Transplantation between individuals of the same species. Usually refers to genetically disparate individuals in contradistinction to isogeneic transplantation for genetically identical individuals.
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.
Tissues, cells, or organs transplanted between genetically different individuals of the same species.
The transference of a heart 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 grafting of skin in humans or animals from one site to another to replace a lost portion of the body surface skin.
The transference of a kidney from one human or animal to another.
Transplantation of tissue typical of one area to a different recipient site. The tissue may be autologous, heterologous, or homologous.
Partial or total replacement of the CORNEA from one human or animal to another.
The grafting of bone from a donor site to a recipient site.
An induced state of non-reactivity to grafted tissue from a donor organism that would ordinarily trigger a cell-mediated or humoral immune response.
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.
Centers for acquiring, characterizing, and storing bones or bone tissue for future use.
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.
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.
Antibodies from an individual that react with ISOANTIGENS of another individual of the same species.
Individuals supplying living tissue, organs, cells, blood or blood components for transfer or transplantation to histocompatible recipients.
Antigens that exist in alternative (allelic) forms in a single species. When an isoantigen is encountered by species members who lack it, an immune response is induced. Typical isoantigens are the BLOOD GROUP ANTIGENS.
The transference of pancreatic islets within an individual, between individuals of the same species, or between individuals of different species.
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).
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.
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.
The transference of a part of or an entire liver from one human or animal to another.
The transference of either one or both of the lungs from one human or animal to another.
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.
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.
Preservation of cells, tissues, organs, or embryos by freezing. In histological preparations, cryopreservation or cryofixation is used to maintain the existing form, structure, and chemical composition of all the constituent elements of the specimens.
Organs, tissues, or cells taken from the body for grafting into another area of the same body or into another individual.
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).
The degree of antigenic similarity between the tissues of different individuals, which determines the acceptance or rejection of allografts.
Elements of limited time intervals, contributing to particular results or situations.
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 large fragment formed when COMPLEMENT C4 is cleaved by COMPLEMENT C1S. The membrane-bound C4b binds COMPLEMENT C2A, a SERINE PROTEASE, to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).
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)
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.
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.
A dead body, usually a human body.
The destroying of all forms of life, especially microorganisms, by heat, chemical, or other means.
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).
A group of antigens that includes both the major and minor histocompatibility antigens. The former are genetically determined by the major histocompatibility complex. They determine tissue type for transplantation and cause allograft rejections. The latter are systems of allelic alloantigens that can cause weak transplant rejection.
A group of closely related cyclic undecapeptides from the fungi Trichoderma polysporum and Cylindocarpon lucidum. They have some antineoplastic and antifungal action and significant immunosuppressive effects. Cyclosporins have been proposed as adjuvants in tissue and organ transplantation to suppress graft rejection.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Centers for acquiring, characterizing, and storing organs or tissue for future use.
The transference of a pancreas from one human or animal to another.
The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) TRANSPLANTATION ANTIGENS, genes which control the structure of the IMMUNE RESPONSE-ASSOCIATED ANTIGENS, HUMAN; the IMMUNE RESPONSE GENES which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
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.
A repeat operation for the same condition in the same patient due to disease progression or recurrence, or as followup to failed previous surgery.
Genetically developed small pigs for use in biomedical research. There are several strains - Yucatan miniature, Sinclair miniature, and Minnesota miniature.
An encapsulated lymphatic organ through which venous blood filters.
A membrane glycoprotein and differentiation antigen expressed on the surface of T-cells that binds to CD40 ANTIGENS on B-LYMPHOCYTES and induces their proliferation. Mutation of the gene for CD40 ligand is a cause of HYPER-IGM IMMUNODEFICIENCY SYNDROME, TYPE 1.
Procedures used to reconstruct, restore, or improve defective, damaged, or missing structures.
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)
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.
Serum containing GAMMA-GLOBULINS which are antibodies for lymphocyte ANTIGENS. It is used both as a test for HISTOCOMPATIBILITY and therapeutically in TRANSPLANTATION.
Combinations of diagnostic or therapeutic substances linked with specific immune substances such as IMMUNOGLOBULINS; MONOCLONAL ANTIBODIES; or ANTIGENS. Often the diagnostic or therapeutic substance is a radionuclide. These conjugates are useful tools for specific targeting of DRUGS and RADIOISOTOPES in the CHEMOTHERAPY and RADIOIMMUNOTHERAPY of certain cancers.
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.
A critical subpopulation of regulatory T-lymphocytes involved in MHC Class I-restricted interactions. They include both cytotoxic T-lymphocytes (T-LYMPHOCYTES, CYTOTOXIC) and CD8+ suppressor T-lymphocytes.
Disease having a short and relatively severe course.
An increased reactivity to specific antigens mediated not by antibodies but by cells.
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.
Transplant comprised of an individual's own tissue, transferred from one part of the body to another.
Transference of tissue within an individual, between individuals of the same species, or between individuals of different species.
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.
CD4-positive T cells that inhibit immunopathology or autoimmune disease in vivo. They inhibit the immune response by influencing the activity of other cell types. Regulatory T-cells include naturally occurring CD4+CD25+ cells, IL-10 secreting Tr1 cells, and Th3 cells.
The longest and largest bone of the skeleton, it is situated between the hip and the knee.
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.
General dysfunction of an organ occurring immediately following its transplantation. The term most frequently refers to renal dysfunction following KIDNEY TRANSPLANTATION.
The immune responses of a host to a graft. A specific response is GRAFT REJECTION.
Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (IMMUNOTHERAPY, ADOPTIVE).
Transference of an organ between individuals of the same species or between individuals of different species.
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.
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.
Antibodies produced by a single clone of cells.
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.
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.
Transplantation of an individual's own tissue from one site to another site.
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 transparent anterior portion of the fibrous coat of the eye consisting of five layers: stratified squamous CORNEAL EPITHELIUM; BOWMAN MEMBRANE; CORNEAL STROMA; DESCEMET MEMBRANE; and mesenchymal CORNEAL ENDOTHELIUM. It serves as the first refracting medium of the eye. It is structurally continuous with the SCLERA, avascular, receiving its nourishment by permeation through spaces between the lamellae, and is innervated by the ophthalmic division of the TRIGEMINAL NERVE via the ciliary nerves and those of the surrounding conjunctiva which together form plexuses. (Cline et al., Dictionary of Visual Science, 4th ed)
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
Partial or total replacement of all layers of a central portion of the cornea.
Single layer of large flattened cells covering the surface of the cornea.
The transfer of lymphocytes from a donor to a recipient or reinfusion to the donor.
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.
The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.
The hemispheric articular surface at the upper extremity of the thigh bone. (Stedman, 26th ed)
A graft consisting of multiple tissues, such as muscle, bone, nerve, vasculature, and skin, comprising a functional unit for reconstructive purposes.
An organism whose body contains cell populations of different genotypes as a result of the TRANSPLANTATION of donor cells after sufficient ionizing radiation to destroy the mature recipient's cells which would otherwise reject the donor cells.
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.
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.
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.
Infections resulting from the implantation of prosthetic devices. The infections may be acquired from intraoperative contamination (early) or hematogenously acquired from other sites (late).
The span of viability of a tissue or an organ.
A trisaccharide occurring in Australian manna (from Eucalyptus spp, Myrtaceae) and in cottonseed meal.
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
The transference of a complete HAND, as a composite of many tissue types, from one individual to another.
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. This also includes animals with a long history of closed colony breeding.
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.
Solutions used to store organs and minimize tissue damage, particularly while awaiting implantation.
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.
An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed)
Membrane glycoproteins consisting of an alpha subunit and a BETA 2-MICROGLOBULIN beta subunit. In humans, highly polymorphic genes on CHROMOSOME 6 encode the alpha subunits of class I antigens and play an important role in determining the serological specificity of the surface antigen. Class I antigens are found on most nucleated cells and are generally detected by their reactivity with alloantisera. These antigens are recognized during GRAFT REJECTION and restrict cell-mediated lysis of virus-infected cells.
Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.
The demonstration of the cytotoxic effect on a target cell of a lymphocyte, a mediator released by a sensitized lymphocyte, an antibody, or complement.
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.
Surgical removal of the thymus gland. (Dorland, 28th ed)
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).
A 302-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c, and C3dg (955-1303) in the presence COMPLEMENT FACTOR H. Serum proteases further degrade C3dg into C3d (1002-1303) and C3g (955-1001).
An INTEFERON-inducible CXC chemokine that is specific for the CXCR3 RECEPTOR.
The procedure of removing TISSUES, organs, or specimens from DONORS for reuse, such as TRANSPLANTATION.
The growth action of bone tissue as it assimilates surgically implanted devices or prostheses to be used as either replacement parts (e.g., hip) or as anchors (e.g., endosseous dental implants).
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.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
Injections into the lymph nodes or the lymphatic system.
The space in the eye, filled with aqueous humor, bounded anteriorly by the cornea and a small portion of the sclera and posteriorly by a small portion of the ciliary body, the iris, and that part of the crystalline lens which presents through the pupil. (Cline et al., Dictionary of Visual Science, 4th ed, p109)
Disorder occurring in the central or peripheral area of the cornea. The usual degree of transparency becomes relatively opaque.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
Non-cadaveric providers of organs for transplant to related or non-related recipients.
A transmembrane protein belonging to the tumor necrosis factor superfamily that was originally discovered on cells of the lymphoid-myeloid lineage, including activated T-LYMPHOCYTES and NATURAL KILLER CELLS. It plays an important role in immune homeostasis and cell-mediated toxicity by binding to the FAS RECEPTOR and triggering APOPTOSIS.
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
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.
Manifestations of the immune response which are mediated by antigen-sensitized T-lymphocytes via lymphokines or direct cytotoxicity. This takes place in the absence of circulating antibody or where antibody plays a subordinate role.
Liquids transforming into solids by the removal of heat.
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.
Glycoproteins found on the membrane or surface of cells.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
Immunized T-lymphocytes which can directly destroy appropriate target cells. These cytotoxic lymphocytes may be generated in vitro in mixed lymphocyte cultures (MLC), in vivo during a graft-versus-host (GVH) reaction, or after immunization with an allograft, tumor cell or virally transformed or chemically modified target cell. The lytic phenomenon is sometimes referred to as cell-mediated lympholysis (CML). These CD8-positive cells are distinct from NATURAL KILLER CELLS and NATURAL KILLER T-CELLS. There are two effector phenotypes: TC1 and TC2.
Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
A subclass of winged helix DNA-binding proteins that share homology with their founding member fork head protein, Drosophila.
Pathological processes involving the URETERS.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.
The major group of transplantation antigens in the mouse.
The aorta from the DIAPHRAGM to the bifurcation into the right and left common iliac arteries.
Allelic alloantigens often responsible for weak graft rejection in cases when (major) histocompatibility has been established by standard tests. In the mouse they are coded by more than 500 genes at up to 30 minor histocompatibility loci. The most well-known minor histocompatibility antigen in mammals is the H-Y antigen.
Death of cells in the KIDNEY CORTEX, a common final result of various renal injuries including HYPOXIA; ISCHEMIA; and drug toxicity.
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.
Pathological processes of the KIDNEY or its component tissues.
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.
Irradiation of the whole body with ionizing or non-ionizing radiation. It is applicable to humans or animals but not to microorganisms.
The second longest bone of the skeleton. It is located on the medial side of the lower leg, articulating with the FIBULA laterally, the TALUS distally, and the FEMUR proximally.
Chelating agent used for heavy metal poisoning and assay. It causes diabetes.
Immunologic techniques based on the use of: (1) enzyme-antibody conjugates; (2) enzyme-antigen conjugates; (3) antienzyme antibody followed by its homologous enzyme; or (4) enzyme-antienzyme complexes. These are used histologically for visualizing or labeling tissue specimens.
One of the protein CROSS-LINKING REAGENTS that is used as a disinfectant for sterilization of heat-sensitive equipment and as a laboratory reagent, especially as a fixative.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi.
Replacement for a hip joint.
A double-walled epithelial capsule that is the bulbous closed proximal end of the kidney tubular system. It surrounds the cluster of convoluted capillaries of KIDNEY GLOMERULUS and is continuous with the convoluted PROXIMAL KIDNEY TUBULE.
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.
An immunological attack mounted by a graft against the host because of tissue incompatibility when immunologically competent cells are transplanted to an immunologically incompetent host; the resulting clinical picture is that of GRAFT VS HOST DISEASE.
The main trunk of the systemic arteries.
An inhibitory T CELL receptor that is closely related to CD28 ANTIGEN. It has specificity for CD80 ANTIGEN and CD86 ANTIGEN and acts as a negative regulator of peripheral T cell function. CTLA-4 antigen is believed to play role in inducing PERIPHERAL TOLERANCE.
An alternative to amputation in patients with neoplasms, ischemia, fractures, and other limb-threatening conditions. Generally, sophisticated surgical procedures such as vascular surgery and reconstruction are used to salvage diseased limbs.
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.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
Malfunction of implantation shunts, valves, etc., and prosthesis loosening, migration, and breaking.
The part of the pelvis that comprises the pelvic socket where the head of FEMUR joins to form HIP JOINT (acetabulofemoral joint).
Method of tissue preparation in which the tissue specimen is frozen and then dehydrated at low temperature in a high vacuum. This method is also used for dehydrating pharmaceutical and food products.
A calcium-dependent pore-forming protein synthesized in cytolytic LYMPHOCYTES and sequestered in secretory granules. Upon immunological reaction between a cytolytic lymphocyte and a target cell, perforin is released at the plasma membrane and polymerizes into transmembrane tubules (forming pores) which lead to death of a target cell.
Acute kidney failure resulting from destruction of EPITHELIAL CELLS of the KIDNEY TUBULES. It is commonly attributed to exposure to toxic agents or renal ISCHEMIA following severe TRAUMA.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
The phenomenon of target cell destruction by immunologically active effector cells. It may be brought about directly by sensitized T-lymphocytes or by lymphoid or myeloid "killer" cells, or it may be mediated by cytotoxic antibody, cytotoxic factor released by lymphoid cells, or complement.
Specialized tissues that are components of the lymphatic system. They provide fixed locations within the body where a variety of LYMPHOCYTES can form, mature and multiply. The lymphoid tissues are connected by a network of LYMPHATIC VESSELS.
A colorless and flammable gas at room temperature and pressure. Ethylene oxide is a bactericidal, fungicidal, and sporicidal disinfectant. It is effective against most micro-organisms, including viruses. It is used as a fumigant for foodstuffs and textiles and as an agent for the gaseous sterilization of heat-labile pharmaceutical and surgical materials. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p794)
CXCR receptors that are expressed on the surface of a number of cell types, including T-LYMPHOCYTES; NK CELLS; DENDRITIC CELLS; and a subset of B-LYMPHOCYTES. The receptors are activated by CHEMOKINE CXCL9; CHEMOKINE CXCL10; and CHEMOKINE CXCL11.
The period following a surgical operation.
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 large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Serum that contains antibodies. It is obtained from an animal that has been immunized either by ANTIGEN injection or infection with microorganisms containing the antigen.
A CXC chemokine that is induced by GAMMA-INTERFERON and is chemotactic for MONOCYTES and T-LYMPHOCYTES. It has specificity for the CXCR3 RECEPTOR.
The alpha subunits of integrin heterodimers (INTEGRINS), which mediate ligand specificity. There are approximately 18 different alpha chains, exhibiting great sequence diversity; several chains are also spliced into alternative isoforms. They possess a long extracellular portion (1200 amino acids) containing a MIDAS (metal ion-dependent adhesion site) motif, and seven 60-amino acid tandem repeats, the last 4 of which form EF HAND MOTIFS. The intracellular portion is short with the exception of INTEGRIN ALPHA4.
A subdiscipline of genetics which deals with the genetic basis of the immune response (IMMUNITY).
The portion of the GASTROINTESTINAL TRACT between the PYLORUS of the STOMACH and the ILEOCECAL VALVE of the LARGE INTESTINE. It is divisible into three portions: the DUODENUM, the JEJUNUM, and the ILEUM.
Antigens expressed primarily on the membranes of living cells during sequential stages of maturation and differentiation. As immunologic markers they have high organ and tissue specificity and are useful as probes in studies of normal cell development as well as neoplastic transformation.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Cells contained in the bone marrow including fat cells (see ADIPOCYTES); STROMAL CELLS; MEGAKARYOCYTES; and the immediate precursors of most blood cells.
Forceful administration into the peritoneal cavity of liquid medication, nutrient, or other fluid through a hollow needle piercing the abdominal wall.
Emission or propagation of acoustic waves (SOUND), ELECTROMAGNETIC ENERGY waves (such as LIGHT; RADIO WAVES; GAMMA RAYS; or X-RAYS), or a stream of subatomic particles (such as ELECTRONS; NEUTRONS; PROTONS; or ALPHA PARTICLES).
Aneurysm due to growth of microorganisms in the arterial wall, or infection arising within preexisting arteriosclerotic aneurysms.
Proteins secreted from an organism which form membrane-spanning pores in target cells to destroy them. This is in contrast to PORINS and MEMBRANE TRANSPORT PROTEINS that function within the synthesizing organism and COMPLEMENT immune proteins. These pore forming cytotoxic proteins are a form of primitive cellular defense which are also found in human LYMPHOCYTES.
Fractures of the femur.
Receptors present on activated T-LYMPHOCYTES and B-LYMPHOCYTES that are specific for INTERLEUKIN-2 and play an important role in LYMPHOCYTE ACTIVATION. They are heterotrimeric proteins consisting of the INTERLEUKIN-2 RECEPTOR ALPHA SUBUNIT, the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT, and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN.
Device constructed of either synthetic or biological material that is used for the repair of injured or diseased blood vessels.
Transference of cells within an individual, between individuals of the same species, or between individuals of different species.
The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.

