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.Complement C9: 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 C6: 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.Complement C8: 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.Antigens, CD59: 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)Complement C7: 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.Complement C5b: 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 System Proteins: 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).Complement Activation: 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.Complement C5: 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.Complement Inactivator Proteins: 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.Complement C3: 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.Complement C4: 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.Antigens, CD55: 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.Complement Pathway, Alternative: 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.Complement Pathway, Classical: 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.Complement C5a: 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.Receptors, Complement: Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.Complement C3b: 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.Complement Factor I: 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.Complement C1q: 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.Receptor, Anaphylatoxin C5a: A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.Complement C3-C5 Convertases: 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.Complement C3a: 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.Complement Factor H: 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).Complement Hemolytic Activity Assay: 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.beta-Aminoethyl Isothiourea: A radiation-protective agent that can inhibit DNA damage by binding to the DNA. It also increases the susceptibility of blood cells to complement-mediated lysis.Avidin: A specific protein in egg albumin that interacts with BIOTIN to render it unavailable to mammals, thereby producing biotin deficiency.Micelles: Particles consisting of aggregates of molecules held loosely together by secondary bonds. The surface of micelles are usually comprised of amphiphatic compounds that are oriented in a way that minimizes the energy of interaction between the micelle and its environment. Liquids that contain large numbers of suspended micelles are referred to as EMULSIONS.HLA-B27 Antigen: A specific HLA-B surface antigen subtype. Members of this subtype contain alpha chains that are encoded by the HLA-B*27 allele family.HLA-B Antigens: Class I human histocompatibility (HLA) surface antigens encoded by more than 30 detectable alleles on locus B of the HLA complex, the most polymorphic of all the HLA specificities. Several of these antigens (e.g., HLA-B27, -B7, -B8) are strongly associated with predisposition to rheumatoid and other autoimmune disorders. Like other class I HLA determinants, they are involved in the cellular immune reactivity of cytolytic T lymphocytes.HIV-1: The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.HIV Infections: Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).HLA-B7 Antigen: A specific HLA-B surface antigen subtype. Members of this subtype contain alpha chains that are encoded by the HLA-B*07 allele family.HLA-B35 Antigen: A specific HLA-B surface antigen subtype. Members of this subtype contain alpha chains that are encoded by the HLA-B*35 allele family.HLA-B51 Antigen: A specific HLA-B surface antigen subtype. Members of this subtype contain alpha chains that are encoded by the HLA-B*51 allele family.Fraxinus: A plant genus of the family OLEACEAE. Members contain secoiridoid glucosides.AxisMicrobiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses.Teaching Materials: Instructional materials used in teaching.Pharmacology, Clinical: The branch of pharmacology that deals directly with the effectiveness and safety of drugs in humans.Competitive Behavior: The direct struggle between individuals for environmental necessities or for a common goal.Video Games: A form of interactive entertainment in which the player controls electronically generated images that appear on a video display screen. This includes video games played in the home on special machines or home computers, and those played in arcades.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Antigens, CD46: 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.Antibody Specificity: 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.Brain Chemistry: Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.Alzheimer Disease: A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)Electrowetting: Reducing the SURFACE TENSION at a liquid/solid interface by the application of an electric current across the interface thereby enhancing the WETTABILITY of the surface.Neurobiology: The study of the structure, growth, activities, and functions of NEURONS and the NERVOUS SYSTEM.Age Factors: Age as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or the effect of a circumstance. It is used with human or animal concepts but should be differentiated from AGING, a physiological process, and TIME FACTORS which refers only to the passage of time.Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.Models, Biological: Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.

Complement-mediated injury reversibly disrupts glomerular epithelial cell actin microfilaments and focal adhesions. (1/554)

BACKGROUND: Foot process effacement and condensation of the glomerular epithelial cell (GEC) cytoskeleton are manifestations of passive Heymann nephritis, a model of complement-mediated membranous nephropathy. METHODS: To study the effects of complement on the actin cytoskeleton in this model, we have used an in vitro system in which GECs are sublethally injured using a combination of complement-fixing anti-Fx1A IgG and human serum as a source of complement. We examined the effects of this injury on the organization of the cytoskeleton and focal contacts using immunohistology and immunochemistry. RESULTS: By immunofluorescence, sublethal complement-mediated injury was accompanied by a loss of actin stress fibers and focal contacts but retention of matrix-associated integrins. Full recovery was seen after 18 hours. Western blot analysis showed no change in the cellular content of the focal contact proteins. Inhibition of the calcium-dependent protease calpain did not prevent injury. In addition, cycloheximide during recovery did not inhibit the reassembly of stress fibers or focal contacts. Injury was associated with a reduction in tyrosine phosphorylation of paxillin and a currently unidentified 200 kDa protein, but inhibition of tyrosine phosphatase activity with sodium vanadate did not prevent injury. Cellular adenosine triphosphate content was significantly reduced in injured cells. CONCLUSION: These results document reversible, complement-dependent disruption of actin microfilaments and focal contacts leading to the dissociation of the cytoskeleton from matrix-attached integrins. This may explain the altered cell-matrix relationship accompanying podocyte effacement in membranous nephropathy.  (+info)

Complement activation and increased systemic and pulmonary vascular resistance indices during infusion of postoperatively drained untreated blood. (2/554)

In nine healthy young patients, operated on for thoracic scoliosis, a pulmonary artery catheter was inserted for the study of haemodynamic variables and blood sampling during autologous transfusion of postoperatively drained blood. At 1-3 h after wound closure, 10 ml kg/body weight of drained untreated blood from the wound was collected and recirculated over a l-h period. The concentration of the complement activation product, C3bc, increased from a mean of 5.4 (SD 1.5) AU ml-1 before infusion to 11.1 (3.9) AU ml-1 during infusion and then returned to 7.8 (2.8) AU ml-1 after infusion. The concentration of the terminal complement complex (TCC) increased from 0.5 (0.2) to 1.3 (0.5) AU ml-1 and was reduced to 0.7 (0.3) AU ml-1 after infusion. Only TCC exceeded the reference values which are 14 AU ml-1 for C3bc and 1.0 AU ml-1 for TCC. Pulmonary vascular resistance index concomitantly increased from a mean of 130 (SD 52) to 195 (88) dyn s cm-5 m-2 and was reduced to 170 (86) dyn s cm-5 m-2 after infusion. Systemic vascular resistance index increased from a mean of 1238 (SD 403) to 1349 (473) dyn s cm-5 m-2 and returned to 1196 (401) dyn s cm-5 m-2 after infusion. White blood cell count (WCC) increased from 14.4 (4.3) x 10(9) litre-1 before infusion to 17.8 (7.2) x 10(9) litre-1 during and after infusion. No change in platelet count during infusion was observed. There were no differences in WCC or platelet count between mixed venous or peripheral arterial blood. Pulmonary and systemic vascular resistance indices may be influenced by activated complement in drained untreated blood when it is recirculated.  (+info)

Synergistic enhancement of chemokine generation and lung injury by C5a or the membrane attack complex of complement. (3/554)

Complement plays an important role in many acute inflammatory responses. In the current studies it was demonstrated that, in the presence of either C5a or sublytic forms of the complement-derived membrane attack complex (MAC), rat alveolar macrophages costimulated with IgG immune complexes demonstrated synergistic production of C-X-C (macrophage inflammatory protein-2 and cytokine-induced neutrophil chemoattractant) and C-C (macrophage inflammatory protein-1alpha and monocyte chemoattractant-1) chemokines. In the absence of the costimulus, C5a or MAC did not induce chemokine generation. In in vivo studies, C5a and MAC alone caused limited or no intrapulmonary generation of chemokines, but in the presence of a costimulus (IgG immune complexes) C5a and MAC caused synergistic intrapulmonary generation of C-X-C and C-C chemokines but not of tumor necrosis factor alpha. Under these conditions increased neutrophil accumulation occurred, as did lung injury. These observations suggest that C5a and MAC function synergistically with a costimulus to enhance chemokine generation and the intensity of the lung inflammatory response.  (+info)

The terminal sequence of complement plays an essential role in antibody-mediated renal cell apoptosis. (4/554)

Mesangial cell (MC) injury is a characteristic feature in the early phase of Thy.1 nephritis. The present study investigates the contribution of complement to MC apoptosis in this experimental model of kidney disease in rats. Thy.1 nephritis was induced by injection of mouse anti-Thy.1 monoclonal antibody (ER4G). To assess the contribution of the terminal sequence of complement on apoptosis, the studies were performed in complement-sufficient PVG/c (PVG/c+) rats and in rats deficient in complement C6 (PVG/c-). Apoptosis was monitored by assessment of the number of condensed nuclei in kidney sections stained with periodic acid-Schiff (PAS) and by the terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) method and expressed as number of apoptotic cells per 50 glomerular cross sections. In the PAS method, 1 h after intravenous injection of ER4G, PVG/c+ rats exhibited 160.9 +/- 49.5 apoptotic cells, whereas PVG/c- rats had only 3.2 +/- 1.4 apoptotic cells. Control rats exhibited 0.9 +/- 0.6 apoptotic cells. These findings were confirmed with the TUNEL method. In PVG/c- rats, a maximum number of 8.8 +/- 3.1 TUNEL-positive (TUNEL+) cells was found at 6 h followed by a decline thereafter. In PVG/c+ rats, apoptosis was associated with deposition of C6 and C5b-9. Restoration of the complement system of PVG/c- rats with purified human C6 resulted in an increase of apoptosis at 1 h after injection of ER4G from minimal numbers to 239.9 +/- 52.4 TUNEL+ cells. These studies appear to indicate for the first time that the terminal sequence of complement is involved in induction of apoptosis.  (+info)

Evidence for enhanced rates of complement activation in serum from patients with newly diagnosed insulin-dependent diabetes mellitus exposed to rat islet cells and complement-dependent induction of islet cell apoptosis. (5/554)

In this paper we report the concentration of terminal complement complexes (TCCs, SC5b-9, an index of complement activation) in newly diagnosed insulin-dependent diabetes mellitus (IDDM) patient serum and normal human serum. In the nine patients studied, levels of serum soluble TCCs were approximately 1.6-fold higher than in sera obtained from normal control individuals. On incubation of rat islet cells with diluted serum (10%, v/v, concentration), complement activation was increased at a significantly faster rate and the total TCC concentration was significantly higher in culture medium containing IDDM patient serum than in medium containing control serum. The concentration of anti-(glutamic acid decarboxylase) autoantibodies in newly diagnosed IDDM patient serum was on average 60-fold higher than in normal human control serum. IDDM patient serum (10%, v/v) induced apoptosis in islet cells, as determined by islet cell density changes and DNA fragmentation patterns. However, serum from IDDM patients was not able to induce apoptosis of the cells when complement components (C1q and C3) or antibodies were depleted. In addition, glutamine and the potent antioxidant 1-pyrrolidinecarbodithioic acid partially reversed cell death induced by IDDM patient serum in a concentration-dependent manner. The ATP concentration in islet cells incubated for 24 h in the presence of diluted IDDM patient serum was reduced to 4.4% of that observed in islet cells incubated in fetal calf serum or 7.3% of that observed in islet cells incubated in normal human serum. On the basis of these observations, we suggest that the pathway of IDDM patient serum-induced islet cell apoptosis may involve antibody-dependent complement activation, free radical generation and a precipitous fall in ATP levels.  (+info)

Complement (C5b-9) induces glomerular epithelial cell DNA synthesis but not proliferation in vitro. (6/554)

BACKGROUND: The C5b-9 membrane attack complex of complement is the principal mediator of injury induced experimentally by antibodies directed at glomerular cell membranes. In experimental membranous nephropathy, C5b-9 induced injury to the glomerular visceral epithelial cell (VEC) is associated with DNA synthesis, but not cytokinesis. In the current study we determined if C5b-9 increases DNA synthesis in VEC in vitro, and defined the mechanisms involved. METHODS: Rat VEC in vitro were divided into three groups: (1) sensitized with anti-VEC antibody and exposed to sublytic concentrations of C +/PVG serum (normal complement components); (2) anti-VEC antibody and control C-/PVG serum (C6 deficient); (3) no anti-VEC antibody. DNA synthesis (BrdU staining), mitosis (mitotic figures) and cytokinesis (cell counts) were measured at 24 and 48 hours. To examine the expression of specific S-phase and M-phase cell cycle regulatory proteins and their inhibitors, immunostaining and Western blot analysis was performed for cyclin A, CDK2, p21 and p27, cyclin B and cdc2. RESULTS: In the absence of growth factors, sublytic C5b-9 attack did not increase proliferation. In contrast, sublytic C5b-9 attack (group 1) augmented growth factor induced DNA synthesis by 50% compared to controls (groups 2 and 3; P < 0.001), and was accompanied by increased levels of cyclin A and CDK2, and a decrease in the cyclin kinase inhibitor p27 (but not p21). Sublytic C5b-9 attack reduced the expression of the M phase cell cycle proteins, cyclin B and cdc2, accompanied by reduced mitosis (mitotic figures) and cytokinesis (cell number). CONCLUSIONS: Our results show that the C5b-9 augmented growth factor entry into the S phase in VEC is regulated by changes in specific cell cycle regulatory proteins. However, antibody and complement decreased the M phase cell cycle proteins, and prevented VEC mitosis and cytokinesis, suggesting a delay or arrest at the G2/M phase.  (+info)

