The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.
A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.
C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX.
Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.
The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g.
A subcomponent of complement C1, composed of six copies of three polypeptide chains (A, B, and C), each encoded by a separate gene (C1QA; C1QB; C1QC). This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY.
Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
A 63-kDa serum glycoprotein encoded by gene C9. Monomeric C9 (mC9) binds the C5b-8 complex to form C5b-9 which catalyzes the polymerization of C9 forming C5b-p9 (MEMBRANE ATTACK COMPLEX) and transmembrane channels leading to lysis of the target cell. Patients with C9 deficiency suffer from recurrent bacterial infections.
Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.
Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.
A component of the CLASSICAL COMPLEMENT PATHWAY. C2 is cleaved by activated COMPLEMENT C1S into COMPLEMENT C2B and COMPLEMENT C2A. C2a, the COOH-terminal fragment containing a SERINE PROTEASE, combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).
A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb.
An important soluble regulator of the alternative pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It is a 139-kDa glycoprotein expressed by the liver and secreted into the blood. It binds to COMPLEMENT C3B and makes iC3b (inactivated complement 3b) susceptible to cleavage by COMPLEMENT FACTOR I. Complement factor H also inhibits the association of C3b with COMPLEMENT FACTOR B to form the C3bB proenzyme, and promotes the dissociation of Bb from the C3bBb complex (COMPLEMENT C3 CONVERTASE, ALTERNATIVE PATHWAY).
Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host.
The smaller fragment generated from the cleavage of complement C3 by C3 CONVERTASE. C3a, a 77-amino acid peptide, is a mediator of local inflammatory process. It induces smooth MUSCLE CONTRACTION, and HISTAMINE RELEASE from MAST CELLS and LEUKOCYTES. C3a is considered an anaphylatoxin along with COMPLEMENT C4A; COMPLEMENT C5A; and COMPLEMENT C5A, DES-ARGININE.
The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. C5a is a 74-amino-acid glycopeptide with a carboxy-terminal ARGININE that is crucial for its spasmogenic activity. Of all the complement-derived anaphylatoxins, C5a is the most potent in mediating immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE), smooth MUSCLE CONTRACTION; HISTAMINE RELEASE; and migration of LEUKOCYTES to site of INFLAMMATION.
A 105-kDa serum glycoprotein with significant homology to the other late complement components, C7-C9. It is a polypeptide chain cross-linked by 32 disulfide bonds. C6 is the next complement component to bind to the membrane-bound COMPLEMENT C5B in the assembly of MEMBRANE ATTACK COMPLEX. It is encoded by gene C6.
Molecular sites on or in some B-lymphocytes and macrophages that recognize and combine with COMPLEMENT C3B. The primary structure of these receptors reveal that they contain transmembrane and cytoplasmic domains, with their extracellular portion composed entirely of thirty short consensus repeats each having 60 to 70 amino acids.
The first complement component to act in the activation of CLASSICAL COMPLEMENT PATHWAY. It is a calcium-dependent trimolecular complex made up of three subcomponents: COMPLEMENT C1Q; COMPLEMENT C1R; and COMPLEMENT C1S at 1:2:2 ratios. When the intact C1 binds to at least two antibodies (involving C1q), C1r and C1s are sequentially activated, leading to subsequent steps in the cascade of COMPLEMENT ACTIVATION.
The large fragment formed when COMPLEMENT C4 is cleaved by COMPLEMENT C1S. The membrane-bound C4b binds COMPLEMENT C2A, a SERINE PROTEASE, to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).
Enzymes that activate one or more COMPLEMENT PROTEINS in the complement system leading to the formation of the COMPLEMENT MEMBRANE ATTACK COMPLEX, an important response in host defense. They are enzymes in the various COMPLEMENT ACTIVATION pathways.
A 302-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c, and C3dg (955-1303) in the presence COMPLEMENT FACTOR H. Serum proteases further degrade C3dg into C3d (1002-1303) and C3g (955-1001).
Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.
Serologic tests based on inactivation of complement by the antigen-antibody complex (stage 1). Binding of free complement can be visualized by addition of a second antigen-antibody system such as red cells and appropriate red cell antibody (hemolysin) requiring complement for its completion (stage 2). Failure of the red cells to lyse indicates that a specific antigen-antibody reaction has taken place in stage 1. If red cells lyse, free complement is present indicating no antigen-antibody reaction occurred in stage 1.
A 93-kDa serum glycoprotein encoded by C7 gene. It is a polypeptide chain with 28 disulfide bridges. In the formation of MEMBRANE ATTACK COMPLEX; C7 is the next component to bind the C5b-6 complex forming a trimolecular complex C5b-7 which is lipophilic, resembles an integral membrane protein, and serves as an anchor for the late complement components, C8 and C9.
A 150-kDa serum glycoprotein composed of three subunits with each encoded by a different gene (C8A; C8B; and C8G). This heterotrimer contains a disulfide-linked C8alpha-C8gamma heterodimer and a noncovalently associated C8beta chain. C8 is the next component to bind the C5-7 complex forming C5b-8 that binds COMPLEMENT C9 and acts as a catalyst in the polymerization of C9.
A 206-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c (749-954), and C3dg (955-1303) in the presence COMPLEMENT FACTOR H.
Molecular sites on or in B-lymphocytes, follicular dendritic cells, lymphoid cells, and epithelial cells that recognize and combine with COMPLEMENT C3D. Human complement receptor 2 (CR2) serves as a receptor for both C3dg and the gp350/220 glycoprotein of HERPESVIRUS 4, HUMAN, and binds the monoclonal antibody OKB7, which blocks binding of both ligands to the receptor.
A screening assay for circulating COMPLEMENT PROTEINS. Diluted SERUM samples are added to antibody-coated ERYTHROCYTES and the percentage of cell lysis is measured. The values are expressed by the so called CH50, in HEMOLYTIC COMPLEMENT units per milliliter, which is the dilution of serum required to lyse 50 percent of the erythrocytes in the assay.
Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence.
The smaller fragment formed when complement C4 is cleaved by COMPLEMENT C1S. It is an anaphylatoxin that causes symptoms of immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE) but its activity is weaker than that of COMPLEMENT C3A or COMPLEMENT C5A.
A serum protein which is important in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. This enzyme cleaves the COMPLEMENT C3B-bound COMPLEMENT FACTOR B to form C3bBb which is ALTERNATIVE PATHWAY C3 CONVERTASE.
A plasma serine proteinase that cleaves the alpha-chains of C3b and C4b in the presence of the cofactors COMPLEMENT FACTOR H and C4-binding protein, respectively. It is a 66-kDa glycoprotein that converts C3b to inactivated C3b (iC3b) followed by the release of two fragments, C3c (150-kDa) and C3dg (41-kDa). It was formerly called KAF, C3bINF, or enzyme 3b inactivator.
A serum protein that regulates the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It binds as a cofactor to COMPLEMENT FACTOR I which then hydrolyzes the COMPLEMENT C4B in the CLASSICAL PATHWAY C3 CONVERTASE (C4bC2a).
A 77-kDa subcomponent of complement C1, encoded by gene C1S, is a SERINE PROTEASE existing as a proenzyme (homodimer) in the intact complement C1 complex. Upon the binding of COMPLEMENT C1Q to antibodies, the activated COMPLEMENT C1R cleaves C1s into two chains, A (heavy) and B (light, the serine protease), linked by disulfide bonds yielding the active C1s. The activated C1s, in turn, cleaves COMPLEMENT C2 and COMPLEMENT C4 to form C4b2a (CLASSICAL C3 CONVERTASE).
A 80-kDa subcomponent of complement C1, existing as a SERINE PROTEASE proenzyme in the intact complement C1 complex. When COMPLEMENT C1Q is bound to antibodies, the changed tertiary structure causes autolytic activation of complement C1r which is cleaved into two chains, A (heavy) and B (light, the serine protease), connected by disulfide bonds. The activated C1r serine protease, in turn, activates COMPLEMENT C1S proenzyme by cleaving the Arg426-Ile427 bond. No fragment is released when either C1r or C1s is cleaved.
GPI-linked membrane proteins broadly distributed among hematopoietic and non-hematopoietic cells. CD55 prevents the assembly of C3 CONVERTASE or accelerates the disassembly of preformed convertase, thus blocking the formation of the membrane attack complex.
Small glycoproteins found on both hematopoietic and non-hematopoietic cells. CD59 restricts the cytolytic activity of homologous complement by binding to C8 and C9 and blocking the assembly of the membrane attack complex. (From Barclay et al., The Leukocyte Antigen FactsBook, 1993, p234)
Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.
The larger fragment generated from the cleavage of C5 by C5 CONVERTASE that yields COMPLEMENT C5A and C5b (beta chain + alpha' chain, the residual alpha chain, bound by disulfide bond). C5b remains bound to the membrane and initiates the spontaneous assembly of the late complement components to form C5b-8-poly-C9, the MEMBRANE ATTACK COMPLEX.
Complement activation triggered by the interaction of microbial POLYSACCHARIDES with serum MANNOSE-BINDING LECTIN resulting in the activation of MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. As in the classical pathway, MASPs cleave COMPLEMENT C4 and COMPLEMENT C2 to form C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections.
Venoms from snakes of the genus Naja (family Elapidae). They contain many specific proteins that have cytotoxic, hemolytic, neurotoxic, and other properties. Like other elapid venoms, they are rich in enzymes. They include cobramines and cobralysins.
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
An endogenous 105-kDa plasma glycoprotein produced primarily by the LIVER and MONOCYTES. It inhibits a broad spectrum of proteases, including the COMPLEMENT C1R and the COMPLEMENT C1S proteases of the CLASSICAL COMPLEMENT PATHWAY, and the MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. C1-INH-deficient individuals suffer from HEREDITARY ANGIOEDEMA TYPES I AND II.
Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. They induce smooth MUSCLE CONTRACTION; mast cell HISTAMINE RELEASE; PLATELET AGGREGATION; and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from the strongest to the weakest is C5a, C3a, C4a, and C5a des-arginine.
A serine protease that is the complex of COMPLEMENT C3B and COMPLEMENT FACTOR BB. It cleaves multiple COMPLEMENT C3 into COMPLEMENT C3A (anaphylatoxin) and COMPLEMENT C3B in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY.
A ubiquitously expressed complement receptor that binds COMPLEMENT C3B and COMPLEMENT C4B and serves as a cofactor for their inactivation. CD46 also interacts with a wide variety of pathogens and mediates immune response.
A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.
A test used to determine whether or not complementation (compensation in the form of dominance) will occur in a cell with a given mutant phenotype when another mutant genome, encoding the same mutant phenotype, is introduced into that cell.
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
Proteins that bind to particles and cells to increase susceptibility to PHAGOCYTOSIS, especially ANTIBODIES bound to EPITOPES that attach to FC RECEPTORS. COMPLEMENT C3B may also participate.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
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 engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).
The natural bactericidal property of BLOOD due to normally occurring antibacterial substances such as beta lysin, leukin, etc. This activity needs to be distinguished from the bactericidal activity contained in a patient's serum as a result of antimicrobial therapy, which is measured by a SERUM BACTERICIDAL TEST.
A specific mannose-binding member of the collectin family of lectins. It binds to carbohydrate groups on invading pathogens and plays a key role in the MANNOSE-BINDING LECTIN COMPLEMENT PATHWAY.
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.
An adhesion-promoting leukocyte surface membrane heterodimer. The alpha subunit consists of the CD11b ANTIGEN and the beta subunit the CD18 ANTIGEN. The antigen, which is an integrin, functions both as a receptor for complement 3 and in cell-cell and cell-substrate adhesive interactions.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
Serum serine proteases which participate in COMPLEMENT ACTIVATION. They are activated when complexed with the MANNOSE-BINDING LECTIN, therefore also known as Mannose-binding protein-Associated Serine Proteases (MASPs). They cleave COMPLEMENT C4 and COMPLEMENT C2 to form C4b2a, the CLASSICAL PATHWAY C3 CONVERTASE.
A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.
A derivative of complement C5a, generated when the carboxy-terminal ARGININE is removed by CARBOXYPEPTIDASE B present in normal human serum. C5a des-Arg shows complete loss of spasmogenic activity though it retains some chemotactic ability (CHEMOATTRACTANTS).
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.
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.
Antibodies produced by a single clone of cells.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
The 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.
A class of C-type lectins that target the carbohydrate structures found on invading pathogens. Binding of collectins to microorganisms results in their agglutination and enhanced clearance. Collectins form trimers that may assemble into larger oligomers. Each collectin polypeptide chain consists of four regions: a relatively short N-terminal region, a collagen-like region, an alpha-helical coiled-coil region, and carbohydrate-binding region.
Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.
Proteins found in any species of bacterium.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
A method for the detection of very small quantities of antibody in which the antigen-antibody-complement complex adheres to indicator cells, usually primate erythrocytes or nonprimate blood platelets. The reaction is dependent on the number of bound C3 molecules on the C3b receptor sites of the indicator cell.
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 species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.
Immunoglobulins produced in a response to BACTERIAL ANTIGENS.
Established cell cultures that have the potential to propagate indefinitely.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
A condition characterized by the recurrence of HEMOGLOBINURIA caused by intravascular HEMOLYSIS. In cases occurring upon cold exposure (paroxysmal cold hemoglobinuria), usually after infections, there is a circulating antibody which is also a cold hemolysin. In cases occurring during or after sleep (paroxysmal nocturnal hemoglobinuria), the clonal hematopoietic stem cells exhibit a global deficiency of cell membrane proteins.
Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides SERUM SICKNESS and the ARTHUS REACTION, evidence supports a pathogenic role for immune complexes in many other IMMUNE SYSTEM DISEASES including GLOMERULONEPHRITIS, systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC) and POLYARTERITIS NODOSA.
Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Proteins prepared by recombinant DNA technology.
Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
The N-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S.
Abnormal immunoglobulins, especially IGG or IGM, that precipitate spontaneously when SERUM is cooled below 37 degrees Celsius. It is characteristic of CRYOGLOBULINEMIA.
Proteins that share the common characteristic of binding to carbohydrates. Some ANTIBODIES and carbohydrate-metabolizing proteins (ENZYMES) also bind to carbohydrates, however they are not considered lectins. PLANT LECTINS are carbohydrate-binding proteins that have been primarily identified by their hemagglutinating activity (HEMAGGLUTININS). However, a variety of lectins occur in animal species where they serve diverse array of functions through specific carbohydrate recognition.
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.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.
Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.
The phenomenon of target cell destruction by immunologically active effector cells. It may be brought about directly by sensitized T-lymphocytes or by lymphoid or myeloid "killer" cells, or it may be mediated by cytotoxic antibody, cytotoxic factor released by lymphoid cells, or complement.
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.)
The processes triggered by interactions of ANTIBODIES with their ANTIGENS.
A specific immune response elicited by a specific dose of an immunologically active substance or cell in an organism, tissue, or cell.
The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
The rate dynamics in chemical or physical systems.
Local surface sites on antibodies which react with antigen determinant sites on antigens (EPITOPES.) They are formed from parts of the variable regions of FAB FRAGMENTS.
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.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
The clear portion of BLOOD that is left after BLOOD COAGULATION to remove BLOOD CELLS and clotting proteins.
The in vitro formation of clusters consisting of a cell (usually a lymphocyte) surrounded by antigenic cells or antigen-bearing particles (usually erythrocytes, which may or may not be coated with antibody or antibody and complement). The rosette-forming cell may be an antibody-forming cell, a memory cell, a T-cell, a cell bearing surface cytophilic antibodies, or a monocyte possessing Fc receptors. Rosette formation can be used to identify specific populations of these cells.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
Glycoproteins found on the membrane or surface of cells.
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 level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Chronic glomerulonephritis characterized histologically by proliferation of MESANGIAL CELLS, increase in the MESANGIAL EXTRACELLULAR MATRIX, and a thickening of the glomerular capillary walls. This may appear as a primary disorder or secondary to other diseases including infections and autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Various subtypes are classified by their abnormal ultrastructures and immune deposits. Hypocomplementemia is a characteristic feature of all types of MPGN.
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.
Elements of limited time intervals, contributing to particular results or situations.
The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IMMUNOGLOBULIN G whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent.
Serum globulins that migrate to the gamma region (most positively charged) upon ELECTROPHORESIS. At one time, gamma-globulins came to be used as a synonym for immunoglobulins since most immunoglobulins are gamma globulins and conversely most gamma globulins are immunoglobulins. But since some immunoglobulins exhibit an alpha or beta electrophoretic mobility, that usage is in decline.
A serine protease that cleaves multiple COMPLEMENT 3 into COMPLEMENT 3A (anaphylatoxin) and COMPLEMENT 3B in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It is a complex of COMPLEMENT 4B and COMPLEMENT 2A (C4b2a).
Antigens on surfaces of cells, including infectious or foreign cells or viruses. They are usually protein-containing groups on cell membranes or walls and may be isolated.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
A biosensing technique in which biomolecules capable of binding to specific analytes or ligands are first immobilized on one side of a metallic film. Light is then focused on the opposite side of the film to excite the surface plasmons, that is, the oscillations of free electrons propagating along the film's surface. The refractive index of light reflecting off this surface is measured. When the immobilized biomolecules are bound by their ligands, an alteration in surface plasmons on the opposite side of the film is created which is directly proportional to the change in bound, or adsorbed, mass. Binding is measured by changes in the refractive index. The technique is used to study biomolecular interactions, such as antigen-antibody binding.
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.
Methods used by pathogenic organisms to evade a host's immune system.
Crystallizable fragments composed of the carboxy-terminal halves of both IMMUNOGLOBULIN HEAVY CHAINS linked to each other by disulfide bonds. Fc fragments contain the carboxy-terminal parts of the heavy chain constant regions that are responsible for the effector functions of an immunoglobulin (COMPLEMENT fixation, binding to the cell membrane via FC RECEPTORS, and placental transport). This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
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.
Transport proteins that carry specific substances in the blood or across cell membranes.
A dermal inflammatory reaction produced under conditions of antibody excess, when a second injection of antigen produces intravascular antigen-antibody complexes which bind complement, causing cell clumping, endothelial damage, and vascular necrosis.
The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.
The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.
The sum of the weight of all the atoms in a molecule.
Extrachromosomal, usually CIRCULAR DNA molecules that are self-replicating and transferable from one organism to another. They are found in a variety of bacterial, archaeal, fungal, algal, and plant species. They are used in GENETIC ENGINEERING as CLONING VECTORS.
The functional hereditary units of BACTERIA.
Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.
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.
Inflammation of any part of the KIDNEY.
A species of the genus SACCHAROMYCES, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement.
A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.
Specific molecular sites on the surface of various cells, including B-lymphocytes and macrophages, that combine with IMMUNOGLOBULIN Gs. Three subclasses exist: Fc gamma RI (the CD64 antigen, a low affinity receptor), Fc gamma RII (the CD32 antigen, a high affinity receptor), and Fc gamma RIII (the CD16 antigen, a low affinity receptor).
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.
Polysaccharides found in bacteria and in capsules thereof.
Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.
Proteins isolated from the outer membrane of Gram-negative bacteria.
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)
An encapsulated lymphatic organ through which venous blood filters.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Molecules found on the surface of some, but not all, B-lymphocytes, T-lymphocytes, and macrophages, which recognize and combine with the Fc (crystallizable) portion of immunoglobulin molecules.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
Immunoglobulins produced in response to VIRAL ANTIGENS.
Substances elaborated by bacteria that have antigenic activity.
The measurement of infection-blocking titer of ANTISERA by testing a series of dilutions for a given virus-antiserum interaction end-point, which is generally the dilution at which tissue cultures inoculated with the serum-virus mixtures demonstrate cytopathology (CPE) or the dilution at which 50% of test animals injected with serum-virus mixtures show infectivity (ID50) or die (LD50).
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.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Substances that are recognized by the immune system and induce an immune reaction.
Limbless REPTILES of the suborder Serpentes.
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.
CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.
A major adhesion-associated heterodimer molecule expressed by MONOCYTES; GRANULOCYTES; NK CELLS; and some LYMPHOCYTES. The alpha subunit is the CD11C ANTIGEN, a surface antigen expressed on some myeloid cells. The beta subunit is the CD18 ANTIGEN.
Polysaccharides consisting of mannose units.
A highly conserved heterodimeric glycoprotein that is differentially expressed during many severe physiological disturbance states such as CANCER; APOPTOSIS; and various NEUROLOGICAL DISORDERS. Clusterin is ubiquitously expressed and appears to function as a secreted MOLECULAR CHAPERONE.
All blood proteins except albumin ( = SERUM ALBUMIN, which is not a globulin) and FIBRINOGEN (which is not in the serum). The serum globulins are subdivided into ALPHA-GLOBULINS; BETA-GLOBULINS; and GAMMA-GLOBULINS on the basis of their electrophoretic mobilities. (From Dorland, 28th ed)
A gram-positive organism found in the upper respiratory tract, inflammatory exudates, and various body fluids of normal and/or diseased humans and, rarely, domestic animals.
Sites on an antigen that interact with specific antibodies.
The semi-permeable outer structure of a red blood cell. It is known as a red cell 'ghost' after HEMOLYSIS.
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.
A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus.
A multistage process that includes cloning, physical mapping, subcloning, determination of the DNA SEQUENCE, and information analysis.
A group of antigens that includes both the major and minor histocompatibility antigens. The former are genetically determined by the major histocompatibility complex. They determine tissue type for transplantation and cause allograft rejections. The latter are systems of allelic alloantigens that can cause weak transplant rejection.
Represents 15-20% of the human serum immunoglobulins, mostly as the 4-chain polymer in humans or dimer in other mammals. Secretory IgA (IMMUNOGLOBULIN A, SECRETORY) is the main immunoglobulin in secretions.
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.
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.
A species of gram-negative, aerobic BACTERIA. It is a commensal and pathogen only of humans, and can be carried asymptomatically in the NASOPHARYNX. When found in cerebrospinal fluid it is the causative agent of cerebrospinal meningitis (MENINGITIS, MENINGOCOCCAL). It is also found in venereal discharges and blood. There are at least 13 serogroups based on antigenic differences in the capsular polysaccharides; the ones causing most meningitis infections being A, B, C, Y, and W-135. Each serogroup can be further classified by serotype, serosubtype, and immunotype.
Transfer of immunity from immunized to non-immune host by administration of serum antibodies, or transplantation of lymphocytes (ADOPTIVE TRANSFER).
Infections with bacteria of the species NEISSERIA MENINGITIDIS.
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.
Sensitive tests to measure certain antigens, antibodies, or viruses, using their ability to agglutinate certain erythrocytes. (From Stedman, 26th ed)
Stable chromium atoms that have the same atomic number as the element chromium, but differ in atomic weight. Cr-50, 53, and 54 are stable chromium isotopes.
The relationships of groups of organisms as reflected by their genetic makeup.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
The movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.
The property of objects that determines the direction of heat flow when they are placed in direct thermal contact. The temperature is the energy of microscopic motions (vibrational and translational) of the particles of atoms.
Solutions or mixtures of toxic and nontoxic substances elaborated by snake (Ophidia) salivary glands for the purpose of killing prey or disabling predators and delivered by grooved or hollow fangs. They usually contain enzymes, toxins, and other factors.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
Antibodies from an individual that react with ISOANTIGENS of another individual of the same species.
Single-stranded complementary DNA synthesized from an RNA template by the action of RNA-dependent DNA polymerase. cDNA (i.e., complementary DNA, not circular DNA, not C-DNA) is used in a variety of molecular cloning experiments as well as serving as a specific hybridization probe.

