Biomedical subjects
Publications and source records attributed to Z Xu.
OBJECTIVE: To study the risk and benefits of using compination-type oral contraceptives (COC) for diseases. METHOD: Meta-analysis was used to estimate the summary relative risk (SRR) for diseases. RESULTS: The SRR for cardiovascular diseases was > 1 (P < 0.05). The SRR for endometrial cancer and ovarian cancer were < 1 (P < 0.05). CONCLUSION: COC may increase the risk of cardiovascular diseases and may protect from endometrial and ovarian cancer.
The feasibility of CO2 enhanced ultrasound (CO2-EUS) was evaluated in two-stage operation patients with hepatic tumors. CO2-EUS was carried out in nine patients with indwelling catheter within hepatic artery for two-stage operation of liver cancer. CO2 microbubbles mixing by 5 ml of 5% NaHCO3 and 2.5 ml of 5% Vitamine C were injected into the indwelling catheter. The computed sonography of ACUSON 128XP/10 with a 3.5 MHz convex transducer was used for this study. The enhanced parenchyma of the liver obtained by CO2-EUS and the lasting time of enhancement was about 8 minutes. The hepatic tumors, after chemotherapeutic treatment via indwelling catheter, were variously enhanced by CO2 microbubbles. The enhanced sonogram of the tumors took the forms of hypoechoic, ring-like, or spotty enhanced pattern lasting for more than 30 minutes. The margin of the enhanced tumors was very clear in CO2-EUS. CO2-EUS detected five more lesions (size 1-3 cm) besides 9 lesions by conventional ultrasound. CO2-EUS was extremely useful in evaluating curative effects of tumor, increasing detection rates of small tumor, and improving thoroughness of two-stage operation.
We analyed 136 recurrent colorectal cancer cases their recurrence, residual cancer foci, extraintestinal infiltration, and inappropriate pelvic resection in patients receiving mile's procedure. The authors suggest that distal safe margin of the colon should at least be more than 3 cm and thorough dissection of the proximal third grade lymphonodes at the upper root of the mesentery and the lateral lymphonodes. For these 136 recurrent cases, after preoperative comprehensive procedure including intraarterial chemoembolization, radiation adjuvant immunotherapy, the resection rate of the recurrent mass was 84.5%. The five year survival rate of palliative resection was 40% as compared with 44.8% in radical resection.
To investigate the association of human leukocyte antigen (HLA) with susceptibility and clinical manifestations of sarcoidosis. Fifty-five patients with sarcoidosis were studied by using allele group specific polymerase chain reaction technique (PCR). Our data show that: (1) the gene frequency of HLA-DR5 is significantly increased in patients with sarcoidosis, but that of HLA-DR7 decreased. (2) Gene frequencies of HLA-DR9 and HLA-DR5 are relatively increased in male patients and in patients with stage I and stage IIa, respectively. The results suggest that HLA-DR gene might contribute to the susceptibility as well as to the difference of clinical manifestations in sarcoidosis.
OBJECTIVE: To investigate the correlation between sarcoidosis and Borrelia burgdorferi (Bb) infection. METHODS: Flagella DNA of Bb were detected in 23 tissue speciments from patients with confirmed sarcoidosis using polymerase chain reaction in situ technique (in situ PCR) and the antibodies to Bb were examined in 55 serum samples obtained from the patients by indirect immunoflurescence assays. RESULTS: (1) None of granulomatous tissues was found to have Bb DNA in 23 tissue samples. (2) 30 of 55 (54.6%) patients with sarcoidosis were found antibodies to Bb positive, in contrast, six of 60 (10%) normal subjects had antibodies against Bb, the positive rate was remarkably higher in patient group than that in healty group (P < 0.005). CONCLUSIONS: Bb might not be the causative agent of sarcoidosis, the elevated titres of serum antibodies against Bb in patients with sarcoidosis is a nonspecific response.
Based on pharmacological studies in files, mice and rats, the powder of sea pearl (Pteria martensii), mother-of-pearl and freshwater pearl has been proved to have tonic, anti-aging and anti-radiative actions. The effect of the sea pearl and mother-of-pearl powder is higher than that of freshwater pearl powder.
