A serum protein which is important in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. This enzyme cleaves the COMPLEMENT C3B-bound COMPLEMENT FACTOR B to form C3bBb which is ALTERNATIVE PATHWAY C3 CONVERTASE.
Extravasation of blood into the skin, resulting in a nonelevated, rounded or irregular, blue or purplish patch, larger than a petechia.
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.
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.
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).
A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb.
A plasma serine proteinase that cleaves the alpha-chains of C3b and C4b in the presence of the cofactors COMPLEMENT FACTOR H and C4-binding protein, respectively. It is a 66-kDa glycoprotein that converts C3b to inactivated C3b (iC3b) followed by the release of two fragments, C3c (150-kDa) and C3dg (41-kDa). It was formerly called KAF, C3bINF, or enzyme 3b inactivator.
A 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.
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.
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).
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.
Enzymes that activate one or more COMPLEMENT PROTEINS in the complement system leading to the formation of the COMPLEMENT MEMBRANE ATTACK COMPLEX, an important response in host defense. They are enzymes in the various COMPLEMENT ACTIVATION pathways.
A component of the CLASSICAL COMPLEMENT PATHWAY. C2 is cleaved by activated COMPLEMENT C1S into COMPLEMENT C2B and COMPLEMENT C2A. C2a, the COOH-terminal fragment containing a SERINE PROTEASE, combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).
Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence.
A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.
C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX.
Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.
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.
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.
Proteins in the cerebrospinal fluid, normally albumin and globulin present in the ratio of 8 to 1. Increases in protein levels are of diagnostic value in neurological diseases. (Brain and Bannister's Clinical Neurology, 7th ed, p221)
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)
Microtubule-associated proteins that are mainly expressed in neurons. Tau proteins constitute several isoforms and play an important role in the assembly of tubulin monomers into microtubules and in maintaining the cytoskeleton and axonal transport. Aggregation of specific sets of tau proteins in filamentous inclusions is the common feature of intraneuronal and glial fibrillar lesions (NEUROFIBRILLARY TANGLES; NEUROPIL THREADS) in numerous neurodegenerative disorders (ALZHEIMER DISEASE; TAUOPATHIES).
Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.
A fibrous protein complex that consists of proteins folded into a specific cross beta-pleated sheet structure. This fibrillar structure has been found as an alternative folding pattern for a variety of functional proteins. Deposits of amyloid in the form of AMYLOID PLAQUES are associated with a variety of degenerative diseases. The amyloid structure has also been found in a number of functional proteins that are unrelated to disease.
A prodromal phase of cognitive decline that may precede the emergence of ALZHEIMER DISEASE and other dementias. It may include impairment of cognition, such as impairments in language, visuospatial awareness, ATTENTION and MEMORY.
Persons with physical or mental disabilities that affect or limit their activities of daily living and that may require special accommodations.
A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence.
Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.
A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.
Sequential operating programs and data which instruct the functioning of a digital computer.
The portion of an interactive computer program that issues messages to and receives commands from a user.
Organized activities related to the storage, location, search, and retrieval of information.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
A republic stretching from the Indian Ocean east to New Guinea, comprising six main islands: Java, Sumatra, Bali, Kalimantan (the Indonesian portion of the island of Borneo), Sulawesi (formerly known as the Celebes) and Irian Jaya (the western part of New Guinea). Its capital is Djakarta. The ethnic groups living there are largely Chinese, Arab, Eurasian, Indian, and Pakistani; 85% of the peoples are of the Islamic faith.
A parliamentary democracy with a constitutional monarch in southeast Asia, consisting of 11 states (West Malaysia) on the Malay Peninsula and two states (East Malaysia) on the island of BORNEO. It is also called the Federation of Malaysia. Its capital is Kuala Lumpur. Before 1963 it was the Union of Malaya. It reorganized in 1948 as the Federation of Malaya, becoming independent from British Malaya in 1957 and becoming Malaysia in 1963 as a federation of Malaya, Sabah, Sarawak, and Singapore (which seceded in 1965). The form Malay- probably derives from the Tamil malay, mountain, with reference to its geography. (From Webster's New Geographical Dictionary, 1988, p715 & Room, Brewer's Dictionary of Names, 1992, p329)
NATIONAL LIBRARY OF MEDICINE service for health professionals and consumers. It links extensive information from the National Institutes of Health and other reviewed sources of information on specific diseases and conditions.
In Chinese philosophy and religion, two principles, one negative, dark, and feminine (yin) and one positive, bright, and masculine (yang), from whose interaction all things are produced and all things are dissolved. As a concept the two polar elements referred originally to the shady and sunny sides of a valley or a hill but it developed into the relationship of any contrasting pair: those specified above (female-male, etc.) as well as cold-hot, wet-dry, weak-strong, etc. It is not a distinct system of thought by itself but permeates Chinese life and thought. A balance of yin and yang is essential to health. A deficiency of either principle can manifest as disease. (Encyclopedia Americana)
A ubiquitously expressed zinc finger-containing protein that acts both as a repressor and activator of transcription. It interacts with key regulatory proteins such as TATA-BINDING PROTEIN; TFIIB; and ADENOVIRUS E1A PROTEINS.
Information intended for potential users of medical and healthcare services. There is an emphasis on self-care and preventive approaches as well as information for community-wide dissemination and use.
Studies beyond the bachelor's degree at an institution having graduate programs for the purpose of preparing for entrance into a specific field, and obtaining a higher degree.
The teaching staff and members of the administrative staff having academic rank in an educational institution.
Individuals enrolled in a school or formal educational program.
Educational programs for pharmacists who have a bachelor's degree or a Doctor of Pharmacy degree entering a specific field of pharmacy. They may lead to an advanced degree.
The teaching staff and members of the administrative staff having academic rank in a medical school.

Structural basis of profactor D activation: from a highly flexible zymogen to a novel self-inhibited serine protease, complement factor D. (1/132)

The crystal structure of profactor D, determined at 2.1 A resolution with an Rfree and an R-factor of 25.1 and 20.4%, respectively, displays highly flexible or disordered conformation for five regions: N-22, 71-76, 143-152, 187-193 and 215-223. A comparison with the structure of its mature serine protease, complement factor D, revealed major conformational changes in the similar regions. Comparisons with the zymogen-active enzyme pairs of chymotrypsinogen, trypsinogen and prethrombin-2 showed a similar distribution of the flexible regions. However, profactor D is the most flexible of the four, and its mature enzyme displays inactive, self-inhibited active site conformation. Examination of the surface properties of the N-terminus-binding pocket indicates that Ile16 may play the initial positioning role for the N-terminus, and Leu17 probably also helps in inducing the required conformational changes. This process, perhaps shared by most chymotrypsinogen-like zymogens, is followed by a factor D-unique step, the re-orientation of an external Arg218 to an internal position for salt-bridging with Asp189, leading to the generation of the self-inhibited factor D.  (+info)

Calcium-independent haemolysis via the lectin pathway of complement activation in the guinea-pig and other species*. (2/132)

We previously reported that complement-dependent haemolysis of sheep erythrocytes (E) coated with mannan (M) and sensitized with human mannan-binding lectin (MBL) via the lectin pathway in man occurs in Mg-EGTA and requires alternative pathway amplification. Calcium was required for MBL binding to E-M, but once the E-M-MBL intermediate was formed, MBL was retained and haemolysis occurred in the absence of calcium. Comparable or greater lectin pathway haemolysis in the absence of calcium was observed upon incubation of E-M-MBL in guinea-pig, rat, dog and pig sera, and was further investigated in the guinea-pig, in which titres were much higher ( approximately 14-fold) than in man, and in contrast to humans, greater than classical pathway haemolytic activity. As in human serum, no lysis was observed in C4- or C2-deficient guinea-pig serum until purified C4 or C2, respectively, were restored. However, lectin pathway haemolytic activity in the guinea-pig did not require the alternative pathway. Removal (>98%) of factor D activity by three sequential passages through Sephadex G-75, resulting in serum which retained a normal classical pathway but no alternative pathway haemolytic activity, did not reduce the ability of guinea-pig serum to mediate haemolysis via the lectin pathway. Further, the C3-convertase formed via the lectin pathway (E-M-MBL-C4,2) lysed in C2-deficient guinea-pig but not human serum chelated with EDTA, a condition which precludes alternative pathway amplification. Thus, lectin pathway haemolysis occurs efficiently in guinea-pig serum, in the absence of calcium and without requirement for alternative pathway amplification. The guinea-pig provides a model for studying the assembly and haemolytic function of a lectin pathway which contrasts with the lectin pathway of man, and allows for comparisons that may help clarify the role of this pathway in complement biology.  (+info)

The Arthus reaction in rodents: species-specific requirement of complement. (3/132)

We induced reverse passive Arthus (RPA) reactions in the skin of rodents and found that the contribution of complement to immune complex-mediated inflammation is species specific. Complement was found to be necessary in rats and guinea pigs but not in C57BL/6J mice. In rats, within 4 h after initiation of an RPA reaction, serum alternative pathway hemolytic titers decreased significantly below basal levels, whereas classical pathway titers were unchanged. Thus the dermal reaction proceeds coincident with systemic activation of complement. The serine protease inhibitor BCX 1470, which blocks the esterolytic and hemolytic activities of the complement enzymes Cls and factor D in vitro, also blocked development of RPA-induced edema in the rat. These data support the proposal that complement-mediated processes are of major importance in the Arthus reaction in rats and guinea pigs, and suggest that BCX 1470 will be useful as an anti-inflammatory agent in diseases where complement activation is known to be detrimental.  (+info)

Mutational analysis of the primary substrate specificity pocket of complement factor B. Asp(226) is a major structural determinant for p(1)-Arg binding. (4/132)

Factor B is a serine protease, which despite its trypsin-like specificity has Asn instead of the typical Asp at the bottom of the S(1) pocket (position 189, chymotrypsinogen numbering). Asp residues are present at positions 187 and 226 and either one could conceivably provide the negative charge for binding the P(1)-Arg of the substrate. Determination of the crystal structure of the factor B serine protease domain has revealed that the side chain of Asp(226) is within the S(1) pocket, whereas Asp(187) is located outside the pocket. To investigate the possible role of these atypical structural features in substrate binding and catalysis, we constructed a panel of mutants of these residues. Replacement of Asp(187) caused moderate (50-60%) decrease in hemolytic activity, compared with wild type factor B, whereas replacement of Asn(189) resulted in more profound reductions (71-95%). Substitutions at these two positions did not significantly affect assembly of the alternative pathway C3 convertase. In contrast, elimination of the negative charge from Asp(226) completely abrogated hemolytic activity and also affected formation of the C3 convertase. Kinetic analyses of the hydrolysis of a P(1)-Arg containing thioester by selected mutants confirmed that residue Asp(226) is a primary structural determinant for P(1)-Arg binding and catalysis.  (+info)

C/EBPbeta, when expressed from the C/ebpalpha gene locus, can functionally replace C/EBPalpha in liver but not in adipose tissue. (5/132)

