemia and other complications.
5. Sickle cell disease - a genetic disorder that affects the production of hemoglobin, causing red blood cells to become sickle-shaped and prone to breaking down.
6. Polycythemia vera - a rare disorder where there is an overproduction of red blood cells.
7. Myelodysplastic syndrome - a condition where the bone marrow produces abnormal blood cells that do not mature properly.
8. Myeloproliferative neoplasms - a group of conditions where the bone marrow produces excessive amounts of blood cells, including polycythemia vera, essential thrombocythemia, and primary myelofibrosis.
9. Deep vein thrombosis - a condition where a blood clot forms in a deep vein, often in the leg or arm.
10. Pulmonary embolism - a condition where a blood clot travels to the lungs and blocks a blood vessel, causing shortness of breath, chest pain, and other symptoms.

These are just a few examples of hematologic diseases, but there are many others that can affect the blood and bone marrow. Treatment options for these diseases can range from watchful waiting and medication to surgery, chemotherapy, and stem cell transplantation. It is important to seek medical attention if you experience any symptoms of hematologic disease, as early diagnosis and treatment can improve outcomes.

Note: This definition is an excerpt from the "Merck Manual" home edition, which is available online. It may not be current or complete information, and should not be used as a substitute for professional medical advice or diagnosis.

There are several risk factors for developing HCC, including:

* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
* Diabetes
* Obesity

HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:

* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss

If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:

* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope

Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:

* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer

Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.

Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.

Reperfusion injury can be a complicating factor in various medical conditions, including:

1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.

Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.

Flushing can also be a side effect of certain medications, such as beta-blockers, aspirin, and some antidepressants. In addition, flushing can be a sign of an underlying condition that affects blood flow or blood vessels, such as Raynaud's disease or lupus.

Treatment for flushing will depend on the underlying cause. For example, if flushing is caused by an allergic reaction, medications such as antihistamines may be prescribed. If the flushing is caused by a medical condition, treatment will focus on managing that condition. In some cases, lifestyle changes such as avoiding triggers, wearing protective clothing, and using cool compresses can help reduce flushing.

It is important to seek medical attention if flushing is severe, persistent, or accompanied by other symptoms such as fever, chest pain, or difficulty breathing. Your healthcare provider can diagnose the underlying cause of flushing and recommend appropriate treatment.

There are several types of diabetes mellitus, including:

1. Type 1 DM: This is an autoimmune condition in which the body's immune system attacks and destroys the cells in the pancreas that produce insulin, resulting in a complete deficiency of insulin production. It typically develops in childhood or adolescence, and patients with this condition require lifelong insulin therapy.
2. Type 2 DM: This is the most common form of diabetes, accounting for around 90% of all cases. It is caused by a combination of insulin resistance (where the body's cells do not respond properly to insulin) and impaired insulin secretion. It is often associated with obesity, physical inactivity, and a diet high in sugar and unhealthy fats.
3. Gestational DM: This type of diabetes develops during pregnancy, usually in the second or third trimester. Hormonal changes and insulin resistance can cause blood sugar levels to rise, putting both the mother and baby at risk.
4. LADA (Latent Autoimmune Diabetes in Adults): This is a form of type 1 DM that develops in adults, typically after the age of 30. It shares features with both type 1 and type 2 DM.
5. MODY (Maturity-Onset Diabetes of the Young): This is a rare form of diabetes caused by genetic mutations that affect insulin production. It typically develops in young adulthood and can be managed with lifestyle changes and/or medication.

The symptoms of diabetes mellitus can vary depending on the severity of the condition, but may include:

1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Cuts or bruises that are slow to heal
5. Tingling or numbness in hands and feet
6. Recurring skin, gum, or bladder infections
7. Flu-like symptoms such as weakness, dizziness, and stomach pain
8. Dark, velvety skin patches (acanthosis nigricans)
9. Yellowish color of the skin and eyes (jaundice)
10. Delayed healing of cuts and wounds

If left untreated, diabetes mellitus can lead to a range of complications, including:

1. Heart disease and stroke
2. Kidney damage and failure
3. Nerve damage (neuropathy)
4. Eye damage (retinopathy)
5. Foot damage (neuropathic ulcers)
6. Cognitive impairment and dementia
7. Increased risk of infections and other diseases, such as pneumonia, gum disease, and urinary tract infections.

It is important to note that not all individuals with diabetes will experience these complications, and that proper management of the condition can greatly reduce the risk of developing these complications.

There are several possible causes of hyperglycemia, including:

1. Diabetes: This is a chronic condition where the body either does not produce enough insulin or cannot use insulin effectively.
2. Insulin resistance: This occurs when the body's cells become less responsive to insulin, leading to high blood sugar levels.
3. Pancreatitis: This is inflammation of the pancreas, which can lead to high blood sugar levels.
4. Cushing's syndrome: This is a rare hormonal disorder that can cause high blood sugar levels.
5. Medications: Certain medications, such as steroids and some types of antidepressants, can raise blood sugar levels.
6. Stress: Stress can cause the release of hormones such as cortisol and adrenaline, which can raise blood sugar levels.
7. Infections: Certain infections, such as pneumonia or urinary tract infections, can cause high blood sugar levels.
8. Trauma: Traumatic injuries can cause high blood sugar levels due to the release of stress hormones.
9. Surgery: Some types of surgery, such as heart bypass surgery, can cause high blood sugar levels.
10. Pregnancy: High blood sugar levels can occur during pregnancy, especially in women who have a history of gestational diabetes.

Hyperglycemia can cause a range of symptoms, including:

1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Headaches
5. Cuts or bruises that are slow to heal
6. Tingling or numbness in the hands and feet
7. Dry, itchy skin
8. Flu-like symptoms, such as weakness, dizziness, and stomach pain
9. Recurring skin, gum, or bladder infections
10. Sexual dysfunction in men and women

If left untreated, hyperglycemia can lead to serious complications, including:

1. Diabetic ketoacidosis (DKA): A life-threatening condition that occurs when the body produces high levels of ketones, which are acidic substances that can cause confusion, nausea, and vomiting.
2. Hypoglycemia: Low blood sugar levels that can cause dizziness, confusion, and even loss of consciousness.
3. Nerve damage: High blood sugar levels over an extended period can damage the nerves, leading to numbness, tingling, and pain in the hands and feet.
4. Kidney damage: The kidneys may become overworked and damaged if they are unable to filter out the excess glucose in the blood.
5. Eye damage: High blood sugar levels can cause damage to the blood vessels in the eyes, leading to vision loss and blindness.
6. Cardiovascular disease: Hyperglycemia can increase the risk of cardiovascular disease, including heart attacks, strokes, and peripheral artery disease.
7. Cognitive impairment: Hyperglycemia has been linked to cognitive impairment and an increased risk of dementia.

It is essential to manage hyperglycemia by making lifestyle changes, such as following a healthy diet, regular exercise, and taking medication if prescribed by a healthcare professional. Monitoring blood sugar levels regularly can help identify the signs of hyperglycemia and prevent long-term complications.

People with SCID are extremely susceptible to infections, particularly those caused by viruses, and often develop symptoms shortly after birth. These may include diarrhea, vomiting, fever, and failure to gain weight or grow at the expected rate. Without treatment, SCID can lead to life-threatening infections and can be fatal within the first year of life.

Treatment for SCID typically involves bone marrow transplantation or enzyme replacement therapy. Bone marrow transplantation involves replacing the patient's faulty immune system with healthy cells from a donor, while enzyme replacement therapy involves replacing the missing or dysfunctional enzymes that cause the immune deficiency. Both of these treatments can help restore the patient's immune system and improve their quality of life.

In summary, severe combined immunodeficiency (SCID) is a rare genetic disorder that impairs the body's ability to fight infections and can be fatal without treatment. Treatment options include bone marrow transplantation and enzyme replacement therapy.

JXG is a type of benign vascular tumor that often affects children, particularly those under the age of 5 years. It usually appears as a single, firm nodule on the trunk or extremities, and can be either red or purple in color. The nodule may be painful to the touch or sensitive to pressure.

The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. The tumor typically grows slowly and does not spread to other parts of the body. In rare cases, JXG can recur after initial treatment.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. The tumor typically grows slowly and does not spread to other parts of the body. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

Juvenile xanthogranuloma (JXG) is a rare vascular tumor that affects children under the age of 5 years. The exact cause of JXG is not known, but it is thought to be related to genetic mutations that occur during fetal development. Treatment options for JXG include observation, surgical excision, and laser therapy.

