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Biomedical subjects

H Wang

Publications and source records attributed to H Wang.

At least 1,639 records · Page 91Linked to original sources
PubMed1997

Low level expression of basic FGF upregulates Bcl-2 and delays apoptosis, but high intracellular levels are required to induce transformation in NIH 3T3 cells.

We investigated the roles of basic fibroblast growth factor (bFGF) in the transformation and survival of NIH 3T3 cells. We constructed NIH 3T3-derived cell lines expressing human bFGF using retroviral gene transfer with an N2-based vector. Clonally derived cell lines containing a single copy of the vector overexpress bFGF mRNA and produce more immunoreactive protein (0.407 +/- 0.010-3.028 +/- 0.087 ng bFGF/10(6) cells) which is biologically active than nontransduced (0.151 +/- 0.013 ng bFGF/10(6) cells) or N2-transduced (0.211 +/- 0.029 ng bFGF/10(6) cells) NIH 3T3 cells. All cells producing excess amounts of bFGF achieve greater density at confluence, show delayed apoptosis and increased survival and have elevated intracellular levels of Bcl-2. However, only cells expressing from 8-15 times background levels of bFGF are phenotypically transformed. The transformed cells form dense foci at confluence, have decreased adherence to tissue culture plates and grow colonies in soft agar. Exogenous bFGF induces higher Bcl-2 levels in a dose dependent manner and recapitulates the antiapoptotic effects of the overexpressed species but fails to induce changes associated with the transformed phenotype. In this study, we demonstrate a dissociation between phenotypic transformation secondary to bFGF overexpression and upregulation of cellular Bcl-2 that correlates with a delay in programmed cell death. Although low level expression of bFGF or exogenous bFGF is sufficient to upregulate Bcl-2 and delay apoptosis, high intracellular levels are required for cellular transformation. These data suggest that overexpression of bFGF modulates cellular transformation and Bcl-2-mediated inhibition of apoptosis through alternate molecular mechanisms.

3T3 Cells↗
PubMed1997

HIV-1 infection and the developing nervous system: lineage-specific regulation of viral gene expression and replication in distinct neuronal precursors.

Neurologic abnormalities are common in HIV-1 infected patients and often represent the dominant clinical manifestation of pediatric AIDS. Although the neurological dysfunction has been directly related to CNS invasion by HIV-1, the pathogenesis of neurologic disorders remains unclear. Microglia and macrophages are major HIV-1 targets in the brain, whereas HIV-1 infected neurons or glial cells have been rarely reported. This suggests that indirect mechanisms may account for the severe neuronal damage observed in these patients. Nevertheless, immature, mitotically active neuronal and glial cells, which are present during fetal development, are susceptible to HIV-1 infection and replication in vitro, suggesting that HIV-1 infection during organ development may present unique features. To better characterize virus-host cells interactions in the developing CNS, we have examined the susceptibility of embryologically and biochemically distinct neuronal cell lines to HIV-1 infection. Here we show that mitotically active, immature neurons of distinct lineages, have different susceptibilities to HIV-1 infection and replication and different abilities to support viral gene expression. Mutational analysis of HIV-1 LTR reveals that a region of the viral promoter between nucleotide -255 to -166 is responsible for most quantitative and qualitative differences in viral transactivation among different neuroblasts. This suggests that specific regions of the viral promoter and cellular factors, either lineage- or differentiation-dependent, which bind to those regions, may contribute to control the levels of virus replication and possibly restrict the viral tropism in the developing brain. This may contribute to the establishment of a virus reservoir in the immature CNS and participate by either direct or indirect mechanisms to the severity of the AIDS-related pediatric neurological dysfunction.

Cell Line↗
PubMed1997

[A clinicopathological analysis in 46 elderly cases with cor pulmonale].

