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
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
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)

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Here, we reported the case of a patient who experienced persistent bone marrow necrosis after ATRA and IDA induction therapy for APL, despite cessation of ATRA. Although ATRA-induced bone marrow necrosis has been documented,18-20 this case is notable in that our patient demonstrated continual bone marrow necrosis several months subsequent to stopping ATRA therapy. It is interesting to note that the patient had evidence of hematopoietic recovery despite the necrotic effects of ATRA and shifting to ATO treatment.. Bone marrow necrosis is conjectured to result from poor blood supply to the marrow21 or increased oxygen demand of the marrow, as evidenced in necrosis of other tissue types. The most common cause of bone marrow necrosis is malignancy, in particular hematologic malignancy, including acute leukemia.18,21,22 It is reasonable to postulate that the APL by itself could have caused the bone marrow necrosis as evidenced in this patient23; however, one would have expected necrosis on the initial ...
Synonyms for focal necrosis in Free Thesaurus. Antonyms for focal necrosis. 3 synonyms for necrosis: gangrene, mortification, sphacelus. What are synonyms for focal necrosis?
Unlike the other terminology described in this section, Ischemic Necrosis does not refer to a particular morphology of necrosis but instead references a particular necrotic etiology. Ischemic Necrosis refers to necrosis of a tissue due to the etiological process of ischemia. In nearly all tissues, Ischemic Necrosis results in a pattern of Coagulative Necrosis except for the CNS in which it manifests as a pattern of Liquifactive Necrosis. It should be pointed out that necrotic areas caused by ischemia are termed Infarctions ...
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TY - JOUR. T1 - Hydrogen peroxide-induced liver cell necrosis is dependent on AP-1 activation. AU - Yang, X. U.. AU - Bradham, Cynthia. AU - Brenner, David A.. AU - Czaja, Mark J.. PY - 1997. Y1 - 1997. N2 - To deter-mine whether intracellular signaling events involved in apoptosis may also mediate necrosis, the role of the transcription factor AP-1 was investigated in a hepatoma cell model of cellular necrosis induced by oxidant stress. Treatment of the human hepatoma cell line HuH-7 with H2O2 caused dose-dependent necrosis as determined by light microscopy, fluorescent staining, and an absence of DNA fragmentation. H2O2 treatment led to increases in c-fos and c-jun mRNA levels, Jun nuclear kinase activity, and AP-1 DNA binding. AP-1 transcriptional activity measured with an AP-1-driven luciferase reporter gene was also increased. To determine whether this AP-1 activation contributed to H2O2-induced cell necrosis, HuH-7 cells were stably transfected with an antisense c-jun expression vector. ...
Seventy-five cases of hemorrhagic necrosis of the gastrointestinal tract were analyzed and compared with the entire autopsy population as control. The disease occurred most frequently in association with shock, which was present in 80 per cent of the cases with the gastrointestinal lesions.. The incidence of heart disease was higher in the cases of hemorrhagic necrosis than in the control group. The role of cardiac dysfunction in the etiology of hemorrhagic necrosis is emphasized as are the roles played by the bacterial toxins and shock. All three conditions have been shown to result in marked reduction of the intestinal blood flow and venous stasis.. Hemorrhagic necrosis of the gastrointestinal tract probably represents a conglomeration of microinfarcts of the mucosa secondary to markedly decreased local blood flow. Vasopressor agents have produced no beneficial effect; the effect of vasodilators remains to be determined.. ...
Soiffer R, Lynch T, Mihm M, Jung K, Rhuda C, Schmollinger J, et al. 1998. Vaccination with irradiated autologous melanoma cells engineered to secrete human GM-CSF generates potent antitumor immunity in patients with metastatic melanoma. Proc Natl Acad Sci U S A 1998;95: 13141-6 ...
Annexin A1 is an intracellular calcium/phospholipid-binding protein that is involved in membrane organization and the regulation of the immune system. It has been attributed an anti-inflammatory role at various control levels, and recently we could show that annexin A1 externalization during secondary necrosis provides an important fail-safe mechanism counteracting inflammatory responses when the timely clearance of apoptotic cells has failed. As such, annexin A1 promotes the engulfment of dying cells and dampens the postphagocytic production of proinflammatory cytokines. In our current follow-up study, we report that exposure of annexin A1 during secondary necrosis coincided with proteolytic processing within its unique N-terminal domain by ADAM10. Most importantly, we demonstrate that the released peptide and culture supernatants of secondary necrotic, annexin A1-externalizing cells induced chemoattraction of monocytes, which was clearly reduced in annexin A1- or ADAM10-knockdown cells. Thus, ...
Red Bamboos Dr. Toscano from Clearwater Florida finds a way to reverse skin necrosis without surgery and his findings reach national attention.
ALT: 15,360 (rat normal 29-65). Contributors Diagnosis and Comments: Moderate to severe, acute, multifocal to coalescing centrilobular hepatic necrosis.. Acute coagulative necrosis of the centrilobular region (Zone 3 of the liver acinus) is present throughout this section of rat liver. The necrosis of hepatocytes is most severe in zone 3, with complete dissolution of cytoplasmic components, karyorrhexis and karyolysis, and breakdown of sinusoidal endothelium with blood-filled lakes in the immediate vicinity of central veins. Phagocytosis by large cells assumed to be Kupffer cells is evident in the centrilobular region, and by Kupffer cells and intact hepatocytes at the periphery of the necrotic zones. Large numbers of neutrophils and lesser numbers of other mononuclear cells are abundant in or at the periphery of the necrotic zone (often approximating the Zone 2-3 boundary). Increased homogeneity of the hepatocytic cytoplasm with increased finely granular basophilia exists in the midzonal to ...
Official press release:. For a good while now, Akral Necrosis are working on their new full-length, the second in the history of the group. Recordings are still ongoing at Studio148 under the supervision of Marius Costache, but the process is near its end. Time has come for the band to announce the name of the new material:. The title of the second Akral Necrosis opus is Underlight.. The contrasting juxtaposition of the two words is appropriate and necessary to incorporate multiple meanings, evoked by the lyrical content of the material. Unlike the bands debut album, Pandemic Dominion, built around a narrative line, their upcoming effort quits the classic format, but keeps a well-defined conceptual axis, framed by a more violent and elaborate sound.. After the successful collaboration that led to the release of the (inter)SECTION split, Loud Rage Music and Akral Necrosis are joining forces again scheduling the release of this heinous Black Thrash Metal monster titled Underlight at the beginning ...
TY - JOUR. T1 - Assessment of secondary necrosis of Jurkat cells using a new microscopic system and double staining method with annexin V and propidium iodide.. AU - Honda, O.. AU - Kuroda, Masahiro. AU - Joja, I.. AU - Asaumi, Jun-Ichi. AU - Takeda, Yoshihiro. AU - Akaki, S.. AU - Togami, I.. AU - Kanazawa, Susumu. AU - Kawasaki, S.. AU - Hiraki, Y.. PY - 2000/2. Y1 - 2000/2. N2 - Using a new system developed by us for acquiring microscopic images automatically, we compared the morphological changes that apoptotic cells undergo with changes in the staining pattern of annexin V-enhanced green fluorescent protein (AV-EGFP) and propidium iodide (PI) in individual cells. Jurkat cells were treated with 5 mM CaCl2 alone, anti-Fas antibody and heating at 42 degrees C for 30 min or 46 degrees C for 60 min, and then were incubated in medium with 5 mM CaCl2. Time-lapse DNA fragmentation analysis and morphological observation revealed that the anti-Fas antibody and heating at 42 degrees C for 30 min ...
Disruption of the reprogrammed energy management system of malignant cells is a prioritized goal of targeted cancer therapy. Two regulators of this system are the Fer kinase, and its cancer cell specific variant, FerT, both residing in subcellular compartments including the mitochondrial electron transport chain. Here, we show that a newly developed inhibitor of Fer and FerT, E260, selectively evokes metabolic stress in cancer cells by imposing mitochondrial dysfunction and deformation, and onset of energy-consuming autophagy which decreases the cellular ATP level. Notably, Fer was also found to associate with PARP-1 and E260 disrupted this association thereby leading to PARP-1 activation. The cooperative intervention with these metabolic pathways leads to energy crisis and necrotic death in malignant, but not in normal human cells, and to the suppression of tumors growth in vivo. Thus, E260 is a new anti-cancer agent which imposes metabolic stress and cellular death in cancer cells. The tyrosine
Looking for selective myocardial cell necrosis? Find out information about selective myocardial cell necrosis. 1. the death of one or more cells in the body, usually within a localized area, as from an interruption of the blood supply to that part 2. death of plant... Explanation of selective myocardial cell necrosis
Comparison of the culture of C. perfringens to the presence of clostridia-like bacteria observed on ileal smears is shown in Table 2.. Histopathology. The intestines of 36 pigs that had died of haemorrhagic enteropathy were examined histologically. Advanced autolysis of the sampled tissues precluded histological evaluation in seven of these cases.. In all of the remaining cases (29), the histopathological findings were essentially identical, varying only in degree. The three basic lesions that were consistently found in most cases, to varying degrees, were: necrosis of the intestinal mucosa and congestion and haemorrhages in the intestinal wall. Rod-shaped bacterial bacilli were usually, but not always, present on and in the intestinal mucosa.. Mucosal necrosis was present in all cases. It was invariably linear, that is, parallel to the mucosal surface, and was sharply delimited from the underlying non-necrotic mucosa. The comparative severity of mucosal necrosis in the duodenum, jejunum and ...
AIMS--To compare in situ end-labelling (ISEL) of apoptosis in lung carcinoma with quantitative and semiquantitative light microscopic assessment and ultrastructural observations. METHODS--ISEL of apoptosis was evaluated in 42 lung carcinomas (24 squamous cell carcinomas, 12 adenocarcinomas and six small cell carcinomas). Results were correlated semiquantitatively with the extent of apoptosis in haematoxylin and eosin stained sections, with apoptotic indices and with ultrastructural observations (nine cases). RESULTS--In each tumour type the extent of apoptosis identified by ISEL correlated with that observed on light and electron microscopy. Tumour cells undergoing apoptosis showed either uniform nuclear staining with a surrounding halo or peripheral nuclear membrane staining. The latter pattern was more prominent in small cell carcinoma and correlated ultrastructurally with early apoptosis. A variable proportion of apoptotic cells and apoptotic bodies were unlabelled. Necrotic tumour cells ...
In the formation and growth of a primary tumor, cells can released into the bloodstream. There are many researches for these circulating tumor cells(CTC) And recently circulating cell-free tumor DNA(ctDNA) released from apoptotic or necrotic tumor cells has developed. At one report which checked ctDNA level after operation of colon cancer patients, they suggested that ctDNA could show recurrence of cancer several months earlier than the conventional follow up imaging. And several reports suggested that ctDNA can invade host cell and change host cell biology, which can evoke cancer metastasis.. So in this study, the investigator will collect ctDNA of pancreatic cancer patients, benign pancreatic disease patients, and healthy population. And the investigator will evaluate whether peripheral ctDNA can help early screening of cancer recurrence. And we will study about genomic signature of ctDNA to evaluate relationship between ctDNA and clinical outcome of cancer patients. ...
Dendritic cells (DC) loaded with tumor antigens from apoptotic/necrotic tumor cells are commonly used as vaccines for cancer therapy. However, the use of dead tumor cells may cause both tolerance and immunity, making the effect of vaccination unpredictable. To deliver live tumor cargoes into DC, we developed a new approach based on the labeling of tumors with a phospholipid eat-me sign
The factors contributing to poorly regulated inflammatory responses such as those observed in sepsis and gut ischemia are not well understood, but tissue necrosis might provide a major danger signal that inappropriately amplifies inflammation (3). In the present study, significantly fewer necrotic cells were observed in tlr3−/− mice after sepsis. Further, the coincubation of necrotic neutrophils with WT macrophages promoted the release of many chemokines, most notably CXCL10. This effect was restricted to co-cultures of necrotic neutrophils and WT macrophages, because the co-culture of necrotic neutrophils and tlr3−/− macrophages failed to show similar elevations in proinflammatory cytokines and chemokines. Tissue necrosis leads to the release of several cellular components, including heat shock proteins, HMGB1, and nucleic acids. Heat shock proteins and HMGB1 have been shown or suggested to be agonists for TLR2 and TLR4 (41), whereas mRNA is an endogenous ligand for TLR3 (13). More ...
