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Biomedical subjects

Q Feng

Publications and source records attributed to Q Feng.

At least 37 records · Page 2Linked to original sources
PubMed2001

Human ovarian cancer and cisplatin resistance: possible role of inhibitor of apoptosis proteins.

The inhibitor of apoptosis proteins (IAPs) constitutes a family of highly conserved apoptosis suppressor proteins that were originally identified in baculoviruses. Although IAP homologs have recently been demonstrated to suppress apoptosis in mammalian cells, their expression and role in human ovarian epithelial cancer and chemotherapy resistance are unknown. In the present study we used cisplatin-sensitive and -resistant human ovarian surface epithelial (hOSE) cancer cell lines and adenoviral antisense and sense complementary DNA expression to examine the role of IAP in the regulation of apoptosis in human ovarian cancer cells and chemoresistance. Antisense down-regulation of X-linked inhibitor of apoptosis protein (Xiap), but not human inhibitor of apoptosis protein-2 (Hiap-2), induced apoptosis in cisplatin-sensitive and, to a lesser extent, in -resistant cells. Cisplatin consistently decreased Xiap content and induced apoptosis in the cisplatin-sensitive, but not cisplatin-resistant, cells. Hiap-2 expression was either unaffected or inhibited to a lesser extent. The inhibition of IAP protein expression and induction of apoptosis by cisplatin was time and concentration dependent. Infection of cisplatin-sensitive cells with adenoviral sense Xiap complementary DNA resulted in overexpression of Xiap and markedly attenuated the ability of cisplatin to induce apoptosis. Immunohistochemical localization of the IAPs in hOSE tumors demonstrated the presence of Xiap and Hiap-2, with their levels being highest in proliferative, but not apoptotic, epithelial cells. These studies indicate that Xiap is an important element in the control of ovarian tumor growth and may be a point of regulation for cisplatin in the induction of apoptosis. These results suggest that the ability of cisplatin to down-regulate Xiap content may be an important determinant of chemosensitivity in hOSE cancer.

Aged↗
PubMed2001

Attenuation of compensatory right ventricular hypertrophy and heart failure following monocrotaline-induced pulmonary vascular injury by the Na+-H+ exchange inhibitor cariporide.

Pulmonary hypertension results in compensatory right ventricular (RV) hypertrophy. We studied the role of the Na+-H+ exchange (NHE) in the latter process by determining the effect of the NHE-1 inhibitor cariporide after monocrotaline-induced pulmonary artery injury. Sprague-Dawley rats received a control or cariporide diet for 7 days, at which time they were administered either monocrotaline (60 mg/kg) or its vehicle. Twenty-one days later, monocrotaline control, but not cariporide-fed animals, demonstrated increased RV weights and cell size of 65 and 52%, respectively. Monocrotaline alone significantly increased RV systolic pressure and end diastolic pressure by 70 and 94%, respectively, whereas corresponding values with cariporide were significantly reduced to 33 and 42%. Central venous pressure increased by 414% in control animals, which was significantly reduced by cariporide. Monocrotaline treatment produced a decrease in cardiac output of 28 and 8% in the absence or presence of cariporide (P < 0.05 between groups), respectively. Although body weights were significantly lower in both monocrotaline-treated groups compared with vehicle treatment, with cariporide the net gain in body weight was twice that seen in the monocrotaline-treated animals without cariporide. Monocrotaline also increased RV NHE-1 and atrial natriuretic peptide mRNA expression, which was abrogated by cariporide. Monocrotaline-induced myocardial necrosis, fibrosis, and mononuclear infiltration was completely prevented by cariporide. Cariporide had no effect on monocrotaline-induced pulmonary intimal wall thickening. Our results demonstrate that cariporide directly attenuates myocardial dysfunction after monocrotaline administration independent of pulmonary vascular effects. NHE-1 inhibition may represent an effective adjunctive therapy that selectively targets myocardial hypertrophic responses in pulmonary vascular injury.

Animals↗
PubMed2000

A Saccharomyces gene family involved in invasive growth, cell-cell adhesion, and mating.

