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Biomedical subjects

J Yin

Publications and source records attributed to J Yin.

At least 181 records · Page 10Linked to original sources

Frequent loss of heterozygosity at the retinoblastoma locus in human esophageal cancers.

Abnormalities in the retinoblastoma tumor suppressor gene (Rb) have been observed in a large number of human cancers. Loss of heterozygosity is a common mode of allelic inactivation of Rb and other tumor suppressor genes. We investigated DNA from 61 primary human esophageal tumors for loss of heterozygosity at the Rb locus using a polymerase chain reaction-based restriction fragment length polymorphism assay. Of informative cases, we found loss of heterozygosity in 14 of 26 (54%) squamous cell carcinomas and 5 of 14 (36%) adenocarcinomas. These data support the hypothesis that Rb inactivation is involved in the pathogenesis and/or progression of esophageal cancer.

Adenocarcinoma↗

Reduction to homozygosity involving p53 in esophageal cancers demonstrated by the polymerase chain reaction.

Loss of heterozygosity affecting chromosome 17p has been detected at high frequencies in a variety of human tumors, including cancers of the colon, breast, lung, and brain. One presumed target of these losses is p53, a tumor suppressor gene located on 17p. To our knowledge, loss of heterozygosity has not yet been reported at any locus, including p53, in human esophageal cancer. Moreover, current methods of detecting loss of heterozygosity depend on the availability of large amounts of high molecular weight DNA, making the study of small biopsy specimens or paraffin-embedded tissues problematic. We examined 52 primary human esophageal neoplasms for loss of heterozygosity affecting the p53 gene by using the polymerase chain reaction. Loss of one allele was detected in 52% of informative cases and was more common in squamous carcinomas than in adenocarcinomas. Southern blot analysis was used to confirm polymerase chain reaction-derived data. The identification of allelic loss in approximately half of the tumors analyzed supports the hypothesis that inactivation of p53 is involved in the pathogenesis of esophageal cancer.

Base Sequence↗

A quantifiable phenotype of viral propagation.

A system has been identified where a virus, replicating continuously on its host, displays a distinct and quantifiable phenotype, and thereby continuously reports on the state of the virus-host relationship. When bacteriophage T7 is plated out with its host, Escherichia coli, it establishes a constant-velocity infection wave, which is driven by an autocatalytic reaction-diffusion mechanism. The velocity--which is easily measured--continuously reflects the infection environment. The simplicity of the system extends to the investigator an unprecedented ability to monitor and control a viral infection process.

Escherichia coli↗

Covalent labelling of bovine lens multicatalytic proteinase complex with [3H]di-isopropyl fluorophosphate.

Enzymatically active lens multicatalytic proteinase complex bound [3H]iPr2P-F after incubation for 3 hours at ambient temperature. Label was associated with the lowest molecular weight band (Mr 22,000) on sodium dodecyl sulfate polyacrylamide gels. This binding was inhibited by preincubation of the enzyme with the cysteine-directed reagent, p-chloromercuribenzoate, which inhibits all three hydrolytic activities of the enzyme. Leupeptin, which inhibits the arginyl-hydrolyzing component, but not the iPr2P-F-inhibitable leucyl-hydrolyzing component of the enzyme, does not inhibit [3H]iPr2P-F binding. These data suggest that the leucy-hydrolyzing component of the lens multicatalytic proteinase complex is localized to the 22,000 Mr subunit and is a member of the thiol-dependent subclass of serine proteinases.

Amino Acid Sequence↗

[Apolipoproteins AI, B100, CII, CIII and E in human cerebrospinal fluid].

Apolipoproteins AI, B100, CII, CIII and E contents were measured by radial immunodiffusion assay kits developed by our Research Unit. The apolipoprotein in 10 human cerebrospinal fluid samples was determined. Results show that there are no apo B100, CII or trace apo CIII in human cerebrospinal fluid, the levels of apo AI in cerebrospinal fluid are 1.00 +/- 0.54 mg/dl with a range of 0.35-2.00 mg/dl and the apo E content is 0.69 +/- 0.16 mg/dl with a range of 0.51-0.99 mg/dl. The results are discussed.