(MedPage Today) -- Small study finds elevated incidence of high-grade transmural infarcts via Plaque Rupture Linked to Extensive Ischemic Necrosis in STEMI by from Blogger
Cells exist throughout the body and work synergistically to execute their respective functions. These cells undergo mitotic (and in gonads meiotic) transformations in order to sustain the cellular population. When a cell is exposed to a stressful stimulus, it usually makes an attempt to adapt to that environment until the stimulus is removed. Once there is no extenuating damage to the cell, it usually repairs itself and returns to its normal state. However, once the cell is substantially damaged and the injury is irreversible, the cell may undergo programmed cell death - a process known as apoptosis. Apoptosis is a naturally occurring, controlled cell-mediated process where the damaged or worn cell is autophagocytosed. There is another form of cell death that is unplanned and may result in more injury to adjacent cells that is known as cellular necrosis. Here, the death of the cell follows an external agent (i.e. trauma, infections or toxins) that initiates the premature death of the ...
Since oxygen is mainly bound to hemoglobin in red blood cells, insufficient blood supply causes tissue to become hypoxic, or, if no oxygen is supplied at all, anoxic. This can cause necrosis (i.e. cell death). In very aerobic tissues such as heart and brain, at body temperature Necrosis due to ischemia usually takes about 3-4 hours before becoming irreversible. This and typically some collateral circulation to the ischemic area accounts for the efficacy of clot-buster drugs such as Alteplase, given for stroke and heart-attack within this time period. However, complete cessation of oxygenation of such organs for more than 20 minutes typically results in irreversible damage ...
1/day each: plane shift, telekinesis. Actions. Multiattack. The githyanki doorkeeper makes two attacks, using its necrotic greatsword and/or its withering blast if corporeal, or its withering touch and/or its withering blast if incorporeal.. Necrotic Greatsword. Melee Weapon Attack: +9 to hit, reach 5 ft., one target. Hit: 15 (3d6+5) slashing damage plus 7 (2d6) necrotic damage.. Withering Touch. Melee Weapon Attack: +6 to hit, reach 5 ft., one target. Hit: 16 (4d6+2) necrotic damage plus 7 (2d6) cold damage.. Withering Blast. Ranged Spell Attack: +8 to hit, range 120 ft., one target. Hit: 15 (3d6+4) necrotic damage plus 7 (2d6) cold damage.. Tags: 5E D&D, monsters, undead ...
histophotograph of a longitudinal section through the optic nerve showing vitreous inflammatory cells over the optic disc, hemorrhagic necrosis of the retina, subretinal exudation, and an occluded retinal vessel (arrow and inset ...
The model presented here is based on the model we described earlier (10), but we improved it by rewriting the entire set of differential equations to make the model quantitatively more precise, to recognize 3 rather than 2 cell types, and most importantly by including the effect of antigen shedding, which was not included in the original model.. An important advantage of this model is that it can handle tumors of any size and yields total tumor volume information dynamically while considering only one representative unit of a modest and constant size. Because the model assumes that the total cell density is uniform and unchanged, this is not a good model for poorly vascularized, necrotic regions of the tumor. However, the efficacy of RIT is an issue for well vascularized, rapidly growing tumor; it may be less important for slowly growing, necrotic regions of a tumor. Also, although the cell density is assumed constant for any one tumor model, one can study the effect of density changes by doing ...
Learning Point of the Article: Plain radiographs can fail to detect impending soft tissue damage secondary to comminuted calcaneal fractures. Case Report , Volume 9 , Issue 2 , JOCR March - April 2019 , Page 11-14 , Tarek Taha, Karim Mahmoud, Ahmed Khalil Attia, Maged M Mekhaimar. DOI: 10.13107/jocr.2250-0685.1346 Authors: Tarek Taha[1], Karim Mahmoud[2], Ahmed Khalil Attia[2], Maged M Mekhaimar[2] [1]Department of Medical.... Read More ...
He had low-grade elevated temperature. Vital signs were otherwise normal. Tenderness and firmness of the epigastrium and left upper abdominal quadrant were noted. There was no palpable mass.. Leukocytosis was noted. Basic metabolic profile, hepatic chemistries, lipase, lactate, and urinalysis were all normal. Computed tomographic scan of the abdomen and pelvis showed an 8.0 x 9.0 x 9.6 cm, heterogeneous, left-sided abdominal mass, inseparable from adjacent loops of small bowel, with irregular peripheral enhancement and evidence of central necrosis. There was no bowel obstruction. Based on the imaging findings, the interpreting radiologist raised concern for malignancy. Percutaneous biopsy of the abdominal mass was planned. However, fevers persisted, leukocytosis worsened, and repeat imaging showed further enlargement of the mass, with findings suspicious for bowel perforation and abscess. Percutaneous drainage of 650 milliliters of purulent fluid was performed. Culture of this fluid ultimately ...
Ken, I am just as skeptical. Mostly due to the most recent photo taken by a lady who braided Jahis hair about a year ago. Jahi was notably smaller, necrosis on her mouth etc. we have all seen that photo. I think she is posting an old video for a reason. It was recently publicized that they could once again prove that Jahi is alive. I remember reading that in Dr. Popes blog, that the defendants would be allowed to have their own doctors examine Jahi. I really think that Nailah has gone to posting more than normal videos and pics lately thinking that will be enough to convince a judge. She is thinking if she shoves enough material into the media, that no exam will be needed. That is why I think these are old videos. She went from having necrosis on her mouth area to looking plump again with lips that look like they did on day 1?. Delete ...
Treatment of patients with the VEGFR TKIs sorafenib and sunitinib can lead to periods of tumor stability, but resistance to therapy is inevitable. We used a mouse model to define mechanisms by which resistance develops and found that components of the IFNγ signaling pathway are lost with sunitinib or sorafenib therapy. Our data also show that CXCL9 treatment delays resistance to sunitinib in 786-O- and A498-derived tumors and that one mechanism by which this occurs is by prolongation of the antiangiogenic effects of sunitinib. These data suggest that angiostatic pathways are suppressed as a result of VEGFR TKI therapy and set the stage for the subsequent development of resistance to therapy.. In the setting of VEGFR inhibition, RCC tumors undergo extensive necrosis (22). In the setting of this necrosis and accompanying hypoxia/nutrient deprivation, tumors may undergo compensatory changes, including the induction of salvage angiogenesis pathways. We propose that the environmental stress ...
For a good while now, Akral Necrosis are working on their new full-length, the second in the history of the group. Recordings are still ongoing at Studio148 under the supervision of Marius Costache, but the process is near its end. Time has come for the band to announce the name of the new material: The title…. ...
Video interview by Prof. Paolo Vescovi Faculty of Medicine and Surgery, University of Parma, on the danger of jaw necrosis following the use of bisphosphonates: who are the patients at risk. More on
67 year old male, previously a heavy smoker, suffering for 2 months from weakness, diminished appetite and weight loss. Tests showed a mass in right arm, possibly attached to muscle, and tenderness in right ribs. Chest CT showed a mass in LLL, lung foci, suspected secondary spread and masses in upper abdomen. CT guided biopsy from right lung mass was consistent with non small cell carcinoma with extensive necrosis. SPECT bone scan showed many focal findings in the vertebrae L,D2,7, most of the ribs bilaterally and in the limbs- suspected for secondary pathology. ...
67 year old male, previously a heavy smoker, suffering for 2 months from weakness, diminished appetite and weight loss. Tests showed a mass in right arm, possibly attached to muscle, and tenderness in right ribs. Chest CT showed a mass in LLL, lung foci, suspected secondary spread and masses in upper abdomen. CT guided biopsy from right lung mass was consistent with non small cell carcinoma with extensive necrosis. SPECT bone scan showed many focal findings in the vertebrae L,D2,7, most of the ribs bilaterally and in the limbs- suspected for secondary pathology. ...
Previous experience with High Intensity Focused Ultrasound (HIFU) has demonstrated that HIFU induces coagulative necrosis in tumor tissues and controls tumor gr...
Methods and systems for determining patient specific treatment parameters for delivering vapor to the lung to treat lung tissue. In some embodiments vapor is delivered to the lung to cause coagulative necrosis, inducing fibrosis and thereby reducing the volume of at least one segment of the lung. The delivery parameters can be adjusted depending on the desired degree of injury to be induced in the lung tissue.
considered to bring the greatest reduction the enlarged prostate or stop the prostate a coagulative necrosis below the urethral surface that allows for less obstruction is pressing against the urethra is removed to allow urine to flow easily. The procedure receptors. Men are given local anesthesia involves an electrical loop that cuts tissue for the procedure. This procedure involves • Alpha Blockers: These drugs dont ...
Co-financing: the Foundation for Assistance to Small Innovative Enterprises (FASIE) 3.000.000 rubles. One of the purposes of the project is to study an effect of introduction of stem cells in blood channel for different terms after ischemic stroke caused by bandaging the middle-brain artery in rat line «Vistar-Kioto». Thus for an estimation of an effect of introduction of stem cells it was planned to use following basic criteria: histological picture in necrotic zone caused by bandaging an artery; results of behavioral testing of animals. Taking into account the results of preliminary experiments it is possible to approve, that introduction of autologous stem cells on early terms after infringement of blood flow will allow to improve essentially a condition of damaged tissues due to preservation of vascular system, de novo formation of vessels in necrotic zone, restoration of tissues of the damaged organs due to the differentiation of stem cells.. The projects which are carried out at the ...
Ischemia: Lack of oxygen due to inadequate perfusion. Infarction: Tissue necrosis due to sustained loss of perfusion.. Risk Factors for CAD . Male |45Female | 55Family history of premature CADCigarette smokingHypertensionLipid abnormalitiesDiabetesMenopause (esp....
Z-VAD-FMK is a cell-permeable pan caspase inhibitor that irreversibly binds to the catalytic site of caspases and can inhibit induction of apoptosis.
Abstract: Calcium balance was impaired in a body during myocardium necrosis. Emotional stress, which preceded the myocardial necrosis, fortified these impairments. This was manifested as follows: an increased rate of calcium excretion and elevated hypocalcemia, accumulation of calcium in liver tissue, aorta, brain hemispheres and a decrease of its content in the intact tissue of left heart ventricle ...
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PNC-27 anti-cancer peptide, derived from the MDM2 binding site of p53 and linked to a membrane residency peptide (MRP), has been shown to cause necrosis of cancer cells without affecting untransformed cells. PNC-27 was also able to eradicate pancreatic tumor xenografts in mice (Michl et al, Int. J of Cancer, 2006). Recently, we have identified the mechanism of action of this peptide as due to formation of oligomeric pores in the plasma membrane (PM) of cancer cells but not in the PM of untransformed cells. The mechanism of pore-formation by PNC-27 closely resembles the pore-formation process by streptolysin-O, melittin and similar pore-forming agents. We have shown MDM2 as a targeting molecule that leads to PNC-27 selectivity towards cancer cells by its mis-localization to cancer cell PM (Sarafraz-Yazdi et al, PNAS, in press). Examining purified PM of a variety of cancer cells by immunoblotting, we now provide evidence for multiple MDM2 protein variants, and that were absent in the PM of normal ...
Now this is the coolest.. Literally.... New Scientist Tech - Technology - Plasma needle could replace the dentists drill.. According to the article, this plasma needle can target specific types of cells, and cause necrosis, leaving other types of cells intact and unharmed... AWESOME! all without a knife, and at regular temperatures... I love science! ...
(KudoZ) English to Georgian translation of Myocardial necrosis biomarkers sample: მიოკარდიუმის ნეკროზის ბიომარკერების ნიმუში [Name of a Course - Medical (general) (Medical)].
There are 2 main types of cell death: apoptosis (programmed cell death) & necrosis (due to lack of blood flow, ischaemia). But where do these dead cells go?
When students are asked to compare and contrast two types of cell death: necrosis and apoptosis, the same answers come back:. Apoptosis is programmed cell death.. Necrosis is premature cell death.. All the right things are said but when we then look at a biopsy, they are unsure if necrotic areas are showing necrosis or apoptosis. They dont seem to be getting the underlying concepts.. So, what do you think of the following car death analogy?. ...
Filaga Imaging, LLC Induced for example, by mistake during gavage of liquid test formulation into the trachea Irritation of bronchial and alveolar epithelium by chemical(s) As above Can happen even if the technician who treats do take filagra by gavage is experienced Pneumonia (see above) necrosis Do take filagra (irritation) As a consequence of cell Often restitutio ad integrum Page 477 450 Ettlin and Filaga пFigure 1 Liver Focal necrosisвA focus of homogenous eosinophilic (pink) necro- tic hepatocytes (ф) compatability Filagra to a lobular central vein Takee. In compari- son, Yu J, Krasinska KM et al.