The symptoms of JXG can vary depending on the location and size of the tumor. Common symptoms include swelling, redness, and pain in the affected area. In some cases, JXG may not cause any symptoms at all. Treatment options for JXG include observation, surgical excision, and laser therapy. The choice of treatment depends on the size and location of the tumor, as well as the child's overall health.

The diagnosis of JXG is typically made based on a combination of physical examination, medical history, and imaging studies such as ultrasound or MRI. In some cases, a biopsy may be performed to confirm the diagnosis. Treatment options for JXG include observation, surgical excision, and laser therapy.

The prognosis for JXG is generally good, with most children experiencing complete resolution of the tumor without any long-term effects. However, in rare cases, JXG can recur or progress to more aggressive forms of cancer. Regular follow-up appointments with a healthcare provider are important to monitor the child's condition and detect any signs of recurrence or progression.

The treatment of JXG depends on the size and location of the tumor, as well as the child's overall health. Observation may be recommended for small, slow-growing tumors that are not causing any symptoms. Surgical excision is often recommended for larger tumors or those that are causing symptoms. Laser therapy may also be used to treat JXG, particularly in cases where the tumor is located in a sensitive area such as the face or neck.

The choice of treatment for JXG will depend on several factors, including the size and location of the tumor, the child's overall health, and the family's preferences. It is important to discuss the treatment options with a healthcare provider to determine the best course of action for your child. With appropriate treatment, most children with JXG can experience a good outcome and grow up to lead healthy lives.

Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.

Common symptoms of type 2 diabetes include:

* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections

If left untreated, type 2 diabetes can lead to a range of complications, including:

* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation

The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:

* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.

There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

Some common types of skin diseases include:

1. Acne: a condition characterized by oil clogged pores, pimples, and other blemishes on the skin.
2. Eczema: a chronic inflammatory skin condition that causes dry, itchy, and scaly patches on the skin.
3. Psoriasis: a chronic autoimmune skin condition characterized by red, scaly patches on the skin.
4. Dermatitis: a term used to describe inflammation of the skin, often caused by allergies or irritants.
5. Skin cancer: a type of cancer that affects the skin cells, often caused by exposure to UV radiation from the sun or tanning beds.
6. Melanoma: the most serious type of skin cancer, characterized by a mole that changes in size, shape, or color.
7. Vitiligo: a condition in which white patches develop on the skin due to the loss of pigment-producing cells.
8. Alopecia: a condition characterized by hair loss, often caused by autoimmune disorders or genetics.
9. Nail diseases: conditions that affect the nails, such as fungal infections, brittleness, and thickening.
10. Mucous membrane diseases: conditions that affect the mucous membranes, such as ulcers, inflammation, and cancer.

Skin diseases can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as biopsies or blood tests. Treatment options vary depending on the specific condition and may include topical creams or ointments, oral medications, light therapy, or surgery.

Preventive measures to reduce the risk of skin diseases include protecting the skin from UV radiation, using sunscreen, wearing protective clothing, and avoiding exposure to known allergens or irritants. Early detection and treatment can help prevent complications and improve outcomes for many skin conditions.

Myeloid leukemia can be classified into several subtypes based on the type of cell involved and the degree of maturity of the abnormal cells. The most common types of myeloid leukemia include:

1. Acute Myeloid Leukemia (AML): This is the most aggressive form of myeloid leukemia, characterized by a rapid progression of immature cells that do not mature or differentiate into normal cells. AML can be further divided into several subtypes based on the presence of certain genetic mutations or chromosomal abnormalities.
2. Chronic Myeloid Leukemia (CML): This is a slower-growing form of myeloid leukemia, characterized by the presence of a genetic abnormality known as the Philadelphia chromosome. CML is typically treated with targeted therapies or bone marrow transplantation.
3. Myelodysplastic Syndrome (MDS): This is a group of disorders characterized by the impaired development of immature blood cells in the bone marrow. MDS can progress to AML if left untreated.
4. Chronic Myelomonocytic Leukemia (CMML): This is a rare form of myeloid leukemia that is characterized by the accumulation of immature monocytes in the blood and bone marrow. CMML can be treated with chemotherapy or bone marrow transplantation.

The symptoms of myeloid leukemia can vary depending on the subtype and severity of the disease. Common symptoms include fatigue, weakness, fever, night sweats, and weight loss. Diagnosis is typically made through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment options for myeloid leukemia can include chemotherapy, targeted therapies, bone marrow transplantation, and supportive care to manage symptoms and prevent complications. The prognosis for myeloid leukemia varies depending on the subtype of the disease and the patient's overall health. With current treatments, many patients with myeloid leukemia can achieve long-term remission or even be cured.

Examples of OIs include:

1. Pneumocystis pneumonia (PCP): A type of pneumonia caused by the fungus Pneumocystis jirovecii, which is commonly found in the lungs of individuals with HIV/AIDS.
2. Cryptococcosis: A fungal infection caused by Cryptococcus neoformans, which can affect various parts of the body, including the lungs, central nervous system, and skin.
3. Aspergillosis: A fungal infection caused by Aspergillus fungi, which can affect various parts of the body, including the lungs, sinuses, and brain.
4. Histoplasmosis: A fungal infection caused by Histoplasma capsulatum, which is commonly found in the soil and can cause respiratory and digestive problems.
5. Candidiasis: A fungal infection caused by Candida albicans, which can affect various parts of the body, including the skin, mouth, throat, and vagina.
6. Toxoplasmosis: A parasitic infection caused by Toxoplasma gondii, which can affect various parts of the body, including the brain, eyes, and lymph nodes.
7. Tuberculosis (TB): A bacterial infection caused by Mycobacterium tuberculosis, which primarily affects the lungs but can also affect other parts of the body.
8. Kaposi's sarcoma-associated herpesvirus (KSHV): A viral infection that can cause various types of cancer, including Kaposi's sarcoma, which is more common in individuals with compromised immunity.

The diagnosis and treatment of OIs depend on the specific type of infection and its severity. Treatment may involve antibiotics, antifungals, or other medications, as well as supportive care to manage symptoms and prevent complications. It is important for individuals with HIV/AIDS to receive prompt and appropriate treatment for OIs to help prevent the progression of their disease and improve their quality of life.

Types of Kidney Diseases:

1. Acute Kidney Injury (AKI): A sudden and reversible loss of kidney function that can be caused by a variety of factors, such as injury, infection, or medication.
2. Chronic Kidney Disease (CKD): A gradual and irreversible loss of kidney function that can lead to end-stage renal disease (ESRD).
3. End-Stage Renal Disease (ESRD): A severe and irreversible form of CKD that requires dialysis or a kidney transplant.
4. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products.
5. Interstitial Nephritis: An inflammation of the tissue between the tubules and blood vessels in the kidneys.
6. Kidney Stone Disease: A condition where small, hard mineral deposits form in the kidneys and can cause pain, bleeding, and other complications.
7. Pyelonephritis: An infection of the kidneys that can cause inflammation, damage to the tissues, and scarring.
8. Renal Cell Carcinoma: A type of cancer that originates in the cells of the kidney.
9. Hemolytic Uremic Syndrome (HUS): A condition where the immune system attacks the platelets and red blood cells, leading to anemia, low platelet count, and damage to the kidneys.

