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.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.
A tumor necrosis factor receptor subtype that is expressed primarily in IMMUNE SYSTEM cells. It has specificity for membrane-bound form of TUMOR NECROSIS FACTORS and mediates intracellular-signaling through TNF RECEPTOR ASSOCIATED FACTORS.
A condition in which the death of adipose tissue results in neutral fats being split into fatty acids and glycerol.
Aseptic or avascular necrosis of the femoral head. The major types are idiopathic (primary), as a complication of fractures or dislocations, and LEGG-CALVE-PERTHES DISEASE.
A complication of kidney diseases characterized by cell death involving KIDNEY PAPILLA in the KIDNEY MEDULLA. Damages to this area may hinder the kidney to concentrate urine resulting in POLYURIA. Sloughed off necrotic tissue may block KIDNEY PELVIS or URETER. Necrosis of multiple renal papillae can lead to KIDNEY FAILURE.
Death of cells in the KIDNEY CORTEX, a common final result of various renal injuries including HYPOXIA; ISCHEMIA; and drug toxicity.
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.
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.
A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A family of proteins that were originally identified by their ability to cause NECROSIS of NEOPLASMS. Their necrotic effect on cells is mediated through TUMOR NECROSIS FACTOR RECEPTORS which induce APOPTOSIS.
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.
Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)
Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.
A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS.
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.
The type species of AQUABIRNAVIRUS, causing infectious pancreatic necrosis in salmonid fish and other freshwater and marine animals including mollusks.
A tumor necrosis factor family member that is released by activated LYMPHOCYTES. Soluble lymphotoxin is specific for TUMOR NECROSIS FACTOR RECEPTOR TYPE I; TUMOR NECROSIS FACTOR RECEPTOR TYPE II; and TUMOR NECROSIS FACTOR RECEPTOR SUPERFAMILY, MEMBER 14. Lymphotoxin-alpha can form a membrane-bound heterodimer with LYMPHOTOXIN-BETA that has specificity for the LYMPHOTOXIN BETA RECEPTOR.
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 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.)
Established cell cultures that have the potential to propagate indefinitely.
A subclass of tumor necrosis family receptors that lack cell signaling domains. They bind to specific TNF RECEPTOR LIGANDS and are believed to play a modulating role in the TNF signaling pathway. Some of the decoy receptors are products of distinct genes, while others are products of ALTERNATIVE SPLICING of the MRNA for the active receptor.
A transmembrane-protein belonging to the TNF family of intercellular signaling proteins. It is a widely expressed ligand that activates APOPTOSIS by binding to TNF-RELATED APOPTOSIS-INDUCING LIGAND RECEPTORS. The membrane-bound form of the protein can be cleaved by specific CYSTEINE ENDOPEPTIDASES to form a soluble ligand form.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Mild to fulminant necrotizing vaso-occlusive retinitis associated with a high incidence of retinal detachment and poor vision outcome.
Proteins prepared by recombinant DNA technology.
Elements of limited time intervals, contributing to particular results or situations.
Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
The type species of NOVIRHABDOVIRUS, in the family RHABDOVIRIDAE. It is a major pathogen of TROUT and SALMON.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Antibodies produced by a single clone of cells.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
A family of serine-threonine kinases that plays a role in intracellular signal transduction by interacting with a variety of signaling adaptor proteins such as CRADD SIGNALING ADAPTOR PROTEIN; TNF RECEPTOR-ASSOCIATED FACTOR 2; and TNF RECEPTOR-ASSOCIATED DEATH DOMAIN PROTEIN. Although they were initially described as death domain-binding adaptor proteins, members of this family may contain other protein-binding domains such as those involving caspase activation and recruitment.
Glycoproteins found on the membrane or surface of cells.
A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
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.
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.
An interleukin-1 subtype that is synthesized as an inactive membrane-bound pro-protein. Proteolytic processing of the precursor form by CASPASE 1 results in release of the active form of interleukin-1beta from the membrane.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
A large group of proteins that control APOPTOSIS. This family of proteins includes many ONCOGENE PROTEINS as well as a wide variety of classes of INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS such as CASPASES.
Drugs that are used to treat RHEUMATOID ARTHRITIS.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).
A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.
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.
Tumor necrosis factor receptor family members that are widely expressed and play a role in regulation of peripheral immune responses and APOPTOSIS. The receptors are specific for TNF-RELATED APOPTOSIS-INDUCING LIGAND and signal via conserved death domains that associate with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Substances that reduce or suppress INFLAMMATION.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
A long pro-domain caspase that contains a death effector domain in its pro-domain region. Caspase 8 plays a role in APOPTOSIS by cleaving and activating EFFECTOR CASPASES. Activation of this enzyme can occur via the interaction of its N-terminal death effector domain with DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS.
Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells.
A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, and chemicals from the environment.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
The action of a drug in promoting or enhancing the effectiveness of another drug.
Intracellular signaling peptides and proteins that bind directly or indirectly to the cytoplasmic portion of TUMOR NECROSIS FACTOR RECEPTORS.
A signal transducing tumor necrosis factor receptor associated factor that is involved in TNF RECEPTOR feedback regulation. It is similar in structure and appears to work in conjunction with TNF RECEPTOR-ASSOCIATED FACTOR 1 to inhibit APOPTOSIS.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 9. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
A severe form of acute INFLAMMATION of the PANCREAS characterized by one or more areas of NECROSIS in the pancreas with varying degree of involvement of the surrounding tissues or organ systems. Massive pancreatic necrosis may lead to DIABETES MELLITUS, and malabsorption.
A family of inhibitory proteins which bind to the REL PROTO-ONCOGENE PROTEINS and modulate their activity. In the CYTOPLASM, I-kappa B proteins bind to the transcription factor NF-KAPPA B. Cell stimulation causes its dissociation and translocation of active NF-kappa B to the nucleus.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Diseases of freshwater, marine, hatchery or aquarium fish. This term includes diseases of both teleosts (true fish) and elasmobranchs (sharks, rays and skates).
A signal transducing tumor necrosis factor receptor associated factor that is involved in TNF RECEPTOR feedback regulation. It is similar in structure and appears to work in conjunction with TNF RECEPTOR-ASSOCIATED FACTOR 2 to inhibit APOPTOSIS.
A METHYLXANTHINE derivative that inhibits phosphodiesterase and affects blood rheology. It improves blood flow by increasing erythrocyte and leukocyte flexibility. It also inhibits platelet aggregation. Pentoxifylline modulates immunologic activity by stimulating cytokine production.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
Death of a bone or part of a bone, either atraumatic or posttraumatic.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A cell-surface ligand involved in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue.
Mature LYMPHOCYTES and MONOCYTES transported by the blood to the body's extravascular space. They are morphologically distinguishable from mature granulocytic leukocytes by their large, non-lobed nuclei and lack of coarse, heavily stained cytoplasmic granules.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
A cell line derived from cultured tumor cells.
A protein serine-threonine kinase that catalyzes the PHOSPHORYLATION of I KAPPA B PROTEINS. This enzyme also activates the transcription factor NF-KAPPA B and is composed of alpha and beta catalytic subunits, which are protein kinases and gamma, a regulatory subunit.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A subgroup of mitogen-activated protein kinases that activate TRANSCRIPTION FACTOR AP-1 via the phosphorylation of C-JUN PROTEINS. They are components of intracellular signaling pathways that regulate CELL PROLIFERATION; APOPTOSIS; and CELL DIFFERENTIATION.
A family of membrane-anchored glycoproteins that contain a disintegrin and metalloprotease domain. They are responsible for the proteolytic cleavage of many transmembrane proteins and the release of their extracellular domain.
A CALCIUM-independent subtype of nitric oxide synthase that may play a role in immune function. It is an inducible enzyme whose expression is transcriptionally regulated by a variety of CYTOKINES.
Death of pulp tissue with or without bacterial invasion. When the necrosis is due to ischemia with superimposed bacterial infection, it is referred to as pulp gangrene. When the necrosis is non-bacterial in origin, it is called pulp mummification.
A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.
A subunit of NF-kappa B that is primarily responsible for its transactivation function. It contains a C-terminal transactivation domain and an N-terminal domain with homology to PROTO-ONCOGENE PROTEINS C-REL.
A tumor necrosis factor receptor subtype with specificity for TUMOR NECROSIS FACTOR LIGAND SUPERFAMILY MEMBER 15. It is found in tissues containing LYMPHOCYTES and may play a role in regulating lymphocyte homeostasis and APOPTOSIS. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
Disease having a short and relatively severe course.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).
Splitting the DNA into shorter pieces by endonucleolytic DNA CLEAVAGE at multiple sites. It includes the internucleosomal DNA fragmentation, which along with chromatin condensation, are considered to be the hallmarks of APOPTOSIS.
The inner membrane of a joint capsule surrounding a freely movable joint. It is loosely attached to the external fibrous capsule and secretes SYNOVIAL FLUID.
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.
An encapsulated lymphatic organ through which venous blood filters.
Endogenous and exogenous compounds and that either inhibit CASPASES or prevent their activation.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
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.
Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include, but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
A signal transducing tumor necrosis factor receptor associated factor that is involved in regulation of NF-KAPPA B signalling and activation of JNK MITOGEN-ACTIVATED PROTEIN KINASES.
An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.
Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.
Transport proteins that carry specific substances in the blood or across cell membranes.
Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.
Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC 2.6.1.2.
A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.
Cytokine-induced cell adhesion molecule present on activated endothelial cells, tissue macrophages, dendritic cells, bone marrow fibroblasts, myoblasts, and myotubes. It is important for the recruitment of leukocytes to sites of inflammation. (From Pigott & Power, The Adhesion Molecule FactsBook, 1993, p154)
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
A chemokine that is a chemoattractant for MONOCYTES and may also cause cellular activation of specific functions related to host defense. It is produced by LEUKOCYTES of both monocyte and lymphocyte lineage and by FIBROBLASTS during tissue injury. It has specificity for CCR2 RECEPTORS.
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).
INFLAMMATION of the PANCREAS. Pancreatitis is classified as acute unless there are computed tomographic or endoscopic retrograde cholangiopancreatographic findings of CHRONIC PANCREATITIS (International Symposium on Acute Pancreatitis, Atlanta, 1992). The two most common forms of acute pancreatitis are ALCOHOLIC PANCREATITIS and gallstone pancreatitis.
A secreted tumor necrosis factor receptor family member that has specificity FAS LIGAND and TUMOR NECROSIS FACTOR LIGAND SUPERFAMILY MEMBER 14. It plays a modulating role in tumor necrosis factor signaling pathway.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Caspase 9 is activated during cell stress by mitochondria-derived proapoptotic factors and by CARD SIGNALING ADAPTOR PROTEINS such as APOPTOTIC PROTEASE-ACTIVATING FACTOR 1. It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES.
Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli.
Biologically active substances whose activities affect or play a role in the functioning of the immune system.
A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
An acidic glycoprotein of MW 23 kDa with internal disulfide bonds. The protein is produced in response to a number of inflammatory mediators by mesenchymal cells present in the hemopoietic environment and at peripheral sites of inflammation. GM-CSF is able to stimulate the production of neutrophilic granulocytes, macrophages, and mixed granulocyte-macrophage colonies from bone marrow cells and can stimulate the formation of eosinophil colonies from fetal liver progenitor cells. GM-CSF can also stimulate some functional activities in mature granulocytes and macrophages.
A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.
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.
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
The rate dynamics in chemical or physical systems.
Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis.
Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C; (CHEMOKINES, C); CC; (CHEMOKINES, CC); and CXC; (CHEMOKINES, CXC); according to variations in a shared cysteine motif.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
Adherence of cells to surfaces or to other cells.
A family of bullet-shaped viruses of the order MONONEGAVIRALES, infecting vertebrates, arthropods, protozoa, and plants. Genera include VESICULOVIRUS; LYSSAVIRUS; EPHEMEROVIRUS; NOVIRHABDOVIRUS; Cytorhabdovirus; and Nucleorhabdovirus.
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.
Round, granular, mononuclear phagocytes found in the alveoli of the lungs. They ingest small inhaled particles resulting in degradation and presentation of the antigen to immunocompetent cells.
A ligand that binds to but fails to activate the INTERLEUKIN 1 RECEPTOR. It plays an inhibitory role in the regulation of INFLAMMATION and FEVER. Several isoforms of the protein exist due to multiple ALTERNATIVE SPLICING of its mRNA.
Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.
A signal-transducing adaptor protein that associates with TNF RECEPTOR complexes. It contains a death effector domain that can interact with death effector domains found on INITIATOR CASPASES such as CASPASE 8 and CASPASE 10. Activation of CASPASES via interaction with this protein plays a role in the signaling cascade that leads to APOPTOSIS.
A heterodimeric cytokine that plays a role in innate and adaptive immune responses. Interleukin-12 is a 70 kDa protein that is composed of covalently linked 40 kDa and 35 kDa subunits. It is produced by DENDRITIC CELLS; MACROPHAGES and a variety of other immune cells and plays a role in the stimulation of INTERFERON-GAMMA production by T-LYMPHOCYTES and NATURAL KILLER CELLS.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
A human cell line established from a diffuse histiocytic lymphoma (HISTIOCYTIC LYMPHOMA, DIFFUSE) and displaying many monocytic characteristics. It serves as an in vitro model for MONOCYTE and MACROPHAGE differentiation.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
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.
A sarcoma derived from deep fibrous tissue, characterized by bundles of immature proliferating fibroblasts with variable collagen formation, which tends to invade locally and metastasize by the bloodstream. (Stedman, 25th ed)
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.
A pattern recognition receptor that interacts with LYMPHOCYTE ANTIGEN 96 and LIPOPOLYSACCHARIDES. It mediates cellular responses to GRAM-NEGATIVE BACTERIA.
An APOPTOSIS-regulating protein that is structurally related to CASPASE 8 and competes with CASPASE 8 for binding to FAS ASSOCIATED DEATH DOMAIN PROTEIN. Two forms of CASP8 and FADD-like apoptosis regulating protein exist, a long form containing a caspase-like enzymatically inactive domain and a short form which lacks the caspase-like domain.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
A 34 kDa signal transducing adaptor protein that associates with TUMOR NECROSIS FACTOR RECEPTOR TYPE 1. It facilitates the recruitment of signaling proteins such as TNF RECEPTOR-ASSOCIATED FACTOR 2 and FAS ASSOCIATED DEATH DOMAIN PROTEIN to the receptor complex.
Venous vessels in the umbilical cord. They carry oxygenated, nutrient-rich blood from the mother to the FETUS via the PLACENTA. In humans, there is normally one umbilical vein.
A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents.
An anti-inflammatory 9-fluoro-glucocorticoid.
Cell adhesion molecule and CD antigen that mediates neutrophil, monocyte, and memory T-cell adhesion to cytokine-activated endothelial cells. E-selectin recognizes sialylated carbohydrate groups related to the Lewis X or Lewis A family.
A plasma protein that circulates in increased amounts during inflammation and after tissue damage.
Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC 1.11.1.7.
Virus diseases caused by RHABDOVIRIDAE. Important infections include RABIES; EPHEMERAL FEVER; and vesicular stomatitis.
Tongues of skin and subcutaneous tissue, sometimes including muscle, cut away from the underlying parts but often still attached at one end. They retain their own microvasculature which is also transferred to the new site. They are often used in plastic surgery for filling a defect in a neighboring region.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
ENDOPEPTIDASES which use a metal such as ZINC in the catalytic mechanism.
A soluble factor produced by activated T-LYMPHOCYTES that induces the expression of MHC CLASS II GENES and FC RECEPTORS on B-LYMPHOCYTES and causes their proliferation and differentiation. It also acts on T-lymphocytes, MAST CELLS, and several other hematopoietic lineage cells.
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
The hemispheric articular surface at the upper extremity of the thigh bone. (Stedman, 26th ed)
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
Pathological processes of the LIVER.