Monocyte/macrophages contribute centrally to wound healing. Their known functions include removal of necrotic debris, propagation of angiogenesis, and regulation of extracellular matrix turnover (23,25). These phagocytes elaborate regulatory cytokines, chemokines, and proteolytic enzymes, all of which participate in tissue repair (1-4). Experimental (16,26) and clinical data (27) show that abrogation of monocytes compromises infarct healing. However, little is known about the downregulation of innate immune cell activity and associated inflammation after the initial burst triggered by ischemic myocardial injury. Here we show that effective infarct healing necessitates timely and coordinated resolution of inflammation. The endogenous repair response that follows MI requires immune cell populations that are profoundly altered during atherosclerosis, the condition that causes MI in most patients. Specifically, we found that Ly-6Chimonocytes, which are chronically expanded in the blood pool of ...
TY - JOUR. T1 - Expect skin necrosis following penile replantation. AU - Tuffaha, Sami. AU - Budihardjo, Joshua D.. AU - Sarhane, Karim A.. AU - Azoury, Saïd C.. AU - Redett, Richard. PY - 2014. Y1 - 2014. UR - UR - U2 - 10.1097/PRS.0000000000000901. DO - 10.1097/PRS.0000000000000901. M3 - Article. C2 - 25415107. AN - SCOPUS:84922482148. VL - 134. SP - 1000e-1004e. JO - Plastic and Reconstructive Surgery. JF - Plastic and Reconstructive Surgery. SN - 0032-1052. IS - 6. ER - ...
The effect of propranolol on the severity of myocardial necrosis following 40 minutes of temporary coronary artery occlusion was assessed in dogs. The circumflex coronary artery was occluded 1-2 cm from the aorta in open-chest dogs anesthetized with sodium pentobarbital. One group of dogs was untreated and a second group received propranolol (5.0 mg/kg, iv) 10 minutes prior to the occlusion. After 40 minutes the clamp was removed and arterial perfusion was restored. Dogs which survived this procedure were killed 2-5 days later for gross and histologic assessment of the necrosis. The relative area of necrosis (percent of fibers involved) in the posterior papillary muscle of each heart was quantified from stained histologic sections prepared from serial longitudinal slices of each posterior papillary muscle. Dogs treated with propranolol showed significantly less necrosis than did untreated controls, but the mechanism of the drugs action remains unknown. During coronary artery occlusion, ...
TY - JOUR. T1 - Retinal necrosis following varicella-zoster vaccination. AU - Gonzales, John A.. AU - Levison, Ashleigh L.. AU - Stewart, Jay M.. AU - Acharya, Nisha R.. AU - Margolis, Todd P.. PY - 2012/10. Y1 - 2012/10. UR - UR - U2 - 10.1001/archophthalmol.2012.2255. DO - 10.1001/archophthalmol.2012.2255. M3 - Article. C2 - 23044970. AN - SCOPUS:84867390202. VL - 130. SP - 1355. EP - 1356. JO - JAMA Ophthalmology. JF - JAMA Ophthalmology. SN - 2168-6165. IS - 10. ER - ...
Intravenous injection of 25 micrograms of bacterial endotoxin on day 9 of growth of the SA1 sarcoma results in extensive necrosis of the core of this tumor and in its subsequent complete regression. Tumor hemorrhagic necrosis and regression failed to occur in mice that were given a subcutaneous injection of cortisone acetate or dexamethasone 12 h before being giving endotoxin. Inhibition of tumor hemorrhagic necrosis and regression by glucocorticoids was associated with inhibition of endotoxin-induced intratumor TNF production that normally takes place several h after endotoxin is given. In contrast, glucocorticoids had no effect on the ability of intravenously injected rTNF to cause tumor hemorrhagic necrosis and regression. The results lend further support to the belief that TNF is the predominant mediator of endotoxin-induced hemorrhagic necrosis of established murine tumors, and that hemorrhagic necrosis is a prerequisite for the immunologically mediated regression that follows. ...
SOTO-DOMINGUEZ, Adolfo et al. Early Administration of Peroxisomicine A1 (T-514 Extracted from K. parvifolia Seeds) Causes Necrosis of Implanted TC-1 Cells without Affecting Target Organs in a Murine Model. Int. J. Morphol. [online]. 2012, vol.30, n.1, pp.284-289. ISSN 0717-9502. Peroxisomicine A1 (PA1), one of the toxins isolated from seeds of plants of the Karwinskia genus, whose targets organs are the liver, kidney, and lungs. There is a selective toxicity in vitro to cancer-cell lines derived from the lungs, liver, and colon, compared to normal cell lines. PA1 caused apoptosis in several cancer-cell lines in culture. In toxic doses to rodents, it causes extensive apoptosis in the liver, kidney, and lungs. In our study we were interested in evaluating, for the first time, the morphological effects of administration of PA1 to implanted TC-1 cells and in the target organs in vivo. The TC-1 cells were cultured and injected into the hind limb of ...
We made a straight incision at the dorsal MTP joint. We expanded the joint capsule to avoid the inward extensor hallucis longus (EHL) tendon. Articular cartilage of the great toe was invaded by synovitis of rheumatoid arthritis. We closed the skin without significant problems. The patient began indoor walking with full weight‐bearing 1 week after surgery. All stitches were removed 14 days after surgery. The wound of the right foot presented no issues, but we found that the wound of the left foot was macerated, and the EHL tendon was exposed from the wound site. The wound was 3 × 4 cm in size. NPWT was performed on the wound site on the same day, but the wound did not close. Three weeks later, secondary wound closure was attempted and the implant was removed. We immobilized the MTP joint by K‐wire; however, the EHL tendon remained exposed (Figure 1B). By the end of October 2014 (1 month postsurgery), an extensor digitorum brevis (EDB) flap was used to cover skin necrosis (Figure 1C,D). Bone ...
Results The cancer developed from orthotopic transplantation of YD-10Bmod cells into nude mouse oral tongue show invasion and central necrosis of the tumor, similar to the cancers developed human oral tongue cancer. The difference in tumor size and the time of central necrosis development depending on the number of transplanted tumor cells shows the feasibility of extending the survival period of the nude mouse by limiting the transplanted tumor cells to ,5×104 cells/mouse or under per nude mouse.. ...
TY - JOUR. T1 - Idiopathic and diabetic skeletal muscle necrosis. T2 - Evaluation by magnetic resonance imaging. AU - Kattapuram, Taj M.. AU - Suri, Rajeev. AU - Rosol, Michael S.. AU - Rosenberg, Andrew. AU - Kattapuram, Susan V.. PY - 2005/4/1. Y1 - 2005/4/1. N2 - Objective: Idiopathic and diabetic-associated muscle necrosis are similar, uncommon clinical entities requiring conservative management and minimal intervention to avoid complications and prolonged hospitalization. An early noninvasive diagnosis is therefore essential. We evaluated the magnetic resonance imaging (MRI) characteristics of muscle necrosis in 14 patients, in eight of whom the diagnoses were confirmed histologically. Design and patients: Two experienced musculos keletal radiologists performed retrospective evaluations of the MRI studies of 14 patients with the diagnoses of skeletal muscle infarction. In 10 cases gadolinium-enhanced (T1-weighted fat-suppressed) sequences were available along with T1-weighted, T2-weighted ...
MRI brain with different protocols showing high signal selectively in T1, T1+C along cortical and subcortical regions of right side superior, middle and inferior temporal gyri suggesting cortical laminar necrosis . Absent giral enhancement in T2 sequences as well as DWI suspecting acute or late acute stages of necrosis. Also absence of cortical atrophy exclude chronic stage. ...
Radiation necrosis: Find the most comprehensive real-world symptom and treatment data on radiation necrosis at PatientsLikeMe. 19 patients with radiation necrosis experience fatigue, depressed mood, pain, anxious mood, and insomnia and use Bevacizumab, Physiotherapy, and Therapeutic brace to treat their radiation necrosis and its symptoms.
Internal factors causing necrosis include: trophoneurotic disorders (diseases that occur due to defective nerve action in a part of an organ which results in failure of nutrition); injury and paralysis of nerve cells. Pancreatic enzymes (lipases) are the major cause of fat necrosis.[12] Necrosis can be activated by components of the immune system, such as the complement system; bacterial toxins; activated natural killer cells; and peritoneal macrophages.[1] Pathogen-induced necrosis programs in cells with immunological barriers (intestinal mucosa) may alleviate invasion of pathogens through surfaces affected by inflammation.[1] Toxins and pathogens may cause necrosis; toxins such as snake venoms may inhibit enzymes and cause cell death.[12] Necrotic wounds have also resulted from the stings of Vespa mandarinia.[14] Pathological conditions are characterized by inadequate secretion of cytokines. Nitric oxide (NO) and reactive oxygen species (ROS) are also accompanied by intense necrotic death of ...
TY - JOUR. T1 - Response-driven imaging biomarkers for predicting radiation necrosis of the brain. AU - Zadeh, Mohammad Reza Nazem. AU - Chapman, Christopher H.. AU - Chenevert, Thomas. AU - Lawrence, Theodore S.. AU - Ten Haken, Randall K.. AU - Tsien, Christina I.. AU - Cao, Yue. PY - 2014/5/21. Y1 - 2014/5/21. N2 - Radiation necrosis is an uncommon but severe adverse effect of brain radiation therapy (RT). Current predictive models based on radiation dose have limited accuracy. We aimed to identify early individual response biomarkers based upon diffusion tensor (DT) imaging and incorporated them into a response model for prediction of radiation necrosis. Twenty-nine patients with glioblastoma received six weeks of intensity modulated RT and concurrent temozolomide. Patients underwent DT-MRI scans before treatment, at three weeks during RT, and one, three, and six months after RT. Cases with radiation necrosis were classified based on generalized equivalent uniform dose (gEUD) of whole brain ...
REVIEW Open Access Fat necrosis in the Breast: A systematic review of clinical Narges Vasei1, Azita Shishegar1*, Forouzan Ghalkhani1 and Mohammad Darvishi2 Abstract Breast fat necrosis (FN) originates from aseptic fat saponification, which is a typical lipid cyst or a spiculated lesion. eaimofthispaperisto review the histopathological and radiological features of fat necrosis of the breast which distinguishes it from a cancer. Most of patients with sterile necrosis can generally be managed conservatively and the mortality rate is relatively low (12 percent) [1, 3]. Breast ultrasound fat necrosis Clinica Ginecologica Dr. After reviewing the reports and images he said he thought I may have fat necrosis of the tissue and lession in the. Necrosis was present in 36. Introduction. The patient will need treatment for the kidney disease, including monitoring of kidney function. No enlarged ipsilateral axillary nodes. The problem with fat necrosis in the breast is that it often looks like breast cancer, ...
Severe myocardial necrosis was produced in virgin Sprague-Dawley rats without preexisting arteriosclerosis and in breeder Sprague-Dawley rats with various degrees of arteriosclerosis by giving two subcutaneous injections of isoproterenol; the virgin rats received 50 mg/100 g and the breeder rats 25 mg/100 g body weight. Breeder rats withstood the stress and shock of myocardial necrosis with fewer untoward effects than the virgin animals. Changes in the thymus and adrenal glands also indicated that the arteriosclerotic breeder rats responded with a different pattern of adrenocortical activity. There were marked differences between the nonarteriosclerotic and arteriosclerotic rats in the fluctuation of serum transaminases and lactic dehydrogenase levels during the stress of myocardial necrosis. During the acute stages of myocardial necrosis there was intense activation of lipid metabolism with gross and microscopic evidence of intense fatty infiltration of the liver; during myocardial repair this ...
Leiomyoma with bizarre nuclei (LBN) have significant cytologic atypia, but high mitotic rate and tumor cell necrosis are absent. Although it is a benign leiomyoma variant, recurrent cases have been described. In this study, we investigated the clinical and pathologic features of LBN and compared them with related studies. A total of 30 patients diagnosed with LBN in our department were included in this study. In all cases, clinical data (age, complaint, surgery type), macroscopic features (size, location, number of leiomyomas, necrosis, and hemorrhage), microscopic features (bizarre cell distribution, bizarre cell density, cellularity, mitotic rate, tumor margin, necrosis, nuclear pseudoinclusions, karyorrhectic nuclei, prominent eosinophilic nucleoli with perinucleolar clearing, cytoplasmic eosinophilic inclusions, staghorn vessels, and alveolar-type edema), and follow-up data (recurrence and survival period) were evaluated ...
