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Biomedical subjects

H Wei

Publications and source records attributed to H Wei.

At least 127 records · Page 7Linked to original sources
PubMed1998

The inhibitory effects of IFN alpha-2b on EGFR expression and growth of cultured subconjunctival fibroblasts.

To investigate to what extent the growth of cultured subconjunctival fibroblasts was regulated by epidermal growth factor receptor (EGFR), we observed the expression of EGFR inhibited by interferon alpha-2b (IFN alpha-2b) and determined the growth of cultured subconjunctival fibroblasts by immunohistochemical and MTT methods. The linear relationships between the concentration of IFN alpha-2b and EGFR expression or growth were y = 1252.7-554.61 lgx (r = -0.98, P < 0.01), y = 0.523-0.0421 lgx (r = -0.93, P < 0.05) respectively. The concentration of IFN alpha-2b at doubled IC50 to EGFR (6.55 x 10(3) IU/ml) only inhibited the cell growth by 25.13%. The results suggested that the growth of subconjunctival fibroblasts may be controlled by many other growth factors because it was only partially inhibited by decreasing EGFR expression.

Animals↗
PubMed1998

A differential modulation of allodynia, hyperalgesia and nociception by neuropeptide FF in the periaqueductal gray of neuropathic rats: interactions with morphine and naloxone.

The effect of neuropeptide FF in the periaqueductal gray on pain behaviour was studied in rats with a chronic neuropathy induced by unilateral ligation of two spinal nerves. Neuropeptide FF produced in a non-monotonic fashion a significant attenuation of tactile allodynia. The antiallodynic effect was not significantly modulated by naloxone administered systemically or intracerebrally. The dose of neuropeptide FF producing a significant antiallodynic effect was not antinociceptive in a test of mechanical or thermal nociception. The thermal antinociceptive effect induced by morphine administered in the periaqueductal gray was significantly attenuated by neuropeptide FF, whereas that induced by systemically administered morphine was not. The interaction of neuropeptide FF with intracerebrally or systemically administered morphine in a test of tactile allodynia was not significant. The results indicate that neuropeptide FF in the periaqueductal gray may produce a selective attenuation of tactile allodynia in neuropathic rats. This antiallodynic effect is at least partly independent of naloxone-sensitive opioid receptors. Furthermore, neuropeptide FF in the periaqueductal gray attenuates antinociception induced by intracerebrally but not systemically administered morphine.

Animals↗
PubMed1998

Alterations of antioxidant enzymes and oxidative damage to macromolecules in different organs of rats during aging.

Oxygen free radicals have been hypothesized to play an important role in the aging process. To investigate the correlation between the oxidative stress and aging, we have determined the levels of oxidative protein damage and lipid peroxidation in the brain and liver, and activities of antioxidant enzymes in the brain, liver, heart, kidney, and serum from the Fisher 344 rats at ages of 1, 6, 12, 18, and 24 months. The results showed that the level of oxidative protein damage (measured as carbonyl content) in the brain and liver was significantly higher in older animals than in young animals. No statistical difference was observed in the lipid peroxidation of the liver and brain between young and old animals. The activities of antioxidant enzymes in most tissues displayed an age-dependent decline. Superoxide dismutases in the heart, kidney, and serum, glutathione peroxidase activities in the serum and kidney, and catalase activities in the brain, liver, and kidney, significantly decreased during aging. Cytochrome c oxidase, an enzyme involved in electron transport in mitochondria, initially increased, but subsequently decreased in the aged brain, whereas no significant alteration was observed in the liver mitochondrial antioxidant enzymes. The present studies suggest that the accumulation of oxidized proteins during aging is most likely to be linked with an age-related decline of antioxidant enzyme activities, whereas lipid peroxidation is less sensitive to predict the aging process.

Aging↗
PubMed1998

Bcl-2 protects against apoptosis in neuronal cell line caused by thapsigargin-induced depletion of intracellular calcium stores.

