Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies of gene expression often examine a pool of RNA extracted from the diverse cell types making up a tissue. We have developed a method for isolating vessels from the brain in order to understand the changes occurring in the vessels during the pathogenesis of cerebral malaria. Vessels were visualised by incubating sections of mouse brain with a substrate for alkaline phosphatase. Vessels were collected by laser capture microdissection and the specificity was monitored by measuring the expression of cell-specific markers. RNA from the captured vessels was highly enriched in mRNA for genes associated with endothelial cells and pericytes. Measurement of indoleamine 2,3-dioxygenase mRNA indicated it was possible to detect changes in gene expression, due to malaria infection, occurring specifically within the vessels. Laser capture microdissection can be used to study changes in gene expression occurring at the blood-brain barrier.
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PMID:Isolating vessels from the mouse brain for gene expression analysis using laser capture microdissection. 1211 80

The pathogenicity of Plasmodium falciparum is due to the unique ability of infected erythrocytes (IRBCs) to adhere to vascular endothelium. We investigated whether adhesion of IRBCs to CD36, the major cytoadherence receptor on human dermal microvascular endothelial cells (HDMECs), induces intracellular signaling and regulates adhesion. A recombinant peptide corresponding to the minimal CD36-binding domain from P falciparum erythrocyte membrane protein 1 (PfEMP1), as well as an anti-CD36 monoclonal antibody (mAb) that inhibits IRBC binding, activated the mitogen-activated protein (MAP) kinase pathway that was dependent on Src-family kinase activity. Treatment of HDMECs with a Src-family kinase-selective inhibitor (PP1) inhibited adhesion of IRBCs in a flow-chamber assay by 72% (P <.001). More importantly, Src-family kinase activity was also required for cytoadherence to intact human microvessels in a human/severe combined immunodeficient (SCID) mouse model in vivo. The effect of PP1 could be mimicked by levamisole, a specific alkaline-phosphatase inhibitor. Firm adhesion to PP1-treated endothelium was restored by exogenous alkaline phosphatase. In contrast, inhibition of the extracellular signal-regulated kinase 1/2 (ERK 1/2) and p38 MAP kinase pathways had no immediate effect on IRBC adhesion. These results suggest a novel mechanism for the modulation of cytoadherence under flow conditions through a signaling pathway involving CD36, Src-family kinases, and an ectoalkaline phosphatase. Targeting endothelial ectoalkaline phosphatases and/or signaling molecules may constitute a novel therapeutic strategy against severe falciparum malaria.
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PMID:Src-family kinase signaling modulates the adhesion of Plasmodium falciparum on human microvascular endothelium under flow. 1251 11

The clinical case of one patient with fever of unknown origin, due to granulomatous hepatitis of tuberculous etiology was presented. The patient was a a 50-year-old woman, with 50 days illness characterized by chills, 39 degrees C fever and heavy diaphoresis. She had a record of seven malaria cases. She looked thin and pale at the initial physical examination. During the evolution, she developed pancytopenia, massive hepatosplenomegaly, jaundice, and anasarca. The patient underwent screening tests for infection, neoplasias, collagenosis, and granulomatous diseases. The laboratory tests showed transaminase-alkaline phosphatase dissociation, which led to the final diagnosis of tuberculosis, through the histological examination of the liver parenchyma. The specific treatment against tuberculosis caused remission of fever, ascites, and hepatomegaly and normalization of liver tests, with satisfactory clinical evolution.
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PMID:[Granulomatous tuberculous hepatitis as cause of fever of unknown origin]. 1252 48