OBJECTIVE: To recognize the successful experience in diagnosis of cor pulmonale. METHOD: Autopsy records of 46 elderly patients with cor pulmonale were retrospectively analyzed. RESULTS: The average age of cor pulmonale in aged patients is 65. Most patients were died in the age of 70-79. The rates of incorrect diagnosis and mis diagnoss of cor pulmonale in elderly patients were 27% and 6% respectively. Chronic bronchitis and chronic obstructive emphysema were the most commen causes of cor pulmonale in elderly patients with a rate of 84%. The main cause of death were respiratory failure and heart failure with a rate of 53%. The average thickness of right ventricle wall increased with the course of cor pulmonale and the age of death. About 41% cor pumonale cases were combined with coronary heart disease. CONCLUSIONS: These results indicated that the rate of incorrect diagnoses of cor pulmonale in elderly patients was high, and great effort should be made to draw the clinician's attention for diagnose this illness correctly. The best way to reduce the incidence of cor pulmonale is to prevent and treat chronic bronchitis and chronic obstructive emphysema. Prevent and treat respiratory failure and heart failure effectively may decrease the mortality of cor pulmonale in elderly patients.

Aged↗
PubMed1997

Modulation of phosphatidylinositol turnover on central nicotinic receptors.

AIM: To study the modulatory effects of phosphatidylinositol (PI) turnover on nicotinic receptors in CNS, and to study the relationship between brain nicotinic receptors and PI turnover. METHODS: Effects of inositol phosphatase inhibitor lithium chloride (LiCl) and muscarinic receptor agonist oxotremorine (Oxo) on nicotine-induced convulsions were investigated in mice. RESULTS: The effects of nicotine for producing convulsions were modified by LiCl 2.5-10 mmol.kg-1, revealing the convulsive effects of nicotine > 0.8 mg.kg-1 were increased by acute pretreatment with LiCl rather than oxotremorine. Mice were given LiCl 5.0 mmol.kg-1 once a day for 7 d, the ED50 value of nicotine for producing convulsions was increased from 0.58 to 0.97 mg.kg-1, suggesting that the sensitivity of central nicotinic receptors for mediating convulsions was decreased by chronic treatment with LiCl. CONCLUSION: The functions of central nicotinic receptors were modulated by PI turnover.

Animals↗
PubMed1997

[Changes of [Ca2+]i in colorectal cancer cells induced by some chemicals].

Changes of [Ca2+]i in CCL229 cells induced by retionoic acid (RA), 1,25(OH)2VD3 and PMA were measured by spectrofluorometry. The effects of endoplasmic reticulum (ER)-specific Ca(2+)-ATPase inhibitor thapsigargin (TG) and IP3 receptor inhibitor heparin on RA-induced changes of [Ca2+]i were observed and the relationship between RA-induced changes of [Ca2+]i and ER was also investigated. The results showed that [Ca2+]i increased markedly in several seconds after treated by RA and 1,25(OH)2VD3. When cells were pretreated with EGTA and verapamil (Ca2+ entry blocker drug), TG could not inhibit RA-stimulated Ca2+ release from intracellular calcium pools and TG could increase [Ca2+]i after pretreated by RA. In addition, heparin could not completely inhibit RA-induced [Ca2+]i increase. The results suggest that RA might stimulate IP3-sensitive pool or IP3-insensitive pool on ER to increase [Ca2+]i, or there might be RA-sensitive calcium pools except ER in cells.

Antineoplastic Agents↗
PubMed1997

[Effects of repeated nicotine uptake on brain inositol levels].

In the acute experiments, 30 minutes after nicotine was intraperitoneally injected at the doses of 0.5, 1.0, 1.0, 2.0, 2.0 mg/kg with 5 min interval, the inositol levels were increased in rats cerebral cortex and hippocampus rather than striatum. While the inositol level was decreased in rat cerebral cortex 30 minutes after lithium chloride was given at the dose of 10 mmol/kg. In the chronic experiments, after nicotine at the doses of 2.0-5.0 mg/kg was subcutaneouly injected twice a day for 14 days the inositol level was increased in rat cerebral cortex. In other experiments, nicotine was orally given at the dosese of 2.69, 6.26, 11.53 mg/kg.d for 64 days, the inositol level of rat cerebral cortex was also increased. These indicated that the effects of nicotine on inositol level of rat brain are different from those of lithium chloride, the inositol level of rat cerebral cortex can be increased by repeated administration of nicotine.

Animals↗
PubMed1997

[Cloning and sequencing of the gene for premature beta nerve growth factor].

The entire coding sequence of premature nerve growth factor (NGF) beta subunit was amplified from Genomic DNA extracted from peripheral white blood cells of Chinese by polymerase chain reaction (PCR). The PCR products were cloned into a premade T-vector (linearized plasmid pBluescript II SK (+) with a T base at 3' terminal), followed by automatic sequencing with double strand plasmids. The nucleotide sequence coding for the mature NGF is the same as that reported by Europeans, but there is a base difference within the proper region, resulting in an amino acid replacement in premature NGF.

