Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used monoclonal anti-idiotypes (anti-Id) 63.14, previously shown to mimic polymeric human serum albumin (polyHSA) and bind its receptor on hepatitis B surface antigen (HBsAg), to produce syngeneic monoclonal anti-anti-Id (Ab3) which could bear the internal image of HBsAg and mimic its immunogenicity in vivo. Nine hybridomas obtained from spleen cells of BALB/c mice immunized with 63.14 were isolated, which were able to inhibit the binding of alkaline phosphatase-conjugated 63.14 to HBsAg. Both direct and competition enzyme-linked immunosorbent assay (ELISA) showed that 4 of these clones were able to mimic HBsAg since they reacted with polyHSA and inhibited the binding of monoclonal and polyclonal anti-HBsAg to the viral antigen. To determine whether these Ab3 could induce an immune response against HBsAg in vivo, we injected a series of rabbits with Ab3 G11 or HBsAg and tested their sera after the second boost. ELISA, radioimmunoassay and Western blot experiments showed that G11 was as effective as HBsAg in inducing a specific anti-HBsAg immune response. These data indicate that our Ab3 can mimic HBsAg both in vitro and in vivo and might be useful as alternative vaccine for HBV infection.
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PMID:Interactions between hepatitis B virus and polymeric human serum albumin. II. Development of syngeneic monoclonal anti-anti-idiotypes which mimic hepatitis B surface antigen in the induction of immune responsiveness. 356 4

The hepatoprotective antioxidant bioflavonoid cianidanol has beneficial therapeutic and immunomodulatory effects in chronic hepatitis. Its action on natural killer (NK) cell activity has not yet been studied in hepatitis B virus (HBV) infection. In the present study, the in vitro and in vivo effects of the drug on NK cell activity have been determined in six patients with chronic HBV hepatitis and in ten healthy control subjects. Two methods were used: an enzyme release assay and a cytotoxicity test based on the assessment of endogenous alkaline phosphatase activity of the target cells. The in vitro effect of the drug was assessed using cianidanol at 10(-6), 10(-5) and 10(-4) M concentrations. For in vivo studies, HBV hepatitis patients were treated with cianidanol at a daily dose of 3.0 g cianidanol for seven days and were investigated before and after the treatment. Chronic HBV hepatitis patients showed a moderate decrease in NK cell activity compared to the controls, but after the cianidanol therapy their NK cell activity significantly rose to 68.0% +/- 9.5% (p less than 0.01). Cianidanol in vitro inhibited the NK cell activity both in hepatitis and healthy groups when using K-562 target cells and the lactic acid dehydrogenase enzyme release assay, but did not influence or even slightly enhance the NK activity when human embryonic fibroblast cells and alkaline phosphatase assay were used for the test. After the 7-day in vivo treatment, the in vitro inhibitory action of the drug was diminished or absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of cianidanol on natural killer cell activity in patients with chronic B virus hepatitis. 359 73

Short synthetic oligonucleotides have been covalently cross-linked to alkaline phosphatase using the homobifunctional reagent disuccinimidyl suberate. The oligomers, twenty-one to twenty-six bases in length, are complementary to unique sequences found in herpes simplex virus, hepatitis B virus, Campylobacter jejuni and enterotoxigenic Escherichia coli. Each oligomer contains a single modified base with a 12-atom "linker arm" terminating in a reactive primary amine. Cross-linking through this amine results in oligomer-enzyme conjugates composed of one oligomer per enzyme molecule that have full alkaline phosphatase activity and can hybridize to target DNA fixed to nitrocellulose within 15 minutes. The hybrids are detected directly with a dye precipitation assay at a sensitivity of 10(6) molecules (2 X 10(-18) mol) of target DNA in 4 hours development time. The enzyme has no apparent effect on selectivity or kinetics of oligonucleotide hybridization and the conjugates can be hybridized and melted off in a conventional manner.
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PMID:Preparation of oligodeoxynucleotide-alkaline phosphatase conjugates and their use as hybridization probes. 374 5