Systemic infection with Alaria americana (Trematoda). (1/6081)

Alaria americana is a trematode, the adult of which is found in mammalian carnivores. The first case of disseminated human infection by the mesocercarial stage of this worm occurred in a 24-year-old man. The infection possibly was acquired by the eating of inadequately cooked frogs, which are intermediate hosts of the worm. The diagnosis was made during life by lung biopsy and confirmed at autopsy. The mesocercariae were present in the stomach wall, lymph nodes, liver, myocardium, pancreas and surrounding adipose tissue, spleen, kidney, lungs, brain and spinal cord. There was no host reaction to the parasites. Granulomas were present in the stomach wall, lymph nodes and liver, but the worms were not identified in them. Hypersensitivity vasculitis and a bleeding diathesis due to disseminated intravascular coagulation and a circulating anticoagulant caused his death 8 days after the onset of his illness.  (+info)

Daunorubicin-induced apoptosis in rat cardiac myocytes is inhibited by dexrazoxane. (2/6081)

-The clinical efficacy of anthracycline antineoplastic agents is limited by a high incidence of severe and usually irreversible cardiac toxicity, the cause of which remains controversial. In primary cultures of neonatal and adult rat ventricular myocytes, we found that daunorubicin, at concentrations /=10 micromol/L induced necrotic cell death within 24 hours, with no changes characteristic of apoptosis. To determine whether reactive oxygen species play a role in daunorubicin-mediated apoptosis, we monitored the generation of hydrogen peroxide with dichlorofluorescein (DCF). However, daunorubicin (1 micromol/L) did not increase DCF fluorescence, nor were the antioxidants N-acetylcysteine or the combination of alpha-tocopherol and ascorbic acid able to prevent apoptosis. In contrast, dexrazoxane (10 micromol/L), known clinically to limit anthracycline cardiac toxicity, prevented daunorubicin-induced myocyte apoptosis, but not necrosis induced by higher anthracycline concentrations (>/=10 micromol/L). The antiapoptotic action of dexrazoxane was mimicked by the superoxide-dismutase mimetic porphyrin manganese(II/III)tetrakis(1-methyl-4-peridyl)porphyrin (50 micromol/L). The recognition that anthracycline-induced cardiac myocyte apoptosis, perhaps mediated by superoxide anion generation, occurs at concentrations well below those that result in myocyte necrosis, may aid in the design of new therapeutic strategies to limit the toxicity of these drugs.  (+info)

Changes in the total number of neuroglia, mitotic cells and necrotic cells in the anterior limb of the mouse anterior commissure following hypoxic stress. (3/6081)

The effects of hypoxic stress (390 mmHg) on the total number of glia, cell division, and cell death in the anterior limb of the anterior commissure were studied. There was a significant (P less than 0-01) fall in the total number of glia following exposure to hypoxia at 390 mmHg for two days. No significant change was observed in the total number of glia between the hypoxic and recovery group one week after return to sea level (ca. 760 mmHg). No change was observed in the number of mitotic figures in the control, hypoxic or recovery groups, but significant falls were observed in the mean number of necrotic cells between both the control and hypoxic groups (P less than 0-05) and the hypoxic and recovery groups (P less than 0-012). The decrease in necrotic cells may be due to a large number of elderly and effete cells, which would normally have undergone degeneration over a period of weeks, dying rapidly after the onset of hypoxia, thus temporarily reducing the daily cell death rate.  (+info)

A photodynamic pathway to apoptosis and necrosis induced by dimethyl tetrahydroxyhelianthrone and hypericin in leukaemic cells: possible relevance to photodynamic therapy. (4/6081)

The mechanism of cell death induction by dimethyl tetrahydroxyhelianthrone (DTHe), a new second-generation photodynamic sensitizer, is analysed in human leukaemic cell lines in comparison with the structurally related hypericin. DTHe has a broad range of light spectrum absorption that enables effective utilization of polychromatic light. Photosensitization of HL-60 cells with low doses of DTHe (0.65 microM DTHe and 7.2 J cm(-2) light energy) induced rapid apoptosis of > or =90% of the cells. At doses > or =2 microM, dying cells assumed morphological necrosis with perinucleolar condensation of chromatin in HL-60 and K-562 cell lines. Although nuclear fragmentation that is characteristic to apoptosis was prevented, DNA digestion to oligonucleosomes proceeded unhindered. Such incomplete apoptosis was more prevalent with the related analogue hypericin throughout most doses of photosensitization. Despite hypericin being a stronger photosensitizer, DTHe exhibited advantageous phototoxic properties to tumour cells, initiating apoptosis at concentrations about threefold lower than hypericin. Photosensitization of the cells induced dissociation of the nuclear envelope, releasing lamins into the cytosol. DTHe also differed from hypericin in effects exerted on the nuclear lamina, causing release of an 86-kDa lamin protein into the cytosol that was unique to DTHe. Within the nucleus, nuclear envelope lamin B underwent covalent polymerization, which did not affect apoptotic nuclear fragmentation at low doses of DTHe. At higher doses, polymerization may have been extensive enough to prevent nuclear collapse. Hut-78, CD4+ cells were resistant to the photodynamically activated apoptotic pathway. Beyond the tolerated levels of photodynamic damage, these cells died exclusively via necrosis. Hut-78 cells overexpress Bcl-X(L) as well as a truncated Bcl-X(L)tr isoform that could contribute to the observed resistance to apoptosis.  (+info)

Diet and risk of ethanol-induced hepatotoxicity: carbohydrate-fat relationships in rats. (5/6081)

Nutritional status is a primary factor in the effects of xenobiotics and may be an important consideration in development of safety standards and assessment of risk. One important xenobiotic consumed daily by millions of people worldwide is alcohol. Some adverse effects of ethanol, such as alcohol liver disease, have been linked to diet. For example, ethanol-induced hepatotoxicity in animal models requires diets that have a high percentage of the total calories as unsaturated fat. However, little attention has been given to the role of carbohydrates (or carbohydrate to fat ratio) in the effects of this important xenobiotic on liver injury. In the present study, adult male Sprague-Dawley rats (8-10/group) were infused (intragastrically) diets high in unsaturated fat (25 or 45% total calories), sufficient protein (16%) and ethanol (38%) in the presence or absence of adequate carbohydrate (21 or 2.5%) for 42-55 days (d). Animals infused ethanol-containing diets adequate in carbohydrate developed steatosis, but had no other signs of hepatic pathology. However, rats infused with the carbohydrate-deficient diet had a 4-fold increase in serum ALT levels (p < 0.05), an unexpectedly high (34-fold) induction of hepatic microsomal CYP2E1 apoprotein (p < 0.001), and focal necrosis. The strong positive association between low dietary carbohydrate, enhanced CYP2E1 induction and hepatic necrosis suggests that in the presence of low carbohydrate intake, ethanol induction of CYP2E1 is enhanced to levels sufficient to cause necrosis, possibly through reactive oxygen species and other free radicals generated by CYP2E1 metabolism of ethanol and unsaturated fatty acids.  (+info)

Tumor suppression in human skin carcinoma cells by chromosome 15 transfer or thrombospondin-1 overexpression through halted tumor vascularization. (6/6081)

The development of skin carcinomas presently is believed to be correlated with mutations in the p53 tumor suppressor and ras gene as well as with the loss of chromosome 9. We now demonstrate that, in addition, loss of chromosome 15 may be a relevant genetic defect. Reintroduction of an extra copy of chromosome 15, but not chromosome 4, into the human skin carcinoma SCL-I cells, lacking one copy of each chromosome, resulted in tumor suppression after s.c. injection in mice. Transfection with thrombospondin-1 (TSP-1), mapped to 15q15, induced the same tumor suppression without affecting cell proliferation in vitro or in vivo. Halted tumors remained as small cysts encapsulated by surrounding stroma and blood vessels. These cysts were characterized by increased TSP-1 matrix deposition at the tumor/stroma border and a complete lack of tumor vascularization. Coinjection of TSP-1 antisense oligonucleotides drastically reduced TSP-1 expression and almost completely abolished matrix deposition at the tumor/stroma border. As a consequence, the tumor phenotype reverted to a well vascularized, progressively expanding, solid carcinoma indistinguishable from that induced by the untransfected SCL-I cells. Thus, these data strongly suggest TSP-1 as a potential tumor suppressor on chromosome 15. The data further propose an unexpected mechanism of TSP-1-mediated tumor suppression. Instead of interfering with angiogenesis in general, in this system TSP-1 acts as a matrix barrier at the tumor/stroma border, which, by halting tumor vascularization, prevents tumor cell invasion and, thus, tumor expansion.  (+info)

Mycophenolate mofetil inhibits rat and human mesangial cell proliferation by guanosine depletion. (7/6081)

BACKGROUND: Mycophenolate mofetil (MMF) is used for immunosuppression after renal transplantation because it reduces lymphocyte proliferation by inhibiting inosine monophosphate dehydrogenase (IMPDH) in lymphocytes and GTP biosynthesis. In the present study we asked if therapeutic concentrations of MMF might interfere with mesangial cell (MC) proliferation which is involved in inflammatory proliferative glomerular diseases. METHODS: Rat and human MCs were growth-arrested by withdrawal of fetal calf serum (FCS) and stimulated by addition of FCS, platelet-derived growth factor (PDGF) or lysophosphatidic acid (LPA). Different concentrations of MMF (0.019-10 microM) were added concomitantly in the presence or absence of guanosine. MC proliferation was determined by [3H]thymidine incorporation. Cell viability was assessed by trypan blue exclusion. Apoptotic nuclei were stained using the Hoechst dye H33258. Cytosolic free Ca2+ concentrations were determined with the fluorescent calcium chelator fura-2-AM. RESULTS: MMF inhibited mitogen-induced rat MC proliferation with an IC50 of 0.45 +/- 0.13 microM. Human MCs proved to be even more sensitive (IC50 0.19 +/- 0.06 microM). Inhibition of MC proliferation was reversible and not accompanied by cellular necrosis or apoptosis. Addition of guanosine prevented the antiproliferative effect of MMF, indicating that inhibition of IMPDH is responsible for decreased MC proliferation. Early signalling events of GTP-binding-protein-coupled receptors, such as changes in intracellular Ca2+ levels were not affected by MMF. CONCLUSIONS: The results show that MMF has a concentration-dependent antiproliferative effect on cultured MCs in the therapeutic range, which might be a rationale for the use of this drug in the treatment of mesangial proliferative glomerulonephritis.  (+info)