Complement and atherogenesis: binding of CRP to degraded, nonoxidized LDL enhances complement activation. (7/554)

Complement activation occurs in temporal correlation with the subendothelial deposition of LDL during early atherogenesis, and complement also plays a pathogenetic role in promoting lesion progression. Two lesion components have been identified that may be responsible for complement activation. First, enzymatic degradation of LDL generates a derivative that can spontaneously activate complement, and enzymatically degraded LDL (E-LDL) has been detected in the lesions. Second, C-reactive protein (CRP) colocalizes with complement C5b-9, as evidenced by immunohistological studies of early atherosclerotic lesions, so the possibility exists that this acute phase protein also fulfills a complement-activating function. Here, we report that addition of LDL and CRP to human serum did not result in significant C3 turnover. Addition of E-LDL provoked complement activation, which was markedly enhanced by CRP. Binding of CRP to E-LDL was demonstrated by sucrose flotation experiments. Binding was Ca(2+)-dependent and inhibitable by phosphorylcholine, and the complement-activating property of E-LDL was destroyed by treatment with phospholipase C. These results indicated that CRP binds to phosphorylcholine groups that become exposed in enzymatically degraded LDL particles. Immunohistological studies complemented these findings in showing that CRP colocalizes with E-LDL in early human atherosclerotic lesions. Thus enzymatic, nonoxidative modification of tissue-deposited LDL can be expected to confer CRP-binding capacity onto the molecule. The ensuing enhancement of complement activation may be relevant to the development and progression of the atherosclerotic lesion.  (+info)

Complement activation in patients with systemic lupus erythematosus without nephritis. (8/554)

OBJECTIVE: To study the association between disease activity and complement activation prospectively in patients with systemic lupus erythematosus (SLE). PATIENTS AND METHODS: Twenty-one SLE patients were examined monthly for 1 yr. Disease activity, autoantibodies, conventional complement tests and the following complement activation products were investigated: C1rs-C1inh complexes, C4bc, Bb, C3a, C3bc, C5a and the terminal SC5b-9 complement complex (TCC). RESULTS: Modest variation in disease activity was noted. None of the patients had nephritis. Flare was observed at 27 visits. Four patients had anti-C1q antibodies in conjunction with modestly low C1q concentrations. The complement parameters were rather constant during the observation period. Slightly to moderately decreased C4 (0.05-0.10 g/l) was found in 10 patients and severely decreased C4 (<0.05 g/l) in seven patients. Decreased C4 was not associated with increased complement activation. Complement activation products were either normal or slightly elevated. TCC was the only activation product correlating significantly with score for disease activity at flare. None of the variables tested predicted flares. CONCLUSION: Complement tests are of limited importance in routine examination of SLE without nephritis, although TCC is suggested to be one of the most sensitive markers for disease activity.  (+info)

*Complement membrane attack complex

The membrane attack complex (MAC) or terminal complement complex (TCC) is a structure typically formed on the surface of ... two regulators of complement. The membrane attack complex is initiated when the complement protein C5 convertase cleaves C5 ... Complement Membrane Attack Complex at the US National Library of Medicine Medical Subject Headings (MeSH). ... The membrane-attack complex (MAC) forms transmembrane channels. These channels disrupt the cell membrane of target cells, ...

*Terminal complement pathway deficiency

... is a genetic condition affecting the complement membrane attack complex (MAC). It ... Initial complement tests often include C3 and C4, but not C5 through C9. Instead, the CH50 result may play a role in diagnosis ... Suspect terminal complement pathway deficiency with patients who have more than one episode of Neisseria infection. ... Lint TF, Zeitz HJ, Gewurz H (November 1980). "Inherited deficiency of the ninth component of complement in man". J. Immunol. ...

*Complement component 5

C5b forms the first part of the complement membrane attack complex. Deficiency is thought to cause Leiner's disease. Complement ... and this complex is the basis for formation of the membrane attack complex, which includes additional complement components. ... DiScipio RG (1992). "Formation and structure of the C5b-7 complex of the lytic pathway of complement". J. Biol. Chem. 267 (24 ... Complement component 5 is involved in the complement system. It is cleaved into C5a and C5b: C5a plays an important role in ...

*Complement component 9

C9 is a member of the complement membrane attack complex (MAC) and induces pores on cell membranes, causing lysis. There are 10 ... molecules of C9 in a single membrane attack complex (MAC), along with one of each of the complement components C5b, C6, C7 and ... Complement component 9 (C9) is a protein involved in the complement system, which is part of the innate immune system. ... 2001). "The complement system and innate immunity". Immunobiology: The Immune System in Health and Disease. New York: Garland ...

*CD59

... can prevent C9 from polymerizing and forming the complement membrane attack complex. It may also signal the cell to ... regulates the action of the complement membrane attack complex on homologous cells". J. Exp. Med. 170 (3): 637-654. doi:10.1084 ... Tandon N, Morgan BP, Weetman AP (1992). "Expression and function of membrane attack complex inhibitory proteins on thyroid ... Rooney IA, Morgan BP (1992). "Characterization of the membrane attack complex inhibitory protein CD59 antigen on human amniotic ...

*Index of biochemistry articles

... complement 3A - complement 5A - complement factor B - complement membrane attack complex - complement receptor - complex - ... membrane glycoprotein - Membrane protein - Membrane topology - Membrane transport - memory B cell - memory T cell - Mendelian ... plasma membrane - plasmid - plasmin - plasminogen - platelet glycoprotein GPIb-IX complex - platelet membrane glycoprotein - ... cell membrane - cell membrane transport - cell nucleus - cell surface receptor - cellular respiration - cellulose - centriole ...

*Cold agglutinin disease

In the formation of the membrane attack complex, several complement proteins are inserted into the red blood cell membrane, ... If the complement response is sufficient, red blood cells are damaged by the membrane attack complex, an effector of the ... In lieu of the membrane attack complex, complement proteins (particularly C3b and C4b) are deposited on red blood cells. This ... If the complement response is insufficient to form membrane attack complexes, then extravascular lysis will be favored over ...

*Outline of immunology

Classical complement pathway Mannan-binding lectin pathway Alternate complement pathway Complement membrane attack complex ... C5a C3-convertase C5-convertase Late stage Membrane attack complex (MAC) C6 C7 C8 C9 Complement pathway inhibitors C1-inhibitor ... Classical complement pathway C1Q complex - C1R / C1S C4 - C4a C2 Mannan-binding lectin pathway MASP1 / MASP2 Mannan-binding ... Secreted PRRs Complement system (see complement proteins section) Collectins Mannan-binding lectin (MBL) Surfactant protein A ( ...

*Coombs test

IgM mediated activation of classical complement pathway and Membrane attack complex, MAC) (A memory device to remember that the ... Complement proteins may subsequently bind to the bound antibodies and cause RBC destruction.[citation needed] The direct Coombs ... The direct Coombs test (also known as the direct antiglobulin test or DAT) is used to detect if antibodies or complement system ... A positive Coombs test indicates that an immune mechanism is attacking the patient's own RBCs. This mechanism could be ...

*C5-convertase

... proteolytic cleavage of C5 is the only known enzymatic event in assembly of the cytolytic membrane attack complex of complement ... CFHR1 blocks C5 convertase activity and interferes with C5b surface deposition and membrane attack complex (MAC) formation. ... C5 is activated by CVFBb in the presence of complement component C6 and the C5b6 complex is formed. However, when C6 is added ... in reduced inhibition of terminal complex formation and in reduced protection of endothelial cells upon complement attack. ...

*TCC

Cambridge Tulsa Community College Terminal complement complex, the membrane attack complex of the complement system. ...

*Antibody

... in which antibodies that are latched onto a foreign cell encourage complement to attack it with a membrane attack complex, ... Second, some complement system components form a membrane attack complex to assist antibodies to kill the bacterium directly ( ... The membrane-bound form of an antibody may be called a surface immunoglobulin (sIg) or a membrane immunoglobulin (mIg). It is ... complement system. This results in the killing of bacteria in two ways. First, the binding of the antibody and complement ...

*Decay-accelerating factor

DAF indirectly blocks the formation of the membrane attack complex. This glycoprotein is broadly distributed among ... Complement decay-accelerating factor, also known as CD55 or DAF, is a protein that, in humans, is encoded by the CD55 gene. DAF ... DAF is a 70 kDa membrane protein that attaches to cell membrane via a glycophosphatidylinositol (GPI) anchor. DAF contains four ... Thus, by limiting the amplification convertases of the complement cascade, ...

*Germinal center B-cell like diffuse large B-cell lymphoma

Initiates the complement system which activates the membrane attack complex causing cell lysis and death. Delivers chemotherapy ... Musilova, K; Mraz, M (2014). "MicroRNAs in B cell lymphomas: How a complex biology gets more complex". Leukemia. 29: 1004-17. ... Cell death does not appear to be mediated by complement, but modest antibody-dependent cellular cytotoxicity and direct killing ... and natural killer cells to destroy the targeted cells Complement-dependent cytotoxicity (CDC)-- ...

*MACPF

Complement proteins C6-C9 all contain a MACPF domain and assemble into the membrane attack complex. C6, C7 and C8β appear to be ... is named after a domain that is common to the membrane attack complex (MAC) proteins of the complement system (C6, C7, C8α, C8β ... 2004). "A new membrane-attack complex/perforin (MACPF) domain lethal toxin from the nematocyst venom of the Okinawan sea ... The Membrane Attack Complex/Perforin (MACPF) superfamily, sometimes referred to as the MACPF/CDC superfamily, ...

*C8 complex

Complement component 8 is a protein involved in the complement system. It is part of the membrane attack complex (MAC). A ... Figure created in Pymol Complement C8 at the US National Library of Medicine Medical Subject Headings (MeSH) The crystal ...

*Primary immunodeficiency

MASP2 deficiency Complement receptor 3 (CR3) deficiency Membrane cofactor protein (CD46) deficiency Membrane attack complex ... it is a group of circulating proteins that can bind pathogens and form a membrane attack complex. Complement deficiencies are ... Others predispose to autoimmune disease, where the immune system attacks the body's own tissues, or tumours (sometimes specific ... The complement system is part of the innate as well as the adaptive immune system; ...

*Complement system

C5b initiates the membrane attack pathway, which results in the membrane attack complex (MAC), consisting of C5b, C6, C7, C8, ... and activation of the cell-killing membrane attack complex. Over 30 proteins and protein fragments make up the complement ... Polymorphisms of complement component 3, complement factor B, and complement factor I, as well as deletion of complement factor ... C8 and multiple C9 molecules to assemble the membrane attack complex. This creates a hole or pore in the membrane that can kill ...

*Apoptosis

... not to be confused with the membrane attack complex formed by complement activation, also commonly denoted as MAC), also called ... Later these can grow into larger so-called dynamic membrane blebs. An important regulator of apoptotic cell membrane blebbing ... There are three recognized steps in apoptotic cell disassembly: Membrane blebbing: The cell membrane shows irregular buds known ... thin extensions of the cell membrane called membrane protrusions. Three types have been described: microtubule spikes, ...

*Alternative complement pathway

C5b binds sequentially to C6, C7, C8 and then to multiple molecules of C9 to form membrane attack complex. Since C3b is free ... Factor I requires a C3b-binding protein cofactor such as complement factor H, CR1, or Membrane Cofactor of Proteolysis (MCP or ... Age related macular degeneration (AMD) is now believed to be caused, at least in part, by complement mediated attack on ocular ... The complex is believed to be unstable until it binds properdin, a serum protein. The addition of properdin forms the complex ...

*Complement component 6

... is a protein involved in the complement system. It is part of the membrane attack complex which can ... 2009). "Complement production by trophoblast cells at the feto-maternal interface". J. Reprod. Immunol. 82 (2): 119-25. doi: ... Gancz D, Donin N, Fishelson Z (2009). "Involvement of the c-jun N-terminal kinases JNK1 and JNK2 in complement-mediated cell ... Complement component 6 is a protein that in humans is encoded by the C6 gene. ...