Aflatoxin carcinogenesis appears to relate to multiple factors. This includes bulky adduct formation at DNA guanine N-7. The process also requires more extensive physiological degradation, possibly by the toxin alone as the active principle, but in instances also involving other assaults (e.g., hepatitis B virus). Since aflatoxin carcinogenesis involves complex effects, we have undertaken to define the range of influence of this common food contaminant upon a susceptible model, the broiler-type chick. Aflatoxicosis in two treated groups was indicated by jaundice, coagulopathy, dehydration of combs and shanks, retardation of body weight, and decrease in bursa weight. Blood clotting time, hemoglobin content, erythrocyte and packed-cell volume were affected. Hepatocytes were swollen and had undergone fatty degeneration. Bile duct hyperplasia was evident. Total serum protein, alkaline phosphatase, creatine, lactate dehydrogenase, serum glutamic oxalacetic transaminase and glutamyl transpeptidase were similarly abnormal in birds receiving the contaminated (0.5 and 2.5 micrograms/g aflatoxin B1) feed rations. The aflatoxin B1 and its metabolites were isolated by HPLC from chick serum, liver and muscle.
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PMID:Clinical and biochemical effects of aflatoxin in feed ration of chicks. 392 39

The clinical features of 77 patients with primary liver cell carcinoma seen over a nine-year period were examined. Eighty per cent of the patients had underlying cirrhosis, of alcoholic origin in most cases. In nine of the patients hepatitis B surface antigen was found in the serum; all nine patients were born in areas where hepatitis B virus infection is endemic. Abdominal pain and ascites were the most common presenting symptoms; they are due mainly to the locally invasive nature of the tumour. A confirmatory laboratory finding in the diagnosis is the observation of raised alkaline phosphatase levels and the presence of alpha-fetoprotein in the serum. The diagnosis should be established without performing a laparotomy and should seriously be considered in a previously stable patient with cirrhosis who deteriorates clinically without obvious cause.
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PMID:Primary liver cell carcinoma. Clinical features. 396 17

Mild abnormalities of liver function tests are frequently seen in pregnancy but return to normal after delivery. A raised serum alkaline phosphatase is common, along with a decline in the serum albumin, but the aminotransferases remain within normal limits. The physician must interpret abnormal liver function tests in pregnancy with these changes in mind, but most liver diseases in pregnancy result in more marked alterations. Viral hepatitis is the most common cause of jaundice in pregnancy, and the maternal prognosis is generally good. Perinatal transmission of hepatitis B virus is likely when the mother is positive for HBsAg. Concurrent administration of hepatitis B vaccine and HBIG to the infant has an efficacy of 90 per cent in preventing transmission to the infant. ICP is the second most common cause of jaundice in pregnancy. The condition is generally benign, although maternal and fetal mortality occasionally result, probably due to premature delivery and the bleeding tendency of cholestatic patients. Vitamin K administration may correct the coagulopathy, and cholestyramine is effective in controlling pruritus. AFLP is rare but carries a high mortality rate for both the mother and the fetus. Early diagnosis, correction of the coagulopathy, and prompt delivery may improve the outcome significantly. Patients with cirrhosis have reduced fertility, and in those who become pregnant, fetal loss is high. The effect of pregnancy or hepatocellular function is variable, but, when evidence of liver failure is present in the first trimester, termination should be considered. Variceal size and the risk of bleeding may be assessed by endoscopy. Pregnant cirrhotic patients with large esophageal varices and a history of bleeding can undergo shunt surgery. Conservative management may be appropriate for patients with small varices and no history of bleeding.
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PMID:Liver diseases in pregnancy. 405 85