The toxicity of thapsigargin, a selective inhibitor of endoplasmic reticular Ca2+-ATPase, was investigated in GT1-7 cells, a murine hypothalamic cell line. Treatment of these cells with 50 or 100 nM thapsigargin greatly reduced cell viability at 24 and 48 h. These doses of thapsigargin induced a rapid rise in free cytosolic Ca2+ ([Ca2+]i), followed by a sustained increase. Addition of EGTA to chelate extracellular Ca2+ diminished somewhat the size of the initial increase of [Ca2+]i caused by thapsigargin, and abolished the sustained increase. The sustained increase could also be abolished by addition of La3+ and by SKF 96365, a drug selective for receptor-mediated calcium entry, but not by verapamil or flunarizine. Pretreatment with 50 microM BAPTA/AM, a cytosolic Ca2+ chelator, inhibited the peak [Ca2+]i caused by thapsigargin but did not inhibit the sustained elevation of [Ca2+]i. Neither EGTA nor BAPTA/AM inhibited the cell death induced by thapsigargin. The cell death was characterized by DNA fragmentation ("laddering"), nuclear condensation and fragmentation, and was inhibited by protein synthesis inhibitor cycloheximide, all characteristic of apoptotic cell death. Overexpression of the protooncogene bcl-2 in GT1-7 cells inhibited significantly DNA fragmentation, nuclear condensation and fragmentation, and cell death induced by thapsigargin. However, Bcl-2 did not alter either basal [Ca2+]i or the elevation of [Ca2+]i induced by thapsigargin. Our results suggest that abnormal Ca2+ release from endoplasmic reticulum caused by thapsigargin induces GT1-7 death by apoptosis and that this effect does not depend on Ca2+ influx from the extracellular space. Bcl-2 inhibited apoptosis induced by thapsigargin, but the mechanism is unlikely to be inhibition of endoplasmic reticular Ca2+ release in GT1-7 neuronal cells.

Animals↗
PubMed1998

Differential regulation of P53 and Bcl-2 expression by ultraviolet A and B.

The induction of apoptosis by ultraviolet (UV) radiation and other DNA damaging agents plays a critical role in monitoring the accumulation of genetic damage and the suppression of tumor development. We hypothesize that UVA and UVB induce apoptosis by modulating balances between p53 and/or bcl-2 genes. Using MCF-7 cells that express both wild-type P53 and Bcl-2 proteins, we demonstrated that UVA and UVB induced apoptosis through regulating expression of apoptosis promoting or inhibiting genes. UVA induced immediate apoptosis and downregulated bcl-2 expression. Bcl-2 expression was reduced by approximately 40% at 4 h post-150 kJ UVA irradiation per m2 with a maximum downregulation (over 70%) at 24 h. The dose-response studies revealed that significant reduction of bcl-2 expression was observed at UVA doses ranging from 50 to 200 kJ per m2; however, p53 levels were not affected by UVA. In contrast, UVB exhibited a entirely different action than UVA in that UVB substantially induced p53 expression, but had no effect on bcl-2 expression. The induction of P53 by UVB was dose and time dependent with the maximum expression at 24 h post-2 and post-4 kJ UVB irradiation per m2. Down-regulation of bcl-2 and fragmentation of DNA induced by UVA occurred earlier (approximately at 4 h) than upregulation of p53 and DNA fragmentation by UVB (12-24 h). These results suggest that UVA and UVB cause cell damage through different mechanisms and that the balances between the expression of p53 and bcl-2 may play an important role in regulating the apoptosis induced by UV irradiation.

Apoptosis↗
PubMed1998

The relationship between objective life status and subjective life satisfaction with quality of life.

A locally developed quality of life inventory was used to examine the relationship between objective life status and subjective satisfaction with quality of life in 8,550 participants from Hunan, China. The inventory included 112 items in 4 dimensions-physical health, psychological health, social functional status, and living conditions. Objective life status was the principal factor affecting subjective satisfaction, but discrepancies were found in some participants, especially when objective status was at the extremes of the distribution. Young, urban, or more educated participants with higher scores on objective status often had lower subjective satisfaction scores in spite of comparatively high objective status scores. Participants who ranked lower on objective status (old, rural, or less educated people) sometimes ranked higher in subjective satisfaction. Scores for subjective satisfaction always showed a normal distribution, whatever the objective satisfaction of the population. Divergence between individual objective status and subjective satisfaction was associated with hierarchy of life needs and the reference standards used for the comparison.

Adult↗
PubMed1998

Inhibition of ultraviolet B (UVB)-induced c-fos and c-jun expression in vivo by a tyrosine kinase inhibitor genistein.

We reported the inhibitory effects of genistein, an inhibitor of tyrosine protein kinase (TPK), on ultraviolet B (UVB)-induced expression of c-fos and c-jun in SENCAR mouse skin. UVB irradiation substantially increased transcript levels of c-fos and c-jun mRNA in mouse skin. Topical application of genistein 60 min before UVB radiation reduced c-fos and c-jun expression in the mouse skin in dose-dependent manner. Inhibition was more pronounced in skin exposed to the low dose (5 kJ/m2) than to the high dose (15 kJ/m2) of UVB radiation. In addition, genistein exhibited more inhibition of c-fos than that of c-jun. Post-application of genistein after UVB exposure down-regulated the expressions of c-fos and c-jun, but to a lesser extent compared with pre-application. A431 human epidermoid carcinoma cells, which excessively express epidermal growth factor receptors (EGF-R), were used to investigate the possible mechanism of genistein's action. The results showed that genistein down-regulated the UVB-mediated phosphorylation of TPK-dependent EGF-R in a dose-dependent manner. We concluded that inhibition of UVB-induced c-fos and c-jun expression in mouse skin by genistein may, at least in part, result from the inhibition of TPK activities and down-regulation of EGF-R phosphorylation. Suppression of UVB-induced proto-oncogene expression in mouse skin suggests that genistein may serve as a potential preventative agent against photodamage and photocarcinogenesis.