Apolipoprotein A-I↗

Effect of a traditional Chinese medicine, yin zhi huang, on bilirubin clearance and conjugation.

Oral administration of Yin Zhi Huang (YZH) daily for 3 days in rabbits accelerated plasma clearance of infused unconjugated bilirubin. A similar but less dramatic effect resulted from 3 days pretreatment with phenobarbital, 70 mg/kg/day orally. Similar doses were injected intraperitoneally in rats for 3 days, following which the bile ducts were ligated and bilirubin infused intravenously. Plasma clearance of unconjugated bilirubin and plasma appearance of conjugated bilirubin were faster, and hepatic bilirubin content was higher in both YZH- and phenobarbital-treated rats than in control animals. These observations indicate that YZH is as effective as phenobarbital in stimulating bilirubin metabolic pathways and suggest that the drugs may share common mechanisms of action.

Administration, Oral↗

Induction of hepatic bilirubin-metabolizing enzymes by the traditional Chinese medicine yin zhi huang.

Daily administration of either phenobarbital (60 mg/kg) or yin zhi huang (YZH, 30-60 ml/kg) for 5 days to rats similarly accelerated the clearance and conjugation of intravenously infused bilirubin. However, the two drugs had quite different effects on liver enzyme activities associated with xenobiotic metabolism and with bilirubin metabolism. Phenobarbital markedly increased cytochrome P-450 levels and the cytochrome-P-450-mediated formation of 4-hydroxybiphenyl whereas YZH had a slightly depressive effect on this enzyme system. Both drugs increased glucuronyl transferase activity using bilirubin and alpha-naphthol as substrates. Bilirubin conjugation in microsomes activated by uridine diphosphate-N-acetylglucosamine (NAG) was greater in YZH- than in phenobarbital-treated rats whereas phenobarbital was a more effective inducer in digitonin-activated enzyme. When alpha-naphthol was used as substrate (NAG-activated glucuronyl transferase), pretreatment with phenobarbital produced a greater increase in activity than did YZH. Glutathione-S-transferase activity (using chlorodinitrobenzene as substrate) was increased more than 2-fold by phenobarbital but only slightly (1.29 X) by YZH. In contrast, YZH (60 ml/kg) was more effective than phenobarbital in increasing glutathione peroxidase activity using cumene hydroperoxide as substrate. YZH appears to be a relatively specific inducer of enzymes involved in bilirubin metabolism.

Animals↗

[Studies on molluscicidal effect of bromoacetamide against Ganesella virgo].

Molluscicidal effect of bromoacetamide against the snails in laboratory and field trials were observed. Grassland of Guiliu River in Keerqinyouyiquanqi District, Neimengol Autonomous Region was selected for field trials. The results showed that bromoacetamide was fairly effective against Ganesella virgo, the intermediate host of Dicrocoelium chinensis and Eurytrema pancreaticum. In field trials, 7 days after spraying at a dosage of 0.5g/m2, 74.7-84.7% of snails were killed. When a dosage of 1g/m2 was used, the mortality of snails reached 84.8-95.7%.

Acetamides↗

[Effect of yin zhi huang on bilirubin excretion in animals with unconjugated hyperbilirubinemia].

Yin Zhi Huang (YZH) given stomach perfusion daily for three days in rabbits accelerated plasma clearance of infused unconjugated bilirubin. A similar but less dramatic effect could be obtained by using YZH or phenobarbital i. p. daily for three days in rats employing simultaneously with the method of bile duct ligation, plasma indirect bilirubin levels was lower but hepatic bilirubin content and plasma direct bilirubin levels were higher in both YZH and phenobarbital treated rats than those in the control animals. These observations suggested that YZH and phenobarbital shared a common mechanism of acting in lowering the indirect bilirubin levels of serum.

Animals↗

Airways obstruction associated with graft versus host disease after bone marrow transplantation.