Symptoms of Kidney Diseases:

1. Blood in urine or hematuria
2. Proteinuria (excess protein in urine)
3. Reduced kidney function or renal insufficiency
4. Swelling in the legs, ankles, and feet (edema)
5. Fatigue and weakness
6. Nausea and vomiting
7. Abdominal pain
8. Frequent urination or polyuria
9. Increased thirst and drinking (polydipsia)
10. Weight loss

Diagnosis of Kidney Diseases:

1. Physical examination
2. Medical history
3. Urinalysis (test of urine)
4. Blood tests (e.g., creatinine, urea, electrolytes)
5. Imaging studies (e.g., X-rays, CT scans, ultrasound)
6. Kidney biopsy
7. Other specialized tests (e.g., 24-hour urinary protein collection, kidney function tests)

Treatment of Kidney Diseases:

1. Medications (e.g., diuretics, blood pressure medication, antibiotics)
2. Diet and lifestyle changes (e.g., low salt intake, increased water intake, physical activity)
3. Dialysis (filtering waste products from the blood when the kidneys are not functioning properly)
4. Kidney transplantation ( replacing a diseased kidney with a healthy one)
5. Other specialized treatments (e.g., plasmapheresis, hemodialysis)

Prevention of Kidney Diseases:

1. Maintaining a healthy diet and lifestyle
2. Monitoring blood pressure and blood sugar levels
3. Avoiding harmful substances (e.g., tobacco, excessive alcohol consumption)
4. Managing underlying medical conditions (e.g., diabetes, high blood pressure)
5. Getting regular check-ups and screenings

Early detection and treatment of kidney diseases can help prevent or slow the progression of the disease, reducing the risk of complications and improving quality of life. It is important to be aware of the signs and symptoms of kidney diseases and seek medical attention if they are present.

Hodgkin Disease can spread to other parts of the body through the lymphatic system, and it can affect people of all ages, although it is most common in young adults and teenagers. The symptoms of Hodgkin Disease can vary depending on the stage of the disease, but they may include swollen lymph nodes, fever, night sweats, fatigue, weight loss, and itching.

There are several types of Hodgkin Disease, including:

* Classical Hodgkin Disease: This is the most common type of Hodgkin Disease and is characterized by the presence of Reed-Sternberg cells.
* Nodular Lymphocytic predominant Hodgkin Disease: This type of Hodgkin Disease is characterized by the presence of nodules in the lymph nodes.
* Mixed Cellularity Hodgkin Disease: This type of Hodgkin Disease is characterized by a mixture of Reed-Sternberg cells and other immune cells.

Hodgkin Disease is usually diagnosed with a biopsy, which involves removing a sample of tissue from the affected lymph node or other area and examining it under a microscope for cancer cells. Treatment for Hodgkin Disease typically involves chemotherapy, radiation therapy, or a combination of both. In some cases, bone marrow or stem cell transplantation may be necessary.

The prognosis for Hodgkin Disease is generally good, especially if the disease is detected and treated early. According to the American Cancer Society, the 5-year survival rate for people with Hodgkin Disease is about 85%. However, the disease can sometimes recur after treatment, and the long-term effects of radiation therapy and chemotherapy can include infertility, heart problems, and an increased risk of secondary cancers.

Hodgkin Disease is a rare form of cancer that affects the immune system. It is most commonly diagnosed in young adults and is usually treatable with chemotherapy or radiation therapy. However, the disease can sometimes recur after treatment, and the long-term effects of treatment can include infertility, heart problems, and an increased risk of secondary cancers.

In medical terms, death is defined as the irreversible cessation of all bodily functions that are necessary for life. This includes the loss of consciousness, the absence of breathing, heartbeat, and other vital signs. Brain death, which occurs when the brain no longer functions, is considered a definitive sign of death.

The medical professionals use various criteria to determine death, such as:

1. Cessation of breathing: When an individual stops breathing for more than 20 minutes, it is considered a sign of death.
2. Cessation of heartbeat: The loss of heartbeat for more than 20 minutes is another indicator of death.
3. Loss of consciousness: If an individual is unresponsive and does not react to any stimuli, it can be assumed that they have died.
4. Brain death: When the brain no longer functions, it is considered a definitive sign of death.
5. Decay of body temperature: After death, the body's temperature begins to decrease, which is another indicator of death.

In some cases, medical professionals may use advanced technologies such as electroencephalography (EEG) or functional magnetic resonance imaging (fMRI) to confirm brain death. These tests can help determine whether the brain has indeed ceased functioning and if there is no hope of reviving the individual.

It's important to note that while death is a natural part of life, it can be a difficult and emotional experience for those who are left behind. It's essential to provide support and care to the family members and loved ones of the deceased during this challenging time.

Disease progression can be classified into several types based on the pattern of worsening:

1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.

Disease progression can be influenced by various factors, including:

1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.

Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.

Pancreatic adenocarcinoma is the most common type of malignant pancreatic neoplasm and accounts for approximately 85% of all pancreatic cancers. It originates in the glandular tissue of the pancreas and has a poor prognosis, with a five-year survival rate of less than 10%.

Pancreatic neuroendocrine tumors (PNETs) are less common but more treatable than pancreatic adenocarcinoma. These tumors originate in the hormone-producing cells of the pancreas and can produce excess hormones that cause a variety of symptoms, such as diabetes or high blood sugar. PNETs are classified into two main types: functional and non-functional. Functional PNETs produce excess hormones and are more aggressive than non-functional tumors.

Other rare types of pancreatic neoplasms include acinar cell carcinoma, ampullary cancer, and oncocytic pancreatic neuroendocrine tumors. These tumors are less common than pancreatic adenocarcinoma and PNETs but can be equally aggressive and difficult to treat.

The symptoms of pancreatic neoplasms vary depending on the type and location of the tumor, but they often include abdominal pain, weight loss, jaundice, and fatigue. Diagnosis is typically made through a combination of imaging tests such as CT scans, endoscopic ultrasound, and biopsy. Treatment options for pancreatic neoplasms depend on the type and stage of the tumor but may include surgery, chemotherapy, radiation therapy, or a combination of these.

Prognosis for patients with pancreatic neoplasms is generally poor, especially for those with advanced stages of disease. However, early detection and treatment can improve survival rates. Research into the causes and mechanisms of pancreatic neoplasms is ongoing, with a focus on developing new and more effective treatments for these devastating diseases.

There are several types of lymphoma, including:

1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.

The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:

* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching

Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.

Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.

There are several types of biliary tract diseases, including:

1. Gallstones: Small, pebble-like deposits that form in the gallbladder and can cause pain and blockages.
2. Cholangitis: An infection of the bile ducts that can cause fever, chills, and abdominal pain.
3. Biliary cirrhosis: Scarring of the liver and bile ducts that can lead to liver failure.
4. Pancreatitis: Inflammation of the pancreas that can cause abdominal pain and digestive problems.
5. Cancer of the biliary tract: Cancer that affects the liver, gallbladder, or bile ducts.

Biliary tract diseases can be caused by a variety of factors, including genetics, obesity, alcohol consumption, and certain medications. Diagnosis is typically made through a combination of imaging tests, such as CT scans and endoscopic ultrasound, and laboratory tests, such as blood tests and liver function tests.

Treatment for biliary tract diseases depends on the underlying cause and severity of the condition. In some cases, treatment may involve medications to dissolve gallstones or treat infections. In more severe cases, surgery may be necessary to remove the gallbladder or repair damaged bile ducts.

Prevention is key in avoiding biliary tract diseases, and this includes maintaining a healthy diet and lifestyle, managing risk factors such as obesity and alcohol consumption, and getting regular medical check-ups. Early detection and treatment of biliary tract diseases can help to improve outcomes and reduce the risk of complications.

There are several types of dermatitis, including:

1. Atopic dermatitis: a chronic condition characterized by dry, itchy skin and a tendency to develop allergies.
2. Contact dermatitis: a localized reaction to an allergen or irritant that comes into contact with the skin.
3. Seborrheic dermatitis: a condition characterized by redness, itching, and flaking skin on the scalp, face, or body.
4. Psoriasis: a chronic condition characterized by thick, scaly patches on the skin.
5. Cutaneous lupus erythematosus: a chronic autoimmune disorder that can cause skin rashes and lesions.
6. Dermatitis herpetiformis: a rare condition characterized by itchy blisters or rashes on the skin.

Dermatitis can be diagnosed through a physical examination, medical history, and sometimes laboratory tests such as patch testing or biopsy. Treatment options for dermatitis depend on the cause and severity of the condition, but may include topical creams or ointments, oral medications, phototherapy, or lifestyle changes such as avoiding allergens or irritants.

There are several types of hepatitis C, including genotype 1, which is the most common and accounts for approximately 70% of cases in the United States. Other genotypes include 2, 3, 4, 5, and 6. The symptoms of hepatitis C can range from mild to severe and may include fatigue, fever, loss of appetite, nausea, vomiting, joint pain, jaundice (yellowing of the skin and eyes), dark urine, pale stools, and itching all over the body. Some people with hepatitis C may not experience any symptoms at all.