Animals↗
PubMed1998

Tamoxifen reduces endogenous and UV light-induced oxidative damage to DNA, lipid and protein in vitro and in vivo.

We have investigated the effect of tamoxifen (TAM) on endogenous or ultraviolet radiation (UVR)-induced oxidative damage to macromolecules in vitro and in vivo. In a system containing calf thymus DNA exposed to a germicidal UV lamp, both TAM and 4-hydroxytamoxifen (4-OH-TAM) inhibited UVR-induced the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in DNA in a dose-dependent manner. At low concentrations, 4-OH-TAM quenched 8-OHdG more potently than TAM. However, the reduction of 8-OHdG by TAM and 4-OH-TAM became similar at a concentration of 10 microM. In contrast, ascorbic acid had the similar effect to TAM, whereas glutathione exhibited little effect on UVR-induced 8-OHdG. The order of quenching efficacy was: 4-OH-TAM > TAM approximately = ascorbic acid > glutathione. We have further determined the effect of TAM on endogenous 8-OHdG formation, lipid peroxidation, and protein oxidation in the skin of SENCAR mice. Topical application of 5 micromol TAM significantly reduced the level of 8-OHdG in mouse epidermis by approximately 27% (P < 0.05). Endogenous lipid peroxidation and protein oxidation, measured as malondialdehyde (MDA) and carbonyl groups, were also substantially reduced by topical TAM. Further study was conducted to evaluate the effect of TAM on UVR-induced 8-OHdG and MDA in skin of hairless mice. In mice subacutely exposed to low dose (3.4 kJ/m2 x six doses) and high dose (16.8 kJ/m2 x three doses) of UVB irradiation, TAM significantly blocked the formation of 8-OHdG in mouse epidermis by 57-81% and MDA by 37-65%, respectively. Our studies suggest that reduction of oxidative damages to biological macromolecules in vitro and in vivo may at least in part explain the anti-carcinogenic and chemopreventive actions of tamoxifen.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1998

Genistein modulates neuroblastoma cell proliferation and differentiation through induction of apoptosis and regulation of tyrosine kinase activity and N-myc expression.

Genistein is a specific inhibitor of protein tyrosine kinase (PTK) and is considered as a therapeutic candidate for various cancers. In this paper we investigate the effects of genistein on cell proliferation and differentiation in neuroblastoma (NB) cell lines and its possible mechanism of action. Genistein substantially inhibited the growth of five (N2A, JC, SKNSH, MSN and Lan5) of the six tumor cell lines examined in a dose-dependent manner with an IC50 value of approximately 5 microg/ml. The exception was GC cells. N2A cells were treated with genistein for 6 days and exhibited morphological features of differentiation, as evidenced by the development of dendritic extensions. Terminal deoxynucleotidyl transferase (TDT) histochemical staining showed a significant elevation in darkly stained nuclei in genistein-treated N2A cells compared with controls, indicating the occurrence of apoptosis. Fluorescent quantitation of DNA fragments confirmed apoptosis in genistein-treated N2A cells. To further elucidate the possible mechanisms by which genistein modulates NB cell growth and differentiation we investigated the effect of genistein on the activities of PTK and mitogen-activated protein (MAP) kinase and N-myc proto-oncogene expression in N2A cells. The results showed that genistein down-regulated intrinsic PTK activity by approximately 33% and inhibited insulin-like growth factor (IGF)-stimulated PTK activity by 75%. The effect of genistein on the intrinsic activity of MAP kinase was insignificant. In addition, genistein significantly reduced N-myc expression in a dose-dependent fashion. Our study suggests that genistein arrests cell growth and induces NB cell differentiation by mediating apoptosis and modulating PTK activity and N-myc proto-oncogene expression.

Apoptosis↗
PubMed1998

Isoflavone genistein inhibits the initiation and promotion of two-stage skin carcinogenesis in mice.

