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)

Renal involvement is known to occur in leprosy. In the present study the possible role of reactive oxygen species (ROS) in causation of renal damage in mice infected with Mycobacterium leprae has been investigated. At least six animals from each group (control and infected) were killed at 0 day, 3, 6 and 9 months postinfection. The results showed a significant increase in the chemiluminescence (CL) response of peritoneal macrophages which was maximum between 3 and 6 months. No significant increase was observed in CL response of blood neutrophils. A significant increase in lipid peroxidation was observed at 3 and 6 months as evident by an increase in malondialdehyde levels. The increased ROS production might be the cause of lipid peroxidation. The renal damage is alos evident by decrease in the activity of renal brush border membrane enzymes, namely, alkaline phosphatase, leucine aminopeptidase and r-glutamyl transpeptidase. Thus ROS might play a role during early stages of M. leprae infection but in the later stages other immunological mechanisms may overpower the effect of ROS.
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PMID:Role of reactive oxygen species in renal damage in experimental leprosy. 750 Aug 14

Previously, nine fecal isolates from wild birds and a domestic swine were identified as helicobacters by phenotypic characterization and reaction with a helicobacter genus-specific DNA probe. These isolates fell into three biotypes by analysis of phenotypic traits. To further characterize these isolates, full 16S rRNA sequences were determined for strains representing each biotype, and sequence comparison indicated that the strains represented three novel, phylogenetically defined Helicobacter species. Three 16S rRNA-based DNA probes were designed and used to identify the remaining strains. Probe reactivity divided the strains into the same three groups identified phenotypically. Six of the isolates represented a new species of the genus Helicobacter for which we propose the name Helicobacter pametensis sp. nov. The following phenotypic features distinguished H. pametensis from other Helicobacter and Campylobacter species: positive tests for oxidase, catalase, alkaline phosphatase, nitrate reduction, growth at 42 degrees C, and growth in the presence of 1% glycine; negative tests for urease, gamma glutamyl transpeptidase, indoxyl acetate hydrolysis, and hippurate hydrolysis; and susceptibility to nalidixic acid and cephalothin. H. pametensis cells were motile and possessed one subterminal sheathed flagellum at each end. The two additional Helicobacter species were similar to H. pametensis except that they were urease positive, hydrolyzed indoxyl acetate, and were resistant to cephalothin. Because these two additional species are phenotypically similar and are represented by only two isolates for one species and one isolate for the other, they are not formally named but are referred to as Helicobacter sp. "Bird-B" and Helicobacter sp. "Bird-C."(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phylogeny of Helicobacter isolates from bird and swine feces and description of Helicobacter pametensis sp. nov. 752 Jul 43

The hypothesis was tested that goats allowed ad libitum access to feed during the dry period develop higher post partum hepatic triacylglycerol concentrations than do goats given a restricted amount of feed during the dry period. Goats in their second or more pregnancies were either given a restricted amount of hay, maize silage and concentrate (n = 5) or had free access to this feed mixture while the composition was kept constant (n = 11). After parturition both groups were allowed ad libitum access to feed. Post partum liver triacylglycerol concentrations, as measured in liver biopsies, were significantly raised in goats allowed ad libitum access to feed during the dry period. The increase in liver triacylglycerols was associated with slightly higher plasma concentrations of non-esterified fatty acids but lower serum 3-hydroxybutyrate concentrations. The feeding regimen during the dry period did not significantly influence post partum liver glycogen concentrations and serum levels of glucose, cholesterol, and insulin. The increase in post partum liver triacylglycerol concentrations in the goats allowed ad libitum access to feed instead of a restricted ration during the dry period, was associated with a significant rise in serum alkaline phosphatase activities, whereas other liver function and cell damage indicators in serum, i.e. aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transpeptidase, and bilirubin, were unchanged. Feed intake after parturition tended to be higher in the goats allowed ad libitum access to feed during the dry period but milk production was significantly raised.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver triacylglycerol concentrations around parturition in goats with either pre-partum restricted or free access to feed. 757 Dec 80