Eight patients, five with chronic granulocytic leukaemia and three with severe aplastic anaemia, developed moderately severe airflow obstruction after allogeneic bone marrow transplantation. All eight had clinically and radiologically normal lungs before undergoing transplantation. Treatment in the patients with chronic granulocytic leukaemia before transplantation included high dose total body irradiation. All eight patients developed acute and chronic graft versus host disease after transplantation. The pulmonary syndrome consisted of cough, dyspnoea, and wheezing beginning six to 20 weeks after transplantation, with ratios of forced expiratory volume in one second (FEV1) to vital capacity (VC) falling to 60% or less of predicted values. The three patients with severe aplastic anaemia had relatively mild graft versus host disease and acute chest infection may have initiated or contributed to their airways obstruction, which subsequently resolved. The five patients with chronic granulocytic leukaemia had more severe graft versus host disease and more progressive respiratory problems; two died and three continued to have persistent airflow obstruction 11, 15, and 20 months after transplantation. None of those with chronic granulocytic leukaemia improved. Transfer factor (TLCO) was reduced in all patients after bone marrow transfer and did not improve; in the patients with chronic granulocytic leukaemia the reduction in TLCO preceded the fall in FEV1/VC ratio. Open lung biopsy in one of the patients with chronic granulocytic leukaemia showed obliterative bronchiolitis with lymphocytic infiltration consistent with graft versus host disease. Bronchodilators were of no benefit in the management of these patients, but prompt treatment of infection and early use of corticosteroids may have contributed to the improvement seen in the patients with severe aplastic anaemia.

Adolescent↗

Reconstitution of intercalator-induced DNA scission by an active component from nuclear extracts.

Treatment with intercalating agents causes formation of protein-associated DNA breaks in mammalian cells in culture and in the nuclei isolated from these cells. We found that this effect, when induced by the intercalator m-AMSA, required a component which could be dissociated from nuclei by 0.3 M NaCl. The effect was restored by combining the extracted nuclei with the nuclear extract. The active component of the extract eluted in gel filtration at a point corresponding to a molecular weight of 800 000. During its reaction with DNA, DNA-protein links and DNA breaks appeared in approximately equal frequencies. In this respect the reaction stimulated by m-AMSA resembled the reaction of a topoisomerase with DNA. However, intercalator-stimulated formation of protein-associated DNA breaks differed from the activity of the nuclear topoisomerase I in that there was a different optimum salt concentration and a different apparent molecular weight.

Aminoacridines↗

Topoisomerase I activities in L-1210 cell nuclei.

Topoisomerase was extracted from L-1210 nuclei by 0.35 M sodium chloride Extract fractionation by molecular weight revealed two activities. The activities were quantitatively determined using a technique based on the electrophoretic separation of 3H-labelled DNA product from substrate. This technique enables the determination of topoisomerase activity in extracts where nuclease activity is also present.

Animals↗

Interaction of serum lipoproteins with the intestine. Evidence for specific high density lipoprotein-binding sites on isolated rat intestinal mucosal cells.

To determine if plasma lipoproteins interact and therefore possibly regulate intestinal lipoprotein metabolism, we investigated the binding, internalization, and degradation of 125I-labeled low density lipoprotein (LDL) and high density lipoprotein (HDL) by enzyme-dispersed rat intestinal mucosal cells. Both human and rat LDL and HDL were bound, internalized, and degraded in a concentration-dependent manner with calculated half-saturation occurring at approximately 30, 35, 35, and 15 micrograms/ml for human LDL, rat LDL, human HDL, and rat HDL, respectively. Isolated brush border membranes had no saturable or specific binding sites for 125I-labeled HDL or LDL, suggesting that lipoproteins may be bound to receptors on lateral or basal membranes of mucosal cells. Compared with HDL, LDL binding was characterized by a large non-specific component. LDL of human and the rat were not only displaced by excess LDL but at least as effectively by excess HDL of their own species. Labeled HDL was displaced by corresponding unlabeled lipoproteins, but human LDL could produce only minor displacement of human HDL3. ApoE-deficient rat HDL, separated by heparin-Sepharose affinity chromatography also showed highly specific saturable binding to intestinal cells. Thus, apparently two different lipoprotein binding sites exist in intestinal plasma membranes, one recognizing B and/or E apoproteins present in human and rat LDL and rat HDL while another binds human HDL3 and apoE-deficient rat HDL which contain A apoproteins as major components.

Animals↗