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Biomedical subjects

L S Zhang

Publications and source records attributed to L S Zhang.

At least 19 recordsLinked to original sources
PubMed2001

Cloning and characterization of a novel gene (C17orf25) from the deletion region on chromosome 17p13.3 in hepatocelular carcinoma.

Using a combination of hybridization of PAC to a cDNA library and RACE technique, we isolated a novel cDNA, designated as C17orf25 (Chromosome 17 open reading frame 25, previously named it HC71A), from the deletion region on chromosome 17p13.3. The cDNA encodes a protein of 313 amino acids with a calculated molecular mass of 34.8 kDa. C17orf25 is divided into 10 exons and 9 introns, spanning 23 kb of genomic DNA. Northern blot analysis showed that the mRNA expression of C17orf25 was decreased in hepatocellular carcinoma samples as compared to adjacent noncancerous liver tissues from the same patients. The transfection of C17orf25 into the hepatocellular carcinoma cell SMMC7721 and overexpression could inhibit the cell growth. The above results indicate that C17orf25 is a novel human gene, and the cloning and preliminary characterization of C17orf25 is a prerequisite for further functional analysis of this novel gene in human hepatocellular carcinoma.

Amino Acid Sequence↗
PubMed2000

[Nasopharyngeal stenosis following uvulopalatopharyngoplasty].

OBJECTIVE: To report nasopharyngeal stenosis following UPPP and our treatment experience. METHOD: Two clinical cases were analysised. RESULT: In this paper, the complications were attributed to excessive excision palapharyngeal arches, which juried mucous membrane of nasopharyngeal inlet during the long management time as bleeding and the laser used. Surgical management was performed in two cases. One failed. One was treated successfully by rotation palato-pharyngeal flap and prolonged nasopharyngeal stent, Follow-up 20 months there was no recurrence of stenosis. CONCLUSION: Surgical correction of nasopharyngeal stenosis following UPPP is challenging and the best treatment is prevention.

Constriction, Pathologic↗
PubMed1997

Illegitimate recombination leading to allelic loss and unbalanced translocation in p53-mutated human lymphoblastoid cells.

Allelic loss and translocation are critical mutational events in human tumorigenesis. Allelic loss, which is usually identified as loss of heterozygosity (LOH), is frequently observed at tumor suppressor loci in various kinds of human tumors. It is generally thought to result from deletion or mitotic recombination between homologous chromosomes. In this report, we demonstrate that illegitimate (nonhomologous) recombination strongly contributes to the generation of allelic loss in p53-mutated cells. Spontaneous and X-ray-induced LOH mutations at the heterozygous thymidine kinase (tk) gene, which is located on the long arm of chromosome 17, from normal (TK6) and p53-mutated (WTK-1) human lymphoblastoid cells were cytogenetically analyzed by chromosome 17 painting. We observed unbalanced translocations in 53% of LOH mutants spontaneously arising from WTK-1 cells but none spontaneously arising from TK6 cells. We postulate that illegitimate recombination was occurring between nonhomologous chromosomes after DNA replication, leading to allelic loss and unbalanced translocations in p53-mutated WTK-1 cells. X-ray irradiation, which induces DNA double-strand breaks (DSBs), enhanced the generation of unbalanced translocation more efficiently in WTK-1 than in TK6 cells. This observation implicates the wild-type p53 protein in the regulation of homologous recombination and recombinational DNA repair of DSBs and suggests a possible mechanism by which loss of p53 function may cause genomic instability.

Alleles↗
PubMed1997

Echocardiography of the right ventricle-to-pulmonary artery homograft conduit of patients with transposition of the great arteries or double outlet right ventricle undergoing the Rastelli procedure.

BACKGROUND: Aortic valved homograft conduits have been valuable in right ventricular outflow tract (RVOT) reconstruction in complex congenital heart disease. METHODS: Since 1995, 12 patients ranging in age from 3 to 22 years, with transposition of the great arteries or double outlet right ventricle associated with pulmonary stenosis and ventricular septal defect, underwent the Rastelli procedure with the RVOT reconstruction utilizing cryopreserved aortic valved homograft conduits. RESULTS: Operative deaths for three patients were caused by the complexity of the heart defects (25%). One late death (8.33%) occurred as a result of pulmonary embolism one month after conduit implantation. The remaining eight patients (66.67%) survived asymptomatically with a mean postoperative hospitalization of 22 days. Preoperative Doppler echocardiographic flow visualization distinguished not only the corresponding location among the atrium, ventricle and great arteries, but also intracardiac. Mosaic flow pattern could be detected in the right ventricle and right atrium (n = 11). Postoperative echocardiographic flow visualization showed the valved homograft extracardiac conduit lay between the right ventricle and the pulmonary artery, and the valve inside the conduit could faintly be seen. Mosaic flow pattern could be observed with the systole and diastole jet in the cardiac circle (n = 8). Peak velocity and pressure gradient across the pulmonary valve after the Rastelli procedure were significantly decreased when compared with those before operation (4.13 +/- 0.44 m/s vs. 3.15 +/- 1.13 m/s, p = 0.032; 72.46 +/- 15.79 mmHg vs. 39.87 +/- 23.23 mmHg, p = 0.003). However, there were no significant differences between pre- and postoperative peak velocity and pressure gradient beyond the pulmonary valve. CONCLUSIONS: Apart from operative mortality, the application of aortic valved homograft conduits were all excellent choice for the correction of complex congenital heart disease.

