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Biomedical subjects

S Yu

Publications and source records attributed to S Yu.

At least 397 records · Page 22Linked to original sources
PubMed1993

[Anoxia-reperfusion injury to endothelial cells: mechanism and protection].

Endothelial cells in the aortic walls of inbred SD rats were cultured in MEM culture medium containing 10% calf serum, and an anoxia-reperfusion injury model was established. The effect of anoxia-reperfusion injury on cultured endothelial cells was studied by measurements of membrane fluidity, intracellular Ca content, the release rate of 51Cr and the uptake rate of trypan-blue. The effect of fructose 1-6 diphosphate (FDP) and captopril (Cap) on cultured endothelial cells was also investigated. The findings indicated that the two drugs might protect cultured endothelial cells from anoxia-reperfusion injury. The mechanism of anoxia-reperfusion injury and the protective effect of the two drugs on cultured endothelial cells were briefly discussed.

Animals↗
PubMed1992

Priority among air pollution factors for preventing chronic obstructive pulmonary disease in Shanghai.

The problems that city environmental protection planners face are how important the air pollution exposures are in relation to chronic obstructive pulmonary disease (COPD) in local residents and which factor should be controlled most urgently. The purpose of our study is to determine the control priority among ambient sulphur dioxide (SO2) inhalable particulates (IP) and indoor use of coal to prevent COPD in residents of the city. Ambient air pollution is mainly from SO2 and IP(< 10 nm). Indoor air pollution is mainly from the use of coal for heating and/or cooking. Distribution of ambient SO2, and IP concentrations were described using a quartic trend surface simulation. When stratified by two extreme levels of ambient SO2 and IP and types of fuel used indoors, eight local area populations in four communities with different combinations of exposure levels were selected. In each community a local area population mostly using coal and one mostly burning gas was chosen. Chronic obstructive pulmonary diseases (COPD, ICD 490-493) including chronic bronchitis, asthma and emphysema, are a major cause of death in residents of Shanghai. The relationship between the three air pollution factors and their health effects were analyzed at the level of mortality (1978-1987, 232,459 person-years), prevalence of symptoms (12,037 persons) of COPD, lung function and non-specific immunologic function (514 women). The results show that indoor use of coal has stronger associations with health than estimated exposure to ambient SO2 or IP.

Adult↗
PubMed1992

Assembly and secretion of fibrinogen. Degradation of individual chains.

Hep G2 cells produce surplus A alpha and gamma fibrinogen chains. These excess chains, which are not secreted, exist primarily as free gamma chains and as an A alpha-gamma complex. We have determined the intracellular location and the degradative fate of these polypeptides by treatment with endoglycosidase-H and by inhibiting lysosomal enzyme activity, using NH4Cl, chloroquine, and leupeptin. Free gamma chain and the gamma component of A alpha-gamma are both cleaved by endoglycosidase-H, indicating that the gamma chains accumulate in a pre-Golgi compartment. Lysosomal enzyme inhibitors did not affect the disappearance of free gamma chains but inhibited A alpha-gamma by 50%, suggesting that A alpha-gamma is degraded in lysosomes. The degradative fate of individual chains was determined in transfected COS cells which express but do not secrete single chains. Leupeptin did not affect B beta chain degradation, had very little affect on gamma chain, but markedly inhibited A alpha chain degradation. Antibody to immunoglobulin heavy chain-binding protein (GRP 78) co-immunoprecipitated B beta but not A alpha or gamma chains. Preferential binding of heavy chain-binding protein to B beta was also noted in Hep G2 cells and in chicken hepatocytes. Taken together these studies indicate that B beta and gamma chains are degraded in the endoplasmic reticulum, but only B beta is bound to BiP. By contrast A alpha chains and the A alpha-gamma complex undergo lysosomal degradation.

Ammonium Chloride↗
PubMed1992

Optical isomers of a leukotriene B4 antagonist have differential effects on granulocyte diapedesis in the guinea pig dermis.

Leukotriene B4 (LTB4) is a proinflammatory product of arachidonic acid metabolism that has been implicated in a number of inflammatory diseases. When injected intradermally into the guinea pig, LTB4 has been shown to elicit a dose-dependent infiltration of granulocytes as assessed by the level of the neutrophil marker enzyme myeloperoxidase. SC-41930 [7-[3-(4-acetyl-3-methoxy-2-propylphenoxy)propoxy]-3,4-dihydro-8- propyl-2H-1-benzopyran-2-carboxylic acid] is a potent LTB4 receptor antagonist. When compounds were coadministered along with LTB4 (35 ng) into the dermal site, racemic SC-41930, (+)-SC-41930, and (-)-SC-41930 each inhibited granulocyte accumulation with ED50 values of 340 +/- 30, 98 +/- 5.7, and 1000 +/- 142 ng, respectively; when given intravenously inhibited with ED50 values of 0.5 +/- 0.06, 0.3 +/- 0.04, and 1.4 +/- 0.19 mg/kg, respectively; and when given intragastrically inhibited with ED50 values of 1.7 +/- 0.20, 1.4 +/- 0.23, and 3.0 +/- 0.41 mg/kg, respectively.

Animals↗
PubMed1992

Dietary iron loading does not influence biliary iron excretion in rats.

The effect of dietary iron loading on biliary iron excretion was investigated with male Wistar rats aged 6 wk. The rats were fed purified diets with either 174 or 1740 mg FeSO4. 7H2O/kg diet and demineralized water for 6 wk. Blood haemoglobin, hematocrit, and iron concentrations in kidney and heart were not affected and iron concentrations in liver, spleen, and tibia were significantly raised after feeding the high-iron diet. The high-iron diet did not raise biliary iron excretion, suggesting that biliary iron excretion does not play an important role in regulating iron metabolism in rat after dietary iron loading.