In this study we measured some parameters that are associated with ethanol damage to the liver. The method allowed us to determine the injury that chronic and acute ethanol treatments produce at the cellular level without interference from homeostatic or compensatory mechanisms. The system used is a hepatic fetal human cell line, WRL-68, which retains, in culture, many of the liver-specific functions. WRL-68 cells do not metabolise ethanol, and consequently we could evaluate the effect of ethanol alone. We explored two different conditions: 30 days with 0.1 M ethanol (chronic treatment) and 24 h in the presence of 0.5 M ethanol (acute treatment). 1. The transmission electron microscopy studies revealed, in both treatments, the presence of granules not usually present in the cytoplasm of control cells and morphological mitochondrial alterations in chronically treated cells. 2. Lipid peroxidation, measured as the rate of malondialdehyde production, increased three and a half times in acutely treated cells and about twofold in chronically treated cells. 3. The percentage of total activity (activity in the medium/(activity in the medium + activity of the cells). 100) and the enzymatic activity in the culture medium of gamma glutamyl transpeptidase (GGT), alanine amino transferase (ALAT), aspartate amino transferase (ASAT) and alkaline phosphatase (AI-P), increased. 4. We measured some parameters related to the transport of sodium across the membrane. Cells chronically treated with ethanol had higher rate constants and effluxes than control cells. There was no difference between the total and passive efflux. Ethanol treated cells apparently lacked the ouabain sensitive pathway. In acutely treated cells, the total sodium efflux and the rate constant were enhanced. Sodium pools in the acutely treated cells were diminished and active sodium pumping was seven times higher than in control cells. 5. We determined the number of high affinity ouabain binding sites per cell. Ethanol did not alter the number of pumps, rather it seems to induce a functional alteration. Our results indicate that ethanol per se induces lipid peroxidation, alters enzymatic activities, sodium transport systems, sodium pools and cellular morphology, and that all these changes may be partly responsible for ethanol-induced hepatotoxicity. The data compare favourably with those reported in the literature for many different systems. Therefore our model for studying the mechanism of alcohol effects appears to be valid, with the advantage of being able to compare experiments that can be done in the same system and under the same conditions.
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PMID:The effect of chronic and acute ethanol treatment on morphology, lipid peroxidation, enzyme activities and Na+ transport systems on WRL-68 cells. 759 92

Antimitochondrial antibodies are of considerable importance for the diagnosis of primary biliary cirrhosis. Several subtypes of antimitochondrial antibodies have been identified and the pattern has been associated with prognosis of the disease in the long term course. 22 patients with primary biliary cirrhosis (19 female, 3 male; age 29-66, mean 49 years) were examined for the occurrence of the subtypes of antimitochondrial antibodies anti M2, anti M4 and anti M9. Diagnosis of primary biliary cirrhosis was based on elevated cholestatic enzymes, antimitochondrial antibodies, histology and exclusion of other chronic liver disease in all patients and elevated serum IgM concentration in 18/22 patients. Most patients were included in a study protocol of the Swiss Association for the Study of the Liver and treated with 10 mg/kg/day oral ursodeoxycholic acid. According to the subtype pattern of antimitochondrial antibodies, patients were divided into 4 groups A to D (A: anti M2-, anti M4-, anti M9+; B: anti M2+, anti M4-, anti M9+; C: anti M2+, anti M4-, anti M9- and D: anti M2+, anti M4+, anti M9-). The groups were compared with respect to the prognostically relevant parameters age, bilirubin, albumin, prothrombin time and peripheral edema, as well as the occurrence of granulomas in liver biopsy, galactose elimination capacity and response to treatment with ursodeoxycholic acid during one year. Treatment response was expressed as decrease of the serum concentration of IgM, GPT, alkaline phosphatase, gamma glutamyl transpeptidase and bilirubin. No significant differences between the four groups were found with respect to the prognostically relevant parameters, histology and galactose elimination capacity at study entry.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Significance of subtype pattern of antimitochondrial antibodies in primary biliary cirrhosis for prognostic parameters and response to ursodeoxycholic acid]. 774 Feb 90

Hepatic arteritis is a rare complication in systemic lupus erythematosus (SLE). Information about its clinical manifestations is still very limited. Elevated serum r-glutamyl transpeptidase and alkaline phosphatase levels, but without elevated bilirubin and transaminase levels, were found in the present report to be the clinical presentation of hepatic arteritis. This clinical picture originally suggested a disease of the biliary tree. Hepatic arteritis must be included in the differential diagnosis of biliary tract disorders in SLE.
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PMID:Clinical manifestations of hepatic arteritis in systemic lupus erythematosus. 779 21

Primary sclerosing cholangitis (PSC) is a cholestatic liver disease characterized by inflammation and obliterative fibrosis of bile ducts leading to their progressive destruction (1-4). As a consequence, cholestasis with elevated serum levels of alkaline phosphatase (AP) and gamme glutamyl transpeptidase (GGT) and bilirubin in more advanced disease is the most prominent feature of this disease. The diagnosis of PSC is primarily based on endoscopic retrograde cholangiography with demonstration of irregular strictures and dilatations. In liver biopsy, typical findings are portal and periodical inflammation and fibrosis. Since PSC is a focal disease, the characteristic histological findings may or may not be seen in a single liver biopsy. The cause of PSC is still unknown. The association with histocombatibility antigens indicates that immunological mechanisms may be involved but it is still unclear whether the disease is immunogenic. Alternatively, bacteria and bacterial toxins from the colon might play a role (3, 4). In 70% of cases PSC is associated with ulcerative colitis (5) and, therefore, in all patients with this intestinal disease who also have elevated levels of liver enzymes, a cholangiography should be performed. Recently, in up to 80% of patients with PSC anti-neutrophil-cytoplasmatic-antigens (ANCA) were found to be elevated (6) and, in future, this test may help to diagnose the disease more easily. Up to now, however, the disease is usually diagnosed at a relatively advanced stage when the patients have jaundice.
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PMID:Ursodeoxycholic acid in the treatment of primary sclerosing cholangitis. 782 95