TY - JOUR. T1 - Inhibition of selectin- and integrin-mediated inflammatory response after burn injury. AU - Nwariaku, Fiemu E.. AU - Sikes, Patricia J.. AU - Lightfoot, Ellis. AU - Mileski, William J.. PY - 1996/6. Y1 - 1996/6. N2 - Inflammation and microvascular injury in the areas adjacent to burn wounds produces extension of postburn tissue necrosis. Leukocytes are potent mediators of the local inflammatory response preceding tissue necrosis, and the selectin and integrin adhesion molecules have been implicated in leukocyte-mediated tissue destruction. We sought to examine the role of L- selectin (CD62-L) and CD18 in leukocyte accumulation and tissue necrosis following burn injury. New Zealand White rabbits (n = 36) were subjected to burn injury and were randomized to treatment with saline (control) or monoclonal antibodies to L-selectin or CD18. Animals given the anti-L- selectin antibody demonstrated reduced immunohistochemical evidence of leukocyte accumulation at 24 hr postinjury but did ...
Ischemic necrosis of the muscles of the anterior tibial compartment of the leg occurs only infrequently, but when it does occur permanent impairment of the func
Nix is a pro-apoptotic gene that is regulated by Histotoxic hypoxia. It expresses a signaling protein related to the BH3-only family. This protein induces autophagy, an intracellular function by which cytoplasmic components are delivered to the lysosome to be broken down and used elsewhere or excreted from the cell.[1] This protein is important in development because it allows cells to have a consistent store of cellular components.[2] It also holds an important role in the differentiation and maturation of erythrocytes and lymphocytes by the process of mitophagy with the help of its regulator BNIP3.[3] Using a gene knockout technique in mice, scientists have been able to attribute this pruning of mitochondria and induction of cellular necrosis to the expression of the Nix gene.[1]. Not only does it hold a role in the differentiation of these immune and oxygen-carrying cells, but it also affects the development and maintenance of heart tissue. It has been found to be a cause of pathologic ...
The main event observed in our study was the replacement of a necrotic muscle fibre with an essentially new muscle fibre, formed through myogenesis. As the muscle fibre itself undergoes necrosis, macrophages infiltrate the dead tissue and begin the process of phagocytosis (Figs. 4 and 5). This occurs simultaneously at many sites along the length of the muscle fibre, rather than beginning at one end of the fibre. It is likely that the narrower regions observed to intersperse with the necrotic regions represent areas where the macrophages have already removed the necrotic tissue, and are thus at more advanced stage of regeneration. It can be speculated that this pattern is fully attributable to the 7-day time point at which the tissue samples were collected, rather than being specific to the electrical stimulation model employed in this study. Had we taken a muscle biopsy a few days after day 7, it can be speculated that the necrotic zones of the injured fibres would have all been removed, leaving ...
Absolute decrease in fibrin and necrotic tissue (a). Cumulative distribution of the absolute change in the amount of fibrin and necrotic tissue at day 14 after
Results 3 days after pristane application the proportion of cells positive for cleaved caspase 3 was highly increased in draining inguinal lymph nodes of DA.1F rats indicating apoptosis. Interestingly, the apoptosis rate decreased to normal levels as seen as in naïve animals within 2 weeks but draining lymph nodes became extremely hypercellular. In peripheral blood both apoptosis and necrosis rates doubled during the first week after pristane injection. In the acute disease phase four times increased apoptosis and necrosis rates were observed which was in contrast to the draining lymph nodes which normalised during the disease course. The authors could not observe any phagoytosis deficiency in pristane-injected animals rather a strongly increased phagocytosis activity was seen in the acute disease phase. In line with this in vivo data, pristane induced pronounced apoptosis and secondary necrosis in a dose dependent manner when added to cultured rat splenocytes.. ...
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With needle biopsies mostly used for diagnosis these days, we are seeing less and less gross fat necrosis compared with 20 years ago. The protean manifestations of fat necrosis on mammogram and ultrasound can confuse if you are not aware of the d...
We demonstrated that maintaining normoglycemia with insulin-dextrose infusion in the first 24 h following AMI attenuated the rise of serum CRP. It is possible that insulin inhibits the release of CRP through an anti-inflammatory effect, but the positive correlation between mean glucose level during first 24 h and serum CRP on day 2 suggests that the lowering of glucose level from insulin infusion contributes to the suppression of infarct-related inflammatory response.. Myocardial necrosis following AMI induces free radical generation and triggers the inflammatory cascade. Reperfusion therapy may also lead to further intensification of the inflammatory reaction, with the recruitment of neutrophils into the reperfused myocardium (1). Although this inflammatory response is important in the healing process, it can also extend myocardial injury, and anti-inflammatory strategies have been successful in reducing infarct size in animal models (13,14).. Hyperglycemia is associated with increased ...
I had a fairly young patient once who used Blood Root Salve for her breast cancer. Continued to grow until it replaced her whole breast. By the time she came to a real doc, it had invaded the ribs into the pleural cavity & all the breast skin was gone. Necrotic tumor was growing out of her armpit like a cauliflower. It bled & oozed & smelled so horrible that the Hospice House had to kick her out. She was so skinny & the tumor on her chest was just huge sucking up all her nutrients & life. She hurt like hell. She didnt tolerate chemo & antiestrogens didnt do much. As a desperate measure we irradiated it which slowed the bleeding & debulked as much as possible surgically without leaving to much of her heart & lungs exposed. Helped the pain a lot & improved the smell enough that her family could visit ...
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The MoAb E4 is a promising radiotracer for prostate cancer and may be used in radioimmunotherapy. As in earlier studies, TS1 shows significant radioimmunolocalization into necrotic tumor tissue, which also exists in prostate cancer.. ...
The same time, preisvergleich levitra 5 mg in general. In: Antony mm and stein mb, eds, handbook of clinical research, there is clinical suspicion of malignancy seen in type type iv. Similarly with the following drugs x adenosine, mg in weeks,, and, followed by voiding symptoms signs of chest pain the natural history of a painful, swollen leg, usually accompanied by parental anxieties as well as the main nding. Knowing that death will occur more frequently,, this injection is not yet been subject to compulsion part the consent cannot be assumed if reckless. Invasive cancer is starting with iu of fsh or human menopausal gonadotrophins: Response is monitored when parenteral nutrition and growth. Granulomatous inammation with extensive necrosis. Table. The most common sites of progressive descent with each drug is known as one-sample t test. Chapter legal issues mental health services have a catecholamine surge during delivery or miscarriage. Oxford university press. We could use a burst of oxygen ...
As this eMedTV segment explains, treating avascular necrosis may involve medications, exercises, surgery, or other options. This article explains the treatment options in detail, including when each type is generally used.
Hypergel contains a high concentration of sodium chloride that effectively hydrates and facilitates natural debridement of necrotic tissue. Apply Hypergel to the dry necrotic tissue but not on the surrounding skin. The high concentration sodium chloride gel effectively hydrates and facilitates natural Debridement of necrotic tissue. The environment for healing is optimised when necrotic tissue is removed.. ...
Breast fat tissue necrosis | Partial resection. Mammalogy: Treatment in Erlangen, Germany ✈. Prices on - booking treatment online!
T34.99XA is a billable diagnosis code used to specify a medical diagnosis of frostbite with tissue necrosis of other sites, initial encounter. Code valid for the fiscal year 2021
Liquefactive necrosis (or colliquative necrosis) is a type of necrosis which results in a transformation of the tissue into a liquid viscous mass. Often it is associated with focal bacterial or fungal infections. In liquefactive necrosis, the affected cell is completely digested by hydrolytic enzymes, resulting in a soft, circumscribed lesion consisting of pus and the fluid remains of necrotic tissue. Dead leukocytes will remain as a creamy yellow pus. After the removal of cell debris by white blood cells, a fluid filled space is left. It is generally associated with abscess formation and is commonly found in the central nervous system. For unclear reasons, hypoxic death of cells within the central nervous system can result in liquefactive necrosis. This is a process in which lysosomes turn tissues into pus as a result of lysosomal release of digestive enzymes. Loss of tissue architecture means that the tissue can be liquefied. This process is not associated with bacterial action or infection. ...
The pathogenesis involves Ebola virus entering through mucous membranes, breaks in the skin, or parenteral exposure. It infects multiple cell types, including monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells, and epithelial cells. There may be a relationship between the incubation period and the infection route (eg, 6 days for injection vs 10 days for contact). From the initial infection site, Ebola virus migrates to regional lymph nodes and then to the liver, spleen, and adrenal glands. Lymphocytes undergo apoptosis, resulting in decreased lymphocyte counts. Hepatocellular necrosis can occur, which is associated with clotting factor dysregulation and subsequent coagulopathy. It is also possible to find adrenocortical necrosis, which is associated with hypotension and steroid synthesis impairment. Multiorgan failure and shock typically result from the vascular leaking and impairment of clotting that occurs after the virus triggers a ...
An experimental study upon the demonstrable effects of large doses of dried thyroid gland and thyroxin upon the myocardium of rabbits has been made. Animals under such treatment show characteristic clinical symptoms with definite, although relatively slight, myocardial lesions. Similarly treated animals which have, in addition, been subjected to chloroform anesthesia show more striking, widespread myocardial necrosis.. These experiments indicate very distinctly that chloroform as an anesthetic in cases of hyperthyroidism is apt to be exceptionally detrimental to the myocardium, and should be avoided.. ...
Testing of Gacyclidine was performed on animals in a study. In concluding hours (18-96 h) no necrotic neurons were discovered in animals with dosages of 1, 5, 10, 20 milligrams of Gacyclidine. At 20 milligrams the presence of a few cytoplasmic vacuoles were present. In a study conducted to find possible neurotoxicity in dosages, scientists tested the effects of Gacyclidine in comparison to MK-801 and CNS-1102, and finalized more positive effects on animals from Gacyclidine. When given MK-801 at dosages of 1 or 5 milligrams of Gacyclidine, effects were harmless and behaved similarly to untreated animals. At dosages between 5 and 10 milligrams, the animals began to experience behaviors of tremors, sedation and exophthalmos. With CNS-1102, at all doses tested, the animals exhibited some excitation. At the highest doses (10 and 20 milligrams) they suffered from severe akinesia 1 hour after drug administration. Animals that received 1 or 5 milligrams of Gacyclidine or its enantiomers behave similarly ...
One of the major consequences of shock is that the tissues dont get enough oxygen and nutrients, a condition known as ischaemia. This begins a cascade of bad things that can eventually cause necrosis. The hypoxia causes the tissues to switch to glycolysis, which is anaerobic. This switch has two consequences: the tissues produce much less ATP than normal and lactic acid is produced, causing lactic acidosis.. Many enzymes are dependent on ATP to work, most notably the Na+/K+ ATPase which upholds the resting membrane potential. Water will start to enter the cells along with Na+, causing intracellular swelling and damage to the lysosomes and cell membrane. Lysosomal enzymes will be released out of the cell, damaging cells in the vicinity.. Because Na+ accumulates in the cell will the cell try to get rid of it by pumping out Na+ in exchange for Ca2+, which causes intracellular Ca2+ to also increase. Calcium enters and damages the mitochondria and activates proteases which cause further membrane ...
Mixed lineage kinase domain-like pseudokinase (MLKL) mediates necroptosis by translocating to the plasma membrane and inducing its rupture. The activation of MLKL occurs in a multimolecular complex (the necrosome), which is comprised of MLKL, receptor-interacting serine/threonine kinase (RIPK)-3 ( …
Application of a plaster cast seems to be easy. But it is only a make-believe. The wrong use of this kind of dressing may cause many complications, for instance local skin maceration, skin injuries or pressure on the blood vessels which may cause necrosis. That is why we have to do everything we can to protect the skin and the outgrowths under the cast against abrasions and prevent the itching, providing the patient with comfort. A correctly applied cast may free the patient from the pain and enable to move the limb despite the trauma.. ...
Short term complications included: 1. Skin Necrosis that required a number of skin grafts. 2. Temporary loss of use of the leg. This was due to the nerve damage caused by the surgery. I literally had to teach my leg to move again. 3. Reaction to loss of blood. I might add that these surgeries also required from 5 - 8 pints of blood. In the second surgery I had severe cardiac problems and for several days, it wasnt clear that I would make it. These are some of the long term complications I experienced: 1. Massive, permenant nerve damage. Parts of my leg are so nerve dead you could literally put a knife into and not feel it. Other parts are so sensitive that even to touch it feels like your digging into it with a shovel. If my knee itches, I scratch my thigh. 2. The swelling will return. Can you imagine trying to have MLD with this kind of nerve damage? And because the leg is so disfigured, even wearing compression garments is a challenge. So when the swelling returns you may well be stuck with ...
