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)

Prior studies identified a cell-surface antigen, p75/150, that exclusively associated with the tumorigenic phenotype of the HeLa parent and the tumorigenic phenotype of the HeLa parent and the tumorigenic segregants of suppressed, nontumorigenic HeLa x human fibroblast cell hybrids. Candidate p75/150 cDNA clones were isolated from a D98/AH.2 (HeLa) cDNA library using oligonucleotide probes derived from p75/150 partial peptide sequence data. A data base search revealed close similarity of p75/150 with intestinal alkaline phosphatase (IAP) [Berger, J., Garantini, E., Hua, J. C. & Udenfriend, S. (1987) Proc. Natl. Acad. Sci. USA 84, 695-698]. We demonstrate that p75/150 is identical to HeLa IAP by the following criteria: (i) 47/49 amino acid identity of p75 peptide sequence with IAP, (ii) restriction maps for the p75/150 candidate cDNA clone and IAP are identical, (iii) partial DNA sequence analysis of p75/150 candidate cDNA clones revealed complete nucleotide identity with IAP, except for a single nucleotide substitution in the 5' untranslated region, (iv) transfection of a p75/150 cDNA expression vector into the nontumorigenic hybrid, CGL1, yielded p75/150 antibody-positive transfectants that also expressed partially heat-resistant alkaline phosphatase activity. Northern blot analysis demonstrated that high levels of HeLa IAP mRNA were expressed in D98/AH.2 and the tumorigenic segregant CGL4; however, no mRNA was detected in CGL1. Nuclear run-on analyses indicate that HeLa IAP mRNA expression in the HeLa x fibroblast hybrids is regulated at the level of transcription initiation. Furthermore, evidence is discussed supporting the involvement of a chromosome 11 tumor suppressor locus in the regulation of HeLa IAP gene expression.
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PMID:Identification of the HeLa tumor-associated antigen, p75/150, as intestinal alkaline phosphatase and evidence for its transcriptional regulation. 230 98

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 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

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

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

A prospective study of the initial liver laboratory tests was carried out in the following patients: 55 patients with alcoholic liver disease, 53 with cholangitis, 41 with hepatocellular carcinoma, 65 with acute viral hepatitis, and 49 with hepatitis-B surface antigen-positive chronic active hepatitis. There was considerable overlap in the levels of the serum gamma-glutamyl transpeptidase (GT) and alkaline phosphatase (AP) among the five groups. However, the ratio of GT to AP was significantly higher in the group with alcoholic liver disease than in any of the other four groups. When the ratio was higher than 1.4, the diagnostic efficiency for distinguishing the alcohol group from the other four groups was 78% (the normal upper limit for GT and AP being 35 and 115 U/1, respectively). A possible explanation for this higher ratio in alcoholic liver disease is suggested. We conclude that when the GT and AP is greater than 1.4, it is of greater diagnostic value than either variable alone in differentiating alcoholic from other liver diseases.
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PMID:The diagnostic value of the ratio of serum gamma-glutamyl transpeptidase to alkaline phosphatase in alcoholic liver disease. 612 89

The monoclonal antibodies (mAb) H315, H317, and OKT9 have been used in immunofluorescence to investigate the expression of fetal trophoblast membrane antigens by cells within human term amniochorionic membranes and the marginal area of term placental bed tissue. OKT9 reacted only with trophoblast of placental chorionic villi and did not react with any nonvillous cytotrophoblast population: this mAb is known to identify the cell surface receptor for transferrin. H315 identifies a trophoblast-specific cell-surface antigen and strongly stained both placental villous trophoblast and the cytotrophoblastic layer of amniochorion. This mAb also stained some extravillous cytotrophoblast in the term placental bed, notable interstitial cytotrophoblast within maternal decidua. H317, which identifies placental-type alkaline phosphatase, gave the same distribution pattern as H315.
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PMID:Localization in human term placental bed and amniochorion of cells bearing trophoblast antigens identified by monoclonal antibodies. 631 18

The biotin/avidin system was incorporated into the enzyme-linked immunosorbent assay (ELISA) technique to increase the sensitivity of the standard ELISA for the detection of mouse antibody to hepatitis B surface antigen ((anti-HBs and HBsAg, respectively). Two biotin/avidin ELISA designs were studied. In both assays, 96-well polystyrene plates were coated with HBsAg, post-coated with 0.5% gelatin and incubated with dilutions of mouse anti-HBs. In the biotin/avidin (BA) ELISA, reagents were added to antibody reacted wells in the following sequence: biotinylated goat anti-mouse IgG (b-GAMG), avidin-alkaline phosphatase (Av-AP) and substrate. The order of reactants after mouse antibody in the biotin/avidin/biotin (BAB) ELISA was b-GAMG, avidin, biotinylated alkaline phosphatase (b-AP) and substrate. The sensitivities of BA ELISA, BAB ELISA and a standard ELISA using a glutaraldehyde conjugated goat anti-mouse enzyme were compared to AUSAB (a commercial radioimmunoassay) using a panel of 23 mouse anti-HBs sera. All 3 ELISAs were more sensitive than AUSAB; the standard ELISA, BAB ELISA and BA ELISA were respectively 50, 1173 and 4134 times more sensitive than AUSAB for detection of mouse anti-HBs activity.
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PMID:Utilization of the biotin/avidin system to amplify the sensitivity of the enzyme-linked immunosorbent assay (ELISA). 683 65

The employees of the Japan National Railways Co. working in the Tokyo area, comprising 98% men over the age of 40 yr, were examined for hepatitis B virus seromarkers and routine liver function tests (serum glutamic oxaloacetic transaminase, alkaline phosphatase, and zinc turbidity test) and were followed for 5 yr. The examinees included 202 hepatitis B surface antigen carriers, 502 positive for hepatitis B surface antibody, and 2426 negative for both. We found that the frequency of continuously abnormal liver function test was higher in hepatitis B surface antigen carriers compared with noncarriers. Of the 202 carriers, 4 (1.98%) died from hepatocellular carcinoma with or without cirrhosis, whereas in 2928 noncarriers only 2 (0.07%) died from liver diseases unrelated to hepatitis B virus, the difference being 28.3-fold. Three of the 4 who died from hepatocellular carcinoma initially had normal liver function tests. Mortality in carriers with initially normal liver function tests was 44.5 times higher than that in noncarriers with normal tests. Thus, asymptomatic carriers carry a high risk of dying from chronic liver disease. Routine liver function tests appear of limited value in predicting prognosis.
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PMID:Prognosis of hepatitis B virus surface antigen carriers in relation to routine liver function tests: a prospective study. 707 36

Forty-one Egyptian schoolchildren (36 boys and five girls; age, 12-16 years) who were heavily infected with Schistosoma mansoni were studied. Symptomatic subjects had swimmer's itch and hematochezia. Hepatomegaly was found in 39 and splenomegaly in 31 children. All subjects had eosinophilia, 13 had anemia, 31 had elevated levels of serum globulins, and nine had elevated levels of alkaline phosphatase. All but one subject had antibody to hepatitis A virus, and 26 had antibody to hepatitis B core antigen, antibody to hepatitis B surface antigen, or both. Oxamniquine was given in single daily doses of 20 mg/kg of body weight for either two or three days and cured 50% and 85%, respectively, of subjects treated; ova excretion was reduced by 86%-93% for up to 12 months. Morbidity was associated with heavy S. mansoni infection. Therapy with oxamniquine was safe and efficacious.
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PMID:Clinical characteristics and response to therapy in Egyptian children heavily infected with Schistosoma mansoni. 708 3


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