Adolescent↗
PubMed1997

[Expression of c-fos in spinal cord, medulla oblongata and thalamus following epicardial application of adenosine].

Effects of epicardial application of adenosine on the expression of c-fos proto-oncogene in spinal cord, medulla oblongata and thalamus were examined in 12 sinoaortic denervated and vagotomized anesthetized rats. The results showed that following epicardial application of adenosine the Fos-like protein immunoreactive (FLI) neurons were remarkably increased in the dorsal horn of T3 spinal segment, nucleus paragigantocellularis lateralis (PGL) of medulla oblongata, ventral postero-lateral thalamic nucleus (VPL), posterior thalamic nucleus (Po), parafascicular thalamic nucleus (PF) and centrolateral thalamic nucleus (CL), while the blood pressure and heart rate were not affected. Only a few FLI neurons were found in the vehicle-control rats. The results indicate that epicardial application of adenosine may activate the pain-related neurons in spinal cord, medulla oblongata and thalamus.

Adenosine↗
PubMed1996

Chromosome painting analysis of spontaneous and methyl methanesulfonate-induced trifluorothymidine-resistant L5178Y cell colonies.

Spontaneous and methyl methanesulfonate-induced trifluorothymidine-resistant mutants in mouse lymphoma L5178Y cells were analyzed using fluorescence in situ hybridization with mouse probes specific for chromosome 11, on which the tk gene is located, and chromosome 3, as the control. 76.5% (13/17) of small-colony mutants (thought to be the result of chromosomal mutation) and 28.6% (4/14) of large-colony mutants (thought to be the result of gene mutation) showed rearranged chromosome 11. Of the mutants with abnormal chromosome 11 painting pattern, 5 small- and 2 large-colony mutants carried clonal aberrations, while the remaining 8 small- and 2 large-colony mutants showed mosaic aberrations. Most abnormalities in the small-colony mutants involved the distal region of one painted chromosome 11, where the tk+ gene maps. An increase, rather than a decrease, in chromosome 11 material was found in a majority of abnormally painted mutants. On the contrary, no rearrangements involving chromosome 3 were found in any small- and large-colony mutants analyzed except one large-colony mutant, which showed chromosome rearrangements involving both chromosome 11 and 3. The present study confirms that the majority of small-colony mutants in L5178Y cells have chromosome 11 rearrangements that can be detected by chromosome painting and that the majority of the chromosomal abnormalities in TFT-resistant mutants involved complex rearrangements.

Animals↗
PubMed1995

A comparative study of TK6 human lymphoblastoid and L5178Y mouse lymphoma cell lines in the in vitro micronucleus test.

Micronucleus induction was compared in human lymphoblastoid TK6 and mouse lymphoma L5178Y cell lines treated with model clastogens and spindle poisons, i.e., X-rays, methyl methanesulfonate, ethyl methanesulfonate, mitomycin C, colcemid, and vincristine. The spontaneous micronucleated cell (MNC) frequency was stable and reproducible in both cell lines. All clastogens and spindle poisons studied here induced micronuclei in both cell lines. They increased MNC frequency at lower concentrations or caused a greater increase at the same concentration in TK6 cells. These clastogens and spindle poisons, however, were also more toxic to TK6 than to L5178Y cells and when comparison was based on cytotoxicity, they showed more efficient MNC induction in L5178Y cells. In conclusion, neither cell line was superior to the other, and both of them can be used as target cells in the in vitro micronucleus assay.

Animals↗
PubMed1994

[Mitochondrial DNA mutation in Leber's hereditary optic neuropathy in China].

Leber's hereditary optic neuropathy (LHON), a typical maternally inherited disease, is caused by a single nucleotide change of G to A at the site of nucleotide 11,788 of mtDNA. We used PCR method to analysis mtDNA from 102 individuals of nineteen pedigrees. The results showed that 67% of the patients (30/45) and 55% (29/53) of the maternal relatives have such a mutation, while no mutation exists in the four normal individuals. The results show that Wallace's mutation is a main cause of LHON in China.