Bhaijee, F et al. Warfarin-induced skin necrosis in HIV-1-infected patients with tuberculosis and venous thrombosis. SAMJ, S. Afr. med. j., June 2010, vol.100, no.6, p.372-377. ISSN 0256- ...
I am one of those folks like Judy, who posted on 5/17, who always have the most severe reactions to every drug I remember taking. I developed severe lipoatrophy and nearly reached skin necrosis with Copaxone (sad, because it had an amazingly positive effect against my MS). I had severe flu symptoms for 5/7 days with Avonex (even after 4 months of treatment). And with other non-MS medications, I always need about a quarter of the dose to feel twice the side effects, and sometimes before the doctors say I should be able to feel anything. But Tecfidera, not the same story. Disclaimer: Im only on week two, so maybe I have a surprise in store. Ive had no flushing and very mild GI symptoms, which is amazing, because I have a host of GI problems independent of MS, and nausea, vomiting, cramping, etc are commonly exacerbated by medications. I have taken zofran for the nausea, which also helps slow my GI action, so Im sure thats helped, but Ive only taken it about three out of my 10 days of ...
I am one of those folks like Judy, who posted on 5/17, who always have the most severe reactions to every drug I remember taking. I developed severe lipoatrophy and nearly reached skin necrosis with Copaxone (sad, because it had an amazingly positive effect against my MS). I had severe flu symptoms for 5/7 days with Avonex (even after 4 months of treatment). And with other non-MS medications, I always need about a quarter of the dose to feel twice the side effects, and sometimes before the doctors say I should be able to feel anything. But Tecfidera, not the same story. Disclaimer: Im only on week two, so maybe I have a surprise in store. Ive had no flushing and very mild GI symptoms, which is amazing, because I have a host of GI problems independent of MS, and nausea, vomiting, cramping, etc are commonly exacerbated by medications. I have taken zofran for the nausea, which also helps slow my GI action, so Im sure thats helped, but Ive only taken it about three out of my 10 days of ...
*Necrosis* *Divine Boon* *Property*: You can change any damage you deal to necrotic damage. *Power (daily):* trigger, you hit with an attack that deals necr
The nuclear factor-kappaB (NF-kappaB) transcription factors have emerged as major regulators of programmed cell death (PCD) whether via apoptosis or necrosis. In this context, NF-kappaBs activity has important ramifications for normal tissue development, homoeostasis and the physiological functions of various cell systems including the immune, hepatic, epidermal and nervous systems. However, improper regulation of PCD by NF-kappaB can have severe pathologic consequences, ranging from neurodegeneration to cancer, where its activity often precludes effective therapy. Although NF-kappaB generally protects cells by inducing the expression genes encoding antiapoptotic and antioxidizing proteins, its role in apoptosis and necrosis can vary markedly in different cell contexts, and NF-kappaB can sensitize cells to death-inducing stimuli in some instances. This article describes our current knowledge of the role of NF-kappaB in apoptosis and necrosis, and focuses on the many advances since we last ...
Hypoglycaemia, liver necrosis and perinatal death in mice lacking all isoforms of phosphoinositide 3-kinase p85α Academic Article ...
TNF, DIF, TNF-alpha, TNFA, TNFSF2, Tumour necrosis factor, TNF-α, tumor necrosis factor, TNLG1F, Tumor necrosis factor alpha. ... Tumor necrosis factor (TNF, tumor necrosis factor alpha, TNFα, cachexin, or cachectin) is a cell signaling protein (cytokine) ... tumor necrosis factor receptor binding. • cytokine activity. • identical protein binding. Cellular component. • membrane. • ... tumor necrosis factor-mediated signaling pathway. • positive regulation of I-kappaB kinase/NF-kappaB signaling. • necroptotic ...
Necrosis Coagulative necrosis. Liquefactive necrosis. Gangrenous necrosis. Caseous necrosis. Fat necrosis. Fibrinoid necrosis. ... Necrosis[edit]. Necrosis is characterised by cytoplasmic swelling, irreversible damage to the plasma membrane, and organelle ... Gangrenous necrosis. Apoptosis[edit]. Apoptosis is the programmed cell death of superfluous or potentially harmful cells in the ... "What Is Necrosis? - Definition & Types - Video & Lesson Transcript ,". Retrieved 2016-04-16.. ...
Zonal Necrosis[edit]. This is the most common type of drug-induced liver cell necrosis where the injury is largely confined to ... Drug-induced hepatic necrosis. Drug induced hepatic fibrosis. Drug induced hepatic granuloma. Toxic liver disease with ... In this pattern, hepatocellular necrosis is associated with infiltration of inflammatory cells. There can be three types of ... B) in focal or non-specific hepatitis, scattered foci of cell necrosis may accompany lymphocytic infiltration. (C) chronic ...
... Coagulative necrosis. Liquefactive necrosis. Gangrenous necrosis. Caseous necrosis. Fat necrosis. Fibrinoid necrosis. ... Liquefactive necrosis (or colliquative necrosis), in contrast to coagulative necrosis, is characterized by the digestion of ... There are many causes of necrosis, and as such treatment is based upon how the necrosis came about. Treatment of necrosis ... Fat necrosis is specialized necrosis of fat tissue,[8] resulting from the action of activated lipases on fatty tissues such as ...
Necrosis (1988-1992)[edit]. Necrosis was formed in April 1988[5] by drummer Mike Atkin, guitarist Steve Thibault and vocalist ... Todds also left Necrosis shortly thereafter, retiring from music to focus on his family. Guitarist Dave Galea also joined the ... The band released several demos, including Mastication and Heterodontism (1989), Realms Of Pathogenia (1991) and Necrosis (1992 ... The band then changed their name to Necrosis, opting for a "more metal" name. John Todds later joined on bass. ...
Radiation necrosis is the death of healthy tissue near the irradiated site. It is a type of coagulative necrosis that occurs ... "Radiation Necrosis: Background, Pathophysiology, Epidemiology". 2019-11-09.. *^ Nieder C, Milas L, Ang KK (July 2000). "Tissue ...
Stem necrosis (water berry, grape peduncle necrosis) Physiological disorder Nematodes, parasitic[edit]. Nematodes, parasitic. ...
Tumor necrosis factor Monocytes Necrosis of tumor cells 9 Interleukin-1 Monocytes, Leukocytes Stimulate synthesis of IL-2 ...
renal papillary necrosis. *sickle cell disease or trait. Children[edit]. In many cases of asymptomatic microscopic hematuria ...
Centrilobular necrosis occurs. Macroscopically, the liver has a pale and spotty appearance in affected areas, as stasis of the ...
1989 Play Fast Or Die 12". Necrosis Records (#19). Re-issue of the band's half of the split LP with Generic. ...
Necrosis (2004). Lamented Souls[editar , editar código-fonte]. *Soulstorm (demo) (1993). *Demo (demo) (1995) ...
blood: Anticoagulant-induced skin necrosis. *Warfarin necrosis. *Vitamin K reaction. *Texier's disease ...
The tissue can become irreversibly damaged, a process known as necrosis. This can affect any organ; for instance, arterial ... ischemia and necrosis). A piece of either an arterial or a venous thrombus can break off as an embolus which can travel through ... which unless treated very quickly will lead to tissue necrosis (an infarction) in the area past the occlusion. Venous ...
tumor necrosis factor alpha. Genetics[edit]. It is typically believed that lupus is influenced by multiple genes. Lupus is ...
Fatty livers, focal necrosis No studies Skin No exposure assessment data available Swollen vacuolated epidermal cells, damage ...
blood: Anticoagulant-induced skin necrosis. *Warfarin necrosis. *Vitamin K reaction. *Texier's disease ...
blood: Anticoagulant-induced skin necrosis. *Warfarin necrosis. *Vitamin K reaction. *Texier's disease ...
"Maxillary necrosis by mucormycosis. a case report and literature review" (PDF). Med Oral Patol Oral Cir Bucal. 12 (5): E360-4 ...
Bell suffers from avascular necrosis. He has had both hips replaced, which keeps him from "pogoing around" in more recent ...
Redspotted grouper nervous necrosis virus(RGNNV), Striped Jack nervous necrosis virus (SJNNV) and Tiger puffer nervous necrosis ... Betanodavirus or nervous necrosis virus (NNV) is a viral genus classified in the family Nodaviridae. It contains four ... Viral nervous necrosis can have a clinical or sub-clinical presentation. Signs include: abnormal behaviour like lethargy, ... The crystal structure of a betanodavirus- T=3 Grouper nervous necrosis virus (GNNV)-like particle has been determined by X-ray ...
Osteonecrosis - same as avascular necrosis. *Insomnia. *Severe joint pain. *Cataracts or glaucoma ...
... causing tiny clots throughout the body and possibly ischemic necrosis (tissue death due to lack of circulation/perfusion to ...
Necrosis and New Beginnings. 21. Okt. 2015. 28. Mär. 2017. Eric Laneuville. Nkechi Okoro Carroll. 5,27 Mio. ...
Pulpal necrosis[edit]. Pulp necrosis usually occurs either as ischaemic necrosis (infarction) caused by disruption to the blood ... Potential sequelae can involve pulpal necrosis, pulp obliteration and root resorption.[10] Necrosis is the most common ... Dental trauma often lead to the main complication such as pulpal necrosis, and it's nearly impossible to predict the long-term ... Teeth that have multiple traumatic events also showed to have higher chance of pulp necrosis (61.9%) compared to teeth that ...
Post-partum necrosis of anterior pituitary. The Journal of Pathology and Bacteriology, Chichester, 1937, 45: 189-214. Sheehan's ... Sheehan's syndrome, also known as postpartum pituitary gland necrosis, is hypopituitarism (decreased functioning of the ... Cortisol and ACTH depending on the extent of necrosis MRI of the pituitary and hypothalamus: this helps to exclude tumor or ... pituitary gland), caused by ischemic necrosis due to blood loss and hypovolemic shock during and after childbirth. The various ...
Pain and other local effects worsen 12 to 36 hours after the bite, and the necrosis develops over the next few days.[37] Over ... In presumed cases of recluse bites, dapsone is often used for the treatment of necrosis, but controlled clinical trials have ... When both types of loxoscelism do result, systemic effects may occur before necrosis, as the venom spreads throughout the body ... Purportedly application of nitroglycerin stopped necrosis.[56] However, one scientific animal study found no benefit in ...
Infectious hypodermal and haematopoietic necrosis (PDF). pp. 78-95. Archived from the original (PDF) on September 7, 2012. ... Infectious hypodermal and hematopoietic necrosis (IHHN) is a disease that causes mass mortality among P. stylirostris (as high ...
Necrosis is increased in T lymphocytes.. Tingible body macrophages (TBMs) - large phagocytic cells in the germinal centers of ... It leads to a progression of the apoptosis process and finally to secondary necrosis of the cells if this ability is disturbed ... and tumor necrosis factor α (TNFα) are involved in the inflammatory process and are potential therapeutic targets.[4][60][61] ... Necrosis, a pro-inflammatory form of cell death, is increased in T lymphocytes, due to mitochondrial dysfunction, oxidative ...
Tumor necrosis factor-alpha (TNF-α). *Vascular endothelial growth factor (VEGF). *Wnt Signaling Pathway ...
Necrosis Coagulative necrosis. Liquefactive necrosis. Gangrenous necrosis. Caseous necrosis. Fat necrosis. Fibrinoid necrosis. ... Liquefactive necrosis (or colliquative necrosis), in contrast to coagulative necrosis, is characterized by the digestion of ... There are many causes of necrosis, and as such treatment is based upon how the necrosis came about. Treatment of necrosis ... Fat necrosis is specialized necrosis of fat tissue,[8] resulting from the action of activated lipases on fatty tissues such as ...
Caseous necrosis is a specific form of coagulation necrosis typically caused by mycobacteria (e.g., tuberculosis), fungi, and ... Fatty necrosis results from the action of lipases on fatty tissues (e.g., acute pancreatitis, breast tissue necrosis). ... Liquefactive necrosis (or colliquative necrosis) is usually associated with cellular destruction and pus formation (e.g., ... There are seven distinctive morphologic patterns of necrosis:. *Coagulative necrosis is typically seen in hypoxic (low-oxygen) ...
... is not cancer, but it can cause lumps and pulling of the tissues. When this happens in the breast, it can be ... fat necrosis. Phonetic. nuh-c,b,row,/b,-sis. Description. the death of fat cells, usually following injury. Fat necrosis is not ...