Knockout of C/EBPalpha causes a severe loss of liver function and, subsequently, neonatal lethality in mice. By using a gene replacement approach, we generated a new C/EBPalpha-null mouse strain in which C/EBPbeta, in addition to its own expression, substituted for C/EBPalpha expression in tissues. The homozygous mutant mice C/ebpalpha(beta/beta) are viable and fertile and show none of the overt liver abnormalities found in the previous C/EBPalpha-null mouse line. Levels of hepatic PEPCK mRNA are not different between C/ebpalpha(beta/beta) and wild-type mice. However, despite their normal growth rate, C/ebpalpha(beta/beta) mice have markedly reduced fat storage in their white adipose tissue (WAT). Expression of two adipocyte-specific factors, adipsin and leptin, is significantly reduced in the WAT of C/ebpalpha(beta/beta) mice. In addition, expression of the non-adipocyte-specific genes for transferrin and cysteine dioxygenase is reduced in WAT but not in liver. Our study demonstrates that when expressed from the C/ebpalpha gene locus, C/EBPbeta can act for C/EBPalpha to maintain liver functions during development. Moreover, our studies with the C/ebpalpha(beta/beta) mice provide new insights into the nonredundant functions of C/EBPalpha and C/EBPbeta on gene regulation in WAT.  (+info)

Induction of adipocyte-specific gene expression is correlated with mammary tumor regression by the retinoid X receptor-ligand LGD1069 (targretin). (6/132)

Targretin (LGD1069; a high-affinity ligand for the retinoid X receptors) is an efficacious chemotherapeutic and chemopreventive agent in the N-nitroso-N-methylurea-induced rat mammary carcinoma model. To evaluate the molecular action of LGD1069 in mammary carcinoma we have examined gene expression patterns in controls and nonresponding tumors compared with tumors undergoing regression (responding) by LGD1069. When compared with controls or nonresponding tumors, the expression of adipocyte-related genes such as adipocyte P2 (aP2), adipsin, peroxisome proliferator-activated receptor gamma (PPARgamma), and lipoprotein lipase was elevated in LGD1069-responding tumors. Further analysis showed that gene expression changes occurred rapidly, in as little as 6 h, after the first dose of LGD1069. Immunohistochemical analysis showed that aP2 protein was also highly expressed in responding tumors when compared with control or nonresponding tumors. More importantly, aP2 protein was localized in the tumor cells in addition to the adipocytes present in the tumors. Similar changes in gene expression and inhibition in growth were seen in tumor cells (cloned from N-nitroso-N-methylurea-induced carcinoma) exposed to LGD1069 in vitro. These data suggest that tumor regression by LGD1069 involves differentiation induction along the adipocyte lineage.  (+info)

A comparison of on-line hemodiafiltration and high-flux hemodialysis: a prospective clinical study. (7/132)

Some of the morbidity associated with chronic hemodialysis is thought to result from retention of large molecular weight solutes that are poorly removed by diffusion in conventional hemodialysis. Hemodiafiltration combines convective and diffusive solute removal in a single therapy. The hypothesis that hemodiafiltration provides better solute removal than high-flux hemodialysis was tested in a prospective, randomized clinical trial. Patients were randomized to either on-line postdilution hemodiafiltration or high-flux hemodialysis. The groups did not differ in body size, treatment time, blood flow rate, or net fluid removal. The filtration volume in hemodiafiltration was 21 +/-1 L. Therapy prescriptions were unchanged for a 12-mo study period. Removal of both small (urea and creatinine) and large (ss(2)-microglobulin and complement factor D) solutes was significantly greater for hemodiafiltration than for high-flux hemodialysis. The increased urea and creatinine removal did not result in lower pretreatment serum concentrations in the hemodiafiltration group. Pretreatment plasma beta(2)-microglobulin concentrations decreased with time (P< 0.001); however, the decrease was similar for both therapies (P = 0.317). Pretreatment plasma complement factor D concentrations also decreased with time (P<0.001), and the decrease was significantly greater with hemodiafiltration than with high-flux hemodialysis (P = 0.010). The conclusion is that on-line hemodiafiltration provides superior solute removal to high-flux hemodialysis over a wide molecular weight range. The improved removal may not result in lower pretreatment plasma concentrations, however, possibly because of limitations in mass transfer rates within the body.  (+info)

A family with complement factor D deficiency. (8/132)

A complement factor D deficiency was found in a young woman who had experienced a serious Neisseria meningitidis infection, in a deceased family member with a history of meningitis, and in three relatives without a history of serious infections. The patient and these three relatives showed a normal activity of the classical complement pathway, but a very low activity of the alternative complement pathway and a very low capacity to opsonize Escherichia coli and N. meningitidis (isolated from the patient) for phagocytosis by normal human neutrophils. The alternative pathway-dependent hemolytic activity and the opsonizing capacity of these sera were restored by addition of purified factor D. The family had a high degree of consanguinity, and several other family members exhibited decreased levels of factor D. The gene encoding factor D was found to contain a point mutation that changed the TCG codon for serine 42 into a TAG stop codon. This mutation was found in both alleles of the five completely factor D-deficient family members and in one allele of 21 other members of the same family who had decreased or low-normal factor D levels in their serum. The gene sequence of the signal peptide of human factor D was also identified. Our report is the first, to our knowledge, to document a Factor D gene mutation. The mode of inheritance of factor D deficiency is autosomal recessive, in accordance with the localization of the Factor D gene on chromosome 19. Increased susceptibility for infections in individuals with a partial factor D deficiency is unlikely.  (+info)

Complement Factor D is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Specifically, Factor D is a serine protease that is involved in the alternative pathway of the complement system.

In this pathway, Factor D helps to cleave another protein called Factor B, which then activates a complex called the C3 convertase. The C3 convertase cleaves complement component 3 (C3) into C3a and C3b, leading to the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, causing its lysis and removal from the body.

Deficiencies or mutations in Complement Factor D can lead to an impaired alternative pathway and increased susceptibility to certain infections, particularly those caused by Neisseria bacteria. Additionally, abnormal regulation of the complement system has been implicated in a variety of diseases, including autoimmune disorders, inflammatory conditions, and neurodegenerative diseases.

Ecchymosis is a medical term that refers to a discoloration of the skin caused by the leakage of blood from ruptured blood vessels into the tissues beneath. It is typically caused by trauma or injury to the affected area, which results in the escape of blood from the damaged blood vessels. The escaped blood collects under the skin, causing a bruise or a purple, blue, or blackish patch on the skin's surface.

Ecchymosis can occur anywhere on the body and can vary in size and shape depending on the extent of the injury. While ecchymosis is generally harmless and resolves on its own within a few days to a week, it can be a sign of an underlying medical condition, such as a bleeding disorder or a blood vessel abnormality. In these cases, further evaluation and treatment may be necessary.

A Complement Hemolytic Activity Assay is a laboratory test used to measure the functionality and activity level of the complement system, which is a part of the immune system. The complement system is a group of proteins that work together to help eliminate pathogens from the body.

The assay measures the ability of the complement system to lyse (break open) red blood cells. This is done by mixing the patient's serum (the liquid portion of the blood) with antibody-coated red blood cells and incubating them together. The complement proteins in the serum will then bind to the antibodies on the red blood cells and cause them to lyse.

The degree of hemolysis (red blood cell lysis) is directly proportional to the activity level of the complement system. By measuring the amount of hemolysis, the assay can determine whether the complement system is functioning properly and at what level of activity.

This test is often used to diagnose or monitor complement-mediated diseases such as autoimmune disorders, infections, and some types of cancer. It may also be used to evaluate the effectiveness of treatments that target the complement system.

The alternative complement pathway is one of the three initiating pathways of the complement system, which is a part of the innate immune system that helps to clear pathogens and damaged cells from the body. The other two pathways are the classical and lectin pathways.

The alternative pathway is continuously activated at a low level, even in the absence of infection or injury, through the spontaneous cleavage of complement component C3 into C3a and C3b by the protease factor D in the presence of magnesium ions. The generated C3b can then bind covalently to nearby surfaces, including pathogens and host cells.

On self-surfaces, regulatory proteins like decay-accelerating factor (DAF) or complement receptor 1 (CR1) help to prevent the formation of the alternative pathway convertase and thus further activation of the complement system. However, on foreign surfaces, the C3b can recruit more complement components, forming a complex called the alternative pathway convertase (C3bBb), which cleaves additional C3 molecules into C3a and C3b.

The generated C3b can then bind to the surface and participate in the formation of the membrane attack complex (MAC), leading to the lysis of the target cell. The alternative pathway plays a crucial role in the defense against gram-negative bacteria, fungi, and parasites, as well as in the clearance of immune complexes and apoptotic cells. Dysregulation of the alternative complement pathway has been implicated in several diseases, including autoimmune disorders and atypical hemolytic uremic syndrome (aHUS).

Complement Factor H is a protein involved in the regulation of the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Specifically, Complement Factor H helps to regulate the activation and deactivation of the complement component C3b, preventing excessive or unwanted activation of the complement system and protecting host tissues from damage.

Complement Factor H is a crucial protein in maintaining the balance between the protective effects of the complement system and the potential for harm to the body's own cells and tissues. Deficiencies or mutations in Complement Factor H have been associated with several diseases, including age-related macular degeneration (AMD), atypical hemolytic uremic syndrome (aHUS), and C3 glomerulopathy.

Complement Factor B is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. Specifically, Factor B is a component of the alternative pathway of the complement system, which provides a rapid and amplified response to microbial surfaces.

Factor B is cleaved by another protease called Factor D into two fragments, Ba and Bb. The formation of the C3 convertase (C3bBb) is essential for the activation of the alternative pathway. This complex can cleave and activate more C3 molecules, leading to a cascade of reactions that result in the formation of the membrane attack complex (MAC), which forms pores in the membranes of target cells, causing their lysis and elimination.

Deficiencies or mutations in Complement Factor B can lead to various complement-mediated diseases, such as atypical hemolytic uremic syndrome (aHUS) and age-related macular degeneration (AMD).

Complement Factor I is a protein involved in the regulation of the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Specifically, Complement Factor I is a serine protease that regulates the complement component C3b by cleaving it into inactive fragments, thereby preventing the excessive activation of the complement system and protecting host tissues from damage.

Complement Factor I functions in conjunction with other regulatory proteins, such as complement receptor 1 (CR1) and membrane cofactor protein (MCP), to control the activity of the complement system at various stages. Deficiencies or mutations in Complement Factor I have been associated with several diseases, including atypical hemolytic uremic syndrome (aHUS), age-related macular degeneration (AMD), and systemic lupus erythematosus (SLE).

Complement C3 is a protein that plays a central role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C3 can be activated through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Once activated, it breaks down into two fragments, C3a and C3b.

C3a is an anaphylatoxin that helps to recruit immune cells to the site of infection or injury, while C3b plays a role in opsonization, which is the process of coating pathogens or damaged cells with proteins to make them more recognizable to the immune system. Additionally, C3b can also activate the membrane attack complex (MAC), which forms a pore in the membrane of target cells leading to their lysis or destruction.

In summary, Complement C3 is an important protein in the complement system that helps to identify and eliminate pathogens and damaged cells from the body through various mechanisms.

Complement activation is the process by which the complement system, a part of the immune system, is activated to help eliminate pathogens and damaged cells from the body. The complement system consists of a group of proteins that work together to recognize and destroy foreign substances.