The cell wall of bakers' yeast contains a family of glycosyl-phosphatidylinositol (GPI)-linked glycoproteins of domain structure similar to the adhesins of pathogenic fungi. In wild-type cells each of these proteins has a unique function in different developmental processes (mating, invasive growth, cell-cell adhesion, or filamentation). What unifies these developmental events is adhesion, either to an inert substrate or to a cell. Although they differ in their specificities, many of these proteins can substitute for each other when overexpressed. For example, Flo11p is required during vegetative growth for haploid invasion and diploid filamentation, whereas Fig2p is required for mating. When overexpressed, Flo11p and Fig2p can function in mating, invasion, filamentation, and flocculation. The ability of Flo11p to supply Fig2p function in mating depends on its intracellular localization to the mating projection, where Fig2p normally functions in the adhesion of mating cells. Our data show that even distant family members retain the ability to carry out disparate functions if localized and expressed appropriately.

Cell Adhesion↗
PubMed2000

Tumor necrosis factor-alpha induces apoptosis via inducible nitric oxide synthase in neonatal mouse cardiomyocytes.

OBJECTIVE: It has been demonstrated that tumor necrosis factor-alpha (TNF alpha) induces apoptosis in cardiac myocytes. However, its mechanism of action is still not well understood. In the present study, we hypothesized that TNF alpha induces myocardial apoptosis by induction of inducible nitric oxide synthase (iNOS). METHODS: Neonatal cardiac myocytes were isolated from iNOS (-/-) mutant and C57BL6 wild type mice. Cells were cultured for 3 days before treatment with an NO donor or TNF alpha. Following treatment with S-nitroso-N-acetyl-penicillamine (SNAP) or TNF-alpha, cells were tested for apoptosis by terminal deoxynucleotidyl transfer-mediated end labeling (TUNEL) staining and cell death detection ELISA. NO production was measured by nitrite concentration in the culture medium. Cardiomyocyte expression of iNOS and TNF type 1 receptor (TNFR1) mRNA was determined by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: SNAP (0.01-100 microM) induced apoptosis of cardiac myocytes in a concentration-dependent manner in the wild type mice (n = 5, P < 0.01). TNFR1 mRNA was expressed in neonatal cardiomyocytes from both wild type and iNOS (-/-) mutant mice. TNF alpha induced a concentration-dependent increase in iNOS mRNA expression and nitrite production as well as significant apoptosis of cardiomyocytes in the wild type mice (n = 4, P < 0.01). However, without iNOS expression, the apoptotic effects of TNF-alpha were significantly attenuated in cardiomyocytes from iNOS (-/-) mutant mice (n = 4, P < 0.05). CONCLUSION: TNF alpha induces apoptosis via iNOS expression and NO production in neonatal mouse cardiomyocytes.

Analysis of Variance↗
PubMed2000

Venous neuropeptide Y receptor responsiveness in patients with chronic heart failure.

BACKGROUND: Chronic heart failure is associated with increased sympathetic nerve activity and elevated plasma neuropeptide Y levels. The aim of this study was to investigate whether increased neuropeptide Y release altered vascular neuropeptide Y responses in the dorsal hand veins in patients with chronic heart failure. METHODS AND RESULTS: Neuropeptide Y responsiveness was studied in vivo with use of a hand vein tonometry technique in 14 patients with chronic heart failure and left ventricular ejection fraction (LVEF) values <20%, 16 patients with LVEF values from 20% to 35%, and 16 age-similar healthy control subjects. Plasma norepinephrine and neuropeptide Y levels were significantly elevated in patients with chronic heart failure and LVEF values <20% compared with control subjects (P < .01). Plasma neuropeptide Y but not norepinephrine levels were significantly elevated in patients with chronic heart failure and LVEF values from 20% to 35% compared with control subjects (P < .01). Increasing doses of neuropeptide Y (25 to 2,000 pmol/min) were infused into a dorsal hand vein of each subject. Dose-dependent venoconstriction to neuropeptide Y was observed in all subjects studied. The neuropeptide Y dose-response curve in patients with LVEF values from 20% to 35% was significantly shifted to the left compared with patients with LVEF values <20% and control subjects (P < .01), whereas no significant difference was observed between the control subjects and the patients with LVEF values <20%. No significant difference in neuropeptide Y dose responses was observed between patients with chronic heart failure with plasma neuropeptide Y levels above the median and patients with chronic heart failure with plasma neuropeptide Y levels below the median. CONCLUSIONS: In vivo venous neuropeptide Y receptor responsiveness is increased in patients with chronic heart failure and LVEF values from 20% to 35%. This increased neuropeptide Y responsiveness may contribute to venoconstriction at this stage of heart failure.