AIM: To study the effects of oxymatrine (Oxy) on arrhythmia in dogs with myocardial infarction. METHODS: Partly ligating the left anterior descending coronary artery in the open-chest dogs produced myocardial infarction of left anterior ventricular wall. After 5-8 d, the diastolic excitability threshold (DET), the effective refractory periods (ERP) and arrhythmias were determined by programmed electric stimulation (PES). RESULTS: Oxy (i.v. 50 mg.kg-1) increased DET from 2.53 +/- 1.28 to 3.19 +/- 1.62 V, lengthened ERP from 182 +/- 25 to 219 +/- 43 ms at normal region and from 206 +/- 49 to 235 +/- 55 ms at infarct region in left ventricle, but had no effects on dispersion of ERP, QTc interval and ventricular tachycardia (VT) or ventricular fibrillation (VF). Procainamide (Pro) (i.v. 25 mg.kg-1) increased DET and lengthened ERP and QTc interval, but decreased the dispersion of ERP. Pro prevented PES-induced VT/VF and spontaneous ischemia-related VF. CONCLUSION: The increased DET and lengthened ERP of Oxy are its anti-arrhythmic mechanism.
Allantoate amidohydrolase from Bacillus fastidiosus was purified 170-fold to homogeneity as judged by isoelectric focusing and nondenaturing and sodium dodecyl sulfate polyacrylamide gel electrophoresis. The molecular mass was estimated to be 128 kDa. The enzyme appeared to be a homodimer with a subunit molecular mass of 66 kDa. The enzyme has an isoelectric point of 5.6. Allantoate amidohydrolase is a Mn(2+)-dependent enzyme exhibiting a pH optimum around 8.8. Its Km value for allantoate was estimated to be 9 mM. Similar to other microbial allantoate amidohydrolases the enzyme can be reversibly activated and inactivated. No indication for the involvement of arginine, lysine, and cysteine residues in the catalytic action of the enzyme was obtained. Diethylpyrocarbonate strongly inhibited the enzyme activity, indicating the involvement of histidine or tyrosine residues in catalytic action. However, no recovery was obtained by treatment with hydroxylamine as would be expected if such residues were modified. The enzyme could be reversibly denatured by urea, guanidine, and sodium dodecyl sulfate.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Human alpha 1-->3fucosyltransferases constitute a family of closely related membrane-bound enzymes distinguished by differences in acceptor specificities and inherent protein biochemical properties. One such biochemical property is sensitivity to enzyme inactivation by sulfhydral-group modifying reagents such as N-ethylmaleimide. The basis for this property has been studied using a fusion protein of FucT-III and FucT-V composed of Protein A coupled to the catalytic domain of the enzyme. The results indicate that modification of FucT-V by 5,5'-dithiobis(2-nitrobenzoic acid) resulted in efficient enzyme inactivation that could be reversed by excess thiol reagent suggesting that the free sulfhydral group on the enzyme was required for activity. Recombinant forms of both FucT-III and FucT-V were irreversibly inactivated by N-ethylmaleimide and could be effectively protected from inactivation by GDP-fucose and GDP but not by UDP-galactose, fucose, or N-acetyllactosamine. Analysis of the distribution of Cys residues in aligned sequences of cloned human alpha 1-->3fucosyltransferases indicated one site, Cys143 of FucT-III and Cys156 of FucT-V, corresponded to the highly conservative replacement of Ser178 in FucT-IV, an enzyme insensitive to N-ethylmaleimide. A site-directed mutagenesis experiment was performed to replace Ser178 of FucT-IV with a Cys residue. The mutant FucT-IV enzyme was active; however, the Km for GDP-fucose was increased about 3-fold compared to the native enzyme to 28 +/- 3 microM. This enzyme was N-ethylmaleimide sensitive and could be partially protected by GDP-fucose but not N-acetyllactosamine. These results support the importance of Ser178 of FucT-IV in donor substrate binding and strongly suggest analogous Cys residues are the GDP-fucose protectable, N-ethylmaleimide-sensitive sites present in FucT-III and -V.