Homograft banking in Singapore: two years of cardiovascular tissue banking in Southeast Asia. (1/86)

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Burnei's procedure in the treatment of long bone pseudarthrosis in patients having osteogenesis imperfecta or congenital pseudarthrosis of tibia - preliminary report. (2/86)

RATIONALE: given the recalcitrant behaviour of pseudarthrosis in osteogenesis imperfecta (OI) and congenital pseudarthrosis of the tibia (CPT), there is no ideal solution to treat such challenging deformities. The reconsideration of the already known principles, by using the modern technology, may generate new treatment methods. AIM: the present paper presents the preliminary results of an original reconstruction procedure used to treat large bone defects in paediatric orthopaedics. A case series study, the surgical technique, complications and illustrative cases are presented. METHODS AND RESULTS: 3 cases of pseudarthrosis in OI and 2 cases of CPT were operated by using this technique. The principles of the method are to create an optimal osteoconductive and osteoinductive environment by using a bone autograft, bone allograft and bone graft substitutes and to provide a good stabilisation of the bones. We operated 3 patients with OI and 2 patients with CPT. Four patients had multiple previous surgeries. The follow-up period ranged from 3 to 28 months. Four of the five patients are able to ambulate independently at the moment this paper was written. DISCUSSION: we believe that the present technique could be a reliable alternative to other procedures, especially in cases of repeated failures.  (+info)

Matricellular proteins and matrix metalloproteinases mark the inflammatory and fibrotic response in human cardiac allograft rejection. (3/86)

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Aseptically processed and chemically sterilized BTB allografts for anterior cruciate ligament reconstruction: a prospective randomized study. (4/86)

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Pilot study of patient and caregiver out-of-pocket costs of allogeneic hematopoietic cell transplantation. (5/86)

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Effects of spleen status on early outcomes after hematopoietic cell transplantation. (6/86)

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Evaluation of safety and efficacy of radiation-sterilized bone allografts in reconstructive oral surgery. (7/86)

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Allografts with autogenous platelet-rich plasma for tibial defect reconstruction: a rabbit study. (8/86)

PURPOSE: To evaluate the effect of autogenous platelet-rich plasma (PRP) for fresh-frozen allografts in tibial defect reconstruction in rabbits. METHODS: 40 adult New Zealand white rabbits underwent tibial defect reconstruction with autografts (n=12), allografts without PRP (n=12), or allografts with PRP (n=12) and were observed for 12, 16, and 24 weeks (4 for each period). Tibias of the remaining 4 rabbits were used as donor allografts, and the remaining allografts were procured from recipient rabbits. A 1.5- cm cortical segment of the tibia was osteotomised, and then fixed with a 9-hole mini-compression plate and 2 cerclage wires. Allografts were stripped off the periosteum and soft tissues and medullary contents, and then stored in a freezer at -80 masculineC. All allografts were deep frozen for at least 4 weeks before transplantation. 7 ml of whole blood was drawn to prepare 1 ml of PRP. The PRP was then mixed with 1.0 ml of human thrombin to form a platelet gel. The PRP gel was then packed into the medullary canal of the allograft and applied on the cortical surface before tibial defect reconstruction. Rabbits were sacrificed at 12, 16, and 24 weeks. The specimens were assessed for bone union at host-graft junctions and for bone resorption, new bone formation, callus encasement, and viable osteocyte counts. RESULTS: There were 4 specimens in each group at each observation period. Osteoid bridging the gap at host-graft junctions was noted in all specimens in the autograft and allograft-with-PRP groups at week 12 and in the allograft-without-PRP group at week 24. Bone union in allografts without PRP was delayed. All indices for biological incorporation (resorption index, new bone formation index, callus encasement index, and viable osteocyte count) were significantly greater in the autograft than allograft-without-PRP groups, except for the resorption index at week 24, whereas the differences were not significant between the autograft and allograft-with-PRP groups. The differences between the 2 allograft groups were usually not significant, except for the resorption index. CONCLUSION: PRP-augmented allografts behaved similarly to autografts for tibial defect reconstruction in rabbits. PRP increased bone union and bone resorption.  (+info)

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.

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.

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.

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.

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.

Examples of delayed hypersensitivity reactions include contact dermatitis (a skin reaction to an allergic substance), tuberculin reactivity (a reaction to the bacteria that cause tuberculosis), and sarcoidosis (a condition characterized by inflammation in various organs, including the lungs and lymph nodes).

Delayed hypersensitivity reactions are important in the diagnosis and management of allergic disorders and other immune-related conditions. They can be detected through a variety of tests, including skin prick testing, patch testing, and blood tests. Treatment for delayed hypersensitivity reactions depends on the underlying cause and may involve medications such as antihistamines, corticosteroids, or immunosuppressants.

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.

There are several types of prosthesis-related infections, including:

1. Bacterial infections: These are the most common type of prosthesis-related infection and can occur around any type of implanted device. They are caused by bacteria that enter the body through a surgical incision or other opening.
2. Fungal infections: These types of infections are less common and typically occur in individuals who have a weakened immune system or who have been taking antibiotics for another infection.
3. Viral infections: These infections can occur around implanted devices, such as pacemakers, and are caused by viruses that enter the body through a surgical incision or other opening.
4. Parasitic infections: These types of infections are rare and occur when parasites, such as tapeworms, infect the implanted device or the surrounding tissue.

Prosthesis-related infections can cause a range of symptoms, including pain, swelling, redness, warmth, and fever. In severe cases, these infections can lead to sepsis, a potentially life-threatening condition that occurs when bacteria or other microorganisms enter the bloodstream.

Prosthesis-related infections are typically diagnosed through a combination of physical examination, imaging tests such as X-rays or CT scans, and laboratory tests to identify the type of microorganism causing the infection. Treatment typically involves antibiotics or other antimicrobial agents to eliminate the infection, and may also involve surgical removal of the infected implant.

Prevention is key in avoiding prosthesis-related infections. This includes proper wound care after surgery, keeping the surgical site clean and dry, and taking antibiotics as directed by your healthcare provider to prevent infection. Additionally, it is important to follow your healthcare provider's instructions for caring for your prosthesis, such as regularly cleaning and disinfecting the device and avoiding certain activities that may put excessive stress on the implant.

Overall, while prosthesis-related infections can be serious, prompt diagnosis and appropriate treatment can help to effectively manage these complications and prevent long-term damage or loss of function. It is important to work closely with your healthcare provider to monitor for signs of infection and take steps to prevent and manage any potential complications associated with your prosthesis.

Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.

There are many different types of fibrosis, including:

* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.

Fibrosis can be diagnosed through a variety of methods, including:

* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.

There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:

* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.

It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.

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.

Femoral neoplasms refer to abnormal growths or tumors that occur in the femur, which is the longest bone in the human body and runs from the hip joint to the knee joint. These tumors can be benign (non-cancerous) or malignant (cancerous), and their impact on the affected individual can range from minimal to severe.

Types of Femoral Neoplasms:

There are several types of femoral neoplasms, including:

1. Osteosarcoma: This is a type of primary bone cancer that originates in the femur. It is rare and tends to affect children and young adults.
2. Chondrosarcoma: This is another type of primary bone cancer that arises in the cartilage cells of the femur. It is more common than osteosarcoma and affects mostly older adults.
3. Ewing's Sarcoma: This is a rare type of bone cancer that can occur in any bone, including the femur. It typically affects children and young adults.
4. Giant Cell Tumor: This is a benign tumor that occurs in the bones, including the femur. While it is not cancerous, it can cause significant symptoms and may require surgical treatment.

Symptoms of Femoral Neoplasms:

The symptoms of femoral neoplasms can vary depending on the type and location of the tumor. Common symptoms include:

1. Pain: Patients with femoral neoplasms may experience pain in the affected leg, which can be worse with activity or weight-bearing.
2. Swelling: The affected limb may become swollen due to fluid accumulation or the growth of the tumor.
3. Limited mobility: Patients may experience limited mobility or stiffness in the affected joint due to pain or swelling.
4. Fracture: In some cases, femoral neoplasms can cause a fracture or weakening of the bone, which can lead to further complications.

Diagnosis and Treatment of Femoral Neoplasms:

The diagnosis of femoral neoplasms typically involves a combination of imaging studies and biopsy. Imaging studies, such as X-rays, CT scans, or MRI scans, can help identify the location and extent of the tumor. A biopsy may be performed to confirm the diagnosis and determine the type of tumor.

Treatment for femoral neoplasms depends on the type and location of the tumor, as well as the patient's age and overall health. Treatment options may include:

1. Observation: Small, benign tumors may not require immediate treatment and can be monitored with regular imaging studies to ensure that they do not grow or change over time.
2. Surgery: Many femoral neoplasms can be treated with surgery to remove the tumor and any affected bone tissue. In some cases, this may involve removing a portion of the femur or replacing it with a prosthetic implant.
3. Radiation therapy: This may be used in combination with surgery to treat more aggressive tumors or those that have spread to other areas of the body.
4. Chemotherapy: This may also be used in combination with surgery and radiation therapy to treat more aggressive tumors or those that have spread to other areas of the body.
5. Targeted therapy: This is a type of chemotherapy that targets specific molecules involved in the growth and progression of the tumor. Examples include denintuzumab mafodotin, which targets a protein called B-cell CD19, and olaratumab, which targets a protein called platelet-derived growth factor receptor alpha (PDGFR-alpha).
6. Immunotherapy: This is a type of treatment that uses the body's own immune system to fight cancer. Examples include pembrolizumab and nivolumab, which are checkpoint inhibitors that work by blocking proteins on T cells that prevent them from attacking cancer cells.

The prognosis for patients with femoral neoplasms depends on the type and location of the tumor, as well as the patient's age and overall health. In general, the prognosis is better for patients with benign tumors than those with malignant ones. However, even for patients with malignant tumors, there are many treatment options available, and the prognosis can vary depending on the specifics of the case.

It's important to note that these are general treatment options and the best course of treatment will depend on the specifics of each individual case. Patients should discuss their diagnosis and treatment options with their healthcare provider to determine the most appropriate course of action for their specific situation.

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.

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.

Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.

There are several types of arteriosclerosis, including:

1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.

Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.

1. Ureteral stones: Small, hard mineral deposits that form in the ureters and can cause pain, bleeding, and blockage of urine flow.
2. Ureteral tumors: Abnormal growths that can be benign or cancerous and can cause symptoms such as blood in the urine, pain, and difficulty urinating.
3. Ureteral strictures: Narrowing of the ureters due to scarring or inflammation, which can cause pain and blockage of urine flow.
4. Ureteral injuries: Trauma to the ureters during surgery or other medical procedures can cause damage and lead to ureteral diseases.
5. Ureteral ectopia: A rare condition in which the ureters do not properly connect to the bladder, leading to urine leakage and other symptoms.
6. Ureteral tuberculosis: A type of bacterial infection that affects the ureters and can cause symptoms such as fever, weight loss, and blood in the urine.
7. Ureteral cancer: Cancer that affects the ureters and can cause symptoms such as blood in the urine, pain, and difficulty urinating.
8. Ureteral calculus: A small, hard deposit that forms in the ureters and can cause pain, bleeding, and blockage of urine flow.
9. Ureteral stenosis: A narrowing of the ureters due to scarring or inflammation, which can cause pain and blockage of urine flow.
10. Ureteral obstruction: A blockage of the ureters that can be caused by a variety of factors, such as tumors, stones, or inflammation.