*CD59 antigen

... inhibits formation of membrane attack complex (MAC), thus protecting cells from complement-mediated lysis. It has a signaling ... A domain structure belonging to a novel superfamily of glycolipid-anchored membrane proteins". J. Biol. Chem. 268 (23): 17539- ... in plasma membranes. Genetic defects in GPI-anchor attachment that cause a reduction or loss of both CD59 and CD55 on ...

*Complement component 7

C7 is part of the membrane attack complex (MAC) which creates a hole on pathogen surfaces, leading to cell lysis and death. Its ... Terminal complement pathway deficiency Complement C7 at the US National Library of Medicine Medical Subject Headings (MeSH). ... Complement component 7 is a protein involved in the complement system of the innate immune system. ... primary task is to bind the C5bC6 complex together. This junction alters the configuration of the protein molecules, exposing a ...

*List of MeSH codes (D12.776.124)

... complement c4b-binding protein MeSH D12.776.124.486.274.930 -- complement membrane attack complex MeSH D12.776.124.486.274.965 ... complement c6 MeSH D12.776.124.486.274.650 -- complement c7 MeSH D12.776.124.486.274.750 -- complement c8 MeSH D12.776.124.486. ... complement c4a MeSH D12.776.124.486.274.024.270 -- complement c5a MeSH D12.776.124.486.274.024.270.255 -- complement c5a, des- ... complement c1r MeSH D12.776.124.486.274.050.290 -- complement c1s MeSH D12.776.124.486.274.150 -- complement c2 MeSH D12.776. ...

*CD93

... which leads to the formation of the membrane attack complex. C1q is also involved in other immunological processes such as ... C1q belongs to the complement activation proteins and plays a major role in the activation of the classical pathway of the ... 2001). "Interaction between complement receptor gC1qR and hepatitis C virus core protein inhibits T-lymphocyte proliferation". ...