Four chelating agents that have been used most commonly for the treatment of humans intoxicated with lead, mercury, arsenic or other heavy metals and metalloids are reviewed as to their advantages, disadvantages, metabolism and specificity. Of these, CaNa2EDTA and dimercaprol (British anti-lewisite, BAL) are becoming outmoded and can be expected to be replaced by meso-2,3-dimercaptosuccinic acid (DMSA, succimer) for treatment of lead intoxication and by the sodium salt of 2,3-dimercapto-1-propanesulfonic acid (DMPS, Dimaval) for treating lead, mercury or arsenic intoxication. Meso-2,3-DMSA and DMPS are biotransformed differently in humans. More than 90% of the DMSA excreted in the urine is found in the form of a mixed disulfide in which each of the sulfur atoms of DMSA is in disulfide linkage with an L-cysteine molecule. After DMPS administration, however, acyclic and cyclic disulfides of DMPS are found in the urine. The Dimaval-mercury challenge test holds great promise as a diagnostic test for mercury exposure, especially for low level mercurialism. Urinary mercury after Dimaval challenge may be a better biomarker of low level mercurialism than unchallenged urinary mercury excretion.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Mutation in superoxide dismutase 1 (SOD1), a Cu/Zn enzyme that removes oxygen radicals and protects against oxidative injury, has been implicated in some cases of familial amyotrophic lateral sclerosis (FALS). As a first approach to examining the mechanism(s) through which these mutations cause specific degeneration of motor neurons, we have used immunocytochemistry to identify the distribution of SOD1 in populations of cells in the peripheral and central nervous systems. In the spinal cord, intense SOD1 immunoreactivity was present in motor neurons, interneurons, and substantia gelatinosa. In motor neurons, SOD1 immunoreactivity was abundant in perikarya, dendrites, and axons; most of this activity appeared to be free in the cytoplasm, although a portion was associated with membranous vesicles, presumably peroxisomes. Since a variety of central nervous system neurons, including pyramidal cells in cerebral cortex and neurons of the CA3 and CA4 sectors of the hippocampus, showed high immunoreactivity but are unaffected in ALS, the apparent abundance of SOD1 does not predict vulnerability of neurons to mutations in SOD1. Rather, SOD1 accumulates in many neuronal populations but is particularly abundant in motor neurons. Consistent with recent studies of FALS-linked SOD1 mutations in vitro and in transgenic mice, our findings offer further support for the view that the mutations confer a gain of adverse function. In this view, high, rather than limiting, levels of SOD1 may place motor neurons selectively at risk in FALS.
The hypoxanthine-guanine phosphoribosyltransferase (hprt) locus has been widely used as a selectable genetic marker for studies of mammalian cell mutagenesis. We report here the spontaneous mutation spectrum at the hprt locus in 64 independently isolated mutants of Chinese hamster ovary (CHO) cells. All nine hprt exons were simultaneously analyzed via multiplex polymerase chain reaction (PCR) for rapid detection of gene deletions or insertions. Structural point mutations were identified by direct sequence analysis of the PCR amplified cDNA. The molecular nature of RNA splicing errors and insertions was analyzed by solid-phase direct exon sequencing. Single base substitutions were found in 24 mutants (38%), of which 21 were missense and 3 were nonsense mutations. Transversions were about twice as frequent as transitions. Fifteen mutants (23%) had deletions involving either intragenic small fragments (2), single exons (9), or multiple exons (4). The majority of deletion breakpoints (71%) were located in regions surrounding exons 4, 5, and 6. RNA splicing mutations were observed in 15 mutants (23%) and affected exons 3-8; most (6/15) resulted in the loss of exon 7. Two insertion mutants, one with a 209 bp insert in exon 4 and the other with a 88 bp insert accompanied by a 24 bp deletion in exon 6, represent novel mutations reported for the first time in spontaneous mutants of the mammalian hprt gene.
Explore the source record for details and available documents.