Base Sequence↗
PubMed1993

[A molecular genetic study of Leber's disease].

That Leber's hereditary optic neuropathy is caused by a single nucleotide change in the mitochondrial DNA (mtDNA) was first verified by Wallace and his colleagues in 1988. The mtDNA of 11 patients with Leber's disease from different families and of normal persons are analyzed with polymerase chain reaction by the authors, with results that confirm those of Wallace. The procedure is simple and speedy, and hence recommended for clinical utilization.

Base Sequence↗
PubMed1992

Molecular dosimetry of urinary aflatoxin-DNA adducts in people living in Guangxi Autonomous Region, People's Republic of China.

Hepatocellular carcinoma is one of the five leading human cancers causing at least 250,000 deaths each year. One of the major risk factors for this disease is exposure to dietary aflatoxins, and the development of appropriate molecular dosimetry biomarkers would facilitate the identification of individuals at risk. This study was undertaken to explore the relationship between dietary intake of aflatoxins and the excretion of the major aflatoxin-DNA adduct and other metabolites into the urine of chronically exposed people. The following protocol was developed for this investigation in Guangxi Autonomous Region, People's Republic of China, where the diets of 30 males and 12 females (ages, 25-64 years) were monitored for 1 week and aflatoxin intake levels determined each day. Starting on the fourth day, total urine volumes were obtained in consecutive 12-h fractions for 3 or 4 days. High performance liquid chromatography and competitive radioimmunoassay analyses were done on each of the urine samples, and the relationships between excretion of total aflatoxin metabolites, aflatoxin-N7-guanine, aflatoxin M1, aflatoxin P1, and aflatoxin B1, and aflatoxin B1 intake values were determined. The average intake of aflatoxin B1 by men was 48.4 micrograms/day, giving a total mean exposure during the study period of 276.8 micrograms. The average daily intake by women was 77.4 micrograms/day, resulting in a total average exposure during the 7-day period of 542.6 micrograms aflatoxin B1. Initial efforts to characterize aflatoxin metabolites in urine samples were with an analysis by competitive radioimmunoassay. The analysis by linear regression of the association between aflatoxin B1 intake/day and total aflatoxin metabolite excretion/day showed a correlation coefficient of only 0.26. These findings stimulated the immunoaffinity/analytical high performance liquid chromatography analysis for individual metabolites. When the data were analyzed by linear regression analysis, the aflatoxin N7-guanine excretion and aflatoxin B1 intake from the previous day showed a correlation coefficient of 0.65 and P less than 0.000001. Similar analysis for aflatoxin M1 resulted in a correlation coefficient of 0.55 and P less than 0.00001, whereas there was no positive statistical association between exposure in the diet and aflatoxin P1 excretion, despite aflatoxin P1 being quantitatively a major metabolite. Analysis of the total aflatoxin-N7-guanine excretion in the urine during the complete collection period plotted against the total aflatoxin B1 exposure in the diet for each of the individuals, smoothing the day to day variations, revealed a correlation coefficient of 0.80 and P less than 0.0000001.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1991

Bufalin as a potent inducer of differentiation of human myeloid leukemia cells.

Bufalin was found to be a potent inducer of differentiation in human erythroleukemia K562 cells by examination of various differentiation markers (as assessed by the morphology, histochemistry, and the abilities to phagocytose latex particles, to reduce nitro-blue tetrazolium and to develop Fc receptors). Bufalin, at a concentration as low as 10 nM, also produced a strong differentiation-inducing activity in three other human leukemia-derived cell lines (human promyelocytic HL60, monoblastic U937 and myeloblastic ML1). Treatment of K562 cells with other cardiotonic steroids, such as cinobufagin, ouabain and digitoxigenin, at the concentration of 10 nM for four days resulted in weak or no effect on the cells. These findings suggest that bufalin might have potentiality as a new agent in the differentiation therapy for human myelogenous leukemia.

Bufanolides↗
PubMed1991

Bacteriological study of juvenile periodontitis in China.

The predominant cultivable bacteria associated with juvenile periodontitis (JP) in China were studied for the first time. Subgingival plaque samples were taken on paper points from 23 diseased sites in 15 JP patients and from 7 healthy sites in 7 control subjects. Serially diluted plaque samples were plated on nonselective blood agar and on MGB agar, a selective medium for the isolation of Actinobacillus actinomycetemcomitans. Fifteen or more isolated colonies from each sample (in sequence without selection) were purified for identification. The results indicated that the microflora in healthy sulci of the 7 control subjects was significantly different from that in diseased sites of JP patients. The predominant species in healthy sulci were Streptococcus spp. and Capnocytophaga gingivalis. In JP patients, Eubacterium sp. was found in significantly higher frequency and proportion. Actinobacillus actinomycetemcomitans was not detected in any samples. It appears that this species is not associated with juvenile periodontitis in China.