*Lyme disease

Panic attacks and anxiety can occur; also, delusional behavior may be seen, including somatoform delusions, sometimes ... Spirochetes are surrounded by peptidoglycan and flagella, along with an outer membrane similar to other Gram-negative bacteria ... The resistance of a genospecies of Lyme disease spirochetes to the bacteriolytic activities of the alternative complement ... Richard Ostfeld (2012). Lyme Disease: The Ecology of a Complex System. New York: Oxford University Press. ISBN 0199928479. ...
A novel cell surface antigen has been identified on a wide range of lymphoid cells and erythrocytes. A mAb YTH 53.1 (CD59) against this antigen enhanced the lysis of human red cells and lymphocytes by homologous complement. Studies of reactive lysis using different species of C56, and of whole serum used as a source of C7-9, indicated that the inhibitory activity of the CD59 antigen is directed towards the homologous membrane attack complex. CD59 antigen was purified from human urine and erythrocyte stroma by affinity chromatography using the mAb YTH 53.1 immobilized on Sepharose, and, following transient expression of a human T cell cDNA library in COS cells, the corresponding cDNA also identified using the antibody. It was found that the CD59 antigen is a small protein (approximately 20 kD as judged by SDS-PAGE, 11.5 kD predicted from the isolated cDNA) sometimes associated with larger components (45 and 80 kD) in urine. The sequence of CD59 antigen is unlike that of other complement ...
Background In the rat brain, a single intracerebroventricular injection of neuraminidase from Clostridium perfringens induces ependymal detachment and death. This injury occurs before the infiltration of inflammatory blood cells; some reports implicate the complement system as a cause of these injuries. Here, we set out to test the role of complement. Methods The assembly of the complement membrane attack complex on the ependymal epithelium of rats injected with neuraminidase was analyzed by immunohistochemistry. Complement activation, triggered by neuraminidase, and the participation of different activation pathways were analyzed by Western blot. In vitro studies used primary cultures of ependymal cells and explants of the septal ventricular wall. In these models, ependymal cells were exposed to neuraminidase in the presence or absence of complement, and their viability was assessed by observing beating of cilia or by trypan blue staining. The role of complement in ependymal damage induced by ...
[A type of glomerulonephritis that is characterized by the accumulation of immune deposits ( COMPLEMENT MEMBRANE ATTACK COMPLEX) on the outer aspect of the GLOMERULAR BASEMENT MEMBRANE. It progresses from subepithelial dense deposits, to basement membrane reaction and eventual thickening of the basement membrane., A slowly progressive inflammation of the glomeruli characterized by immune complex deposits at the glomerular basement membrane, resulting in a thickened membrane, and nephrotic syndrome.]
TY - JOUR. T1 - The membrane attack complex of complement. T2 - Relation of C7 to the metastable membrane binding site of the intermediate complex C5b-7. AU - Preissner, K. T.. AU - Podack, E. R.. AU - Muller-Eberhard, H. J.. PY - 1985/1/1. Y1 - 1985/1/1. N2 - Isolated C7 (m.w. 120,000) in 1% deoxycholate (DOC) forms dimers with an apparent m.w. of 230,000 and a DOC-binding capacity of 82 mol per mol of dimer. Dimerization of C7 also occurs in the presence of DOC-phospholipid mixed micelles and eventuates in the insertion of C7 dimers into the lipid bilayer upon the removal of the detergent, C5b-7 complex formation in the fluid phase or on lipid vesicles likewise involves polymerization, C5b-7 sedimented with 17-40S, which suggests a dimeric to hexameric composition. In avidin-biotin binding experiments in which two differentially labeled forms of C5b,6 (biotinyl 125I-C5b,6, and 131I-C5b,6) were used in equimolar amounts to assemble C5b-7, more than 50% of the biotinyl 125I-C5b,6-containing ...
Understanding tumor resistance to T cell immunotherapies is critical to improve patient outcomes. Our study revealed a role for transcriptional suppression of the tumor-intrinsic HLA class I (HLA-I) antigen processing and presentation machinery (APM) in therapy resistance. Low HLA-I APM mRNA levels in melanoma metastases prior to immune checkpoint blockade (ICB) correlated with non-responsiveness to therapy and poor clinical outcome. Patient-derived melanoma cells with silenced HLA-I APM escaped recognition by autologous CD8+ T cells. However, targeted activation of the innate immunoreceptor RIG-I initiated de novo HLA-I APM transcription thereby overcoming T cell resistance. Antigen presentation was restored in interferon (IFN)-sensitive but also immunoedited IFN-resistant melanoma models through RIG-I-dependent stimulation of an IFN-independent salvage pathway involving IRF1 and IRF3. Likewise, enhanced HLA-I APM expression was detected in RIG-I (DDX58)-high melanoma biopsies, correlating with ...
The C5b-9 complex (Terminal Complement Complex-TCC) is the final product of the terminal complement pathway. In this study, using the monoclonal antibody MCaE11 (specific for a C9 neoantigen) and an immunohistochemical technique, we examined the TCC deposits in synovial tissues from 4 patients affected by rheumatoid arthritis (RA) and 6 patients affected by osteoarthritis (OA). Synovial tissues from 8 patients affected by acute joint trauma were examined as controls. Furthermore, plasma TCC levels were measured in 44 RA patients and 51 controls, using the above mentioned antibody and a sandwich ELISA. Eight synovial fluids were also included in this study. Abundant TCC deposits were detected in the cytoplasm of the synovial lining cells and of large stromal mononuclear cells in all the RA and in 3 out of 6 OA synovial tissues characterized by histological signs of inflammation. No TCC deposits were found in non-inflamed synovial tissues from patients with joint trauma. In agreement with previous ...
Herein reported is the case of a 15-year-old female without a relevant medical history, who developed severe headaches, speech problems, dizziness, weakness, inability to walk, depressed consciousness, confusion, amnesia and vomiting, 14 days after receiving her first qHPV vaccine injection. After the second vaccine booster, her symptoms worsened and she expired 15 days later. Autopsy revealed cerebral oedema and cerebellar herniation indicative of a focally disrupted blood-brain barrier.. There was no evidence of an active brain infection. Immunohistochemistry (IHC) examination of the brainstem, hippocampus and the cerebellum showed prominent infiltration of T-lymphocytes and macrophages in all brain areas examined. Notably, marked activation of the complement membrane attack complex (MAC) was detected in the cerebellar Purkinje cells, hippocampal neurons and portions of the brainstem. This pattern of MAC activation in the absence of an active brain infection indicates an abnormal triggering of ...
Regenesance is developing nanoparticle formulations of inhibitors of the complement membrane attack complex (MAC) for the treatment of peripheral neuropathy.
Purpose: : Uncontrolled activation of the alternative complement pathway is thought to be associated with age-related macular degeneration (AMD). Previously, we have shown that in retinal pigmented epithelium (RPE) monolayers, oxidative stress reduced complement inhibitor expression and function on the cell surface, resulting in sublytic activation of the membrane attack complex . Here we examined the potential ligand and pathway(s) involved in initiating complement-dependent RPE cell damage by oxidative stress. Methods: : ARPE-19 cells were grown as monolayers on transwell plates. Sublytic complement activation was induced by challenging monolayers with H2O2 in the presence of complement-sufficient normal human serum (NHS). Since sublytic complement activation results in VEGF release, which in turn reduces barrier function, transepithelial electrical resistance (TER) measurements were used as a measure of cell injury. Results: : (1) TER deteriorated rapidly in H2O2-exposed monolayers upon ...
During sublytic complement attack on human neutrophils, plasma-membrane vesicles are shed from the cell surface as a cell-protection mechanism. By using surface-iodinated neutrophils it was found that less than 2% of surface label was recovered in shed vesicles under conditions where 40% of complement component C9 was shed. SDS/PAGE of 125I-labelled shed vesicles and plasma membranes showed differences in iodination pattern, demonstrating the sorting of membrane proteins into the shed vesicles. Analysis of 32P-labelled phospholipids after labeling of neutrophils with [32P]Pi before sublytic complement attack showed the presence of phosphatidic acid, phosphatidylcholine, phosphatidyl-ethanolamine, phosphatidylinositol and polyphosphoinositides in shed vesicles. Quantitative analysis using [3H]acetic anhydride-labelling method showed that the molar proportions of phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine and sphingomyelin were the same in shed vesicles as in plasma ...
Assembly of the terminal C5b-C9 complement components into the cytolytic C5b-9 complex is accompanied by exposure of characteristic neoantigens on the macromolecule. We report the production and characterization of mouse monoclonal antibodies to C9-dependent neoantigens of human C5b-9. Binding-inhibition assays with EDTA-human plasma and micro-ELISA assays with purified C9 showed that the antibodies did not react with native complement components and thus confirmed the specificity of the antibodies for the neoantigens. The monoclonal antibodies did, however, cross-react with cytolyticaIly inactive, fluid-phase C5b-9 complexes, Thus, expression of the neoantigenic determinants was not dependent on the formation of high molecular weight C9 polymers with the complex, since these are absent in fluid-phase C5b-9. Radioiodinated antibodies could be utilized in immunoradiometric assays for the detection and quantitation of C5b-9 on cell membranes. Cross-reactivities of the antibodies with C9-dependent ...
Isolated C7 (m.w. 120,000) in 1% deoxycholate (DOC) forms dimers with an apparent m.w. of 230,000 and a DOC-binding capacity of 82 mol per mol of dimer. Dimerization of C7 also occurs in the presence of DOC-phospholipid mixed micelles and eventuates in the insertion of C7 dimers into the lipid bilayer upon the removal of the detergent. C5b-7 complex formation in the fluid phase or on lipid vesicles likewise involves polymerization. C5b-7 sedimented with 17-40S, which suggests a dimeric to hexameric composition. In avidin-biotin binding experiments in which two differentially labeled forms of C5b,6 (biotinyl 125I-C5b,6, and 131I-C5b,6) were used in equimolar amounts to assemble C5b-7, more than 50% of the biotinyl 125I-C5b,6-containing complexes also contained 131I label; again suggesting that C5b-7 consisted of oligomers rather than monomers. The conformation of C7 in C5b-7 and in dimeric C7 appeared similar by the following criteria. On formation of C5b-7 from C5b,6 and C7, a 20% increase in ...
When the complement system is activated, it triggers a variety of events leading to cleavage of one component known as C5. Once C5 is cleaved, a variety of events occur that propagate the formation of the membrane attack complex. This member attack complex generates pores, or holes, in cells ultimately leading to the cells demise. So when you have such a powerful system, regulators of the system are needed. These regulators sit on the outer membrane of cells, so the complement system recognizes that these cells are of the self. When those regulators are missing, as is the case in PNH, this leads to the destructions of the cells that are missing these protein shields.. Some of those shields, (2 proteins known as CD 55 and CD 59) are anchored the cell surface by a tail. We call this tail a GPI anchor - but in PNH this GPI anchor is missing because of a mutation in a gene called PIG-A. This defective gene leads to cause the cells inability to form this GPI anchor. So the complement regulator ...
Purpose.: Increasing evidence supports a role for complement in the pathogenesis of age-related macular degeneration (AMD). This study evaluated retinal microglia, T-lymphocytes, and complement deposition in a light-induced retinopathy model. The effect of a serotonin (5-hydroxytryptamine, 5-HT1A) agonist on these processes was investigated. Methods.: Rats were dark adapted for 24 hours before a 6-hour blue light exposure. Some animals were predosed subcutaneously with AL-8309A. Retinas were evaluated at different times after light exposure. Paraffin sections were stained with antibody for a microglial marker (Iba1), a T-lymphocyte marker (CD3), and complement components C1q, C3, factor B, factor H, and membrane attack complex (MAC). Results.: Light exposure resulted in substantial photoreceptor and RPE loss. Robust microglia activation and migration to the outer retina occurred rapidly. Substantial T-lymphocyte recruitment did not occur. Complement alternative pathway was strongly activated, ...
Background Glaucoma is an age-related neurodegenerative disorder involving the loss of retinal ganglion cells (RGCs), which results in blindness. Studies in animal models have shown that activation of inflammatory processes occurs early in the disease. In particular, the complement cascade is activated very early in DBA/2J mice, a widely used mouse model of glaucoma. A comprehensive analysis of the role of the complement cascade in DBA/2J glaucoma has not been possible because DBA/2J mice are naturally deficient in complement component 5 (C5, also known as hemolytic complement, Hc), a key mediator of the downstream processes of the complement cascade, including the formation of the membrane attack complex. Methods To assess the role of C5 in DBA/2J glaucoma, we backcrossed a functional C5 gene from strain C57BL/6J to strain DBA/2J for at least 10 generations. The prevalence and severity of glaucoma was evaluated using ocular examinations, IOP measurements, and assessments of optic nerve damage and RGC
Complement C7: 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.
This study demonstrates that anti-ganglioside Abs, including experimental mAbs and GBS patient serum, induce sequential nodal and/or axonal injury in a new passive transfer mouse model that recapitulates the salient pathologic features found in axonal GBS (Griffin et al., 1996b). We found that the breakdown of BNB induced by L5SNT was essential for Ab-mediated nerve injury. Furthermore, this anti-ganglioside Abs-mediated neuropathy (injury to intact nerve fibers) depends on activating FcγRs bearing macrophages/microglia-mediated inflammation triggered by ICs formed by anti-ganglioside Abs and their target antigens on the nerves. Notably, we found that the terminal complement complex was not involved in the anti-ganglioside Abs-mediated axonal degeneration in this animal model. Overall, our study supports the notion that cellular elements of innate immunity are required for Ab-mediated nerve injury and involved in the pathogenesis of GBS. The identification of activating FcγRs in ...
Granulocytic infiltrate occurs in the absence of demyelination, terminal complement complex formation, and overt tissue destruction in NMO white matter. a H&
Complement component C9 binds to the C5b-8 complex as the final protein of the membrane attack complex. After binding, it undergoes a conformational change and inserts itself into the cell membrane, forming transmembrane channels.
Complement C6, 50 µg. C6 is a component of complement cascade. It is part of the membrane attack complex which can insert into the cell membrane and cause cell to lyse.
Constituent of the membrane attack complex (MAC) that plays a key role in the innate and adaptive immune response by forming pores in the plasma membrane of target cells (PubMed:9634479, PubMed:9212048, PubMed:26841934). C9 is the pore-forming subunit of the MAC (PubMed:4055801, PubMed:26841934, PubMed:30111885).
Constituent of the membrane attack complex (MAC) that plays a key role in the innate and adaptive immune response by forming pores in the plasma membrane of target cells.
Membrane attack complex (MAC) is formed under the combined stimulation of amyloid beta (Aβ) and normal human serum (NHS), immunolabeled with a monoclonal mouse anti-human C5b-9 antibody and subsequently visualized by Cy3 (red). RPE cell nuclei are counter-stained with DAPI. Scale bars: 20 μm. See full article online. Read More ...
Die genetische Anfälligkeit für Meningokokken-Infektionen liegt vor allem in Störungen des Komplementsystems begründet, vor allem der terminale membrane attack complex (MAC), der von C8 und C9 gebildet wird, aber auch Teile des Komplementsystems, die die Bildung des MAC steuern, können betroffen sein (C3, C5, C6, C7).. ...
Dr. Elias Reichel, of Tufts University School of Medicine and a founder of Hemera Biosciences, Inc., of Boston, MA, presented on a new approach to treating the dry form of age-related macula degeneration. His paper was based on the research being done by Hemera Biosciences on HMR59, a naturally occurring protein that protects retinal cells from damage by MAC (Membrane Attack Complex), that can be delivered for long-lasting activity via a gene therapy approach. ...
Complex C DailyFoods Vitamin Formula All The C Factors As Nature Intended In Nature, Vitamin C is only found as a complex food with all the beneficial factors, such as bioflavonoids, intact. This formula contains 250 mg of Cold Fusion FoodState Vitamin C in its optimal form ~ FOOD. Cold Fusion FoodState Vitamin C is 10 times less acidic than regular Vitamin C (ascorbic acid), therefore it is Naturally Buffered and gentler on the stomach. Complex C DailyFoods is formulated with 100% Cold Fusion FoodState nutrients, developed by Durham Research, Inc. Cold Fusion FoodState nutrients have the inherent benefits of Vital Food Factors, known as Nutrient Chaperones. Nutrient Chaperones contain the plant intelligence necessary for all nutrient delivery and utilization. These nutrients have Food Chaperones, which facilitate utilization and reduce the potential for side-effects. Benefits are enhanced with the addition of phytonutrient rich concentrated fruit and vegetable extracts. Cold Fusion
Hi, Weird issue has cropped up. I have a total of 4 X Cisco 6509 switches in 2 data-centres. Multiple VLANs exist on each switch... However, I have a problem on 6 individual ports.....Really weird issue in that every 30 minutes without fail the
Fetal development inside the womb has many benefits, including protection from fluctuations in nourishment, temperature, and oxygen levels (41). Beyond the safety from external threats, fetal in utero existence, however, entails problems. Among the biggest challenges for mother and fetus is the establishment of immunologic coexistence of 2 genetically distinct entities while simultaneously ensuring potent immune defense against pathogens. To date, several maternal and fetal mechanisms contributing to the establishment and maintenance of fetal-maternal immune homeostasis have been described (11). Yet, numerous non-pathogen-related inflammatory reactions leading to pregnancy complications exist, which represent major threats to the developing fetus and its mother (42). Using a CMP-Sia-negative mouse model, we demonstrated sialylation to be crucial for protection of fetal extraembryonic tissue from maternal complement attack, thereby guaranteeing its proper development, which ultimately ensures ...
Name:C.I.Reactive Black 8,C.I.18207 Molecular Structure: Single azo,Metal Complexes C.I.Reactive Black 8,C.I.18207,CAS 12225-26-2,656.90,C19H11ClN8Na2O10S2,Reactive Black K-BR,Black HN C.I.Reactive Black 8,C.I.18207,CAS 12225-26-2,656.90,C19H11ClN8Na2O10S2,Reactive Black K-BR,Black HN Molecular Formula:C19H11ClN8Na2O10S2 Molecular Weight: CAS Registry Number:12225-26-2
In addition to being a component of innate immunity and an ancient defense mechanism against invading pathogens, complement activation also participates in the adaptive immune response, inflammation, hemostasis, embryogenesis, and organ repair and development. Activation of the complement system via classical, lectin, or alternative pathways generates anaphylatoxins (C3a and C5a) and membrane attack complex (C5b-9) and opsonizes targeted cells. Complement activation end products and their receptors mediate cell-cell interactions that regulate several biological functions in the extravascular tissue. Signaling of anaphylatoxin receptors or assembly of membrane attack complex promotes cell dedifferentiation, proliferation, and migration in addition to reducing apoptosis. As a result, complement activation in the tumor microenvironment enhances tumor growth and increases metastasis. In this Review, I discuss immune and nonimmune functions of complement proteins and the tumor-promoting effect of ...