Ureteral diseases can be diagnosed through a combination of physical examination, imaging studies such as X-rays and CT scans, and endoscopic procedures such as ureteroscopy. Treatment options vary depending on the specific condition and may include antibiotics, surgery, or other interventions to address the underlying cause of the disease. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can help prevent complications and improve outcomes.

Kidney cortex necrosis is a condition where there is death of the cells in the outer layer of the kidney, known as the renal cortex. This can occur due to various reasons such as injury, infection, or inflammation. The symptoms of kidney cortex necrosis may include fever, pain in the flank or abdomen, nausea, vomiting, and blood in the urine.

Diagnosis is typically made through a combination of imaging studies such as CT scans or ultrasound, and laboratory tests to evaluate kidney function. Treatment may involve supportive care to manage symptoms and address any underlying causes, as well as medications to help protect the remaining healthy kidney tissue. In severe cases, dialysis or a kidney transplant may be necessary.

Kidney cortex necrosis can be acute or chronic, and the prognosis depends on the underlying cause and the extent of the damage. Prompt medical attention is essential to prevent further damage and improve outcomes.

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.

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.

It is important to identify and address prosthesis failure early to prevent further complications and restore the functionality of the device. This may involve repairing or replacing the device, modifying the design, or changing the materials used in its construction. In some cases, surgical intervention may be necessary to correct issues related to the implantation of the prosthetic device.

Prosthesis failure can occur in various types of prosthetic devices, including joint replacements, dental implants, and orthotic devices. The causes of prosthesis failure can range from manufacturing defects to user error or improper maintenance. It is essential to have a comprehensive understanding of the factors contributing to prosthesis failure to develop effective solutions and improve patient outcomes.

In conclusion, prosthesis failure is a common issue that can significantly impact the quality of life of individuals who rely on prosthetic devices. Early identification and addressing of prosthesis failure are crucial to prevent further complications and restore functionality. A comprehensive understanding of the causes of prosthesis failure is necessary to develop effective solutions and improve patient outcomes.

In this answer, we will explore the definition of 'Kidney Tubular Necrosis, Acute' in more detail, including its causes, symptoms, diagnosis, and treatment options.

What is Kidney Tubular Necrosis, Acute?
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Kidney Tubular Necrosis, Acute (ATN) is a condition that affects the tubules of the kidneys, leading to inflammation and damage. The condition is often caused by various factors such as sepsis, shock, toxins, or medications.

The term "acute" refers to the sudden and severe nature of the condition, which can progress rapidly within hours or days. The condition can be life-threatening if left untreated, and it is important to seek medical attention immediately if symptoms persist or worsen over time.

Causes of Kidney Tubular Necrosis, Acute
--------------------------------------

There are various factors that can cause Kidney Tubular Necrosis, Acute, including:

### 1. Sepsis

Sepsis is a systemic inflammatory response to an infection, which can lead to damage to the tubules of the kidneys.

### 2. Shock

Shock can cause a decrease in blood flow to the kidneys, leading to damage and inflammation.

### 3. Toxins

Exposure to certain toxins, such as heavy metals or certain medications, can damage the tubules of the kidneys.

### 4. Medications

Certain medications, such as antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs), can cause damage to the tubules of the kidneys.

### 5. Infection

Infections such as pyelonephritis or perinephric abscess can spread to the kidneys and cause inflammation and damage to the tubules.

### 6. Radiation necrosis

Radiation therapy can cause damage to the kidneys, leading to inflammation and scarring.

### 7. Kidney transplant rejection

Rejection of a kidney transplant can lead to inflammation and damage to the tubules of the transplanted kidney.

Symptoms of Kidney Tubular Necrosis, Acute
------------------------------------------

The symptoms of acute tubular necrosis can vary depending on the severity of the condition and the underlying cause. Some common symptoms include:

### 1. Fatigue

Fatigue is a common symptom of acute tubular necrosis, as the condition can lead to a decrease in the kidneys' ability to filter waste products from the blood.

### 2. Nausea and vomiting

Nausea and vomiting can occur due to electrolyte imbalances and changes in fluid levels in the body.

### 3. Decreased urine output

Acute tubular necrosis can cause a decrease in urine production, as the damaged tubules are unable to filter waste products from the blood effectively.

### 4. Swelling (edema)

Swelling in the legs, ankles, and feet can occur due to fluid buildup in the body.

### 5. Abdominal pain

Abdominal pain can be a symptom of acute tubular necrosis, as the condition can cause inflammation and scarring in the kidneys.

### 6. Fever

Fever can occur due to infection or inflammation in the kidneys.

### 7. Blood in urine (hematuria)

Hematuria, or blood in the urine, can be a symptom of acute tubular necrosis, as the damaged tubules can leak blood into the urine.

## Causes and risk factors

The exact cause of acute tubular necrosis is not fully understood, but it is believed to be due to damage to the kidney tubules, which can occur for a variety of reasons. Some possible causes and risk factors include:

1. Sepsis: Bacterial infections can spread to the kidneys and cause inflammation and damage to the tubules.
2. Toxins: Exposure to certain toxins, such as heavy metals or certain medications, can damage the kidney tubules.
3. Medications: Certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics, can cause kidney damage and increase the risk of acute tubular necrosis.
4. Hypotension: Low blood pressure can reduce blood flow to the kidneys and increase the risk of acute tubular necrosis.
5. Shock: Severe shock can lead to damage to the kidney tubules.
6. Burns: Severe burns can cause damage to the kidneys and increase the risk of acute tubular necrosis.
7. Trauma: Traumatic injuries, such as those caused by car accidents or falls, can damage the kidneys and increase the risk of acute tubular necrosis.
8. Surgery: Major surgery can cause damage to the kidneys and increase the risk of acute tubular necrosis.
9. Kidney disease: People with pre-existing kidney disease are at increased risk of developing acute tubular necrosis.
10. Chronic conditions: Certain chronic conditions, such as diabetes and high blood pressure, can increase the risk of developing acute tubular necrosis.

It is important to note that acute tubular necrosis can occur in people with no underlying medical conditions or risk factors, and it is often a diagnosis of exclusion, meaning that other potential causes of the person's symptoms must be ruled out before the diagnosis can be made.

Infection in an aneurysm can occur through bacteria entering the bloodstream and traveling to the site of the aneurysm. This can happen during surgery or other medical procedures, or as a result of a skin infection or other illness. Once the bacteria have entered the aneurysm, they can cause inflammation and potentially destroy the blood vessel wall, leading to further complications.

Symptoms of an infected aneurysm may include fever, chills, weakness, and pain in the affected limb or organ. Treatment typically involves antibiotics to clear the infection and repair or replace the damaged blood vessel. In severe cases, surgery may be necessary to remove the infected tissue and prevent further complications.

Early detection and treatment of an infected aneurysm are important to prevent serious complications and improve outcomes for patients.

The symptoms of a femoral fracture may include:

* Severe pain in the thigh or groin area
* Swelling and bruising around the affected area
* Difficulty moving or straightening the leg
* A visible deformity or bone protrusion

Femoral fractures are typically diagnosed through X-rays, CT scans, or MRIs. Treatment for these types of fractures may involve immobilization with a cast or brace, surgery to realign and stabilize the bone, or in some cases, surgical plate and screws or rods may be used to hold the bone in place as it heals.

In addition to surgical intervention, patients may also require physical therapy to regain strength and mobility in the affected leg after a femoral fracture.

Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.

There are several types of necrosis, including:

1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.

The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.

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.

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.

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.

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.

There are several types of fistulas, including:

1. Anal fistula: a connection between the anus and the skin around it, usually caused by an abscess or infection.
2. Rectovaginal fistula: a connection between the rectum and the vagina, often seen in women who have had radiation therapy for cancer.
3. Vesicovaginal fistula: a connection between the bladder and the vagina, often caused by obstetric injuries or surgery.
4. Enterocutaneous fistula: a connection between the intestine and the skin, often seen in patients with inflammatory bowel disease or cancer.
5. Fistula-in-ano: a connection between the rectum and the skin around the anus, often caused by chronic constipation or previous surgery.

Symptoms of fistulas can include pain, bleeding, discharge, and difficulty controlling bowel movements. Treatment depends on the type and location of the fistula, but may include antibiotics, surgery, or other interventional procedures.

CNV can cause vision loss and blindness if left untreated. It can also increase the risk of complications such as cataracts, glaucoma, and corneal ulcers.

There are several treatment options for CNV, including:

1. Anti-vascular endothelial growth factor (VEGF) injections: These medications can help reduce the growth of new blood vessels and preserve vision.
2. Photodynamic therapy: This involves the use of a light-sensitive medication and low-intensity laser to damage and shrink the new blood vessels.
3. Corneal transplantation: In severe cases, a corneal transplant may be necessary to replace the damaged or diseased cornea with a healthy one.
4. Surgical removal of the neovascularized tissue: This can be done through a surgical procedure called vitrectomy, where the new blood vessels are removed and the eye is filled with a gas or oil bubble.

Early detection and treatment of CNV are crucial to prevent vision loss and improve outcomes. Ophthalmologists use a range of diagnostic tests such as imaging studies and visual acuity assessments to diagnose and monitor the progression of the condition.

The term "segmental" refers to the fact that the scarring or hardening occurs in a specific segment of the glomerulus. Focal segmental glomerulosclerosis can be caused by a variety of factors, including diabetes, high blood pressure, and certain infections or injuries.

Symptoms of focal segmental glomerulosclerosis may include proteinuria (excess protein in the urine), hematuria (blood in the urine), and decreased kidney function. Treatment options vary depending on the underlying cause, but may include medications to control high blood pressure or diabetes, as well as immunosuppressive drugs in cases where the condition is caused by an autoimmune disorder. In severe cases, dialysis or kidney transplantation may be necessary.

1. Keratoconus: This is a progressive thinning of the cornea that can cause it to bulge into a cone-like shape, leading to blurred vision and sensitivity to light.
2. Fuchs' dystrophy: This is a condition in which the cells in the innermost layer of the cornea become damaged, leading to clouding and blurred vision.
3. Bullous keratopathy: This is a condition in which there is a large, fluid-filled bubble on the surface of the cornea, which can cause blurred vision and discomfort.
4. Corneal ulcers: These are open sores on the surface of the cornea that can be caused by infection or other conditions.
5. Dry eye syndrome: This is a condition in which the eyes do not produce enough tears, leading to dryness, irritation, and blurred vision.
6. Corneal abrasions: These are scratches on the surface of the cornea that can be caused by injury or other conditions.
7. Trachoma: This is an infectious eye disease that can cause scarring and blindness if left untreated.
8. Ocular herpes: This is a viral infection that can cause blisters on the surface of the cornea and lead to scarring and vision loss if left untreated.
9. Endophthalmitis: This is an inflammation of the inner layer of the eye that can be caused by bacterial or fungal infections, and can lead to severe vision loss if left untreated.
10. Corneal neovascularization: This is the growth of new blood vessels into the cornea, which can be a complication of other conditions such as dry eye syndrome or ocular trauma.

These are just a few examples of the many different types of corneal diseases that can affect the eyes. It's important to seek medical attention if you experience any symptoms such as pain, redness, or blurred vision in one or both eyes. Early diagnosis and treatment can help prevent complications and preserve vision.

Some common types of bone neoplasms include:

* Osteochondromas: These are benign tumors that grow on the surface of a bone.
* Giant cell tumors: These are benign tumors that can occur in any bone of the body.
* Chondromyxoid fibromas: These are rare, benign tumors that develop in the cartilage of a bone.
* Ewing's sarcoma: This is a malignant tumor that usually occurs in the long bones of the arms and legs.
* Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow.

Symptoms of bone neoplasms can include pain, swelling, or deformity of the affected bone, as well as weakness or fatigue. Treatment options depend on the type and location of the tumor, as well as the severity of the symptoms. Treatment may involve surgery, radiation therapy, chemotherapy, or a combination of these.

1. Aneurysms: A bulge or ballooning in the wall of the aorta that can lead to rupture and life-threatening bleeding.
2. Atherosclerosis: The buildup of plaque in the inner lining of the aorta, which can narrow the artery and restrict blood flow.
3. Dissections: A tear in the inner layer of the aortic wall that can cause bleeding and lead to an aneurysm.
4. Thoracic aortic disease: Conditions that affect the thoracic portion of the aorta, such as atherosclerosis or dissections.
5. Abdominal aortic aneurysms: Enlargement of the abdominal aorta that can lead to rupture and life-threatening bleeding.
6. Aortic stenosis: Narrowing of the aortic valve, which can impede blood flow from the heart into the aorta.
7. Aortic regurgitation: Backflow of blood from the aorta into the heart due to a faulty aortic valve.
8. Marfan syndrome: A genetic disorder that affects the body's connective tissue, including the aorta.
9. Ehlers-Danlos syndrome: A group of genetic disorders that affect the body's connective tissue, including the aorta.
10. Turner syndrome: A genetic disorder that affects females and can cause aortic diseases.

Aortic diseases can be diagnosed through imaging tests such as ultrasound, CT scan, or MRI. Treatment options vary depending on the specific condition and may include medication, surgery, or endovascular procedures.

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.

The exact cause of OD is not fully understood, but it is thought to be due to a combination of genetic and environmental factors. It can occur as a result of repetitive trauma or injury to the joint, such as from sports or other physical activities, or it may develop gradually over time without any specific incident.

Symptoms of OD can include:

* Pain in the affected joint, which may be exacerbated by activity or movement
* Swelling and stiffness in the joint
* Limited range of motion in the joint
* A popping or snapping sensation in the joint

To diagnose OD, a healthcare provider will typically perform a physical examination of the affected joint and order imaging tests, such as X-rays or an MRI, to confirm the presence of the condition. Treatment for OD depends on the severity of the condition and may include:

* Rest and avoidance of activities that exacerbate the condition
* Physical therapy to improve joint mobility and strength
* Medications such as pain relievers or anti-inflammatory drugs to manage symptoms
* Surgery in more severe cases to repair or remove the damaged cartilage and bone.

The term "intestinal fistula" encompasses several different types of fistulas that can occur in the gastrointestinal tract, including:

1. Enterocutaneous fistula: This type of fistula occurs between the intestine and the skin, typically on the abdominal wall.
2. Enteroenteric fistula: This type of fistula occurs between two segments of the intestine.
3. Enterofistulous intestinal tract: This type of fistula occurs when a segment of the intestine is replaced by a fistula.
4. Fecal fistula: This type of fistula occurs between the rectum and the skin, typically on the perineum.