Hepatitis C is diagnosed through a combination of blood tests that detect the presence of antibodies against HCV or the virus itself. Treatment typically involves a combination of medications, including interferon and ribavirin, which can cure the infection but may have side effects such as fatigue, nausea, and depression. In recent years, new drugs known as direct-acting antivirals (DAAs) have become available, which can cure the infection with fewer side effects and in a shorter period of time.

Prevention measures for hepatitis C include avoiding sharing needles or other drug paraphernalia, using condoms to prevent sexual transmission, and ensuring that any tattoos or piercings are performed with sterilized equipment. Vaccines are also available for people who are at high risk of contracting the virus, such as healthcare workers and individuals who engage in high-risk behaviors.

Overall, hepatitis C is a serious and common liver disease that can lead to significant health complications if left untreated. Fortunately, with advances in medical technology and treatment options, it is possible to manage and cure the virus with proper care and attention.

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

Boschero AC, Negreiros de Paiva CE (1977). "Transplantation of islets of Langerhans in diabetic rats". Acta Physiol Lat Am. 27 ...

https://en.wikipedia.org/wiki/Neurexin

Scharp DW, Murphy JJ, Newton WT, Ballinger WF, Lacy PE (January 1975). "Transplantation of islets of Langerhans in diabetic ... Islet transplantation is the transplantation of isolated islets from a donor pancreas into another person. It is an ... The goal of islet transplantation is to infuse enough islets to control the blood glucose level removing the need for insulin ... and the limited supply of islets for transplantation. Current immunosuppressive regimens are capable of preventing islet ...

https://en.wikipedia.org/wiki/Islet_cell_transplantation

2003). "Inflammatory mediators expressed in human islets of Langerhans: implications for islet transplantation". Biochem. ...

https://en.wikipedia.org/wiki/TMSB10

Islet cell Transplantation Moving the beta (islet) cells from a donor pancreas and putting them into a person whose pancreas ... Islets of Langerhans Groups of cells in the pancreas. Some of them make and secrete hormones that help the body break down and ... Beta cell transplantation See: Islet cell transplantation. Biosynthetic human insulin A man-made insulin that is chemically ... Insulin a hormone produced by the beta cells in the Islet of Langerhans' beta cells. It is a very small protein and has effects ...

https://en.wikipedia.org/wiki/Glossary_of_diabetes

Insulin originates from beta cells located in the islets of Langerhans. Since each islet contains up to 2000 beta cells and ... Pulsatile insulin delivery to the portal vein or islet cell transplantation to the liver of diabetic patients are therefore ... The islets of Langerhans. Md. Shahidul Islam. Dordrecht: Springer. 2010. ISBN 978-90-481-3271-3. OCLC 663096203. Insulin ... within an islet of Langerhans the oscillations become synchronized by electrical coupling between closely located beta cells ...

https://en.wikipedia.org/wiki/Insulin_oscillation

"Three-yr follow-up of a type 1 diabetes mellitus patient with an islet xenotransplant". Clinical Transplantation. 21 (3): 352- ... "Xenotransplantation of porcine neonatal islets of Langerhans and Sertoli cells: a 4-year study". European Journal of ...

https://en.wikipedia.org/wiki/Animal_testing

... s have been successful for transplanting a number of cells including islets of Langerhans for diabetes treatment ... April 1994). "Insulin independence in a type 1 diabetic patient after encapsulated islet transplantation". Lancet. 343 (8903): ... Current status of artificial devices and hepatocyte transplantation". Transplantation. 87 (4): 457-466. doi:10.1097/TP. ... This principle has been used to remove blood group antibodies from plasma for bone marrow transplantation and for the treatment ...

https://en.wikipedia.org/wiki/Artificial_cell

... with enough islet recovery from the original tissue, for safe and effective islet transplantation in humans. Because Ficoll- ... Ficoll was used in an attempt to separate islets of Langerhans from enzyme (collagenase) digested human pancreatic tissue. The ... theory was that separated islets could then be used for transplantation into patients with type 1 diabetes. In practice, using ... At one time, fairly early in the research for diabetes treatment by transplantation, ...

https://en.wikipedia.org/wiki/Ficoll

Islets of Langerhans (pancreas islet cells) (deceased-donor and living-donor) Bone marrow or adult stem cell (living-donor and ... Thyroid transplantation became the model for a whole new therapeutic strategy: organ transplantation. After the example of the ... "ABO Incompatible Heart Transplantation in Young Infants". American Society of Transplantation. 30 July 2009. Archived from the ... Kidney Transplantation, Bioengineering, and Regeneration: Kidney Transplantation in the Regenerative Medicine Era, edited by ...

https://en.wikipedia.org/wiki/Organ_transplantation

... islets of langerhans transplantation MeSH E04.936.225.687 - stem cell transplantation MeSH E04.936.225.687.155 - bone marrow ... islets of langerhans transplantation MeSH E04.270.694 - parathyroidectomy MeSH E04.270.856 - thyroidectomy MeSH E04.292.413 - ... heart transplantation MeSH E04.936.450.475.450 - heart-lung transplantation MeSH E04.936.450.485 - kidney transplantation MeSH ... lung transplantation MeSH E04.936.450.495.450 - heart-lung transplantation MeSH E04.936.450.650 - pancreas transplantation MeSH ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(E04)

"Xenotransplantation of porcine neonatal islets of Langerhans and Sertoli cells: a 4-year study". European Journal of ... Upon xenogenic transplantation, Sertoli cells have been shown to regain the ability to proliferate. Recently (2016), ... By treating spontaneously diabetic and obese mice with the transplantation of microencapsulated Sertoli cells in subcutaneous ... Korbutt GS, Elliott JF, Rajotte RV (February 1997). "Cotransplantation of allogeneic islets with allogeneic testicular cell ...

https://en.wikipedia.org/wiki/Sertoli_cell

... islet cells are obtained from the patient, whereas in the allogeneic pancreatic islet cell transplantation islet cells were ... Schmidt observed inflammation caused by lymphocytic infiltration in the islets of Langerhans in the periphery of islets (peri- ... Due to the islets of Langerhans being small clusters of cells in the pancreas, it is difficult to study and diagnose insulitis ... Insulitis is an inflammation of the islets of Langerhans, a collection of endocrine tissue located in the pancreas that helps ...

https://en.wikipedia.org/wiki/Insulitis

In 2008 started the only currently active program of islet transplantation in Germany. This treatment is a great benefit for ... and one of the coordinators of the Paul-Langerhans-Institute Dresden. Since 2012, he has been scientific secretary of the DFG ... stem cell research and advances in islet cell transplantation as a therapy for diabetes. This is why, presently, Dresden is the ... DFG TRansregio 127 Transplantation of human islets without immunosuppression CV Bornstein (Orphaned articles from June 2014, ...

https://en.wikipedia.org/wiki/Stefan_R._Bornstein

Insulin independence after islet transplantation into type I diabetic patient. Diabetes 1990; 39: 515-518. "Pancreatic Islet ... That work resulted in a better understanding of how beta cells in the pancreatic islets of Langerhans produced and exported ... He is often credited as the originator of islet transplantation. Lacy was born in Trinway, Ohio in February, 1924. He was ... Ballinger WF II, Lacy PE: Transplantation of intact pancreatic islets in rats. Surgery 1972; 72: 175-186. Ballinger WF II, Lacy ...

https://en.wikipedia.org/wiki/Paul_Eston_Lacy

Langerhans islet beta-cells, cardiomyocytes and neurons. Drug screen are performed on miniaturized cell culture in multiwell- ... Source material can be normal healthy cells from another donor (heterologous transplantation) or genetically corrected from the ... cell replacement and transplantation following acute injuries and reconstructive surgery. These applications are limited to the ... "Differentiation of embryonic stem cells to insulin-secreting structures similar to pancreatic islets". Science. 292 (5520): ...

https://en.wikipedia.org/wiki/Directed_differentiation

... while leaving the islets of Langerhans intact. He reasoned that a relatively pure extract could be made from the islets once ... or by islet cell transplantation to the liver. The blood insulin level can be measured in international units, such as µIU/mL ... Beta cells in the islets of Langerhans release insulin in two phases. The first-phase release is rapidly triggered in response ... The function of the "little heaps of cells", later known as the islets of Langerhans, initially remained unknown, but Édouard ...