Bcl-2 alters the balance between apoptosis and necrosis, but does not prevent cell death induced by oxidized low density lipoproteins. (8/6081)

Oxidized low density lipoproteins (oxLDL) participate in atherosclerosis plaque formation, rupture, and subsequent thrombosis. Because oxLDL are toxic to cultured cells and Bcl-2 protein prevents apoptosis, the present work aimed to study whether Bcl-2 may counterbalance the toxicity of oxLDL. Two experimental model systems were used in which Bcl-2 levels were modulated: 1) lymphocytes in which the (high) basal level of Bcl-2 was reduced by antisense oligonucleotides; 2) HL60 and HL60/B (transduced by Bcl-2) expressing low and high Bcl-2 levels, respectively. In cells expressing relatively high Bcl-2 levels (lymphocytes and HL60/B), oxLDL induced mainly primary necrosis. In cells expressing low Bcl-2 levels (antisense-treated lymphocytes, HL60 and ECV-304 endothelial cells), the rate of oxLDL-induced apoptosis was higher than that of primary necrosis. OxLDL evoked a sustained calcium rise, which is a common trigger to necrosis and apoptosis since both types of cell death were blocked by the calcium chelator EGTA. Conversely, a sustained calcium influx elicited by the calcium ionophore A23187 induced necrosis in cells expressing high Bcl-2 levels and apoptosis in cells expressing low Bcl-2 levels. This suggests that Bcl-2 acts downstream from the calcium peak and inhibits only the apoptotic pathway, not the necrosis pathway, thus explaining the apparent shift from oxLDL-induced apoptosis toward necrosis when Bcl-2 is overexpressed.  (+info)

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.

The symptoms of fat necrosis can vary depending on the location and extent of the affected tissue. In some cases, there may be no symptoms at all, while in others, there may be pain, swelling, redness, and warmth in the affected area. If the condition becomes severe, it can lead to the formation of a fat necrosis mass or abscess, which can be painful and tender to the touch.

Fat necrosis is typically diagnosed through imaging studies such as ultrasound, CT scan, or MRI. A biopsy may also be performed to confirm the diagnosis and rule out other conditions.

Treatment of fat necrosis depends on the severity of the condition and can range from conservative measures such as rest, ice, compression, and elevation (RICE) to surgical intervention in more severe cases. In some cases, antibiotics may be prescribed if there is an underlying infection.

Preventing fat necrosis is challenging, but it can be minimized by avoiding trauma or injury to the affected area, maintaining good wound care, and managing any underlying medical conditions that may contribute to the development of the condition.

This can cause pain, stiffness, and difficulty walking. In severe cases, it can lead to complete hip joint dislocation. FHN is typically caused by trauma or aseptic conditions such as osteonecrosis (death of bone cells due to lack of blood supply), sickle cell disease, Gaucher's disease, and long-term use of steroids. Treatment options include conservative management with pain management, physical therapy, and avoiding activities that exacerbate the condition; or surgical intervention such as femoral head osteotomy (cutting and realigning the bone) or hip replacement.

The prognosis for FHN depends on the severity of the condition, with more severe cases carrying a worse prognosis. Early diagnosis and treatment are key to improving outcomes.

Symptoms:

* Blood in urine
* Pain in the back or flank
* Fever
* Nausea and vomiting

Diagnosis:

* Imaging tests like ultrasound, CT scan, or MRI to visualize the papillae and assess any damage
* Biopsy to examine kidney tissue under a microscope for signs of inflammation and scarring

Treatment:

* Antibiotics for infections
* Corticosteroids to reduce inflammation
* Immunosuppressive drugs for autoimmune disorders
* Dialysis in severe cases

Prognosis:

* Mild cases may resolve on their own, but severe cases can lead to chronic kidney disease and potentially kidney failure.

Complications:

* Chronic kidney disease
* Kidney failure
* High blood pressure
* Recurrent infections

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.

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?
------------------------------------------

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.

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.

The symptoms of acute RNS may include:

1. Severe eye pain
2. Blurred vision or loss of vision
3. Sensitivity to light
4. Redness and swelling of the eye
5. Floaters (specks or cobwebs in vision)
6. Flashes of light

The exact cause of acute RNS is not known, but it is believed to be related to a viral or bacterial infection, trauma, or systemic diseases such as diabetes, high blood pressure, and autoimmune disorders.

Diagnosis of acute RNS typically involves a comprehensive eye exam, including imaging tests such as fluorescein angiography and optical coherence tomography (OCT) to evaluate the retina and optic nerve. Laboratory tests may also be ordered to rule out other causes of vision loss.

Treatment for acute RNS is focused on addressing the underlying cause and managing symptoms. This may include antiviral or antibacterial medications, corticosteroids, and pain management. In severe cases, surgery may be necessary to remove damaged tissue or repair the retina.

Prognosis for acute RNS varies depending on the underlying cause and severity of the condition. In some cases, vision loss may be permanent, while in others, vision can improve with treatment. Prompt medical attention is essential to minimize visual loss and prevent complications.

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.

There are several symptoms of RA, including:

1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)

RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.

There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.

The definition of DILI has been revised several times over the years, but the most recent definition was published in 2013 by the International Consortium for DILI Research (ICDCR). According to this definition, DILI is defined as:

"A clinically significant alteration in liver function that is caused by a medication or other exogenous substance, and is not related to underlying liver disease. The alteration may be biochemical, morphological, or both, and may be acute or chronic."

The ICDCR definition includes several key features of DILI, including:

1. Clinically significant alteration in liver function: This means that the liver damage must be severe enough to cause symptoms or signs of liver dysfunction, such as jaundice, nausea, vomiting, or abdominal pain.
2. Caused by a medication or other exogenous substance: DILI is triggered by exposure to certain drugs or substances that are not related to underlying liver disease.
3. Not related to underlying liver disease: This means that the liver damage must not be caused by an underlying condition such as hepatitis B or C, alcoholic liver disease, or other genetic or metabolic disorders.
4. May be acute or chronic: DILI can occur as a sudden and severe injury (acute DILI) or as a slower and more insidious process (chronic DILI).

The ICDCR definition provides a standardized way of defining and diagnosing DILI, which is important for clinicians and researchers to better understand the cause of liver damage in patients who are taking medications. It also helps to identify the drugs or substances that are most likely to cause liver injury and to develop strategies for preventing or treating DILI.

The symptoms of ANP can include:

1. Severe abdominal pain that worsens rapidly within a few days
2. Fever
3. Nausea and vomiting
4. Diarrhea or constipation
5. Blood in stools or vomitus
6. Signs of organ failure, such as decreased blood pressure, tachycardia, and tachypnea
7. Sepsis or infection
8. Pleural effusion or ascites
9. Rhabdomyolysis (breakdown of muscle tissue)
10. Elevated serum levels of inflammatory markers, such as CRP and WBC.

The diagnosis of ANP is based on a combination of clinical features, laboratory tests, and imaging studies. Laboratory tests may include:

1. Elevated serum levels of amylase and lipase
2. Elevated blood urea nitrogen (BUN) and creatinine
3. Increased white blood cell count and elevated C-reactive protein (CRP)
4. Electrolyte imbalance
5. Renal failure
6. Hepatic dysfunction
7. Cardiovascular instability
8. Coagulopathy
9. Hypocalcemia
10. Hyperglycemia

Imaging studies, such as CT scans or MRI, may show:

1. Widespread pancreatic necrosis
2. Inflammation in the surrounding tissues
3. Abscesses or fluid collections in the pancreas or peripancreatic tissues
4. Obstruction of the pancreatic duct
5. Intestinal ischemia or perforation
6. Peritonitis or retroperitoneal abscess

The treatment of ANP involves a multidisciplinary approach, including surgical, medical, and radiological interventions. The goals of treatment are to:

1. Stabilize the patient's vital signs and correct any electrolyte imbalances
2. Manage infection and sepsis
3. Provide supportive care for any organ dysfunction or failure
4. Remove any obstructions or necrotic tissue from the pancreas
5. Promote pancreatic tissue healing and regeneration
6. Prevent further complications, such as pancreatic fibrosis or pseudocyst formation

Surgical interventions may include:

1. Pancreatectomy: removal of the necrotic or infarcted pancreatic tissue
2. Drainage of abscesses or fluid collections
3. Repair of any obstructions in the pancreatic duct
4. Debridement of any infected or necrotic tissue
5. Reconstruction of the pancreas and surrounding tissues

Medical interventions may include:

1. Antibiotics to treat infection and sepsis
2. Pain management with analgesics and sedatives
3. Management of diabetes or other endocrine disorders
4. Supportive care for any organ dysfunction or failure
5. Monitoring of vital signs and laboratory values

Radiological interventions may include:

1. Imaging studies to evaluate the extent of the inflammation and assess the response to treatment
2. Therapeutic interventions, such as endoscopic retrograde cholangiopancreatography (ERCP) or percutaneous drainage of abscesses

The prognosis for ANP depends on several factors, including the severity of the inflammation, the presence of any complications, and the timeliness and effectiveness of treatment. In general, the sooner treatment is initiated, the better the prognosis. Mortality rates for ANP have been reported to range from 5-20%, with higher mortality rates associated with more severe disease and delayed treatment.

Prevention of ANP involves prompt management of any underlying conditions or risk factors that may lead to pancreatitis. This includes:

1. Proper management of gallstones, including cholecystectomy if necessary
2. Treatment of chronic alcoholism and cessation of alcohol consumption
3. Management of hyperlipidemia with appropriate medications and lifestyle modifications
4. Avoiding certain medications that may increase the risk of pancreatitis, such as certain antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs)
5. Maintaining good overall health and avoiding any other potential risk factors for pancreatitis, such as smoking and excessive physical activity.

Some common types of fish diseases include:

1. Bacterial infections: These are caused by bacteria such as Aeromonas, Pseudomonas, and Mycobacterium. Symptoms can include fin and tail rot, body slime, and ulcers.
2. Viral infections: These are caused by viruses such as viral hemorrhagic septicemia (VHS) and infectious hematopoietic necrosis (IHN). Symptoms can include lethargy, loss of appetite, and rapid death.
3. Protozoan infections: These are caused by protozoa such as Cryptocaryon and Ichthyophonus. Symptoms can include flashing, rapid breathing, and white spots on the body.
4. Fungal infections: These are caused by fungi such as Saprolegnia and Achlya. Symptoms can include fuzzy growths on the body and fins, and sluggish behavior.
5. Parasitic infections: These are caused by parasites such as Ichthyophonus and Cryptocaryon. Symptoms can include flashing, rapid breathing, and white spots on the body.

Diagnosis of fish diseases is typically made through a combination of physical examination, laboratory tests, and observation of the fish's behavior and environment. Treatment options vary depending on the type of disease and the severity of symptoms, and can include antibiotics, antifungals, and medicated baths. Prevention is key in managing fish diseases, and this includes maintaining good water quality, providing a balanced diet, and keeping the fish in a healthy environment.

Note: The information provided is a general overview of common fish diseases and their symptoms, and should not be considered as professional medical advice. If you suspect your fish has a disease, it is recommended that you consult with a veterinarian or a qualified aquarium expert for proper diagnosis and treatment.

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.

The symptoms of dental pulp necrosis can include:

* Toothache pain that is often severe and throbbing
* Sensitivity to hot or cold foods and drinks
* Swelling and redness in the gum tissue near the affected tooth
* A bad taste or smell in the mouth
* Discharge of pus from the gums near the affected tooth

If left untreated, dental pulp necrosis can lead to more serious complications such as an abscessed tooth, bone loss, and even sepsis. Treatment options for dental pulp necrosis include root canal therapy, extraction of the affected tooth, or antibiotic therapy if the infection has spread beyond the tooth.

It is important to seek professional dental care if you experience any symptoms of dental pulp necrosis to prevent further complications and maintain good oral health.

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.

Shock refers to a severe and sudden drop in blood pressure, which can lead to inadequate perfusion of vital organs such as the brain, heart, and lungs. There are several types of shock, including hypovolemic shock (caused by bleeding or dehydration), septic shock (caused by an overwhelming bacterial infection), and cardiogenic shock (caused by a heart attack or other cardiac condition).

Septic refers to the presence of bacteria or other microorganisms in the bloodstream, which can cause a range of symptoms including fever, chills, and confusion. Sepsis is a serious and potentially life-threatening condition that can lead to organ failure and death if left untreated.