Activation of the complement system can occur through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteolytic reactions that ultimately result in the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, leading to its lysis and removal.

The classical pathway is typically activated by the binding of antibodies to antigens on the surface of a pathogen or damaged cell. The lectin pathway is activated by the recognition of specific carbohydrate structures on the surface of microorganisms. The alternative pathway can be spontaneously activated and serves as an amplification loop for both the classical and lectin pathways.

Complement activation plays a crucial role in the immune response, but uncontrolled or excessive activation can also lead to tissue damage and inflammation. Dysregulation of complement activation has been implicated in various diseases, including autoimmune disorders, inflammatory conditions, and neurodegenerative diseases.

The complement system is a group of proteins found in the blood and on the surface of cells that when activated, work together to help eliminate pathogens such as bacteria, viruses, and fungi from the body. The proteins are normally inactive in the bloodstream. When they encounter an invading microorganism or foreign substance, a series of reactions take place leading to the activation of the complement system. Activation results in the production of effector molecules that can punch holes in the cell membranes of pathogens, recruit and activate immune cells, and help remove debris and dead cells from the body.

There are three main pathways that can lead to complement activation: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteins that work together in a cascade-like manner to amplify the response and generate effector molecules. The three main effector molecules produced by the complement system are C3b, C4b, and C5b. These molecules can bind to the surface of pathogens, marking them for destruction by other immune cells.

Complement proteins also play a role in the regulation of the immune response. They help to prevent excessive activation of the complement system, which could damage host tissues. Dysregulation of the complement system has been implicated in a number of diseases, including autoimmune disorders and inflammatory conditions.

In summary, Complement System Proteins are a group of proteins that play a crucial role in the immune response by helping to eliminate pathogens and regulate the immune response. They can be activated through three different pathways, leading to the production of effector molecules that mark pathogens for destruction. Dysregulation of the complement system has been linked to various diseases.

Complement C3b is a protein fragment that plays a crucial role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. C3b is generated during the activation of the complement system, particularly via the classical, lectin, and alternative pathways.

Once formed, C3b can bind covalently to the surface of microbes or other target particles, marking them for destruction by other components of the immune system. Additionally, C3b can interact with other proteins in the complement system to generate the membrane attack complex (MAC), which forms pores in the membranes of targeted cells, leading to their lysis and removal.

In summary, Complement C3b is a vital protein fragment involved in the recognition, tagging, and elimination of pathogens and damaged cells during the immune response.

Complement activating enzymes are proteins that play a crucial role in the activation of the complement system, which is a part of the immune system. The complement system is a complex series of biochemical reactions that help to eliminate pathogens and damaged cells from the body.

There are several types of complement activating enzymes, including:

1. Classical pathway activators: These include the C1, C4, and C2 components of the complement system. When activated, they trigger a series of reactions that lead to the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, leading to its lysis.
2. Alternative pathway activators: These include factors B, D, and P. They are constantly active at low levels and can be activated by surfaces that are not normally found in the body, such as bacterial cell walls. Once activated, they also trigger the formation of the MAC.
3. Lectin pathway activators: These include mannose-binding lectin (MBL) and ficolins. They bind to carbohydrates on the surface of microbes and activate the complement system through the MBL-associated serine proteases (MASPs).

Overall, complement activating enzymes play a critical role in the immune response by helping to identify and eliminate pathogens and damaged cells from the body.

Complement C2 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. Specifically, C2 is a component of the classical complement pathway, which is activated by the binding of antibodies to antigens on the surface of foreign particles or cells.

When the classical pathway is activated, C2 is cleaved into two fragments: C2a and C2b. C2a then binds to C4b to form the C3 convertase (C4b2a), which cleaves C3 into C3a and C3b. C3b can then go on to form the membrane attack complex, which creates a pore in the membrane of the target cell, leading to its lysis.

In summary, Complement C2 is a protein that helps to activate the complement system and destroy foreign particles or cells through the formation of the C3 convertase and the membrane attack complex.

Complement C3b inactivator proteins, also known as complement regulators or decay-accelerating factor (DAF), are a group of proteins that play a crucial role in regulating the complement system. The complement system is a part of the immune system that helps to eliminate pathogens and damaged cells from the body.

The complement C3b inactivator proteins include two main types: complement receptor 1 (CR1) and decay-accelerating factor (DAF). These proteins work by regulating the formation of the membrane attack complex (MAC), a protein structure that forms pores in the cell membrane, leading to cell lysis.

Complement C3b inactivator proteins bind to C3b and C4b components of the complement system, preventing them from forming the MAC. By doing so, they help to prevent excessive activation of the complement system, which can damage healthy cells and tissues.

Deficiencies or dysfunction of complement C3b inactivator proteins have been associated with several diseases, including autoimmune disorders, inflammatory diseases, and infectious diseases. Therefore, understanding the role of these proteins in regulating the complement system is essential for developing new therapies to treat these conditions.

Complement C4 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C4 is involved in the early stages of the complement activation cascade, where it helps to identify and tag foreign or abnormal cells for destruction by other components of the immune system.

Specifically, Complement C4 can be cleaved into two smaller proteins, C4a and C4b, during the complement activation process. C4b then binds to the surface of the target cell and helps to initiate the formation of the membrane attack complex (MAC), which creates a pore in the cell membrane and leads to lysis or destruction of the target cell.

Deficiencies or mutations in the Complement C4 gene can lead to various immune disorders, including certain forms of autoimmune diseases and susceptibility to certain infections.

Complement C5 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. The complement system is a complex series of biochemical reactions that help to identify and destroy foreign substances, such as bacteria and viruses.

Complement C5 is one of several proteins in the complement system that are activated in a cascading manner in response to an activating event, such as the binding of an antibody to a pathogen. Once activated, Complement C5 can be cleaved into two smaller proteins, C5a and C5b.

C5a is a powerful anaphylatoxin, which means it can cause the release of histamine from mast cells and basophils, leading to inflammation and increased vascular permeability. It also acts as a chemoattractant, drawing immune cells to the site of infection or injury.

C5b, on the other hand, plays a role in the formation of the membrane attack complex (MAC), which is a protein structure that can punch holes in the membranes of pathogens, leading to their lysis and destruction.

Overall, Complement C5 is an important component of the immune system's response to infection and injury, helping to eliminate pathogens and damaged cells from the body.

Macular degeneration, also known as age-related macular degeneration (AMD), is a medical condition that affects the central part of the retina, called the macula. The macula is responsible for sharp, detailed vision, which is necessary for activities such as reading, driving, and recognizing faces.

In AMD, there is a breakdown or deterioration of the macula, leading to gradual loss of central vision. There are two main types of AMD: dry (atrophic) and wet (exudative). Dry AMD is more common and progresses more slowly, while wet AMD is less common but can cause rapid and severe vision loss if left untreated.

The exact causes of AMD are not fully understood, but risk factors include age, smoking, family history, high blood pressure, obesity, and exposure to sunlight. While there is no cure for AMD, treatments such as vitamin supplements, laser therapy, and medication injections can help slow its progression and reduce the risk of vision loss.

Complement C3-C5 convertases are proteins that play a crucial role in the activation of the complement system, which is a part of the immune system. The complement system helps to eliminate pathogens and damaged cells from the body by marking them for destruction and attracting immune cells to the site of infection or injury.

The C3-C5 convertases are formed during the activation of the complement component 3 (C3) protein, which is a central player in the complement system. The formation of the C3-C5 convertase involves two main steps:

1. C3 convertase formation: In this step, a complex of proteins called the C3 convertase is formed by the cleavage of C3 into C3a and C3b fragments. This complex can then cleave additional C3 molecules into C3a and C3b fragments, amplifying the complement response.
2. C5 convertase formation: In this step, the C3b fragment from the C3 convertase binds to another protein called C4b2a, forming a new complex called the C5 convertase. The C5 convertase can then cleave the C5 protein into C5a and C5b fragments.

The C5b fragment goes on to form the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, leading to its lysis or destruction. The C3a and C5a fragments are small proteins called anaphylatoxins that can cause inflammation and attract immune cells to the site of infection or injury.

Overall, the formation of Complement C3-C5 convertases is a critical step in the activation of the complement system and plays a key role in the body's defense against pathogens and damaged cells.

Complement C5a is a protein fragment that is generated during the activation of the complement system, which is a part of the immune system. The complement system helps to eliminate pathogens and damaged cells from the body by tagging them for destruction and attracting immune cells to the site of infection or injury.

C5a is formed when the fifth component of the complement system (C5) is cleaved into two smaller fragments, C5a and C5b, during the complement activation cascade. C5a is a potent pro-inflammatory mediator that can attract and activate various immune cells, such as neutrophils, monocytes, and eosinophils, to the site of infection or injury. It can also increase vascular permeability, promote the release of histamine, and induce the production of reactive oxygen species, all of which contribute to the inflammatory response.

However, excessive or uncontrolled activation of the complement system and generation of C5a can lead to tissue damage and inflammation, contributing to the pathogenesis of various diseases, such as sepsis, acute respiratory distress syndrome (ARDS), and autoimmune disorders. Therefore, targeting C5a or its receptors has been explored as a potential therapeutic strategy for these conditions.

Cerebrospinal fluid (CSF) proteins refer to the proteins present in the cerebrospinal fluid, which is a clear, colorless fluid that surrounds and protects the brain and spinal cord. The protein concentration in the CSF is much lower than that in the blood, and it contains a specific set of proteins that are produced by the brain, spinal cord, and associated tissues.

The normal range for CSF protein levels is typically between 15-45 mg/dL, although this can vary slightly depending on the laboratory's reference range. An elevation in CSF protein levels may indicate the presence of neurological disorders such as meningitis, encephalitis, multiple sclerosis, or Guillain-Barre syndrome. Additionally, certain conditions such as spinal cord injury, brain tumors, or neurodegenerative diseases can also cause an increase in CSF protein levels.

Therefore, measuring CSF protein levels is an important diagnostic tool for neurologists to evaluate various neurological disorders and monitor disease progression. However, it's essential to interpret the results of CSF protein tests in conjunction with other clinical findings and laboratory test results to make an accurate diagnosis.

Alzheimer's disease is a progressive disorder that causes brain cells to waste away (degenerate) and die. It's the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently.

The early signs of the disease include forgetting recent events or conversations. As the disease progresses, a person with Alzheimer's disease will develop severe memory impairment and lose the ability to carry out everyday tasks.

Currently, there's no cure for Alzheimer's disease. However, treatments can temporarily slow the worsening of dementia symptoms and improve quality of life.

Tau proteins are a type of microtubule-associated protein (MAP) found primarily in neurons of the central nervous system. They play a crucial role in maintaining the stability and structure of microtubules, which are essential components of the cell's cytoskeleton. Tau proteins bind to and stabilize microtubules, helping to regulate their assembly and disassembly.

In Alzheimer's disease and other neurodegenerative disorders known as tauopathies, tau proteins can become abnormally hyperphosphorylated, leading to the formation of insoluble aggregates called neurofibrillary tangles (NFTs) within neurons. These aggregates disrupt the normal function of microtubules and contribute to the degeneration and death of nerve cells, ultimately leading to cognitive decline and other symptoms associated with these disorders.