Cardiac Output, Low↗
PubMed2000

Long-term effects of cis and trans monounsaturated (18:1) and saturated (16:0) fatty acids on the synthesis and secretion of apolipoprotein A-I- and apolipoprotein B-containing lipoproteins in HepG2 cells.

The objective of this study was to compare the long-term effects of oleic (cis 18:1), elaidic (trans 18:1), and palmitic (16:0) acids on hepatic lipoprotein production, using HepG2 cells as an experimental model. The net accumulation in the medium of apolipoprotein A-I (apoA-I) was not significantly altered by fatty acids, whereas that of apoB was increased with oleic and elaidic acids. Oleic acid, and to a lesser extent elaidic and palmitic acids, increased the mass of triglycerides in the medium and the incorporation of [(3)H]glycerol into secreted triglycerides. The incorporation of [(14)C]acetate into cellular and secreted total cholesterol was stimulated by 96% and 83%, respectively, with elaidic acid but was not significantly modified by oleic or palmitic acid. Relative to oleic acid, the secretion of (14)C-labeled phospholipids and triglycerides was decreased 28% to 31% with elaidic and palmitic acids whereas that of free cholesterol and cholesteryl esters was enhanced 93% and 73%, respectively, with elaidic acid but remained unchanged with palmitic acid. Compared with oleic acid, elaidic acid stimulated the secretion of very low density lipoprotein cholesterol (VLDL-Chol), low density lipoprotein cholesterol (LDL-Chol), and high density lipoprotein cholesterol (HDL-Chol) by 43%, 70%, and 34%, respectively, whereas palmitic acid decreased VLDL-Chol but had no significant effect on LDL-Chol and HDL-Chol. The ratios of total cholesterol to HDL-Chol were 3.17, 3.60, and 3.25 with oleic, elaidic, and palmitic acids, respectively; the corresponding ratios of LDL-Chol to HDL-Chol were 0.87, 1.10, and 0.93, respectively. Compared with oleic and palmitic acids, the LDL and HDL particles secreted in the presence of elaidic acid contained higher levels of free cholesterol and cholesteryl esters and a lower content of phospholipids. The phospholipid-to-total cholesterol ratios of HDL were 1.05, 0.40, and 0.76 with oleic, elaidic, and palmitic acids, respectively. Our results indicate that in comparison with cis monounsaturated and saturated fatty acids, trans fatty acids have more adverse effects on the concentration and composition of lipoproteins secreted by HepG2 cells.

Apolipoprotein A-I↗
PubMed2000

[Clinical significance of beta-hCG and human placental lactogen in serum of normal pregnancies and patients with pregnancy induced hypertension].

OBJECTIVE: To examine the level of beta-hCG and Human Placental Lactogen (HPL) in maternal serum of normal pregnancies and patients with pregnancy induced hypertension (PIH) and to study the clinical significance and effects of them on the pathogenesis of the disease. METHODS: Serum levels of beta-hCG and HPL of 142 normal pregnant women and 43 patients with PIH (16 mild, 12 moderate and 15 severe) were determined by radioimmunossay. RESULTS: (1) Serum levels of beta-hCG in all PIH subgroups [(25.33 +/- 17.80) micrograms/L in mild, (33.12 +/- 4.91) micrograms/L in moderate, (42.19 +/- 17.47) micrograms/L in severe] were significantly higher than the normal pregnant group [(12.33 +/- 7.92) micrograms/L; P < 0.001]. There is positive correlation between levels of beta-hCG and degrees of PIH (r = 0.677, P < 0.05). (2) Serum levels of HPL in all PIH subgroups [(14.73 +/- 3.26) mg/L in mild, (11.44 +/- 4.02) mg/L in moderate, (12.73 +/- 4.18) mg/L in severe] did not show significant difference when compared with that of normal pregnant group [(12.78 +/- 4.67) mg/L; P > 0.05]. Furthermore, there was no correlation between levels of HPL and degrees of PIH (r = -0.300, P > 0.05). CONCLUSIONS: Serum beta-hCG could reflect the degree of functional imbalance of the placental trophoblasts on PIH and it may be used as a clinical detecting index of PIH. On the other hand, HPL is not such a useful factor.