The causes of intestinal fistulas are varied and can include:

1. Inflammatory bowel disease (IBD): Both Crohn's disease and ulcerative colitis can lead to the development of intestinal fistulas.
2. Diverticulitis: This condition can cause a fistula to form between the diverticula and the surrounding tissues.
3. Infection: Bacterial or parasitic infections can cause the formation of fistulas in the intestine.
4. Radiation therapy: This can damage the intestinal tissue and lead to the formation of a fistula.
5. Trauma: Blunt or penetrating trauma to the abdomen can cause a fistula to form between the intestine and surrounding tissues.
6. Cancer: Malignancies in the intestine or surrounding tissues can erode through the bowel wall and form a fistula.
7. Rare genetic conditions: Certain inherited conditions, such as familial polyposis syndrome, can increase the risk of developing intestinal fistulas.
8. Other medical conditions: Certain medical conditions, such as tuberculosis or syphilis, can also cause intestinal fistulas.

The symptoms of intestinal fistulas can vary depending on the location and severity of the fistula. Common symptoms include:

1. Abdominal pain
2. Diarrhea
3. Rectal bleeding
4. Infection (fever, chills, etc.)
5. Weakness and fatigue
6. Abdominal distension
7. Loss of appetite
8. Nausea and vomiting

The diagnosis of an intestinal fistula is typically made through a combination of physical examination, medical history, and diagnostic tests such as:

1. Imaging studies (X-rays, CT scans, MRI scans) to visualize the fistula and surrounding tissues.
2. Endoscopy to examine the inside of the intestine and identify any damage or abnormalities.
3. Biopsy to obtain a tissue sample for further examination.
4. Blood tests to check for signs of infection or inflammation.

Treatment of an intestinal fistula depends on the underlying cause and the severity of the condition. Treatment options may include:

1. Antibiotics to treat any underlying infections.
2. Surgery to repair the fistula and remove any damaged tissue.
3. Nutritional support to help the body heal and recover.
4. Management of any underlying medical conditions, such as diabetes or Crohn's disease.
5. Supportive care to manage symptoms such as pain, nausea, and vomiting.

The prognosis for intestinal fistulas varies depending on the underlying cause and the severity of the condition. In general, with prompt and appropriate treatment, many people with intestinal fistulas can experience a good outcome and recover fully. However, in some cases, complications such as infection or bleeding may occur, and the condition may be challenging to treat.

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 types of ischemia, including:

1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.

Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.

Also known as nonunion or malunion.

Note: This term is not intended to be used as a substitute for proper medical advice. Do you have a specific question about your condition? Please ask your healthcare provider for more information.

1. Atherosclerosis: A condition in which plaque builds up inside the arteries, causing them to narrow and harden. This can lead to heart disease, heart attack, or stroke.
2. Hypertension: High blood pressure that can damage blood vessels and increase the risk of heart disease, stroke, and other conditions.
3. Peripheral artery disease (PAD): A condition in which the blood vessels in the legs and arms become narrowed or blocked, leading to pain, cramping, and weakness in the affected limbs.
4. Raynaud's phenomenon: A condition that causes blood vessels in the hands and feet to constrict in response to cold temperatures or stress, leading to discoloration, numbness, and tissue damage.
5. Deep vein thrombosis (DVT): A condition in which a blood clot forms in the deep veins of the legs, often caused by immobility or injury.
6. Varicose veins: Enlarged, twisted veins that can cause pain, swelling, and cosmetic concerns.
7. Angioplasty: A medical procedure in which a balloon is used to open up narrowed blood vessels, often performed to treat peripheral artery disease or blockages in the legs.
8. Stenting: A medical procedure in which a small mesh tube is placed inside a blood vessel to keep it open and improve blood flow.
9. Carotid endarterectomy: A surgical procedure to remove plaque from the carotid arteries, which supply blood to the brain, to reduce the risk of stroke.
10. Bypass surgery: A surgical procedure in which a healthy blood vessel is used to bypass a blocked or narrowed blood vessel, often performed to treat coronary artery disease or peripheral artery disease.

Overall, vascular diseases can have a significant impact on quality of life and can increase the risk of serious complications such as stroke, heart attack, and amputation. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can help to prevent long-term damage and improve 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.

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.

Arteritis can lead to a range of symptoms including fever, fatigue, joint pain, skin rashes, and difficulty speaking or swallowing. In severe cases, it can also cause cardiovascular complications such as heart attack, stroke, or organ failure.

There are several types of arteritis, each with different causes and symptoms. Some common forms of arteritis include:

1. Giant cell arteritis (GCA): This is the most common form of arteritis and primarily affects older adults. It is caused by inflammation of the medium-sized arteries, particularly those in the head and neck. Symptoms may include headaches, vision loss, and pain in the face and jaw.
2. Takayasu arteritis (TA): This is a rare form of arteritis that affects the aorta and its branches. It is more common in women than men and typically affects young adults. Symptoms may include high blood pressure, chest pain, and weakness or numbness in the limbs.
3. Polyarteritis nodosa (PAN): This is a rare form of arteritis that affects multiple arteries throughout the body. It can cause symptoms such as fever, fatigue, joint pain, and skin rashes.
4. Kawasaki disease: This is a rare inflammatory disease that primarily affects children under the age of 5. It causes inflammation in the blood vessels, particularly those in the heart and can lead to cardiovascular complications if left untreated.

Arteritis can be diagnosed through various tests such as blood tests, imaging studies like CT or MRI scans, and biopsies. Treatment options vary depending on the type of arteritis and its severity but may include corticosteroids, immunosuppressive medications, and antibiotics. Early diagnosis and treatment are crucial to prevent long-term damage and improve outcomes.

Surgical wound infections can be caused by a variety of factors, including:

1. Poor surgical technique: If the surgeon does not follow proper surgical techniques, such as properly cleaning and closing the incision, the risk of infection increases.
2. Contamination of the wound site: If the wound site is contaminated with bacteria or other microorganisms during the surgery, this can lead to an infection.
3. Use of contaminated instruments: If the instruments used during the surgery are contaminated with bacteria or other microorganisms, this can also lead to an infection.
4. Poor post-operative care: If the patient does not receive proper post-operative care, such as timely changing of dressings and adequate pain management, the risk of infection increases.

There are several types of surgical wound infections, including:

1. Superficial wound infections: These infections occur only in the skin and subcutaneous tissues and can be treated with antibiotics.
2. Deep wound infections: These infections occur in the deeper tissues, such as muscle or bone, and can be more difficult to treat.
3. Wound hernias: These occur when the intestine bulges through the incision site, creating a hernia.
4. Abscesses: These occur when pus collects in the wound site, creating a pocket of infection.

Surgical wound infections can be diagnosed using a variety of tests, including:

1. Cultures: These are used to identify the type of bacteria or other microorganisms causing the infection.
2. Imaging studies: These can help to determine the extent of the infection and whether it has spread to other areas of the body.
3. Physical examination: The surgeon will typically perform a physical examination of the wound site to look for signs of infection, such as redness, swelling, or drainage.

Treatment of surgical wound infections typically involves a combination of antibiotics and wound care. In some cases, additional surgery may be necessary to remove infected tissue or repair damaged structures.

Prevention is key when it comes to surgical wound infections. To reduce the risk of infection, surgeons and healthcare providers can take several steps, including:

1. Proper sterilization and disinfection of equipment and the surgical site.
2. Use of antibiotic prophylaxis, which is the use of antibiotics to prevent infections in high-risk patients.
3. Closure of the incision site with sutures or staples to reduce the risk of bacterial entry.
4. Monitoring for signs of infection and prompt treatment if an infection develops.
5. Proper wound care, including keeping the wound clean and dry, and changing dressings as needed.
6. Avoiding unnecessary delays in surgical procedure, which can increase the risk of infection.
7. Proper patient education on wound care and signs of infection.
8. Use of biological dressings such as antimicrobial impregnated dressings, which can help reduce the risk of infection.
9. Use of negative pressure wound therapy (NPWT) which can help to promote wound healing and reduce the risk of infection.
10. Proper handling and disposal of sharps and other medical waste to reduce the risk of infection.

It is important for patients to follow their healthcare provider's instructions for wound care and to seek medical attention if they notice any signs of infection, such as redness, swelling, or increased pain. By taking these precautions, the risk of surgical wound infections can be significantly reduced, leading to better outcomes for patients.

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.

1. Types of Polyomaviruses: There are several types of polyomaviruses that can infect humans, including the common cold virus (Rhinovirus), respiratory syncytial virus (RSV), human metapneumovirus (HMPV), and the newly identified Parechovirus.
2. Infection: Polyomaviruses can be transmitted through contact with an infected person's respiratory secretions, such as mucus and saliva, or through contaminated surfaces. Inhaling the virus can lead to an infection in the respiratory tract.
3. Symptoms: The symptoms of polyomavirus infections can vary depending on the type of virus and the individual's age and overall health. Common symptoms include runny nose, cough, fever, sore throat, headache, and fatigue. In severe cases, polyomaviruses can cause pneumonia, bronchiolitis, and other respiratory disorders.
4. Diagnosis: A diagnosis of a polyomavirus infection is typically made based on the symptoms and medical history of the individual, as well as through laboratory tests such as PCR (polymerase chain reaction) or viral culture.
5. Treatment: There is no specific treatment for polyomavirus infections, but antiviral medications may be prescribed to help manage symptoms and prevent complications. Supportive care, such as rest, hydration, and over-the-counter pain relievers, may also be recommended.
6. Prevention: Preventing the spread of polyomaviruses can be challenging, but good hygiene practices such as frequent handwashing, avoiding close contact with people who are sick, and disinfecting surfaces can help reduce the risk of transmission. Vaccines are also being developed to protect against certain types of polyomaviruses.
7. Prognosis: In most cases, polyomavirus infections are mild and self-limiting, with symptoms resolving on their own within a few days to a week. However, severe infections can be life-threatening, particularly in individuals with weakened immune systems or underlying medical conditions.
8. Epidemiology: Polyomaviruses are common and widespread, with the majority of individuals worldwide being infected at some point in their lives. Outbreaks of polyomavirus infections can occur in settings such as hospitals, long-term care facilities, and daycare centers, where individuals with weakened immune systems are more susceptible to infection.
9. Research: Research on polyomaviruses is ongoing to better understand the viruses, their transmission, and their clinical impact. This includes development of vaccines and antiviral medications, as well as studies to identify risk factors for severe infections and to improve diagnostic tests.
10. Public health: Polyomaviruses are a public health concern, particularly in settings where individuals with weakened immune systems are more susceptible to infection. Prevention strategies include practicing good hygiene, such as frequent handwashing, and avoiding close contact with individuals who are sick.

Overall, polyomaviruses are a diverse group of viruses that can cause a range of diseases, from mild and self-limiting to severe and life-threatening. Understanding the clinical features, diagnosis, treatment, prognosis, epidemiology, research, and public health implications of polyomavirus infections is essential for providing appropriate care and preventing outbreaks.

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.

There are several types of joint instability, including:

1. Ligamentous laxity: A condition where the ligaments surrounding a joint become stretched or torn, leading to instability.
2. Capsular laxity: A condition where the capsule, a thin layer of connective tissue that surrounds a joint, becomes stretched or torn, leading to instability.
3. Muscular imbalance: A condition where the muscles surrounding a joint are either too weak or too strong, leading to instability.
4. Osteochondral defects: A condition where there is damage to the cartilage and bone within a joint, leading to instability.
5. Post-traumatic instability: A condition that develops after a traumatic injury to a joint, such as a dislocation or fracture.

Joint instability can be caused by various factors, including:

1. Trauma: A sudden and forceful injury to a joint, such as a fall or a blow.
2. Overuse: Repeated stress on a joint, such as from repetitive motion or sports activities.
3. Genetics: Some people may be born with joint instability due to inherited genetic factors.
4. Aging: As we age, our joints can become less stable due to wear and tear on the cartilage and other tissues.
5. Disease: Certain diseases, such as rheumatoid arthritis or osteoarthritis, can cause joint instability.

Symptoms of joint instability may include:

1. Pain: A sharp, aching pain in the affected joint, especially with movement.
2. Stiffness: Limited range of motion and stiffness in the affected joint.
3. Swelling: Swelling and inflammation in the affected joint.
4. Instability: A feeling of looseness or instability in the affected joint.
5. Crepitus: Grinding or crunching sensations in the affected joint.

Treatment for joint instability depends on the underlying cause and may include:

1. Rest and ice: Resting the affected joint and applying ice to reduce pain and swelling.
2. Physical therapy: Strengthening the surrounding muscles to support the joint and improve stability.
3. Bracing: Using a brace or splint to provide support and stability to the affected joint.
4. Medications: Anti-inflammatory medications, such as ibuprofen or naproxen, to reduce pain and inflammation.
5. Surgery: In severe cases, surgery may be necessary to repair or reconstruct the damaged tissues and improve joint stability.

There are different types of hyperplasia, depending on the location and cause of the condition. Some examples include:

1. Benign hyperplasia: This type of hyperplasia is non-cancerous and does not spread to other parts of the body. It can occur in various tissues and organs, such as the uterus (fibroids), breast tissue (fibrocystic changes), or prostate gland (benign prostatic hyperplasia).
2. Malignant hyperplasia: This type of hyperplasia is cancerous and can invade nearby tissues and organs, leading to serious health problems. Examples include skin cancer, breast cancer, and colon cancer.
3. Hyperplastic polyps: These are abnormal growths that occur in the gastrointestinal tract and can be precancerous.
4. Adenomatous hyperplasia: This type of hyperplasia is characterized by an increase in the number of glandular cells in a specific organ, such as the colon or breast. It can be a precursor to cancer.

The symptoms of hyperplasia depend on the location and severity of the condition. In general, they may include:

* Enlargement or swelling of the affected tissue or organ
* Pain or discomfort in the affected area
* Abnormal bleeding or discharge
* Changes in bowel or bladder habits
* Unexplained weight loss or gain

Hyperplasia is diagnosed through a combination of physical examination, imaging tests such as ultrasound or MRI, and biopsy. Treatment options depend on the underlying cause and severity of the condition, and may include medication, surgery, or other interventions.

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.