https://en.wikipedia.org/wiki/Insulin

II MHC gene products are expressed at higher levels or de novo on the insulin-producing beta cells of the islets of Langerhans ... At Harvard, he served as head of the Inflammation, Immunity and Transplantation Focus Group at the Schepens Eye Research ... Enhanced MHC class I heavy-chain gene expression in pancreatic islets". Diabetes. 37 (10): 1411-8. doi:10.2337/diabetes.37.10. ...

https://en.wikipedia.org/wiki/Santa_Ono

the T cell did not encounter in the thymus (such as, tissue-specific molecules like those in the islets of Langerhans, brain, ... Braza, F; Soulillou JP; Brouard S. (Sep 2012). "Gene expression signature in transplantation tolerance". Clin Chim Acta. 413 ( ... Immune recognition of non-self-antigens typically complicates transplantation and engrafting of foreign tissue from an organism ... which could be rescued by transplantation of CD4+ T cells. A more specific depletion and reconstitution experiment established ...

https://en.wikipedia.org/wiki/Immune_tolerance

Selawry HP, Cameron DF (1993). "Sertoli cell-enriched fractions in successful islet cell transplantation". Cell Transplantation ... islets of Langerhans), resulting in increased graft survival. Molecules released by the Sertoli cells are predicted to protect ... ISBN 978-0-12-515401-7. Setchel BP (1990). "The testis and tissue transplantation: historical aspects". Journal of Reproductive ... Korbutt GS, Elliott JF, Rajotte RV (1997). "Cotransplantation of allogeneic islets with allogeneic testicular cell aggregates ...

https://en.wikipedia.org/wiki/Testicular_immunology

The pancreas contains the islets of Langerhans, which are responsible for making insulin, a hormone that helps regulate blood ... October 2005). "Simultaneous liver and pancreas transplantation in patients with cystic fibrosis". Transplantation Proceedings ... Damage to the pancreas can lead to loss of the islet cells, leading to a type of diabetes unique to those with the disease. ... Lung transplantation may be an option if lung function continues to worsen. Pancreatic enzyme replacement and fat-soluble ...

https://en.wikipedia.org/wiki/Cystic_fibrosis

... islet cell - islet cell cancer - islet of Langerhans cell - isoflavone - isointense - isolated hepatic perfusion - isolated ... syngeneic bone marrow transplantation - syngeneic stem cell transplantation - synovial membrane - synovial sarcoma - synthetic ... allogeneic bone marrow transplantation - allogeneic stem cell transplantation - allogenic - allopurinol - Allovectin-7 - aloe- ... autologous bone marrow transplantation - autologous lymphocyte - autologous stem cell transplantation - autologous tumor cell ...

https://en.wikipedia.org/wiki/Index_of_oncology_articles

Paul Langerhans: Islets of Langerhans, Langerhans cells Max von Laue: Discoveries regarding the diffraction of X-rays in ... Pioneer of skin transplantation and cosmetic surgery. Ernst Dickmanns: Developer of the first driverless car. Otto Diels: Diels ...

https://en.wikipedia.org/wiki/List_of_German_inventors_and_discoverers

Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to ... "Pancreas Transplantation". American Diabetes Association. Archived from the original on 13 April 2014. Retrieved 9 April 2014. ... Type 1 diabetes is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin ... sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the ...

https://en.wikipedia.org/wiki/Diabetes

An experimental procedure to treat type 1 diabetes is pancreas transplantation or isolated transplantation of islet cells to ... also called islets of Langerhans) that are distributed throughout the pancreas. Pancreatic islets contain alpha cells, beta ... more numerous and found throughout the islet. Enterochromaffin cells are also scattered throughout the islets. Islets are ... The pancreatic islets form as the endocrine cells migrate from the duct system to form small clusters around capillaries. This ...

https://en.wikipedia.org/wiki/Pancreas

... polypeptide receptor List of terms associated with diabetes Guangxitoxin Alpha cell Pancreatic development Islets of Langerhans ... "Differentiation and transplantation of functional pancreatic beta cells generated from induced pluripotent stem cells derived ... Beta cells make up 50-70% of the cells in human islets. In patients with Type 1 diabetes, beta-cell mass and function are ... Cilia deletion can lead to islet dysfunction and type 2 diabetes. Beta cells are the only site of insulin synthesis in mammals ...

https://en.wikipedia.org/wiki/Beta_cell

July 2000). "Islet transplantation in seven patients with type 1 diabetes mellitus using a glucocorticoid-free ... have been dedicated towards the development of bioartificial pancreas involving the immobilization of islets of Langerhans ... "Considerations for successful transplantation of encapsulated pancreatic islets". Diabetologia. 45 (2): 159-73. doi:10.1007/ ... The use of microencapsulation would protect the islet cells from immune rejection as well as allow the use of animal cells or ...

https://en.wikipedia.org/wiki/Cell_encapsulation

Allotransplantation of cells of Islets of Langerhans. 52.86 Transplantation of cells of Islets of Langerhans, not otherwise ...

https://www.aapc.com/codes/icd9-codes-vol3-range/11/

However, a majority of patients resume insulin treatment in the first 5 years after transplantation. Several mechanisms have ... insulin independence can reproducibly be achieved after islet transplantation. ... Islets of Langerhans Transplantation* Actions. * Search in PubMed * Search in MeSH * Add to Search ... Noninvasive imaging techniques in islet transplantation Sophie Borot 1 , Lindsey A Crowe, Christian Toso, Jean-Paul Vallée, ...

https://pubmed.ncbi.nlm.nih.gov/21800023

... at 1 year post-initial islet transplantation. The same subjects reported consistent, statistically significant, and clinically ... Islets of Langerhans Transplantation* Actions. * Search in PubMed * Search in MeSH * Add to Search ... Clinical Islet Transplantation Consortium: Beth Begley, Jose Cano, Sallie Carpentier, Jennifer Hutchinson, Christian P Larsen, ... Clinical Islet Transplantation Consortium: Beth Begley, Jose Cano, Sallie Carpentier, Jennifer Hutchinson, Christian P Larsen, ...

https://www.ncbi.nlm.nih.gov/pubmed/29563196

Healthy islets are taken from a donated pancreas and placed in a recipient. ... Overview of islet transplantation, an experimental treatment for type 1 diabetes. ... What are islets?. Pancreatic islets, also called islets of Langerhans, are groups of cells in your pancreas. The pancreas is an ... In the type of islet transplantation used to treat type 1 diabetes, also called islet allo-transplantation, doctors take islets ...

https://www.niddk.nih.gov/health-information/diabetes/overview/insulin-medicines-treatments/pancreatic-islet-transplantation

7. Islet of Langerhans allogeneic transplantation at the University of Geneva in the steroid free era in islet after kidney and ... Focus on Islets of Langerhans transplantation].. Bayle F. Presse Med; 2001 Sep; 30(24 Pt 2):19-20. PubMed ID: 11577579. [TBL] ... Improved human pancreatic islet isolation for a prospective cohort study of islet transplantation vs best medical therapy in ... 4. Islet transplantation in type 1 diabetes mellitus using cultured islets and steroid-free immunosuppression: Miami experience ...

https://pubmedhh.nlm.nih.gov/biomarkers/search.php?id=16515432&mod=related&page=1&outid=&proj=

islets of langerhans transplantation (1) * pancreatic beta cell (1) * positron-emission tomography (1) ... Click here to open pdf in another window PDF for Monitoring beta cell survival after intrahepatic islet transplantation using ... Monitoring beta cell survival after intrahepatic islet transplantation using dynamic exendin PET imaging: a proof-of-concept ... View article titled, Monitoring beta cell survival after intrahepatic islet transplantation using dynamic exendin PET imaging: ...

https://diabetesjournals.org/diabetes/search-results?f_AllAuthors=Michiel+F.+Nijhoff

Grafting, Islets of Langerhans Islands of Langerhans Transplantation Islands of Pancreas Transplantation Islet Transplantation ... Transplantation, Islet Transplantation, Islets of Langerhans Transplantation, Pancreatic Islets NLM Classification #. WK 800. ... Transplantation [E04.936] * Cell Transplantation [E04.936.225] * Islets of Langerhans Transplantation [E04.936.225.375] ... Cell Transplantation [E02.095.147.500] * Islets of Langerhans Transplantation [E02.095.147.500.250] * Stem Cell Transplantation ...

