Pathogenesis

Schistosomiasis is an endemic disease in Egypt caused by the trematode Schistosoma which has different species. c the best known form of chronic disease with a wide range of clinical manifestations. The pathogenesis of schistosomiasis is related to the host cellular immune response. This leads to granuloma formation and neo angiogenesis with subsequent periportal fibrosis manifested as portal hypertension, splenomegaly and esophageal varices. Intestinal schistosomiasis is another well identified form of chronic schistosomal affection.

8p kethamoi1 17-11-2019 29 2   Download

Document "Constipation: A global perspective" introduction of content: Cascades—a resource-sensitive approach, pathogenesis and risk factors, associated conditions and medication, diagnostic criteria for functional constipation, patient evaluation,... Invite you to consult.

13p vovanvovan2013 13-05-2016 36 2   Download

In the course of trying to understand the pathogenesis of leishmaniasis in relation to extracellular matrix (ECM) elements, laminin, a major ECM protein, has been found to bind saturably and with high affinity to a 67-kDa cell surface protein of Leishmania donovani. This interaction involves a single class of binding sites, which are ionic in nature, conformation-dependent and possibly involves sulfhydryls. Binding activity was significantly enhanced by Zn2+, an effect possibly mediated through Cys-rich zinc finger-like sequences on laminin....

8p system191 01-06-2013 41 4   Download

The immune coagulant fgl2/fibroleukin has been previously shown to play a pivotal role in the pathogenesis of murine and human fulminant hepatitis and fetal loss syndrome. Constitutive expression of fgl2 transcripts at low levels are seen in cytotoxic T cells, endothelial, intestinal and tropho-blast cells, while specific factors (such as virus and cytokines) are required to induce high levels of fgl2 expression in other cell types including monocytes/macrophages.

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Flexibacter maritimus, a Gram-negative bacterium, is a fish pathogenresponsible fordisease infinfishspecies andacause of cutaneous erosiondisease in sea-caged salmonids. For the development of serology based diagnostics, protective vac-cines, and a study of pathogenesis, the structural analysis of the lipopolysaccharide (LPS) producedby the bacteriumhas been undertaken. We now report that an acidic O-specific polysaccharide, obtained by mild acid degradation of the F. maritimusLPSwas found to be composed of a disac-...

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The Goodpasture antigen-binding protein, GPBP, is a serine⁄threonine kinase whose relative expression increases in autoimmune processes. Tumor necrosis factor (TNF) is a pro-inflammatory cytokine implicated in auto-immune pathogenesis. Here we show that COL4A3BP, the gene encoding GPBP, maps head-to-head withPOLK, the gene encoding for DNA polymerase kappa (polj), and shares with it a 140-bp promoter containing a Sp1 site, a TATA-like element, and a nuclear factor kappa B (NFjB)-like site

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Tobacco pathogenesis-related protein 1a (PR-1a) is induced in plants during the hypersensitive response (HR) after exposure of plants to salicylic acid (SA) and by develop-mental cues.Gene activation by these diverse stimuli is mediated via anas-1-like element in the PR-1aupstream region.To further analyze the significance of thiscis-acting sequence, an authentic as-1element from the cauliflower mosaic virus 35S RNA promoter was inserted into the PR-1apromoter in place of theas-1-like motif.

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The pathogenesis of formation of neurofibrillary tangles (NFTs) in Alzhei-mer’s disease (AD) brains is unknown. One of the possibilities might be that translation of tau mRNA is aberrantly regulated in AD brains.

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Fibrillization ofa-synuclein (a-Syn) is closely associated with the formation of Lewy bodies in neurons and dopamine (DA) is a potent inhibitor for the process, which is implicated in the causative pathogenesis of Parkin-son’s disease (PD). To elucidate any molecular mechanism that may have biological relevance, we tested the inhibitory abilities of DA and several analogs including chemically synthetic and natural polyphenols in vitro.

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Recently, a novel plaque-associated protein, collagenous Alzheimer amy-loid plaque component (CLAC), was identified in brains from patients with Alzheimer’s disease. CLAC is derived from a type II transmembrane colla-gen precursor protein, termed CLAC-P (collagen XXV). The biological function and the contribution of CLAC to the pathogenesis of Alzheimer’s disease and plaque formation are unknown.