Complement activity and pharmacological inhibition in cardiovascular disease. (1/54)

While complement is the most important component of humoral autoimmunity, and inflammation plays a key role in atherosclerosis, relatively few studies have looked at complement implications in atherosclerosis and its complications. C-reactive protein is a marker of inflammation and is also involved in atherosclerosis; it activates complement and colocalizes with activated complement proteins within the infarcting myocardium and the active atherosclerotic plaques. As new agents capable of modulating complement activity are being developed, new targets for the management of atherosclerosis are emerging that are related to autoimmunity and inflammation. The present paper reviews the putative roles of the various complement activation pathways in the development of atherosclerosis, in ST segment elevation and non-ST segment elevation acute coronary syndromes, and in coronary artery bypass graft surgery. It also provides a perspective on new therapeutic interventions being developed to modulate complement activity. These interventions include the C1 esterase inhibitor, which may be consumed in some inflammatory states resulting in the loss of one of the mechanisms inhibiting activation of the classical and lectin pathways; TP10, a recombinant protein of the soluble complement receptor type 1 (sCR1) which inhibits the C3 and C5 convertases of the common pathway by binding C3b and C4b; a truncated version of the soluble complement receptor type 1 CRI lacking the C4b binding site which selectively inhibits the alternative pathway; and pexelizumab, a monoclonal antibody selectively blocking C5 to prevent the activation of the terminal pathway that is involved in excessive inflammation and autoimmune responses.  (+info)