Isoflavone genistein is a specific inhibitor of protein tyrosine kinase (PTK) and has been shown to have a variety of anticancer activities in cultured cells and animal models. We report here that genistein significantly inhibits 7,12-dimethylbenz[a]anthracene (DMBA)-initiated and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-promoted skin tumorigenesis in a two-stage carcinogenesis model. In an initiation study, 10 micromol genistein was applied daily to female SENCAR mouse skin for 1 week, followed by initiation with 10 nmol DMBA. Mice were then treated with twice weekly 4 microg TPA. Genistein was shown to reduce tumor incidence and multiplicity in DMBA-initiated skin tumors by approximately 20 (P < 0.05) and 50% (P < 0.01), respectively. Two promotion studies were conducted using CD-1 and SENCAR mice. In experiment 1, CD-1 mice were initiated with 100 nmol DMBA and followed by a twice weekly regimen of 1 and 5 micromol genistein/4 microg TPA. In experiment 2, SENCAR mice were initiated with 10 nmol DMBA and followed by a regimen of 5, 10 and 20 micromol genistein/2 microg TPA. Both studies consistently showed that genistein substantially inhibited TPA-promoted skin tumorigenesis by reducing the tumor multiplicity by approximately 60 and 75%, respectively (P < 0.01). However, the tumor incidence appeared to be less affected. Mechanistic studies showed that genistein inhibited DMBA-induced bulky DNA adduct formation and substantially suppressed TPA-stimulated H2O2 and inflammatory responses in mouse skin by >60% (P < 0.01). In contrast, genistein only exhibited a moderate inhibition of TPA-induced ornithine decarboxylase activity (P > 0.05). Our results suggest that genistein exerts its anti-initiational and anti-promotional effects on skin carcinogenesis probably through blockage of DNA adduct formation and inhibition of oxidative and inflammatory events in vivo.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1998

Genistein alters the ontogeny of mammary gland development and protects against chemically-induced mammary cancer in rats.

Breast cancer is the most common cancer in US females and is the second leading cause of cancer death among women. By contrast, Asian women consuming a traditional diet high in soy products have a relatively low incidence of breast cancer. Asians who emigrate to the United States and adopt a Western diet lose this protection. Soy-based diets are high in phytoestrogens, and one of these components is genistein. Using the dimethylbenz(a)anthracene (DMBA) mammary cancer rodent model, we have investigated the breast cancer protective potential of genistein. Our results demonstrate that neonatal and prepubertal genistein treatments altered the ontogeny of the mammary gland and rendered the adult animals less susceptible to chemically-induced mammary cancer. Neonatal genistein treatment did not significantly alter the rate of formation and persistence of DMBA-DNA adducts in the mammary gland. While high concentrations of genistein during the neonatal period caused adverse effects on ovarian follicular development, prepubertal genistein treatment did not appear to be toxic in either the female reproductive tract or the endocrine system.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1998

Cloning and expression of phenylalanine ammonia lyase cDNA in Escherichia coli.

The phenylalanine ammonia lyase (PAL) cDNA was amplified from Petroselinum crispum RNA by using the RT-PCR technique. The amplified 2.2 kb DNA fragment was sequenced and inserted into expression vector pET23b. The resulting plasmid pET23bPAL was then transformed into E. coli JM109DE3. The expressed PAL protein in JM109DE3 (pET23bPAL) accounted for more than 15% of total proteins in the engineering E. coli cells. The activity and specificity of the expressed PAL was identified and tested by using HPLC technique. The results indicated that the PAL activity was good enough for application to enzymatic therapy of phenylketonurea (PKU).

Apiaceae↗
PubMed1998

Protective effect of recombinant human augmenter of liver regeneration on CCl4-induced hepatitis in mice.

OBJECTIVE: To observe the anti-injury role of recombinant human augmenter of liver regeneration. METHODS: To establish liver injury models induced by CCl4 in vivo and in vitro, cell survival rates and LDH release rates served as observing index in experiments in vitro. Survival rates of liver failure animals, serum concentration of ALT, LDH, DNA and pathological examination were selected as parameters in experiment in vivo. RESULTS: rhALR could increase the survival rates and decrease the LDH release rates of injured hepatocytes in vitro. rhALR could also increase the survival rates of liver failure animal, promote hepatocyte proliferation and decrease the serum level of ALT and LDH in vivo. CONCLUSION: ALR is an important stimulator for liver regeneration and may play important role in liver damage repair.

Animals↗
PubMed1998

[Breathing control of patients with obstructive sleep apnea syndrome (OSAS) during sleep].