Graft occlusion can occur due to a variety of factors, including:

1. Blood clots forming within the graft
2. Inflammation or infection within the graft
3. Narrowing or stenosis of the graft
4. Disruption of the graft material
5. Poor blood flow through the graft

The signs and symptoms of vascular graft occlusion can vary depending on the location and severity of the blockage. They may include:

1. Pain or tenderness in the affected limb
2. Swelling or redness in the affected limb
3. Weakness or numbness in the affected limb
4. Difficulty walking or moving the affected limb
5. Coolness or discoloration of the skin in the affected limb

If you experience any of these symptoms, it is important to seek medical attention as soon as possible. A healthcare professional can diagnose vascular graft occlusion using imaging tests such as ultrasound, angiography, or MRI. Treatment options for vascular graft occlusion may include:

1. Medications to dissolve blood clots or reduce inflammation
2. Surgical intervention to repair or replace the graft
3. Balloon angioplasty or stenting to open up the blocked graft
4. Hyperbaric oxygen therapy to improve blood flow and promote healing.

Preventive measures to reduce the risk of vascular graft occlusion include:

1. Proper wound care and infection prevention after surgery
2. Regular follow-up appointments with your healthcare provider
3. Avoiding smoking and other cardiovascular risk factors
4. Taking medications as directed by your healthcare provider to prevent blood clots and inflammation.

It is important to note that vascular graft occlusion can be a serious complication after surgery, but with prompt medical attention and appropriate treatment, the outcome can be improved.

There are several factors that can contribute to bone resorption, including:

1. Hormonal changes: Hormones such as parathyroid hormone (PTH) and calcitonin can regulate bone resorption. Imbalances in these hormones can lead to excessive bone resorption.
2. Aging: As we age, our bones undergo remodeling more frequently, leading to increased bone resorption.
3. Nutrient deficiencies: Deficiencies in calcium, vitamin D, and other nutrients can impair bone health and lead to excessive bone resorption.
4. Inflammation: Chronic inflammation can increase bone resorption, leading to bone loss and weakening.
5. Genetics: Some genetic disorders can affect bone metabolism and lead to abnormal bone resorption.
6. Medications: Certain medications, such as glucocorticoids and anticonvulsants, can increase bone resorption.
7. Diseases: Conditions such as osteoporosis, Paget's disease of bone, and bone cancer can lead to abnormal bone resorption.

Bone resorption can be diagnosed through a range of tests, including:

1. Bone mineral density (BMD) testing: This test measures the density of bone in specific areas of the body. Low BMD can indicate bone loss and excessive bone resorption.
2. X-rays and imaging studies: These tests can help identify abnormal bone growth or other signs of bone resorption.
3. Blood tests: Blood tests can measure levels of certain hormones and nutrients that are involved in bone metabolism.
4. Bone biopsy: A bone biopsy can provide a direct view of the bone tissue and help diagnose conditions such as Paget's disease or bone cancer.

Treatment for bone resorption depends on the underlying cause and may include:

1. Medications: Bisphosphonates, hormone therapy, and other medications can help slow or stop bone resorption.
2. Diet and exercise: A healthy diet rich in calcium and vitamin D, along with regular exercise, can help maintain strong bones.
3. Physical therapy: In some cases, physical therapy may be recommended to improve bone strength and mobility.
4. Surgery: In severe cases of bone resorption, surgery may be necessary to repair or replace damaged bone tissue.

There are several types of atrophy that can occur in different parts of the body. For example:

1. Muscular atrophy: This occurs when muscles weaken and shrink due to disuse or injury.
2. Neuronal atrophy: This occurs when nerve cells degenerate, leading to a loss of cognitive function and memory.
3. Cardiac atrophy: This occurs when the heart muscle weakens and becomes less efficient, leading to decreased cardiac output.
4. Atrophic gastritis: This is a type of stomach inflammation that can lead to the wasting away of the stomach lining.
5. Atrophy of the testes: This occurs when the testes shrink due to a lack of use or disorder, leading to decreased fertility.

Atrophy can be diagnosed through various medical tests and imaging studies, such as MRI or CT scans. Treatment for atrophy depends on the underlying cause and may involve physical therapy, medication, or surgery. In some cases, atrophy can be prevented or reversed with proper treatment and care.

In summary, atrophy is a degenerative process that can occur in various parts of the body due to injury, disease, or disuse. It can lead to a loss of function and decreased quality of life, but with proper diagnosis and treatment, it may be possible to prevent or reverse some forms of atrophy.

Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.

Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.

Example sentence: The patient was diagnosed with experimental sarcoma and underwent a novel chemotherapy regimen that included a targeted therapy drug.

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.

Nephritis is often diagnosed through a combination of physical examination, medical history, and laboratory tests such as urinalysis and blood tests. Treatment for nephritis depends on the underlying cause, but may include antibiotics, corticosteroids, and immunosuppressive medications. In severe cases, dialysis may be necessary to remove waste products from the blood.

Some common types of nephritis include:

1. Acute pyelonephritis: This is a type of bacterial infection that affects the kidneys and can cause sudden and severe symptoms.
2. Chronic pyelonephritis: This is a type of inflammation that occurs over a longer period of time, often as a result of recurrent infections or other underlying conditions.
3. Lupus nephritis: This is a type of inflammation that occurs in people with systemic lupus erythematosus (SLE), an autoimmune disorder that can affect multiple organs.
4. IgA nephropathy: This is a type of inflammation that occurs when an antibody called immunoglobulin A (IgA) deposits in the kidneys and causes damage.
5. Mesangial proliferative glomerulonephritis: This is a type of inflammation that affects the mesangium, a layer of tissue in the kidney that helps to filter waste products from the blood.
6. Minimal change disease: This is a type of nephrotic syndrome (a group of symptoms that include proteinuria, or excess protein in the urine) that is caused by inflammation and changes in the glomeruli, the tiny blood vessels in the kidneys that filter waste products from the blood.
7. Membranous nephropathy: This is a type of inflammation that occurs when there is an abnormal buildup of antibodies called immunoglobulin G (IgG) in the glomeruli, leading to damage to the kidneys.
8. Focal segmental glomerulosclerosis: This is a type of inflammation that affects one or more segments of the glomeruli, leading to scarring and loss of function.
9. Post-infectious glomerulonephritis: This is a type of inflammation that occurs after an infection, such as streptococcal infections, and can cause damage to the kidneys.
10. Acute tubular necrosis (ATN): This is a type of inflammation that occurs when there is a sudden loss of blood flow to the kidneys, causing damage to the tubules, which are tiny tubes in the kidneys that help to filter waste products from the blood.

There are several types of osteosarcomas, including:

1. High-grade osteosarcoma: This is the most common type of osteosarcoma and tends to grow quickly.
2. Low-grade osteosarcoma: This type of osteosarcoma grows more slowly than high-grade osteosarcoma.
3. Chondrosarcoma: This is a type of osteosarcoma that arises in the cartilage cells of the bone.
4. Ewing's family of tumors: These are rare types of osteosarcoma that can occur in any bone of the body.

The exact cause of osteosarcoma is not known, but certain risk factors may increase the likelihood of developing the disease. These include:

1. Previous radiation exposure
2. Paget's disease of bone
3. Li-Fraumeni syndrome (a genetic disorder that increases the risk of certain types of cancer)
4. Familial retinoblastoma (a rare inherited condition)
5. Exposure to certain chemicals, such as herbicides and industrial chemicals.

Symptoms of osteosarcoma may include:

1. Pain in the affected bone, which may be worse at night or with activity
2. Swelling and redness around the affected area
3. Limited mobility or stiffness in the affected limb
4. A visible lump or mass on the affected bone
5. Fractures or breaks in the affected bone

If osteosarcoma is suspected, a doctor may perform several tests to confirm the diagnosis and determine the extent of the disease. These may include:

1. Imaging studies, such as X-rays, CT scans, or MRI scans
2. Biopsy, in which a sample of tissue is removed from the affected bone and examined under a microscope for cancer cells
3. Blood tests to check for elevated levels of certain enzymes that are produced by osteosarcoma cells
4. Bone scans to look for areas of increased activity or metabolism in the bones.

Example sentence: "The patient underwent surgery to create a vascular fistula in her arm to improve the flow of blood to her kidneys."

1. Meniscal tears: The meniscus is a cartilage structure in the knee joint that can tear due to twisting or bending movements.
2. Ligament sprains: The ligaments that connect the bones of the knee joint can become stretched or torn, leading to instability and pain.
3. Torn cartilage: The articular cartilage that covers the ends of the bones in the knee joint can tear due to wear and tear or trauma.
4. Fractures: The bones of the knee joint can fracture as a result of a direct blow or fall.
5. Dislocations: The bones of the knee joint can become dislocated, causing pain and instability.
6. Patellar tendinitis: Inflammation of the tendon that connects the patella (kneecap) to the shinbone.
7. Iliotibial band syndrome: Inflammation of the iliotibial band, a ligament that runs down the outside of the thigh and crosses the knee joint.
8. Osteochondritis dissecans: A condition in which a piece of cartilage and bone becomes detached from the end of a bone in the knee joint.
9. Baker's cyst: A fluid-filled cyst that forms behind the knee, usually as a result of a tear in the meniscus or a knee injury.

Symptoms of knee injuries can include pain, swelling, stiffness, and limited mobility. Treatment for knee injuries depends on the severity of the injury and may range from conservative measures such as physical therapy and medication to surgical intervention.

Osteonecrosis can be caused by a variety of factors, including:

* Trauma or injury to the bone
* Blood vessel disorders, such as blood clots or inflammation
* Certain medications, such as corticosteroids
* Alcohol consumption
* Avascular necrosis can also be a complication of other conditions, such as osteoarthritis, rheumatoid arthritis, and sickle cell disease.

There are several risk factors for developing osteonecrosis, including:

* Previous joint surgery or injury
* Family history of osteonecrosis
* Age, as the risk increases with age
* Gender, as women are more likely to be affected than men
* Certain medical conditions, such as diabetes and alcoholism.

Symptoms of osteonecrosis can include:

* Pain in the affected joint, which may worsen over time
* Limited mobility or stiffness in the joint
* Swelling or redness in the affected area
* A grinding or cracking sensation in the joint.

To diagnose osteonecrosis, a doctor may use a combination of imaging tests such as X-rays, CT scans, and MRI scans to evaluate the bone and joint. Treatment options for osteonecrosis depend on the severity of the condition and can include:

* Conservative management with pain medication and physical therapy
* Bone grafting or surgical intervention to repair or replace the damaged bone and joint.

First-degree burns are the mildest form of burn and affect only the outer layer of the skin. They are characterized by redness, swelling, and pain but do not blister or scar. Examples of first-degree burns include sunburns and minor scalds from hot liquids.

Second-degree burns are more severe and affect both the outer and inner layers of the skin. They can cause blisters, redness, swelling, and pain, and may lead to infection. Second-degree burns can be further classified into two subtypes: partial thickness burns (where the skin is damaged but not completely destroyed) and full thickness burns (where the skin is completely destroyed).

Third-degree burns are the most severe and affect all layers of the skin and underlying tissues. They can cause charring of the skin, loss of function, and may lead to infection or even death.

There are several ways to treat burns, including:

1. Cooling the burn with cool water or a cold compress to reduce heat and prevent further damage.
2. Keeping the burn clean and dry to prevent infection.
3. Applying topical creams or ointments to help soothe and heal the burn.
4. Taking pain medication to manage discomfort.
5. In severe cases, undergoing surgery to remove damaged tissue and promote healing.

Prevention is key when it comes to burns. Some ways to prevent burns include:

1. Being cautious when handling hot objects or substances.
2. Keeping a safe distance from open flames or sparks.
3. Wearing protective clothing, such as gloves and long sleeves, when working with hot materials.
4. Keeping children away from hot surfaces and substances.
5. Installing smoke detectors and fire extinguishers in the home to reduce the risk of fires.

Overall, burns can be a serious condition that requires prompt medical attention. By understanding the causes, symptoms, and treatments for burns, individuals can take steps to prevent them and seek help if they do occur.

Open fracture: The bone breaks through the skin, exposing the bone to the outside environment.

Closed fracture: The bone breaks, but does not penetrate the skin.

Comminuted fracture: The bone is broken into many pieces.

Hairline fracture: A thin crack in the bone that does not fully break it.

Non-displaced fracture: The bone is broken, but remains in its normal position.

Displaced fracture: The bone is broken and out of its normal position.

Stress fracture: A small crack in the bone caused by repetitive stress or overuse.

Types of Arterial Occlusive Diseases:

1. Atherosclerosis: Atherosclerosis is a condition where plaque builds up inside the arteries, leading to narrowing or blockages that can restrict blood flow to certain areas of the body.
2. Peripheral Artery Disease (PAD): PAD is a condition where the blood vessels in the legs and arms become narrowed or blocked, leading to pain or cramping in the affected limbs.
3. Coronary Artery Disease (CAD): CAD is a condition where the coronary arteries, which supply blood to the heart, become narrowed or blocked, leading to chest pain or a heart attack.
4. Carotid Artery Disease: Carotid artery disease is a condition where the carotid arteries, which supply blood to the brain, become narrowed or blocked, leading to stroke or mini-stroke.
5. Renal Artery Stenosis: Renal artery stenosis is a condition where the blood vessels that supply the kidneys become narrowed or blocked, leading to high blood pressure and decreased kidney function.

Symptoms of Arterial Occlusive Diseases:

1. Pain or cramping in the affected limbs
2. Weakness or fatigue
3. Difficulty walking or standing
4. Chest pain or discomfort
5. Shortness of breath
6. Dizziness or lightheadedness
7. Stroke or mini-stroke

Treatment for Arterial Occlusive Diseases:

1. Medications: Medications such as blood thinners, cholesterol-lowering drugs, and blood pressure medications may be prescribed to treat arterial occlusive diseases.
2. Lifestyle Changes: Lifestyle changes such as quitting smoking, exercising regularly, and eating a healthy diet can help manage symptoms and slow the progression of the disease.
3. Endovascular Procedures: Endovascular procedures such as angioplasty and stenting may be performed to open up narrowed or blocked blood vessels.
4. Surgery: In some cases, surgery may be necessary to treat arterial occlusive diseases, such as bypass surgery or carotid endarterectomy.

Prevention of Arterial Occlusive Diseases:

1. Maintain a healthy diet and lifestyle
2. Quit smoking and avoid exposure to secondhand smoke
3. Exercise regularly
4. Manage high blood pressure, high cholesterol, and diabetes
5. Avoid excessive alcohol consumption
6. Get regular check-ups with your healthcare provider

Early detection and treatment of arterial occlusive diseases can help manage symptoms, slow the progression of the disease, and prevent complications such as heart attack or stroke.