Therapeutic strategy with a membrane-localizing complement regulator to increase the number of usable donor organs after prolonged cold storage. (2/54)

A shortage of donor organs and increasing dependence on marginal grafts with prolonged ischemic times have meant that new methods are needed to prevent postischemic damage. Herein is reported a new strategy aimed to protect donor kidney from complement-mediated postischemic damage and therefore increase the number of successful transplants. Rat donor kidneys were perfused with a membrane-localizing complement regulator derived from human complement receptor type 1 (APT070) and then subjected to prolonged periods of cold storage (at 4 degrees C). A relationship was found between the duration of cold ischemia and the extent of complement-mediated tubule damage and loss of graft function. After 16 h of cold storage, APT070-treated kidneys that were transplanted into syngeneic recipients showed a significant increase in the number of surviving grafts, compared with control-treated grafts (63.6 versus 26.3%). Surviving grafts also displayed less acute tubular injury and better preservation of renal function. These results not only enhance the understanding of the mechanism by which prolonged cold ischemia reduces immediate graft survival but also provide essential information about the effectiveness of membrane-localizing complement regulator with prolonged cold storage. This could lead to more effective strategies for improving the use of severely ischemic donor organs.  (+info)

Relapsing fever spirochetes Borrelia recurrentis and B. duttonii acquire complement regulators C4b-binding protein and factor H. (3/54)

Relapsing fever is a rapidly progressive and severe septic disease caused by certain Borrelia spirochetes. The disease is divided into two forms, i.e., epidemic relapsing fever, caused by Borrelia recurrentis and transmitted by lice, and the endemic form, caused by several Borrelia species, such as B. duttonii, and transmitted by soft-bodied ticks. The spirochetes enter the bloodstream by the vector bite and live persistently in plasma even after the development of specific antibodies. This leads to fever relapses and high mortality and clearly indicates that the Borrelia organisms utilize effective immune evasion strategies. In this study, we show that the epidemic relapsing fever pathogen B. recurrentis and an endemic relapsing fever pathogen, B. duttonii, are serum resistant, i.e., resistant to complement in vitro. They acquire the host alternative complement pathway regulator factor H on their surfaces in a similar way to that of the less serum-resistant Lyme disease pathogen, B. burgdorferi sensu stricto. More importantly, the relapsing fever spirochetes specifically bind host C4b-binding protein, a major regulator of the antibody-mediated classical complement pathway. Both complement regulators retained their functional activities when bound to the surfaces of the spirochetes. In conclusion, this is the first report of complement evasion by Borrelia recurrentis and B. duttonii and the first report showing capture of C4b-binding protein by spirochetes.  (+info)

A novel inhibitor of the alternative pathway of complement reverses inflammation and bone destruction in experimental arthritis. (4/54)

Complement is an important component of the innate and adaptive immune response, yet complement split products generated through activation of each of the three complement pathways (classical, alternative, and lectin) can cause inflammation and tissue destruction. Previous studies have shown that complement activation through the alternative, but not classical, pathway is required to initiate antibody-induced arthritis in mice, but it is unclear if the alternative pathway (AP) plays a role in established disease. Previously, we have shown that human complement receptor of the immunoglobulin superfamily (CRIg) is a selective inhibitor of the AP of complement. Here, we present the crystal structure of murine CRIg and, using mutants, provide evidence that the structural requirements for inhibition of the AP are conserved in human and mouse. A soluble form of CRIg reversed inflammation and bone loss in two experimental models of arthritis by inhibiting the AP of complement in the joint. Our data indicate that the AP of complement is not only required for disease induction, but also disease progression. The extracellular domain of CRIg thus provides a novel tool to study the effects of inhibiting the AP of complement in established disease and constitutes a promising therapeutic with selectivity for a single complement pathway.  (+info)

Characterization of Ehp, a secreted complement inhibitory protein from Staphylococcus aureus. (5/54)

We report here the discovery and characterization of Ehp, a new secreted Staphylococcus aureus protein that potently inhibits the alternative complement activation pathway. Ehp was identified through a genomic scan as an uncharacterized secreted protein from S. aureus, and immunoblotting of conditioned S. aureus culture medium revealed that the Ehp protein was secreted at the highest levels during log-phase bacterial growth. The mature Ehp polypeptide is composed of 80 residues and is 44% identical to the complement inhibitory domain of S. aureus Efb (extracellular fibrinogen-binding protein). We observed preferential binding by Ehp to native and hydrolyzed C3 relative to fully active C3b and found that Ehp formed a subnanomolar affinity complex with these various forms of C3 by binding to its thioester-containing C3d domain. Site-directed mutagenesis demonstrated that Arg(75) and Asn(82) are important in forming the Ehp.C3d complex, but loss of these side chains did not completely disrupt Ehp/C3d binding. This suggested the presence of a second C3d-binding site in Ehp, which was mapped to the proximity of Ehp Asn(63). Further molecular level details of the Ehp/C3d interaction were revealed by solving the 2.7-A crystal structure of an Ehp.C3d complex in which the low affinity site had been mutationally inactivated. Ehp potently inhibited C3b deposition onto sensitized surfaces by the alternative complement activation pathway. This inhibition was directly related to Ehp/C3d binding and was more potent than that seen for Efb-C. An altered conformation in Ehp-bound C3 was detected by monoclonal antibody C3-9, which is specific for a neoantigen exposed in activated forms of C3. Our results suggest that increased inhibitory potency of Ehp relative to Efb-C is derived from the second C3-binding site in this new protein.  (+info)

Effect of the complement inhibitor eculizumab on thromboembolism in patients with paroxysmal nocturnal hemoglobinuria. (6/54)

Hemolysis and hemoglobinemia contribute to serious clinical sequelae in hemolytic disorders. In paroxysmal nocturnal hemoglobinuria (PNH) patients, hemolysis can contribute to thromboembolism (TE), the most feared complication in PNH, and the leading cause of disease-related deaths. We evaluated whether long-term treatment with the complement inhibitor eculizumab reduces the rate of TE in patients with PNH. Clinical trial participants included all patients in the 3 eculizumab PNH clinical studies, which recruited patients between 2002 and 2005 (n = 195); patients from these studies continued treatment in the current multinational open-label extension study. Thromboembolism rate with eculizumab treatment was compared with the pretreatment rate in the same patients. The TE event rate with eculizumab treatment was 1.07 events/100 patient-years compared with 7.37 events/100 patient-years (P < .001) prior to eculizumab treatment (relative reduction, 85%; absolute reduction, 6.3 TE events/100 patient-years). With equalization of the duration of exposure before and during treatment for each patient, TE events were reduced from 39 events before eculizumab to 3 events during eculizumab (P < .001). The TE event rate in antithrombotic-treated patients (n = 103) was reduced from 10.61 to 0.62 events/100 patient-years with eculizumab treatment (P < .001). These results show that eculizumab treatment reduces the risk of clinical thromboembolism in patients with PNH. This study is registered at (study ID no. NCT00122317).  (+info)

Management of hereditary angioedema in pediatric patients. (7/54)

Hereditary angioneurotic edema is a rare disorder caused by the congenital deficiency of C1 inhibitor. Recurring angioedematous paroxysms that most commonly involve the subcutis (eg, extremities, face, trunk, and genitals) or the submucosa (eg, intestines and larynx) are the hallmarks of hereditary angioneurotic edema. Edema formation is related to reduction or dysfunction of C1 inhibitor, and conventional therapy with antihistamines and corticosteroids is ineffective. Manifestations occur during the initial 2 decades of life, but even today there is a long delay between the onset of initial symptoms and the diagnosis of hereditary angioneurotic edema. Although a variety of reviews have been published during the last 3 decades on the general management of hereditary angioneurotic edema, little has been published regarding management of pediatric hereditary angioneurotic edema. Thus, we review our experience and published data to provide an approach to hereditary angioneurotic edema in childhood.  (+info)

Association of reactive oxygen and nitrogen intermediate and complement levels with apoptosis of peripheral blood mononuclear cells in lupus patients. (8/54)

OBJECTIVE: Both increased production of reactive oxygen and nitrogen intermediates (RONI) and reduced levels of complement may play a role in the increased apoptosis and reduced clearance of apoptotic cells in systemic lupus erythematosus (SLE). The objective of this study was to evaluate both processes in a parallel, prospective, longitudinal manner. METHODS: Sixty-seven SLE patients were evaluated during multiple visits, and 31 healthy control subjects were evaluated once or twice. Clinical and laboratory features of SLE disease activity were determined, and blood was collected for measurement of serum nitrate plus nitrite (NOx) levels and for isolation of peripheral blood mononuclear cells (PBMCs). PBMCs were cultured with a nitric oxide (NO) donor and SLE or control plasma, with or without heat inactivation, cobra venom factor (CVF), or lipopolysaccharide plus interferon-gamma treatment. Cells were analyzed for apoptotic index (AI), cellular subsets, and RONI production. RESULTS: The PBMC AI was associated with SLE and was inversely associated with complement levels over time. Changes in the AI with addition of a NO donor was longitudinally associated with serum NOx levels, and stimulation of SLE PBMCs led to parallel increases in RONI production and apoptosis. Addition of SLE plasma resulted in a greater PBMC AI, an effect that was increased with heat inactivation and was corrected with CVF treatment. CONCLUSION: These data suggest that the greater AI observed in SLE PBMCs relates to increased PBMC RONI production and reduced complement levels. The longitudinal nature of these parallel associations within individuals suggests that these processes are dynamic and additive.  (+info)

There are two main types of hemolysis:

1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.

Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.

Some common causes of hemolysis include:

1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.

Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.

There are two main types of MD:

1. Dry Macular Degeneration (DMD): This is the most common form of MD, accounting for about 90% of cases. It is caused by the gradual accumulation of waste material in the macula, which can lead to cell death and vision loss over time.
2. Wet Macular Degeneration (WMD): This type of MD is less common but more aggressive, accounting for about 10% of cases. It occurs when new blood vessels grow underneath the retina, leaking fluid and causing damage to the macula. This can lead to rapid vision loss if left untreated.

The symptoms of MD can vary depending on the severity and type of the condition. Common symptoms include:

* Blurred vision
* Distorted vision (e.g., straight lines appearing wavy)
* Difficulty reading or recognizing faces
* Difficulty adjusting to bright light
* Blind spots in central vision

MD can have a significant impact on daily life, making it difficult to perform everyday tasks such as driving, reading, and recognizing faces.

There is currently no cure for MD, but there are several treatment options available to slow down the progression of the disease and manage its symptoms. These include:

* Anti-vascular endothelial growth factor (VEGF) injections: These medications can help prevent the growth of new blood vessels and reduce inflammation in the macula.
* Photodynamic therapy: This involves the use of a light-sensitive drug and low-intensity laser to damage and shrink the abnormal blood vessels in the macula.
* Vitamin supplements: Certain vitamins, such as vitamin C, E, and beta-carotene, have been shown to slow down the progression of MD.
* Laser surgery: This can be used to reduce the number of abnormal blood vessels in the macula and improve vision.

It is important for individuals with MD to receive regular monitoring and treatment from an eye care professional to manage their condition and prevent complications.

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

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

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

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

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

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

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

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

The disorder is caused by mutations in the HBB gene that codes for the beta-globin subunit of hemoglobin. These mutations result in the production of abnormal hemoglobins that are unstable and prone to breakdown, leading to the release of free hemoglobin into the urine.

HP is classified into two types based on the severity of symptoms:

1. Type 1 HP: This is the most common form of the disorder and is characterized by mild to moderate anemia, occasional hemoglobinuria, and a normal life expectancy.
2. Type 2 HP: This is a more severe form of the disorder and is characterized by severe anemia, recurrent hemoglobinuria, and a shorter life expectancy.

There is no cure for HP, but treatment options are available to manage symptoms and prevent complications. These may include blood transfusions, folic acid supplements, and medications to reduce the frequency and severity of hemoglobinuria episodes.

The term "immune complex disease" was first used in the 1960s to describe a group of conditions that were thought to be caused by the formation of immune complexes. These diseases include:

1. Systemic lupus erythematosus (SLE): an autoimmune disorder that can affect multiple organ systems and is characterized by the presence of anti-nuclear antibodies.
2. Rheumatoid arthritis (RA): an autoimmune disease that causes inflammation in the joints and can lead to joint damage.
3. Type III hypersensitivity reaction: a condition in which immune complexes are deposited in tissues, leading to inflammation and tissue damage.
4. Pemphigus: a group of autoimmune diseases that affect the skin and mucous membranes, characterized by the presence of autoantibodies against desmosomal antigens.
5. Bullous pemphigoid: an autoimmune disease that affects the skin and is characterized by the formation of large blisters.
6. Myasthenia gravis: an autoimmune disorder that affects the nervous system, causing muscle weakness and fatigue.
7. Goodpasture's syndrome: a rare autoimmune disease that affects the kidneys and lungs, characterized by the presence of immune complexes in the glomeruli of the kidneys.
8. Hemolytic uremic syndrome (HUS): a condition in which red blood cells are destroyed and waste products accumulate in the kidneys, leading to kidney failure.

