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Biomedical subjects

X W Wang

Publications and source records attributed to X W Wang.

At least 19 recordsLinked to original sources
PubMed1992

Structural and functional analysis of the amdR regulatory gene of Aspergillus oryzae.

We have isolated the Aspergillus oryzae homologue of the amdR regulatory gene of Aspergillus nidulans by cross hybridization. Sequence analysis and functional studies have shown that the amdR genes are highly conserved and functionally interchangeable between the two species. The homology between the two genes extends throughout most of the coding sequences, including sequences encoding the DNA-binding domain and putative activation domains. Two regions of nonconserved sequence were also identified. Studies using various amdS::lacZ fusion constructs indicate that the A. oryzae gene product binds similar sequences and responds to inducer in a similar manner to the A. nidulans protein. Inactivation of the A. oryzae gene results in the inability to grow on gamma-amino-butyric acid (GABA) as a carbon and/or nitrogen source indicating that GABA utilization is amdR-dependent in A. oryzae as it is in A. nidulans.

Amino Acid Sequence↗
PubMed1992

A conserved region in human and Chinese hamster X chromosomes can induce cellular senescence of nickel-transformed Chinese hamster cell lines.

Cellular senescence is the genetically programmed cessation of cellular proliferation. We have recently mapped a putative senescence gene(s) on the X chromosome of Chinese hamster embryo (CHE) cells. In the present study, we have utilized microcell-mediated chromosome transfer (microcell fusion) to test whether: (i) the human X chromosome exhibits similar genetic potential to induce senescence and (ii) the deletion or inactivation of the X-linked senescence gene(s) in CHE cells is associated with nickel-induced immortalization. A normal CHE or human X chromosome was first introduced into mouse-cell hybrids, then transferred by microcell fusion into a nickel-transformed, immortal male CHE cell line (Ni-2/TGR) with an X deletion (Xq1). Microcell fusion of the normal CHE X chromosome into tumorigenic Ni-2/TGR cells yielded senescence of all X recipient clones. The normal human X chromosome induced dominant senescence of tumorigenic Ni-2/TGR cells in only 17% of the resulting microcell hybrids (14/81). Karyotypic analyses of 13 non-senescing human X chromosome-derived microcell hybrid clones revealed that none of these clones retained the complete X. A normal CHE X chromosome induced senescence of 75% of hybrids obtained with another immortal and tumorigenic nickel-transformed male CHE cell line (Ni-6/TGR), which exhibited no visible deletion of the X chromosome, while the normal human X chromosome, only induced senescence in 19% of these hybrids. Transfer of the normal CHE or human X chromosome into spontaneously transformed and tumorigenic cell lines, CHO/TGR or V79/TGR, had little or no effect on their growth. These data suggest that both human and CHE cells possess similar X-linked genetic activities that regulate the process of cellular senescence, and that in Chinese hamster cells nickel-induced immortalization but not that of CHO or V79 cells is associated with inactivation of an X-linked senescence gene.

Animals↗
PubMed1992

[Anti-lipid peroxidation and protective effects of phenytoin sodium on ischemic myocardium of mice].

Isoproterenol (Iso, 20 mg.kg-1 x d-1 x 2 d) induced widespread and severe myocardial damages at ultrastructural level, decreased the myocardial Se-glutathione peroxidase (Se-GSH-Px) and superoxide dismutase (SOD) activities, increased the serum creatine phosphokinase (CPK) concentration and myocardial malondialdehyde (MDA) content. Phenytoin sodium (Phe) 15 or 30 mg.kg-1 ip pretreatment diminished the CPK release and MDA production, protected the Se-GSH-Px activity in the Iso-induced damage of mouse heart. The pretreatment with 30 mg.kg-1 abated the reduction of SOD activity. However, Phe 15 mg.kg-1 did not show such an effect. Phe (15 or 30 mg.kg-1) reduced the ultrastructural cardiotoxicity of Iso, and the membrane structure of ischemic myocardium was protected. The protective effects of verapamil pretreatment 3 mg.kg-1 ip were weaker than those of Phe on ultrastructural changes, but biochemical changes were similar to those of Phe. The results suggested that Phe possessed anti-lipid peroxidation and protective effects on ischemic myocardium.

Animals↗
PubMed1992

[A laboratory and clinical study of induced differentiation therapy by all trans-retinoic acid in acute promyelocytic leukemia].