Animals↗
PubMed1992

Effects of acute pentobarbital administration on GABAA receptor-regulated chloride uptake in rat brain synaptoneurosomes.

Effects of acute pentobarbital administration on GABAA receptor-regulated muscimol-stimulated, pentobarbital-stimulated, or flunitrazepam-enhanced, muscimol-stimulated chloride uptake were studied in the brains of Sprague-Dawley rats. Animals received sodium pentobarbital, 60 mg/kg IP, and cerebral cortical and cerebellar synaptoneurosomes were isolated at 10 min, 1 h, and when animals had awakened. The basal uptake of chloride was not changed in either cerebral cortex or cerebellum at different time periods after pentobarbital administration. Ten minutes after sodium pentobarbital administration, muscimol-stimulated chloride uptake was significantly reduced in cerebellum when the muscimol concentration was 2.5, 5, or 20 microM and in cerebral cortex when the concentration of muscimol was 5 or 10 microM (p less than 0.05, Duncan multiple-range test). One hour after pentobarbital administration or after animals had awakened, chloride uptake in brains from pentobarbital-treated animals was less at low concentration of muscimol (2.5 microM). No significant difference was found in either cerebral cortex or cerebellum in pentobarbital-(125-1,000 microM) stimulated or flunitrazepam-(2.5-20 microM) enhanced, muscimol-(3 microM) stimulated chloride uptake at different time periods after pentobarbital administration. Saline treatment had no effects on the basal or muscimol-stimulated chloride uptake in cerebellar synaptoneurosomes when compared with naive animals. The results demonstrate that GABAA receptor-regulated chloride uptake is decreased after acute pentobarbital administration, an effect that is reversible.

Animals↗
PubMed1992

Fragile X syndrome without CCG amplification has an FMR1 deletion.

We describe a patient with typical clinical features of the fragile X syndrome, but without cytogenetic expression of the fragile X or an amplified CCG trinucleotide repeat fragment. The patient has a previously uncharacterized submicroscopic deletion encompassing the CCG repeat, the entire FMR1 gene and about 2.5 megabases of flanking sequences. This finding confirms that the fragile X phenotype can exist, without amplification of the CCG repeat or cytogenetic expression of the fragile X, and that fragile X syndrome is a genetically homogeneous disorder involving FMR1. We also found random X-inactivation in the mother of the patient who was shown to be a carrier of this deletion.

Adult↗
PubMed1992

Experience with direct molecular diagnosis of fragile X.

The utility of the pfxa3 probe for direct molecular diagnosis of the fragile X (FRAXA) has been established. This probe detects amplification of an unstable DNA element consisting of variable length CCG repeats. The size of the amplified fragment is correlated with phenotype and was determined using PstI digested DNA in family members. In 35 families with the fragile X, there was correspondence in 183 cases between the presence of an amplified unstable element and the presence of the fragile X chromosome independently determined by cytogenetics, position in the pedigree, or linked DNA markers flanking the fragile X. There was also correspondence in 124 cases between the presence of the normal 1.0 kb PstI fragment and absence of the fragile X chromosome independently determined by linked flanking markers. Six additional families considered to be isolated cases of 'fragile X' had been diagnosed before recognition of FRAXD. The pfxa3 probe confirmed the cytogenetic diagnosis in three families, the other three being rediagnosed as non-fragile X. A further two families had consistent expression of a different folate sensitive fragile site, FRAXE, close to FRAXA but not associated with fragile X syndrome and not detectable with the pfxa3 probe. Subsequent referrals were received from additional family members or from members of new families for whom carrier status had not been predetermined by linked markers. Direct pfxa3 diagnosis for the 135 females within these 222 additional cases was confirmed by dosage analysis with the control probe pS8.(ABSTRACT TRUNCATED AT 250 WORDS)

Artifacts↗
PubMed1992

Quantitative risk assessment for lung cancer from exposure to metal ore dust.

To quantitatively assess risk for lung cancer of metal miners, a historical cohort study was conducted. The cohort consisted of 1113 miners who were employed to underground work for at least 12 months between January 1, 1960 and December 12, 1974. According to the records of dust concentration, a cumulative dust dose of each miner in the cohort was estimated. There were 162 deaths in total and 45 deaths from lung cancer with a SMR of 2184. The SMR for lung cancer increased from 1019 for those with cumulative dust dose of less than 500 mg-year to 2469 for those with the dose of greater than 4500 mg-year. Furthermore, the risk in the highest category of combined cumulative dust dose and cigarette smoking was 46-fold greater than the lowest category of dust dose and smoking. This study showed that there was an exposure-response relationship between metal ore dust and lung cancer, and an interaction of lung cancer between smoking and metal ore dust exposure.

Adult↗
PubMed1992

Fragile-X syndrome: unique genetics of the heritable unstable element.

The fragile site at Xq27.3 is an unstable microsatellite repeat, p(CCG)n. In fragile-X syndrome pedigrees, this sequence exhibits variable amplification, the length of which correlates with fragile-site expression. There is a direct relationship between increased p(CCG)n copy number and propensity for instability: individuals having large amplifications exhibit somatic variation due to increased instability. The instability of the p(CCG)n repeat, when transmitted through affected pedigrees, explains the unusual segregation patterns of fragile-X phenotype, referred to as the Sherman paradox. All individuals of fragile-X genotype were found (where testing was possible) to have a parent with amplified p(CCG)n repeat, indicating that few, if any, cases of fragile-X syndrome are not familial.

Blotting, Southern↗