Background/Purpose: The influence of complement-mediated innate immune responses on cartilage and bone homeostasis in the ageing joint have not been studied. Inappropriate complement-mediated cell damage is prevented by membrane regulators such as CD59. Synovial tissue expression of CD59 is altered during inflammatory arthritis; elevated CD59 levels may be necessary to protect joint tissues. Roles of CD59 in maintaining tissue equilibrium and structural architecture within the synovial joint have not been described previously. Since CD59a is the primary regulator of membrane attack complex assembly in mice; we used CD59a-gene-deleted mice (CD59a-/-) as tools to unravel the function of CD59a in modulating age-related joint degeneration. Methods: Hind limbs were collected from C57BL/6J wild type (WT) and CD59a-/- mice at 8-, 20- and 50- weeks of age (6 to 10 mice/group). The Mankin score was used to classify the histopathological severity of osteoarthritic (OA) lesions. Three dimensional ...
Cerebral IR injury produces a profound inflammatory response characterized by neutrophil, macrophage, and platelet accumulation, upregulation of adhesion molecules, blood-brain barrier destruction, and cytokine production.5 During central nervous system inflammation, complement activation plays a direct role in neuronal cell death6 and has been implicated in many disease processes, including subarachnoid hemorrhage,9 Alzheimer disease,10 trauma,11 and stroke.12,13 In a study of patients who died after ischemic stroke, Lindsberg et al9 demonstrated complement deposition within areas of necrosis and concluded that activation of the terminal complement pathway with membrane attack complex assembly occurs within cerebral infarct zones. Others have shown that complement depletion before cerebral IR injury may have neuroprotective effects in animal models.12,14 Huang et al12 used a mouse model of middle cerebral artery occlusion and reperfusion to demonstrate that administering a potent inhibitor of ...
C5a is a protein fragment released from cleavage of complement component C5 by protease C5-convertase into C5a and C5b fragments. C5b is important in late events of the complement cascade, an orderly series of reactions which coordinates several basic defense mechanisms, including formation of the Membrane Attack Complex (MAC), one of the most basic weapons of the innate immune system, formed as an automatic response to intrusions from foreign particles and microbial invaders. It essentially pokes microscopic pinholes in these foreign objects, causing loss of water and sometimes death. C5a, the other cleavage product of C5, acts as a highly inflammatory peptide, encouraging complement activation, formation of the MAC, attraction of innate immune cells, and histamine release involved in allergic responses. The origin of C5 is in the hepatocyte, but its synthesis can also be found in macrophages, where it may cause local increase of C5a. C5a is a chemotactic agent and an anaphylatoxin; it is ...
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. . ...
Porcine complement regulators protect aortic smooth muscle cells poorly against human complement-induced lysis and proliferation: consequences for xenotransplantation. Xenotransplantation 12 (3) , pp. 217-226. 10.1111/j.1399-3089.2005.00217.x ...
c-C3BP or rGAPDH was observed (Figure 3c, d). The H.c-C3BP or rGAPDH interaction with C3 was specific and strong, which was evident from the fact that the column-bound C3 was eluted at high salt wash (0·5 m NaCl) or by lowering the pH to 2·2. To test whether H.c-C3BP or rGAPDH binding to C3 would influence complement function, a simple haemolytic assay was performed where the lysis of sensitized sheep erythrocytes by serum complement proteins was measured. As shown in Figure 3(e, f), a dose-dependent inhibition of erythrocyte lysis by H.c-C3BP and rGAPDH was observed. To rule out that the observed inhibition was not due to suppression of the classical pathway, binding of C1q protein by H.c-C3BP was. measured. No interaction among these proteins was evident in the microtitre plate assay (not shown). To confirm check details whether the inhibition of erythrocyte lysis by H.c-C3BP or rGAPDH was due to suppression of C3 activation, the formation of membrane attack complex (MAC) was measured on the ...
When antigens enter into the body, normally this antigen will be recognized by the antibody that has been generated before during first exposure. The antibody binds to the soluble antigen forming the antibody-antigen complexes in the circulation in order to clear up all of the pathogens. According to Levinson (n.d), the reticuloendothelial system or macrophages system and other phagocytes have the ability to remove the immune antibody-antigen complexes very effectively in a normal condition. However, in type III hypersensitivity, these systems are not capable to remove these complexes. As a result, this antigen-antibody complexes tends to deposit on the wall of the blood vessels. Some of the immune complex deposition on the blood vessel will activate the complement protein such as C1, C4, C3 and C5-9 resulting membrane attack complex, leukocytes chemotaxis, leukocytes polymorphism and phagocytosis as well as inflammation. So that, in classical pathway C1 binds to the antigen-antibody complex and ...
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterised by the production of IgG autoantibodies that are specific for self-antigens, such as DNA, nuclear proteins and certain cytoplasmic components, in association with a diverse array of clinical manifestations. The primary pathological findings in patients with SLE are those of inflammation, vasculitis, immune complex deposition, and vasculopathy. Immune complexes comprising autoantibody and self-antigen is deposited particulary in the renal glomeruli and mediate a systemic inflammatory response by activating complement or via Fc{gamma}R-mediated neutrophil and macrophage activation. Activation of complement (C5) leads to injury both through formation of the membrane attack complex (C5b-9) or by generation of the anaphylatoxin and cell activator C5a. Neutrophils and macrophages cause tissue injury by the release of oxidants and proteases ...
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterised by the production of IgG autoantibodies that are specific for self-antigens, such as DNA, nuclear proteins and certain cytoplasmic components, in association with a diverse array of clinical manifestations. The primary pathological findings in patients with SLE are those of inflammation, vasculitis, immune complex deposition, and vasculopathy. Immune complexes comprising autoantibody and self-antigen is deposited particulary in the renal glomeruli and mediate a systemic inflammatory response by activating complement or via Fc{gamma}R-mediated neutrophil and macrophage activation. Activation of complement (C5) leads to injury both through formation of the membrane attack complex (C5b-9) or by generation of the anaphylatoxin and cell activator C5a. Neutrophils and macrophages cause tissue injury by the release of oxidants and proteases ...
The complement system (Chap. 308) consists of a group of serum proteins functioning as a cooperative, self-regulating cascade of enzymes that adhere to- and in some cases disrupt-the surface of invading organisms. Some of these surface-adherent proteins (e.g., C3b) can then act as opsonins for destruction of microbes by phagocytes. The later, "terminal" components (C7, C8, and C9) can directly kill some bacterial invaders (notably, many of the neisseriae) by forming a membrane attack complex and disrupting the integrity of the bacterial membrane, thus causing bacteriolysis. ...
Melted terminal components on Red Brick battery - posted in Batteries/Power: Hi All, I know this isnt really Steadicam related, but I was hoping I could draw on your experience and knowledge with this nasty situation. We hired a RED from one of my freinds to use at the BSC show, and he has just told me that a terminal on the charger and on one battery has melted. I have seen no photos so im not sure exactly what he means, but he is saying hte plastic parts around the power terminal...
The present invention provides modified IgG3 containing human constant regions which has a shorter total-hinge region compared with normal human IgG3. Also described is a method for assaying an antibody against a specific antigen or hapten for its effectiveness in complement activation in an animal species, wherein the antibody is contacted with the immobilized antigen or hapten to form an immobilized antibody/antigen or hapten complex which is then contacted with complement from the relevant animal species, followed by assay of components of the complement complex thereby formed; whereby the extent and nature of complement activation by the antibody in the sample may be determined.
I did that trip as a quick turn, assembling a roughly 24-hour itinerary to fly Newark - Montreal - Amsterdam - Newark. I took only my messenger bag with a camera, laptop and a clean t-shirt and underwear. I breezed through the Global Entry kiosks at Newark to the Customs exit where the agent was either suspicious or confused, suggesting to me twice that I go get my bags before presenting myself. And he was none to happy when I smiled and just stood there. I handed over the Global Entry receipt and explained that I was a journalist covering an event and was only gone 24 hours so I had no bags. I made an impression, but not a good one. I was escorted to the secondary screening area at Newarks Terminal C where I did my best to not fall asleep waiting for whatever would come next.. I was not sent into the "Green Room" which is definitely a good thing. It meant that I got to watch as the agent spent 20 minutes on his computer. Turns out he was looking for questions to ask me about the MD-11 and why ...
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The invention describes a platform technology that increases MHC presentation of oncogene derived peptide neoantigens that do not normally occur in the cell. The platform has already been used to identify a method of increasing KRAS G12 D/V derived peptide presentation on MHC- I.
The presence of lytic antibodies in the circulation of patients with chronic Chagas disease might lead to their cure. It has been shown that amastigotes of Trypanosoma cruzi activate complement and accumulate large amounts of the terminal complement components, but without killing the parasites. One plausible explanation for this observation is that the insertion of the membrane attack complex of complement is prevented by inhibitors present in the parasite membrane. To explore this possibility, we raised a panel of monoclonal antibodies (MAbs) against the surface molecules of T. cruzi amastigotes. One of these, MAb M4C12, induced complement-mediated lysis of amastigotes as detected with a 86Rb-release assay. The antigen molecule from the membrane lysate of amastigotes that was recognized by MAb M4C12 was purified, characterized, and designated M4C12Ag. It is a 92-kD molecule structurally related to Ssp4, a previously characterized amastigote surface molecule. However, M4C12Ag is more basic (pI 6.9-7.1
Background: C reactive protein (CRP), an important serum marker of atherosclerotic vascular disease, has recently been reported to be active inside human atherosclerotic plaques.. Aims: To investigate the simultaneous presence of macrophages, CRP, membrane attack complex C5b-9 (MAC), and oxidised low density lipoprotein (oxLDL) in atherectomy specimens from patients with different coronary syndromes.. Methods: In total, 54 patients with stable angina (SA; n = 21), unstable angina (UA; n = 15), and myocardial infarction (MI; n = 18) underwent directional coronary atherectomy for coronary lesions. Cryostat sections of atherosclerotic plaques were immunohistochemically stained with monoclonal antibodies: anti-CD68 (macrophages), anti-5G4 (CRP), aE11 (MAC), and 12E7 (oxLDL). Immunopositive areas were evaluated in relation to fibrous and neointima tissues, atheroma, and media. Quantitative analysis was performed using image cytometry with systematic random sampling (percentage immunopositive/total ...
The key event in complement activation is the proteolytic cleavage of C3 to C3a and C3b. Three pathways can lead to C3 cleavage, namely, classical, alternative, and mannose-binding lectin (MBL) pathways. C3 cleavage leads on to the activation of the terminal complement pathway, causing the generation of the membrane attack complex (MAC), which assembles…
TY - JOUR. T1 - Interaction of complement and clusterin in renal injury. AU - Correa-Rotter, Ricardo. AU - Hostetter, Thomas H.. AU - Nath, Karl A. AU - Manivel, J. Carlos. AU - Rosenberg, Mark E.. PY - 1992/11. Y1 - 1992/11. N2 - Clusterin is a heterodimeric glycoprotein that has been associated with such diverse biologic functions as reproduction, cell regression, cell aggregation, and regulation of the cytolytic activity of the membrane attack complex of complement. Clusterin is a component of glomerular immune deposits in the kidney, and increased Clusterin expression occurs in a number of renal injury states. To further explore the interaction between Clusterin and complement, the requirement for an intact complement system for renal Clusterin induction in an acute (folic acid nephropathy) and a chronic (subtotal renal ablation) model of renal injury was examined. After it was first demonstrated that folic acid increased renal clusterin mRNA in the rat, a species in which renal clusterin ...
Nineteen years after Gasser et al. [1] reported HUS, an interesting report was published in the Lancet [10]. This report indicated that although C3-predominant activity is initiated in the blood vessels in TMA patients, this is not observed in typical cases of HUS, suggesting that complement activation is involved in aHUS onset [12]. Subsequently, numerous researchers have elucidated further information on the pathology of aHUS. At present, the reported causes of aHUS include, complement regulation abnormalities, cobalamin metabolism disorder, infection with Streptococcus pneumoniae and other microorganisms, drugs, pregnancy, and autoimmune diseases.. The complement system plays an important role as part of the immune systems of living organisms. It is activated via 3 pathways, the classical, alternative, and lectin pathways. As a result of the activation of the hosts alternative and classical pathways, C5b-9, a membrane attack complex, is generated and destroys cells by forming transmembrane ...
This gene encodes a plasma glycoprotein that positively regulates the alternative complement pathway of the innate immune system. This protein binds to many microbial surfaces and apoptotic cells and stabilizes the C3- and C5-convertase enzyme complexes in a feedback loop that ultimately leads to formation of the membrane attack complex and lysis of the target cell. Mutations in this gene result in two forms of properdin deficiency, which results in high susceptibility to meningococcal infections. Multiple alternatively spliced variants, encoding the same protein, have been identified.[provided by RefSeq, Feb 2009 ...
... is pseudo-oligosaccharide with a terminal C7-cyclitol patented in 1975 by Bayer. Acarbose is a component of the amylostatin complex produced by species of Actinoplanes and Streptomyces. Acarbose acts as a potent inhibitor of α-glucosidases and saccharases. Since 1990, acarbose has been used therapeutically for the treatment of type 2 diabetes ...
Concerns that the immune system is a two-edged sword that sometimes inhibits and sometimes enhances tumor growth have focused on both the B-cell and T-cell arms of the immune system for over 40 years. While the clinical value of adoptively transfused T cells in a variety of clinical settings is well established (28), recent concerns have focused on regulatory mechanisms able to diminish the antitumor T-cell response and even enhance tumor growth (29). Antibodies and the B-cell response have long been associated with this dichotomy as well (30). Since FDA approval of mAbs such as Rituxan and Herceptin, and their widespread use, there is no doubt about the clinical value of immune effector mechanisms such as complement activation and antibody-dependant cellular cytotoxicity (ADCC), which these antibodies are known to mediate (8, 31). Despite the obvious value of adoptively administered antibodies and T cells, the role of vaccine-induced antibodies and T cells targeting cancer antigens remains less ...
IgG antibody accounts for the vast majority of all antibody mediated protection even though it is the slowest to be produced after the initial insult. Its primary means of protection is to identify the pathogen by attaching to it and marking it for destruction by other immune cells. It can also burst cells by fixing complement. Complement is a group of proteins that build on one another after the initial component has been "fixed", much like the first domino must be tipped over to topple the whole row. Once the "row" has been completed, the complement has the ability to pierce the cell wall of the antigen. Typically only gram negative bacteria can be pierced (lysed) by a particular chain of complement known as the membrane attack (MAC). Gram positives can fall prey to the complement cascade but through the identification route ...
Please ask any questions you may have about this specific product in the field below.. Your question(s) and our corresponding answer(s) will not be confidential and will be posted publically on this specific product page.. Additionally, PureFormulas is unable to directly recommend products in relation to specific health conditions. Please contact your trusted healthcare practitioner for direct product recommendations.. If you have any general questions regarding orders or our policies and programs, please contact our Customer Happiness Team @ 1.800.383.6008. If you are pregnant, nursing, taking any medications or have any medical condition, consult your doctor before use. Your healthcare professional is the best source for guidance before beginning an exercise or nutritional supplement program.. ...
Please ask any questions you may have about this specific product in the field below.. Your question(s) and our corresponding answer(s) will not be confidential and will be posted publically on this specific product page.. Additionally, PureFormulas is unable to directly recommend products in relation to specific health conditions. Please contact your trusted healthcare practitioner for direct product recommendations.. If you have any general questions regarding orders or our policies and programs, please contact our Customer Happiness Team @ 1.800.383.6008. If you are pregnant, nursing, taking any medications or have any medical condition, consult your doctor before use. Your healthcare professional is the best source for guidance before beginning an exercise or nutritional supplement program.. ...
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The neuronal microtubule-associated protein tau becomes hyperphosphorylated and forms aggregates in tauopathies but the processes leading to this pathological hallmark are not understood. Because tauopathies are accompanied by neuroinflammation and the complement cascade forms a key innate immune pathway, we asked whether the complement system has a role in the development of tau pathology. We tested this hypothesis in two mouse models, which expressed either a central inhibitor of complement or lacked an inhibitor of the terminal complement pathway. Complement receptor-related gene/protein y is the natural inhibitor of the central complement component C3 in rodents. Expressing a soluble variant (sCrry) reduced the number of phospho-tau (AT8 epitope) positive neurons in the brain stem, cerebellum, cortex, and hippocampus of aged P301L mutant tau/sCrry double-transgenic mice compared with tau single-transgenic littermates (JNPL3 line). CD59a is the major inhibitor of formation of the membrane attack