https://meshb.nlm.nih.gov/record/ui?ui=D016381

Islets of Langerhans; NAmerica; Predictive Value of Tests; Registries; Transplantation; Transplantation/statistics & numerical ... CONCLUSIONS: Clinical islet transplantation needs to be evaluated using the most clinically relevant endpoints such as glucose ... BACKGROUND: This report summarizes the primary efficacy and the safety outcomes of islet transplantation reported to the NIDDK ... The cumulative results of the registry confirm the inarguably positive impact of islet transplantation on metabolic control in ...

https://emmes.com/publications/705

The major deliverable of the project will represent a major breakthrough compared to islet of Langerhans transplantation, the ... important signs of progress have been made in clinical islet transplantation. However, islet transplantation relies on organ ... the current state of the art in clinical cell therapy for type 1 diabetes has consisted of islet of Langerhans transplantation ... In contrast, VANGUARD will use a stepwise strategy, moving from allogeneic islet cell organoids to a more complex, but still ...

https://cordis.europa.eu/project/id/874700/reporting

HUMAN PANCREATIC ISLET CELL RESOURCES (ICRS) RFA-RR-01-002. NCRR ... relating to islet cell isolation and islet cell transplantation ... "islets of Langerhans" of the pancreas. While injection of exogenous insulin has long been the standard treatment for patients ... investigators in the transplantation of islet cells. If the applicant has had no prior experience with islet transplantation, ... monitoring of potential islet cell transplantation recipients; and d) inpatient or outpatient costs related to islet cell ...

http://grants1.nih.gov/grants/guide/rfa-files/RFA-RR-01-002.html

https://grants.nih.gov/grants/guide/rfa-files/RFA-RR-01-002.html

Transplanted pancreatic islet cells release a unique biomarker that signals the early stages of tissue rejection. The finding ... A mouse pancreatic islet near a blood vessel; insulin in red, nuclei in blue.Jakob Suckale, Solimena lab, Paul Langerhans ... Pancreatic islet transplantation is performed in certain patients whose blood glucose levels are especially difficult to ... The scientists next analyzed blood samples from 5 people with type 1 diabetes who were enrolled in an islet transplantation ...

https://www.nih.gov/news-events/nih-research-matters/biomarkers-early-organ-transplant-rejection

Transplantation, Islet. Transplantation, Islets of Langerhans. Transplantation, Pancreatic Islets. Transplantations, Islet. ... Islands of Langerhans Transplantation Islands of Pancreas Transplantation Islet Transplantation Islet Transplantations Islets ... Islet Transplantation. Islet Transplantations. Islets Transplantation, Pancreatic. Pancreatic Islets Transplantation. ... Transplantation, Islands of Langerhans Transplantation, Islands of Pancreas Transplantation, Islet Transplantation, Islets of ...

https://decs.bvsalud.org/en/ths/resource/?id=28997&filter=ths_exact_term&q=TRANSPLANTE+DAS+ILHOTAS+PANCRE%C3%81TICAS

https://meshb-prev.nlm.nih.gov/record/ui?ui=D016381

EPITA is established to provide a forum for those working in the field of pancreas and islet of Langerhans transplantation or ... Young Professionals in Transplantation. The Young Professionals in Transplantation (YPT) is the Network for Junior Transplant ... EKITA is the Organ Expert Section of ESOT on kidney transplantation in Europe, providing a forum for kidney transplantation ... Transplantation trials from ClinicalTrials.gov. *the Impact of Occupational Therapy : a Multicenter Randomized Controlled Trial ...

https://esot.org/read-the-report-of-the-esot-educational-needs-survey/

Islet and whole pancreas transplantation in type 1 diabetes]. / Greffes dîlots de Langerhans et de pancréas dans le diabète de ...

https://pesquisa.bvsalud.org/perinatal/?lang=es&q=au:Vantyghem,+Marie-Christine

Islets of Langerhans Transplantation Medicine & Life Sciences 21% * Transplants Medicine & Life Sciences 15% ... Islet transplantation results in decreased albuminuria and decreased foot process width, indicating reversibility of these ... Islet transplantation results in decreased albuminuria and decreased foot process width, indicating reversibility of these ... Islet transplantation results in decreased albuminuria and decreased foot process width, indicating reversibility of these ...

https://experts.umn.edu/en/publications/epithelial-cell-foot-process-width-in-intact-and-uninephrectomize

Tra Transplantation. Translation:AnimalsCells * Nonviral transfection of isolated islets of Langerhans. Transplant Proc. 1998 ... Transplantation. 2003 Jun 27; 75(12):2128-30. McVicar JP, Albertson TE, Troppmann C, Kappes J, Perez RV. PMID: 12829923. ... Multiple organ transplantation after suicide by acetaminophen and gunshot wound. West J Emerg Med. 2010 Dec; 11(5):506-9. ... Improved pig islet yield and post-culture recovery using Liberase PI purified enzyme blend. Transplant Proc. 1998 Mar; 30(2): ...

https://profiles.ucdavis.edu/timothy.albertson

Palavras-chave : Diabetes Mellitus type I; Transplantation; Islets of Langerhans; Psychology; clinical. ... PEREIRA, Ester et al. Psychological aspects of diabetic patients candidates to the pancreatic islet transplantation. Arq. bras ... Diabetic patients see the pancreatic islet transplantation (IT) as an idealized form of cure of the disease, and put great ...

http://pepsic.bvsalud.org/scielo.php?script=sci_abstract&pid=S1809-52672007000100007&lng=pt&nrm=is&tlng=en

Islets of Langerhans Transplantation. Male. Middle Aged. Pancreatectomy. Pancreatitis, Chronic. Perioperative Care. ...

https://profiles.musc.edu/display/person/christopheraskorke/network/researchareas/timeline

Insulin is produced by specialized cells of the pancreas called islets of Langerhans. Insulin regulates blood sugar levels. ...

https://medlineplus.gov/ency/presentations/100129_1.htm

Islets of Langerhans Transplantation 14% * Hybrid Cells 13% * Streptozocin 11% * Kidney Transplantation 10% ... Dive into the research topics of Electrofusion of Mesenchymal Stem Cells and Islet Cells for Diabetes Therapy: A Rat Model. ... Electrofusion of Mesenchymal Stem Cells and Islet Cells for Diabetes Therapy: A Rat Model. ...

https://hub.tmu.edu.tw/en/publications/electrofusion-of-mesenchymal-stem-cells-and-islet-cells-for-diabe/fingerprints/

Islets of Langerhans Transplantation 60% * Peptides 60% * Transplants 59% * Apoptosis 57% * Carrier Proteins 40% ... Novel cell-permeable p38-MAPK inhibitor efficiently prevents porcine islet apoptosis and improves islet graft function. ... Novel cell-permeable p38-MAPK inhibitor efficiently prevents porcine islet apoptosis and improves islet graft function. ...

https://okayama.elsevierpure.com/en/publications/novel-cell-permeable-p38-mapk-inhibitor-efficiently-prevents-porc/fingerprints/

Liver Transplantation Medicine & Life Sciences 41% * Allografts Medicine & Life Sciences 37% * Islets of Langerhans ... the HOPE in Action Investigators, Mar 2022, In: American Journal of Transplantation. 22, 3, p. 853-864 12 p.. Research output: ... Patient and Graft Survival After A1/A2-incompatible Living Donor Kidney Transplantation. Bisen, S. S., Getsin, S. N., Chiang, P ... Successful kidney transplantation from a deceased donor with severe COVID-19 respiratory illness with undetectable SARS-CoV-2 ...

https://pure.johnshopkins.edu/en/persons/niraj-desai

AN - /transpl: do not routinely coordinate with ISLETS OF LANGERHANS TRANSPLANTATION HN - 2006; use ISLETS OF LANGERHANS 1980- ... AN - /transpl: do not routinely coordinate with ISLETS OF LANGERHANS TRANSPLANTATION HN - 2006; use ISLETS OF LANGERHANS 1980- ... AN - /transpl: do not routinely coordinate with ISLETS OF LANGERHANS TRANSPLANTATION HN - 2006 BX - PP Cells, Pancreatic MH - ... transplantation. The term most frequently refers to renal dysfunction following KIDNEY TRANSPLANTATION. HN - 2006 FX - Graft ...