According to investigations, it was shown that peripheral blood WBC count increased, percentage of promyelocytes increased, differentiation features emerged, protein kinase C (PK-C) activity elevated, intracellular lysozyme content increased, CFU-F productivity increased and typical t (15; 17) disappeared, when induced differentiation therapy with all trans-retinoic acid (RA) was carried out in patients with acute promyelocytic leukemia. Comparison between RA group and RA+Harringtonin/Ara-C group showed no significant difference in most of the parameters; the curative effect was same in both groups. Complete remission (CR) rate was achieved in 92.6% (25/27 cases) of the patients in the entire group. In order to increase CR rate, prevention and treatment for haemorrhagic complications are critical. Patients with hyperleukocytosis (WBC > or = 100 x 10(9)/L) should be treated with intensive combined therapy as well as aggressive prevention of haemorrhage and pathological changes of lung and brain.

Adolescent↗
PubMed1992

Corneal surface after deepithelialization using a sharp and a dull instrument.

Manual removal of the corneal epithelium currently precedes excimer laser photorefractive keratectomy. To assess the smoothness of the corneal surface following this procedure, six paired human eye-bank eyes (12 eyes) were manually deepithelialized using a blunt instrument (Paton spatula) on one eye and a sharp instrument (surgical blade) on the contralateral eye; all deepithelializations were done by the same surgeon. The 12 corneas were then resected and processed in an identical fashion for scanning electron microscopy. The microphotographs obtained showed that among the corneas deepithelialized with the blunt spatula, two had a smooth surface, and four had variable amounts of residual epithelial cells and basement membrane, confirmed by light microscopy. The surface of five corneas deepithelialized with the sharp instrument were slightly rougher than the former, with occasional linear scratches; one cornea retained a small amount of basement membrane. Removal of epithelium appears to be more complete when a sharp instrument is used. These findings may have clinical relevance, since residual epithelium and basement membrane after deepithelialization may influence the depth of ablation subsequently achieved with the excimer laser.

Basement Membrane↗
PubMed1991

Senescence of nickel-transformed cells by an X chromosome: possible epigenetic control.

Transfer of a normal Chinese hamster X chromosome (carried in a mouse A9 donor cell line) to a nickel-transformed Chinese hamster cell line with an Xq chromosome deletion resulted in senescense of these previously immortal cells. At early passages of the A9/CX donor cells, the hamster X chromosome was highly active, inducing senescence in 100% of the colonies obtained after its transfer into the nickel-transformed cells. However, senescence was reduced to 50% when Chinese hamster X chromosomes were transferred from later passage A9 cells. Full senescing activity of the intact hamster X chromosome was restored by treatment of the donor mouse cells with 5-azacytidine, which induced demethylation of DNA. These results suggest that a senescence gene or genes, which may be located on the Chinese hamster X chromosome, can be regulated by DNA methylation, and that escape from senescence and possibly loss of tumor suppressor gene activity can occur by epigenetic mechanisms.

Animals↗
PubMed1991

Changes in protein phosphorylation in wild-type and nickel-resistant cells and their involvement in morphological elongation.

Treatment of wild-type Balb/c-3T3 cells with NiCl2 or N6,2-O-dibutyl-adenosine 3',5'-monophosphate (Bt2-cAMP) resulted in a high degree and frequency of cellular elongation. Nickel-resistant Balb/c-3T3 cells (B200) treated with Bt2-cAMP elongated at the same exposure concentration as wild-type cells. In contrast, treatment of the nickel-resistant cells with both non-cytotoxic and cytotoxic doses of NiCl2 failed to induce elongation. Nickel-resistant cells had two-thirds of the total protein-phosphorylation activity of wild-type cells. Both cAMP and NiCl2 enhanced phosphorylation of specific proteins in intact wild-type cells as detected by 32p autoradiography of these proteins separated on two-dimensional gels. A nickel-dependent phosphorylation of specific proteins is seen following NiCl2 treatment of wild-type cells but was not observed in B200 cells. In contrast, the pattern of Bt2-cAMP-stimulated protein phosphorylation was quite similar in both wild-type and nickel-resistant cells. Although it is unclear at present how nickel ions affect the cellular protein-phosphorylation system, these results suggested that targets controlling cellular elongation are sensitive to nickel, are altered in nickel-resistant cells and appear to involve protein phosphorylation. Further characterization of these targets may help in understanding the mechanisms of nickel carcinogenesis.

3T3 Cells↗
PubMed1990

[Protective effect of 2-[p-(dimethylamino) styryl] pyridine methiodide (DSPM) on acute experimental myocardial ischemia].

ip DSPM 5 mg/kg 1 or 4 h before excision of the heart was found to prevent damage to the heart due to global myocardial ischemia. Compared with the controls, the heart rate, coronary resistance, contractile force and edema of the heart were all greatly improved during the 60 min reflow after 25 min of no-flow, especially the heart pretreated with DSPM 4 h prior to excision. In addition, DSPM 1.5, 6 mg/kg markedly reduced the myocardial Ca2+ content measured by isoproterenol in mice. DSPM at higher dosage also lowered the normal myocardial Ca2+ content. These results suggest that DSPM may have a protective effect on myocardial ischemia which might be associated with its calcium antagonistic action.