Evasion of complement-mediated killing is a common phenotype for many different types of pathogens, but the mechanism is still poorly understood. Most of the clinic isolates of Edwardsiella tarda, an important pathogen infecting both of human and fish, are commonly found serum-resistant. To explore the potential mechanisms, we applied GC-MS based metabolomics approaches to profile the metabolomes of E. tarda EIB202 in the presence or absence of serum stress. We found that TCA cycle was greatly enhanced in the presence of serum. The QRT-PCR and enzyme activity assays validated this result. Furthermore, exogenous succinate that promoting TCA cycle increased serum resistance, while TCA cycle inhibitors (bromopyruvate and propanedioic acid) that inhibit TCA cycle, attenuated serum resistance. Moreover, the enhanced TCA cycle increased membrane potential, thus decreased the formation of membrane attack complex at cell surface, resulting serum resistance. These evidences suggested a previously unknown
Saliva of the blood feeding sand fly Lutzomyia longipalpis was previously shown to inhibit the alternative pathway (AP) of the complement system. Here, we have identified Lufaxin, a protein component in saliva, as the inhibitor of the AP. Lufaxin inhibited the deposition of C3b, Bb, Properdin, C5b and C9b on agarose-coated plates in a dose dependent manner. It also inhibited the activation of factor B in normal serum, but had no effect on the components of the membrane attack complex. Surface plasmon resonance (SPR) experiments demonstrated that Lufaxin stabilizes the C3b-B proconvertase complex when passed over a C3b surface in combination with factor B. Lufaxin was also shown to inhibit the activation of factor B by factor D in a reconstituted C3b-B, but did not inhibit the activation of C3 by reconstituted C3b-Bb. Proconvertase stabilization does not require the presence of divalent cations, but addition of Ni2+ increases the stability of complexes formed on SPR surfaces. Stabilization of the C3b-B
The general aim of this study was to evaluate the disease spectrum in patients presenting with a pure polymyositis (pPM) phenotype. Specific objectives were to characterize clinical features, autoantibodies (aAbs), and membrane attack complex (MAC) in muscle biopsies of patients with treatment-responsive, statin-exposed necrotizing autoimmune myositis (NAM). Patients from the Centre hospitalier de lUniversité de Montréal autoimmune myositis (AIM) Cohort with a pPM phenotype, response to immunosuppression, and follow-up ≥3 years were included. Of 17 consecutive patients with pPM, 14 patients had a NAM, of whom 12 were previously exposed to atorvastatin (mean 38.8 months). These 12 patients were therefore suspected of atorvastatin-induced AIM (atorAIM) and selected for study. All had aAbs to 3-hydroxy-3-methylglutaryl coenzyme A reductase, and none had overlap aAbs, aAbs to signal recognition particle, or cancer. Three stages of myopathy were recognized: stage 1 (isolated serum creatine ...
CH50 and CH100 measures the integrity of the classical and terminal complement pathways. Indicated in the investigation of suspected immune deficiency associated with recurrent pyogenic infections, recurrent/atypical meningococcal infections and atypical immune complex disorders.AP100 measures the integrity of the alternative and terminal complement pathways. Rare deficiencies of AP components predispose to neisserial infections.AP100 measures the integrity of the alternative and terminal complement pathways. Rare deficiencies of AP components predispose to neisserial infections ...
CD46 is a transmembrane protein that is known as a complement membrane cofactor protein, MCP, and measles virus receptor. It is widely expressed on leukocytes, platelets, epithelial cells, and fibroblasts. Multiple isoforms of CD46 have been reported with molecular weights ranging from 45-75 kD. CD4
Background The immune system has been shown to be important in the pathophysiology of MDS. Adaptive immunity relies on T cells ability to discriminate between self and non-self antigens in the context of a surface bound MHC protein structure. Genomic changes occurring in acquired somatic mutations can encode novel amino acid sequences, which if translated and presented by the MHC are termed a neoantigen. To establish the impact of neoantigens in MDS we have combined a predictive algorithm to screen cases for the presence of neoantigens together with mass cytometry by time of flight (CyTOF) to identify neoantigen-related immune signatures. Results Mutation screening was performed on 204 MDS patients using our established gene panel targeting mutations commonly occurring in MDS (Mohemdali, Leukaemia 2015). Neoantigen-MHC affinity was predicted using NetMHCpan3.0 with neoantigen affinities ranked against 400,000 naturally occurring peptides. Those in the top 2% of peptides were classed as predicted ...
Security video shows the officer walking away from his post about four minutes after he asked an unidentified man to stay behind the rope line. Moments later, the man ducks under the rope and walks the wrong way through security to greet a woman, prompting a security breach that shut down Terminal C for hours and forced the rescreening of thousands of passengers.. Cameras dont work, procedures are not known and employees wont or cant do their jobs. Were not in good hands. ...
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These studies suggested that cell lysates and supernatant collected from cultured PMNs that were exposed to cytokines or C. albicans hyphae opsonized with normal human serum had elevated levels of C6 and C7 proteins [18,19]; however, it was not conclusive that these proteins were produced by PMNs in culture because (1) the rise in C6 or C7 in culture could have been released by C. albicans hyphae or derived from normal human serum, (2) the inhibition of protein biosynthesis by cycloheximide did not affect the rise in C6 or C7 in PMN cultures [18], and (3) conclusive evidence showing that PMNs are actively expressing these terminal complement mRNAs or proteins has been lacking in the literature ...
If youre lucky to have two or more Macs in your home or office, you no doubt find occasions where you would like to remote control a Mac either from another room or from another part of the country. You probably know that you can use the Shared feature to remotely control another Mac on the same network. But by creating some simple AppleScript commands you can control a remote Mac much faster, alleviating the need to open the Shared screen feature. If you have never worked with AppleScript before, dont fret. The following Mac remote control scripts are very Read more. ...
The 13" Retina Mac on the other hand looks a little more pedestrian in terms of specs. For $1,699 you get a dual core full mobile Intel Core i5 CPU clocked at 2.5GHz (not the slower ULV CPU used in Ultrabooks and the MacBook Air). It has a healthy 8 gigs of DDR3 1600MHz RAM soldered on the motherboard and a skimpy 128 gig SSD drive. The optical drive is gone to make the machine so thin and light. Basically, its a 13" MacBook Pro standard model with a seriously upgraded display and the SSD option. A similarly configured standard 13" MBP would set you back $1,499, and Id say $200 for the 2560 x 1600 Retina panel is a fair price ...
The 13" Retina Mac on the other hand looks a little more pedestrian in terms of specs. For $1,699 you get a dual core full mobile Intel Core i5 CPU clocked at 2.5GHz (not the slower ULV CPU used in Ultrabooks and the MacBook Air). It has a healthy 8 gigs of DDR3 1600MHz RAM soldered on the motherboard and a skimpy 128 gig SSD drive. The optical drive is gone to make the machine so thin and light. Basically, its a 13" MacBook Pro standard model with a seriously upgraded display and the SSD option. A similarly configured standard 13" MBP would set you back $1,499, and Id say $200 for the 2560 x 1600 Retina panel is a fair price ...
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Doctors give trusted, helpful answers on causes, diagnosis, symptoms, treatment, and more: Dr. Mack on symptoms of pregnancy in the tubes: Pelvic/abdominal pain and vaginal bleeding are most common symptoms. These are rarely present with an early ectopic though, so if theres reason for concern about ectopic consult your doctor, do not rely on symptoms.
this suit was fun to wear and i got a lot of complements on the fringe beads. the beads didnt get annoying in the water either! throw on some shorts and it becomes a cute top ...
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Host defense mechanisms can counteract the antiphagocytic bacterial capsule. Unlike classical complement pathway, the alternative complement pathway is not antibody-mediated and can easily overwhelm encapsulated bacteria. It is triggered by the cleavage of C3 into C3a and C3b and the attachment of C3b to MAMPs (Microbe Associated Molecular Patterns), such as the capsular polysaccharides. The C3b molecules osponsize the pathogen, facilitating its phagocytosis and intravascular clearance. Furthermore, the complement cascade leads to the formation of proteolytic C3and C5 convertases and the terminal membrane attack complex, which lyses the pathogen. However, a potentially fatal drawback from lysing the pathogen is the release of endotoxic lipopolysaccharides, which elicit an out-of-control immune response. [2 ...
Since the 1980s, plasma exchange therapy has been the mainstay method for management of aHUS. This therapy aims to eliminate abnormal complement regulatory proteins and anti-CFH antibodies, while supplementing normal complement regulatory proteins. Eculizumab is a humanized monoclonal antibody that binds to C5 complement protein. Eculizumab suppresses C5 cleavage to C5a and C5b and thereby prevents the production of the membrane attack complement complex (MAC).. In practical terms, when a patient presents with TMA and is negative for STEC-HUS and invasive pneumococcal infection (the latter of which is not indicated for plasma exchange), the treating physician should start the empirical treatments described below, while continuing diagnostic efforts. Physicians should also pay attention to systemic management such as fluid and electrolyte control, blood pressure control, and supportive therapies for AKI.. If the physician considers plasma exchange appropriate, it should be started immediately. ...
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OBJECTIVE: The complement system has been suggested to play a role in reperfusion injury which may result from an enhanced destruction of myocardial tissue or from an impairment of reflow. We investigated the influence of the C5b-9 complement complex
By Gerard V. Smith. The positive aspects of this publication to be able to be of unique curiosity to educational natural chemists are the creation (Chapter 1), which offers a brief direction at the thoughts and language of heterogeneous catalysis, covers natural response mechanisms of hydrogenation (Chapter 2), hydrogenolysis (Chapter 4), and oxidation (Chapter 6), a provides difficulties and ideas particular for operating heterogeneous catalytic natural reactions in resolution. those fabrics can complement complex chemistry courses.. Most artificial natural chemists use a number of "protecting teams" which they connect to useful teams (reactive teams of atoms) whereas a few response is being performed on one other a part of the molecule. those maintaining teams hinder reactions of the practical teams in the course of different reactions and are got rid of later via a heterogeneous catalytic procedure referred to as hydrogenolysis. One targeted function of this ebook, now not present in ...
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CONCLUSION: The molecular functions of candidate proteins suggest that SAPDS of NSCLC is involved in the activity of complement, protease inhibitor, transcription factor and structural constituent of ribosome. Biological process analysis shows the different between different syndromes of NSCLC in regulation of nucleobase, nucleoside, nucleotide and nucleic acid metabolism, protein metabolism and immune response. The SAPDS of NSCLC also plays an important role in the biological pathway of the complement cascade; terminal pathway of complement; innate immune system; initial triggering of complement; FOXA1 transcription factor network and immune system.. ...
Attack speed is a measurement of how long it takes to attack with a weapon. Skills can either increases your own or an allys attack speed (IAS), or decrease an enemys attack speed. The activation time of an attack skill is equal to the attack speed, except when the attack skill has an activation time listed. Attack speeds are measured in seconds between attacks. Changes in attack speeds are capped at 133% total for IAS (100% being your normal attack speed) and 50% total for DAS from normal. ...
Frequencies of verified positive TIL responses from selected fragment cultures (some patients had ,1) to p53 R175H, Y220C, G245S, R248Q, R248W, and R282W neoantigens. The upregulation of 41BB minus the background in response to mutated p53 peptide (CD4) or TMG (CD8) is reported. Types of T cell responses can be found in ...
Increased exposure of the tubular epithelium to filtered protein is a proposed mechanism of progressive renal failure associated with glomerular disease, but how this protein overload translates into tubular damage remains unclear. We have examined a model of adriamycin-induced proteinuria to determine the effect of locally synthesized C3, the central proinflammatory protein of the complement cascade. C3(-/-) kidney isografts placed in wild-type C3+/+ mice were protected from proteinuria-associated complement activation, tubular damage, and progressive renal failure despite the presence of abundant circulating C3. The quantity of urinary protein was unaffected by the absence of C3, and thus the influence of C3 was not explained by alteration in the filtered protein load. These results suggest that local synthesis of complement from renal epithelial cells is a critical mediator of tubular damage in proteinuria-associated renal disease. Our results concur with previous findings of increased ...
0029] Please refer to FIG. 7. FIG. 7 is a schematic top view of a variant of the finger-type, 3T-MOM capacitor according to another embodiment of this invention. As shown in FIG. 7, the finger-type, 3T-MOM capacitor 4a comprises a plurality of parallel-arranged vertical metal plates 142a, 142b, 142c, which are connected to a common terminal A, for example, ground or an output terminal. A segmental metal plate 144a and a segmental metal plate 146a intervene between the vertical metal plates 142a and 142b, wherein the segmental metal plate 144a is connected to a terminal B and the segmental metal plate 146a is connected to a terminal C. The segmental metal plate 144a is substantially aligned with the segmental metal plate 146a in a lateral direction. More specifically, the segmental metal plate 144a and the segmental metal plate 146a are arranged side-by-side along the lateral direction. A pair of segmental metal plates 144a and a pair of segmental metal plates 146a sandwich about the vertical ...
Learn how uncontrolled or excessive complement activation may play a role in several autoimmune and inflammatory diseases, and why APL-2 (pegcetacoplan) targeting of complement proteins at the level of C3 is being investigated as a treatment.
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Endocytosed GzmB is released into the cytosol within ~10 min of PFN loading(a) Within 5-10 min of treatment with sublytic native rat PFN and native human GzmB
At least 29 people were killed and many others injured when gunmen suspected to be members of the Boko Haram attacked Gwoza and Gamboru-Ngala in Borno State.
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In vitro studies have proved the presence of epitopes of CD59 in the surface of trophozoites of Entamoeba histolytica (E. histolytica). However, it has not been proved if CD59 molecules are expressed in the surface during the trophozoites tissue invasion. The aim of the present study was to determine whether the complement-regulatory protein CD59 is present on trophozoites of E. histolytica in human colon. Eleven specimens of amoebic colitis were studied by immunohistochemistry and electron microscopy techniques with a monoclonal antibody against human CD59 molecule. Our results show that a CD59-like molecule is expressed in trophozoites of E. histolytica found in colonic amebic lesions. Also, a CD59-like molecule was detected by western blot analysis in whole lysate of E. histolytica as well as on the plasma membrane by immunocytochemistry. These results suggest that E. histolytica can use CD59-like protein against the lytic action of membrane attack complex.
We have been interested in developing a complement dependent opsonophagocytic assay for Neisseria meningitidis serogroups A and C. Our problem is that when we add a complement source (baby rabbit) we get (as expected) bactericidal killing. We have tried to remove one of the terminal complement components but without much success (can remove component(s) but the removal process reduces the lytic complement activity when we reconstitute with the purified complement component). We have had success using a serum from a C7 defficient patient, however, this complement source is in limited supply. QUESTIONS: 1. is anyone else working on this? have you had success? 2. is there a method to remove terminal components in human sera that does not reduce complement activity when the component is added back? can this method be used for large vols. (600 ml)? 3. did I miss something in the literature? 4. any ideas or suggestions? P#: (404)639-3622 F#: (404)639-3115 George ...
Objective: Complement proteins have been associated with atherosclerosis and cardiovascular risk factors. Recent data suggest a potential role of complement protein C3 in clot stability with hypofibrinolytic and prothrombotic features. Women after menopause are at greater risk of cardiovascular disease and have significantly higher levels of C3 compared with younger women. To better understand the association between complement proteins and atherosclerosis we evaluated the cross-sectional associations between complement proteins C3 and C4 and hemostatic markers (factor VIIc, fibrinogen, plasminogen activator inhibitor-1 (PAI-1) antigen and tissue plasminogen activator (tPA) antigen) in a sample of midlife women.. Design: Pilot data from the Study of Womens Health Across the Nation (SWAN) Pittsburgh site were used. Both C3 and C4 were measured using frozen serum specimens by immunoturbidimetric assay. Data for hemostatic markers were available in SWAN Core data (factor VIIc and fibrinogen were ...
The objective of our study was the investigation of differential pathways in cardiac and skeletal muscles that protect one tissue and render the other susceptible to damage within a single organism. This approach might help to identify relevant pathways and possible candidates for therapeutic intervention. Dysferlin-deficient muscular dystrophy appeared to be a suitable model for this approach, because dysferlin is expressed in skeletal and cardiac muscles, but, clinically, the heart is thought to be unaffected in LGMD2B (25, 26). We demonstrate down-regulation of DAF/CD55 on mRNA and protein levels in dysferlin-deficient mice and LGMD2B patients, leading to activation of the MAC of the complement cascade on skeletal muscle cells. In vitro, dysferlin-deficient human myotubes are highly susceptible to complement attack, whereas normal human myoblasts/myotubes are not (19). The underlying mechanism appears to be a lack of myostatin, leading to down-regulation of SMAD proteins, with a negative ...
106. Abstract Protoplasts of Boergesenia forbesii (Hanvey) were treated with inhibitors of protein synthesis in order to investigate their effects on cellulose synthesis. Cellulose synthesis was reversibly inhibited by 10 M cycloheximide as assayed by fluorescence microscopy of Tinopal binding to cellulose. Freeze fracture and image analysis of cycloheximide-treated cells indicated a reduction in the number of intramembrane particles; however, the terminal synthesizing complexes remained at all times. Treatment with 10 M actinomycin D, when applied during the first hour of protoplast formation, irreversibly inhibits cellulose synthesis and terminal complex formation. De novo protein synthesis is required for cell wall regeneration by protoplasts. The data suggest that the structural subunits visualized in the terminal complex do not undergo signifi-cant turnover, but that there may exist an essential proteinaceous component of cellulose synthesis which must be continually renewed ...