https://nlmpubs.nlm.nih.gov/projects/mesh/.newterms/.bkup/mshnew2006.10-03-2005.txt

Isolation of Islets of Langerhans for Transplantation in Type-1 Diabetic Patients 20191213 ... Cover , Pancreatic islet transplantation , ISBN 9789080216402 20221024 * Blurb , Pancreatic islet transplantation , 20221023 ... Pancreatic islet transplantation Thesis Repository Leiden University , 20221125 20221125 * Jews and the Resistance , Marc ... Lancet Letter 1989 UW Solution Islet Isolation , 20220823 20220823 * Minneapolis 1989 Poster UW Solution Islet Isolation , ...

https://michelvanderburg.com/2020/04/19/virtual-opera-push-epilogue-ma-vie-nest-que-miracles/

Islets of Langerhans Transplantation. *Animals, Genetically Modified. _. Top Journals Top journals in which articles about this ...

https://connects.catalyst.harvard.edu/Profiles/display/Concept/Triiodothyronine

Diabetes Mellitus, Type 1, Humans, Insulin Infusion Systems, Islets of Langerhans Transplantation, Pancreas Transplantation ... Report from the 11th Workshop of Artificial Insulin Delivery Systems, Pancreas and Islet Transplantation Study Group of the ... Report from the 11th Workshop of Artificial Insulin Delivery Systems, Pancreas and Islet Transplantation Study Group of the ...

https://www.rdm.ox.ac.uk/publications/72910?cdc418fe-07f5-11ee-9765-06ee384a3ad0

... system proliferated and partly differentiated into endocrine cells that subsequently formed many new islets of Langerhans as ... The structures of P-, a-, 8-, and pancreatic polypeptide cells were found to be intact even 1.5 years after transplantation. In ... In addition to this, the organization of these cells inside the islets is similar to that of normal pancreatic tissue. The ... In addition to this, the organization of these cells inside the islets is similar to that of normal pancreatic tissue. The ...

https://research.uaeu.ac.ae/en/publications/morphological-findings-in-long-term-pancreatic-tissue-transplants-2

The limitations of islet transplantation include a shortage of donors, fibrosis of transplanted islets, and various side ... A minor subset of Batf3-dependent antigen-presenting cells in islets of Langerhans is essential for the development of ... Islet transplantation in seven patients with type 1 diabetes mellitus using a glucocorticoid-free immunosuppressive regimen. N ... International trial of the Edmonton protocol for islet transplantation. N Engl J Med. 2006;355(13):1318-1330.. View this ...

https://www.jci.org/articles/view/87388?key=bbb2df2018c8c18d1e0b

At 3 years post-first infusion, 23% of islet-alone recipients were insulin independent (II>or=2 weeks), 29% were insulin dependent with detectable C-peptide, 26% had lost function, and 22% had missing data. (emmes.com)
Insulin is produced by specialized cells of the pancreas called islets of Langerhans. (medlineplus.gov)
The loss of insulin-producing β cells within islets results in diabetes, and islet transplantation from cadaveric donors can cure the disease. (harvard.edu)
The viability was assessed by the content of LDH, content of cAMP, glucose output, insulin output, response to ionophore A23187, and the ability to preserve islets in isosmolar solution and after freeze-thawing. (estatezone.net)
In vitro, islets responded to the drug and ionophore with a significant decrease in insulin release. (estatezone.net)
Type 1 diabetes is caused when the insulin-producing beta cells in the endocrinal part of the pancreas - the islets of Langerhans - are destroyed by an autoimmune attack. (ki.se)
For islet transplants to complete the transition from clinical research to clinical care restoration of insulin independence must be achieved-as with pancreas transplants-with a single donor. (umn.edu)
Hering, BJ 2005, ' Achieving and maintaining insulin independence in human islet transplant recipients ', Transplantation , vol. 79, no. 10, pp. 1296-1297. (umn.edu)

EPITA is established to provide a forum for those working in the field of pancreas and islet of Langerhans transplantation or any other alternative form of beta cell replacement in Europe, to exchange scientific information and views related primarily to providing the best service for patients in Europe requiring pancreas or islet transplantation. (esot.org)
His lab studies the developmental biology of the pancreas, using that information to grow and develop pancreatic cells (islets of Langerhans). (harvard.edu)

The mission of ECTORS is to provide a forum for discussing and stimulating novel developments in the fields of cellular therapies in organ transplantation, organ regeneration and generation of new organs from stem cells and biomaterials. (esot.org)
The pancreatic acinar cells degenerated and were not observed at this stage of transplantation. (uaeu.ac.ae)
The ductal system proliferated and partly differentiated into endocrine cells that subsequently formed many new islets of Langerhans as well. (uaeu.ac.ae)
The structures of P-, a-, 8-, and pancreatic polypeptide cells were found to be intact even 1.5 years after transplantation. (uaeu.ac.ae)
In addition to this, the organization of these cells inside the islets is similar to that of normal pancreatic tissue. (uaeu.ac.ae)
In vitro production of whole islets, not just β cells, will benefit from a better understanding of endocrine differentiation and islet morphogenesis. (harvard.edu)
Finally, we induce peninsula-like structures in differentiating human embryonic stem cells, laying the ground for the generation of entire islets in vitro. (harvard.edu)
Now, using an innovative transplantation technique, researchers at Karolinska Institutet and University of Miami Miller School of Medicine have been able to intervene to save the beta cells in mice by discovering early signs of the disease. (ki.se)
The infiltration of immune cells took place concurrently with the signs of autoimmunity, namely inflammation in the islets and later hyperglycaemia. (ki.se)
and/or 3) failure of islet neogenesis in the absence of an adequate mass and viability of cotransplanted/engrafted islet precursor cells. (umn.edu)
overcame many these obstacles and expanded the encapsulation field when they effectively encapsulated islets of Langerhans and various cells with poly (ethylene glycol) (PEG) in the early 1990s [ 4 , 5 , 6 ]. (biomedcentral.com)
Yet dissociation of islets into individual cells destroys cellular interactions important to islet physiology. (biomedcentral.com)
This enabled the effective modulation of two central growth control pathways resulting in the phenotypic outcome of cell cycle reentry in postmitotic islet cells. (biomedcentral.com)
The study of human islets is hindered by obstacles including difficulty of maintaining islet cells in vitro but within their native complex tissue environment, the intact islet, and difficulty modulating gene expression in a majority of islet cells without significantly damaging islet viability, function and architecture. (biomedcentral.com)
In this review, we provide an overview of the heterogeneity of islet cells during embryogenesis and differentiation as demonstrated by scRNA-seq studies on the developing and adult pancreata, with implications for the future application of regenerative medicine for diabetes. (e-dmj.org)
In addition, the presence of undesired cells, including undifferentiated cells and non-pancreatic lineage cells, can lead to tumorigenesis, which is one of the biggest safety concerns of cell transplantation. (e-dmj.org)

CONCLUSIONS: Clinical islet transplantation needs to be evaluated using the most clinically relevant endpoints such as glucose stabilization and severe hypoglycemia prevention. (emmes.com)
Our study demonstrates the possibility of using eye-transplanted islets of Langerhans as a tool for improving the development of new drugs and, in combination with the local administration of immunosuppressive drugs, as a new clinical transplantation strategy for patients with type 1 diabetes," says Professor Berggren. (ki.se)
Transient exposure to multiple siRNAs is an effective approach to modify islets for study with the potential to aid clinical applications. (biomedcentral.com)
Translational efforts towards clinical applications using intact islets could also benefit from the advances described here. (biomedcentral.com)
As transplantation of intact islets advances in clinical trials, clinical applications requiring direct modification of gene expression to improve islet survival and engraftment would likely rely on transient modifications that do not result in permanent integration of genetic constructs. (biomedcentral.com)

Cryopreserved islets of Langerhans were investigated in vitro and in vivo to detect the long-term viability, functional response, and survival after transplantation. (estatezone.net)
The PEG encapsulated islets introduced the ability of immunosuppression while maintaining cell viability and allowing selective permeability. (biomedcentral.com)

Electroporation of intact human cadaveric islets resulted in robust and specific suppression of gene expression. (biomedcentral.com)