Actinobacillus↗
PubMed1991

[Bayesian and RFLP linkage analysis on a DMD family].

Three methods were applied to estimate the carrier risk of the daughter of an obligate carrier of the Duchenne gene in a pedigree of Duchenne muscular dystrophy (DMD). According to Mendel's law of segregation, the daughter (III-3) of the obligate carrier (II-2) has a 50% chance of being a carrier. III-3 is also found to have a normal value in a carrier test, creatine phosphate kinase (CPK), and so the Bayesian analysis in risk estimation shows that the posterior probability that she is a carrier (25%). The restriction fragment length polymorphism (RFLP) linkage analysis indicates that the probability that III-3 is a carrier less than 5%. This result can be included in the Bayesian analysis to give an even lower risk of less than 2%. Our study demonstrates that the best result of carrier risk estimation can be obtained by a simultaneous application of Mendel's law, RFLP linkage analysis and the Bayesian analysis.

Bayes Theorem↗
PubMed1991

Effects of high erucic acid rapeseed oil on fatty acid oxidation in rat liver.

The effects of high erucic acid rapeseed oil (HER) on fatty acid oxidation in rat liver compared with low erucic acid rapeseed oil (LER) were studied. Weanling male SD rats were fed diets containing 20% HER or LER for 1 week or 4 weeks, or 5% HER diet for 4 weeks. The hepatic oxidation capacity of butyric acid or palmitic acid was determined by titrating the propanone produced by their oxidation. The results showed that feeding HER to rats led to an increase in the weight of liver and a decrease in the hepatic oxidation capacity of palmitic acid. Hepatic oxidation of butyric acid was not influenced by the intake of HER. The inhibitory action of HER on the oxidation of long-chain fatty acids probably resulted from the incorporation of erucic acid into mitochondrial membranes, interfering the fatty acyl-CoA transferring system on the membranes, but not from the beta-oxidation enzyme system in mitochondria being directly inhibited.

Animals↗
PubMed1990

Influences of refined konjac meal on the levels of tissue lipids and the absorption of four minerals in rats.

This paper reports a study on the hypocholesterolemic effect of the refined konjac meal (RKM) containing about 80% glucomannan prepared from the tubers of Amorphophallus konjac K. Koch. Male and female Sprague-Dawley rats, 5 weeks old, were divided into five groups and fed a normal basal diet, a hypercholesterolemic diet (control diet), and three test diets (RKM added to the control diet at levels of 2.5, 5, and 10%, respectively) for 12 weeks. The results obtained indicate that RKM could markedly lower the cholesterol levels in the serum and the liver of rats eating hypercholesterolemic diets. At the end of the 4th week of feeding experiment, the serum cholesterol levels in the 5 and the 10% RKM groups and the liver cholesterol level in the 10% RKM group were significantly lower than those in the control groups. At the end of the 12th week, the serum cholesterol levels of all the three RKM groups were lowered to a normal level as was the liver cholesterol level of the 10% RKM group. The lipotropic effect of RKM was also confirmed by histopathologic examination of the livers. In addition to the hypocholesterolemic effects, RKM diets also increased stool bulk. Minor effects on the absorption and utilization of Ca, Fe, Zn, and Cu were found.

Animals↗
PubMed1988

The measurement of platelet aggregation and ATP-release in mice with liver damage induced by carbon tetrachloride (CCl4) using a whole blood aggregometer.

Time course change in platelet function on liver damaged mice was studied by a whole blood aggregometer. The liver damaged animals were produced by single and multiple injections (p.o.) of 20% CCl4 in olive oil to ddY mice (6 weeks). Platelet aggregation and ATP-release were induced with collagen (final conc. of 2 micrograms/ml), ADP (final conc. of 20 microM) and arachidonic acid (AA: final conc. of 100 microM). After a single injection of CCl4, platelet counts increased at 5 and 12 hr, and then they decreased from 24 to 120 hr. Multiple injections of CCl4 resulted in a significant increase in platelet counts. A single injection of CCl4 suppressed aggregation by collagen at 24 and 48 hr and diminished the rate of ATP-release from 12 to 48 hr. AA-induced platelet aggregation was depressed at 48 hr, and ATP-release was also diminished from 24 to 72 hr after a single injection. ADP-induced platelet aggregation was decreased 24 and 48 hr after a single injection and at 48 hr after multiple injections, while, the rate of ATP-release by ADP was significantly increased after single and multiple injections. These changes in platelet functions might be consistent with our original report on the alterations in coagulative and fibrinolytic activities with CCl4-induced liver injury.

Adenosine Diphosphate↗