Animals↗
PubMed1990

[Effects of 2-[p-(dimethylamino)styryl] pyridine methiodide on conduction and refractory period of atrioventricular node in rat].

The effects of 2-[p-(dimethylamino)styryl] pyridine methiodide (DSPM) on rat ECG and HBE were studied. The P-R and R-R intervals of ECG were lengthened 40.3% and 115.4% respectively, after iv injection of DSPM 2 mg/kg. DSPM (1.5 and 2 mg/kg) affected the A-H interval in a dose-dependent manner with no change in the H-V interval of HBE. DSPM 0.5 mumol/L lengthened the A-H interval of isolated perfused hearts in frequency-dependent manner, with greater prolongation at higher frequency. The effect of verapamil on the A-H interval was less than that of DSPM. Propranolol had no effect on the frequency-dependent delay of atrioventricular node. DSPM 0.5 mumol/L lengthened the functional and effective refractory periods of atrioventricular node by 26.8% and 31% respectively. These phenomena support that DSPM may be a calcium antagonist.

Animals↗
PubMed1990

[Effects of 2-[p-(dimethylamino)styryl]pyridine methiodide on contractive response of rabbit aortic strips].

The effects of 2-[p-(dimethylamino) styryl]pyridine methiodide (DSPM) on rabbit aortic contraction induced by high K+, norepinephrine (NE) and Ca2+ were studied. On rabbit thoracic aortic strips, DSPM inhibited the contraction induced by KCl and NE in normal modified Tyrode's solution. DSPM shifted the dose-response relationships of KCl and NE to the right, and depressed their maximal responses; the pD'2 values were 5.09 and 5.16 respectively. After the strip had been exposed to Ca2(+)-free Tyrode's solution for 2 h, the NE-induced responses were further inhibited by DSPM, whereas the KCl-induced responses were not significantly affected. On depolarized vessels, the dose-response relationships of CaCl2 were also shifted to the right and their maximal responses were also depressed by DSPM, suggesting that DSPM is a non-competitive antagonist. The pD'2 value was 6.86. These results suggest that DSPM is a calcium antagonist. It not only inhibited the influx of extracellular calcium, but also has an inhibitory effect on the release of sequestered calcium in the rabbit aortic smooth muscle.

Animals↗
PubMed1989

Second virial coefficient of alpha-crystallin.

Light scattering studies were performed on bovine alpha-crystallin measuring the scattering intensities as a function of scattering angle, concentration, and temperature. The data yielded the molecular weight, radius of gyration, and second virial coefficient of alpha-crystallin at different temperatures. The second virial coefficient increased with increasing temperature. Both the enthalpy and entropy of solution of alpha-crystallin are positive. The Flory theta temperature was found to be 271 K.

Animals↗
PubMed1989

Studies on the relationship between protein kinase C and differentiation of human promyelocytic leukemia cells induced by retinoic acid.

We studied the differentiation of acute promyelocytic leukemia (APL) cells in 14 patients with APL. After the induction by retinoic acid (RA) the mature cells rose to 60 +/- 11.8% compared to 0.7 +/- 1% of the control, while the promyelocytes declined to 8.7 +/- 6.4% (93.3 +/- 5.6% in the control group). Protein kinase C (PKC) activity was significantly increased to 149.3 +/- 156.2 pmol/mg per min compared to 47 +/- 40.9 of the control (p less than 0.01). In HL-60 cells, the activity of PKC increased also from 52.3 +/- 35 to 129.2 +/- 64.6 pmol/mg per min (n = 10, p less than 0.01) after the induction of differentiation with RA. If the leukemia cells were pretreated with a kind of PKC inhibitor such as trifluoperazine, the increase of PKC activity was inhibited, and the rate of nitroblue tetrazolium reduction decreased from 89.9 +/- 7.7% to 62 +/- 25% (n = 6, p less than 0.01) and the mature cells reduced from 63.1 +/- 11.7% to 19.7 +/- 12.2% (p less than 0.01). We presumed that the activity of PKC is closely related to the differentiation of human promyelocytic leukemia cells induced by all-trans-retinoic acid.

Adult↗
PubMed1989

Alteration of nickel-binding proteins in nickel-resistant cells.