A key problem in organ transplantation is the problem of transplant rejection, such as the body's immune response to the transplanted organ, based on the possible failure of transplantation, and the need for immediate removal of the organ from the recipient. (hermesclinics.com)
Organ transplantation raises several ethical questions, including the medical definition of death, when and how consent must be given for an organ transplant, donor consent, and whether there is monetary compensation for organs taken for transplant. (hermesclinics.com)

RESULTS: As of April 2008, the CITR registry comprised 325 adult recipients of 649 islet infusions derived from 712 donors. (emmes.com)

Guided by these early symptoms of an autoimmune reaction, the researchers were able to retard the attack on the islets with both systemic and local immunosuppression. (ki.se)

Atypical features including extracapsular, as well as parenchymal invasion, simulation of islet cell tumors, calcifications, ductal obstruction, and metastasis are suspicious for malignant degradation. (emorysurgicalfocus.com)

Contrary to the prevailing dogma, we find islet morphology and endocrine differentiation to be directly related. (harvard.edu)

While the study of cellular coatings on islets of Langerhans for diabetes treatment continues [ 7 , 8 , 9 ], improved understanding of cellular properties and coating techniques has expanded the application space for cellular coatings. (biomedcentral.com)

The present study shows that the islets of Langerhans transplanted to the anterior chamber of the eye can be important reporters of autoimmunity and the development of type 1 diabetes. (ki.se)

One monkey had an autoimmune disorder that is probably responsible for the immune rejection that occurred after transplantation. (estatezone.net)

A Peninsular Structure Coordinates Asynchronous Differentiation with Morphogenesis to Generate Pancreatic Islets. (harvard.edu)

The cumulative results of the registry confirm the inarguably positive impact of islet transplantation on metabolic control in T1 diabetes. (emmes.com)

EDTCO aims to support health care professionals to provide clinically effective programmes on organ and tissue donation, procurement and transplantation. (esot.org)
Organ and tissue transplantation can be carried out in several ways, depending on who the recipient is. (hermesclinics.com)
Approaches that improve transient targeting of gene expression in intact human islets are needed in order to effectively perturb intracellular pathways to achieve biological effects in the most relevant tissue contexts. (biomedcentral.com)

On monitoring the graft in real time before and after the development of type 1 diabetes, Professor Berggren and his colleague Dr Midhat Abdulreda at the Diabetes Research Institute, University of Miami Miller School of Medicine, found that the transplanted islets were attacked by the immune system in a way similar to those in the liver during type 1 diabetes. (ki.se)
Although isografts are similar to allografts in terms of anatomical procedures, they generally do not elicit an immune response, unlike other types of transplantation. (hermesclinics.com)

BACKGROUND: This report summarizes the primary efficacy and the safety outcomes of islet transplantation reported to the NIDDK and JDRF funded Collaborative Islet Transplant Registry (CITR), currently the most comprehensive collection of human-to-human islet transplant data. (emmes.com)
Pancreatic islet transplantation : studies on the technique and efficacy of islet isolation and transplantation. (michelvanderburg.com)

Its membership represents the expertise on liver and intestinal transplantation in Europe. (esot.org)

An active basic science community and an efficient translation of innovation into the clinic are crucial for the future of transplantation medicine. (esot.org)

We used single-cell mRNA sequencing to obtain a detailed description of pancreatic islet development. (harvard.edu)
Simultaneous targeting of RB and p53 pathway members resulted in cell cycle reentry as measured by EDU incorporation in 10% of islet nuclei. (biomedcentral.com)
By contrast, modification of islet cell gene expression in the context of intact intercellular relationships should increase the relevance of the information obtained. (biomedcentral.com)
Islet study also has inherent technical challenges shared by other cell types. (biomedcentral.com)

In the case of islet transplantation the period of ex vivo culture prior to transplantation affords an opportunity for transient delivery of siRNA to modulate gene expression in efforts to improve transplantation protocols [ 6 , 7 ]. (biomedcentral.com)

At least three genes can be effectively suppressed simultaneously in cultured intact human pancreatic islets without disruption of islet architecture or overt alterations in function. (biomedcentral.com)

We report the simultaneous suppression of multiple genes in intact adult human pancreatic islets. (biomedcentral.com)

Organs or tissues for transplantation can be taken from living bodies or cadavers. (hermesclinics.com)
It is possible to use organs removed from the body for transplantation within 24 hours after cardiac arrest or brain death. (hermesclinics.com)
Xenograft and xenotransplantation This is the name given to the transplantation of tissues and organs between two different types of organisms. (hermesclinics.com)

Other ethical issues associated with this situation include transplant tourism and, more broadly, the socio-economic conditions in which organ harvesting or transplantation can be created or considered as a solution. (hermesclinics.com)

Diabetic patients see the pancreatic islet transplantation (IT) as an idealized form of cure of the disease, and put great expectations in this treatment. (bvsalud.org)

Thus, the establishment of techniques that expand our ability to study intact islets is merited. (biomedcentral.com)

Human pancreatic islet structure poses challenges to investigations that require specific modulation of gene expression. (biomedcentral.com)

By studying transplanted islets of Langerhans in a mouse model with type 1 diabetes, the researchers found that the islets showed signs of inflammation long before other indicators of the disease appeared. (ki.se)

METHODS: CITR collects and monitors comprehensive data on allogeneic islet transplantation in North America, Europe, and Australia since 1999. (emmes.com)

The transference of pancreatic islets within an individual, between individuals of the same species, or between individuals of different species. (bvsalud.org)

Autocad Mdx 2009 Key Generator Free Download.Autodesk 3ds Max 2009 Crack Features/Overview/X-Force Activation Tool.Design Review 2009 8.36 (x86x64) Keygen Crack download pc.Limitations of cryopreserved pancreatic islets for transplantation. (estatezone.net)

Higher number of infusions, greater number of total islet equivalents infused, lower pretransplant HbA1c levels, processing centers related to the transplant center, and larger islet size are factors that favor the primary outcomes. (emmes.com)

The Young Professionals in Transplantation (YPT) is the Network for Junior Transplant professionals of ESOT, representing all young transplant clinicians and scientists who are beginning a career in transplantation and organ donation. (esot.org)

The two animals without a response to the treatment had the largest number of remaining islets. (estatezone.net)

American Journal of Transplantation. (johnshopkins.edu)

Islets of Langerhans Transplantation

Langerhans Cells

Islets of Langerhans

Liver Transplantation

Transplantation, Homologous

Kidney Transplantation

Histiocytosis, Langerhans-Cell

Bone Marrow Transplantation

Hematopoietic Stem Cell Transplantation

Heart Transplantation

Transplantation, Autologous

Lung Transplantation

Graft Survival

Stem Cell Transplantation

Transplantation Conditioning

Organ Transplantation

Graft Rejection

Pancreas Transplantation

Tissue Donors

Transplantation

Transplantation Immunology

Cell Transplantation

Transplantation Chimera

Immunosuppressive Agents

Transplantation, Isogeneic

Islet Amyloid Polypeptide

Transplantation, Heterotopic

Insulin

Graft vs Host Disease

Epidermis

Treatment Outcome

Living Donors

Cord Blood Stem Cell Transplantation

Heart-Lung Transplantation

Insulin-Secreting Cells

Time Factors

Immunosuppression

Mannose-Binding Lectins

Transplantation Tolerance

Langerhans Cell Sarcoma

Tissue and Organ Procurement

Skin

Skin Transplantation

Glucose

Retrospective Studies

Peripheral Blood Stem Cell Transplantation

Transplantation, Heterologous

Fetal Tissue Transplantation

Histocompatibility Testing

Liver Failure

Mice, Inbred C57BL

Diabetes Mellitus, Type 1

Corneal Transplantation

Postoperative Complications

Dermatitis, Contact

Antigens, CD1

Glucagon-Secreting Cells

Cells, Cultured

Pancreas

Mice, Inbred BALB C

Waiting Lists

Recurrence

Mesenchymal Stem Cell Transplantation

Diabetes Mellitus, Experimental

Tacrolimus

Histocompatibility

Cell Differentiation

Cyclosporine

Hematologic Neoplasms

Tissue Transplantation

Cadaver

Organ Preservation

Follow-Up Studies

Whole-Body Irradiation

Glucagon

Dendritic Cells

T-Lymphocytes

Insulinoma

Survival Analysis

Survival Rate