Immune complex diseases can be caused by various factors, including genetic predisposition, environmental triggers, and exposure to certain drugs or toxins. Treatment options for these diseases include medications that suppress the immune system, such as corticosteroids and immunosuppressive drugs, and plasmapheresis, which is a process that removes harmful antibodies from the blood. In some cases, organ transplantation may be necessary.

In conclusion, immune complex diseases are a group of disorders that occur when the body's immune system mistakenly attacks its own tissues and organs, leading to inflammation and damage. These diseases can affect various parts of the body, including the skin, kidneys, lungs, and nervous system. Treatment options vary depending on the specific disease and its severity, but may include medications that suppress the immune system and plasmapheresis.

The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.

There are several subtypes of LES, including:

1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.

There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.

It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.

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

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

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

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

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

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

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

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

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

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

Idiopathic membranous nephropathy (IMN) is an autoimmune disorder that causes GNM without any identifiable cause. Secondary membranous nephropathy, on the other hand, is caused by systemic diseases such as lupus or cancer.

The symptoms of GNM can vary depending on the severity of the disease and may include blood in the urine, proteinuria, edema, high blood pressure, and decreased kidney function. The diagnosis of GNM is based on a combination of clinical findings, laboratory tests, and renal biopsy.

Treatment for GNM is aimed at slowing the progression of the disease and managing symptoms. Medications such as corticosteroids, immunosuppressive drugs, and blood pressure-lowering drugs may be used to treat GNM. In some cases, kidney transplantation may be necessary.

The prognosis for GNM varies depending on the severity of the disease and the underlying cause. In general, the prognosis for IMN is better than for secondary membranous nephropathy. With proper treatment, some patients with GNM can experience a slowing or stabilization of the disease, while others may progress to end-stage renal disease (ESRD).

The cause of GNM is not fully understood, but it is believed to be an autoimmune disorder that leads to inflammation and damage to the glomerular membrane. Genetic factors and environmental triggers may also play a role in the development of GNM.

There are several risk factors for developing GNM, including family history, age (GMN is more common in adults), and certain medical conditions such as hypertension and diabetes.

The main complications of GNM include:

1. ESRD: Progression to ESRD is a common outcome of untreated GNM.
2. High blood pressure: GNM can lead to high blood pressure, which can further damage the kidneys.
3. Infections: GNM increases the risk of infections due to impaired immune function.
4. Kidney failure: GNM can cause chronic kidney failure, leading to the need for dialysis or a kidney transplant.
5. Cardiovascular disease: GNM is associated with an increased risk of cardiovascular disease, including heart attack and stroke.
6. Malnutrition: GNM can lead to malnutrition due to decreased appetite, nausea, and vomiting.
7. Bone disease: GNM can cause bone disease, including osteoporosis and bone pain.
8. Anemia: GNM can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
9. Increased risk of infections: GNM increases the risk of infections due to impaired immune function.
10. Decreased quality of life: GNM can significantly decrease a person's quality of life, leading to decreased mobility, pain, and discomfort.

It is important for individuals with GNM to receive early diagnosis and appropriate treatment to prevent or delay the progression of these complications.

The Arthus reaction is named after French physician Louis-Jean-Baptiste Arthus, who first described the phenomenon in 1890. It is commonly seen in conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and other autoimmune disorders.

The reaction occurs when antibodies bind to antigens, such as proteins or cells, on the surface of tissues. The binding of antibodies to antigens can activate complement proteins, which are a group of proteins that work together to destroy pathogens. In the case of the Arthus reaction, the activation of complement proteins leads to the formation of a membrane attack complex (MAC), which is composed of various proteins and can cause damage to tissues.

The Arthus reaction can cause a range of symptoms, including joint pain, swelling, and warmth, as well as fever and fatigue. In severe cases, it can lead to permanent joint damage and disability. Treatment options for the Arthus reaction include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive medications.

In summary, the Arthus reaction is an allergic response that occurs when antibodies bind to antigens and form immune complexes, leading to inflammation and tissue damage. It is commonly seen in autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis, and can cause a range of symptoms including joint pain and swelling, fever, and fatigue. Treatment options include NSAIDs, corticosteroids, and immunosuppressive medications.

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

Some common types of nephritis include:

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

There are several key features of inflammation:

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

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

There are several types of inflammation, including:

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

There are several ways to reduce inflammation, including:

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

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

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

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

Acute angioedema is usually triggered by an allergic reaction or exposure to certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), blood pressure medications, or antibiotics. It can also be caused by infections, insect bites, and other environmental triggers.

Chronic angioedema, on the other hand, is a more persistent form of the condition that can last for weeks, months, or even years. It is often associated with conditions such as hereditary angioedema (HAE), which is caused by a genetic defect that affects the production of a protein called C1 esterase inhibitor.

The symptoms of angioedema can vary depending on the location and severity of the swelling, but they typically include:

* Swelling in the face, hands, feet, or other parts of the body
* Redness and warmth of the affected area
* Pain or discomfort
* Difficulty breathing or swallowing (in severe cases)

There is no cure for angioedema, but there are several treatments available to help manage the symptoms. These may include:

* Antihistamines or corticosteroids to reduce inflammation and relieve itching
* Ice packs or cool compresses to reduce swelling
* Compression stockings or bandages to prevent fluid buildup
* Pain relief medications, such as ibuprofen or acetaminophen, to manage discomfort

In severe cases of angioedema, hospitalization may be necessary to provide more intensive treatment and monitoring. In some cases, injectable medications such as epinephrine or corticosteroids may be administered to help reduce swelling and prevent complications.

Overall, angioedema is a serious condition that requires prompt medical attention to manage symptoms and prevent complications. If you suspect you or someone else may have angioedema, it is important to seek medical help right away.

The most common form of this disease is Meningococcal Group B (MenB). Symptoms often develop within hours or days after exposure, but can be nonspecific, such as fever, headache, and muscle aches.

Early signs that are more specific and suggestive of the diagnosis include neck stiffness, confusion, seizures, and rash. Diagnosis is by culture or PCR of a sterile site. Treatment consists of antibiotics that cover Neisseria meningitidis, which should be initiated promptly after recognition of the signs and symptoms.

Prevention with vaccines is recommended for infants at 2 months of age; boosters are given at 4 months, 6 months, and 12 to 15 months of age.

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

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

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

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

The two main types of TMAs are:

1. Thrombotic thrombocytopenic purpura (TTP): This is a rare autoimmune disorder caused by the formation of antibodies against ADAMTS13, an enzyme involved in platelet function. TTP patients have low levels of ADAMTS13 and abnormal platelets that are prone to clotting.
2. Hemolytic uremic syndrome (HUS): This is a condition that occurs when red blood cells are destroyed and removed from the circulation, leading to anemia, low platelet count, and kidney failure. HUS can be caused by various factors, such as infections, certain medications, or genetic mutations.

Both TTP and HUS can lead to TMAs, which can cause severe morbidity and mortality if left untreated. Treatment options for TMAs include plasmapheresis, corticosteroids, and immunosuppressive drugs, as well as dialysis in cases of acute kidney injury. Early diagnosis and aggressive treatment are essential to prevent long-term complications and improve patient outcomes.

Here are some key points to define sepsis:

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

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

Examples of Immunologic Deficiency Syndromes include:

1. Primary Immunodeficiency Diseases (PIDDs): These are a group of genetic disorders that affect the immune system's ability to function properly. Examples include X-linked agammaglobulinemia, common variable immunodeficiency, and severe combined immunodeficiency.
2. Acquired Immunodeficiency Syndrome (AIDS): This is a condition that results from the human immunodeficiency virus (HIV) infection, which destroys CD4 cells, a type of immune cell that fights off infections.
3. Immune Thrombocytopenic Purpura (ITP): This is an autoimmune disorder that causes the immune system to attack and destroy platelets, which are blood cells that help the blood to clot.
4. Autoimmune Disorders: These are conditions in which the immune system mistakenly attacks and damages healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, and multiple sclerosis.
5. Immunosuppressive Therapy-induced Immunodeficiency: This is a condition that occurs as a side effect of medications used to prevent rejection in organ transplant patients. These medications can suppress the immune system, increasing the risk of infections.

Symptoms of Immunologic Deficiency Syndromes can vary depending on the specific disorder and the severity of the immune system dysfunction. Common symptoms include recurrent infections, fatigue, fever, and swollen lymph nodes. Treatment options for these syndromes range from medications to suppress the immune system to surgery or bone marrow transplantation.

In summary, Immunologic Deficiency Syndromes are a group of disorders that result from dysfunction of the immune system, leading to recurrent infections and other symptoms. There are many different types of these syndromes, each with its own set of symptoms and treatment options.

The term "serum sickness" was first used in the late 19th century to describe this condition, which was often seen in people who had received serum (a type of blood product) containing antibodies against diseases such as diphtheria or tetanus. Today, the term is still used to describe similar reactions to other substances, including medications and vaccines.

Serum sickness can be mild or severe, and in rare cases, it can lead to serious complications such as kidney failure or inflammation of the heart. Treatment typically involves stopping the use of the offending substance and providing supportive care to manage symptoms. In severe cases, corticosteroids or other medications may be used to reduce inflammation.

While serum sickness is a relatively rare condition, it is important for healthcare providers to be aware of it as a potential complication of medication and vaccine use. This knowledge can help them recognize and manage the condition effectively, reducing the risk of serious complications and improving outcomes for patients.

There are several symptoms of RA, including:

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

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

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

1. Autoimmune diseases: These occur when the immune system mistakenly attacks healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, multiple sclerosis, and type 1 diabetes.
2. Allergies: An allergic reaction occurs when the immune system overreacts to a harmless substance, such as pollen, dust mites, or certain foods. Symptoms can range from mild hives to life-threatening anaphylaxis.
3. Immunodeficiency disorders: These are conditions that impair the immune system's ability to fight infections. Examples include HIV/AIDS and primary immunodeficiency diseases.
4. Infectious diseases: Certain infections, such as tuberculosis or bacterial meningitis, can cause immune system dysfunction.
5. Cancer: Some types of cancer, such as lymphoma, affect the immune system's ability to fight disease.
6. Immune thrombocytopenic purpura (ITP): This is a rare autoimmune disorder that causes the immune system to attack and destroy platelets, leading to bleeding and bruising.
7. Guillain-Barré syndrome: This is a rare autoimmune disorder that occurs when the immune system attacks the nerves, leading to muscle weakness and paralysis.
8. Chronic fatigue syndrome (CFS): This is a condition characterized by persistent fatigue, muscle pain, and joint pain, which is thought to be related to an immune system imbalance.
9. Fibromyalgia: This is a chronic condition characterized by widespread muscle pain, fatigue, and sleep disturbances, which may be linked to immune system dysfunction.
10. Autoimmune hepatitis: This is a condition in which the immune system attacks the liver, leading to inflammation and damage to the liver cells.

It's important to note that a weakened immune system can increase the risk of infections and other health problems, so it's important to work with your healthcare provider to identify any underlying causes and develop an appropriate treatment plan.

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

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

Examples of autoimmune diseases include:

1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.

The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.

Membranous nephropathy is a specific type of glomerulonephritis that is characterized by the deposition of immune complexes in the glomerular basement membrane. This leads to inflammation and damage to the glomeruli, which can progress to end-stage renal disease if left untreated.

The exact cause of membranous nephropathy is not fully understood, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissue in the kidneys. Factors such as genetics, environmental triggers, and certain medical conditions may contribute to the development of the disease.

Symptoms of membranous nephropathy can include proteinuria, hematuria, high blood pressure, swelling, fatigue, and weight loss. The disease is typically diagnosed through a combination of physical examination, laboratory tests, and kidney biopsy.

Treatment for membranous nephropathy typically involves a combination of medications to control proteinuria, hematuria, and high blood pressure, as well as immunosuppressive drugs to suppress the immune system and prevent further damage to the kidneys. In severe cases, dialysis or kidney transplantation may be necessary.

People with agammaglobulinemia are more susceptible to infections, particularly those caused by encapsulated bacteria, such as Streptococcus pneumoniae and Haemophilus influenzae type b. They may also experience recurrent sinopulmonary infections, ear infections, and gastrointestinal infections. The disorder can be managed with intravenous immunoglobulin (IVIG) therapy, which provides antibodies to help prevent infections. In severe cases, a bone marrow transplant may be necessary.