Amyloid beta-peptides (Aβ) are small protein fragments that are crucially involved in the pathogenesis of Alzheimer's disease. They are derived from a larger transmembrane protein called the amyloid precursor protein (APP) through a series of proteolytic cleavage events.

The two primary forms of Aβ peptides are Aβ40 and Aβ42, which differ in length by two amino acids. While both forms can be harmful, Aβ42 is more prone to aggregation and is considered to be the more pathogenic form. These peptides have the tendency to misfold and accumulate into oligomers, fibrils, and eventually insoluble plaques that deposit in various areas of the brain, most notably the cerebral cortex and hippocampus.

The accumulation of Aβ peptides is believed to initiate a cascade of events leading to neuroinflammation, oxidative stress, synaptic dysfunction, and neuronal death, which are all hallmarks of Alzheimer's disease. Although the exact role of Aβ in the onset and progression of Alzheimer's is still under investigation, it is widely accepted that they play a central part in the development of this debilitating neurodegenerative disorder.

Amyloid is a term used in medicine to describe abnormally folded protein deposits that can accumulate in various tissues and organs of the body. These misfolded proteins can form aggregates known as amyloid fibrils, which have a characteristic beta-pleated sheet structure. Amyloid deposits can be composed of different types of proteins, depending on the specific disease associated with the deposit.

In some cases, amyloid deposits can cause damage to organs and tissues, leading to various clinical symptoms. Some examples of diseases associated with amyloidosis include Alzheimer's disease (where amyloid-beta protein accumulates in the brain), systemic amyloidosis (where amyloid fibrils deposit in various organs such as the heart, kidneys, and liver), and type 2 diabetes (where amyloid deposits form in the pancreas).

It's important to note that not all amyloid deposits are harmful or associated with disease. However, when they do cause problems, treatment typically involves managing the underlying condition that is leading to the abnormal protein accumulation.

Mild Cognitive Impairment (MCI) is a medical term used to describe a stage between the cognitive changes seen in normal aging and the more serious decline of dementia. It's characterized by a slight but noticeable decline in cognitive abilities, such as memory or thinking skills, that are greater than expected for an individual's age and education level, but not significant enough to interfere with daily life.

People with MCI have an increased risk of developing dementia, particularly Alzheimer's disease, compared to those without MCI. However, it's important to note that not everyone with MCI will develop dementia; some may remain stable, and others may even improve over time.

The diagnosis of MCI is typically made through a comprehensive medical evaluation, including a detailed medical history, cognitive testing, and sometimes brain imaging or laboratory tests.

According to the World Health Organization (WHO), "disabled persons" are those who have long-term physical, mental, intellectual or sensory impairments which may hinder their participation in society on an equal basis with others. The term "disability" is not meant to be understood as a 'personal tragedy' but rather as a complex interaction between the features of a person's body and mind, the activities they wish to perform and the physical and social barriers they encounter in their environment.

It's important to note that the term 'disabled persons' has been largely replaced by 'people with disabilities' or 'persons with disabilities' in many contexts, as it is considered more respectful and empowering to put the person first, rather than focusing on their disability. The United Nations Convention on the Rights of Persons with Disabilities (CRPD) uses the term "persons with disabilities" throughout its text.

Pediatrics is a branch of medicine that deals with the medical care and treatment of infants, children, and adolescents, typically up to the age of 18 or sometimes up to 21 years. It covers a wide range of health services including preventive healthcare, diagnosis and treatment of physical, mental, and emotional illnesses, and promotion of healthy lifestyles and behaviors in children.

Pediatricians are medical doctors who specialize in this field and have extensive training in the unique needs and developmental stages of children. They provide comprehensive care for children from birth to young adulthood, addressing various health issues such as infectious diseases, injuries, genetic disorders, developmental delays, behavioral problems, and chronic conditions like asthma, diabetes, and cancer.

In addition to medical expertise, pediatricians also need excellent communication skills to build trust with their young patients and their families, and to provide education and guidance on various aspects of child health and well-being.

Electronic mail, often abbreviated as email or e-mail, is a method of exchanging digital messages between people using computer networks. The term "electronic mail" is a direct comparison to traditional paper-based mail systems and has been in use since the creation of the first email system in 1971.

In medical terms, email is commonly used as a means of communication between healthcare professionals, patients, and other stakeholders in the healthcare industry. For example, physicians may use email to communicate with colleagues or staff members, while hospitals and clinics may use email to send appointment reminders or test results to patients.

Email messages can include text, images, videos, and attachments, making them a versatile tool for communication. However, it is important to note that email is not considered a secure means of transmitting sensitive medical information due to the risk of interception or unauthorized access. As such, healthcare professionals must follow established guidelines and regulations when using email to communicate protected health information (PHI) in order to maintain patient privacy and confidentiality.

I'm sorry for any confusion, but "Internet" is a term that pertains to the global network of interconnected computers and servers that enable the transmission and reception of data via the internet protocol (IP). It is not a medical term and does not have a specific medical definition. If you have any questions related to medicine or health, I'd be happy to try to help answer them for you!

I am not aware of a widely accepted medical definition for the term "software," as it is more commonly used in the context of computer science and technology. Software refers to programs, data, and instructions that are used by computers to perform various tasks. It does not have direct relevance to medical fields such as anatomy, physiology, or clinical practice. If you have any questions related to medicine or healthcare, I would be happy to try to help with those instead!

A User-Computer Interface (also known as Human-Computer Interaction) refers to the point at which a person (user) interacts with a computer system. This can include both hardware and software components, such as keyboards, mice, touchscreens, and graphical user interfaces (GUIs). The design of the user-computer interface is crucial in determining the usability and accessibility of a computer system for the user. A well-designed interface should be intuitive, efficient, and easy to use, minimizing the cognitive load on the user and allowing them to effectively accomplish their tasks.

'Information Storage and Retrieval' in the context of medical informatics refers to the processes and systems used for the recording, storing, organizing, protecting, and retrieving electronic health information (e.g., patient records, clinical data, medical images) for various purposes such as diagnosis, treatment planning, research, and education. This may involve the use of electronic health record (EHR) systems, databases, data warehouses, and other digital technologies that enable healthcare providers to access and share accurate, up-to-date, and relevant information about a patient's health status, medical history, and care plan. The goal is to improve the quality, safety, efficiency, and coordination of healthcare delivery by providing timely and evidence-based information to support clinical decision-making and patient engagement.

An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.

I'm sorry for any confusion, but "Indonesia" is not a medical term. It is a country located in Southeast Asia and Oceania, between the Indian and Pacific oceans. It is the world's largest island country, with more than thirteen thousand islands. If you have any questions about medical terms or concepts, I would be happy to help with those!

I'm sorry for any confusion, but "Malaysia" is not a medical term or concept. It is a country located in Southeast Asia, consisting of thirteen states and three federal territories. If you have any questions about Malaysia's geography, culture, or people, I would be happy to try to help answer those! However, if you have a question related to medicine or healthcare, please provide more details so I can give you an accurate and helpful response.

MedlinePlus is not a medical term, but rather a consumer health website that provides high-quality, accurate, and reliable health information, written in easy-to-understand language. It is produced by the U.S. National Library of Medicine, the world's largest medical library, and is widely recognized as a trusted source of health information.

MedlinePlus offers information on various health topics, including conditions, diseases, tests, treatments, and wellness. It also provides access to drug information, medical dictionary, and encyclopedia, as well as links to clinical trials, medical news, and patient organizations. The website is available in both English and Spanish and can be accessed for free.

I'm sorry for any confusion, but the concept of Yin and Yang does not have a medical definition. It is a philosophical concept from Chinese culture, often used in traditional Chinese medicine, that describes how seemingly opposite or contrary forces may actually be interconnected and interdependent in the natural world. In this context, yin and yang are used to describe the complementary aspects of and interdependence between various phenomena.

Yin is characterized as feminine, passive, receptive, and associated with night, darkness, and cold. Yang, on the other hand, is characterized as masculine, active, creative, and associated with day, light, and warmth. The concept of yin and yang is often used to describe the balance and harmony in health and well-being, and any imbalance between these two forces is believed to cause disease or illness. However, it's important to note that this concept is not a medical diagnosis or treatment approach and should not be considered as such.

The YY1 transcription factor, also known as Yin Yang 1, is a protein that plays a crucial role in the regulation of gene expression. It functions as a transcriptional repressor or activator, depending on the context and target gene. YY1 can bind to DNA at specific sites, known as YY1-binding sites, and it interacts with various other proteins to form complexes that modulate the activity of RNA polymerase II, which is responsible for transcribing protein-coding genes.

YY1 has been implicated in a wide range of biological processes, including embryonic development, cell growth, differentiation, and DNA damage response. Mutations or dysregulation of YY1 have been associated with various human diseases, such as cancer, neurodevelopmental disorders, and heart disease.

Consumer health information (CHI) refers to the resources and materials that provide health information and education to the general public, who are not necessarily healthcare professionals. CHI is designed to be understandable and accessible to laypeople, and it covers a wide range of topics related to health and wellness, including:

* Diseases and conditions
* Preventive care and healthy lifestyles
* Medications and treatments
* Medical tests and procedures
* Healthcare services and facilities
* Patient rights and responsibilities

CHI can be found in various formats, such as pamphlets, brochures, websites, videos, podcasts, and social media. It is essential to ensure that CHI is accurate, unbiased, and up-to-date to help consumers make informed decisions about their health and healthcare. The goal of CHI is to empower individuals to take an active role in managing their health and making healthcare choices that are right for them.

Graduate education typically refers to educational programs beyond the undergraduate level that lead to an advanced degree, such as a master's, doctoral, or professional degree. These programs usually require completion of a Bachelor's degree as a prerequisite and involve more specialized and in-depth study in a particular field. Graduate education may include coursework, research, examinations, and the completion of a thesis or dissertation. The specific requirements for graduate education vary depending on the field of study and the institution offering the degree program.

In a medical context, "faculty" most commonly refers to the inherent abilities or powers of a normal functioning part of the body or mind. For example, one might speak of the "faculties of perception" to describe the senses of sight, hearing, touch, taste, and smell. It can also refer to the teaching staff or body of instructors at a medical school or other educational institution. Additionally, it can be used more generally to mean a capability or skill, as in "the faculty of quick thinking."

I apologize for any confusion, but "students" is not a medical term. It refers to individuals who are engaged in studying or learning at an educational institution, such as a school, college, or university. If you have any questions related to medical terminology or concepts, I would be happy to help clarify those for you.

"Education, Pharmacy, Graduate" generally refers to the completion of a graduate-level program of study in the field of pharmacy. This type of education is typically pursued by individuals who already hold an undergraduate degree and wish to specialize in the preparation, dispensing, and proper use of medications.

In order to become a licensed pharmacist in the United States, for example, an individual must typically complete a Doctor of Pharmacy (Pharm.D.) program, which is a post-baccalaureate degree that typically takes four years to complete. During this time, students learn about various aspects of pharmacy practice, including drug therapy management, patient care, and communication skills. They also gain hands-on experience through internships and other experiential learning opportunities.

