Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well established that Giardia infection causes malabsorption. However, the precise mechanism of such a malabsorption is not known. To investigate this, transport studies, using the tissue accumulation technique, were carried out in mice infected with G. lamblia obtained from human stools. There was a significant fall in the transport of D-glucose, L-alanine and glycine in the infected animals compared with the controls. Kinetics of the D-glucose and glycine transport system were examined by measuring the tissue uptake in the presence of different concentrations of the substrate. For glucose, the affinity constant (Km) for the transport site was the same (4 . 37mM) in normal and infected animals but the maximal transport rate (V max) was considerably reduced in infected animals (158 . 7 mu moles/hr/g tissue) compared with (357 . 1 microgram moles/hr/g tissue) in controls. Results with glycine were similar; the Km was similar in control and infected animals (5 . 7 mM) whereas the V max was reduced in infected animals (27 . 02 microgram moles/hr/g tissue) compared with controls (45 . 5 micrograms moles/hr/g tissue). Analysis of the intestinal enzymes showed a significant decrease in the levels of brush border sucrase, lactase and alkaline phosphatase in infected animals; the cellular enzymes, LDH, GOT and GPT remained unaffected. The observed aberrations in the transport functions and brush border enzymes suggest that G. lamblia causes malabsorption by damaging the epithelial membrane of the enterocyte.
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PMID:Transport studies and enzyme assays in mice infected with human Giardia lamblia. 717 14

Three hundred and sixty day-old commercial broiler chicks were assigned to a 3 x 2 factorial arrangement of treatments to examine the effects of three levels of Saccharomyces cerevisiae 0, .05, and .1% of feed, and two levels of aflatoxin, 0 and 5 ppm, singly and in combination on aflatoxicosis. Each treatment group was replicated three times. The S. cerevisiae and aflatoxin were incorporated in a standard commercial broiler ration and fed to chicks for 4 wk. Data were collected weekly on body weights, and at the end of the experiment on the relative weights of the liver, proventriculus, pancreas, and heart. Serum concentrations of the albumin, total protein, cholesterol, uric acid, triglycerides, and enzyme activities of alanine transaminase, aspartate aminotransferase, lactase dehydrogenase, and creatine phosphokinase were also evaluated. Results showed that chicks receiving aflatoxin-contaminated feed had suppressed body weight (456 g), which significantly improved (516 g) with the inclusion of .1% S. cerevisiae. The relative weights of liver (3.58%), heart (.916%), and proventriculus (.770%), which increased significantly with the addition of 5 ppm of aflatoxin, were restored to 3.00, .783, and .680%, respectively, with the dietary inclusion of .1% S. cerevisiae. The serum concentrations of albumin and total protein (.66 and 1.62 g/100 mL), which were significantly decreased by aflatoxin, were elevated to .88 and 2.24 g/100 mL, respectively, with the inclusion of .1% S. cerevisiae.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The use of Saccharomyces cerevisiae to suppress the effects of aflatoxicosis in broiler chicks. 841 59

Autoimmune hepatitis is a chronic inflammatory disease in the liver with potential to the development of liver fibrosis. Recent evidences suggest that bone marrow derived mesenchymal stem cells (BMSCs) may exert its therapeutic activity through exosomes. Moreover, miR-223 is highly expressed in BMSCs and plays an important role in autoimmune diseases. Therefore, in this study, hepatoprotective role of BMSCs and miR-223 was investigated in both mice and hepatocytes. Liver antigen S100 was used to establish autoimmune hepatitis model in mice while LPS and ATP were used to establish cell injury model in hepatocyte. Before the experiments, BMSCs were infected with pre-miR-223 and transfected with miR-223 inhibitor respectively. Exosomes from bone marrow stem cells were isolated by ultracentrifugation. Liver injury was evaluated by serum levels of ALT and AST as well as liver histology. Inflammation and cell death were examined by inflammatory cytokines and lactase dehydrogenase respectively. Both BMSCs-exo and BMSCs-exomiR-223(+) significantly reversed either S100 or LPS/ATP induced injury in mice and hepatocytes. Meanwhile, the expressions of cytokines, NLRP3 and caspase-1 were also downregulated by BMSCs-exo and BMSCs-exomiR-223(+) at both protein and mRNA levels in mice and hepatocytes. Moreover, BMSCs-exomiR-223(-) reverses the effects of BMSCs-exo and BMSCs-exomiR-223(+) in mouse AIH and in hepatocytes. In conclusion, bone marrow stem cell derived exosomes can protect liver injury in an experimental model of autoimmune hepatitis and the mechanism could be related to exosomal miR-223 regulation of NLRP3 and caspase-1.
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PMID:BMSCs-derived miR-223-containing exosomes contribute to liver protection in experimental autoimmune hepatitis. 2914 57