OBJECTIVE: It is assumed that reduced ventilatory control function during sleep may be one of the mechanisms resulting in obstructive sleep apnea syndrome (OSAS), but the breathing drive has never been measured in patients with OSAS during sleep. METHOD: P0.1, delta P0.1/delta SaO2, delta VE/delta SaO2, delta P0.1/delta PaCO2 and delta VE/delta PaCO2 in sixteen patients with severe OSAS were measured via nasopharyngeal tubes connected with nasal mask to maintain upper airway patent, during wake and NREM I + II, NREM III + IV, REM sleep stages, and the same parameters in eleven normal subjects, non-snorers were also measured, by nasal mask as control. RESULT: (1) During wake: P0.1 in all the OSAS patients was remarkably higher than that of the normal subjects (P < 0.05), but there was no difference in delta VE/delta SaO2, delta P0.1/delta SaO2, delta VE/delta PaCO2 and delta P0.1/delta PaCO2 between the two groups (P > 0.05). (2) The above parameters measured during sleep compared with that measured during wake: In NREM I + II and NREM III + IV, normal subjects showed no significant decrease in P0.1, delta P0.1/delta SaO2, delta P0.1/delta PaCO2 (P > 0.05), but delta VE/delta SaO2 and delta VE/delta PaCO2 decreased significantly (P < 0.05). In REM1 P0.1 maintained the same level as that during wake, but both hypoxic and hypercapnic responses decreased remarkably (P < 0.05). In the OSAS patients, P0.1 decreased during NREM I + II and REM sleep (P < 0.5), but not during NREM III + IV (P > 0.05). delta VE/delta SaO2, delta P0.1/delta SaO2, delta P0.1/delta PaCO2 and delta VE/delta PaCO2 decreased markedly during all sleep stages (P < 0.01). (3) From wake to sleep, delta VE/delta SaO2 decreased by 51.6 +/- 30.4% (Mean +/- SD) in the OSAS patients vs 33.6 +/- 26.0% decreased in the normal subjects; delta VE/delta PaCO2 decreased by 56.9 +/- 25.5% in OSAS vs 40.8 +/- 17.5% in the normal subjects; The hypoxic and hypercapnic responses in OSAS patients decreased much more than those in the normal subjects during sleep (P < 0.05). CONCLUSION: This is the first study to measure the hypoxic and hypercapnic responses successfully in OSAS patients during sleep. It was found that the breathing drive was significantly reduced in sleeping OSAS patients, which may play an important role in the development of OSAS, possibly through the reduced action upon the dilators causing the upper airway in predilection for collapse.

Adult↗
PubMed1998

[Clinical study on the forced oscillatory pulmonary function test].

OBJECTIVE: To discuss the change of airway resistance and phase angle (phi) in normal subjects, patients with COPD, asthma and pulmonary fibrosis when the new technique of the forced oscillatory pulmonary function test was applied to measure them as well as the change of pulmonary function of patients with asthma after using bronchodilator. METHOD: Use Custo-vitm forced oscillation device manufactured in Germany to determine airway resistance and phase angle and to compare their statistical differences between normal subjects and patients with pulmonary disease, and then comparing the improvement rates of their FEV1, F-V curve and airway resistance in patients with asthma after inhaling bricasol. RESULT: The measurements of group COPD and asthma were significantly higher than those of normal group (P < 0.05), and there were obvious frequency dependence in these two groups. The results of phase angle in each group of patients were significantly lower than those of normal group (P < 0.05), and the group of patients with pulmonary fibrosis only demonstrates a decrease in phase angle, and the improvement rate of airway resistance in patients with asthma after inhaling bricasol was significantly higher than FEV1 and F-V curve (P < 0.05). CONCLUSION: Forced oscillation is a convenient, quick, and noninvasive new method when applied to measure airway resistance and phase angle. It is especially suitable for patients with severe COPD and better than conventional pulmonary function test in observing therapeutic effect in asthma.

Adult↗
PubMed1998

[Constituents in petroleum ether and ethyl acetate extract fractions of Dracaena cochinensis (Lour.) S.C. Chen].

OBJECTIVE: To study the chemical constituents of Dracaena cochinensis. METHODS: Compounds were separated by solvent extraction, column chromatography, TLC and HPLC, and their structures were determined by spectral analysis. RESULTS: Ten compounds were isolated from the petroleum ether and ethyl acetate fractions of D. cochinensis and identified as n-heptacosane, lophenol, docosanyl ferulate, tetracosanyl ferulate, hexacosanyl ferulate, octacosanyl ferulate, pterostilbene, dioctyl phthalate, butyl isobutyl phthalate and 4'-methoxy-3',7-dihydroxy-flavone. CONCLUSION: All the compounds were isolated from this plant for the first time.

Coumaric Acids↗