Graduates of pharmacy programs may go on to work in a variety of settings, including community pharmacies, hospitals, clinics, and long-term care facilities. They may also choose to pursue research or academic careers, working as professors or researchers in universities or research institutions.

The term "Faculty, Medical" generally refers to the faculty members who are involved in medical education and training within a medical school or academic institution. These individuals are responsible for teaching and instructing medical students, residents, and fellows in various areas of medical knowledge and clinical skills. They may hold positions such as professor, associate professor, assistant professor, or instructor, and they may specialize in a particular area of medicine such as internal medicine, surgery, pediatrics, or psychiatry. Medical faculty members may also be involved in research, patient care, and administrative duties within the institution.

Factor I deficiency in turn leads to low levels of complement component 3 (C3), factor B, factor H and properdin in blood, due ... Complement factor I (factor I) is a protein of the complement system, first isolated in 1966 in guinea pig serum, that ... Loss of function mutations in the Complement Factor I gene lead to low levels of factor I which results in increased complement ... Complement factor I, also known as C3b/C4b inactivator, is a protein that in humans is encoded by the CFI gene. ...
... is a protein that in humans is encoded by the CFB gene. This gene encodes complement factor B, a component ... CFB complement factor B". Ambrus JL, Peters MG, Fauci AS, Brown EJ (March 1990). "The Ba fragment of complement factor B ... Christie DL, Gagnon J (January 1983). "Amino acid sequence of the Bb fragment from complement Factor B. Sequence of the major ... Upon activation of the alternative pathway, it is cleaved by complement factor D yielding the noncatalytic chain Ba and the ...
"The role of complement factor C3 in lipid metabolism". Molecular Immunology. 15th European Meeting on Complement in Human ... 12th European Meeting on Complement in Human Disease12th European Meeting on CHD12th European Meeting on Complement in Human ... that allows it to bind to a plasma protein called Factor B. This complex is then cleaved by Factor D, a serine protease, to ... Factor I, a serine protease activated by cofactors, can cleave and C3b and C4b, thus preventing convertase formation. C3 ...
Activated C3 can then interact with factor B. Factor B is then activated by factor D, to form Bb. The resultant complex, C3bBb ... "Interactions between human complement components factor H, factor I and C3b". The Biochemical Journal. 326 (2): 553-61. doi: ... Complement component 3 has been shown to interact with Factor H. Deficiencies in C3 lead to genetic infections, usually fatal ... Factor I is the protease cleaves C3b but requires a cofactor (e.g Factor H, CR1, MCP or C4BP) for activity. Several ...
This gene encodes the basic form of complement factor 4, part of the classical activation pathway. The protein is expressed as ... Complement component 4 Complement component 4A HLA A1-B8-DR3-DQ2 haplotype Complement system Complement deficiency ... Aoki H, Takizawa F, Tsuji S, Nagasawa S (Jul 2000). "Elongation factor-1alpha as a homologous complement activator of Jurkat ... Complement component 4B (Chido blood group) is a kind of the Complement component 4 protein that in humans is encoded by the ...
Decay Accelerating Factor, DAF (CD55) Protectin (CD59) Complement C3b/C4b Receptor 1, CR1 (CD35) Complement Regulator of the ... Complement control protein are proteins that interact with components of the complement system. The complement system is ... Complement proteins protect against malignant cells- both by direct complement attack and through initiation of Complement- ... factor H competes with factor B to bind C3b; if it manages to bind, then the convertase is not formed. Factor H can bind C3b ...
PSAP Complement component 4, partial deficiency of; 120790; C1NH Complement factor H deficiency; 609814; HF1 Complement factor ... GLA Factor V and factor VIII, combined deficiency of; 227300; MCFD2 Factor V deficiency; 227400; F5 Factor XI deficiency, ... F11 Factor XII deficiency; 234000; F12 Factor XIIIA deficiency; 613225; F13A1 Factor XIIIB deficiency; 613235; F13B Failure of ... LCAT Fletcher factor deficiency; 612423; KLKB1 Focal cortical dysplasia, Taylor balloon cell type; 607341; TSC1 Focal dermal ...
... complement subgroups factor a group into smaller pieces. As previously mentioned, complements need not exist. A p-complement is ... A Frobenius complement is a special type of complement in a Frobenius group. A complemented group is one where every subgroup ... if K is a complement of H, then H is a complement of K. Neither H nor K need be a normal subgroup of G. Complements need not ... That is, H could have two distinct complements K1 and K2 in G. If there are several complements of a normal subgroup, then they ...
"OMIM Entry - * 300383 - COMPLEMENT FACTOR PROPERDIN; CFP". www.omim.org. Retrieved 2022-03-24. editor., Leung, Donald Y. M., ... The gene responsible for the production of properdin, Complement Factor Properdin (CFP), lies on the X-chromosome at the ... Properdin deficiency is a rare X-linked disease in which properdin, an important complement factor responsible for the ... Pertaining to complement deficiencies, there is no cure and the treatments for complement deficiencies vary widely. The best ...
Like complement factor H, CFHR5 is able to bind to complement C3. A mutation in CHFR5 was found in patients with the disease ... "Entrez Gene: CFHR5 complement factor H-related 5". McRae JL, Duthy TG, Griggs KM, et al. (2005). "Human factor H-related ... 2006). "Variations in the complement regulatory genes factor H (CFH) and factor H related 5 (CFHR5) are associated with ... Complement factor H-related protein 5 is a protein that in humans is encoded by the CFHR5 gene. CFHR5 is structurally related ...
Diaz-Guillen MA, Rodriguez de Cordoba S, Heine-Suner D (Jul 1999). "A radiation hybrid map of complement factor H and factor H- ... CFHR4 complement factor H-related 4". Hageman GS, Hancox LS, Taiber AJ, et al. (2007). "Extended Haplotypes in the Complement ... Complement factor H-related protein 4 is a protein that in humans is encoded by the CFHR4 gene. GRCh38: Ensembl release 89: ... 2000). "Functional properties of complement factor H-related proteins FHR-3 and FHR-4: binding to the C3d region of C3b and ...
Complement factor H-related protein 2) at the PDBe-KB. Zipfel PF, Skerka C (1994). "Complement factor H and related proteins: ... Díaz-Guillén MA, Rodríguez de Córdoba S, Heine-Suñer D (1999). "A radiation hybrid map of complement factor H and factor H- ... "Two additional human serum proteins structurally related to complement factor H. Evidence for a family of factor H-related ... Complement factor H-related protein 2 is a protein that in humans is encoded by the CFHR2 gene. GRCh38: Ensembl release 89: ...
"Cellular adhesion mediated by factor J, a complement inhibitor. Evidence for nucleolin involvement". The Journal of Biological ... Nucleolin is also able to act as a transcriptional coactivator with Chicken Ovalbumin Upstream Promoter Transcription Factor II ...
... is produced when complement factor I cleaves C3b. Complement receptors on white blood cells are able to bind iC3b, so iC3b ... thus preventing amplification of the complement cascade through the alternative pathway. Complement factor I can further cleave ... iC3b is a protein fragment that is part of the complement system, a component of the vertebrate immune system. ... v t e (Complement system, All stub articles, Biochemistry stubs). ...
These SNPs were located in the gene encoding complement factor H, which was an unexpected finding in the research of ARMD. The ... April 2005). "Complement factor H polymorphism in age-related macular degeneration". Science. 308 (5720): 385-9. Bibcode: ... "Complement factor H variant increases the risk of age-related macular degeneration". Science. 308 (5720): 419-21. Bibcode: ... It has been identified different variants associated with transcription factor coding-genes, such as TBX3 and TBX5, NKX2-5 o ...
Wu LC, Morley BJ, Campbell RD (Jan 1987). "Cell-specific expression of the human complement protein factor B gene: evidence for ... the body signals the Complement system and the Complement component 2 protein attaches to Complement system 4 resulting in an ... It is also important to note that Complement component 2 deficiency can be caused by genetic and environmental factors. In ... Gagnon J (Sep 1984). "Structure and activation of complement components C2 and factor B". Philosophical Transactions of the ...
It can also be seen in systemic lupus erythematosus as a result of increased usage of complement factors due to the pathology ... The CH50 is testing the classical complement pathway in an individual thus requiring functioning C1-C9 factors. If an ... Total complement activity (TCA) refers to a series of tests that determine the functioning of the complement system in an ... One can interpret the CH50 value along with the individual's complement factor values to help determine the etiology. For ...
Complement factors are decreased in rheumatoid arthritis and lupus arthritis. Microscopic analysis of synovial fluid is ... Jay, GD; Britt, DE; Cha, CJ (March 2000). "Lubricin is a product of megakaryocyte stimulating factor gene expression by human ...
Markusen, James R. (May 1, 1983). "Factor movements and commodity trade as complements". Journal of International Economics. 14 ... Markusen, James R.; Venables, Anthony J. (November 1, 2007). "Interacting factor endowments and trade costs: A multi-country, ... Markusen's international trade and economics research has contributed to the identification of factors that influence trade ... Markusen's regional economics research has investigated how factors such as infrastructure and education, impact economic ...
Calippe, Bertrand; Guillonneau, Xavier; Sennlaub, Florian (March 2014). "Complement factor H and related proteins in age- ... A SNP in the F5 gene causes Factor V Leiden thrombophilia. rs3091244 is an example of a triallelic SNP in the CRP gene on human ... Other factors, like genetic recombination and mutation rate, can also determine SNP density. SNP density can be predicted by ... LD can be affected by two parameters (among other factors, such as population stratification): 1) The distance between the SNPs ...
Malhotra R, Ward M, Sim RB, Bird MI (July 1999). "Identification of human complement Factor H as a ligand for L-selectin". The ... The embryo secretes human chorionic gonadotropin (hCG), which downregulates anti-adhesion factor, MUC-1, located on the uterine ... Human sell consists of 10 exons and its transcription factor is FOXO 1, on the other hand the mouse sell gene is composed of 9 ... an adjacent epidermal growth factor-like domain, two to the consensus repeat units homologous to those found in C3/C4-binding ...
It is the first drug that selectively inhibits factor B, the active component of the complement's C3 and C5 convertases. In ... April 2019). "Small-molecule factor B inhibitor for the treatment of complement-mediated diseases". Proceedings of the National ... Iptacopan is also investigated as a drug in other complement-mediated diseases, like age-related macular degeneration and some ...
April 2005). "Complement factor H variant increases the risk of age-related macular degeneration". Science. 308 (5720): 419-21 ... Some of the factors that should be considered are the level of efficacy of various genetic tests in the general population, ... Combining molecular scale information with macro-scale clinical data, such as patients' tumor type and other risk factors, ... 2 July 2015). "Race/Ethnic Differences in the Associations of the Framingham Risk Factors with Carotid IMT and Cardiovascular ...
BCX9930, an oral Factor D inhibitor for the treatment of complement-mediated diseases. FDA has granted Fast Track designation ...
In the meantime, notebooks and small form factor desktop computers complement the range. The names of the devices borrow from ... Complementing Tuxedo OS, the company is working on tools to control hardware functions and improve usability. Licensed under ...