Acute Cortical Necrosis. Synonyms. diffuse bilateral renal cortical necrosis (BRCN), diffuse cortical necrosis, acute cortical ... "eMedicine: Renal Cortical Necrosis". Medscape. Retrieved 27 March 2012.. *^ Singh, B.; Gupta, A.; Mahajan, S.; Gupta, R. (2012 ... Cortical necrosis is a severe and life-threatening condition, with mortality rates over 50%.[citation needed] Those mortality ... Renal cortical necrosis (RCN) is a rare cause of acute kidney failure. The condition is "usually caused by significantly ...
Avascular necrosis most commonly affects the epiphyses (ends) of the femur (thigh bone); other commonly affected bones include ... Avascular necrosis, death of bone tissue caused by a lack of blood supply to the affected area. ... Avascular necrosis, also called aseptic necrosis, ischemic bone necrosis, or osteonecrosis, death of bone tissue caused by a ... Location of avascular necrosis. The most common location of avascular necrosis is the anterolateral femoral head. The condition ...
Avascular Necrosis) is marked by a loss of blood supply to the bones, causing bone to break down faster than the body make new ... Avascular Necrosis (Mayo Foundation for Medical Education and Research) Also in Spanish ...
... or Aseptic Necrosis of the hip is caused by a disruption to the hips blood supply which results in the deterioration and often ... 3. Avascular necrosis (AVN) or Aseptic Necrosis of the hip is caused by a disruption to the hips blood supply which results in ... Avascular necrosis (AVN) or Aseptic Necrosis of the hip is caused by a disruption to the hips blood supply which results in ... Some physicians treat avascular necrosis nihilistically, meaning they believe that regardless of the type of avascular necrosis ...
Necrosis after Penicillin. Br Med J 1950; 1 doi: (Published 15 April 1950) Cite this as ...
Avascular necrosis (AVN) is defined as cellular death of bone components due to interruption of the blood supply. The bone ... AVN is also known as osteonecrosis, aseptic necrosis, and ischemic bone necrosis. [1] ... What is avascular necrosis (AVN)?. Updated: Dec 05, 2020 * Author: Sunny B Patel, MD; Chief Editor: Herbert S Diamond, MD more ... Avascular necrosis of the femoral head: role of vascularized bone grafts. Orthop Clin North Am. 2007 Jan. 38(1):13-22, v. [ ...
Avascular necrosis or osteonecrosis is the cellular death of bone in some part of the body due to obstruction of its blood ... Avascular necrosis is a condition that should be caught and treated early to prevent collapse of the bone of the joint. In most ... Avascular necrosis or osteonecrosis is the cellular death of bone in some part of the body due to obstruction of its blood ... Avascular necrosis always progresses with time if over 15% of the bone. Once it involves more than 50% of the bone, the bone ...
Renal papillary necrosis is a disorder of the kidneys in which all or part of the renal papillae die. The renal papillae are ... Renal papillary necrosis is a disorder of the kidneys in which all or part of the renal papillae die. The renal papillae are ... Renal papillary necrosis often occurs with analgesic nephropathy. This is damage to one or both kidneys caused by overexposure ... There is no specific treatment for renal papillary necrosis. Treatment depends on the cause. For example, if analgesic ...
Tumor Necrosis Factor Hairy Cell Leukemia 9ene Cellular Oncogene Tyrosine Specific Kinase ...
Can a dislocated hip cause avascular necrosis (AVN)?. NEXT QUESTION: Can excessive alcohol use cause avascular necrosis (AVN)? ... Can corticosteroids cause avascular necrosis (AVN)?. ANSWER Long-term use of corticosteroids is associated with 35% of all ...
Check out just released Necrosis (Blood Snow) Pics, Images, Clips, Trailers, Production Photos and more from Rotten Tomatoes ... Necrosis (Blood Snow) Pictures and Movie Photo Gallery -- ... Home , Necrosis (Blood Snow) , Pictures Necrosis (Blood Snow) ...
Papillary necrosis can cause ureteral obstruction as sloughed papilla pass down the ureter. Analgesic abuse, liver cirrhosis, ... How does papillary necrosis cause flank pain?. Updated: Dec 11, 2019 * Author: Bradley C Gill, MD, MS; Chief Editor: Bradley ... Papillary necrosis can cause ureteral obstruction as sloughed papilla pass down the ureter. Analgesic abuse, liver cirrhosis, ... The actual sloughing of the renal papilla is caused by vascular ischemia, which leads to coagulative necrosis of the renal ...
Avascular necrosis of the bone (osteonecrosis) is when a bone dies from losing blood supply. Bone grafts and joint replacement ... The treatment of aseptic necrosis is critically dependent on the stage of the condition. Avascular necrosis is caused by a loss ... Early aseptic necrosis (before x-ray changes are evident) can be treated with a surgical operation called a core decompression ... What Is the Treatment for Avascular Necrosis?. *Medical Author: William C. Shiel Jr., MD, FACP, FACR ...
10, cell necrosis apparatus 10 is used to create cell necrosis zones 28 in a turbinate structure 88, which can include the ... 9 and 10, cell necrosis apparatus 10 is used to create one or more cell necrosis zones 28 in uvula 80. Electrode 14 is ... Cell necrosis apparatus 10 can be used to create cell necrosis in other structures that affect airway passages including but ... create controlled cell necrosis zones 28 and reposition soft palate structure 94 in oral cavity 16 with reduced necrosis of an ...
Tumour necrosis factor and cancer.. Balkwill F1.. Author information. 1. Centre for Cancer and Inflammation, Institute of ... Tumour necrosis factor (TNF) is a major inflammatory cytokine that was first identified for its ability to induce rapid ... haemorrhagic necrosis of experimental cancers. When efforts to harness this anti-tumour activity in cancer treatments were ...
Renal cortical necrosis is a rare cause of acute renal failure secondary to ischemic necrosis of the renal cortex. The lesions ... Renal Cortical Necrosis Differential Diagnoses. Updated: Nov 03, 2015 * Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig ... Bilateral renal cortical necrosis in acute pancreatitis. Indian J Nephrol. 2009 Jul. 19(3):125. [Medline]. [Full Text]. ... encoded search term (Renal%20Cortical%20Necrosis) and Renal Cortical Necrosis What to Read Next on Medscape. Related Conditions ...
Acute retinal necrosis was first described in the Japanese literature in 1971 and termed Kirisawa uveitis. ... Acute retinal necrosis (ARN) can lead to uveitis, retinal detachment, and blindness. ... Acute Retinal Necrosis Differential Diagnoses. Updated: Feb 14, 2017 * Author: Andrew A Dahl, MD, FACS; Chief Editor: C Stephen ... Acute retinal necrosis in the United Kingdom: results of a prospective surveillance study. Eye (Lond). 2012 Mar. 26 (3):370-7; ...
Papillary necrosis answers are found in the Diagnosaurus powered by Unbound Medicine. Available for iPhone, iPad, Android, and ... 5minute, Zeiger RF. Papillary necrosis. ... Papillary necrosis is a topic covered in the Diagnosaurus. To view the entire topic, please sign in or purchase a subscription. ... Zeiger, R. F. (2014). Papillary necrosis. In Diagnosaurus (4th edition). McGraw-Hill Education. Retrieved July 04, 2020, from ...
Avascular necrosis answers are found in the Diagnosaurus powered by Unbound Medicine. Available for iPhone, iPad, Android, and ... 5minute, Zeiger RFR. Avascular necrosis. ... Avascular necrosis is a sample topic from the Diagnosaurus. To view other topics, please log in or purchase a subscription. ... Zeiger, Roni F.. "Avascular Necrosis." Diagnosaurus, 4th ed., McGraw-Hill Education, 2015. ...
In 1975 the author found an explanation: the infection stimulates the secretion of tumor necrosis factor (TNF), which has ... Tumor necrosis factor Sci Am. 1988 May;258(5):59-60, 69-75. doi: 10.1038/scientificamerican0588-59. ... In 1975 the author found an explanation: the infection stimulates the secretion of tumor necrosis factor (TNF), which has ...
The present invention relates to ligands which bind to human tumor necrosis factor alpha (TNF) in a manner such that upon ... Tumour necrosis factor binding ligands. US20030139577 *. 3 Oct 2002. 24 Jul 2003. Rathjen Deborah Ann. Tumour necrosis factor ... Tumour necrosis factor binding ligands. US20030162948 *. 3 Oct 2002. 28 Aug 2003. Rathjen Deborah Ann. Tumour necrosis factor ... Tumour necrosis factor binding ligands. US20030171554 *. 15 Jan 2003. 11 Sep 2003. Rathjen Deborah Ann. Tumour necrosis factor ...
Zenkers necrosis definition at, a free online dictionary with pronunciation, synonyms and translation. Look it ...
Tumour necrosis factor domain (IPR006052). Short name: TNF_dom Overlapping homologous superfamilies *Tumour necrosis factor- ... Tumor Necrosis Factor (TNF) (also known as cachectin or TNF-alpha) [PMID: 3061461, PMID: 1850405] is a cytokine which has a ... A 3-D model for the CD40 ligand predicts that it is a compact trimer similar to the tumor necrosis factors.. Int. Immunol. 5 ... A 3-D model for the CD40 ligand predicts that it is a compact trimer similar to the tumor necrosis factors.. Int. Immunol. 5 ...
Peripheral skin necrosis complicating beta-blockade. Br Med J 1979; 1 :955 doi:10.1136/bmj.1.6168.955-b ... Peripheral skin necrosis complicating beta-blockade.. Br Med J 1979; 1 doi: (Published ...
if avascular necrosis is caught early, treatment may involve medications to ease pain or limiting the use of the affected joint ... How is avascular necrosis (AVN) treated before surgery?. ANSWER If avascular necrosis is caught early, treatment may involve ... While these may slow the progression of avascular necrosis, most people with the condition still eventually need surgery. ...
Inflammation and necrosis promote tumour growth.. Vakkila J1, Lotze MT.. Author information. 1. Hospital for Children and ...
... or epipericardial fat necrosis, as it is commonly referred to in the literature, is a rare self-limiting cause of chest pain of ... Mediastinal fat necrosis (MFN) or epipericardial fat necrosis, as it is commonly referred to in the literature, is a rare self- ... The first proposes acute torsion of mediastinal fat causing necrosis [10]. The second proposes that necrosis relates to the ... Imaging Manifestations of Mediastinal Fat Necrosis. Malay Y. Bhatt. ,1 Santiago Martínez-Jiménez. ,1. ,. 2 Melissa L. Rosado-de ...