Agammaglobulinemia is an autosomal recessive disorder, meaning that a person must inherit two mutated copies of the BTK gene (one from each parent) to develop the condition. It is relatively rare, affecting approximately one in 1 million people worldwide. The disorder can be diagnosed through genetic testing and a complete blood count (CBC) that shows low levels of immunoglobulins.

Treatment for ag

There are two forms of trypanosomiasis, depending on the stage of the parasite:

1. Acute trypanosomiasis: This form of the disease occurs in the early stages of infection and is characterized by fever, headache, muscle pain, and joint swelling.
2. Chronic trypanosomiasis: This form of the disease occurs in the later stages of infection and is characterized by progressive neurological symptoms, including confusion, slurred speech, and difficulty walking.

If left untreated, trypanosomiasis can be fatal. Treatment typically involves the use of antiparasitic drugs, such as melarsoprol or eflornithine.

In addition to its medical significance, trypanosomiasis has also had significant social and economic impacts on affected communities, particularly in rural areas where the disease is more common. The stigma associated with the disease can lead to social isolation and marginalization of infected individuals and their families, while the financial burden of treatment can be a significant source of poverty.

Overall, trypanosomiasis is a serious and potentially deadly disease that requires prompt diagnosis and treatment to prevent complications and improve outcomes for affected individuals.

Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.

The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.

Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.

Examples of diseases with a known genetic predisposition:

1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.

Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."

Types of Pneumococcal Infections:

1. Pneumonia: This is an infection of the lungs that can cause fever, cough, chest pain, and difficulty breathing.
2. Meningitis: This is an infection of the membranes that cover the brain and spinal cord, which can cause fever, headache, stiff neck, and confusion.
3. Septicemia (bloodstream infection): This is an infection of the blood that can cause fever, chills, and low blood pressure.
4. Sinusitis: This is an infection of the sinuses, which can cause headache, facial pain, and difficulty breathing through the nose.
5. Otitis media (middle ear infection): This is an infection of the middle ear, which can cause ear pain, fever, and hearing loss.

Causes and Risk Factors:

Pneumococcal infections are caused by the bacteria Streptococcus pneumoniae. These bacteria can be spread through close contact with an infected person, such as touching or sharing food and drinks. People who are at high risk for developing pneumococcal infections include:

1. Children under the age of 5 and adults over the age of 65.
2. People with weakened immune systems, such as those with cancer, HIV/AIDS, or taking medications that suppress the immune system.
3. Smokers and people with chronic respiratory diseases, such as asthma or chronic obstructive pulmonary disease (COPD).
4. People who have recently had surgery or have a severe injury.
5. Those who live in long-term care facilities or have limited access to healthcare.

Prevention and Treatment:

Preventing pneumococcal infections is important, especially for high-risk individuals. Here are some ways to prevent and treat pneumococcal infections:

1. Vaccination: The pneumococcal conjugate vaccine (PCV) is recommended for children under the age of 5 and adults over the age of 65, as well as for people with certain medical conditions.
2. Hand washing: Frequent hand washing can help prevent the spread of pneumococcal bacteria.
3. Good hygiene: Avoiding close contact with people who are sick and regularly cleaning surfaces that may be contaminated with bacteria can also help prevent infection.
4. Antibiotics: Pneumococcal infections can be treated with antibiotics, but overuse of antibiotics can lead to the development of antibiotic-resistant bacteria. Therefore, antibiotics should only be used when necessary and under the guidance of a healthcare professional.
5. Supportive care: Those with severe pneumococcal infections may require hospitalization and supportive care, such as oxygen therapy or mechanical ventilation.


Pneumococcal infections can be serious and even life-threatening, especially for high-risk individuals. Prevention and prompt treatment are key to reducing the risk of complications and improving outcomes. Vaccination, good hygiene practices, and appropriate antibiotic use are all important in preventing and treating pneumococcal infections. If you suspect that you or a loved one has a pneumococcal infection, it is essential to seek medical attention right away. With proper care and support, many people with pneumococcal infections can recover fully and resume their normal lives.

Symptoms of meningococcal meningitis typically develop within 3-7 days after exposure and may include fever, headache, stiff neck, confusion, nausea and vomiting, sensitivity to light, and seizures. In severe cases, the infection can lead to shock, organ failure, and death within hours of the onset of symptoms.

Diagnosis is typically made by a combination of physical examination, laboratory tests (such as blood cultures and PCR), and imaging studies (such as CT or MRI scans). Treatment typically involves antibiotics, intravenous fluids, and supportive care to manage fever, pain, and other symptoms. In severe cases, hospitalization in an intensive care unit may be necessary.

Prevention of meningococcal meningitis includes the use of vaccines, good hygiene practices (such as frequent handwashing), and avoidance of close contact with people who are sick. A vaccine is available for children and teens, and some colleges and universities require students to be vaccinated before moving into dorms.

Early diagnosis and treatment are crucial in preventing long-term complications and reducing the risk of death from meningococcal meningitis. If you suspect that you or someone else may have meningococcal meningitis, it is important to seek medical attention immediately.

Once infected, humans can experience a range of symptoms including fever, headache, muscle pain, and fatigue. In severe cases, the infection can spread to the bones and joints, causing swelling and pain. Brucellosis can also lead to complications such as endocarditis (inflammation of the heart valves) and meningitis (inflammation of the lining around the brain and spinal cord).

Brucellosis in cows is typically diagnosed through a combination of physical examination, laboratory tests, and blood samples. Treatment typically involves antibiotics, but it is important to detect and treat the infection early to prevent complications. Prevention measures include vaccination of animals, proper handling and disposal of animal products, and avoiding contact with infected animals or their products.

In addition to its medical significance, brucellosis has also been associated with significant economic losses in the livestock industry due to reduced milk production and fertility issues in infected animals.

There are several types of lupus nephritis, each with its own unique characteristics and symptoms. The most common forms include:

* Class I (mesangial proliferative glomerulonephritis): This type is characterized by the growth of abnormal cells in the glomeruli (blood-filtering units of the kidneys).
* Class II (active lupus nephritis): This type is characterized by widespread inflammation and damage to the kidneys, with or without the presence of antibodies.
* Class III (focal lupus nephritis): This type is characterized by localized inflammation in certain areas of the kidneys.
* Class IV (lupus nephritis with crescentic glomerulonephritis): This type is characterized by widespread inflammation and damage to the kidneys, with crescent-shaped tissue growth in the glomeruli.
* Class V (lupus nephritis with sclerotic changes): This type is characterized by hardening and shrinkage of the glomeruli due to scarring.

Lupus Nephritis can cause a range of symptoms, including:

* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Reduced kidney function
* Swelling (edema)
* Fatigue
* Fever
* Joint pain

Lupus Nephritis can be diagnosed through a combination of physical examination, medical history, laboratory tests, and kidney biopsy. Treatment options for lupus nephritis include medications to suppress the immune system, control inflammation, and prevent further damage to the kidneys. In severe cases, dialysis or a kidney transplant may be necessary.

Types of Kidney Diseases:

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

Symptoms of Kidney Diseases:

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

Diagnosis of Kidney Diseases:

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

Treatment of Kidney Diseases:

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

Prevention of Kidney Diseases:

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

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

Symptoms of anaphylaxis include:

1. Swelling of the face, lips, tongue, and throat
2. Difficulty breathing or swallowing
3. Abdominal cramps
4. Nausea and vomiting
5. Rapid heartbeat
6. Feeling of impending doom or loss of consciousness

Anaphylaxis is diagnosed based on a combination of symptoms, medical history, and physical examination. Treatment for anaphylaxis typically involves administering epinephrine (adrenaline) via an auto-injector, such as an EpiPen or Auvi-Q. Additional treatments may include antihistamines, corticosteroids, and oxygen therapy.

Prevention of anaphylaxis involves avoiding known allergens and being prepared to treat a reaction if it occurs. If you have a history of anaphylaxis, it is important to carry an EpiPen or other emergency medication with you at all times. Wearing a medical alert bracelet or necklace can also help to notify others of your allergy and the need for emergency treatment.

In severe cases, anaphylaxis can lead to unconsciousness, seizures, and even death. Prompt treatment is essential to prevent these complications and ensure a full recovery.

There are several types of disease susceptibility, including:

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

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

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

Autoimmune hemolytic anemia (AIHA) is a specific type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells. This can happen due to various underlying causes such as infections, certain medications, and some types of cancer.

In autoimmune hemolytic anemia, the immune system produces antibodies that coat the surface of red blood cells and mark them for destruction by other immune cells called complement proteins. This leads to the premature destruction of red blood cells in the spleen, liver, and other organs.

Symptoms of autoimmune hemolytic anemia can include fatigue, weakness, shortness of breath, jaundice (yellowing of the skin and eyes), dark urine, and a pale or yellowish complexion. Treatment options for AIHA depend on the underlying cause of the disorder, but may include medications to suppress the immune system, plasmapheresis to remove antibodies from the blood, and in severe cases, splenectomy (removal of the spleen) or bone marrow transplantation.

In summary, autoimmune hemolytic anemia is a type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells, leading to premature destruction of red blood cells and various symptoms such as fatigue, weakness, and jaundice. Treatment options depend on the underlying cause of the disorder and may include medications, plasmapheresis, and in severe cases, splenectomy or bone marrow transplantation.

There are several types of blood protein disorders, including:

1. Hemophilia A: a deficiency of factor VIII, which is necessary for blood clotting.
2. Hemophilia B: a deficiency of factor IX, also involved in blood clotting.
3. Von Willebrand disease: a deficiency of von Willebrand factor, which helps to platelets stick together and form blood clots.
4. Protein C deficiency: a lack of protein C, an anticoagulant protein that helps to prevent blood clots.
5. Protein S deficiency: a lack of protein S, another anticoagulant protein that helps to prevent blood clots.
6. Antithrombin III deficiency: a lack of antithrombin III, a protein that prevents the formation of blood clots.
7. Fibrinogen deficiency: a lack of fibrinogen, a protein that is essential for blood clotting.
8. Dysproteinemia: an abnormal amount or type of proteins in the blood, which can lead to various symptoms and complications.

Symptoms of blood protein disorders can vary depending on the specific condition and the severity of the deficiency. Common symptoms include easy bruising or bleeding, frequent nosebleeds, prolonged bleeding after injuries or surgery, and joint pain or swelling.

Treatment for blood protein disorders typically involves replacing the missing protein or managing symptoms with medication or lifestyle changes. In some cases, gene therapy may be an option to correct the underlying genetic defect.

It's important for individuals with blood protein disorders to work closely with their healthcare provider to manage their condition and prevent complications such as joint damage, infections, and bleeding episodes.

Examples of acute diseases include:

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

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

This definition of 'Angioedemas, Hereditary' in the medical field is from the Medical Dictionary for the Health Professions and Nursing, provided by the Fortune Company.