Opsonins include Mfge8, Gas6, Protein S, antibodies and complement factors C1q and C3b. Phagoptosis has multiple functions ... Pathogenic cells such as bacteria can be opsonised by antibodies or complement factors, enabling their phagocytosis and ...
1989). "20 KDa homologous restriction factor of complement resembles T cell activating protein". Biochem. Biophys. Res. Commun ... When complement activation leads to deposition of C5b678 on host cells, CD59 can prevent C9 from polymerizing and forming the ... Ninomiya H, Sims PJ (1992). "The human complement regulatory protein CD59 binds to the alpha-chain of C8 and to the "b"domain ... 1992). "Complement regulatory proteins at the feto-maternal interface during human placental development: distribution of CD59 ...
... factor H, factor HR1 or HR3, membrane cofactor protein, factor I, factor B, complement C3, and thrombomodulin). This results in ... The complement system activation may be due to mutations in the complement regulatory proteins (factor H, factor I, or membrane ... of complement can result from production of anti-factor H autoantibodies or from genetic mutations in any of several complement ... "Platelet-associated complement factor H in healthy persons and patients with atypical HUS". Blood. 114 (20): 4538-4545. doi: ...
Lee FJ, Moss J, Vaughan M (1992). "Human and Giardia ADP-ribosylation factors (ARFs) complement ARF function in Saccharomyces ... ADP-ribosylation factor 5 is a protein that in humans is encoded by the ARF5 gene. ADP-ribosylation factor 5 (ARF5) is a member ... Shin, O H; Exton J H (August 2001). "Differential binding of arfaptin 2/POR1 to ADP-ribosylation factors and Rac1". Biochem. ... Tsuchiya M, Price SR, Tsai SC, Moss J, Vaughan M (March 1991). "Molecular identification of ADP-ribosylation factor mRNAs and ...
"Entrez Gene: CFHR3 complement factor H-related 3". Zipfel PF, Skerka C (1994). "Complement factor H and related proteins: an ... Diaz-Guillen MA, Rodriguez de Cordoba S, Heine-Suner D (Jul 1999). "A radiation hybrid map of complement factor H and factor H- ... Complement factor H-related protein 3 is a protein that in humans is encoded by the CFHR3 gene. GRCh38: Ensembl release 89: ... 2000). "Complement factor H: sequence analysis of 221 kb of human genomic DNA containing the entire fH, fHR-1 and fHR-3 genes ...
Factor I deficiency in turn leads to low levels of complement component 3 (C3), factor B, factor H and properdin in blood, due ... Complement factor I (factor I) is a protein of the complement system, first isolated in 1966 in guinea pig serum, that ... Loss of function mutations in the Complement Factor I gene lead to low levels of factor I which results in increased complement ... Complement factor I, also known as C3b/C4b inactivator, is a protein that in humans is encoded by the CFI gene. ...
Molecular defects in complement factor H (CFH), a critical regulatory protein of the complement alternative pathway (AP), are ... for evidence of complement-mediated inflammation revealed widespread deposition of complement-activation fragments throughout ... Little is known regarding the role of CFH in controlling complement activation within the liver. While studying aging CFH- ... These results indicate that CFH is critical for controlling complement activation in the liver, and in its absence, AP ...
View Goat Polyclonal anti-Complement Factor MASP3/MASP1 Antibody (AF1724). Validated Applications: WB, IP. Validated Species: ... Blogs on Complement Factor MASP3/MASP1. There are no specific blogs for Complement Factor MASP3/MASP1, but you can read our ... Reviews for Complement Factor MASP3/MASP1 Antibody (AF1724) (0) There are no reviews for Complement Factor MASP3/MASP1 Antibody ... Additional Complement Factor MASP3/MASP1 Products. Array AF1724 * Complement Factor MASP3/MASP1 Antibodies ...
Crystal structure of human Complement Factor D with anti-Factor D Fab 20D12 ... Crystal structure of human Complement Factor D with anti-Factor D Fab 20D12. Dion, M., Wu, P., Morando, A., Bullen, G., Shatz, ... Complement factor D. I [auth W],. J [auth X],. K [auth Y],. L [auth Z]. 228. Homo sapiens. Mutation(s): 0 Gene Names: CFD, DF, ... Crystal structure of human Complement Factor D with anti-Factor D Fab 20D12. *PDB DOI: https://doi.org/10.2210/pdb6VMJ/pdb ...
The Y402H polymorphism in complement factor H (CFH) gene on chromosome 1, area q31, has been reported to be a risk factor for ... complement factor H) protein is known as a critical regulator of the complement alternative pathway activation. 20 In the ... Na Rae Kim, Ju Hee Kang, Oh Woong Kwon, Seok Joon Lee, Jung Hyub Oh, Hee Seung Chin; Association between Complement Factor H ... Complement factor H variant increases the risk of age-related macular degeneration. Science. 2005;308:419-421. [CrossRef] [ ...
... complement-mediated... (More). Complement factor B (FB) mutant variants are associated with excessive complement activation in ... atypical hemolytic uremic syndrome, C3 glomerulopathy, complement, danicopan, factor B, factor D. in Frontiers in Immunology. ... Factor D Inhibition Blocks Complement Activation Induced by Mutant Factor B Associated With Atypical Hemolytic Uremic Syndrome ... Complement factor B (FB) mutant variants are associated with excessive complement activation in kidney diseases such as ...
... including mutations in complement factor H, complement factor I, or the membrane co-factor protein. We report the case of a 26- ... Approximately 60% of cases of atypical hemolytic uremic syndrome are associated with deficiencies of the complement regulatory ... From: A novel missense mutation in complement factor I predisposes patients to atypical hemolytic uremic syndrome: a case ...
Complement receptor 1 (CR1) has factor H-like activity, permitting factor I to cleave C3b. Membrane cofactor protein also has ... Ehrlich and Morgan termed this factor complement. The complement system as understood today is a multimolecular system composed ... Factor H competes with factor B for binding to C3b and displaces Bb from C3bBb. It accelerates the inactivation of C3b by ... Here, C3b binds to factor B that is cleaved by factor D to Bb. C3bBb complex then acts as the C3 convertase and generates more ...
Variation registry for Complement factor I deficiency Select database by name. ADAbase. AICDAbase. AIREbase. AK2base. AP3B1base ...
Buy online Biotin-Linked Monoclonal Antibody to Complement Factor H (CFH) from cat# primary antibody. Find the Other labeled ... More info about Biotin-Linked Monoclonal Antibody to Complement Factor H (CFH). Product no.: LAA635Ra76. ... Primary antibodies>Other labeled antibodies>Biotin-Linked Monoclonal Antibody to Complement Factor H (CFH) ... Data sheet of Biotin-Linked Monoclonal Antibody to Complement Factor H (CFH). Brand. Cloud Clone. ...
You are here: Home1 / Antibodies2 / Complement Factor D, Human, ELISA kit, 1 x 96 det. ... 31Complement Factor D, Human, ELISA kit, 1 x 96 det.. ... Complement Factor D, Human, ELISA kit, 1 x 96 det.. Product ...
Increased plasma complement factor H is associated with geriatric depression. Cheolmin Shin, Byung Joo Ham, Young Hoon Ko, Chi ... Dive into the research topics of Increased plasma complement factor H is associated with geriatric depression. Together they ...
Complement Factor D (Cfd) is the rate limiting enzyme in the alternative complement pathway. We hypothesize that the loss of ... forms of complement to determine whether the loss of Cfd reduces complement activity. If the loss of Cfd rescues the phenotype ... This project investigates complement activity by developing a western blot assay to measure inactive (C3) and active (C3b) ... caused by the dysregulation of the complement system leading to inflammation in tissue that is critical for vision. ...
Human CFHR3(Complement Factor H Related Protein 3) ELISA Kit. Human CFHR3(Complement Factor H Related Protein 3) ELISA Kit. To ... Human Complement Factor H Related Protein 3 (CFHR3) ELISA Kit. SEL329Hu-10x96wellstestplate Cloud-Clone 10x96-wells test plate ... Human CFHR3(Complement Factor H Related Protein 3) ELISA Kit. *Human CLEC11A(C-Type Lectin Domain Family 11, Member A) ELISA ... Description: A sandwich ELISA kit for detection of Complement Factor H Related Protein 3 from Human in samples from blood, ...
The CFI gene provides instructions for making a protein called complement factor I. Learn about this gene and related health ... Complement factor I deficiency. At least 10 mutations in the CFI gene have been identified in people with complement factor I ... or absent complement factor I.. The lack (deficiency) of functional complement factor I protein allows uncontrolled activation ... Complement factor I and several related proteins protect healthy cells by preventing activation of the complement system when ...
... "complement factor H". Humanized Cobra Venom Factor: Experimental Therapeutics for Targeted Complement Activation and Complement ... Complement and Complement Regulatory Proteins as Potential Molecular Targets for Vascular Diseases. Journal: Current ... Emerging Role of Complement in Ocular Diseases. Journal: Current Immunology Reviews. Volume: 7 Issue: 3 Year: 2011 Page: 360- ... The Host Complement System and Arbovirus Pathogenesis. Journal: Current Drug Targets. Volume: 9 Issue: 2 Year: 2008 Page: 165- ...
The CFHR5 gene provides instructions for making a protein called complement factor H-related 5. Learn about this gene and ... Complement factor H regulates a part of the bodys immune response known as the complement system. The complement system is a ... Complement factor H helps to protect healthy cells by preventing the complement system from being turned on (activated) when it ... Variations in the complement regulatory genes factor H (CFH) and factor H related 5 (CFHR5) are associated with ...
However, little is known in humans about the effects of the complement system and genetic modifiers of AD risk like the ε4 ... As a part of the innate immune system, the complement cascade enhances the bodys ability to destroy and remove pathogens and ... Using linear models, we assessed the relationship between APOE ε4 genotype, CSF Complement 3 (C3), CSF amyloid-β (amyloid) and ... Our results support a conceptual model of the AD pathogenic cascade where a synergistic relationship between the complement ...
Decay accelerating factor (DAF, CD55), a glycosylphosphatidylinositol-anchored membrane protein, is a candidate for autoimmune ... disease susceptibility based on its role in restricting complement activation and evidence that DAF expression modulates the ... Decay accelerating factor (DAF, CD55), a glycosylphosphatidylinositol-anchored membrane protein, is a candidate for autoimmune ... Discovery, linkage disequilibrium and association analyses of polymorphisms of the immune complement inhibitor, decay- ...
Factor I-like modules (FIMs) of complement proteins C6, C7, and factor I participate in protein-protein interactions critical ... N2 - Factor I-like modules (FIMs) of complement proteins C6, C7, and factor I participate in protein-protein interactions ... AB - Factor I-like modules (FIMs) of complement proteins C6, C7, and factor I participate in protein-protein interactions ... abstract = "Factor I-like modules (FIMs) of complement proteins C6, C7, and factor I participate in protein-protein ...
CTRP-12 elisa Test :: Human Complement C1q tumor necrosis factor-related protein 12 (CTRP-12) ELISA Test 95T ... www.cortex-biochem.com/shop/0544-mbs167643-96t-ctrp-12-elisa-test-human-complement-c1q-tumor-necrosis-factor-related-protein-12 ... CTRP-12 elisa Test :: Human Complement C1q tumor necrosis factor-related protein 12 (CTRP-12) ELISA Test 95T. https:// ...
Dive into the research topics of Genetic coding variant in complement factor B (CFB) is associated with increased risk for ... Genetic coding variant in complement factor B (CFB) is associated with increased risk for perianal Crohns disease and leads to ... Genetic coding variant in complement factor B (CFB) is associated with increased risk for perianal Crohns disease and leads to ... Genetic coding variant in complement factor B (CFB) is associated with increased risk for perianal Crohns disease and leads to ...