Proteins from wild-type and nickel-resistant cells (Balb/c-3T3 and B200, respectively) were studied by one- or two-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis and detected either by standard protein staining or by fluorographic analysis of [63Ni] binding. Wild-type cells contained three major nickel-binding proteins with molecular masses of 68 kDa (p68), 55 kDa (p55), and 48 kDa (p48). The p55 was present in high concentrations in the microsomal fraction, whereas the p68 nickel-binding protein predominated in the cytosolic fraction. We were unable to demonstrate that p48 was localized in any subcellular fraction. Both the p55 and p48 proteins appeared to be present in similar amounts in wild-type and nickel-resistant cell lines, based upon silver staining of two-dimensional gels, yet in the nickel-resistant B200 cells, these proteins could not be visualized by [63Ni] binding. This suggested that if nickel binding to these proteins were important for nickel toxicity, then nickel resistance in the B200 cells would be associated with the observed loss of metal binding to these proteins. In addition to the changes in [63Ni]-binding proteins, the total concentration of a 44 kDa protein was increased in B200 cells, but its ability to bind nickel could not be established due to its rapid degradation. Among the nickel-binding proteins studied, the p55 contained nickel-binding sites that were the most resistant to exchange by excess nickel ions. The microsomal fraction that contained the highest concentration of p55 also had the highest nickel-binding activity when standardized for protein concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Effects of 2[p-(dimethylamino)styryl]pyridine methiodide on action potentials of sinoatrial node cells of rabbits].

The effects of 2[p-(dimethyl-amino)styryl]pyridine methiodide (DSPM) on the action potential of dominant pacemaker cells in sinoatrial nodes of rabbits were studied by microelectrode technique. DSPM 45 mumol/L decreased the slope of phase 4, the maximum rate of rise of the action potential and the action potential amplitude by 54% (P less than 0.01), 27% (P less than 0.05) and 13% (P less than 0.05), respectively, and increased the spontaneous sinus cycle length and action potential duration at 90% repolarization by 62 and 26% (P less than 0.01), respectively. These effects of DSPM were similar to that of nifedipine 3.9 mumol/L. The positive chronotropic effect of nicotinamide 33 mmol/L was completedly blocked by DSPM 45 mumol/L while that of isoprenaline 0.11 mumol/L was partially blocked by DSPM 45 mumol/L. The results suggest that DSPM may be a Ca2+ antagonist.

Action Potentials↗
PubMed1989

[Effects of 2[p-(dimethylamino)styryl] pyridine methiodide on mouse and rabbit].

The effects of 2[p-(dimethylamino)styryl] pyridine methiodide on mouse and rabbit ECG and on the contraction of isolated rabbit atrial muscles were studied. DSPM produced long-lasting bradycardia and A-V block in a dose-dependent manner, but did not effect intraventricular conduction. DSPM antagonized the positive chronotropic and dromotropic effects of isoprenaline (Iso) in vivo, and antagonized the inotropic effects of Iso and CaCl2 non-competitively in vitro. The pD'2 were 4.49 and 4.52, respectively. It is suggested that DSPM may be a Ca2+ antagonist.

Animals↗
PubMed1989

[Effects of 2-[p-(dimethylamino) styryl] pyridine methiodide on action potentials of depolarized papillary muscle cells of guinea pig].

Effects of 2-[p-(dimethylamino) styryl] pyridine methiodide (DSPM), nifedipine (Nif), CaCl2 and isoprenaline (Iso) on action potentials (AP) of guinea pig papillary muscle cells depolarized by high K+ (15.4 mmol/L) were studied by microelectrode technique. DSPM 45 mumols/L decreased the Vmaxf and Vmaxs of phasee O of the AP by 14 and 26%, respectively. APD90 was lengthened by 7%, amplitude of action potentials (APA) was decreased by 3%. The effects of CaCl2 on Vmaxs of phase 0 of the AP of depolarized papillary muscle cells were abolished by DSPM 45 mumols/L, but the effects of Iso were not antagonized. Effects of DSPM on Vmaxs of the AP of depolarized papillary muscle cells and the influence of DSPM to the action of CaCl2 and Iso were similar to those of Nif. It further suggests that DSPM may be a calcium antagonist.

Action Potentials↗
PubMed1988

Characterization of mouse cell lines resistant to nickel(II) ions.

BALB/c-3T3 cells have been isolated that are resistant to NiCl2. The degree of resistance is directly dependent upon the NiCl2 exposure concentration and ranges from 6- to 11-fold. Resistance to NiCl2 does not appear to be due to alterations in cellular uptake, since the entry of Ni(II) into wild-type or resistant cells was similar. Resistance does not appear to be due to alterations in metallothionein expression. Resistant cells have a high incidence of heterochromatic abnormalities involving fusions at the centromeres as determined by C-banding and in situ hybridization utilizing a cloned mouse satellite DNA probe. Cells retain nickel resistance for many generations in the absence or presence of NiCl2 selection; however, with time in the absence of NiCl2, the level of resistance decreases. This loss of resistance is associated with a decreased number of centromeric fusions. These results indicate that nickel resistance is involved with changes in heterochromatin and suggest that this effect of nickel on heterochromatin may be important as an early step in nickel carcinogenesis.

Animals↗