Furthermore, BacMam viruses are inactivated by human complement, which reduces risk to researchers. Lastly, viruses used in the ... Baculoviruses are Risk Group 1 agents that have been widely used for over 25 years for insect cell protein production ... "Baculovirus-mediated gene transfer in the presence of human serum or blood facilitated by inhibition of the complement system ...
... immunosuppressive agents MeSH D27.505.696.477.656.500 - complement inactivating agents MeSH D27.505.696.477.656.750 - ... antiviral agents MeSH D27.505.954.122.388.077 - anti-retroviral agents MeSH D27.505.954.122.388.077.088 - anti-hiv agents MeSH ... tocolytic agents MeSH D27.505.954.016 - anti-allergic agents MeSH D27.505.954.122 - anti-infective agents MeSH D27.505.954.122. ... tranquilizing agents MeSH D27.505.696.277.950.015 - anti-anxiety agents MeSH D27.505.696.277.950.025 - antimanic agents MeSH ...
Very Heavy on 28 March 1944 Inactivated on 1 April 1944 Activated on 1 April 1944 Inactivated on 27 December 1945. Redesignated ... These facilities complement the area's cooperative weather, sparsely populated terrain and uncongested airspace. Pilots fly ... The 425th Air Base Squadron provides mission and administrative agent support to US personnel assigned to NATO HQ Allied Land ... Inactivated on 1 April 1944 with the end of heavy bomber training. Reactivated the same day at Smoky Hill Army Airfield, Kansas ...
Importantly, RNA integrity is maintained by inactivating RNases with chaotropic agents such as guanidinium isothiocyanate, ... mRNA is selectively reverse transcribed using oligo-dT primers that are the reverse complement of the poly-adenylated tail on ...
Combining ABT-737 with second agents that inactivate Mcl-1 may reduce this effect. ABT-737 has demonstrated single-agent ... and natural killer cells to destroy the targeted cells Complement-dependent cytotoxicity (CDC)-- Initiates the complement ... Cell death does not appear to be mediated by complement, but modest antibody-dependent cellular cytotoxicity and direct killing ... Reduced susceptibility to apoptosis increases the resistance of cancer cells to radiation and cytotoxic agents. B-cell lymphoma ...
Studies began to look for the possible species that acted as reservoirs for the virus and the agents responsible for ... The vaccine for KFDV consists of formalin-inactivated KFDV. The vaccine has a 62.4% effectiveness rate for individuals who ... Other methods of diagnosis included hemagglutination inhibition (HI), complement fixation, neutralization tests. However, new ...
First, the catalog of infectious agents has grown to the point that virtually all of the significant infectious agents of the ... This process requires immune mechanisms to kill or inactivate the inoculum of the pathogen. Specific acquired immunity against ... such as antibody-initiated complement-dependent bacteriolysis, opsonoization, phagocytosis and killing, as occurs for some ... Second, an infectious agent must grow within the human body to cause disease; essentially it must amplify its own nucleic acids ...
"Janssen's Single-Agent Darzalex (daratumumab) Approved by European Commission for Treatment of Multiple Myeloma (MM)". 23 May ... Daratumumab binds to CD38, causing cells to apoptose via antibody-dependent cellular cytotoxicity, complement-dependent ... DTT also inactivates/destroys many antigens on the red blood cell surface by disrupting disulfide bonds. The only antigen ... Updated trial results presented in December 2012, indicate daratumumab is continuing to show promising single-agent anti- ...
Hence, the classic inflammatory response was viewed as fully regulated by the soluble signaling agents. That is, the agents ... complement components C5a and C3a which are chemotactic factors formed during the activation of the host's blood complement ... However, studies suggest that synthetic SPM that are resistant to being metabolically inactivated hold promise of being ... While initially found to have in vitro activity suggesting that they might act as pro-inflammatory agents, Serhan and ...
Adenylate cyclese toxin binds to target cells by the complement receptor 3 (CD11b/CD18, or Mac-1). Target cell are therefore ... Together with the pertussis toxin it is the most important virulence factor of the causative agent of whooping cough, ... Besides attachment to bacterial proteins, aggregation also inactivates the toxin. This quick inactivation highlights the ...
Tissue plasminogen activator (t-PA) and urokinase are the agents that convert plasminogen to the active plasmin, thus allowing ... Plasmin, in addition to lysing fibrin clots, also cleaves the complement system component C3, and fibrin degradation products ... α2-Antiplasmin and α2-macroglobulin inactivate plasmin. Plasmin activity is also reduced by thrombin-activatable fibrinolysis ... Thrombolysis refers to the dissolution of the thrombus due to various agents while fibrinolysis refers specifically to the ...
... s have the ability to metabolize, detoxify, and inactivate exogenous compounds such as drugs (see drug metabolism), ... in which calcium is removed to disrupt cell-cell tight junctions by the use of a calcium chelating agent. Next, a solution ... complement, and glycoproteins. Hepatocytes manufacture their own structural proteins and intracellular enzymes. Synthesis of ... "Wheat extracts as an efficient cryoprotective agent for primary cultures of rat hepatocytes". Biotechnology and Bioengineering ...
Li W, Qin L, Feng R, Hu G, Sun H, He Y, Zhang R (July 2019). "Emerging senolytic agents derived from natural products". ... Additionally, several types of ubiquitination events parallel and complement the galectin-driven processes: Ubiquitination of ... of the autophagy systems listed above and further inactivates mTORC1, allows for strong autophagy induction and autophagic ... mTOR is inhibited when lysosomal membrane is damaged by various exogenous or endogenous agents, such as invading bacteria, ...
becoming the first approved oncolytic agent in the western world. It is based on herpes simplex virus (HSV-1). It has also been ... Although it poses a hurdle by inactivating viruses, the patient's immune system can also act as an ally against tumors; ... Magge D, Guo ZS, O'Malley ME, Francis L, Ravindranathan R, Bartlett DL (June 2013). "Inhibitors of C5 complement enhance ... Directed evolution was applied on human adenovirus, one of many viruses that are being developed as oncolytic agents, to create ...
Its causative agent is lymphocytic choriomeningitis mammarenavirus (LCMV), a member of the family Arenaviridae. The name was ... However, some authors note that such complement-fixation tests are insensitive and should not be used for diagnosis. Dr. Clare ... In addition, LCMV can also be inactivated by heat, ultraviolet light or gamma irradiation. Studies have indicated that human ... Such agents had been developed in the animal care facility, which periodically screened sentinel animals for extraneous ...
The human genome already contains remnants of retroviral genomes that have been inactivated and harnessed for self-gain. Indeed ... This prevents infection by effectively destroying the foreign DNA introduced by an infectious agent (such as a bacteriophage). ... and excision repair cross complementing 1(ERCC) appear to mimic the action of RM-systems in bacteria, and the non-homologous ... gene transfer agents or generalized transduction in order to move between genomes.[citation needed] Methylation Restriction ...
Next, we try to determine if we can block protein function by treating AB9 with pharmacological agents. The inhibitor in this ... heat inactivated FBS and antibiotics-antimycotics. The cells were then placed poly-L-lysine coverglass and allowing it to grow ... "The zebrafish fibroblast cell line AB9 as a tool to complement gene regulation studies". Musculoskeletal Regeneration. 1. ... "The zebrafish fibroblast cell line AB9 as a tool to complement gene regulation studies". Musculoskeletal Regeneration. 1. ( ...
These agents increase the level of aminopeptidase P, an enzyme that inactivates kinins; kinins (especially bradykinin) are ... All forms of HAE lead to abnormal activation of the complement system, and all forms can cause swelling elsewhere in the body, ... In this analysis, it is usually a reduced complement factor C4, rather than the C1-INH deficiency itself, that is detected. The ... The version related to histamine is due to an allergic reaction to agents such as insect bites, foods, or medications. The ...
... as the electrophilic properties of glutathione allow it to react with cytotoxic agents, inactivating them. In some cases, ... The cisplatin-resistant cells upregulate expression of the excision repair cross-complementing (ERCC1) gene and protein. Some ... In colorectal cancer cells, inhibition of NF-κB or MDR1 caused increased apoptosis in response to a chemotherapeutic agent. ... 2004-07-15). "Oncogenic H-Ras Up-Regulates Expression of ERCC1 to Protect Cells from Platinum-Based Anticancer Agents". Cancer ...
As LF is the agent responsible for the death of infected hosts, it is classified in the group of lethal toxins. Diphtheria ... The diphtheria vaccine contains a diphtheria toxoid, antigenically identical yet inactivated and non-toxic. When the toxoid is ... complement and neutrophils. These secreted virulence factors assist the bacterium in surviving immune response mechanisms. ... Mycotoxins can also play a role in chemical warfare agents, CWA, which are chemicals that contain toxins that are used to cause ...
The squadrons flew agents and supplies into southern France with B-24 Liberators that had all armament removed except in the ... When assigned to Harrington, the 801st Bombardment Group (Provisional) was inactivated in a name-only manner. Headquarters and ... HHS 39th Service Group 18th Weather Squadron 35th Station Complement Squadron Regular Army Station Units included: Headquarters ... However, the Japanese surrender canceled those plans and the Group was inactivated in October. After the war, Harrington ...
A causative agent may not be isolated in about half of cases despite careful testing. In an active population-based ... In the lower airways, reflexes of the glottis, actions of complement proteins and immunoglobulins are important for protection ... attempt to inactivate the bacteria. The neutrophils also release cytokines, causing a general activation of the immune system. ... The causative agent is determined in only 15% of cases with routine microbiological tests. Pneumonitis refers to lung ...
Note below that PARP is inactivated by caspase-3 cleavage during programmed cell death. PARP enzymes are essential in a number ... DNA damage theory of aging Maximum life span PARP1 PARP inhibitor class of anti-cancer agents Parthanatos Senescence Herceg Z, ... and scaffolding proteins such as X-ray cross-complementing gene 1 (XRCC1). After repairing, the PAR chains are degraded via ... Cleavage of PARP, by enzymes such as caspases or cathepsins, typically inactivates PARP. The size of the cleavage fragments can ...
intercalating agent Any chemical compound (e.g. acridine dyes) that disrupts the alignment and pairing of bases in the ... genome The entire complement of genetic material contained within the chromosomes of an organism, organelle, or virus. The term ... back mutation A mutation that reverses the effect of a previous mutation which had inactivated a gene, thus restoring wild-type ... genotype The entire complement of alleles present in a particular individual's genome, which gives rise to the individual's ...
intercalating agent Any chemical compound (e.g. acridine dyes) that disrupts the alignment and pairing of bases in the ... genome The entire complement of genetic material contained within the chromosomes of an organism, organelle, or virus. The term ... back mutation A mutation that reverses the effect of a previous mutation which had inactivated a gene, thus restoring wild-type ... genotype The entire complement of alleles present in a particular individual's genome, which gives rise to the individual's ...
... A71 (EV-A71) is notable as one of the major causative agents for hand, foot and mouth disease (HFMD), and is ... There are two types of vaccines available to prevent polio: inactivated poliovirus vaccine given as an injection in the leg ( ... complement proteins, and proapoptotis proteins have been implicated. There are three serotypes of poliovirus, PV-1, PV-2, and ...
Rather than introducing an inactivated or attenuated micro-organism to an immune system (which would constitute a "whole-agent ... Meri S, Jördens M, Jarva H (December 2008). "Microbial complement inhibitors as vaccines". Vaccine. 26 Suppl 8: I113-117. doi: ... The agent stimulates the body's immune system to recognize the agent as a threat, destroy it, and to further recognize and ... Formaldehyde is used to inactivate bacterial products for toxoid vaccines. Formaldehyde is also used to inactivate unwanted ...
The M-protein aids in immune evasion by inhibiting phagocytosis and inactivating the complement system. Furthermore, ... Second-line agents include macrolides and clindamycin, although increasing resistance, due to both efflux and target ... Antimicrobial Agents and Chemotherapy. 19 (5): 716-725. doi:10.1128/aac.19.5.716. ISSN 0066-4804. PMC 181512. PMID 7027921. ...
Agents Chemother. 49 (1): 269-75. doi:10.1128/AAC.49.1.269-275.2005. PMC 538877. PMID 15616305. Vordenbäumen, S; Sander, O; ... The mechanism(s) by which microorganisms are killed and/or inactivated by defensins is not understood completely. However, it ... Moreover, human alpha-defensins can enhance or suppress the activation of the classical pathway of complement in vitro by ... suppress anti-inflammatory mediators and regulate complement activation argues that defensins upregulate innate host ...
... groups on each monomeric enzyme molecule that react equally fast with the modifying agent, and n e s s e n t i a l {\ ... but it complements Tsou's approach in useful ways. Suppose that an enzyme has two groups G 1 {\displaystyle \mathrm {G_{1}} } ... is inactivated in a first-order reaction with a different rate constant k 2 {\displaystyle k_{2}} , then the remaining activity ... for which modification of just one essential group by diethyl pyrocarbonate was sufficient to inactivate the enzyme. A little ...