Primary: complement. Persistent complement, properdin, or Factor B deficiency. None. Pneumococcal. Meningococcal. Hib (children ... Persons with functional or anatomic asplenia (including sickle cell disease), HIV infection and persistent complement component ... Persons with functional or anatomic asplenia (including sickle cell disease) and persistent complement component deficiency ( ... Other immunosuppressive medications include human immune mediators like interleukins and colony-stimulating factors, immune ...
... transforming growth factor-beta1, tumor necrosis factor-alpha, or interferon-gamma. C3 and factor B proteins were measured in ... In skin the keratinocyte is the major cell type, it is known to produce two soluble complement components, C3 and factor B. In ... Synthesis of complement components C3 and factor B in human keratinocytes is differentially regulated by cytokines. ... Tumor necrosis factor-alpha induced production of C3 and interferon-gamma induced production of factor B were inhibited by ...
... complement 3/cobra venom factor); epididymal secretory protein; hyaluronidase; kallikrein; kunitz; L-amino acid oxidase; ... Venom nerve Growth Factor (VNGF). 1. Partial sequence nearly identical to viperidaes VNGFs. ... Moreover, it complements traditional methods of studying toxin evolution through use of phylogenetic trees and multi-domain ... Their role in venom is not fully understood but they might act as a spreading factor facilitating diffusion of other venom ...
keywords = "AMD, Complement factor H, Complement system",. author = "Robyn Troutbeck and Salmaan Al-Qureshi and Guymer, {Robyn ... the association between AMD and mutations in various complement pathway genes, most notably complement factor H. Increasingly, ... the association between AMD and mutations in various complement pathway genes, most notably complement factor H. Increasingly, ... the association between AMD and mutations in various complement pathway genes, most notably complement factor H. Increasingly, ...
Low complement factor H (i.e., ,70%). 3/69 (4.3). Low complement factor I (i.e., ,70%). 1/69 (1.4). ... Frémeaux-Bacchi V, Sellier-Leclerc A-L, Vieira-Martins P, Limou S, Kwon T, Lahoche A, et al. Complement gene variants and Shiga ... Wong CS, Mooney JC, Brandt JR, Staples AO, Jelacic S, Boster DR, et al. Risk factors for the hemolytic uremic syndrome in ... characterization of isolates and identification of risk factors for haemolytic uremic syndrome. BMC Infect Dis. 2015;15:324. ...
Complement 1q/Tumor Necrosis Factor-Related Proteins (CTRPs): Structure, Receptors and Signaling. Schanbacher C, Hermanns HM, ...
Coagulation Factor III/Tissue Factor. IL-2. RAGE. Complement Component C5/C5a. IL-3. RBP4. ... Krüppel-like Factor 5 Plays an Important Role in the Pathogenesis of Chronic Pancreatitis Authors: Alavi, M;Mejia-Bautista, A; ... Wisp1 is a circulating factor that stimulates proliferation of adult mouse and human beta cells Authors: R Fernandez-, A García ... Liver-derived fibroblast growth factor 21 mediates effects of glucagon-like peptide-1 in attenuating hepatic glucose output ...
Complement Activation and Key Risk Factors in Disease Assessment for IgAN 0.25 CME Credits ...
  • The complement system as understood today is a multimolecular system composed of more than 32 proteins and consisting of serum proteins, serosal proteins, and cell membrane receptors that bind to complement fragments. (medscape.com)
  • The complement system consists of 7 serum and 9 membrane regulatory proteins, 1 serosal regulatory protein, and 8 cell membrane receptors that bind complement fragments. (medscape.com)
  • The complement system is a group of proteins that work together to destroy foreign invaders (such as bacteria and viruses), trigger inflammation, and remove debris from cells and tissues. (medlineplus.gov)
  • Complement factor I and several related proteins protect healthy cells by preventing activation of the complement system when it is not needed. (medlineplus.gov)
  • Factor I-like modules (FIMs) of complement proteins C6, C7, and factor I participate in protein-protein interactions critical to the progress of a complement-mediated immune response to infections and other trauma. (ed.ac.uk)
  • C3 and factor B proteins were measured in culture supernatant by enzyme-linked immunosorbent assay and C3 and factor B transcripts in harvested cells by reverse transcriptase - polymerase chain reaction . (bvsalud.org)
  • Cytokine induced upregulation of C3 and factor B proteins was always associated with the upregulation of levels of C3 and factor B mRNA . (bvsalud.org)
  • In this time, the complement system has featured as a unifying theme for several elements of new evidence: initially, the discovery of complement proteins within drusen and subsequently, the association between AMD and mutations in various complement pathway genes, most notably complement factor H. Increasingly, a wealth of data are pointing towards a role for chronic local inflammation and complement activation in the patho-aetiology of AMD. (monash.edu)
  • thus, PIGA mutations lead to a deficiency of GPI-anchored proteins, such as complement decay-accelerating factor (also known as CD55) and CD59 glycoprotein (CD59), which are both complement inhibitors. (medscape.com)
  • Genes that encode the proteins of complement components or their isotypes are distributed throughout different chromosomes, with 19 genes comprising 3 significant complement gene clusters in the human genome. (medscape.com)
  • The important components of this system are various cell membrane-associated proteins such as complement receptor 1 (CR1), complement receptor 2 (CR2), and decay accelerating factor (DAF). (medscape.com)
  • for example, the proteins factor H and factor I inhibit the formation of the enzyme C3 convertase of the alternative pathway. (medscape.com)
  • Complement dysregulation is usually from a mutation in genes controlling complement proteins or factors but sometimes from acquired autoantibodies to certain complement factors. (msdmanuals.com)
  • Complement factor I (factor I) is a protein of the complement system, first isolated in 1966 in guinea pig serum, that regulates complement activation by cleaving cell-bound or fluid phase C3b and C4b. (wikipedia.org)
  • Factor I deficiency in turn leads to low levels of complement component 3 (C3), factor B, factor H and properdin in blood, due to unregulated activation of C3 convertase, and to low levels of IgG, due to loss of iC3b and C3dg production. (wikipedia.org)
  • Little is known regarding the role of CFH in controlling complement activation within the liver. (jci.org)
  • Examination of fH-/- livers (3-24 months) for evidence of complement-mediated inflammation revealed widespread deposition of complement-activation fragments throughout the sinusoids, elevated transaminase levels, increased hepatic CD8+ and F4/80+ cells, overexpression of hepatic mRNA associated with inflammatory signaling pathways, steatosis, and increased collagen deposition. (jci.org)
  • These results indicate that CFH is critical for controlling complement activation in the liver, and in its absence, AP activation leads to chronic inflammation and promotes hepatic carcinogenesis. (jci.org)
  • Activation of the complement pathway via MBL is initiated by specific MASPs. (novusbio.com)
  • Complement factor B (FB) mutant variants are associated with excessive complement activation in kidney diseases such as atypical hemolytic uremic syndrome (aHUS), C3 glomerulopathy and membranoproliferative glomerulonephritis (MPGN). (lu.se)
  • Activation of the complement pathways. (medscape.com)
  • Binding of factor H to C3b increases its inactivation by factor I. Properdin stabilizes it, preventing its inactivation by factors H and I. The alternate pathway does not result in a truly nonspecific activation of complement because it requires specific types of compounds for activation. (medscape.com)
  • The lack (deficiency) of functional complement factor I protein allows uncontrolled activation of the complement system. (medlineplus.gov)
  • The CFI gene mutations identified in this disorder result in an abnormal or nonfunctional version of complement factor I. The defective protein allows uncontrolled activation of the complement system. (medlineplus.gov)
  • Conclusion pCD-associated rs4151651 in CFB is a loss-of-function mutation that impairs its cleavage, activation of alternative complement pathway, and pathogen phagocytosis thus implicating the alternative complement pathway and CFB in pCD aetiology. (mssm.edu)
  • Inflammation and innate immunity are thought to play a role in the pathogenesis of AMD with complement activation, retinal microglial activation and choroidal macrophage infiltration being key components ( 8 - 11 ). (frontiersin.org)
  • In vitro activation of the alternative pathway of complement by settled grain dust. (cdc.gov)
  • The accumulation of anaphylatoxins (such as C5a) from complement activation might also have a role. (medscape.com)
  • at the same time, the inflammation promoted by complement activation can result in cellular damage when not kept in check. (medscape.com)
  • 2015). This condition is, in part, caused by the dysregulation of the complement system leading to inflammation in tissue that is critical for vision. (uvic.ca)
  • Although several studies have examined the association between inflammation and AD neurodegeneration in humans, it is still unknown whether APOE ε4 influences the relationship between inflammation (specifically the complement cascade) and amyloid and tau pathology. (biomedcentral.com)
  • The complement system plays an important part in host defense and inflammation . (bvsalud.org)
  • The complement system is a central component of host defense but can also contribute to the inflammation seen in pathological conditions. (eurogentec.com)
  • Variations in the complement regulatory genes factor H (CFH) and factor H related 5 (CFHR5) are associated with membranoproliferative glomerulonephritis type II (dense deposit disease). (medlineplus.gov)
  • At least 10 mutations in the CFI gene have been identified in people with complement factor I deficiency, a disorder characterized by immune system dysfunction. (medlineplus.gov)
  • This condition, which may also occur in people with complement factor I deficiency, is characterized by kidney malfunction that can be serious or life-threatening. (medlineplus.gov)
  • Baracho GV, Nudelman V, Isaac L. Molecular characterization of homozygous hereditary factor I deficiency. (medlineplus.gov)
  • Cases of complement deficiency have helped defined the role of complement in host defense. (medscape.com)
  • Loss of function mutations in the Complement Factor I gene lead to low levels of factor I which results in increased complement activity. (wikipedia.org)
  • These results suggest that FD inhibition can effectively block complement overactivation induced by FB gain-of-function mutations. (lu.se)
  • The mutations result in abnormal, nonfunctional, or absent complement factor I. (medlineplus.gov)
  • Characterization of mutations in complement factor I (CFI) associated with hemolytic uremic syndrome. (medlineplus.gov)
  • Genetic mutations in the alternative complement pathway, particularly involving the complement factor H (CFH) gene, are associated with an increased risk of development of AMD ( 12 - 14 ) and infiltrating mononuclear phagocytes have been identified within drusen as well as lesions associated with more late disease ( 15 ). (frontiersin.org)
  • Complement factor I, also known as C3b/C4b inactivator, is a protein that in humans is encoded by the CFI gene. (wikipedia.org)
  • The gene for Factor I in humans is located on chromosome 4. (wikipedia.org)
  • This study was undertaken to investigate the association between the complement factor H ( CFH ) gene and exudative age-related macular degeneration (AMD) in Korean patients. (arvojournals.org)
  • Y402H polymorphism which has been suggested to be a major risk factor of AMD in Caucasians was found to be only marginally associated with exudative AMD with low frequency, whereas three adjacent SNPs in the CFH gene were significantly associated with AMD in Koreans. (arvojournals.org)