Septic shock is a specific type of shock that occurs as a result of sepsis, which is the body's systemic inflammatory response to an infection. Septic shock is characterized by severe vasopressor (a medication used to increase blood pressure) and hypotension (low blood pressure), and it can lead to multiple organ failure and death if not treated promptly and effectively.

In summary, shock refers to a drop in blood pressure, while septic refers to the presence of bacteria or other microorganisms in the bloodstream. Septic shock is a specific type of shock that occurs as a result of sepsis, and it can be a life-threatening condition if not treated promptly and effectively.

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 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.

There are several causes of pancreatitis, including:

1. Gallstones: These can block the pancreatic duct, causing inflammation.
2. Alcohol consumption: Heavy alcohol use can damage the pancreas and lead to inflammation.
3. High triglycerides: Elevated levels of triglycerides in the blood can cause pancreatitis.
4. Infections: Viral or bacterial infections can infect the pancreas and cause inflammation.
5. Genetic factors: Some people may be more susceptible to pancreatitis due to inherited genetic mutations.
6. Pancreatic trauma: Physical injury to the pancreas can cause inflammation.
7. Certain medications: Some medications, such as certain antibiotics and chemotherapy drugs, can cause pancreatitis as a side effect.

Symptoms of pancreatitis may include:

1. Abdominal pain
2. Nausea and vomiting
3. Fever
4. Diarrhea or bloating
5. Weight loss
6. Loss of appetite

Treatment for pancreatitis depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to manage symptoms and address any complications. Treatment options may include:

1. Pain management: Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids may be used to manage abdominal pain.
2. Fluid replacement: Intravenous fluids may be given to replace lost fluids and electrolytes.
3. Antibiotics: If the pancreatitis is caused by an infection, antibiotics may be prescribed to treat the infection.
4. Nutritional support: Patients with pancreatitis may require nutritional support to ensure they are getting enough calories and nutrients.
5. Pancreatic enzyme replacement therapy: In some cases, pancreatic enzyme replacement therapy may be necessary to help the body digest food.
6. Surgery: In severe cases of pancreatitis, surgery may be necessary to remove damaged tissue or repair damaged blood vessels.

It is important to seek medical attention if you experience persistent abdominal pain or other symptoms of pancreatitis, as early treatment can help prevent complications and improve outcomes.

The exact cause of fibrosarcoma is not known, but it is believed to be linked to genetic mutations that occur during a person's lifetime. Some risk factors for developing fibrosarcoma include previous radiation exposure, chronic inflammation, and certain inherited conditions such as neurofibromatosis type 1 (NF1).

The symptoms of fibrosarcoma can vary depending on the location and size of the tumor. In some cases, there may be no symptoms until the tumor has grown to a significant size. Common symptoms include pain, swelling, and limited mobility in the affected limb. If the tumor is near a nerve, it can also cause numbness or tingling sensations in the affected area.

Diagnosis of fibrosarcoma typically involves a combination of imaging tests such as X-rays, CT scans, and MRI scans, as well as a biopsy to confirm the presence of cancer cells. Treatment options for fibrosarcoma may include surgery, radiation therapy, and chemotherapy, depending on the size and location of the tumor, as well as the patient's overall health.

Prognosis for fibrosarcoma is generally good if the tumor is caught early and treated aggressively. However, if the cancer has spread to other parts of the body (metastasized), the prognosis is generally poorer. In some cases, the cancer can recur after treatment, so it is important for patients to follow their doctor's recommendations for regular check-ups and follow-up testing.

Overall, fibrosarcoma is a rare and aggressive form of cancer that can be challenging to diagnose and treat. However, with early detection and appropriate treatment, many people with this condition can achieve long-term survival and a good quality of life.

Granulomas are formed in response to the presence of a foreign substance or an infection, and they serve as a protective barrier to prevent the spread of the infection and to isolate the offending agent. The granuloma is characterized by a central area of necrosis, surrounded by a ring of immune cells, including macrophages and T-lymphocytes.

Granulomas are commonly seen in a variety of inflammatory conditions, such as tuberculosis, leprosy, and sarcoidosis. They can also occur as a result of infections, such as bacterial or fungal infections, and in the context of autoimmune disorders, such as rheumatoid arthritis.

In summary, granuloma is a term used to describe a type of inflammatory lesion that is formed in response to the presence of a foreign substance or an infection, and serves as a protective barrier to prevent the spread of the infection and to isolate the offending agent.

Example sentences:

1. The rhabdoviridae infections in cattle can cause significant economic losses for farmers, as they can lead to reduced milk production and mortality rates.
2. Scientists are working on developing vaccines against rhabdoviridae infections in pigs, which could help reduce the risk of disease transmission to humans.

There are several types of edema, including:

1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.

Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.

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.

1. Influenza (flu): Caused by the influenza virus, which is an RNA virus that affects the respiratory system and can cause fever, cough, sore throat, and body aches.
2. HIV/AIDS: Caused by the human immunodeficiency virus (HIV), which is an RNA virus that attacks the body's immune system and can lead to acquired immunodeficiency syndrome (AIDS).
3. Hepatitis B: Caused by the hepatitis B virus, which is an RNA virus that infects the liver and can cause inflammation, scarring, and cancer.
4. Measles: Caused by the measles virus, which is an RNA virus that affects the respiratory system and can cause fever, cough, and a rash.
5. Rabies: Caused by the rabies virus, which is an RNA virus that attacks the central nervous system and can cause brain damage and death.
6. Ebola: Caused by the Ebola virus, which is an RNA virus that affects the blood vessels and can cause fever, vomiting, diarrhea, and bleeding.
7. SARS-CoV-2: Caused by the severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2), which is an RNA virus that affects the respiratory system and can cause COVID-19.

RNA virus infections are often difficult to treat and can be highly contagious, so it's important to take precautions to prevent transmission and seek medical attention if symptoms persist or worsen over time.

Here are some key points to define sepsis:

1. Inflammatory response: Sepsis is characterized by an excessive and uncontrolled inflammatory response to an infection. This can lead to tissue damage and organ dysfunction.
2. Systemic symptoms: Patients with sepsis often have systemic symptoms such as fever, chills, rapid heart rate, and confusion. They may also experience nausea, vomiting, and diarrhea.
3. Organ dysfunction: Sepsis can cause dysfunction in multiple organs, including the lungs, kidneys, liver, and heart. This can lead to organ failure and death if not treated promptly.
4. Infection source: Sepsis is usually caused by a bacterial infection, but it can also be caused by fungal or viral infections. The infection can be localized or widespread, and it can affect different parts of the body.
5. Severe sepsis: Severe sepsis is a more severe form of sepsis that is characterized by severe organ dysfunction and a higher risk of death. Patients with severe sepsis may require intensive care unit (ICU) admission and mechanical ventilation.
6. Septic shock: Septic shock is a life-threatening condition that occurs when there is severe circulatory dysfunction due to sepsis. It is characterized by hypotension, vasopressor use, and organ failure.

Early recognition and treatment of sepsis are critical to preventing serious complications and improving outcomes. The Sepsis-3 definition is widely used in clinical practice to diagnose sepsis and severe sepsis.

These animal models allow researchers to study the underlying causes of arthritis, test new treatments and therapies, and evaluate their effectiveness in a controlled environment before moving to human clinical trials. Experimental arthritis models are used to investigate various aspects of the disease, including its pathophysiology, immunogenicity, and potential therapeutic targets.

Some common experimental arthritis models include:

1. Collagen-induced arthritis (CIA): This model is induced in mice by immunizing them with type II collagen, which leads to an autoimmune response and inflammation in the joints.
2. Rheumatoid arthritis (RA) models: These models are developed by transferring cells from RA patients into immunodeficient mice, which then develop arthritis-like symptoms.
3. Osteoarthritis (OA) models: These models are induced in animals by subjecting them to joint injury or overuse, which leads to degenerative changes in the joints and bone.
4. Psoriatic arthritis (PsA) models: These models are developed by inducing psoriasis in mice, which then develop arthritis-like symptoms.

Experimental arthritis models have contributed significantly to our understanding of the disease and have helped to identify potential therapeutic targets for the treatment of arthritis. However, it is important to note that these models are not perfect representations of human arthritis and should be used as tools to complement, rather than replace, human clinical trials.

Endotoxemia can occur in individuals who have a severe bacterial infection, such as pneumonia or meningitis, or those who have a prosthetic device or other foreign body that becomes infected with gram-negative bacteria. Treatment of endotoxemia typically involves antibiotics and supportive care to manage symptoms and prevent further complications. In severe cases, medications such as corticosteroids and vasopressors may be used to help reduce inflammation and improve blood flow.

Endotoxemia is a serious medical condition that requires prompt diagnosis and treatment to prevent complications and improve outcomes for patients.

The symptoms of myocarditis can vary depending on the severity of the inflammation and the location of the affected areas of the heart muscle. Common symptoms include chest pain, shortness of breath, fatigue, and swelling in the legs and feet.

Myocarditis can be difficult to diagnose, as its symptoms are similar to those of other conditions such as coronary artery disease or heart failure. Diagnosis is typically made through a combination of physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, and blood tests.

Treatment of myocarditis depends on the underlying cause and severity of the condition. Mild cases may require only rest and over-the-counter pain medication, while more severe cases may require hospitalization and intravenous medications to manage inflammation and cardiac function. In some cases, surgery may be necessary to repair or replace damaged heart tissue.

Prevention of myocarditis is important, as it can lead to serious complications such as heart failure and arrhythmias if left untreated. Prevention strategies include avoiding exposure to viruses and other infections, managing underlying medical conditions such as diabetes and high blood pressure, and getting regular check-ups with a healthcare provider to monitor cardiac function.

In summary, myocarditis is an inflammatory condition that affects the heart muscle, causing symptoms such as chest pain, shortness of breath, and fatigue. Diagnosis can be challenging, but treatment options range from rest and medication to hospitalization and surgery. Prevention is key to avoiding serious complications and maintaining good cardiac health.

There are several types of radiation injuries, including:

1. Acute radiation syndrome (ARS): This occurs when a person is exposed to a high dose of ionizing radiation over a short period of time. Symptoms can include nausea, vomiting, diarrhea, fatigue, and damage to the bone marrow, lungs, and gastrointestinal system.
2. Chronic radiation syndrome: This occurs when a person is exposed to low levels of ionizing radiation over a longer period of time. Symptoms can include fatigue, skin changes, and an increased risk of cancer.
3. Radiation burns: These are similar to thermal burns, but are caused by the heat generated by ionizing radiation. They can cause skin damage, blistering, and scarring.
4. Ocular radiation injury: This occurs when the eyes are exposed to high levels of ionizing radiation, leading to damage to the retina and other parts of the eye.
5. Radiation-induced cancer: Exposure to high levels of ionizing radiation can increase the risk of developing cancer, particularly leukemia and other types of cancer that affect the bone marrow.

Radiation injuries are diagnosed based on a combination of physical examination, medical imaging (such as X-rays or CT scans), and laboratory tests. Treatment depends on the type and severity of the injury, but may include supportive care, medication, and radiation therapy to prevent further damage.

Preventing radiation injuries is important, especially in situations where exposure to ionizing radiation is unavoidable, such as in medical imaging or nuclear accidents. This can be achieved through the use of protective shielding, personal protective equipment, and strict safety protocols.

There are five types of PsA:

1. Asymptomatic psoriatic arthritis - This type of psoriatic arthritis does not cause any symptoms and is typically diagnosed during routine blood tests or imaging studies.

2. Symptomatic psoriatic arthritis - This type of psoriatic arthritis causes painful joints, stiffness, and swelling in the hands and feet.

3. Distal interphalangeal predominant psoriatic arthritis - This type of psoriatic arthritis affects the joints at the tips of the fingers and toes.

4. Polyarticular psoriatic arthritis - This type of psoriatic arthritis causes inflammation in multiple joints throughout the body, including the hands, feet, knees, elbows, and spine.

5. Sulfur-shoulder psoriatic arthritis - This type of psoriatic arthritis primarily affects the shoulders and upper back.

Symptoms of PsA may include:

1. Joint pain and stiffness

2. Swollen and warm joints

3. Redness and warmth in the affected area

4. Fatigue

5. Low-grade fever

6. Loss of range of motion

7. Skin rashes or lesions

PsA is diagnosed based on a combination of physical examination, medical history, and laboratory tests such as blood tests to check for inflammatory markers (e.g., ESR and CRP) and X-rays or imaging studies to assess joint damage. There is no cure for PsA, but various treatments can help manage symptoms, slow the progression of the disease, and improve quality of life. These may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs) or biologic agents that target specific proteins involved in inflammation. In severe cases, surgery may be necessary to repair damaged joints or correct deformities.

It's important for people with PsA to work closely with their healthcare provider to develop a personalized treatment plan that addresses their individual needs and monitors their disease activity over time. With appropriate treatment and self-care, many people with PsA are able to manage their symptoms, maintain joint function, and lead active and fulfilling lives.