In a study of the influence of malaria-associated renal impairment on plasma concentrations of bilirubin, 111 Indian cases of Plasmodium falciparum malaria who had >34.2 microM total bilirubin/litre plasma were investigated. As the aim was to exclude those cases who had concomitant hepatic or (non-malarial) renal dysfunction, 19 cases who had serum concentrations of alanine aminotransferase (ALT) or alkaline phosphatase (AP) that were at least double the normal mean values were withdrawn. Of the remaining 92 patients, 47 showed evidence of renal impairment, the other 45 having plasma concentrations of creatinine that were <177 microM/litre. Plasma concentrations of the liver enzymes ALT and AP were similar for those with and without renal impairment. The plasma concentration of conjugated bilirubin (P<0.02), that of total bilirubin (P<0.05) and the ratio between the two (P<0.01) were, however, all significantly higher in the 47 patients with renal impairment than in the 45 with apparently normal renal function. The plasma concentration of creatinine was found to be not only positively correlated with the plasma concentrations of total (r=0.34; P<0.01) and conjugated (r=0.41; P<0.001) bilirubin but also negatively correlated with the urinary excretion rate for conjugated bilirubin (r=-0.34; P<0.001). The malaria-associated mortality was significantly higher among the patients with renal impairment than among those with apparently normal renal function, with 12 and three deaths, respectively (P<0.001). With increasing renal impairment there therefore appears to be a fall in the renal excretion of conjugated bilirubin. This leads to a disproportionate rise in the plasma concentration of conjugated bilirubin and this, since bilirubin can be toxic to renal tissue, may further worsen the renal impairment.
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PMID:Influence of renal impairment on plasma concentrations of conjugated bilirubin in cases of Plasmodium falciparum malaria. 1451 56

We studied leukocyte alkaline phosphatase in malaria to assess leukocyte defence mechanisms. Twenty-seven patients with malaria were stratified into two classes on the basis of disease severity. Fifteen malaria negative patients were taken as controls. Data showed mild polymorphonucleated cell activation, in the absence of correlation with the severity of the malaria.
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PMID:Leukocyte alkaline phosphatase in Plasmodium falciparum malaria. 1507 85

Disrupted signaling through lymphotoxin beta receptor (LTbetaR) results in severe defects of the spleen and even loss of all other secondary lymphoid tissues, making mice susceptible to diverse infectious agents. Surprisingly, however, we find that female LTbetaR-deficient mice are even more resistant to blood stages of Plasmodium chabaudi malaria than wild-type C57BL/6 mice. Higher resistance of LTbetaR-deficient mice correlates with an earlier onset of reticulocytosis, and the period of anemia is shorter. After surviving fulminant parasitemias of about 35%, mice develop long-lasting protective immunity against homologous rechallenge, with both spleen and liver acting as anti-malaria effectors. Testosterone suppresses resistance, i.e. all mice succumb to infections during or shortly after peak parasitemia. At peak parasitemia, testosterone does not essentially affect cellularity and apoptosis in the spleen, but aggravates liver pathology in terms of increased cell swelling, numbers of apoptotic and binucleated cells and reduced serum alkaline phosphatase levels, and conversely, reduces inflammatory lymphocytic infiltrates in the liver. In the spleen, hybridization of cDNA arrays identified only a few testosterone-induced changes in gene expression, in particular upregulation of INFgamma and IFN-regulated genes. By contrast, a much larger number of testosterone-affectable genes was observed in the liver, including genes involved in regulation of the extracellular matrix, in chemokine and cytokine signaling, and in cell cycle control. Collectively, our data suggest that testosterone dysregulates the inflammatory response in spleen and liver during their differentiation to anti-malaria effectors in malaria-resistant female LTbetaR-deficient mice, thus contributing to the testosterone-induced lethal outcome of malaria.
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PMID:Testosterone responsiveness of spleen and liver in female lymphotoxin beta receptor-deficient mice resistant to blood-stage malaria. 1578 53

Human cerebral malaria is caused by a protozoan parasitic with no cure till date. The isolation of brain capillaries i.e. microvessels has permitted the in vitro study related to cerebral function. Microvessels were isolated from normal and P. yoelii infected mice brain cortex and subjected to biochemical characterization by the following enzyme markers viz alkaline phosphatase, gamma-glutamyI transpeptidase and monoamine oxidase and electron microscopically. Limited studies have been carried out in relation to drug metabolizing enzymes in cerebral microvessels of rodents. The present studies have been carried out in relation to status of drug metabolizing enzymes during P. yoelii infection in cerebral microvessels of mice. The data obtained depicted a clear cut impairment of cytochrome P450 (a terminal monooxygenase) and related indices viz b5, benzopyrene hydroxylase, aminopyrene-n-demethylase, aniline hydroxylase except NADH cytochrome e reductase which increased during P. yoelii infection in mice as compared to normal. Further the oral drug administration (arteether) treatment brought back the altered MFO system normal a week alter cessation of drug treatment.
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PMID:Studies on drug metabolizing enzymes during arteether treatment of Plasmodium yoelii nigeriensis infected mice cerebral microvessels. 1663