  • The CFI gene provides instructions for making a protein called complement factor I. This protein helps regulate a part of the body's immune response known as the complement system. (medlineplus.gov)
  • The CFHR5 gene provides instructions for making a protein called complement factor H-related 5. (medlineplus.gov)
  • However, its structure is similar to that of a protein called complement factor H (which is produced from the CFH gene). (medlineplus.gov)
  • It is unclear how variations in this gene affect the regulation of the complement system, and researchers are still working to determine how these genetic changes contribute to disease risk. (medlineplus.gov)
  • Complement factor H regulates a part of the body's immune response known as the complement system. (medlineplus.gov)
  • As a part of the innate immune system, the complement cascade enhances the body's ability to destroy and remove pathogens and has recently been shown to influence Alzheimer's associated amyloid and tau pathology. (biomedcentral.com)
  • Although the complement system is part of the body's innate, relatively nonspecific defense against pathogens, its role is hardly primitive or easily understood. (medscape.com)
  • Molecular defects in complement factor H (CFH), a critical regulatory protein of the complement alternative pathway (AP), are typically associated with inflammatory diseases of the eye and kidney. (jci.org)
  • MASP3 is a member of the MASPs involved in mannan-binding lectin (MBL) complement pathway (1). (novusbio.com)
  • Depending on the nature of complement activators, the classic pathway, the alternative pathway, or the more recently discovered lectin pathway is activated predominantly to produce C3 convertase. (medscape.com)
  • Complement Factor D (Cfd) is the rate limiting enzyme in the alternative complement pathway. (uvic.ca)
  • targeting of specific molecular constituents in the complement pathway thus producing dampening or inhibition of the inflammatory response. (monash.edu)
  • The complement cascade consists of 3 separate pathways that converge in a final common pathway. (medscape.com)
  • Lectins activate the lectin pathway in a manner similar to the antibody interaction with complement in the classical pathway. (medscape.com)
  • Our results support a conceptual model of the AD pathogenic cascade where a synergistic relationship between the complement cascade (C3) and APOE ε4 results in elevated Alzheimer's neurodegeneration and in turn, amyloid further regulates the effect of the complement cascade on downstream tau pathology. (biomedcentral.com)
  • An intricate system regulates complement activity. (medscape.com)
  • In addition to playing an important role in host defense against infection, the complement system is a mediator in both the pathogenesis and prevention of immune complex diseases, such as systemic lupus erythematosus (SLE). (medscape.com)
  • The complement system functions as an interactive sequence, with one reaction leading to another in the form of a cascade. (medscape.com)
  • The effects of settled grain dust on the human serum complement cascade were investigated. (cdc.gov)
  • Deficiencies in the complement cascade can lead to overwhelming infection and sepsis. (medscape.com)
  • New studies point to the complex interplay between the complement cascade and adaptive immune response, and complement is also being studied in association with ischemic injury as a target of therapy. (medscape.com)
  • Atypical hemolytic uremic syndrome is caused by complement overactivation. (wikipedia.org)
  • We showed that one common strategy is to bind complement inhibitor C4BP, which leads to decreased opsonisation of bacteria with C3b impairing phagocytosis and allowing bacterial survival. (lu.se)
  • The unregulated activity of the complement system decreases blood levels of another complement protein called C3, reducing the immune system's ability to fight infections. (medlineplus.gov)
  • The overactive complement system attacks certain kidney cells, which damages the kidneys and leads to a loss of protein in the urine (proteinuria). (medlineplus.gov)
  • Complement factor H helps to protect healthy cells by preventing the complement system from being turned on (activated) when it is not needed. (medlineplus.gov)
  • Studies suggest that complement factor H-related 5 also plays a role in controlling the complement system. (medlineplus.gov)
  • The duplication alters the structure and function of complement factor H-related 5, preventing it from regulating the complement system effectively. (medlineplus.gov)
  • As a result, the complement system becomes overactive, which damages structures called glomeruli in the kidneys. (medlineplus.gov)
  • However, little is known in humans about the effects of the complement system and genetic modifiers of AD risk like the ε4 allele of apolioprotein E ( APOE ε4) on AD pathobiology. (biomedcentral.com)
  • Here, we investigated the relationship between APOE ε4 and the complement system on amyloid and tau pathology in AD. (biomedcentral.com)
  • In this review we discuss the role of the complement system in AMD, novel therapies in preclinical evaluation and clinical trial, and whether these have a part to play in reducing the burden of disease. (monash.edu)
  • The complement system is part of the innate immune system. (medscape.com)
  • The complement system plays an important part in defense against pyogenic organisms. (medscape.com)
  • These findings underscore the duality of the complement system. (medscape.com)
  • Knowledge about the complement system is expanding. (medscape.com)
  • Aliquots were analyzed for factor-B conversion and hemolytic activity. (cdc.gov)
  • the heavy chain plays an inhibitory role in maintaining the enzyme inactive until it meets the complex formed by the substrate (either C3b or C4b) and a cofactor protein (Factor H, C4b-binding protein, complement receptor 1, and membrane cofactor protein). (wikipedia.org)
  • Conventional protease inhibitors do not completely inactivate Factor I but they can do so if the enzyme is pre-incubated with its substrate: this supports the proposed rearrangement of the molecule upon binding to the substrate. (wikipedia.org)
  • Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Complement Factor H Related Protein 3 (CFHR3) in serum, plasma and other biological fluids. (youngresearch.eu)
  • This peptide employs 5FAM/QXL® 520 FRET pair for quantitation of complement enzyme activity. (eurogentec.com)
  • As a first line of defense against pathogens and a mediator between innate and adaptive immunity, complement is a particular focus of evasion strategies developed by pathogens. (lu.se)
  • https://doronscientific.com/wp-content/uploads/2022/12/doron-scintific-logo.png 0 0 [email protected] https://doronscientific.com/wp-content/uploads/2022/12/doron-scintific-logo.png [email protected] 2023-02-21 13:48:31 2023-02-21 13:48:31 Complement Factor D, Human, ELISA kit, 1 x 96 det. (doronscientific.com)
  • Description: A competitive ELISA for quantitative measurement of Human Complement factor H related protein 3(CFHR3) in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (youngresearch.eu)
  • In addition to the following diseases, low factor I is associated with recurrent bacterial infections in children. (wikipedia.org)
  • Patients with aHUS are currently treated with eculizumab while there is no specific treatment for other complement-mediated renal diseases. (lu.se)
  • [ 3 ] A registry of complement deficiencies has been established as a means to promote joint projects on treatment and prevention of diseases associated with defective complement function. (medscape.com)
  • Mutagenesis was performed to study the effect of factor D (FD) inhibition on C3 convertase-induced FB cleavage, complement-mediated. (lu.se)
  • In the first phase, a series of specific interactions leads to formation of intrinsic complement proteinase, termed C3 convertase. (medscape.com)
  • We also identified a unique mechanism to battle complement used by the respiratory pathogen Moraxella catarrhalis . (lu.se)
  • Using linear models, we assessed the relationship between APOE ε4 genotype, CSF Complement 3 (C3), CSF amyloid-β (amyloid) and CSF hyperphosphorylated tau (ptau). (biomedcentral.com)
  • Recombinant S252 CFB had reduced binding to C3b, its cleavage was impaired, and complement-driven phagocytosis and cytokine secretion were reduced compared with G252 CFB. (mssm.edu)
  • Deficiencies in complement predispose patients to infection via 2 mechanisms: (1) ineffective opsonization and (2) defects in lytic activity (defects in MAC). (medscape.com)
  • Congenital complement disorders may also increase the risk of hemolytic-uremic sydrome (HUS) following infection. (msdmanuals.com)
  • This indicated that, as expected, cytokine -induced enhancement in C3 and factor B levels was due to an increase in synthesis rather than their possible release from intracellular stores. (bvsalud.org)
  • Immunostaining of human HCC biopsies revealed extensive deposition of complement fragments within the tumors. (jci.org)
  • Crystal structure the crystal structure of human Factor I has been deposited as PDB: 2XRC. (wikipedia.org)
  • Detects human Complement Factor MASP3 Catalytic Domain in direct ELISAs and Western blots. (novusbio.com)
  • Synthesis of complement components C3 and factor B in human keratinocytes is differentially regulated by cytokines. (bvsalud.org)
  • Human keratinocytes were cultured in the presence of supernatant of activated peripheral blood mononuclear cells , interleukin-1alpha , interleukin-2 , interleukin-6 , transforming growth factor-beta1 , tumor necrosis factor-alpha , or interferon-gamma . (bvsalud.org)
  • Another important mechanism by which bacteria resist human complement is the production of proteases that efficiently degrade complement components. (lu.se)
  • Variation near complement factor I is associated with risk of advanced AMD. (medlineplus.gov)
  • Tumor necrosis factor-alpha induced production of C3 and interferon-gamma induced production of factor B were inhibited by cycloheximide . (bvsalud.org)
  • This peptide is a second complement component (C2), the physiological substrate for the proenzyme Cls, first complement component. (eurogentec.com)
  • There are currently no images for Complement Factor MASP3/MASP1 Antibody (AF1724). (novusbio.com)
  • The factor I light chain contains only the serine protease domain. (wikipedia.org)
  • Some new clinical entities are linked with partial complement defects. (medscape.com)
  • The factor I heavy chain has four domains: an FI membrane attack complex (FIMAC) domain, CD5 domain, and low density lipoprotein receptor 1 and 2 (LDLr1 and LDLr2) domains. (wikipedia.org)
  • The term "nocturnal" refers to the belief that hemolysis is triggered by acidosis during sleep and activates complement to hemolyze an unprotected and abnormal RBC membrane. (medscape.com)
  • Factor I is a glycoprotein heterodimer consisting of a disulfide linked heavy chain and light chain. (wikipedia.org)
  • Dysregulated factor I activity has clinical implications. (wikipedia.org)
  • This article outlines some of the disease states associated with complement deficiencies and their clinical implications. (medscape.com)
  • Several risk factors, including aging, cigarette smoking, and arterial hypertension, have been proposed, but only a fraction of exudative AMD cases can be attributed to these risk factors. (arvojournals.org)
  • 3 The prevailing view is that AMD is a complex disorder derived from interactions between multiple genetic and environmental risk factors. (arvojournals.org)
  • Hence there is a pressing need to complement programmes that reduce risk factors with policies that create conditions for better health in vulnerable groups. (who.int)
  • This project investigates complement activity by developing a western blot assay to measure inactive (C3) and active (C3b) forms of complement to determine whether the loss of Cfd reduces complement activity. (uvic.ca)
  • In conclusion, synthesis of C3 and factor B in keratinocytes is regulated by some cytokines , known to be produced by inflammatory cells and keratinocytes . (bvsalud.org)