In conclusion, psoriatic arthritis (PsA) is a chronic inflammatory disease that affects both the skin and joints, causing pain, stiffness, and swelling in various parts of the body. Early diagnosis and appropriate treatment can help manage symptoms, slow the progression of the disease, and improve quality of life.

Example sentences:

1. The outbreak of birnaviridae infections in the local wildlife population has been linked to the consumption of contaminated water sources.
2. The researchers are studying the effects of birnaviridae infections on the reproduction rates of infected birds.
3. The veterinarian suspects that the sudden death of several zoo animals may be due to birnaviridae infections.

The definition of AKI has evolved over time, and it is now defined as a syndrome characterized by an abrupt or rapid decrease in kidney function, with or without oliguria (decreased urine production), and with evidence of tubular injury. The RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria are commonly used to diagnose and stage AKI based on serum creatinine levels, urine output, and other markers of kidney damage.

There are three stages of AKI, with stage 1 representing mild injury and stage 3 representing severe and potentially life-threatening injury. Treatment of AKI typically involves addressing the underlying cause, correcting fluid and electrolyte imbalances, and providing supportive care to maintain blood pressure and oxygenation. In some cases, dialysis may be necessary to remove waste products from the blood.

Early detection and treatment of AKI are crucial to prevent long-term damage to the kidneys and improve outcomes for patients.

Symptoms of MHN may include jaundice (yellowing of the skin and eyes), loss of appetite, nausea, vomiting, abdominal pain, fatigue, and confusion. The condition can progress rapidly, leading to multi-organ failure and death if left untreated.

Treatment options for MHN depend on the underlying cause, but may include supportive care such as fluid replacement, antibiotics, and medication to manage symptoms. In severe cases, a liver transplant may be necessary. The prognosis for MHN is generally poor, with high mortality rates reported in some studies.

Prevention measures for MHN include avoiding alcohol, maintaining a healthy diet, and getting vaccinated against hepatitis A and B viruses. Early detection and management of underlying conditions such as viral hepatitis can also help prevent the development of MHN.

Osteoarthritis (OA) is a degenerative condition that occurs when the cartilage that cushions the joints breaks down over time, causing the bones to rub together. It is the most common form of arthritis and typically affects older adults.

Rheumatoid arthritis (RA) is an autoimmune condition that occurs when the body's immune system attacks the lining of the joints, leading to inflammation and pain. It can affect anyone, regardless of age, and is typically seen in women.

Other types of arthritis include psoriatic arthritis, gouty arthritis, and lupus-related arthritis. Treatment for arthritis depends on the type and severity of the condition, but can include medications such as pain relievers, anti-inflammatory drugs, and disease-modifying anti-rheumatic drugs (DMARDs). Physical therapy and lifestyle changes, such as exercise and weight loss, can also be helpful. In severe cases, surgery may be necessary to repair or replace damaged joints.

Arthritis is a leading cause of disability worldwide, affecting over 50 million adults in the United States alone. It can have a significant impact on a person's quality of life, making everyday activities such as walking, dressing, and grooming difficult and painful. Early diagnosis and treatment are important to help manage symptoms and slow the progression of the disease.

Spondylitis, ankylosing can affect any part of the spine, but it most commonly affects the lower back (lumbar spine) and the neck (cervical spine). The condition can also affect other joints, such as the hips, shoulders, and feet.

The exact cause of spondylitis, ankylosing is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissue in the joints. Genetics may also play a role in the development of the condition.

Symptoms of spondylitis, ankylosing can include:

* Back pain and stiffness
* Pain and swelling in the joints
* Limited mobility and flexibility
* Redness and warmth in the affected area
* Fatigue

If you suspect that you or someone you know may have spondylitis, ankylosing, it is important to seek medical attention for proper diagnosis and treatment. A healthcare professional can perform a physical examination and order imaging tests, such as X-rays or MRIs, to confirm the diagnosis and rule out other conditions.

Treatment for spondylitis, ankylosing typically involves a combination of medications and physical therapy. Medications may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). Physical therapy can help improve mobility and flexibility, as well as strengthen the muscles supporting the affected joints.

In severe cases of spondylitis, ankylosing, surgery may be necessary to repair or replace damaged joints. In some cases, the condition may progress to the point where the joints become fused and immobile, a condition known as ankylosis.

While there is no cure for spondylitis, ankylosing, early diagnosis and appropriate treatment can help manage symptoms and slow the progression of the disease. With proper care and support, individuals with spondylitis, ankylosing can lead active and fulfilling lives.

Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.

There are several different types of brain neoplasms, including:

1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.

These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.

The exact cause of cachexia is not fully understood, but it is thought to be related to a combination of factors such as inflammation, hormonal imbalances, and changes in metabolism. Treatment for cachexia often focuses on addressing the underlying cause of the wasting, such as managing cancer or HIV/AIDS, as well as providing nutritional support and addressing any related complications.

In the medical field, cachexia is a serious condition that requires careful management to improve quality of life and outcomes for patients. It is important for healthcare providers to be aware of the signs and symptoms of cachexia and to provide appropriate treatment and support to affected individuals.

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

There are several types of liver neoplasms, including:

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

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

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

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

In animals, hepatitis can be caused by a variety of agents, including:

1. Viral hepatitis: Caused by viruses such as feline infectious peritonitis (FIP) in cats and canine infectious hepatitis (CIH) in dogs.
2. Bacterial hepatitis: Caused by bacteria such as Leptospira spp., which can be transmitted through contact with contaminated water or soil.
3. Parasitic hepatitis: Caused by parasites such as liver flukes (Fasciola spp.) and tapeworms (Taenia spp.).
4. Toxic hepatitis: Caused by exposure to certain drugs, chemicals, or environmental toxins.
5. Genetic hepatitis: Caused by inherited genetic disorders such as hemophilia in dogs and cats.

The clinical signs of animal hepatitis can vary depending on the cause and severity of the disease, but may include lethargy, loss of appetite, vomiting, diarrhea, abdominal pain, and jaundice (yellowing of the skin and eyes). Diagnosis is based on a combination of physical examination, laboratory tests (such as blood tests and liver biopsy), and imaging studies.

Treatment of animal hepatitis depends on the underlying cause and may include supportive care, antibiotics, anti-inflammatory medications, and in some cases, surgery or liver transplantation. In severe cases, animal hepatitis can be fatal if left untreated, so early diagnosis and aggressive treatment are essential for a successful outcome.

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 several types of disease susceptibility, including:

1. Genetic predisposition: This refers to the inherent tendency of an individual to develop a particular disease due to their genetic makeup. For example, some families may have a higher risk of developing certain diseases such as cancer or heart disease due to inherited genetic mutations.
2. Environmental susceptibility: This refers to the increased risk of developing a disease due to exposure to environmental factors such as pollutants, toxins, or infectious agents. For example, someone who lives in an area with high levels of air pollution may be more susceptible to developing respiratory problems.
3. Lifestyle susceptibility: This refers to the increased risk of developing a disease due to unhealthy lifestyle choices such as smoking, lack of exercise, or poor diet. For example, someone who smokes and is overweight may be more susceptible to developing heart disease or lung cancer.
4. Immune system susceptibility: This refers to the increased risk of developing a disease due to an impaired immune system. For example, people with autoimmune disorders such as HIV/AIDS or rheumatoid arthritis may be more susceptible to opportunistic infections.

Understanding disease susceptibility can help healthcare providers identify individuals who are at risk of developing certain diseases and provide preventive measures or early intervention to reduce the risk of disease progression. Additionally, genetic testing can help identify individuals with a high risk of developing certain diseases, allowing for earlier diagnosis and treatment.

In summary, disease susceptibility refers to the predisposition of an individual to develop a particular disease or condition due to various factors such as genetics, environment, lifestyle choices, and immune system function. Understanding disease susceptibility can help healthcare providers identify individuals at risk and provide appropriate preventive measures or early intervention to reduce the risk of disease progression.

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.

Psoriasis can affect any part of the body, including the scalp, elbows, knees, and lower back. The symptoms of psoriasis can vary in severity, and the condition can have a significant impact on quality of life. In addition to physical discomfort, psoriasis can also cause emotional distress and stigma.

There is no cure for psoriasis, but there are several treatment options available, including topical creams and ointments, light therapy, and systemic medications such as biologic drugs. With proper treatment, many people with psoriasis are able to manage their symptoms and improve their quality of life.

Psoriasis is relatively common, affecting approximately 2-3% of the global population, with a higher prevalence in Caucasians than in other races. It can occur at any age, but typically starts in the late teenage years or early adulthood. Psoriasis is often associated with other health conditions, such as diabetes, heart disease, and depression.

Overall, psoriasis is a complex and multifactorial condition that requires a comprehensive approach to management, including both physical and emotional support. With appropriate treatment and self-care, people with psoriasis can lead full and active lives.

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

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

What is a Chronic Disease?

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

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

Impact of Chronic Diseases

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

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

Addressing Chronic Diseases

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

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

Conclusion

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

Crohn disease can occur in any part of the GI tract, from the mouth to the anus, but it most commonly affects the ileum (the last portion of the small intestine) and the colon. The inflammation caused by Crohn disease can lead to the formation of scar tissue, which can cause narrowing or blockages in the intestines. This can lead to complications such as bowel obstruction or abscesses.

The exact cause of Crohn disease is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissue in the GI tract. Genetic factors and environmental triggers such as smoking and diet also play a role in the development of the disease.

There is no cure for Crohn disease, but various treatments can help manage symptoms and prevent complications. These may include medications such as anti-inflammatory drugs, immunosuppressants, and biologics, as well as lifestyle changes such as dietary modifications and stress management techniques. In severe cases, surgery may be necessary to remove damaged portions of the GI tract.

Crohn disease can have a significant impact on quality of life, and it is important for individuals with the condition to work closely with their healthcare provider to manage their symptoms and prevent complications. With proper treatment and self-care, many people with Crohn disease are able to lead active and fulfilling lives.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

The exact mechanism of the Shwartzman Phenomenon is not fully understood, but it is thought that the cancer cells that have spread to other parts of the body may be less susceptible to treatment because they are more aggressive and faster-growing than the original tumor. Additionally, these cells may have developed resistance mechanisms that make them less sensitive to chemotherapy and radiation.

The Shwartzman Phenomenon can make it more difficult to treat certain types of cancer, such as breast cancer, lung cancer, and melanoma. It is particularly common in cases where the cancer has spread to the liver or lymph nodes.

To overcome the Shwartzman Phenomenon, doctors may use higher doses of chemotherapy and radiation, or they may use different combinations of treatments. In some cases, surgery may be necessary to remove tumors that have spread to other parts of the body.

Overall, the Shwartzman Phenomenon is an important consideration for doctors treating cancer patients, as it can affect the success of treatment and the patient's prognosis.

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.

Gastric dilatation can occur for various reasons, including:

1. Eating too quickly or consuming large amounts of food in a short period of time.
2. Swallowing air, which can happen when eating or drinking too quickly or sucking on hard candies.
3. Eating certain types of foods that are difficult to digest, such as beans or cabbage.
4. Medical conditions such as irritable bowel syndrome (IBS), gastroparesis, or hiatal hernia.
5. Inflammation or infection of the stomach lining, such as gastritis.

Symptoms of gastric dilatation may include:

* Bloating and discomfort in the abdomen
* Pain or cramping in the abdomen
* Feeling nauseous or vomiting
* Gas and belching
* Diarrhea or constipation

Treatment for gastric dilatation usually involves making lifestyle changes, such as eating smaller, more frequent meals, avoiding foods that trigger symptoms, and reducing stress. In some cases, medications may be prescribed to help manage symptoms. If the condition is caused by an underlying medical condition, treating the underlying condition can help resolve the gastric dilatation.

In severe cases of gastric dilatation, surgical intervention may be necessary. This may involve laparoscopic or open surgery to repair any anatomical abnormalities or to remove any blockages in the digestive tract.

It's important to note that gastric dilatation can lead to more serious complications, such as gastric rupture or perforation, which can be life-threatening. If you experience severe abdominal pain, fever, or vomiting blood, seek medical attention immediately.

Preventing gastric dilatation involves maintaining a healthy diet and lifestyle, managing stress, and avoiding trigger foods. It's also important to drink plenty of water and exercise regularly to promote digestive health. If you experience any symptoms of gastric dilatation, it's important to seek medical attention promptly to prevent complications.

The term "acute-phase" describes the rapid onset and short duration of this reaction, which typically lasts for hours to days before resolving as the body's inflammatory response subsides. APR is characterized by a series of molecular events that result in altered expression of genes involved in inflammation, immune response, and tissue repair.