There are several possible causes of lymphopenia, including:

1. Viral infections: Many viral infections can cause lymphopenia, such as HIV/AIDS, hepatitis B and C, and influenza.
2. Bacterial infections: Some bacterial infections, such as tuberculosis and leprosy, can also cause lymphopenia.
3. Cancer: Certain types of cancer, such as Hodgkin's disease and non-Hodgkin's lymphoma, can cause lymphopenia by destroying lymphocytes.
4. Autoimmune disorders: Autoimmune disorders, such as rheumatoid arthritis and lupus, can cause lymphopenia by attacking the body's own tissues, including lymphocytes.
5. Radiation therapy: Radiation therapy can destroy lymphocytes and cause lymphopenia.
6. Medications: Certain medications, such as chemotherapy drugs and antibiotics, can cause lymphopenia as a side effect.
7. Genetic disorders: Some genetic disorders, such as X-linked lymphoproliferative disease, can cause lymphopenia by affecting the development or function of lymphocytes.

Symptoms of lymphopenia can include recurring infections, fatigue, and swollen lymph nodes. Treatment of lymphopenia depends on the underlying cause and may involve antibiotics, antiviral medications, or immunoglobulin replacement therapy. In some cases, a bone marrow transplant may be necessary.

Overall, lymphopenia is a condition that can have a significant impact on quality of life, and it is important to seek medical attention if symptoms persist or worsen over time. With proper diagnosis and treatment, many people with lymphopenia can experience improved health outcomes and a better quality of life.

The buildup of plaque in the coronary arteries is often caused by high levels of low-density lipoprotein (LDL) cholesterol, smoking, high blood pressure, diabetes, and a family history of heart disease. The plaque can also rupture, causing a blood clot to form, which can completely block the flow of blood to the heart muscle, leading to a heart attack.

CAD is the most common type of heart disease and is often asymptomatic until a serious event occurs. Risk factors for CAD include:

* Age (men over 45 and women over 55)
* Gender (men are at greater risk than women, but women are more likely to die from CAD)
* Family history of heart disease
* High blood pressure
* High cholesterol
* Diabetes
* Smoking
* Obesity
* Lack of exercise

Diagnosis of CAD typically involves a physical exam, medical history, and results of diagnostic tests such as:

* Electrocardiogram (ECG or EKG)
* Stress test
* Echocardiogram
* Coronary angiography

Treatment for CAD may include lifestyle changes such as a healthy diet, regular exercise, stress management, and quitting smoking. Medications such as beta blockers, ACE inhibitors, and statins may also be prescribed to manage symptoms and slow the progression of the disease. In severe cases, surgical intervention such as coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) may be necessary.

Prevention of CAD includes managing risk factors such as high blood pressure, high cholesterol, and diabetes, quitting smoking, maintaining a healthy weight, and getting regular exercise. Early detection and treatment of CAD can help to reduce the risk of complications and improve quality of life for those affected by the disease.

1. Osteoarthritis: A degenerative condition that causes the breakdown of cartilage in the joints, leading to pain, stiffness, and loss of mobility.
2. Rheumatoid arthritis: An autoimmune disease that causes inflammation in the joints, leading to pain, swelling, and deformity.
3. Gout: A condition caused by the buildup of uric acid in the joints, leading to sudden and severe attacks of pain, inflammation, and swelling.
4. Bursitis: Inflammation of the bursae, small fluid-filled sacs that cushion the joints and reduce friction between tendons and bones.
5. Tendinitis: Inflammation of the tendons, which connect muscles to bones.
6. Synovitis: Inflammation of the synovial membrane, a thin lining that covers the joints and lubricates them with fluid.
7. Periarthritis: Inflammation of the tissues around the joints, such as the synovial membrane, tendons, and ligaments.
8. Spondyloarthritis: A group of conditions that affect the spine and sacroiliac joints, leading to inflammation and pain in these areas.
9. Juvenile idiopathic arthritis: A condition that affects children and causes inflammation and pain in the joints.
10. Systemic lupus erythematosus: An autoimmune disease that can affect many parts of the body, including the joints.

These are just a few examples of the many types of joint diseases that exist. Each type has its own unique symptoms and causes, and they can be caused by a variety of factors such as genetics, injury, infection, or age-related wear and tear. Treatment options for joint diseases can range from medication and physical therapy to surgery, depending on the severity of the condition and its underlying cause.

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.

Types of experimental neoplasms include:

* Xenografts: tumors that are transplanted into animals from another species, often humans.
* Transgenic tumors: tumors that are created by introducing cancer-causing genes into an animal's genome.
* Chemically-induced tumors: tumors that are caused by exposure to certain chemicals or drugs.

The use of experimental neoplasms in research has led to significant advances in our understanding of cancer biology and the development of new treatments for the disease. However, the use of animals in cancer research is a controversial topic and alternatives to animal models are being developed and implemented.

There are several types of cholestasis, including:

1. Obstructive cholestasis: This occurs when there is a blockage in the bile ducts, preventing bile from flowing freely from the liver.
2. Metabolic cholestasis: This is caused by a problem with the metabolism of bile acids in the liver.
3. Inflammatory cholestasis: This occurs when there is inflammation in the liver, which can cause scarring and impair bile flow.
4. Idiopathic cholestasis: This type of cholestasis has no identifiable cause.

Treatment for cholestasis depends on the underlying cause, but may include medications to improve bile flow, dissolve gallstones, or reduce inflammation. In severe cases, a liver transplant may be necessary. Early diagnosis and treatment can help to manage symptoms and prevent complications of cholestasis.

Some common examples of bacterial infections include:

1. Urinary tract infections (UTIs)
2. Respiratory infections such as pneumonia and bronchitis
3. Skin infections such as cellulitis and abscesses
4. Bone and joint infections such as osteomyelitis
5. Infected wounds or burns
6. Sexually transmitted infections (STIs) such as chlamydia and gonorrhea
7. Food poisoning caused by bacteria such as salmonella and E. coli.

In severe cases, bacterial infections can lead to life-threatening complications such as sepsis or blood poisoning. It is important to seek medical attention if symptoms persist or worsen over time. Proper diagnosis and treatment can help prevent these complications and ensure a full recovery.

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 types of vasculitis, each with its own set of symptoms and characteristics. Some common forms of vasculitis include:

1. Giant cell arteritis: This is the most common form of vasculitis, and it affects the large arteries in the head, neck, and arms. Symptoms include fever, fatigue, muscle aches, and loss of appetite.
2. Takayasu arteritis: This type of vasculitis affects the aorta and its major branches, leading to inflammation in the blood vessels that supply the heart, brain, and other vital organs. Symptoms include fever, fatigue, chest pain, and shortness of breath.
3. Polymyalgia rheumatica: This is an inflammatory condition that affects the muscles and joints, as well as the blood vessels. It often occurs in people over the age of 50 and is frequently associated with giant cell arteritis. Symptoms include pain and stiffness in the shoulders, hips, and other joints, as well as fatigue and fever.
4. Kawasaki disease: This is a rare condition that affects children under the age of 5, causing inflammation in the blood vessels that supply the heart and other organs. Symptoms include high fever, rash, swollen lymph nodes, and irritability.

The exact cause of vasculitis is not fully understood, but it is thought to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own blood vessels. Genetic factors may also play a role in some cases.

Diagnosis of vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies (e.g., MRI or CT scans), and biopsies. Treatment options vary depending on the specific type of vasculitis and its severity, but may include medications to reduce inflammation and suppress the immune system, as well as lifestyle modifications such as exercise and stress management techniques. In severe cases, surgery or organ transplantation may be necessary.

In addition to these specific types of vasculitis, there are other conditions that can cause similar symptoms and may be included in the differential diagnosis, such as:

1. Rheumatoid arthritis (RA): This is a chronic autoimmune disorder that affects the joints and can cause inflammation in blood vessels.
2. Systemic lupus erythematosus (SLE): This is another autoimmune disorder that can affect multiple systems, including the skin, joints, and blood vessels.
3. Polyarteritis nodosa: This is a condition that causes inflammation of the blood vessels, often in association with hepatitis B or C infection.
4. Takayasu arteritis: This is a rare condition that affects the aorta and its branches, causing inflammation and narrowing of the blood vessels.
5. Giant cell arteritis: This is a condition that causes inflammation of the large and medium-sized blood vessels, often in association with polymyalgia rheumatica (PMR).
6. Kawasaki disease: This is a rare condition that affects children, causing inflammation of the blood vessels and potential heart complications.
7. Henoch-Schönlein purpura: This is a rare condition that causes inflammation of the blood vessels in the skin, joints, and gastrointestinal tract.
8. IgG4-related disease: This is a condition that can affect various organs, including the pancreas, bile ducts, and blood vessels, causing inflammation and potentially leading to fibrosis or tumor formation.

It is important to note that these conditions may have similar symptoms and signs as vasculitis, but they are distinct entities with different causes and treatment approaches. A thorough diagnostic evaluation, including laboratory tests and imaging studies, is essential to determine the specific diagnosis and develop an appropriate treatment plan.

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.

There are two main types of Renal Insufficiency:

1. Acute Kidney Injury (AKI): This is a sudden and reversible decrease in kidney function, often caused by injury, sepsis, or medication toxicity. AKI can resolve with appropriate treatment and supportive care.
2. Chronic Renal Insufficiency (CRI): This is a long-standing and irreversible decline in kidney function, often caused by diabetes, high blood pressure, or chronic kidney disease. CRI can lead to ESRD if left untreated.

Signs and symptoms of Renal Insufficiency may include:

* Decreased urine output
* Swelling in the legs and ankles (edema)
* Fatigue
* Nausea and vomiting
* Shortness of breath (dyspnea)
* Pain in the back, flank, or abdomen

Diagnosis of Renal Insufficiency is typically made through a combination of physical examination, medical history, laboratory tests, and imaging studies. Laboratory tests may include urinalysis, blood urea nitrogen (BUN) and creatinine levels, and a 24-hour urine protein collection. Imaging studies, such as ultrasound or CT scans, may be used to evaluate the kidneys and rule out other possible causes of the patient's symptoms.

Treatment of Renal Insufficiency depends on the underlying cause and the severity of the condition. Treatment may include medications to control blood pressure, manage fluid balance, and reduce proteinuria (excess protein in the urine). In some cases, dialysis or a kidney transplant may be necessary.

Prevention of Renal Insufficiency includes managing underlying conditions such as diabetes and hypertension, avoiding nephrotoxic medications and substances, and maintaining a healthy diet and lifestyle. Early detection and treatment of acute kidney injury can also help prevent the development of chronic renal insufficiency.

In conclusion, Renal Insufficiency is a common condition that can have significant consequences if left untreated. It is important for healthcare providers to be aware of the causes, symptoms, and diagnosis of Renal Insufficiency, as well as the treatment and prevention strategies available. With appropriate management, many patients with Renal Insufficiency can recover and maintain their kidney function over time.

GN IGA is one of the most common forms of idiopathic membranous nephropathy, which means it has no known cause. It can occur at any age but is more common in adults between the ages of 20 and 40. The disease often progresses slowly over several years, and some people may experience no symptoms at all.

The diagnosis of GN IGA is based on a combination of clinical findings, laboratory tests, and kidney biopsy. Laboratory tests may show abnormal levels of proteins in the urine, such as albumin, and a high level of IgA in the blood. A kidney biopsy is often necessary to confirm the diagnosis and to rule out other kidney diseases.

There is no cure for GN IGA, but treatment can help slow the progression of the disease. Treatment options may include medications to control high blood pressure, reduce proteinuria (excess protein in the urine), and suppress the immune system. In severe cases, dialysis or a kidney transplant may be necessary.

Preventive measures for GN IGA are not well established, but maintaining a healthy lifestyle, including a balanced diet, regular exercise, and avoiding exposure to toxins, may help reduce the risk of developing the disease. It is also important to manage any underlying medical conditions, such as high blood pressure or diabetes, which can increase the risk of kidney damage.

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.

Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.

The symptoms of coronary disease can vary depending on the severity of the condition, but may include:

* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Swelling of the legs and feet
* Pain in the arms and back

Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

Preventative measures for coronary disease include:

* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.

There are several different types of calcinosis, each with its own unique causes and symptoms. Some common forms of calcinosis include:

1. Dystrophic calcinosis: This type of calcinosis occurs in people with muscular dystrophy, a group of genetic disorders that affect muscle strength and function. Dystrophic calcinosis can cause calcium deposits to form in the muscles, leading to muscle weakness and wasting.
2. Metastatic calcinosis: This type of calcinosis occurs when cancer cells spread to other parts of the body and cause calcium deposits to form. Metastatic calcinosis can occur in people with a variety of different types of cancer, including breast, lung, and prostate cancer.
3. Idiopathic calcinosis: This type of calcinosis occurs for no apparent reason, and the exact cause is not known. Idiopathic calcinosis can affect people of all ages and can cause calcium deposits to form in a variety of different tissues.
4. Secondary calcinosis: This type of calcidosis occurs as a result of an underlying medical condition or injury. For example, secondary calcinosis can occur in people with kidney disease, hyperparathyroidism (a condition in which the parathyroid glands produce too much parathyroid hormone), or traumatic injuries.

Treatment for calcinosis depends on the underlying cause and the severity of the condition. In some cases, treatment may involve managing the underlying disease or condition that is causing the calcium deposits to form. Other treatments may include medications to reduce inflammation and pain, physical therapy to improve mobility and strength, and surgery to remove the calcium deposits.

There are several types of thrombosis, including:

1. Deep vein thrombosis (DVT): A clot forms in the deep veins of the legs, which can cause swelling, pain, and skin discoloration.
2. Pulmonary embolism (PE): A clot breaks loose from another location in the body and travels to the lungs, where it can cause shortness of breath, chest pain, and coughing up blood.
3. Cerebral thrombosis: A clot forms in the brain, which can cause stroke or mini-stroke symptoms such as weakness, numbness, or difficulty speaking.
4. Coronary thrombosis: A clot forms in the coronary arteries, which supply blood to the heart muscle, leading to a heart attack.
5. Renal thrombosis: A clot forms in the kidneys, which can cause kidney damage or failure.

The symptoms of thrombosis can vary depending on the location and size of the clot. Some common symptoms include:

1. Swelling or redness in the affected limb
2. Pain or tenderness in the affected area
3. Warmth or discoloration of the skin
4. Shortness of breath or chest pain if the clot has traveled to the lungs
5. Weakness, numbness, or difficulty speaking if the clot has formed in the brain
6. Rapid heart rate or irregular heartbeat
7. Feeling of anxiety or panic

Treatment for thrombosis usually involves medications to dissolve the clot and prevent new ones from forming. In some cases, surgery may be necessary to remove the clot or repair the damaged blood vessel. Prevention measures include maintaining a healthy weight, exercising regularly, avoiding long periods of immobility, and managing chronic conditions such as high blood pressure and diabetes.