In order to evaluate the relative contribution of aflatoxin B1 (AFB1)-induced toxicity towards a methyl-deficient diet influenced AFB1 carcinogenesis, a no-observed-effect-level (NOEL) for AFB1, with reference to liver damage, was determined in rats fed a nutritionally complete amino acid-defined basal (CMS) diet or a choline-methionine-deficient (CMD) diet. After 3 weeks of dietary treatment, male Fischer 344 rats received a single, oral dose of AFB1 in the range of 100-600 pg/kg body weight. At 24, 48 and 72 h after AFB1 treatment, six serum biochemical parameters were analysed in parallel with histological examination of liver sections. In rats fed the CMS diet and receiving 250-600 micrograms/kg AFB1, serum levels of glutamyl oxalo-transaminase (SGOT), glutamyl pyruvic transaminase (SGPT), alkaline phosphatase (ALP) and total bilirubin increased, glucose levels decreased and gamma glutamyl transpeptidase (GGT) levels remained unchanged over the 72-h period following mycotoxin treatment. However, at 100 micrograms/kg AFB1, these serum parameters remained at control levels. Pathological examination of liver sections indicated no significant lesions at 100 micrograms/kg AFB1 confirming this as the non-necrogenic dose or NOEL in CMS diet group rats. In contrast, in CMD diet fed rats, serum or pathology data showed no obvious time- or dose-response to mycotoxin treatment, extensive hepatic lipidosis in response to dietary treatment being the only predominant lesion in this diet group. The milder response of CMD rat livers to a single dose of AFB1 suggest a possible reduction in the susceptibility of these livers to AFB1 toxicity.
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PMID:Acute hepatic response to aflatoxin B1 in rats fed a methyl-deficient, amino acid-defined diet. 809 59

We measured whole blood-associated acetaldehyde (WBAA) levels in 225 teetotalers (123 females, 102 males) between the ages of 18 and 86 years. Values were normally distributed, but mean values for females were significantly lower than for males (7.6 +/- 0.6 vs. 7.9 +/- 0.7 microM, p < 0.0001). There was a significant positive correlation with age for the entire group (r2 = 0.149, p = 0.001) and for both sexes. The correlation with WBAA and age was stronger for females. Significant but lesser positive correlations were found between WBAA and other variables that increase with age, including glucose, fructosamine, cholesterol, alkaline phosphatase, serum glutamate pyruvate transaminase (SGPT), gamma glutamyl transpeptidase (GGT), and creatinine in the entire data set. Partial r analyses indicated that the correlations were mediated through the primary association of WBAA and age. We conclude that in individuals who do not consume ethanol there are significant sex differences in whole blood acetaldehyde and that the values increase throughout life.
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PMID:Studies of whole blood-associated acetaldehyde levels in teetotalers. 821 89

To evaluate the clinical applications of serum thymidine kinase (TK) activity, we compared the results obtained with this parameter with those of other liver function tests in 27 patients with acute viral hepatitis and 16 normal controls. In those in the acute stage, the serum TK activity increased significantly to 55.5 +/- 66.5 U/L. There was no significant correlation between serum TK activity and findings for serum albumin, bilirubin, alkaline phosphatase or r-glutamyl transpeptidase. However, it did correlate significantly well with the serum activity of aspartate aminotransferase (AST) (r = 0.621, P < 0.01), alanine aminotransferase (ALT) (r = 0.551, P < 0.01), and lactate dehydrogenase (LDH) (r = 0.620, P < 0.01). Serum TK activity reached higher than 70 U/L in 8 of 11 patients with hepatitis A; however, no patients with the other types of hepatitis reached such a high level. During the recovery stage, the serum TK activity decreased significantly to 5.9 +/- 1.7 U/L (P < 0.01), and did not correlate with AST, ALT, LDH or other conventional liver function parameters. The data suggest that an elevation of serum TK in patients with acute viral hepatitis results from hepatocellular damage. A marked elevation of serum TK activity may thus provide a marker for acute hepatitis A infection.
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PMID:Elevated serum thymidine kinase activity in patients with acute viral hepatitis. 844 Apr 24


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