CD59, an LY-6-like protein expressed in human lymphoid cells, regulates the action of the complement membrane attack complex on...CD59, an LY-6-like protein expressed in human lymphoid cells, regulates the action of the complement membrane attack complex on...

CD59, an LY-6-like protein expressed in human lymphoid cells, regulates the action of the complement membrane attack complex on ... regulates the action of the complement membrane attack complex on homologous cells.. J Exp Med 1 September 1989; 170 (3): 637- ... Physiologic relevance of the membrane attack complex inhibitory protein CD59 in human seminal plasma: CD59 is present on ... indicated that the inhibitory activity of the CD59 antigen is directed towards the homologous membrane attack complex. CD59 ...
more infohttps://rupress.org/jem/article/170/3/637/50090/CD59-an-LY-6-like-protein-expressed-in-human

Complement membrane attack complex - WikipediaComplement membrane attack complex - Wikipedia

Media related to Complement membrane attack complex at Wikimedia Commons. *Complement+Membrane+Attack+Complex at the US ... The membrane attack complex (MAC) or terminal complement complex (TCC) is a structure typically formed on the surface of ... The membrane attack complex is initiated when the complement protein C5 convertase cleaves C5 into C5a and C5b. All three ... The membrane-attack complex (MAC) forms transmembrane channels. These channels disrupt the cell membrane of target cells, ...
more infohttps://en.wikipedia.org/wiki/Complement_membrane_attack_complex

Bacterial killing by complement requires membrane attack complex formation via surface-bound C5 convertases - BioPortfolio.comBacterial killing by complement requires membrane attack complex formation via surface-bound C5 convertases - BioPortfolio.com

... triggered when complement enzymes cleave C5. At present, it is not ... ... The immune system kills bacteria by the formation of lytic membrane attack complexes (MACs), ... Bacterial killing by complement requires membrane attack complex formation via surface-bound C5 convertases. 15:28 EST 15 Feb ... More From BioPortfolio on "Bacterial killing by complement requires membrane attack complex formation via surface-bound C5 ...
more infohttps://www.bioportfolio.com/news/article/3903035/Bacterial-killing-by-complement-requires-membrane-attack-complex-formation-via-surface-bound.html

Aurintricarboxylic Acid Inhibits Complement Activation, Membrane Attack Complex, and Choroidal Neovascularization in a Model of...Aurintricarboxylic Acid Inhibits Complement Activation, Membrane Attack Complex, and Choroidal Neovascularization in a Model of...

Elevated membrane attack complex in human choroid with high risk complement factor H genotypes. Exp Eye Res . 2011; 93: 565-567 ... Aurintricarboxylic Acid Inhibits Complement Activation, Membrane Attack Complex, and Choroidal Neovascularization in a Model of ... Aurintricarboxylic Acid Inhibits Complement Activation, Membrane Attack Complex, and Choroidal Neovascularization in a Model of ... Selective inhibition of the membrane attack complex of complement by low molecular weight components of the aurin tricarboxylic ...
more infohttp://iovs.arvojournals.org/article.aspx?articleid=2203072

The membrane attack complex of complement: relation of C7 to the metastable membrane binding site of the intermediate complex...The membrane attack complex of complement: relation of C7 to the metastable membrane binding site of the intermediate complex...

The membrane attack complex of complement: relation of C7 to the metastable membrane binding site of the intermediate complex ... The membrane attack complex of complement: relation of C7 to the metastable membrane binding site of the intermediate complex ... The membrane attack complex of complement: relation of C7 to the metastable membrane binding site of the intermediate complex ... The membrane attack complex of complement: relation of C7 to the metastable membrane binding site of the intermediate complex ...
more infohttps://www.jimmunol.org/content/135/1/445?ijkey=316dcf253cc2e2270c7417db352e7d1ae8584b2b&keytype2=tf_ipsecsha

Potential association of LMNA-associated generalized lipodystrophy with juvenile dermatomyositis | SpringerLinkPotential association of LMNA-associated generalized lipodystrophy with juvenile dermatomyositis | SpringerLink

Complement membrane attack complex. CCL21. Chemokine (C-C motif) ligand 21. CD. Cluster of differentiation 3 ... LINC complex alterations in DMD and EDMD/CMT fibroblasts. Eur J Cell Biol. 2012;91:614-28.CrossRefPubMedPubMedCentralGoogle ... Nuclear membrane proteins are present within rimmed vacuoles in inclusion-body myositis. Muscle Nerve. 2006;34:406-16.CrossRef ... C5b9 immunostaining highlights complement deposition in capillaries associated with affected fibers; note normal control does ...
more infohttps://link.springer.com/article/10.1186/s40842-018-0058-3

Heme Flashcards by Stuart Abel | BrainscapeHeme Flashcards by Stuart Abel | Brainscape

MIRL: inhibits the complement membrane attack complex. 53 Indirect Coombs test. Used to detect in-vitro antibody-antigen ... Associated with inherited deficiency of inhibitors of the alternative complement pathway. Endothelial damage due to complement ... Antibodies directed against complex of heparin and platelet factor 4 (PF4). Heparin binding exposes a neoepitope on PF4, which ... Membrane may be excessive in liver disease. Intracellular hemoglobin may be lowered during iron deficiency, thalassemia, ...
more infohttps://www.brainscape.com/flashcards/heme-553791/packs/1099175

MEDLINE - Resultado de la b squeda |p gina  1|
	MEDLINE - Resultado de la b squeda |p gina 1|

The soluble membrane attack complex (sMAC) represents the terminal product of the complement cascade. We enrolled 47 HIV+ ... 0 (Anti-Retroviral Agents); 0 (Complement Membrane Attack Complex); 63231-63-0 (RNA). ... Soluble membrane attack complex in the blood and cerebrospinal fluid of HIV-infected individuals, relationship to HIV RNA, and ... with structures that mimic the native membrane-bound Env spike (gp160). Since engineering trimers can be limited by the ...
more infohttp://bases.bireme.br/cgi-bin/wxislind.exe/iah/online/?IsisScript=iah/iah.xis&base=MEDLINE&lang=e&nextAction=lnk&isisFrom=1&count=10&exprSearch=sida%20or%20vih

Search | IOVS | ARVO JournalsSearch | IOVS | ARVO Journals

TAGS: adenovirus infections, adenoviruses, antigens, cd55, complement system proteins, complement membrane attack complex, age- ... CD46, CD55, And CD59-mediated Attenuation Of Complement-induced Damage On Murine RPE Cells In-vitro And In-vivo: Therapeutic ... Decay Accelerating Factor (CD55)-Mediated Attenuation of Complement: Therapeutic Implications for Age-Related Macular ...
more infohttps://iovs.arvojournals.org/solr/searchresults.aspx?author=Kelly+N.+Ma

Glomerular Deposition of Mannose-Binding Lectin (MBL) Indicates a Novel Mechanism of Complement Activation in IgA Nephropathy -...Glomerular Deposition of Mannose-Binding Lectin (MBL) Indicates a Novel Mechanism of Complement Activation in IgA Nephropathy -...

... which is initiated by the MBL/MASPs complex, evidently contributes to the development of glomerular injury in a significant ... Complement Membrane Attack Complex / analysis Actions. * Search in PubMed * Search in MeSH ... Conclusion: The lectin pathway of complement activation, which is initiated by the MBL/MASPs complex, evidently contributes to ... Activation mechanism of the complement system]. Matsushita M. Matsushita M. Nihon Rinsho. 1999 Feb;57(2):291-7. Nihon Rinsho. ...
more infohttps://pubmed.ncbi.nlm.nih.gov/9719152/

Juvenile Dermatomyositis: Background, Pathophysiology, EtiologyJuvenile Dermatomyositis: Background, Pathophysiology, Etiology

... with capillary thrombosis and deposition of membrane attack complex and complement. [10, 11, 12, 14, 16] Immune complex ... Microvascular deposition of complement membrane attack complex in dermatomyositis. N Engl J Med. 1986 Feb 6. 314(6):329-34. [ ... Evidence suggests a complex interplay of the innate and adaptive immune systems with environmental triggers in a genetically ... Reed AM, Pachman L, Ober C. Molecular genetic studies of major histocompatibility complex genes in children with juvenile ...
more infohttps://emedicine.medscape.com/article/1417215-overview

Free Nursing Flashcards about MicrobiologyFree Nursing Flashcards about Microbiology

The complement membrane attack complex consists of. C6-C7-C8-C9. Acquired immunity has the hallmark of. memory and specificity ...
more infohttps://www.studystack.com/flashcard-192022

Membrane attack complex of complement (MAC): Three-dimensional analysis of MAC-phospholipid vesicle recombinants<...Membrane attack complex of complement (MAC): Three-dimensional analysis of MAC-phospholipid vesicle recombinants<...