The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:

* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure

Glomerulonephritis can be caused by a variety of factors, including:

* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia

The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.

Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:

* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases

The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.

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... (CAV) is a progressive type of coronary artery disease in people who have had a heart transplant ... Cardiac allograft vasculopathy is an accelerated type of coronary artery disease in people who have had a heart transplantation ... Antibody-mediated cardiac allograft rejection (AMR) is a significant factor leading to the rapid progression of CAV. Future ... Hence, regular follow-up and monitoring of the allograft for early signs of disease is advocated. Surveillance is performed by ...
... (CAN) is a kidney disorder which is the leading cause of kidney transplant failure, occurring ... Sep 1999). "Chronic allograft nephropathy: An update". Kidney Int. 56 (3): 783-93. doi:10.1046/j.1523-1755.1999.00611.x. PMID ... Mar 2006). "Chronic allograft nephropathy: current concepts and future directions". Transplantation. 81 (5): 643-54. doi: ... Jul 2005). "Chronic renal allograft rejection: pathophysiologic considerations". Kidney Int. 68 (1): 1-13. doi:10.1111/j.1523- ...
"Entrez Gene: AIF1 allograft inflammatory factor 1". Deininger MH, Meyermann R, Schluesener HJ (March 2002). "The allograft ... Allograft inflammatory factor 1 (AIF-1) also known as ionized calcium-binding adapter molecule 1 (IBA1) is a protein that in ... July 2012). "Serum allograft inflammatory factor-1 is a novel marker for diabetic nephropathy". Diabetes Research and Clinical ... Allograft Inflammatory Factor 1 is found in activated macrophages. Activated macrophages are found in tissues with inflammation ...
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... , referred to as DFDBA, is a bone graft material known for its de novo bone formation ...
... is a protein that is encoded by the AIF1L gene in humans. AIF1L is an actin-binding ... "AIF1L allograft inflammatory factor 1 like [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 3 December ... ". "Aif1l - Allograft inflammatory factor 1-like - Mus musculus (Mouse) - Aif1l gene & protein". www.uniprot.org. Retrieved 3 ...
Elkins RC, Dawson PE, Goldstein S, Walsh SP, Black KS (May 2001). "Decellularized human valve allografts". The Annals of ... Dohmen then created a decellularized cryopreserved pulmonary allograft scaffold and seeded it with human vascular endothelial ...
Autologous grafts and some forms of treated allografts can be left on permanently without rejection. Genetically modified pigs ... Other skin substitutes include Allograft, Biobrane, TransCyte, Integra, AlloDerm, Cultured epithelial autografts (CEA). There ... allograft). Xenogeneic: The donor and recipient are of different species (e.g., bovine cartilage; pig skin; xenograft or ... Allografts, xenografts, and prosthetic grafts are usually used as temporary skin substitutes, that is a wound dressing for ...
2008). "Hand Transplantation: The Innsbruck Experience". Transplantation of Composite Tissue Allografts. pp. 234-250. doi: ...
... if the allograft is sized radiographically by use of anteroposterior and lateral films and the allograft meniscal horns have ... The meniscus to be transplanted is taken from a cadaver, and, as such, is known as an allograft. Meniscal transplantation is ... Meniscal allograft processing, sterilization and storage procedures vary from center to center. Some surgeons, particularly in ... Some surgeons leave the allograft anchored to its bony attachments and fix these bone bridges or plugs into size matched slots ...
Segerer S, Böhmig GA, Exner M, Colin Y, Cartron JP, Kerjaschki D, Schlöndorff D, Regele H (2003). "When renal allografts turn ... Geleff S, Draganovici D, Jaksch P, Segerer S (July 2009). "The role of chemokine receptors in acute lung allograft rejection". ...
Autografts are preferred over allografts. Saddle deformity can also be corrected by synthetic implants of teflon or silicon, ...
Transplants that are recently performed between two subjects of the same species are called allografts. Allografts can either ... Most human tissue and organ transplants are allografts. Due to the genetic difference between the organ and the recipient, the ... The first successful corneal allograft transplant was performed in 1837 in a gazelle model; the first successful human corneal ... For instance, patients who underwent liver transplantation using donation-after-circulatory-death allografts have been shown to ...
Though the allograft (skin transplanted from a member of the same species) is replaced by granulation tissue and is not ... On the most difficult chronic wounds, allografts may not work, requiring skin grafts from elsewhere on the patient, which can ... Snyder RJ (2005). "Treatment of nonhealing ulcers with allografts". Clinics in Dermatology. 23 (4): 388-95. doi:10.1016/j. ...
"Osteochondral Autograft & Allograft". Washington University Orthopedics. Retrieved 26 January 2020. Favinger JL, Ha AS, Brage ... This can either be from the person (autograft) or from a donor (allograft). People undergoing a joint transplant (osteochondral ... allograft) do not need to take immunosuppressants as bone and cartilage tissues have limited immune responses. Autologous ...
Loupy is the author of many major publications including : "System for Predicting the Risk of Allograft Loss in Renal ... Alexandre Loupy's work has focused on allograft rejection and the relationship between the presence of antibodies and the ... "About The Banff Foundation for Allograft Pathology". BANFF. Retrieved 2020-04-29. Science portal Medicine portal (CS1 French- ... "Complement-Binding Anti-HLA Antibodies and Kidney-Allograft Survival". New England Journal of Medicine. 369 (13): 1215-1226. ...
Use of fresh decellularized allografts for pulmonary valve replacement may reduce the reoperation rate in children and young ... single-arm European trial on decellularized allografts for aortic valve replacement: the ARISE study and ARISE Registry data". ... Early systemic cellular immune response in children and young adults receiving decellularized fresh allografts for pulmonary ... "Paediatric aortic valve replacement using decellularized allografts". European Journal of Cardio-Thoracic Surgery. 58 (4): 817- ...
Utans U, Quist WC, McManus BM, Wilson JE, Arceci RJ, Wallace AF, Russell ME (May 1996). "Allograft inflammatory factory-1. A ...
Unlike allografts, such grafts do not corporate into the body. As with many operations, allotransplantation risks some side ... Allograft diseases Medical grafting Surgery For ACL Tears (W. P. Longmire, J. National Cancer Institute 14, 669: The term ... An immune response against an allograft or xenograft is termed rejection. An allogenic bone marrow transplant can result in an ... Most human tissue and organ transplants are allografts. It is contrasted with autotransplantation (from one part of the body to ...
Frootko, N. J. (1985). "Immune Responses in Allograft Tympanoplasty". In Veldman, J. E.; Mc Cabe, B. F.; Huising, E. H.; Mygind ... Frootko, N. J. (1984). Allograft Rejection in the Middle Ear of the Rat. (M.Sc. Thesis). Oxford: Green Templeton College, ... Unfortunately this and all other reconstructive procedures using allografts were abandoned in 1987 because of the potential ... Frootko, N. J. (1985). "Tympanic Allografts--Immunopathology and Applying the Language of "Transplantese" to Tympanoplasty". In ...
With Jean-Michel Dubernard, and Earl Owen, he co-edited the textbook Composite Tissue Allograft. It included an introduction by ... Co-edited with Vassilios E. Papalois Composite Tissue Allograft. Imperial College Press, London (2006). ISBN 1-86094-651-8. Co- ... Kirk, A. D. (2007). "Book review: Composite Tissue Allograft". American Journal of Transplantation. 7 (4): 1036. doi:10.1111/j. ...
His practice has a primary focus on the understanding and treatment of cardiac allograft vasculopathy, a condition affecting ... "Anti-HLA antibodies are associated with restenosis after percutaneous coronary intervention for cardiac allograft vasculopathy ... "Cardiac allograft vasculopathy: a review". Circulation. 96 (6): 2069-77. doi:10.1161/01.cir.96.6.2069. PMID 9323100. C-Mail: A ...
Giglia JS, Ollerenshaw JD, Dawson PE, Black KS, Abbott WM (November 2002). "Cryopreservation prevents arterial allograft ...
Winkler, Heinz; Haiden, Peter (2017-01-01). "Allograft Bone as Antibiotic Carrier". Journal of Bone and Joint Infection. 2 (1 ...
J. Pepper (Ed) Cardiac Valve Allografts : Science and Practice. Steinkopff-Verlag Heidelberg (1997). ISBN 9783642592508. With A ...
In early 1960, Ross and Barratt-Boyes used allografts. Tissue prosthetic valves were introduced in 1965 by Binet in Paris, but ...
Studies investigating renal diseases such as renal allograft dysfunction, lupus nephritis, immunoglobulin A nephropathy (IgAN ... "Role of Magnetic Resonance Elastography as a Noninvasive Measurement Tool of Fibrosis in a Renal Allograft: A Case Report". ... "MR elastography in renal transplant patients and correlation with renal allograft biopsy: a feasibility study". Acad Radiol. 19 ... "Magnetic Resonance Elastography to Assess Fibrosis in Kidney Allografts". Clinical Journal of the American Society of ...
"Cell-Free DNA and Active Rejection in Kidney Allografts". Journal of the American Society of Nephrology. 28 (7): 2221-2232. doi ...
"Extramedullary hematopoiesis in the allograft liver". Modern Pathology. 8 (6): 671-4. PMID 8532704. Schlitt HJ, Schäfers S, ...
Meniscal allograft transplantation is surgery in which a meniscus -- a c-shaped cartilage in the knee -- is placed into your ... Meniscal allograft transplantation is surgery in which a meniscus -- a c-shaped cartilage in the knee -- is placed into your ... Meniscus allograft transplantation is a difficult surgery, and the recovery is hard. But for people who are missing the ...
... Tissue allografts are commonly used in orthopedic ... A case of allograft-associated infection was defined as any surgical site infection (SSI) at the site of allograft implantation ... of the allografts were frozen and two (15%) were fresh (femoral condyles). All allografts were processed aseptically but did ... The three allografts received by these two patients came from the same cadaveric donor (donor A) and were supplied by tissue ...
Kidney Allograft Function Is a Confounder of Urine Metabolite Profiles in Kidney Allograft Recipients ... A) Kaplan-Meier plot of patient survival after kidney allograft loss. Median patient survival after kidney allograft loss was ... Kaplan-Meier estimate of kidney allograft survival, in HIV-positive kidney allograft recipients converted to belatacept ... Patient and kidney allograft survival after belatacept treatment. (A) Kaplan-Meier estimate of patient survival was similar in ...
Full Text PA-97-075 DIRECT VS INDIRECT ANTIGEN RECOGNITION IN ALLOGRAFT SURVIVAL NIH GUIDE, Volume 26, Number 24, July 25, 1997 ... These recognition events are key to understanding subsequent events leading to allograft rejection and are thus the focal point ... Thus additional research is needed to distinguish the contributions of direct and indirect recognition to allograft survival ...
Chronic lung allograft dysfunction (CLAD) is the major limitation of long-term survival after lung t ... Restrictive allograft syndrome (RAS): a novel form of chronic lung allograft dysfunction. J Heart Lung Transplant. 2011;30:735- ... In a murine model of lung transplantation, Col(V)-specific T cells found in the lung allograft mediates allograft rejection.115 ... CONSEQUENCES ON THE LUNG ALLOGRAFT. It is now recognized that the recurrent injuries of the lung allograft, either immune or ...
Kidney Allograft Function Is a Confounder of Urine Metabolite Profiles in Kidney Allograft Recipients ... A) Kaplan-Meier plot of patient survival after kidney allograft loss. Median patient survival after kidney allograft loss was ... Kaplan-Meier estimate of kidney allograft survival, in HIV-positive kidney allograft recipients converted to belatacept ... Patient and kidney allograft survival after belatacept treatment. (A) Kaplan-Meier estimate of patient survival was similar in ...
Facial allograft transplantation, personal identity and subjectivity. J S Swindell, Journal of Medical Ethics, 2007 ... Until they have faces: the ethics of facial allograft transplantation. G J Agich et al., Journal of Medical Ethics, 2005 ...
Clostridium infections were traced to allograft implantation. We provide interim recommendations to enhance tissue- ... Clostridium infections associated with musculoskeletal-tissue allografts Marion A Kainer 1 , Jeanne V Linden, David N Whaley, ... Clostridium infections associated with musculoskeletal-tissue allografts Marion A Kainer et al. N Engl J Med. 2004. . ... New techniques in allograft tissue processing. Vaishnav S, Thomas Vangsness C Jr, Dellamaggiora R. Vaishnav S, et al. Clin ...
Second in a series on managing bone allografts. Bone-graft substitutes in all of their many forms have one purpose-to replicate ...
1145 Freeze Dried Allograft Versus Anorganic Bone Xenograft For Site Preservation Friday, March 23, 2012: 3:30 p.m. - 4:45 p.m. ... The purpose of this study is to compare two different graft materials: a freeze dried bone allograft (FDBA) and an anorganic ...
Allograft GraftLink Implant System, for ,em,Internal,/em,Brace Technique ...
These cells express mRNA for IFN-γ receptor (ifngr) and suppress donor but not third party cardiac allograft rejection mediated ... The rIL-12p70 alloactivated Ts1 cells markedly delayed PVG, but not third party Lewis, cardiac allograft rejection in normal DA ... These cells express mRNA for IFN-γ receptor (ifngr) and suppress donor but not third party cardiac allograft rejection mediated ... These Th1-like Treg delayed specific-donor allograft rejection demonstrating therapeutic potential ...
Survival of subretinal pancreatic islet cell allografts and apoptosis in infiltrating lymphocytes in rats. ... Syngeneic transplants and allografts in SD rats survived up to 60 days without appreciable lymphocytic infiltration. Endocrine ... Survival of subretinal pancreatic islet cell allografts and apoptosis in infiltrating lymphocytes in rats. Journal Article ( ... No difference in distribution of TUNEL+ cells was seen between syngeneic transplants and subretinal allografts in SD rats on ...
... is an allograft spacer designed to minimize disruption to patient anatomy while preserving the natural anatomical profile of ... The allograft spacer portion has a pre-shaped footprint, height, and lordosis, eliminating the need for time-consuming implant ... INDEPENDENCE MIS AGX™ is an integrated ALIF allograft spacer designed to minimize disruption to patient anatomy while ... Titanium frame provides protection of the allograft during insertion and allows for compressive loading. ...
What is the allograft made of?. Allograft is bone taken from a cadaver tissue bank for use in medical procedures. It can be ... How long do allografts last?. In general, osteochondral allografts for the treatment of chondral lesions of the tibial plateau ... Who does allografts?. Since 1987, MTF Biologics has supplied more than 9 million allografts from more than 137,000 donors. ... Is bone grafting an allograft?. The two most common types of bone grafts are: Allografts, which use bone from a deceased donor ...