Amino Acid Sequence↗
PubMed1997

[Effect of experimental immunological otitis media on inner ear].

We observed the change of the Outer Hair Cell (OHC) of the Guinea Pig (GP) in experimental immunological otitis media under a transmission electron microscope. Animals were immunized systemically with Bovine Serum Album (BSA) until high circulation serum levels developed, then were given BSA 1 mg/0.1 ml transtympanic challenge into one middle ear (ME) cleft on four successive weeks, after the 7th day of the ME challenge GP were killed. Under the transmission electron microscope, we observed that of the degeneration of mitochondrion and thinning of the sub membranous cistern, the damage in the 3rd row of OHC is more severe than the 2nd and the 1st rows. It suggested that immune reaction of ME may have an effect on the inner ear.

Animals↗
PubMed1997

[A study on the contralateral suppressive effects of distortion product otoacoustic emissions].

To investigate the physiological properties of contralateral suppressive effects of otoacoustic emissions, the effects of contralateral norrow band noise (NBN) on distortion product otoacoustic emissions (DPOAE) in 23 young subjects (46 ears) with normal hearing were studied using ILO92 otodynamic system. The results showed: 1. The amplitude of DPOAE (2f1-f2) was significantly reduced as the intensity of contralateral NBN increased. They were in significant minus correlation (F2 from 1 to 6 kHz, coefficients were -0.49(-)-0.24, all P < 0.05, the slope 0.26-0.08 dB/10 dB); 2. The suppressive effect was the biggest when the primary F2 was 1 kHz or 2 kHz and between 45 dB SPL and 65 dB SPL of intensity level, and damped as primary frequency increased. The most significant reduction of DPOAE amplitude was 3.85 dB SPL; 3. When contralateral NBN was below 50 dB HL, the suppression was frequency-selective; and the most suppressive effect happened when NBN intensities were between 20 dB HL and 50 dB HL. 4. The noise floor in ipsilateral car canal has not been altered by contralateral noise (20-50 dB HL). The underlying mechanism was discussed in this study. It appears that contralateral suppressive effects of DPOAE can be used as a tool in exploring the function of medial olivocochlear system.

Acoustic Stimulation↗
PubMed1997

[Effects of selective attention on distortion product otoacoustic emissions].

To investigate the effects of upper central nervous system on cochlear micromechanics, distortion product otoacoustic emissions (DPOAE) with and without a visual attention task were studied in 16 young subjects with normal hearing. The results showed that the DPOAE (2f1-f2) amplitude were reduced, and significantly decreased in 1 kHz and 2 kHz of F2. In the underlying mechanism of the effects, it is possible that the upper central nervous system facilitate the olivocochlear efferent system and then modulate the cochlear functions. It is suggested that the whole efferent system (from cerebral cortex to olivocochlear bundle) would be of great importance for cochlear function.

Adult↗
PubMed1997

[Effect of cigarette smoking on lipid peroxidation and antioxidation in rat lens].

The effects of cigarette smoking on lipid peroxidation, the activities of antioxidases, and the level of non-protein sulphydryl group in the rat lenses were investigated. The results showed that compared with the control group, MDA contents were significantly higher, while the wet weight of lenses, the concentration of non-protein sulphydryl group, the activities of superoxide dismutase and glutathione peroxidase were significantly decreased in the smoking rats. This study suggested that cigarette smoking might be involved in the development of cataract.

Animals↗
PubMed1997

[PCR-SSCP and sequencing analysis on mutations of anti-oncogene p53 in asbestos-related lung cancer].

To explore the carcinogenic effect of asbestos at molecular level, we directly analyzed the mutations of exon 5, 7 and 8 of anti-oncogene p53 in paraffin-embedded human lung tissue affected by asbestos for the first time. Mutations of p53 gene located in exon 5, 7 and 8 were detected in 7 of 10 cases by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis. The mutation rate found in this study is 70%. Two cases were analyzed by PCR product direct sequencing and C-->A and T-->A transformations were detected. Mutation of p53 gene may be one of the characteristics of asbestos-related lung cancer.

Asbestos↗