... inactivating key immune components such as complement, and hiding in the extracellular matrix, which may interfere with the ... After the identification of B. burgdorferi as the causative agent of Lyme disease, antibiotics were selected for testing, ... The resistance of a genospecies of Lyme disease spirochetes to the bacteriolytic activities of the alternative complement ... Masuzawa T (December 2004). "Terrestrial distribution of the Lyme borreliosis agent Borrelia burgdorferi sensu lato in East ...
As of 2021[update], no vaccines against hantaviruses have been approved by the U.S. FDA, but whole virus inactivated bivalent ... Integrins are considered to be the main receptors for hantaviruses in vitro, but complement decay-accelerating factor (DAF) and ... Agents of HPS found in South America include the Andes virus (also called Oran, Castelo de Sonhos - Portuguese for "Castle of ... globular heads of complement C1q receptor (gC1qR) have mediated attachment in cultured cells too. Entry may proceed through a ...
The 28th Cavalry was inactivated at Assi-Okba, Algeria, in April 1944 in North Africa, and marked the end of the regiment. ... Due in part to the heightened hysteria caused by World War I, allegations surfaced that German agents fomented this violence ... reducing the black complement to two regiments (the 24th and 25th (Colored) Infantry). The 38th and 41st were reorganized as ... could not substantiate accusations of militant German agents in the Mexican border community and instead traced the origins of ...
When the Scorpion extension binds to its complement on the amplicon, the Scorpion structure opens, prevents FRET, and enables ... Next, place the PCR tube into a thermal cycler for one cycle wherein annealing, extending, and inactivating of reverse ... as simple as quantification of yeast cells in wine to more complex uses as diagnostic tools for detecting infectious agents ... The second cycle is the initial denaturation wherein reverse transcriptase is inactivated. The remaining 40-50 cycles are the ...
These neurons become highly sensitized to convulsant agents. It has been shown that seizures early in life can predispose one ... The increased calcium concentration (and subsequent depolarization of the membrane) inactivates sodium channels and targets ... Intrinsic plasticity contributes to encoding memory and complements other forms of activity-dependent plasticity including ...
Medications commonly associated with rebound hypertension include centrally-acting antihypertensive agents, such as clonidine ... Licht C, Fremeaux-Bacchi V (February 2009). "Hereditary and acquired complement dysregulation in membranoproliferative ... an enzyme that normally inactivates circulating cortisol to the less-active metabolite cortisone. At high concentrations ...
Nutritional yeast is another good source of complete protein, and can also be added to complement the amino acid profile. ... In raw plant ingredients, enzyme attachment sites are more readily available when heat and pressure is used to inactivate ... artificial fibers from edible vegetable protein are formed into bundles using an edible form of binding agent. This is then ... High heat has the effect of denaturing proteins as well as inactivating anti-nutritional factors that decrease digestive ...
Embryonic stem cells have constitutive cyclin E-CDK2 activity, which hyperphosphorylates and inactivates Rb. This leads to a ... Biochemical cascades include: The Complement system The Insulin Signaling Pathway The Sonic hedgehog Signaling Pathway The Wnt ... cascades in lymphocytes is the secretion of molecules that can suppress altered cells or eliminate pathogenic agents, through ... complement, coagulation and fibrinolytic systems and iron homeostasis Regulate iron homeostasis (acute phase independent) Via ...
This plan for 2012-2014 introduced an institutional "life course" approach to vaccination to complement the Italian health ... "Intradermal fractional dose inactivated polio vaccine: A review of the literature". Vaccine. 30 (2): 121-125. doi:10.1016/j. ... requiring individuals to accept the injection of medicine or medicinal agent into their bodies, and it has provoked a spirited ... it must adhere to the Occupational Safety and Health Act involving Biological Agents. Criteria for the recommendation include ...
When the Spanish arrived in South America, the conquistadors at first banned coca as an "evil agent of devil". But after ... It is created by combining norcocaine with inactivated cholera toxin. Indigenous peoples of South America have chewed the ... as the converse effects of the drugs actually complement each other, but may also mask the symptoms of an overdose. It has been ... Topical cocaine is sometimes used as a local numbing agent and vasoconstrictor to help control pain and bleeding with surgery ...
As part of the military drawdown in the 1990s, the Air Force inactivated the 33d Fighter Wing's 59th Fighter Squadron on 15 ... For ten years, 1961 to 1971, 222,530 liters of herbicides (Agents Purple, Orange, White and Blue) were sprayed at a test grid ... This brought the Squadron's strength to 17 officers and 114 airmen (out of the 550th's total complement of 201 officers and 816 ... Returning to Eglin on 12 May 1958, the unit was inactivated 25 June 1958. In 2011, the 37th Bomb Squadron operates B-1B Lancers ...
The WHO states bringing water to rolling boil then naturally cooling is sufficient to inactivate pathogenic bacteria, viruses ... Untreated water may contain potentially pathogenic agents, including protozoa, bacteria, viruses, and some larvae of higher- ... but rather as secondary means to complement another purification technique. It is most commonly implemented for pre- or post- ... Inactivation of microbial agents by chemical disinfectants. Cincinnati: US Environmental Protection Agency; 1986. EPA/600/2-86/ ...
On at least one occasion Boehm and another SEAL smuggled a CIA agent ashore to take pictures of Soviet nuclear missiles being ... rapid demobilization at the conclusion of the war reduced the number of active duty UDTs to two on each coast with a complement ... operationally to JSOC Red Squadron Blue Squadron Gold Squadron Silver Squadron Black Squadron Grey Squadron Inactivated Groups ... The OSS MU mission was "to infiltrate agents and supply resistance groups by sea, conduct maritime sabotage, and develop ...
Then, they appoint qualified agents to handle tenders. These agents are prohibited from having ties with the industry ... This is the first combined inactivated Hepatitis A&B vaccine developed by Chinese scientists, and the vaccine has only one ... Direct marketing to doctors (detailing), which is the basic marketing activity in developed countries, complemented by ... the pharmacy enterprise search for its national or regional general agent and use the agent's market network to sell its ...
Reducing agents are not used with steel casting, because they can carburize the metal during casting. Up to 3% of "cushioning ... At the temperatures that copper and iron are poured, the clay is inactivated by the heat, in that the montmorillonite is ... Besides replacing older methods, additive can also complement them in hybrid models, such as making a variety of AM-printed ... In addition to the sand, a suitable bonding agent (usually clay) is mixed or occurs with the sand. The mixture is moistened, ...
Fibroblasts with inactivated Lig3 gene can be propagated in the media supplemented with uridine and pyruvate. However, these ... "Robust chromosomal DNA repair via alternative end-joining in the absence of X-ray repair cross-complementing protein 1 (XRCC1 ... that the cells lacking nuclear DNA ligase III-alpha did not exhibit significantly increased sensitivity to DNA damaging agent. ... in the DNA ligase I gene of an individual with immunodeficiencies and cellular hypersensitivity to DNA-damaging agents". Cell. ...
Interestingly, some antiviral agents licensed for human use, initially thought to act only as inhibitors of viral replication, ... inactivated whole virus > several expressed proteins > one expressed protein > multiple synthetic peptide antigens > single ... "Dynamics of mutation and recombination in a replicating population of complementing, defective viral genomes". Journal of ... Evolution of viruses in nature and as disease agents can be viewed as succession of mutant spectrum alterations, subjected to ...
... is an alkylating agent and has preference for A->T base transversions and also for AT->GC transitions. However it is also ... Thus if an organism has one functional copy of the gene, then this functional copy is capable of complementing the mutated or ... Generally speaking, ENU is fairly unstable, which makes it easier to inactivate when used as an experimental mutagen, compared ... The chemical is an alkylating agent, and acts by transferring the ethyl group of ENU to nucleobases (usually thymine) in ...
Air Troop inactivated 20 March 1972 in Vietnam; 2d Squadron inactivated 6 April 1972 in Vietnam; Air Troop and 2d Squadron ... They also ensure that all chemical agent monitors and navigational satellite systems are maintained. The Service and Recovery ... arrived in December of the same year with a complement of UH-1C Gunships and UH-1D Command and Control "slicks". Early in ... During the drawdown of U.S. forces in Vietnam in early 1972, the 11th ACR was inactivated in stages (Air Troop inactivated 20 ...
Evid Based Complement Alternat Med. 2008; 5(1): 61-69.). Bromelain is an effective cardioprotective agent. It possesses ... In many types of cancer p53 gene, which induces apoptosis, is inactivated thus apoptotic cell death is evaded in such cancerous ... Anti-inflammatory agent. Inflammation is the bodys attempt of self-protection which takes into account the discharge of ... Anti-Inflammatory agent. Disorders. Observed effects. References. Asthma Change CD4+ to CD8+ T lymphocyte ratio and decreases ...
Complement Inactivating Agents Entry term(s):. Agents, Complement Inactivating. Agents, Complement Inhibiting. Complement ... Complement Inhibiting Agents. Complement Inhibitor. Complement Inhibitors. Inactivating Agents, Complement. Inhibiting Agents, ... Complement C1 Inactivating Proteins. Complement C1 Inhibiting Proteins. Complement C1 Inhibitor Proteins. Complement C1r ... Complement 3b Inactivators. Complement 3b Inhibitors. Complement C3b Inactivators. Complement C3b Inhibitor Proteins. ...
... so it is urgent to develop effective antiviral agents to complement vaccine therapy. In the present study, we investigated the ... In in vitro assays, HJ could directly inactivate PEDV strains; moreover, it inhibited the proliferation of PEDV strains in Vero ...
Complement Deficiencies. Patients with complement deficiencies can receive any live or inactivated vaccine. ... Numerous agents often are given in combination with other agents (especially chemotherapy) and are immunosuppressive when given ... Administer inactivated influenza vaccine beginning ≥6 months after HSCT and annually thereafter. A dose of inactivated ... Biologic Agents. Immunosuppressive or immunomodulatory biologic agents can produce immunocompromise by the mechanisms outlined ...
Mixtures of inactivated unidluted sera an tenfold dilutions of Sedlec virus were incuabted for 90 min. at 37dC and innoculated ... COMPLEMENT-FIXATION. No positive reaction between Sedlec antigen and the following mouse immune ascitic fluids or hyperimmune ... Select Agent. No SALS Level. SALS Basis. Other Information. Antigenic Group. Not listed. ...
Lin JT, Zhang JS, Su N, Xu JG, Wang N, Chen JT, Safety and immunogenicity from a phase I trial of inactivated severe acute ... As supplementary agents, the peptidic fusion inhibitors may be developed as MERS prophylactics and therapeutics. ... To complement active immunization approaches, researchers are also advancing several prophylactic or therapeutic approaches ... Bolles M, Deming D, Long K, Agnihothram S, Whitmore A, Ferris M, A double-inactivated severe acute respiratory syndrome ...
Vaccines, Inactivated, Viral. Class Summary. These agents are used to induce active immunity. ... J Altern Complement Med. 1999 Dec. 5(6):553-65. [QxMD MEDLINE Link]. ... These agents modify the bodys immune response to diverse stimuli. Some authors find benefit in the short-term use of steroids ... These agents stabilize the neuronal membrane so the neuron is less permeable to ions. This prevents the initiation and ...
Complement factor deficiencies are absent, only zinc need routinely be given in alternating fashion. Congenital asplenia is ... To prevent rheumatic fever develops, interventions to improve response rates with lipid envelopes are inactivated however, ... If patients ingest the agent, patients with a daily basis by appropriate laboratory studies are indicated in patients who are ...
... or inactivated vaccine. Other persons should receive the inactivated vaccine. ... Medical indications: adults with anatomic or functional asplenia, or terminal complement component deficiencies. Other ... chemotherapy with alkylating agents, antimetabolites, or high-dose, long-term corticosteroids; and cochlear implants. Other ... or chemotherapy with alkylating agents, antimetabolites, or high-dose, long-term corticosteroids. For persons aged ,65 years, ...
Killed or Inactivated Vaccines. USE OF IMMUNE GLOBULINS. REFERENCES. POINT OF CONTACT FOR THIS DOCUMENT:. SUGGESTED CITATION. ... Immunosuppressive agents should not be administered during postexposure therapy, unless essential for the treatment of other ... Many of these patients have leukopenia, decreased complement activity, chemotactic defects, and impaired cell-mediated immunity ... Killed or Inactivated Vaccines. Diphtheria-Tetanus-Pertussis (DTP/DTaP/DT/Td). For children who are severely immunocompromised ...
... complement, vasomotor regulatory molecules, hemostatic factors, and other agents. Secretory antibodies are typically multimeric ... In addition, disruption of endothelial and alveolar epithelial integrity may allow surfactant to be inactivated by ... 8, 16, 17] Other agents to consider include H influenzae type B (HiB) (very uncommon in immunized children [18] ), S pyogenes, ... Agents of chronic congenital infection, such as CMV, Treponema pallidum (the cause of pneumonia alba), Toxoplasma gondii, and ...
Complement Ther Clin Pract 2019;35:323-8. View abstract.. *Moon SW, Shin YU, Cho H, Bae SH, Kim HK; and for the Mogen Study ... Shivashankara, A. R., Azmidah, A., Haniadka, R., Rai, M. P., Arora, R., and Baliga, M. S. Dietary agents in the prevention of ... Agarwal, C., Tyagi, A., and Agarwal, R. Gallic acid causes inactivating phosphorylation of cdc25A/cdc25C-cdc2 via ATM-Chk2 ... J Altern Complement Med 2004;10:431-7. View abstract.. *Greenblatt DJ, von Moltke LL, Perloff ES, et al. Interaction of ...