  • Avascular necrosis , also called aseptic necrosis, ischemic bone necrosis, or osteonecrosis , death of bone tissue caused by a lack of blood supply to the affected area. (
  • Avascular necrosis (AVN) or Aseptic Necrosis of the hip is caused by a disruption to the hip's blood supply which results in the deterioration and often collapse of the ball of the thigh bone (femoral head). (
  • AVN is also known as osteonecrosis, aseptic necrosis, and ischemic bone necrosis. (
  • For patient education information, see Avascular Necrosis (Aseptic Necrosis or Osteonecrosis) . (
  • It is also called bone infarction or aseptic necrosis of bone. (
  • The treatment of aseptic necrosis is critically dependent on the stage of the condition. (
  • Early aseptic necrosis (before x-ray changes are evident) can be treated with a surgical operation called a core decompression. (
  • Later stages of aseptic necrosis (when X-ray changes have occurred) typically lead to seriously damaged bone and joints, requiring surgical replacement of the hip joint. (
  • Aseptic necrosis is bone death caused by poor blood supply to the area. (
  • Avascular necrosis is also called osteonecrosis, aseptic necrosis, or ischemic bone necrosis. (
  • Avascular necrosis or osteonecrosis is the cellular death of bone in some part of the body due to obstruction of its blood supply, usually to the growing end (epiphysis) of the bone. (
  • Retrieved on January 20, 2020 from (
  • Avascular necrosis, or osteonecrosis of the femoral head, is a condition that results when blood flow to the head ball of the hip is reduced or stopped, resulting in the death of cells in the bone tissue. (
  • Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply. (
  • However, often both osteonecrosis and avascular necrosis are often used interchangeably, which can lead to confusion 7. (
  • Avascular necrosis of the femoral head, also known as osteonecrosis, although this term isn't used that much anymore, is characterized by variable areas of dead trabecular bone and bone marrow, extending to and including the subchondral plate. (
  • Scientists from within the Antibody and Vaccine Group at the University of Southampton have gained novel insights into how an important class of immune receptors called tumour necrosis factor receptors (TNFR) are activated. (
  • Tumour necrosis factor and cancer. (
  • Tumour necrosis factor (TNF) is a major inflammatory cytokine that was first identified for its ability to induce rapid haemorrhagic necrosis of experimental cancers. (
  • Tumor necrosis factor (TNF) (also known as TNF-alpha or cachectin) is a monocyte-derived cytotoxin that has been implicated in tumour regression, septic shock and cachexia [ PMID: 2989794 , PMID: 3349526 ]. (
  • Inflammation and necrosis promote tumour growth. (
  • Tumour necrosis factor (TNF), a messenger substance in the immune system, plays an important role in triggering chronic inflammatory diseases. (
  • In collaboration with researchers from Erlangen and beyond, the working group led by PD Dr. Ulrike Schleicher and Prof. Dr. Christian Bogdan at FAU´s Institute of Microbiology - Clinical Microbiology, Immunology and Hygienedemonstrated through cell culture experiments and an infection model that tumour necrosis factor inhibits arginase 1 synthesis, which depends on the messenger substance interleukin 4. (
  • The tumour necrosis factor (TNF)-like domains are found in both TNF and C1q protein families. (
  • Avascular necrosis (AVN) is defined as cellular death of bone components due to interruption of the blood supply. (
  • Avascular necrosis associated with fracture of the femoral neck after hip resurfacing: histological assessment of femoral bone from retrieval specimens. (
  • Avascular necrosis always progresses with time if over 15% of the bone. (
  • Avascular necrosis is a condition that should be caught and treated early to prevent collapse of the bone of the joint. (
  • The prognosis depends on the part affected, the extent of necrosis and the rate of bone replacement. (
  • Avascular necrosis is caused by a loss of the blood supply to the part of the femur (the upper leg bone) that forms part of the hip joint. (
  • Avascular necrosis may be caused a number of conditions that cut off the supply of blood (and thereby oxygen and nutrients) to the bone, including injuries, such as a broken bone or dislocated joint, narrowed blood vessels, steroid medications, or excessive alcohol intake. (
  • Avascular necrosis (AVN) occurs when bone dies because it doesn't get enough blood flow. (
  • Without enough blood flowing to this joint, the bone dies and the joint weakens resulting in bone necrosis. (
  • Necrosis (death of cells) can occur when the the tissue or bone around the area of radiation has died. (
  • A University of British Columbia and Vancouver Coastal Health Research Institute study has found that a popular class of osteoporosis drugs nearly triples the risk of developing bone necrosis, a condition that can lead to disfigurement and incapacitating pain. (
  • The research is the largest study of bone necrosis and bisphosphonates, a class of drugs used by millions of women worldwide to help prevent bone fractures due to osteoporosis. (
  • It is also the first study to explore the link between bone necrosis and specific brands of bisphosphonates, such as Actonel, Didrocal and Fosamax. (
  • Bone necrosis, a relatively rare disease diagnosed in approximately 1 in 20,000 people per year, leads to permanent loss of blood supply to the bones. (
  • Avascular necrosis is a disease that results from the temporary or permanent loss of blood supply to the bone. (
  • The symptoms of avascular necrosis may look like other medical conditions or bone problems. (
  • As you have probably read, avascular necrosis is the death of bone tissue. (
  • Avascular necrosis is bone death that occurs when the blood supply to the bones is decreased or stopped. (
  • Although any bone can be affected, avascular necrosis most often affects ends of the long bones, such as the upper leg bone at the hip. (
  • In adolescents and young adults with avascular necrosis (AVN), the blood supply to the hip joint is interrupted and the bone begins to die. (
  • Though necrosis can occur in any bone, it most often affects the ends of long bones. (
  • In the course of avascular necrosis, however, the bone tissues break down faster than the body can repair them. (
  • If avascular necrosis progresses and the bone and surrounding joint surface collapse, pain may develop or increase quickly. (
  • The goal in treating avascular necrosis is to improve the patient's use of the affected joint and limit further damage to the bone. (
  • Patients treated with prolonged courses of high-dose steroid hormones are at high risk of developing avascular necrosis. (
  • In an average adult human, between 50 billion and 70 billion cells die off and are replaced every day, but necrosis refers to cell death that is unprogrammed and results from atypical body conditions, such as infections, cancer, serious injury, the presence of venom, severe inflammation, and a variety of diseases. (
  • The release of intracellular content after plasma membrane rupture is the cause of inflammation in necrosis. (
  • There are many causes of necrosis including prolonged exposure to injury , infection , cancer , infarction , poisons , and inflammation . (
  • Coagulative necrosis rimmed by acute inflammation (image B) . (
  • Many Crohn's disease sufferers are prescribed drugs, called tumor necrosis factor inhibitors, which decrease the levels of active TNF in the colon and therefore decrease inflammation to reduce symptoms of the disease. (
  • Necrosis of the cornified epithelium (arrow) and abundant inflammation are present. (
  • Inflammation often accompanies the necrosis, and the type of inflammation present depends on the chronicity and the etiology. (
  • In contrast to necrosis, HMGB1 ablation did not alter inflammation or mortality in response to TNF- or FAS-mediated apoptosis. (
  • While the only diagnostic "gold standard" mechanism of diagnosis en vivo is via kidney biopsy, the clinical conditions and blood clotting disorder often associated with this disease may make it impractical in a clinical setting. (
  • Corticosteroid-associated avascular necrosis: dose relationships and early diagnosis. (
  • Consider the diagnosis of renal cortical necrosis in a pregnant woman with sudden onset of abdominal pain, a tender uterus, and hematuria, especially during the third trimester. (
  • Acute retinal necrosis: a national population-based study to assess the incidence, methods of diagnosis, treatment strategies and outcomes in the UK. (
  • Duker JS, Blumenkranz MS. Diagnosis and management of the acute retinal necrosis (ARN) syndrome. (
  • However, if the necrosis is limited to the epithelium of the tongue, the diagnosis should be "tongue, epithelium - necrosis. (
  • Case Discussion Diagnosis: Avascular necrosis of talus. (
  • Coagulative necrosis is characterized by the formation of a gelatinous (gel-like) substance in dead tissues in which the architecture of the tissue is maintained, [5] and can be observed by light microscopy. (
  • Coagulative necrosis occurs primarily in tissues such as the kidney, heart and adrenal glands. (
  • Liquefactive necrosis (or colliquative necrosis), in contrast to coagulative necrosis, is characterized by the digestion of dead cells to form a viscous liquid mass. [5] This is typical of bacterial, or sometimes fungal, infections because of their ability to stimulate an inflammatory response. (
  • Gangrenous necrosis can be considered a type of coagulative necrosis that resembles mummified tissue. (
  • Caseous necrosis can be considered a combination of coagulative and liquefactive necrosis, [4] typically caused by mycobacteria (e.g. tuberculosis ), fungi and some foreign substances. (
  • It is interesting to note that ischemia (restriction of blood supply) in the brain produces liquefactive, rather than coagulative necrosis due to the lack of any substantial supportive stroma. (
  • It can be considered a combination of coagulative and liquefactive necrosis. (
  • The actual sloughing of the renal papilla is caused by vascular ischemia, which leads to coagulative necrosis of the renal medullary pyramids. (
  • Coagulative necrosis is typically seen in hypoxic environments (e.g. myocardial infarction , infarct of the spleen ). (
  • Because the necrosis is induced by ischemia, it typically has a coagulative appearance (ghost cells). (
  • Widespread coagulative necrosis (preserve ghost cell outlines) of cortex (image B) . (
  • What are the risk factors for avascular necrosis? (
  • Only 3 of the 15 patients in our series had other risk factors for avascular necrosis. (
  • What are symptoms of avascular necrosis (AVN)? (
  • There are no symptoms in the early stages of avascular necrosis. (
  • Maize lethal necrosis disease symptoms. (
  • What are the symptoms of acute tubular necrosis? (
  • Early symptoms of soybean vein necrosis virus (SVNV) are light green to yellow (chlorotic) patches near main leaf veins, where thrips fed. (
  • The following are the most common symptoms of avascular necrosis. (
  • Legg-Calve-Perthes disease is a type of avascular necrosis in children that causes hip symptoms. (
  • Necrosis from diabetes produces specific symptoms. (
  • In necrosis, the necrotic epithelium remains attached to the basement membrane. (
  • If the necrotic lesion is consistent with an infarct, it should be diagnosed as "necrosis," but the pathology narrative should state the lesion is consistent with an infarct. (
  • 12. Trauma such as a femoral neck fracture has also been associated with avascular necrosis. (
  • An injury, such as a forceful impact in an auto accident, or a complication of a hip fracture or dislocation can lead to avascular necrosis. (
  • consequently, the talus is at high risk of avascular necrosis after fracture. (
  • For example, fractures in the subcapital region of the femoral neck frequently interrupt the major part of the blood supply to the head of the femur, which can lead to avascular necrosis. (
  • Diseases such as sickle cell disease , gout , and lupus also may lead to avascular necrosis. (
  • 16. Some physicians treat avascular necrosis nihilistically, meaning they believe that regardless of the type of avascular necrosis or the age of the patient, treatment will not help. (
  • Excessive alcohol intake as a risk factor for the development of avascular necrosis is well established. (
  • Those changes may in turn encourage the formation of fat emboli and lead to blood stasis, thereby contributing to the development of avascular necrosis. (
  • It is clear that some other predisposing condition or concomitant risk factor is responsible for the development of avascular necrosis. (
  • Rather, we are attempting to alert physicians to what we feel is strong presumptive evidence that some association exists between short-course steroid therapy and the development of avascular necrosis. (
  • Other medical conditions have been associated with avascular necrosis. (
  • Renal cortical necrosis ( RCN ) is a rare cause of acute kidney failure . (
  • Rapidly corrected acute renal ischemia leads to acute tubular necrosis , from which complete recovery is possible, while more prolonged ischemia may lead to RCN. (
  • Langman, Craig B, ed. "eMedicine: Renal Cortical Necrosis" . (
  • Sahay M, Swain M, Padua M. Renal cortical necrosis in tropics. (
  • Sepsis-induced acute bilateral renal cortical necrosis. (
  • Renal cortical necrosis and acute kidney injury associated with Plasmodium vivax: a neglected human malaria parasite. (
  • Bilateral acute renal cortical necrosis in SLE-associated antiphospholipid syndrome. (
  • Decreasing incidence of renal cortical necrosis in patients with acute renal failure in developing countries: a single-centre experience of 22 years from Eastern India. (
  • Prakash J, Pant P, Singh AK, Sriniwas S, Singh VP, Singh U. Renal cortical necrosis is a disappearing entity in obstetric acute kidney injury in developing countries: our three decade of experience from India. (
  • Bilateral renal cortical necrosis in acute pancreatitis. (
  • Defined as necrosis of papillae and inner portions of renal medulla (which receives 10% of renal blood flow). (
  • Gross: necrosis of renal papillae/medullary portion (image A) . (
  • La NTA es una causa común de insuficiencia renal en personas hospitalizadas. (
  • Bilateral avascular necrosis occurs in about 40-80% of patients, but 10 years later in women on average, than in men. (
  • Decrease in the risk of bilateral acute retinal necrosis by acyclovir therapy. (
  • Similar regionally selective bilateral brain necrosis of the parietal cortex area 1 (blue arrow), thalamus (arrowhead), and retrosplenial cortex (white arrow) in a treated male F344/N rat from a 4-day study, all resulting from the same toxic compound as used in Figure 3. (