Membrane attack complex of complement (MAC) : Three-dimensional analysis of MAC-phospholipid vesicle recombinants. / Podack, E ... Podack ER, Muller-Eberhard HJ, Horst H, Hoppe W. Membrane attack complex of complement (MAC): Three-dimensional analysis of MAC ... title = "Membrane attack complex of complement (MAC): Three-dimensional analysis of MAC-phospholipid vesicle recombinants", ... Podack, E. R., Muller-Eberhard, H. J., Horst, H., & Hoppe, W. (1982). Membrane attack complex of complement (MAC): Three- ...
more infohttps://miami.pure.elsevier.com/en/publications/membrane-attack-complex-of-complement-mac-three-dimensional-analy

Differential Killing of Salmonella enterica Serovar Typhi by Antibodies Targeting
         Vi and Lipopolysaccharide O:9...Differential Killing of Salmonella enterica Serovar Typhi by Antibodies Targeting Vi and Lipopolysaccharide O:9...

Complement C3. dc.subject. Complement Membrane Attack Complex. dc.subject. Humans. dc.subject. Immune Sera. ... Here we investigate the role of Vi capsule and antibodies against Vi and O:9 in antibody-dependent complement- and phagocyte- ... Our findings support a protective role for Vi capsule in preventing complement and phagocyte killing of Salmonella that can be ... However, purified human anti-Vi antibodies in the presence of complement are able to kill Vi-expressing Salmonella, while ...
more infohttps://dukespace.lib.duke.edu/dspace/handle/10161/13763?show=full

CD59 - CD59 glycoprotein precursor - Homo sapiens (Human) - CD59 gene & proteinCD59 - CD59 glycoprotein precursor - Homo sapiens (Human) - CD59 gene & protein

Potent inhibitor of the complement membrane attack complex (MAC) action. Acts by binding to the C8 and/or C9 complements of the ... Potent inhibitor of the complement membrane attack complex (MAC) action. Acts by binding to the C8 and/or C9 complements of the ... Plasma Membrane. *anchored component of external side of plasma membrane Source: MGI ,p>Inferred from Direct Assay,/p> ,p>Used ... Cell membrane, Membrane, Secreted. ,p>This section provides information on the disease(s) and phenotype(s) associated with a ...
more infohttps://www.uniprot.org/uniprot/P13987

The membrane attack complex of complement: Relation of C7 to the metastable membrane binding site of the intermediate complex...The membrane attack complex of complement: Relation of C7 to the metastable membrane binding site of the intermediate complex...

The membrane attack complex of complement: Relation of C7 to the metastable membrane binding site of the intermediate complex ... The membrane attack complex of complement: Relation of C7 to the metastable membrane binding site of the intermediate complex ... The membrane attack complex of complement : Relation of C7 to the metastable membrane binding site of the intermediate complex ... The membrane attack complex of complement: Relation of C7 to the metastable membrane binding site of the intermediate complex ...
more infohttps://miami.pure.elsevier.com/en/publications/the-membrane-attack-complex-of-complement-relation-of-c7-to-the-m

Recombinant Human CD59 protein (ab168079) | AbcamRecombinant Human CD59 protein (ab168079) | Abcam

Potent inhibitor of the complement membrane attack complex (MAC) action. Acts by binding to the C8 and/or C9 complements of the ... Membrane attack complex (MAC) inhibition factor. *Membrane attack complex inhibition factor. *Membrane inhibitor of reactive ... The soluble form from urine retains its specific complement binding activity, but exhibits greatly reduced ability to inhibit ... The N-glycosylation mainly consists of a family of biantennary complex-type structures with and without lactosamine extensions ...
more infohttps://www.abcam.com/recombinant-human-cd59-protein-ab168079.html

Frontiers | Secondary Hematoma Expansion and Perihemorrhagic Edema after Intracerebral Hemorrhage: From Bench Work to Practical...Frontiers | Secondary Hematoma Expansion and Perihemorrhagic Edema after Intracerebral Hemorrhage: From Bench Work to Practical...

These complex cascades lead to apoptosis or neuronal injury. By identifying the major modulators of cerebral edema after ICH, a ... These complex cascades lead to apoptosis or neuronal injury. By identifying the major modulators of cerebral edema after ICH, a ... Inflammatory cellular mediators, activation of the complement, by-products of coagulation and hemolysis such as thrombin and ... Inflammatory cellular mediators, activation of the complement, by-products of coagulation and hemolysis such as thrombin and ...
more infohttps://www.frontiersin.org/articles/10.3389/fneur.2017.00074/full

Frontiers | Potential Role of Myeloid-Derived Suppressor Cells (MDSCs) in Age-Related Macular Degeneration (AMD) | ImmunologyFrontiers | Potential Role of Myeloid-Derived Suppressor Cells (MDSCs) in Age-Related Macular Degeneration (AMD) | Immunology

Role of complement and complement membrane attack complex in laser-induced choroidal neovascularization. J Immunol. (2005) 174: ... Age-related increases in amyloid beta and membrane attack complex: evidence of inflammasome activation in the rodent eye. J ... Laser photocoagulation has also shown to induce the deposition of C3 and membrane attack complex (MAC) in the neovascular ... Down-regulation of human complement factor H sensitizes non-small cell lung cancer cells to complement attack and reduces in ...
more infohttps://www.frontiersin.org/articles/10.3389/fimmu.2020.00384/full

WikiPremed MCAT Course - The Lymphatic System and ImmunityWikiPremed MCAT Course - The Lymphatic System and Immunity

Complement membrane attack complex. The membrane attack complex is typically formed on the surface of intruding pathogenic ... Understand the various modes of activity of the complement system including the classical pathway, membrane attack complex, and ... Complement system. The complement system is a biochemical cascade which helps clear pathogens from an organism consisting of a ... Classical complement pathway. The classical pathway of activation of the complement system is a group of blood proteins that ...
more infohttps://www.wikipremed.com/mcat_course.php?code=040708

CD59 / Complement Regulatory Protein / Protectin Antibody - With BSA and Azide - Mouse Monoclonal Antibody [Clone 193-27 ] IF,...CD59 / Complement Regulatory Protein / Protectin Antibody - With BSA and Azide - Mouse Monoclonal Antibody [Clone 193-27 ] IF,...

CD59 / Complement Regulatory Protein / Protectin Antibody - With BSA and Azide, Mouse Monoclonal Antibody [Clone 193-27 ] ... This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during ... Potent inhibitor of the complement membrane attack complex (MAC) action. Acts by binding to the C8 and/or C9 complements of the ... Membrane attack complex inhibition factor, MACIF, Membrane inhibitor of reactive lysis, MIRL, Protectin, CD59, CD59, MIC11, ...
more infohttp://www.abgent.com/products/AH12764-CD59--Complement-Regulatory-Protein--Protectin-Antibody-With-BSA-and-Azide

CD59 / Complement Regulatory Protein / Protectin Antibody - Without BSA and Azide - Mouse Monoclonal Antibody [Clone SPM616 ]...CD59 / Complement Regulatory Protein / Protectin Antibody - Without BSA and Azide - Mouse Monoclonal Antibody [Clone SPM616 ]...

CD59 / Complement Regulatory Protein / Protectin Antibody - Without BSA and Azide, Mouse Monoclonal Antibody [Clone SPM616 ] ... This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during ... Potent inhibitor of the complement membrane attack complex (MAC) action. Acts by binding to the C8 and/or C9 complements of the ... Membrane attack complex inhibition factor, MACIF, Membrane inhibitor of reactive lysis, MIRL, Protectin, CD59, CD59, MIC11, ...
more infohttp://www.abgent.com/products/AH12772-CD59--Complement-Regulatory-Protein--Protectin-Antibody-Without-BSA-and-Azide

JCI -
Volume 77, Issue 3JCI - Volume 77, Issue 3

Complement membrane attack complex stimulates production of reactive oxygen metabolites by cultured rat mesangial cells.. ... Complement membrane attack complex stimulates production of reactive oxygen metabolites by cultured rat mesangial cells.. ... To explore possible mechanisms by which complement membrane attack complexes (MAC) that are deposited in the glomerular ... A T cell surface membrane-associated glycoprotein, Tp40 (40,000 mol wt), also designated as CD-7, was not expressed by the T ...
more infohttps://www.jci.org/77/3

Amebiasis Medication: Antibiotics, OtherAmebiasis Medication: Antibiotics, Other

Inhibition of the complement membrane attack complex by the galactose-specific adhesion of Entamoeba histolytica. J Clin Invest ...
more infohttps://emedicine.medscape.com/article/212029-medication

des-Arg-(77) complement C3a
     Summary Report | CureHunterdes-Arg-(77) complement C3a Summary Report | CureHunter

... complement C3a: C3a without the COOH-terminal arginine at the 77-position; also known as the acylation-stimulating protein or ... Complement Membrane Attack Complex (Membrane Attack Complex) 7. Leukotrienes 8. Uric Acid (Urate) ... Complement System Proteins: 21537*Complement C3: 812*Complement C3a: 43*des-Arg-(77) complement C3a: 14 ... complement C3a, des-Arg-(77); C3a des-Arg; C3a des-Arg(77); C3a des-Arg77; complement 3a, des-Arg-; complement 3a, des-arginine ...
more infohttp://www.curehunter.com/public/keywordSummaryC044541.do
  • Autoantibodies directed against an unknown endothelial antigen may cause vascular injury, resulting in ischemia and subsequent muscle damage with increased expression of major histocompatibility complex (MHC) class I and II. (medscape.com)
  • Understand the mechanisms of the CD (cluster of differentiation) system, MHC (major histocompatibility complex), B cell receptor, and T cell receptor in antigen presentation and recognition. (wikipremed.com)
  • Cooperation between major histocompatibility complex mismatched mononuclear cells from a human chimera in the production of antigen-specific antibody. (jci.org)
  • This finding is in contrast with the concept that antigen recognition by T cells is major histocompatibility complex (MHC) restricted. (jci.org)
  • The lymphatic system is a complex network of lymphoid organs, lymph nodes, lymph ducts, tissues, lymph capillaries and lymph vessels that produce and transport lymph fluid from tissues to the circulatory system. (wikipremed.com)
  • Here we investigate the role of Vi capsule and antibodies against Vi and O:9 in antibody-dependent complement- and phagocyte-mediated killing of Salmonella. (duke.edu)
  • However, purified human anti-Vi antibodies in the presence of complement are able to kill Vi-expressing Salmonella, while killing by anti-O:9 antibodies is inversely related to Vi expression. (duke.edu)
  • Our findings support a protective role for Vi capsule in preventing complement and phagocyte killing of Salmonella that can be overcome by specific anti-Vi antibodies, but only to a limited extent by anti-O:9 antibodies. (duke.edu)
  • The N-glycosylation mainly consists of a family of biantennary complex-type structures with and without lactosamine extensions and outer arm fucose residues. (abcam.com)
  • Subsequently, the Bruch's membrane of adult mice was damaged using an argon laser, followed by intravitreal injection of ATA. (arvojournals.org)
  • Urate crystals are able to directly initiate, to amplify, and to sustain an intense inflammatory attack because of their ability to stimulate the synthesis and release of humoral and cellular inflammatory mediators. (goutpal.com)
  • Potent inhibitor of the complement membrane attack complex (MAC) action. (uniprot.org)
  • While in vitro and in some cases in vivo studies provide good support for these models, the complex nature of the sand fly bite makes it difficult to ascertain the quantitative importance of these to the final parasitic outcome. (hindawi.com)
  • Individuals homozygous for a Y402H polymorphism in Factor H have elevated levels of membrane attack complex (MAC) in their choroidal blood vessels and RPE relative to individuals homozygous for the wild-type allele. (arvojournals.org)
  • The results strongly suggest that structures of C7 are responsible for the expression of the membrane binding site of metastable C5b-7. (jimmunol.org)