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Oxidative stress and imbalance between free radical generation and detoxi-fication may play a pivotal role in the pathogenesis of Leber’s hereditary optic neuropathy (LHON). Mitochondria, carrying the homoplasmic 11778⁄ND4, 3460⁄ND1 and 14484⁄ND6 mtDNA point mutations associ-ated with LHON, were used to generate osteosarcoma-derived cybrids. Enhanced mitochondrial production of reactive oxygen species has recently been demonstrated in these cybrids [Beretta S, Mattavelli L, Sala G, Trem-olizzo L, Schapira AHV, Martinuzzi A, Carelli V & Ferrarese C (2004) Brain127, 2183–2192]. ...

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The urea cycle enzyme arginase (EC 3.5.3.1) hydrolyzes L-arginine to L-ornithine and urea. Mammalian arginases require manganese, have a highly alkaline pH optimum and are resistant to reducing agents. The gastric human pathogen,Helicobacter pylori, also has a complete urea cycle and contains therocFgene encoding arginase (RocF), which is involved in the pathogenesis ofH. pyloriinfection. Its arginase is specifically involved in acid resistance and inhibits host nitric oxide production.

11p dell39 03-04-2013 50 5   Download

Programmed cell death is a major component of both normal development and disease. The roles of cell death during either embryogenesis or pathogenesis, the signals that modulate this event, and the mechanisms of cell demise are the major subjects that drive research in this field. Increasing evidence obtained both in vitro and in vivo supports the hypothesis that a variety of cell death programs maybe triggered in distinct circumstances.

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Homocysteine (Hcy) is anonprotein-forming sulphur amino acid that plays an important role in remethylation and trans-sulphuration processes. In recent years, it has been suggested that increased levels of plasma Hcy may play a role in the pathogenesis of various diseases, particularly at the cardiovascular level. The pathogenic mechanism of hyperhomocysteinemia, however, has not been clarified.

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Ouabain, a sodiumpump (Na + /K + -ATPase) inhibitor, has been shown to act as a hormone and is possibly involved in the pathogenesis of hypertension. The mechanismby which ouabain may act was investigated using primary cultures of human umbilical artery endothelial cells (HUAECs), which are known to express and release the vasoconstrictive hor-mone endothelin (ET-1). Fiveminutes after application, low concentrations of ouabain induced Ca 2+ oscillations and stimulated ET-1 release from endothelial cells into the medium.

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Mitochondrial fatty acid oxidation deficiencies are due to genetic defects in enzymes of fatty acidb-oxidation and transport proteins.Genetic defects have been identified in most of the genes where nearly all types of sequence vari-ations (mutation types) have beenassociatedwithdisease.In this paper, we will discuss the effects of the various types of sequence variations encountered and review current know-ledge regarding the genotype–phenotype relationship, espe-cially in patients with acyl-CoA dehydrogenase deficiencies where sufficient material exists for a meaningful discussion....

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Bermuda grass pollen (BGP) contains a very complex mixture of allergens, but only a few have been characterized. One of the allergens, with an apparent molecular mass of 21 kDa, has been shown to bind serum IgE from 29% of patients with BGP allergy. A combination of chromato-graphic techniques (ion exchange and reverse phase HPLC) was used to purify the 21 kDa allergen.

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The amyloidbpeptide (Ab) is crucial for the pathogenesis of Alzheimer’s disease. Aggregation of monomeric Ab into insoluble amyloid fibrils proceeds through several soluble Abintermediates, including protofibrils, which are believed to be central in the disease process. The main reason for this is their implication in familial Alzheimer’s disease with the Arctic amyloid precursor protein mutation (E693G).

13p inspiron33 26-03-2013 46 4   Download

During pathogenesis of transmissible spongiform encephalopathies (TSEs) an abnormal form (PrP Sc ) of the host encoded prion protein (PrP C ) accu-mulates in insoluble fibrils and plaques. The two forms of PrP appear to have identical covalent structures, but differ in secondary and tertiary structure.

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Neurodegenerative disorders are associated with oxidative stress. Low den-sity lipoprotein (LDL) exists in the brain and is especially sensitive to oxi-dative damage. Oxidative modification of LDL has been implicated in the pathogenesis of neurodegenerative diseases. Therefore, protecting LDL from oxidation may be essential in the brain.

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