Some key components of an acute-phase reaction include:

1. Cytokine production: Cytokines are signaling molecules released by immune cells, such as white blood cells, that coordinate the immune response. During an APR, cytokine levels increase, triggering a cascade of downstream effects.
2. Leukocyte trafficking: White blood cells migrate towards sites of inflammation or infection, where they phagocytose (engulf and digest) pathogens and cellular debris. This process helps to limit the spread of infection and initiate tissue repair.
3. Coagulation cascade: The APR triggers a complex series of events involving blood coagulation factors, leading to the formation of blood clots and preventing excessive bleeding.
4. Anti-inflammatory response: As the APR progresses, anti-inflammatory cytokines, such as interleukin-10 (IL-10), are produced to dampen the inflammatory response and promote tissue repair.
5. Cellular proliferation: To replace damaged cells and tissues, the APR stimulates cellular proliferation and tissue regeneration.
6. Nutrient mobilization: The APR enhances nutrient uptake and utilization by immune cells, allowing them to mount an effective response to the stress.
7. Hormonal changes: The APR is accompanied by changes in hormone levels, such as the increase in corticotropin-releasing factor (CRF) and cortisol, which help to mobilize energy resources and regulate metabolism.
8. Immune tolerance: The APR helps to establish immune tolerance, preventing excessive or inappropriate immune responses that can lead to autoimmune diseases or allergies.
9. Tissue remodeling: The APR stimulates the remodeling of damaged tissues, allowing for the restoration of normal tissue function.
10. Memory formation: The APR sets the stage for the formation of immunological memory, which enables the immune system to mount a more effective response to future infections or stressors.

The most common type of colitis is ulcerative colitis, which affects the rectum and lower part of the colon. The symptoms of ulcerative colitis can include:

* Diarrhea (which may be bloody)
* Abdominal pain and cramping
* Rectal bleeding
* Weight loss
* Fever
* Loss of appetite
* Nausea and vomiting

Microscopic colitis is another type of colitis that is characterized by inflammation in the colon, but without visible ulcers or bleeding. The symptoms of microscopic colitis are similar to those of ulcerative colitis, but may be less severe.

Other types of colitis include:

* Infantile colitis: This is a rare condition that affects babies and young children, and is characterized by diarrhea, fever, and vomiting.
* Isomorphic colitis: This is a rare condition that affects the colon and rectum, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Radiation colitis: This is a condition that occurs after radiation therapy to the pelvic area, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Ischemic colitis: This is a condition where there is a reduction in blood flow to the colon, which can lead to inflammation and symptoms such as abdominal pain and diarrhea.

The diagnosis of colitis typically involves a combination of physical examination, medical history, and diagnostic tests such as:

* Colonoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the colon and rectum.
* Endoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the esophagus, stomach, and duodenum.
* Stool tests: These are tests that analyze stool samples for signs of inflammation or infection.
* Blood tests: These are tests that analyze blood samples for signs of inflammation or infection.
* Biopsy: This is a test that involves taking a small sample of tissue from the colon and examining it under a microscope for signs of inflammation or infection.

Treatment for colitis depends on the underlying cause, but may include medications such as:

* Aminosalicylates: These are medications that help to reduce inflammation in the colon and relieve symptoms such as diarrhea and abdominal pain. Examples include sulfasalazine (Azulfidine) and mesalamine (Asacol).
* Corticosteroids: These are medications that help to reduce inflammation in the body. They may be used short-term to control acute flares of colitis, or long-term to maintain remission. Examples include prednisone and hydrocortisone.
* Immunomodulators: These are medications that help to suppress the immune system and reduce inflammation. Examples include azathioprine (Imuran) and mercaptopurine (Purinethol).
* Biologics: These are medications that target specific proteins involved in the inflammatory response. Examples include infliximab (Remicade) and adalimumab (Humira).

In addition to medication, lifestyle changes such as dietary modifications and stress management techniques may also be helpful in managing colitis symptoms. Surgery may be necessary in some cases where the colitis is severe or persistent, and involves removing damaged portions of the colon and rectum.

It's important to note that colitis can increase the risk of developing colon cancer, so regular screening for colon cancer is recommended for people with chronic colitis. Additionally, people with colitis may be more susceptible to other health problems such as osteoporosis, osteopenia, and liver disease, so it's important to work closely with a healthcare provider to monitor for these conditions and take steps to prevent them.

Example sentence: The patient had a hemorrhage after the car accident and needed immediate medical attention.

There are several types of gliomas, including:

1. Astrocytoma: This is the most common type of glioma, accounting for about 50% of all cases. It arises from the star-shaped cells called astrocytes that provide support and nutrients to the brain's nerve cells.
2. Oligodendroglioma: This type of glioma originates from the oligodendrocytes, which are responsible for producing the fatty substance called myelin that insulates the nerve fibers.
3. Glioblastoma (GBM): This is the most aggressive and malignant type of glioma, accounting for about 70% of all cases. It is fast-growing and often spreads to other parts of the brain.
4. Brain stem glioma: This type of glioma arises in the brain stem, which is responsible for controlling many of the body's vital functions such as breathing, heart rate, and blood pressure.

The symptoms of glioma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory, or speech.

Gliomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and tissue biopsy to confirm the presence of cancer cells. Treatment options for glioma depend on the type and location of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment to remove as much of the tumor as possible, followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells.

The prognosis for glioma patients varies depending on the type and location of the tumor, as well as the patient's overall health. In general, the prognosis is better for patients with slow-growing, low-grade tumors, while those with fast-growing, high-grade tumors have a poorer prognosis. Overall, the 5-year survival rate for glioma patients is around 30-40%.

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

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.

Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.

Types of Neoplasms

There are many different types of neoplasms, including:

1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.

Causes and Risk Factors of Neoplasms

The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:

1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.

Signs and Symptoms of Neoplasms

The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:

1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.

Diagnosis and Treatment of Neoplasms

The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.

The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:

1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.

Prevention of Neoplasms

While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:

1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.

It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.

The main symptoms of FMF include:

1. Recurrent fever, usually during childhood and adolescence, which can range from 38°C to 40°C (100°F to 104°F).
2. Serositis, which can involve the heart (endocarditis), lungs (pleuritis), and/or peritoneum (peritonitis).
3. Painful joints, particularly in the hands, knees, and ankles.
4. Abdominal pain, diarrhea, and vomiting.
5. Rash, which may be present during fever episodes.
6. Enlarged spleen and liver.
7. Elevated levels of inflammatory markers in the blood, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).
8. Skin rashes or lesions, which may be present during fever episodes.
9. Kidney problems, such as kidney stones or chronic kidney disease.
10. Eye problems, such as uveitis or retinal vasculitis.

There is no cure for FMF, but the symptoms can be managed with medications and other therapies. Treatment typically involves colchicine, a drug that reduces inflammation and prevents flares. Other medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids, may also be used to manage symptoms. In some cases, surgery may be necessary to remove the affected organ or to repair damaged tissue.

It is important for individuals with FMF to work closely with their healthcare provider to develop a treatment plan that is tailored to their specific needs and symptoms. With proper management, many people with FMF are able to lead active and fulfilling lives. However, it is important to note that FMF can be a chronic condition, and ongoing management is typically necessary to control symptoms and prevent complications.

Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.

There are several different types of pathologic neovascularization, including:

* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.

The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.

In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.