Liver function tests were performed in 61 vivax, 54 malariae and 15 ovale malaria patients who were admitted to Bangkok Hospital for Tropical Diseases between 2001 and 2004. The objective of the study was to evaluate changes in hepatic biochemical indices before and after treatment with artemisinin derivatives. On admission and prior to treatment, hepatic dysfunction was found among the 3 groups. Serum liver function tests and physical examinations were performed weekly during the 28-day follow-up period. Initially elevated serum bilirubin and diminished albumin returned to normal within 2 weeks of treatment. Serum alkaline phosphatase and aminotransferases returned to within normal limits within 3 weeks. We conclude that patients with Plasmodium vivax, P. malariae and P. ovale infections had slightly elevated serum bilirubin, aminotransferase and alkaline phosphatase levels, and hypoalbuminemia. These minor abnormalities returned to normal within a few weeks after treatment with therapies based on artemisinin derivatives.
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PMID:Minor liver profile dysfunctions in Plasmodium vivax, P. malaria and P. ovale patients and normalization after treatment. 1717 May 71

Malaria leads to pathophysiological and biochemical alterations in placenta and blood of pregnant mice. A significant decrease in the sugar, protein and lipid levels in the placental homogenate of pregnant-infected mice was observed compared to the pregnant mice. However, serum protein content was not altered much in the pregnant-infected mice as compared to the levels in control mice. The serum lipid level enhanced significantly in both pregnant and non pregnant-infected mice. The enzymatic activities of alkaline phosphatase and acid phosphatase altered significantly in malaria-infected placenta. Our study clearly highlights the possible role of these enzymes in damaging the placenta which in turn may jeoparadise the fetal growth together with altered biochemistry of placenta. Therefore biochemical along with pathological alterations occurring during malaria infection in pregnancy may account for compromised maternal fetal relationship.
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PMID:Plasmodium berghei induced biochemical alterations in pregnant mice. 1759 79

A prospective study among the patients (n = 301) belonging to the coastal districts of Orissa having complicated falciparum malaria with multiorgan failure fulfilling modified APACHE II criteria, for a period of two years in this hospital setting was carried out with particular emphasis on hepatic involvement. There were 206 males and the rest females. Hepatic involvement in the form of raised serum bilirubin levels > or = 6 mg% and prothombin time > 4 compared to controls was found in 192 cases (63.8%). On analysis out of 192 cases predominantly conjugated hyperbilirubinaemia, mixed patterns and unconjugated hyperbilirubinaemia were seen in 115 (59.9%), 64 (33.3%) and 13 (6.8%) cases respectively. Serum bilirubin ranged from 6 to 38 mg%. Aminotransferase aspartate (AST, SGOT) and aminotransferase alkaline (ALT, SGPT) were raised almost two-fold in 98% cases of multiorgan failure with hepatic failure with mean values of 78 +/- 30.4 IU/l and 81 +/- 29.06 IU/l respectively. Nearly three-fold elevation of alkaline phosphatase was observed in 80% cases with mean (315 +/- 39.4 IU/l). Prothombin time was prolonged with mean 7 +/- 3 seconds. Serum proteins and albumin/globulin ratio were normal. There was no difference in glycaemic status over controls. In selected cases, liver histopathological study showed abnormalities in the form of Kupffer cell hyperplasia, mononuclear cell infiltration, hepatocyte necrosis, fatty changes and cholestasis. Majority of patients in multiorgan failure who died, had hepatic failure.
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PMID:Malarial hepatitis as a component of multiorgan failure--a bad prognostic sign. 1791 92


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