A physician's personal series of 10 women treated from 1970-1979 for oral contraceptive-associated liver tumors is presented. Of the 10 women treated, 7 had hepatocellular carcinoma and 3 had benign adenomas. Symptomatology is described. Problems with diagnosis of liver dysfunctions included misleading biopsies and liver scans. The erythrocyte sedimentation rate was raised in all but 1 woman, and it was above 70 mm/h in 7. Changes in liver function tests were consistent with an intrahepatic tumor, with a striking increase in alkaline phosphatase in 9 (1170 IU/ml), and with only a slight rise in serum aspartate transaminase (mean 55 IU/ml). None of the patients had alpha fetoprotein levels above the upper limit of normal, and all patients were negative for hepatitis B surface antigen and antibody and anticore antibody. The carcinoma characteristics were similar in 7 patients (irregular trabecular arrangement with basophilic and dysplastic cells with nuclear pleomorphism and increased mitotic figures). When these oral contraceptive users were compared with 7 women diagnosed with hepatocellular tumors who had never used oral contraceptives, several striking differences were found. None of the poll users with carcinoma had raised alpha fetoproteins, whereas 4/7 nonpill users did. By arteriography, tumors in nonusers were much less vascular and less well defined. Survival rates also differed, with a 50% survival time of 1-8 years in nonusers compared with 4-8 years in pill users. The striking feature of this series is the delay in reaching a diagnosis in most of the 10 cases treated.
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PMID:Oral-contraceptive-associated liver tumours: occurrence of malignancy and difficulties in diagnosis. 610 35

An enzyme histochemical study was performed to investigate abnormal enzyme activity in human hepatocellular carcinoma (HCC) and, by application of these staining reactions to noncancerous liver disorders, to clarify the true nature of putative percancerous lesions. The enzyme activity of hepatocytes in cirrhotic livers, hepatitis B virus (HBV)-positive cells, and dysplastic liver cells was investigated. Although the tumor cells in HCC gave an intensively positive reaction for gamma-glutamyl transpeptidase activity at the cytoplasm and the whole-cell membrane, they were essentially deficient in glucose-6-phosphatase, alkaline phosphatase, acid phosphatase, and nonspecific esterase activities. Cirrhotic liver showed loss of the orderly zonal difference of enzyme activity that is present in normal liver. However, a pattern of enzyme deviation similar to that of HCC was not recognized anywhere. Neither HBV-positive hepatocytes nor dysplastic liver cells were shown enzymatically to be direct precusors of HCC.
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PMID:Human hepatocellular carcinoma and putative precancerous disorders: their enzyme histochemical study. 611 3

During an outbreak of trichinosis, two young men--one with established trichinosis and the other with suspected infection--were found to have clinical, radiologic and histologic stigmata of a systemic necrotizing vasculopathy equivalent to classic polyarteritis nodosa. The parasitosis manifested as a pentad of fever, myalgias, facial edema, eosinophilia and hyperimmunoglobulinemia E. Features of the arteritis included mononeuritis multiplex, pain in the abdomen and joints, weight loss, hypertension, leukocytosis, thrombocytosis, microhematuria and raised alkaline phosphatase levels. A sustained remission was achieved by the administration of thiabendazole, prednisone and cyclophosphamide. Pathogenetic links between the two diseases are presented: (1) deposition of circulating immune complexes in the vessel wall; (2) adjuvant activity with cross reaction between parasitic antigen and human vessel wall; (3) immunoglobulin E (IgE) aggregates and soluble antigen IgE complexes precipitation in vessel wall; and (4) hypereosinophilia-induced tissue damage. A causal relationship of trichinosis to polyarteritis nodosa is persuasive, and we suggest that cases of hepatitis B surface antigen (HBsAg) negative polyarteritis nodosa, especially those in which myalgias and eosinophilia are prominent, may be related to trichinosis and that, conversely, patients with trichinosis and multiorgan disease should be studied for polyarteritis nodosa.
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PMID:Trichinosis-related polyarteritis nodosa. 611 36

In 1964 a 42-year-old woman was hospitalized with clinical and laboratory signs of posttransfusion hepatitis five weeks after administration of six whole blood transfusions. During the following 17 years anicteric chronic liver disease was repeatedly documented by elevations of serum aspartate aminotransferase (SGOT) and alkaline phosphatase enzymes. In 1981 hepatomegaly, progressive jaundice, and a serum alphafetoprotein level of 516,000 ng/ml were observed. Percutaneous liver biopsy showed a primary hepatocellular carcinoma (PHC). Serologic examinations failed to reveal markers for hepatitis B virus including HBsAg, anti-HBs, and anti-HBc by radioimmunoassay; antibody to hepatitis A virus was also absent. This sequence of events demonstrates a presumptive association of PHC and the agent(s) of non-A, non-B viral hepatitis.
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PMID:Primary hepatocellular carcinoma following non-A, non-B posttransfusion hepatitis. 619 33


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