Liquefactive necrosis (or colliquative necrosis), in contrast to coagulative necrosis, is characterized by the digestion of ... Some granulomas contain this pattern of necrosis. Fat necrosis is specialized necrosis of fat tissue, resulting from the action ... Fibrinoid necrosis is a special form of necrosis usually caused by immune-mediated vascular damage. It is marked by complexes ... Until recently, necrosis was thought to be an unregulated process. However, there are two broad pathways in which necrosis may ...
... is a cutaneous condition and usually occurs between days 5 and 10 of heparin therapy. Warfarin necrosis List ...
... generally refers to a necrosis that occurs in fragments. Piecemeal necrosis in liver aka interface hepatitis ... When used in relation to the [nibbling necrosis and interface necrosis) refers specifically to a loss and degeneration of ( ... Necrosis: Renamed Troxis Necrosis". Experimental and Molecular Pathology. 71 (2): 137-146. doi:10.1006/exmp.2001.2397. PMID ... Piecemeal necrosis of the liver is associated with a lymphocytic infiltrate into the adjacent parenchyma, and with destruction ...
Necrosis is the fourth studio album by the Norwegian death metal band Cadaver. A video was released for the song "Decomposed ... "Necrosis - Cadaver - Songs, Reviews, Credits - AllMusic". AllMusic. Retrieved 2016-08-07. v t e (Articles with short ...
... refers to the necrosis of the centrilobular tissue of the hepatic lobule. The centrilobular zone of the ... v t e (Necrosis, All stub articles, Disease stubs). ... will bind to the liver cells causing centrilobular necrosis. ...
... is not limited to the immune-mediated vasculitides; many pathologic processes can lead to areas of fibrinoid ... Fibrinoid necrosis is a specific pattern of irreversible, uncontrolled cell death that occurs when antigen-antibody complexes ... OCLC 879416939.{{cite book}}: CS1 maint: others (link) (CS1 maint: others, Histopathology, Necrosis, Cellular processes). ... which may show prominent fibrinoid necrosis. Also it's seen in rheumatoid nodules with similar pathology. Also seen in Serum ...
... may be a symptom of other diseases too. It also has been observed as an adverse event related to a medical ... Acral necrosis is a symptom common in bubonic plague. The striking black discoloration of skin and tissue, primarily on the ... However, acral necrosis occurs when blood supply is disrupted for prolonged periods, blackening and damaging the affected area ... With appropriate medical treatment, areas with acral necrosis may be successfully restored to function and lead a normal life. ...
... (or colliquative necrosis) is a type of necrosis which results in a transformation of the tissue into a ... Liquefactive necrosis can also occur in the lung, especially in the context of lung abscesses. Liquefactive necrosis can also ... In liquefactive necrosis, the affected cell is completely digested by hydrolytic enzymes, resulting in a soft, circumscribed ... Due to excitotoxicity, hypoxic death of cells within the central nervous system can result in liquefactive necrosis. This is a ...
... is a type of accidental cell death typically caused by ischemia or infarction. In coagulative necrosis, ... Different diseases are associated with coagulative necrosis, including acute tubular necrosis and acute myocardial infarction. ... Coagulative necrosis can also be induced by high local temperature; it is a desired effect of treatments such as high intensity ... Coagulative necrosis is most commonly caused by conditions that do not involve severe trauma, toxins or an acute or chronic ...
In Japan, Necrosis was released to film theaters on 5 March 2010. The Donner Party - a 2009 film based on the ill-fated Donner ... Necrosis (released internationally as Blood Snow) is a 2009 independent psychological thriller film directed by Jason Robert ... in April Story Page American World Pictures Trailer Necrosis Brings the Dead back to Life April 20 Official website Necrosis at ... Party expedition Cannibalism in popular culture Necrosis Hitting DVD ...
Osteonecrosis / Avascular Necrosis at the National Institute of Health Osteonecrosis / Avascular necrosis at Merck Manual for ... The intravertebral vacuum cleft sign (at white arrow) is a sign of avascular necrosis. Avascular necrosis of a vertebral body ... Pathology of avascular necrosis, with a photograph of a cross-section of the involved bone at top left. The reactive zone shows ... Avascular necrosis of the hip was also identified in a routine medical check-up on quarterback Brett Favre following his trade ...
This causes necrosis. Necrosis is a histological term that means death of the pulp. It does not occur suddenly unless there has ... Pulp necrosis may or may not arise with symptoms. Signs and symptoms of pulpal necrosis include; Pain Crown discolouration ... There are a plethora of ways to diagnose pulp necrosis in a tooth. The diagnosis of pulp necrosis can be based on the following ... The pulp can respond (reversible pulpitis, irreversible pulpitis, partial necrosis, total necrosis) in a variety of ways to ...
Warfarin-induced skin necrosis is a condition in which skin and subcutaneous tissue necrosis (tissue death) occurs due to ... Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of ... While skin necrosis in patients had been previously described, Verhagen was the first to publish a paper on this relationship ... Warfarin necrosis is also different from another drug eruption associated with warfarin, purple toe syndrome, which usually ...
... in the pleura Caseous necrosis in the kidney "caseous degeneration". TheFreeDictionary.com. Retrieved 2019-09- ... Microscope images of caseous necrosis Image of a hilar lymph node demonstrating caseous necrosis Image of a caseating granuloma ... which is why this type of necrosis is often depicted as a combination of both coagulative and liquefactive necrosis.[citation ... Caseous necrosis or caseous degeneration (/ˈkeɪsiəs/) is a unique form of cell death in which the tissue maintains a cheese- ...
Necrosis may also refer to: Necrosis (album), a 2004 album by the Norwegian death metal band Cadaver Necrosis (film), a 2009 ... Necrosis is a form of cell injury that results in the premature death of cells in living tissue. ... a sublabel of Earache Records This disambiguation page lists articles associated with the title Necrosis. If an internal link ... independent film directed by Jason Robert Stephens Necrosis, ...
Caseous necrosis Coagulative necrosis Liquefactive necrosis Myospherulosis Necrosis "Cell Injury". Kumar, Vinay; Abbas, Abul K ... Fat necrosis is a form of necrosis characterized by the action upon fat by digestive enzymes. In fat necrosis the enzyme lipase ... To keep track of benign fat necrosis a yearly mammogram is taken in order to observe it. However, if fat necrosis consists of ... that give fat necrosis its characteristic chalky-white appearance. Fat necrosis is an example of dystrophic calcification ...
Acute interstitial nephritis Renal cortical necrosis Renal papillary necrosis Desanti De Oliveira, B., Xu, K., Shen, T.H. et al ... Acute tubular necrosis is classified as a "renal" (i.e. not pre-renal or post-renal) cause of acute kidney injury. Diagnosis is ... Because necrosis is often not present, the term acute tubular injury (ATI) is preferred by pathologists over the older name ... Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules ...
... (UDN) is a chronic dermatological disease of cold water salmonid fish that had a severe impact on ... Ulcerative dermal necrosis". In Roberts, Ronald J. (ed.). Fish pathology (4th ed.). Wiley Blackwell. pp. 435-438. ISBN ... Mills, Derek (1989). "Ulcerative dermal necrosis". Ecology and management of Atlantic salmon. London: Chapman and Hall. pp. 81- ...
... is a late-stage and serious complication usually occurring in persons who have undergone radiation ... Dassarath, M; Yin, Z; Chen, J; Liu, H; Yang, K; Wu, G (2011). "Temporal lobe necrosis: a dwindling entity in a patient with ... Chen, J; Dassarath, M; Yin, Z; Liu, H; Yang, K; Wu, G (2011). "Radiation induced temporal lobe necrosis in patients with ... Many patients who experience temporal lobe necrosis are asymptomatic. This demonstrates a need for consistent imaging follow up ...
... was first described by Goldenberg et al. in 1990. Cases have emerged since 1960, but have never been ... Necrosis can be found mostly between the three distals of the esophagus, but stops abruptly at the gastroesophageal junction. ... Acute esophageal necrosis made an appearance on an American medical drama show, Dr. G: Medical Examiner. Jan Garavaglia, the ... Acute esophageal necrosis (AEN), black esophagus, or Gurvits syndrome is a rare esophageal disorder. AEN defines itself with ...
... , also known as cortical laminar necrosis and simply laminar necrosis, is the (uncontrolled) ... Histologically, grey matter is more vulnerable than white matter to necrosis due to lack of oxygen. The third layer of the grey ... Samain, J.; Haven, F.; Gille, M.; Mathys, P. (2011-06-18). "Typical CT and MRI features of cortical laminar necrosis". Journal ... Hypoxic-ischemic encephalopathy - principles (neuropathology-web.org) Laminar necrosis on MRI (rochester.edu) (Pathology). ...
... is a cutaneous condition that is rapidly fatal, characterized by skin erosions and ulcerations ...
... (IPN) is a severe viral disease of salmonid fish. It is caused by infectious pancreatic necrosis ... On necropsy, internal damage (viral necrosis) to the pancreas and thick mucus in the intestines often is present. Surviving ... "Product Information Database - Home". Infectious pancreatic necrosis - The Scottish Government: Marine and Fisheries Infectious ... Necrosis, accessed 09/09/2011. (Articles with short description, Short description is different from Wikidata, Articles with ' ...
... (TNF, cachexin, or cachectin; formerly known as tumor necrosis factor alpha or TNF-α) is an adipokine and ... "Tumor Necrosis Factor-alpha". Drug Information Portal. U.S. National Library of Medicine. Tumor Necrosis Factor-alpha at the US ... Ghada A. Abd El Latif, Tumor necrosis factor alpha and keratin 17 expression in oral submucous fibrosis in rat model, E.D.J. ... Salomon BL, Leclerc M, Tosello J, Ronin E, Piaggio E, Cohen JL (2018). "Tumor Necrosis Factor α and Regulatory T Cells in ...
Cytomegalovirus retinitis Progressive outer retinal necrosis Forster, David (1990). "Rapidly Progressive Outer Retinal Necrosis ... Acute retinal necrosis (ARN) is a medical inflammatory condition of the eye. The condition presents itself as a necrotizing ... The combination of the conditions was given the name acute retinal necrosis. The first reports of ARN came about in 1971. It is ... "Acute retinal necrosis - EyeWiki". eyewiki.aao.org. Retrieved 2015-10-27. Lau, Chun H.; Missotten, Tom; Salzmann, Joel; ...
... and rot is a soft rot disease caused by the bacterium Pectobacterium carotovorum subsp. betavasculorum, ... Saleh, O.I.; Huang, P.-Y.; J.-S. Huang (1996). "Bacterial Vascular Necrosis and Root Rot Disease of Sugar Beet in Egypt". ... 1977). "Beet Vascular Necrosis and Rot of Sugarbeet: General Description and Etiology" (PDF). Phytopathology. 67 (10): 1183- ... Whitney, E.D.; R.T. Lewellen (1977). "Bacterial Vascular Necrosis and Rot of Sugar Beet: Effects on Cultivars and Quality". ...
... is a form of nephropathy involving the necrosis of the renal papilla. Lesions that characterize renal ... Ultimately, necrosis of the papillae results in sloughing into the lumen, causing hematuria. If the degree of necrosis is ... Jung, Dae Chul; Kim, Seung Hyup; Jung, Sung Il; Hwang, Sung Il; Kim, Sun Ho (November 2006). "Renal Papillary Necrosis: Review ... Individuals with renal papillary necrosis due to excess use of analgesic have an elevated risk of epithelial tumors, hence a ...
... is a type of uncontrolled cell death (necrosis) unique to cardiac myocytes and thought to arise in ... Contraction band necrosis. H&E stain. Contraction band necrosis. PTAH. Myocardial infarction Timeline of myocardial infarction ... Contraction band necrosis is thought to arise by two mechanisms: a calcium-dependent mechanism - activation of the contractile ... November 1997). "Gap junction uncoupler heptanol prevents cell-to-cell progression of hypercontracture and limits necrosis ...
... may refer to: Pancreatic panniculitis Subcutaneous fat necrosis of the newborn This disambiguation ... page lists articles associated with the title Subcutaneous fat necrosis. If an internal link led you here, you may wish to ...
... (CoNV) is a plant pathogenic virus of the genus nepovirus that infects Theobroma cacao en natura causing ... Cacao necrosis virus is restricted to systemic infection of Theobroma cacao in nature. Symptoms on cacao include an acute stage ... Specificity in the life cycle of cacao necrosis virus, in contrast to other plant pathogenic viral pathogens, has not yet been ... The exact mechanism of pathogenesis for cacao necrosis virus is not yet understood. The virus is not infective in sap after ...
Necrosis Coagulative necrosis. Liquefactive necrosis. Gangrenous necrosis. Caseous necrosis. Fat necrosis. Fibrinoid necrosis. ... Coagulative necrosis is a type of accidental cell death typically caused by ischemia or infarction. In coagulative necrosis, ... also induces coagulative necrosis in target tumors.[3] Both of these treatments use coagulative necrosis in treatment of cancer ... Coagulative necrosis is most commonly caused by conditions that do not involve severe trauma, toxins or an acute or chronic ...
Renal cortical necrosis is a rare cause of acute renal failure secondary to ischemic necrosis of the renal cortex. The lesions ... Renal cortical necrosis is a rare cause of acute renal failure secondary to ischemic necrosis of the renal cortex. The lesions ... More prolonged vasospasm can cause necrosis and thrombosis of the distal arterioles and glomeruli, and renal cortical necrosis ... In childhood, renal cortical necrosis equally affects both sexes. In adults, renal cortical necrosis occurs more frequently in ...
Necrosis is the death of body tissue. It occurs when too little blood flows to the tissue. This can be from injury, radiation, ... Necrosis is the death of body tissue. It occurs when too little blood flows to the tissue. This can be from injury, radiation, ...
Learn about pulp necrosis, including symptoms and treatments. ... With pulp necrosis and its treatment, youre at risk for:. * ... Pulp necrosis refers to a condition where the pulp inside your teeth die. This is often the last stage of chronic pulpitis. It ... If you have no feeling in your tooth at all, this could be a sign of necrosis. A tooth can be necrotic due to untreated decay, ... If pulpitis or necrosis are suspected, your dentist may use a tool called an electric pulp tester. This tool delivers small ...
Anti-tumour necrosis factor agents and tuberculosis risk: mechanisms of action and clinical management. Lancet Infect Dis 2003; ... Tumor necrosis factor-a inhibitors and the reactivation of latent tuberculosis infection. CMAJ 2003;168:1153--6. ... Tuberculosis associated with infliximab, a tumor necrosis factor-alpha neutralizing agent. N Engl J Med 2001;345:1098--104. ... Tuberculosis Associated with Blocking Agents Against Tumor Necrosis Factor-Alpha --- California, 2002--2003. ...
Subcutaneous fat necrosis of the newborn (SFNN) is an uncommon disorder characterized by firm, erythematous nodules and plaques ... encoded search term (Subcutaneous Fat Necrosis of the Newborn) and Subcutaneous Fat Necrosis of the Newborn What to Read Next ... Subcutaneous Fat Necrosis of the Newborn. Updated: May 15, 2018 * Author: Sungat K Grewal; Chief Editor: William D James, MD ... Subcutaneous fat necrosis of the newborn (SFNN) occurs in the first several weeks of life. [1, 2, 4] Hypercalcemia, if it ...
Skin necrosis is a recognised complication of amiodarone infusion, but how does it compare with the risks of central venous ... Skin necrosis is a recognised complication of amiodarone infusion, but how does it compare with the risks of central venous ...
... prospectively in 198 attacks of acute pancreatitis with specific attention to their ability to predict pancreatic necrosis. The ... Prognostic markers in acute pancreatitis: can pancreatic necrosis be predicted? Ann R Coll Surg Engl. 1988 Jul;70(4):227-32. ... These methods are unlikely to distinguish pancreatic necrosis from other severe outcomes, but they may supplement clinical ... None of the measured parameters were helpful in distinguishing patients who subsequently developed pancreatic necrosis from ...