We previously developed a model system to study the mechanisms governing inhibition of chronic rejection of heart allografts. ... CONCLUSIONS: The function of allochimeric molecule in the abrogation of heart allograft rejection may rely on the ... We previously developed a model system to study the mechanisms governing inhibition of chronic rejection of heart allografts. ... CONCLUSIONS: The function of allochimeric molecule in the abrogation of heart allograft rejection may rely on the ...
Chronic rejection of human face allografts. (Am J Transplant. 2019 Apr;19(4):1168-1177. doi: 10.1111/ajt.15143. Epub 2018 Nov ... "Chronic rejection of human face allografts.". (Am J Transplant. 2019 Apr;19(4):1168-1177. doi: 10.1111/ajt.15143. Epub 2018 Nov ... Chronic rejection of human face allografts. Presented live on Tuesday, October 15th, 2019 • Hosted by the Vascularized ... Face vascularized composite allografts (FVCAs) have helped patients with severe facial disfigurement, with acute rejection now ...
Loss of living donor renal allograft survival advantage in children with focal segmental glomerulosclerosis. Go back to ...
A decellularized and sterilized human meniscus allograft: towards off-the-shelf meniscus replacement. Velthuijs, W. A. K. ( ...
https://TopgradeApp.com/playQuiz/allografts-pd. Other share options Embed In Website. If your website allows iFrames add the ...
Allograft So, you were recently told by your doctor that you need a bone graft, but you arent quite sure what that means. A ...
Low-dose carbon monoxide inhalation prevents development of chronic allograft nephropathy. Joao Seda Neto, Atsunori Nakao, ... Dive into the research topics of Low-dose carbon monoxide inhalation prevents development of chronic allograft nephropathy. ...
Clark, D. S., Foker, J. E., Good, R. A., & Varco, R. L. (1968). Humoral factors in canine renal allograft rejection. Lancet, 1( ... Humoral factors in canine renal allograft rejection. / Clark, D. S.; Foker, J. E.; Good, R. A. et al. In: Lancet, Vol. 1, No. ... Clark, DS, Foker, JE, Good, RA & Varco, RL 1968, Humoral factors in canine renal allograft rejection., Lancet, vol. 1, no. ... title = "Humoral factors in canine renal allograft rejection.",. author = "Clark, {D. S.} and Foker, {J. E.} and Good, {R. A.} ...
Category: Renuva Allograft. Sep 21 2017 Renuva Allograft Adipose for Permanent Natural Filling. Thursday, September 21st, 2017 ... Renuva allograft adipose matrix is a new product we now have in our arsenal of anti aging treatment. It is unique new ...
Natural killer cell subsets in allograft rejection and tolerance. Curr Opin Organ Transplant. 2007 Feb; 12(1):10-16. ...
Bone Fiber Bullets Provide Improved Allograft Delivery By HospiMedica International staff writers. Posted on 28 Jan 2021. ... The allograft also has an osteoinductive potential and enhanced handling properties that are ideal for spinal fusion and other ... DBF is an autograft, allograft, or xenograft bone product prepared by removing inorganic minerals and leaving a matrix ... Bone Fiber Bullets Provide Improved Allograft Delivery ...
Homeostatic Proliferation of Lymphocytes Results in Augmented Memory-Like Function and Accelerated Allograft Rejection ... Homeostatic Proliferation of Lymphocytes Results in Augmented Memory-Like Function and Accelerated Allograft Rejection ...
Structural Allograft Implant - Custom allograft implant includes a large trans-joint graft window for accommodating a biologic ... Tag Archive for: allograft implant. Sacroiliac Joint Fusion with TransFasten - Patient Experience. /by Captiva Spine. Captiva ... A posterior approach coupled with the proprietary QuadraCentric™ Joint Preparation and unique structural allograft implant ...
Osteochondral allograft transplantations (OCAs) are becoming a mainstay of treatment for knee-cartilage injuries. To help ...
  • Face vascularized composite allografts (FVCAs) have helped patients with severe facial disfigurement, with acute rejection now largely controlled through iatrogenic immunosuppression. (nih.gov)
  • The rIL-12p70 alloactivated Ts1 cells markedly delayed PVG, but not third party Lewis, cardiac allograft rejection in normal DA recipients. (frontiersin.org)
  • These Th1-like Treg delayed specific donor allograft rejection demonstrating therapeutic potential. (frontiersin.org)
  • 1:1 of nTreg:effector CD4 + T cells to inhibit organ allograft rejection ( 2 , 8 ) or graft versus host disease (GVHD) ( 11 ). (frontiersin.org)
  • Thus, extremely large numbers of nTreg are required in vivo to prevent allograft rejection and GVHD in unmodified recipients ( 13 ). (frontiersin.org)
  • Allochimeric molecules and mechanisms in abrogation of cardiac allograft rejection. (inserm.fr)
  • We previously developed a model system to study the mechanisms governing inhibition of chronic rejection of heart allografts. (inserm.fr)
  • CONCLUSIONS: The function of allochimeric molecule in the abrogation of heart allograft rejection may rely on the downregulation of RhoB pathway components that regulate the structure and function of the ER/Golgi/vesicular trafficking pathways involved in antigen processing and presentation by dendritic cells. (inserm.fr)
  • Humoral factors in canine renal allograft rejection. (umn.edu)
  • The importance of antibodies in allograft rejection has hitherto been diffiicult to assess. (umn.edu)
  • Other experi-ments demonstrating an effect of passive transfer of sensitised serum have measured only the accelerating effect on the rejection of allografts. (umn.edu)
  • Our demonstration that humoral components can precipitate an allograft rejection does not lessen the importance of the cellular infiltration seen in the usual process of rejection but does suggest that most of its activity may be non-specific. (umn.edu)
  • The gross features of renal allograft rejection-decreased urinary output, increased size, and decreased blood-flow- correlated well in time with the interstitial infiltration of polymorphs and platelets. (umn.edu)
  • Natural killer cell subsets in allograft rejection and tolerance. (uchicago.edu)
  • In our cohort of patients, we examine demographic and clinical characteristics, as well as differential levels of cell free DNA, to explore outcomes of allograft failure, acute cellular rejection, and chronic lung allograft dysfunction in individuals of European and non-European ancestry. (nih.gov)
  • Maintenance of immunosuppression after solid-organ transplant is essential in order to prevent short-and long-term complications such as acute cellular rejection and chronic lung allograft dysfunction. (nih.gov)
  • Renal allograft rejection. (nih.gov)
  • The incidence of postransplant diabetes mellitus (PTDM) was compared in two groups of renal allograft recipients. (northwestern.edu)
  • The current study suggests that CsA may be diabetogenic when administered with methylprednisolone to renal allograft recipients. (northwestern.edu)
  • Acute jejunal obstruction in a renal allograft recipient. (who.int)
  • Meniscal allograft transplantation is surgery in which a meniscus -- a c-shaped cartilage in the knee -- is placed into your knee. (medlineplus.gov)
  • Thus additional research is needed to distinguish the contributions of direct and indirect recognition to allograft survival and to determine how this knowledge could lead to improvements in existing therapies as well as the development of new therapies to prolong graft survival. (nih.gov)
  • Chronic lung allograft dysfunction (CLAD) is the major limitation of long-term survival after lung transplantation. (lww.com)
  • Survival of subretinal pancreatic islet cell allografts and apoptosis in infiltrating lymphocytes in rats. (duke.edu)
  • The adverse effect on allograft survival requires further investigation. (northwestern.edu)
  • For the published notice of special interest, check the February 23, 2022 Guide notice, Notice of Special Interest (NOSI)-Optimizing Vascularized Composite Allograft Survival . (nih.gov)
  • Transcriptionally Distinct B Cells Infiltrate Allografts After Kidney Transplantation. (bvsalud.org)
  • The purpose of this study is to compare two different graft materials: a freeze dried bone allograft (FDBA) and an anorganic bovine bone mineral (ABBM) in clinical and histological level. (umich.edu)
  • This surgical defect allowed the use of magnetized (test group) and non-magnetized (control group) metal devices associated with molar apices and distal stump of the lower incisor, where the lyophilized bone allograft was performed. (bvsalud.org)
  • In the test and control groups, there was gradual integration of the lyophilized bone allograft, maintenance of pulp vitality of the molars and proximal stump of the lower incisor, in addition to continuous eruption of the lower incisor. (bvsalud.org)
  • Lyophilized bone allograft. (bvsalud.org)
  • Identification of relevant pathways and genes, such as JunB and c-Fos, may provide new targets for preventative therapies for chronic immune-mediated changes in vascularized composite allografts. (myast.org)
  • Facial allograft transplants: where's the catch? (bmj.com)
  • Syngeneic transplants and allografts in SD rats survived up to 60 days without appreciable lymphocytic infiltration. (duke.edu)
  • No difference in distribution of TUNEL+ cells was seen between syngeneic transplants and subretinal allografts in SD rats on day 60. (duke.edu)
  • Chronic lung allograft dysfunction manifests as bronchiolitis obliterans syndrome or the recently described restrictive allograft syndrome. (lww.com)
  • Chronic lung allograft dysfunction is a multifactorial disease that remains irreversible and unpredictable so far. (lww.com)
  • Royer et al review the immune mechanisms involved in the development chronic lung allograft dysfunction (CLAD), which manifests as bronchiolitis obliterans syndrome (BOS) or restrictive allograft syndrome (RAS), concluding that CLAD is a multifactorial disease that remains irreversible and unpredictable. (lww.com)
  • We explore the innate or adaptive immune reactions induced by the allograft itself or by the environment and how they lead to allograft dysfunction. (lww.com)
  • Class-switched intragraft B cells are rare but can be donor -specific and produce IgG capable of binding to the kidney allograft . (bvsalud.org)
  • As of March 11, 2002, CDC has received 26 reports of bacterial infections associated with musculoskeletal tissue allografts including the previously reported cases ( 2 , 3 ). (cdc.gov)
  • The three allografts received by these two patients came from the same cadaveric donor (donor A) and were supplied by tissue processor A (TP-A). Based on records from the medical examiner, no evidence indicated that donor A was septic or had risk factors for Clostridium spp. (cdc.gov)
  • The two most common types of bone grafts are: Allografts, which use bone from a deceased donor or cadaver that has been cleaned and placed in a tissue bank. (vintage-kitchen.com)
  • What is the difference between an allograft and an autograft? (vintage-kitchen.com)
  • DBF is an autograft, allograft, or xenograft bone product prepared by removing inorganic minerals and leaving a matrix containing mainly collagen, and also allowing exposure of bone morphogenetic proteins (BMPs) that retain their biological activities. (hospimedica.com)
  • In rat models, CD4 + CD25 + T regulatory cells (Treg) play a key role in the induction and maintenance of antigen-specific transplant tolerance, especially in DA rats with PVG cardiac allografts ( 1 , 2 ). (frontiersin.org)
  • An algorithm using PET/CT imaging with regadenoson and Rb-82 imaging with myocardial blood flow (MBF) quantification offers a high negative predictive value to rule out significant cardiac allograft vasculopathy (CAV) in patients with heart transplant. (acc.org)
  • were isolated, patients were excluded unless additional epidemiologic or microbiologic evidence suggested allograft contamination. (cdc.gov)
  • 11 (85%) of these patients received tissue processed by TP-A. Allografts that were implicated in Clostridium spp. (cdc.gov)
  • A case of allograft-associated infection was defined as any surgical site infection (SSI) at the site of allograft implantation occurring within 12 months of allograft implantation in an otherwise healthy patient with no known risk factors for SSI (e.g., diabetes). (cdc.gov)
  • ABSTRACT Objective: the objective of this paper is to provide a descriptive histological analysis of the use of a buried, static and permanent magnetic field in lyophilized bone allografts in a dentoalveolar area associated with surgical defects in rat mandibles. (bvsalud.org)
  • Through innovation and a commitment to clinical results and positive outcomes, JRF Ortho is redefining the standard for allograft joint repair. (jrfortho.org)
  • After the reported death of a recipient of an allograft contaminated with Clostridium spp. (cdc.gov)
  • What is the diagnostic and prognostic value of a previously published algorithm for diagnosing cardiac allograft vasculopathy (CAV) via positron emission tomography/computed tomography (PET/CT) scan with myocardial blood flow (MBF) in a larger population? (acc.org)
  • The allograft also has an osteoinductive potential and enhanced handling properties that are ideal for spinal fusion and other orthopedic applications. (hospimedica.com)
  • Therefore, once the initial recognition phase has passed, allografts can be rejected in a system where the only sensitised components are humoral. (umn.edu)
  • Although sterilization and preservation techniques have been improved to limit the amount of structural damage to allograft tissue, it is not as strong as tissue that has not undergone these processes. (vintage-kitchen.com)
  • This allograft both resembles human-like melanoma and has features that will stimulate a normal immunological response in the mouse. (nih.gov)
  • This is problematic both in models in which the cancer spontaneously develops in the animal as well as models in which cancerous cells or tumors, i.e. allografts (derived from cells of the same organism) or xenografts (derived from cells of different organism, usually humans) are transplanted into an otherwise cancer-free animal. (nih.gov)
  • To identify additional cases of allograft-associated infections, CDC solicited case reports through electronic listservers and MMWR ( 2 , 3 ) and by contacting the Food and Drug Administration (FDA) and state regulatory authorities ( 2 ). (cdc.gov)
  • In our study, skin allografts are evaluated as a permanent cover for deep burns. (vintage-kitchen.com)
  • INDEPENDENCE MIS AGX™ is an integrated ALIF allograft spacer designed to minimize disruption to patient anatomy while preserving the natural anatomical profile of the lumbar spine. (globusmedical.com)
  • Allografts are primarily used to repair broken and damaged bones in the knees, hips, arms, and legs (long bone reconstruction). (vintage-kitchen.com)
  • Renuva allograft adipose matrix is a new product we now have in our arsenal of anti aging treatment. (drgailhumble.com)
  • On November 7, 2001, a man aged 23 years underwent reconstructive knee surgery at a hospital in Minnesota using a femoral condyle (bone-cartilage) allograft. (cdc.gov)
  • After suspension of the allograft and companion tissue in an antibiotic/antifungal solution, the companion tissue was cultured. (cdc.gov)