  • depicts acute bilateral necrosis in the parietal cortex area 1 (blue arrow), thalamus (arrowhead), and retrosplenial cortex (white arrow). (
  • The present invention relates to ligands which bind to human tumor necrosis factor alpha (TNF) in a manner such that upon binding of these ligands to TNF the biological activity of TNF is modified. (
  • High resolution crystal structure of a human tumor necrosis factor-alpha mutant with low systemic toxicity. (
  • Necrosis (from the Greek νέκρωσις "death, the stage of dying, the act of killing" from νεκρός "dead") is a form of cell injury which results in the premature death of cells in living tissue by autolysis . (
  • Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma which result in the unregulated digestion of cell components. (
  • Thus, untreated necrosis results in a build-up of decomposing dead tissue and cell debris at or near the site of the cell death. (
  • [5] Hypoxic infarcts in the brain presents as this type of necrosis, because the brain contains little connective tissue but high amounts of digestive enzymes and lipids, and cells therefore can be readily digested by their own enzymes. (
  • Fat necrosis is specialized necrosis of fat tissue, [8] resulting from the action of activated lipases on fatty tissues such as the pancreas . (
  • Necrosis (from the Greek νεκρός , "dead", νέκρωσις , "death, the stage of dying, the act of killing") is the premature death of cells and living tissue . (
  • Haemorrhagic necrosis is due to blockage of the venous drainage of an organ or tissue (e.g., in testicular torsion ). (
  • Fatty necrosis results from the action of lipases on fatty tissues (e.g., acute pancreatitis , breast tissue necrosis). (
  • Necrosis is the death of body tissue. (
  • Myocardial infarction, or heart attacks, play a large part in heart diseases and the necrosis of cardiac tissue after blood supply is decreased or stopped. (
  • Lipase activation produces the necrosis of fat tissue in pancreatic and peripancreatic spaces as well as vessel damage. (
  • First, unlike subcutaneous adipose tissue, visceral adipose cells produce significant amounts of proinflammatory such as tumor necrosis factor-alpha ( ), and -1 and −6, etc. (
  • Necrosis (in Greek Νεκρός = Dead ) is the name given to accidental death of cells and living tissue . (
  • A main cause of necrosis is from the Brown Recluse Spiders, who's venom causes significant cutaneous injureis with tissue loss and necrosis. (
  • Note that the substance of the olfactory bulb is lost (arrows) as a result of marked tissue necrosis, leaving only cellular debris and hemorrhage. (
  • Somewhat confusingly, patches of dead tissue are identified as necroses, even when the cause of the cell death is unknown. (
  • While diabetic necrosis is frightening, you do have some control over diabetes, tissue death and anxiety . (
  • Like necrosis, gangrene is the death of tissue or organs. (
  • Resurfacing arthroplasty of the hip for avascular necrosis of the femoral head: a minimum follow-up of four years. (
  • Fat-cell changes as a mechanism of avascular necrosis of the femoral head in cortisone-treated rabbits. (
  • Ninomiya S. An epidemiological survey of idiopathic avascular necrosis of the femoral head in Japan. (
  • Bisphosphonate combination therapy for non-femoral avascular necrosis. (
  • In the initial stages, avascular necrosis is asymptomatic, but pain sets in when the weight is borne by the joint, and in the later stages, joint pain occurs at rest also. (
  • Avascular necrosis occurs most often in men between 40 and 50 years old. (
  • Heparin necrosis is a cutaneous condition and usually occurs between days 5 and 10 of heparin therapy. (
  • Piecemeal necrosis generally refers to a necrosis that occurs in fragments. (
  • By contrast, patients who receive short-term steroids, including pulse-dosing and steroid injections into a joint, rarely develop avascular necrosis. (
  • A dose-response relationship exists between alcohol intake and avascular necrosis risk such that the more alcohol a person consumes regularly, the more likely he or she is to develop avascular necrosis. (
  • 2 We included these patients in our article to illustrate the point that of the many patients who receive a short course of corticosteroid medication only a small percentage develop avascular necrosis. (
  • 11. People most at risk for avascular necrosis include children who have been exposed to second hand cigarette smoke, those who drink excessively, and individuals who have blood clotting disorders (ex: factor V Leiden, protein C and protein S deficiency, etc). (
  • In the late 1990s, the mouse and human nomenclature committees and basic researchers met and combined efforts to standardize the nomenclature of the tumor necrosis factor (TNF) superfamily. (
  • Tumor necrosis factor (TNF) is a member of the TNF ligand superfamily that also includes lymphotoxins alpha (LTA) and beta (LTB), tumor necrosis factor (ligand) superfamily, member 5 (TNFSF5) and the FAS ligand (FASL). (
  • [4] Severe ischemia most commonly causes necrosis of this form. (
  • The extent of the necrosis is a major determinant of the prognosis, which in turn is dependent on the duration of ischemia , duration of oliguria , and the severity of the precipitating conditions. (
  • The problem of human myocardial infarction passed through stage 2 when everybody was happy with the explanation that the syndrome was produced by a sudden occlusion ofa branch ofa coronary artery with subsequent acute ischemia and necrosis ofthe area supplied by the occluded vessel. (
  • arrows), depending on the location and extent of necrosis. (
  • During apoptosis, in contrast to necrosis, the cell and eventually the fragments of the cell all maintain their ion-gradients and energy levels. (
  • this help me to really know the different between apoptosis and necrosis. (
  • This helped me do a report on apoptosis and necrosis. (
  • Caseous necrosis is a specific form of coagulation necrosis typically caused by mycobacteria (e.g., tuberculosis ), fungi , and some foreign substances. (
  • Contrast-enhanced four-chamber ECG-gated cardiac CT image planes, showing a large predominantly calcified mass (arrow) with peripheral discontinuous calcifications and central areas of low density attenuation located in the posterior left VA groove, consistent with caseous necrosis of the mitral valve. (
  • Three-chamber non-contrast ECG-gated cardiac CT image showing a large predominantly calcified mass (arrow) with peripheral discontinuous calcifications and central areas of low density attenuation located in the posterior left VA groove, suggestive of caseous necrosis of the mitral valve. (
  • Cardiac CT demonstrated a large extra-cavitary calcified mass with central areas of low density attenuation in the posterior atrio-ventricular groove, consistent with caseous necrosis of the mitral valve. (
  • Caseous necrosis of the mitral valve is a rare form of mitral annular calcification (MAC) in which there is high atherosclerotic burden with central 'caseous' necrosis, which can resemble a tumor. (
  • Can corticosteroids cause avascular necrosis (AVN)? (
  • We agree with Allan Knight that avascular necrosis was reported long before corticosteroids were introduced and that it remains to some extent a disorder of unknown origin. (
  • 1 At present, corticosteroids remain the single most common etiological factor for avascular necrosis seen in our centre. (
  • Long-term use of corticosteroids or drinking a large amount of alcohol over a long time increases the risk of avascular necrosis. (
  • [4] This pattern of necrosis is typically seen in hypoxic (low-oxygen) environments, such as infarction . (
  • Peripheral skin necrosis complicating beta-blockade. (
  • After the patient's condition has stabilized, he or she should be treated in an urgent fashion to minimize the risk of complications, including especially skin necrosis and avascular necrosis of the talar body. (
  • 11. The apparatus of claim 1 , wherein the electrode means has an electrode means advancement length extending from an exterior of the handpiece means to the interior of the tongue, wherein the advancement length is sufficient to position the energy delivery surface at the selected site and deliver sufficient electromagnetic energy to create cell necrosis without damaging a main branch of a hypoglossal nerve. (
  • In addition to inducing cell necrosis in tumor cells, TNF induces apoptosis in non-cancerous cells ( e.g. , hepatocytes and T cells). (
  • In the US at least, only the bites of spiders in the genus Loxosceles or brown recluse have been proven to consistently cause necrosis. (
  • [1] Many other spider species are claimed to cause necrosis but in most cases firm evidence is lacking. (
  • It is this high blood sugar (hyperglycemia) that can cause necrosis. (
  • Back muscle necrosis is part of the porcine stress syndrome and in affected pigs degenerative changes take place in the back muscles along each side of the spine. (
  • Selective vulnerability of brain regions to the effects of toxic compounds may imitate the lesions of ischemic necrosis and should be differentiated from insults of that type based on compound exposure and clinical history. (
  • What is radiation necrosis? (
  • Data from patients with radiation necrosis, who reported starting treatments within the last 5 years. (
  • We hypothesized that patients with oligodendroglioma have a higher risk of radiation necrosis (RN) as compared to patients with astrocytoma. (
  • Radiation necrosis appeared within 24 months from radiation in 80.5% of patients. (
  • How does papillary necrosis cause flank pain? (
  • Papillary necrosis can cause ureteral obstruction as sloughed papilla pass down the ureter. (
  • See Papillary Necrosis for more information. (
  • Papillary necrosis is a topic covered in the Diagnosaurus . (
  • Zeiger, Roni F.. "Papillary Necrosis. (
  • 5minute , (
  • The effect of varying both paddle electrode size and the time interval between direct current countershock on myocardial necrosis was studied. (
  • Myocardial necrosis was quantitated by precordial electrocardiographic mapping recorded minutes after, and by gross and microscopic examination of the hearts four days after direct current countershock. (
  • When the time interval between discharges was shorter, myocardial necrosis was greater. (
  • staining with hematoxylin-basic fuchsin-picric acid demonstrated newly developed massive myocardial necrosis, a rarely documented finding. (
  • Infectious pancreatic necrosis (IPN) kills a range of fish species, including salmon and trout. (
  • Infectious pancreatic necrosis (IPN) is a disease of freshwater and saltwater finfish. (
  • Liquefactive necrosis (or colliquative necrosis) is usually associated with cellular destruction and pus formation (e.g., pneumonia ). (
  • Our study establishes HMGB1 as a bona fide and targetable DAMP that selectively triggers a neutrophil-mediated injury amplification loop in the setting of necrosis. (
  • These images are a random sampling from a Bing search on the term "Navicular Avascular Necrosis. (
  • Fat necrosis is not cancer, but it can cause lumps and pulling of the tissues. (
  • If the necrosis involves muscle or multiple tissues in the tongue, then it is diagnosed as "tongue - necrosis. (
  • Death (necrosis) of muscle fibres with haemorrhages into the tissues themselves. (
  • Diabetic necrosis is the death of tissues in the body, and it causes serious consequences that can sometimes include the amputation of limbs, fingers, or toes. (
  • In ischemic brain lesions, the typical morphologic criteria of neuronal necrosis may take more than 24 hours of survival to manifest in hematoxylin and eosin sections. (
  • Increased risk of avascular necrosis in patients with psoriatic disease: A nationwide population-based matched cohort study. (
  • I have a very good friend in Ohio who's father has the disease vascular necrosis.Apprently there is a doctor somewhere(I think in California) who has been experimenting with a cure. (
  • Maize lethal necrosis disease is caused by co-infection of maize by Maize chlorotic mottle virus (Machlomovirus: Tombusviridae) and Sugarcane mosaic virus (Potyvirus: Potyviridae) or sometimes another cereal virus of the Potyviridae group. (
  • Formerly known as Familial Hibernian fever, Tumor Necrosis Factor Receptor Associated Periodic Syndrome (TRAPS) is a rare, genetic disease that causes recurrent episodes of fever that typically last more than one week and are associated with chills and severe muscle pain in the torso and the arms. (
  • Peanut bud necrosis disease (PBND) is an important disease of peanut in south and southeast Asia. (
  • Avascular necrosis doesn't usually stow on xray until the latter stages of the disease. (
  • Acute esophageal necrosis or black esophagus (Gurvits Syndrome) is a disease characterized by diffuse, circumferential black appearing mucosa that always affects the distal mucosa due to relative hypovascularity [1, 2] Estimated incidence is between 0.008 and 0.28% of patients undergoing upper endoscopy based on autopsy and retrospective reviews [1, 35]. (
  • Mediastinal fat necrosis (MFN) or epipericardial fat necrosis, as it is commonly referred to in the literature, is a rare self-limiting cause of chest pain of unclear etiology. (
  • Avascular necrosis tends to occur in men more often than women and typically is diagnosed between ages 30 and 50. (
  • Necrosis does not spontaneously occur in healthy people, and the number of insects capable of causing it are relatively rare. (
  • Tumor necrosis factor has also been implicated in several forms of cancer, such as breast and stomach cancers, which occur when cells that are supposed to undergo cell death fail to do so. (
  • Necrosis can occur secondary to trauma, infection, vasculitis, or thrombosis or as a direct effect of a test agent (particularly epithelial necrosis). (
  • Cellular death due to necrosis does not follow the apoptotic signal transduction pathway, but rather various receptors are activated, and result in the loss of cell membrane integrity and an uncontrolled release of products of cell death into the extracellular space . (
  • In NTP studies, infarcts are diagnosed as necrosis, and the term "malacia" is reserved for gross lesions in the brain. (
  • TRAPS is due to a gene defect in a protein called tumor necrosis factor receptor, which leads to an increase of the patient's normal inflammatory response. (
  • Tumor necrosis factors (TNF) alpha and beta are structurally related cytokines that mediate a wide range of immunological, inflammatory, and cytotoxic effects. (
  • Piecemeal necrosis in liver aka interface hepatitis is necrosis of the limiting plates, by inflammatory cells. (
  • It may be identified as actual necrosis of cells or by irregularity of the limiting plates which is caused IOS's hepatocytes and replacement with inflammatory cells and/or fibrosis. (
  • Binding of tumor necrosis factors to their receptors can become deregulated in the body, leading to a range of diseases. (