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... Course Description. Bisphosphonates, as a class, reduce bone loss associated with diseases such as osteoporosis ...
Teschovirus encephalomyelitis, neuronal necrosis. An area of mild perivascular cuffing and gliosis is adjacent to a ...
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Weinblatt ME, Keystone EC, Furst DE, Moreland LW, Weisman MH, Birbara CA, Adalimumab, a fully human anti-tumor necrosis factor ... haemophilum infection in a woman who had been immunosuppressed by tumor necrosis factor-α antagonist (TNF-αA) (adalimumab) ... Nontuberculous Mycobacterium Infection and Tumor Necrosis Factor-α Antagonists. Emerging Infectious Diseases. 2009;15(10):1700- ... Nontuberculous Mycobacterium Infection and Tumor Necrosis Factor-α Antagonists On This Page ...
negative regulation of tumor necrosis factor superfamily cytokine production. 86. negative regulation of tumor necrosis factor ... down regulation of tumor necrosis factor production; downregulation of tumor necrosis factor production; negative regulation ... inhibition of cachectin production; inhibition of tumor necrosis factor production; negative regulation of tumor necrosis ... negative regulation of tumor necrosis factor production. go back to main search page ...
Tumor Necrosis Factor Receptor Superfamily, Member 11A. *Home*Tumor Necrosis Factor Receptor Superfamily, Member 11A. ...
Mucosal tumour necrosis factor alpha and interleukin-6 in patients with Helicobacter pylori associated gastritis. ... Mucosal tumour necrosis factor alpha and interleukin-6 in patients with Helicobacter pylori associated gastritis. ... The production of tumour necrosis factor alpha (TNF alpha) and interleukin-6 by human antral mucosa during short term culture ...
Tumor Necrosis Factor-Alpha Inhibitor Etanercept Does Not Alter Methotrexate-Induced Gastrointestinal Mucositis in Rats. ... We aimed to determine the effect of the tumor necrosis factor-alpha (TNF-α) inhibitor etanercept on the severity of mucositis ... Tumor Necrosis Factor-Alpha Inhibitor Etanercept Does Not Alter Methotrexate-Induced Gastrointestinal Mucositis in Rats. ...
Inhibition of Soluble Tumor Necrosis Factor Prevents Chemically Induced Carcinogenesis in Mice Andrea Sobo-Vujanovic; Andrea ... Tumor necrosis factor-α blocks differentiation and enhances suppressive activity of immature myeloid cells during chronic ... Essential role of tumor necrosis factor α (TNF-α) in tumor promotion as revealed by TNF-α-deficient mice ... Discovered as an endotoxin-induced serum factor causing hemorrhagic necrosis of tumors, and applied with limited use in ...
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... DSpace Repository. Login ... A Truncated Singleton NLR Causes Hybrid Necrosis in Arabidopsis thaliana. de_DE. ...
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You can see tissue and bone much better in person when viewing these X-rays with the naked eye. Pictures shown here are not showing 100% quality of the X-rays you will receive. Your X-rays will most likely be much better than pictured in this listing.
Necrosis aseptica de la cabeza femoral. Translated title of the contribution. : Necrosis aseptica de la cabeza femoral. ... Necrosis aseptica de la cabeza femoral. / Díaz-Bertrana, C; Tordesilla, C.. In: Revista del Grupo de especialistas veterinarios ... Díaz-Bertrana C, Tordesilla C. Necrosis aseptica de la cabeza femoral. Revista del Grupo de especialistas veterinarios en ... Díaz-Bertrana, C ; Tordesilla, C. / Necrosis aseptica de la cabeza femoral. In: Revista del Grupo de especialistas veterinarios ...
You searched for: Journal Vaccine Remove constraint Journal: Vaccine Subject Infectious spleen and kidney necrosis virus Remove ... Infectious spleen and kidney necrosis virus; Seriola dumerili; Seriola quinqueradiata; antibodies; antigens; blood serum; case ... constraint Subject: Infectious spleen and kidney necrosis virus Subject Seriola dumerili Remove constraint Subject: Seriola ...
KIRCHHOFF, Alison Luís; VIAPIANA, Raqueli and RIBEIRO, Rodrigo Gonçalves. Periapical repercussion of pulpal necrosis. RGO, Rev ... Pulp necrosis occurs when the pulps vital functions are interrupted, starting a degenerative process. If this degenerative ... These periapical lesions related to pulp necrosis result from the same etiologic factors, but they present particular clinical ... Keywords : Periapical abscess.; Periapical radicular.; Endodontics.; Periapical granuloma.; Dental pulp necrosis.; Periapical ...
Avascular necrosis is a condition in which bone tissue becomes ischemic and begins to suffer pathologic decomposition, leading ... Specific types of avascular necrosis Overview of special types of avascular necrosis. ... Avascular necrosis is a condition in which bone tissue becomes ischemic and begins to suffer pathologic decomposition, leading ... Avascular necrosis (AVN) affects all age groups and is caused by direct trauma, medications, cellular insult, or mechanical ...
Blocking of the Tumor Necrosis Factor (TNF) activity is a successful therapeutic approach for 50-60% of rheumatoid arthritis ( ... Mechanism of action of certolizumab pegol (CDP870): in vitro comparison with other anti-tumor necrosis factor α agents. Inflamm ... Interactions between rheumatoid arthritis antibodies are associated with the response to anti-tumor necrosis factor therapy. * ... Blocking of the Tumor Necrosis Factor (TNF) activity is a successful therapeutic approach for 50-60% of rheumatoid arthritis ( ...
Avascular Necrosis. Avascular necrosis is defined as the localized death of cells in the bone due to lack of blood supply to it ... It is also called osteonecrosis or ischemic bone necrosis and most commonly occurs in the hip. The other common sites include ... Joint-preservation operations: These procedures are done in early avascular necrosis of the hip to improve blood supply to the ... Management & treating of underlying cause of avascular necrosis to minimize progression of disease ...
  • Avascular necrosis is a condition in which bone tissue becomes ischemic and begins to suffer pathologic decomposition , leading to joint dysfunction. (amboss.com)
  • Avascular necrosis ( AVN ) affects all age groups and is caused by direct trauma, medications, cellular insult, or mechanical compression, often in the context of predisposing conditions. (amboss.com)
  • Glucocorticoid use and chronic heavy drinking are the most common causes of nontraumatic avascular necrosis . (amboss.com)
  • Avascular necrosis is defined as the localized death of cells in the bone due to lack of blood supply to it. (drnaveenreddyortho.com)
  • We aimed to determine the effect of the tumor necrosis factor-alpha (TNF-α) inhibitor etanercept on the severity of mucositis in a previously established methotrexate (MTX)-induced GI mucositis rat model. (eur.nl)
  • Tumor necrosis factor-alpha. (who.int)
  • Pulp necrosis refers to a condition where the pulp inside your teeth die. (healthline.com)
  • Once pulp necrosis develops, you can't feel cold at all. (healthline.com)
  • Before testing for pulp necrosis, your dentist will first perform an examination of your teeth, gums, and other surrounding tissues. (healthline.com)
  • Dental X-rays are also helpful in narrowing down areas of decay or abscess that may be harboring pulp necrosis. (healthline.com)
  • Pulp necrosis usually starts off with tooth decay. (healthline.com)
  • Another cause of pulp necrosis is chronic pulpitis. (healthline.com)
  • Treatment options for pulp necrosis may vary based on the stage and severity of the condition. (healthline.com)
  • This is a method of treatment used in pulp necrosis from irreversible pulpitis. (healthline.com)
  • Depending on the severity of pulp necrosis, your dentist may remove the entire tooth. (healthline.com)
  • Pulp necrosis occurs when the pulp's vital functions are interrupted, starting a degenerative process. (bvsalud.org)
  • These periapical lesions related to pulp necrosis result from the same etiologic factors, but they present particular clinical and radiographical features and diverse symptoms that are important to differentiate the diagnosis that will determine the treatment. (bvsalud.org)
  • Prognostic markers in acute pancreatitis: can pancreatic necrosis be predicted? (nih.gov)
  • The value of six prognostic markers was assessed prospectively in 198 attacks of acute pancreatitis with specific attention to their ability to predict pancreatic necrosis. (nih.gov)
  • None of the measured parameters were helpful in distinguishing patients who subsequently developed pancreatic necrosis from patients who had other severe outcomes. (nih.gov)
  • These methods are unlikely to distinguish pancreatic necrosis from other severe outcomes, but they may supplement clinical judgment in selecting a high risk group of patients for contrast enhanced computed tomography. (nih.gov)
  • Endotherapy for pancreatic necrosis: An update. (bvsalud.org)
  • Approximately 20% of patients with acute pancreatitis develop pancreatic necrosis . (bvsalud.org)
  • Pancreatic necrosis is associated with high mortality and morbidity . (bvsalud.org)
  • In the last few decades, there has been a significant revolution in the treatment of infected pancreatic necrosis . (bvsalud.org)
  • Endoscopic intervention for pancreatic necrosis is being increasingly performed with good success and a lower complication rate. (bvsalud.org)
  • However, techniques of endotherapy are still not uniform and vary as per local expertise, and there are still many unresolved questions with regard to the interventions in patients with pancreatic necrosis . (bvsalud.org)
  • The objective of this paper is to critically review the literature and update the concepts of endoscopic interventional therapy of pancreatic necrosis . (bvsalud.org)
  • Renal cortical necrosis is a rare cause of acute renal failure secondary to ischemic necrosis of the renal cortex. (medscape.com)
  • Many cases of subcutaneous fat necrosis of the newborn have been reported in newborns who sustained perinatal hypoxic-ischemic injury and were treated by hypothermia to prevent encephalopathy and serious brain injury. (medscape.com)
  • It is also called osteonecrosis or ischemic bone necrosis and most commonly occurs in the hip. (drnaveenreddyortho.com)
  • Coagulative necrosis occurs in most bodily organs, excluding the brain. (wikipedia.org)
  • Subcutaneous fat necrosis of the newborn (SFNN) occurs in the first several weeks of life. (medscape.com)
  • Focal neuronal degeneration with necrosis occurs, leading to the development of glial nodules. (medscape.com)
  • Mucosal tumour necrosis factor alpha and interleukin-6 in patients with Helicobacter pylori associated gastritis. (bmj.com)
  • The production of tumour necrosis factor alpha (TNF alpha) and interleukin-6 by human antral mucosa during short term culture in vitro has been measured by enzyme linked immunosorbent assay. (bmj.com)
  • Details for: Tumour necrosis factor and related cytotoxins. (who.int)
  • The bone tissue ischemia and necrosis characteristic of AVN most commonly affect the epiphysis of long bones . (amboss.com)
  • Coagulative necrosis is a type of accidental cell death typically caused by ischemia or infarction . (wikipedia.org)
  • It is important to note that while ischemia in most tissues of the body will cause coagulative necrosis, in the central nervous system ischemia causes liquefactive necrosis , as there is very little structural framework in neural tissue. (wikipedia.org)
  • Subcutaneous fat necrosis of the newborn (SFNN) is an uncommon disorder characterized by firm, mobile, erythematous nodules and plaques over the trunk, arms, buttocks, thighs, and cheeks of full-term newborns. (medscape.com)
  • Subcutaneous fat necrosis of the newborn usually runs a self-limited course, but it may be complicated by hypercalcemia and other metabolic abnormalities. (medscape.com)
  • The exact pathogenesis of subcutaneous fat necrosis of the newborn (SFNN) is not known. (medscape.com)
  • when the PGE1 was discontinued, the subcutaneous fat necrosis of the newborn resolved. (medscape.com)
  • The cause of subcutaneous fat necrosis of the newborn (SFNN) is not known. (medscape.com)
  • IMSEAR at SEARO: Hypercalcemia and metastatic calcification in a neonate with subcutaneous fat necrosis. (who.int)
  • Nair Sajitha, Nair Sathyajith G, Borade Ashwin, Ramakrishnan K. Hypercalcemia and metastatic calcification in a neonate with subcutaneous fat necrosis. (who.int)
  • We report a 30-day-old baby with subcutaneous fat necrosis and symptomatic hypercalcemia, who developed metastatic calcification in the subcutaneous tissue, kidneys, pericardium and brain. (who.int)
  • Protein denaturation results in exposure of hydrophobic regions normally sequestered within the three-dimensional center of the molecules and may explain why necrotic cells display an increased capacity to bind the hydrophobic Eosin pigment) [4] Also, it is characteristic of coagulative necrosis to not have a zone in between necrotic cells and viable cells. (wikipedia.org)
  • Acute renal failure is typical in patients with renal cortical necrosis, with associated complications (eg, hyperkalemia, fluid overload). (medscape.com)
  • Histopathology of a pheochromocytoma with coagulative necrosis, displayed at gross pathology (upper left) and light microscopy at low (upper right), medium (lower left) and high magnification (lower right). (wikipedia.org)
  • Coagulative necrosis is most commonly caused by conditions that do not involve severe trauma , toxins or an acute or chronic immune response . (wikipedia.org)
  • Díaz-Bertrana, C & Tordesilla, C 2007, ' Necrosis aseptica de la cabeza femoral ', Revista del Grupo de especialistas veterinarios en ortopedia , vol. 11, pp. (uab.cat)
  • Like most types of necrosis , if enough viable cells are present around the affected area, regeneration will usually occur. (wikipedia.org)
  • Renal cortical necrosis is usually extensive, although focal and localized forms occur. (medscape.com)
  • Most of the symptoms that indicate issues with your tooth and inner pulp occur before necrosis. (healthline.com)
  • This is because once the onset of necrosis happens, the nerves may stop sending signals that alert you to any pain or discomfort, because the pulp has died. (healthline.com)
  • [3] Both of these treatments use coagulative necrosis in treatment of cancer. (wikipedia.org)
  • We report pulmonary M . haemophilum infection in a woman who had been immunosuppressed by tumor necrosis factor-α antagonist (TNF-αA) (adalimumab) treatment for rheumatoid arthritis. (cdc.gov)
  • In coagulative necrosis, the architectures of dead tissue are preserved for at least a couple of days. (wikipedia.org)
  • The macroscopic appearance of an area of coagulative necrosis is a pale segment of tissue contrasting against surrounding well vascularized tissue and is dry on cut surface. (wikipedia.org)
  • To achieve coagulative necrosis in tumor tissue, it only takes around 20 minutes of application with the RF probe. (wikipedia.org)
  • Necrosis is the death of body tissue. (medlineplus.gov)
  • Coagulative necrosis can be induced for treatments of cancers. (wikipedia.org)
  • Studies have shown that patients with HUS with thrombotic microangiopathy (TMA) involving arteries have a higher likelihood of progressing into acute cortical necrosis compared with patients with predominant glomerular TMA. (medscape.com)
  • Blocking of the Tumor Necrosis Factor (TNF) activity is a successful therapeutic approach for 50-60% of rheumatoid arthritis (RA) patients. (biomedcentral.com)
  • Cette étude a permis de déterminer la fréquence et l'étiologie de l'insuffisance rénale aiguë chez des patients hospitalisés en Arabie saoudite sur une période de 2 ans. (who.int)
  • The objective of this study was to expose and discuss, through a review, the etiological factors and histological, clinical and radiographical features of the periapical illnesses resulting from necrosis. (bvsalud.org)
  • Renal cortical necrosis was detected by postmortem examination in 5% of infants aged 3 months or younger at death. (medscape.com)
  • If this vasospasm is brief and vascular flow is reestablished, acute tubular necrosis results. (medscape.com)
  • It is postulated that cold or stress-induced injury to immature fat cells results in the development of solidification and necrosis. (medscape.com)
  • Tumor necrosis factor (TNF) is a proinflammatory cytokine that is central to the inflammatory process of RA. (biomedcentral.com)