... in persons with certain complement deficiencies and those receiving treatment that inhibits terminal complement activation (eg ... Immunosuppressants (eg, irradiation, antimetabolites, alkylating agents, cytotoxic drugs, high-dose steroids) may reduce the ... inactivated polio types 1, 2, and 3; hepatitis B; Haemophilus influenzae type b antigens; pentavalent rotavirus; 7-valent ... Complement deficiency, eculizumab recipients; increased risk of invasive meningococcal disease despite vaccination with Menveo ... Treatment: Anticoagulant agents, Fibrinolytic agents, Antiplatelet agents. 4.5. Myeloid Leukemias, Myelodysplasia, ... presence of ANA (not specific), antibodies to dsDNA, ssDNA, Sm, Ro, LA, histone, Complement levels (C3, C4, CH50), serum ... Prevention: After exposure ( immune globulin 0.02mL/kg IM within 2 weeks) Before exposure (inactivated HAV vaccine ... for Type 2 DM, maged with diet and exercise alone or in conjunction with oral glucose-loweing agents, insulin or oral agents + ...
Heating serum to 52˚C for 10 min inactivated complement before use in experiments. ... RPTEC were cultured in dMCM in the presence of TGF-β1-blocking and BIGH3-blocking agents (Figure 7(A)). A pharmacological ... and the antibiotic and anti-fungal agents (gentamicin sulfate and amphotericin B) were purchased from Clonetics/Lonza ( ...
Complement fixation Samples. Isolation and identification of the agent *Living animals: blood in heparin ... Inactivated by iodophores and phenolic compounds. Survival: Very stable in the presence of protein (e.g. has survived for years ... Identification of the agent *Plaque reduction serum neutralisation (for serotyping - many cross-reactions) ...
The risk appears to be related to the intensity and duration of immunosuppression rather than to the use of any specific agent ... Inactivated vaccines noted to be safe for administration after transplantation may not be sufficiently immunogenic during ... Whenever possible, administer the complete complement of vaccines before transplantation and treatment with PROGRAF. The use of ... Calcium-channel blocking agents may increase tacrolimus blood concentrations and require dosage reduction of ASTAGRAF XL. ...
... heat inactivated preparations, and complement-depleted preparations. ... Plant tissue culture reagents, including gelling agents, plant growth regulators, auxins, cytokinins, and other supplements for ...
The risk appears to be related to the intensity and duration of immunosuppression rather than to the use of any specific agent ... Inactivated vaccines noted to be safe for administration after transplantation may not be sufficiently immunogenic during ... Whenever possible, administer the complete complement of vaccines before transplantation and treatment with PROGRAF. The use of ... Calcium-channel blocking agents may increase tacrolimus blood concentrations and require dosage reduction of ASTAGRAF XL. ...
The T-antigen partners with two growth silencer proteins, p53 and the retinoblastoma protein pRb, and inactivates them. ... many hare counter acting agent CDRs have a place with no recently known canonic designs, causing demonstrated erroneously. ... ABBEXA Human Complement C4 Protein. *MARKET SCK6 Bacillus subtilis Strains. *Mouse Anti-Canine Distemper Virus Surface Envelope ... Acculturated antibodies or counter acting agent adaptation are intended to lessen immunogenicity reaction while keeping up with ...
Causative agent of tetanus*Gram positive*obligate anaerobe with prominent terminal spore (drumstick appearance)*Vegetative cell ... Complement initiates phagocytosis*Phagolysosome fusion is inhibited*Cells replicate and lyse cell ... inactivated vaccine available for at risk populations * Spirochetes *Thin, helical, gram negitive bacteria*Order: ... Etiological agent of Rocky Mountain Spotted Fever*500-1000 casesannually in U.S.*First described in Idaho and Montana*Primarily ...
... economically and environmentally sustainable alternative to treatments that often involve the adoption of pharmaceutical agents ... Complement. Med. 2003, 9, 251-256. [Google Scholar] [CrossRef]. *Bocci, V.; Di Paolo, N. Oxygen-ozone therapy in medicine: An ... Hoagland, D.T.; Liu, J.; Lee, R.B.; Lee, R.E. New agents for the treatment of drug-resistant Mycobacterium tuberculosis. Adv. ... Low environmental impact approaches to inactivate microorganisms in fish farming plants. Mar. Drugs 2009, 7, 268-313. [Google ...
These agents embody: Such an acidosis will inevitably end in a Fresh frozen plasma worsening coagulopathy and in the end an ... The medical content of preconception care: an overview and preparation of this complement. Oxygen should not be given in Assess ... Inactivated vaccines are composed of micro-organisms which have been killed with chemicals and/or heat and are not infectious. ... An agent could also be assigned to this cat- egory if it clearly belongs, based mostly on mechanistic considerations, to a ...
They confirmed the presence of mumps virus strains by the complement fixation test with a specific antiserum. They also tested ... Infection with live (but not inactivated) mumps and rubella viruses, and coxsackievirus B4 has been found to lead to increased ... Koch J, Leer C, McCarthy R, Carter A, Cuff W. Adverse events temporally associated with immunizing agents-1987 report/ ... Oldstone MBA, Ahmed R, Salvato M. Viruses as therapeutic agents II. Viral reassortants map prevention of insulin-dependent ...
As such, it shows great promise to complement and potentially replace SRID in a pandemic when strain-specific reagents may not ... Cryptosporidium felis is the major etiologic agent of cryptosporidiosis in felines and has been reported in numerous human ... Hemagglutinin (HA), as the main antigen in inactivated influenza vaccines (IIVs), elicits functional neutralizing antibodies ... Thus, LTD-IDMS is a promising alternative in vitro potency assay for influenza vaccines to complement and potentially replace ...
The total cellular complements of adipocyte GLUT1 and GLUT4 were determined by Western blotting. Metformin had no effect on ... Combination therapy with these agents is an increasingly popular approach because multiple defects are often present in ... responsible for increased insulin-stimulated phosphorylation of Akt is uncertain but may involve control of an inactivating ... on maximal doses of any sulfonylurea agents were recruited. Except for diabetes, the subjects were healthy and on no other ...
Complement C5a receptor 1 exacerbates the pathophysiology of N. meningitidis sepsis and is a potential target for disease ... The metacestode larval stage of the fox tapeworm Echinococcus multilocularis is the causative agent of alveolar echinococcosis ... Conclusions/Significance We conclude that BI 2536 effectively inactivates E. multilocularis germinative cells in parasite ... The complement system is generally accepted as the most important innate immune determinant against invasive meningococcal ...
  • PNH results from expansion of a clone of hematopoietic cells that, as a consequence of an inactivating mutation of the X-linked gene PIG-A, are deficient in glycosylphosphatidylinositol (GPI)-linked proteins: since these include the surface membrane complement-regulatory proteins CD55 and CD59, the red cells arising from this clone are exquisitely sensitive to lysis by activated complement. (
  • Certain proteins in the blood potential points of entry and inside (such as proteins of the complement the body (see figure). (
  • The T-antigen partners with two growth silencer proteins, p53 and the retinoblastoma protein pRb, and inactivates them. (
  • The complement inhibitor eculizumab has dramatically improved the outcome of atypical hemolytic uremic syndrome. (
  • Killed or inactivated vaccines do not represent a danger to immunocompromised persons and generally should be administered as recommended for healthy persons. (
  • Renal recovery under eculizumab was equally good in patients with and those without complement gene variants detected. (
  • Since 2007, PNH has received renewed and much wider attention because a new form of treatment has become available, namely complement blockade through the anti-C5 monoclonal antibody eculizumab . (
  • Although treatment with antiviral agents has proven a very effective way to improve the health and survival of infected individuals, as we discuss here, the epidemic will continue to grow unless greatly improved prevention strategies can be developed and implemented. (
  • Whereas there were once no effective therapies for herpes zoster (shingles), the advent of oral antiviral agents has made the treatment of this condition possible. (
  • Antiviral agents exert a direct antiviral effect on varicella-zoster virus (VZV). (
  • Meanwhile, microscale thermophoresis (MST) indicated that compound 4l have strong binding capability to tobacco mosaic virus coat protein (TMV-CP) with dissociation constant (Kd) values of 0.34 μmol/L, which was better than ningnamycin (0.52 μmol/L). These results suggest that novel myricetin derivatives bearing ferulic acid amide scaffolds may be considered as an activator for antiviral agents. (
  • 13. Gedunin inactivates the co-chaperone p23 protein causing cancer cell death by apoptosis. (
  • Oxytocin may specifically inactivate SARS-COV-2 spike protein and block viral entry into cells via angiotensin-converting enzyme 2 by suppressing serine protease and increasing interferon levels and number of T-lymphocytes. (
  • Human serum is used to culture human cells and is available as plasma-derived AB human serum, clotted whole blood AB human serum, heat inactivated preparations, and complement-depleted preparations. (
  • Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION . (
  • Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. (
  • Antibodies, gamma globulin, agglutinins, complement, neutralizers] And the internal body defenses, the antibodies and other materials found in the body fluids and tissues. (
  • Within days or and inactivate them in an intense for example, by lymphocytes of the weeks, the adaptive immune system chemical shower of reactive oxygen adaptive immune systems, and they manufactures antibodies tailored species cal ed the respiratory burst. (
  • Acculturated antibodies or counter acting agent adaptation are intended to lessen immunogenicity reaction while keeping up with high explicitness. (
  • Utilizing our restrictive innovations (broad immunizer information base, bioinformatics programming, extraordinary counter acting agent humanness score guidelines) and for quick creation of cell lines communicating full length recombinant antibodies, arrangements of the neutralizer variable spaces which decide its limiting explicitness are integrated into human contributor groupings, making a board of full length adapted antibodies for articulation. (
  • While chemicals are not disease-producing agents, they may cause injury to body tissues and increase susceptibility to infection. (
  • Coccus, virus, spirochete] The nurse must know that plant-like agents including bacteria, fungi, molds, and yeasts can cause disease, as well as those without distinctive plant or animal characteristics such as the viruses and rickettsiae. (
  • Severe immunosuppression can be due to a variety of conditions, including congenital immunodeficiency, human immunodeficiency virus (HIV) infection, leukemia, lymphoma, generalized malignancy or therapy with alkylating agents, antimetabolites, radiation, or large amounts of corticosteroids. (
  • Plant tissue culture reagents, including gelling agents, plant growth regulators, auxins, cytokinins, and other supplements for supporting the growth and development of plant cells and tissues in culture. (
  • The complement system, along with natural killer cells and dendritic cells, straddles both innate and adaptive immunity. (
  • agents involve two interrelated systems: body. (
  • In addition, oxytocin can promote parasympathetic outflow and the secretion of body fluids that could dilute and even inactivate SARS-CoV-2 on the surface of cornea, oral cavity and gastrointestinal tract. (
  • Mixtures of inactivated unidluted sera an tenfold dilutions of Sedlec virus were incuabted for 90 min. (
  • In particular, compound 4l possessed significant protection activity against tobacco mosaic virus (TMV), with an half maximal effective concentration (EC50) value of 196.11 μg/mL, which was better than commercial agent ningnamycin (447.92 μg/mL). (
  • Twenty-one patients (55%) carried novel or rare complement genes variants. (
  • If patients ingest the agent, patients with a daily basis by appropriate laboratory studies are indicated in patients who are too large will cause distended neck veins, rales, abnormal heart and leads to bone marrow failure. (
  • 1] Available chelation therapy agents include deferoxamine (parenterally administered) and deferiprone and deferasirox (both orally administered). (
  • It also assist digestion, enhance absorption of other drugs and is a potential postoperatively agent that promote wound healing and reduce postsurgical discomfort and swelling. (
  • She must also be familiar with the portals of entry and exit of an infective agent. (
  • The risk appears to be related to the intensity and duration of immunosuppression rather than to the use of any specific agent. (
  • She must know the various types of disease- producing agents. (
  • Not only must the nurse know that agents can cause disease, she must also be familiar with the methods by which disease is produced, whether by direct invasion of tissue, as in streptococcal infections, or through the liberation of toxin, as in diphtheria. (
  • These agents modify the body's immune response to diverse stimuli. (
  • Oak Biosciences have been conveyed counter acting agent acculturation administration beginning around 2008, and north of 300 effective undertakings have been finished. (
  • Furthermore, VHL deficiency conferred increased sensitivity to PARP inhibitors, analogous to the synthetic lethality observed between hypoxia and these agents. (
  • IVIG may work via several mechanisms, including the blockage of macrophage receptors, the inhibition of antibody production, the inhibition of complement binding, and the neutralization of pathologic antibodies. (
  • Severe immunosuppression can be due to a variety of conditions, including congenital immunodeficiency, human immunodeficiency virus (HIV) infection, leukemia, lymphoma, generalized malignancy or therapy with alkylating agents, antimetabolites, radiation, or large amounts of corticosteroids. (