Adult↗
PubMed2000

[Ligand of platelet and T cell activation antigen 1 (PTA1) expressed on Colo205 cell surface].

OBJECTIVE: To confirm the existence of PTA1 ligand (PTA1L). METHODS: PTA1/Ig fusion protein was prepared by gene recombination and expression in COS-7 cells by DEAE-dextran transfection. The fusion protein was used as a probe in the investigation of PTA1L by immunohistochemical staining. Existence of PTA1L was further identified by adhesion experiment. RESULTS: Colo205 cells could be stained by PTA1/Ig fusion protein specifically but not by hIg, and the adhesion of activated Jurkat cells with Colo205 could be blocked by PTA1/Ig and PTA1 mAb. CONCLUSION: PTA1 ligand is present on the surface of Colo205 cells. These results provide a solid basis for further investigation of the role of PTA1-PTA1L interaction in the pathogenesis of neoplasm.

Animals↗
PubMed2000

[Study on the in vitro cleavage abilities of ribozymes specific to different sites of bcr-abl fusion gene and their induction of apoptosis in K562 cells].

OBJECTIVE: To investigate the in vitro cleavage abilities of ribozymes specific to different sites of bcr-abl fusion gene and their effects on K562 cell. METHODS: First, three single-ribozymes specific to the fusion point were designed. After recombination, 6 vectors including single-, double- and triple- ribozymes were constructed and their in vitro cleavage abilities were compared. Then the triple-unit ribozyme retroviral vector was transfected into K562 cell to test its effect on cell cycle, apoptosis and cell structure. RESULTS: These ribozymes can cleave the template in vitro with different efficiency. The triple-unit ribozyme, with an efficiency of 70.8%, was the most efficient one. The cleavage efficiency of single-unit RZ1, RZ2 and RZ3 was 54.6%, 25.3% and 3.6%, respectively. Those of double-unit RZ12 and RZ23 were 60.7% and 30.3% respectively. The triple-unit ribozyme could inhibit the K562 cell growth by inducing apoptosis. CONCLUSION: It is a new way to treat CML by ribozymes specific to bcr-abl fusion gene, which made it available to purge bone marrow by bcr-abl specific ribozymes.

Apoptosis↗
PubMed2000

[A comparative study on the expressions of IL-4, IFN-gamma and TNF-alpha in BMMNC of acute and chronic aplastic anemia patients].

OBJECTIVE: To detect the induced levels of IL-4, IFN-gamma and TNF-alpha in the supernatant of bone marrow mononuclear cells (BMMNC) and compare the difference of immune status between acute (SAA) and chronic (CAA) aplastic anemia patients. METHODS: Concentrations of IL-4, IFN-gamma and TNF-alpha in PHA-P-induced BMMNC supernatants were determined by ELISA assay in 11 SAA and 13 CAA patients as well as 16 controls. Concentration differences between the two groups were compared. RESULTS: (1) The IFN-gamma and TNF-alpha levels in AA patients studied were much higher than that in controls, and IL-4 levels were normal in SAA group but elevated in CAA group. (2) TNF-alpha levels were comparable between the two AA groups, but both IL-4 and IFN-gamma levels were significantly different between them. CONCLUSION: Enhanced cellular immunity seems to play an important role in the pathogenesis of SAA, and enhancement of both cellular and humoral immunity might contribute to the pathogenesis of CAA.

Acute Disease↗
PubMed2000

[Studies on the effect-increasing components for molluscacides in nut of Areca catech L].

OBJECTIVE: To investigate the effect-increasing action of Areca catech for molluscacide. METHOD: Experiments were conducted on the effect-increasing components isolated from the dry nut of A. catech. RESULT: Arecoline has been proved the most effect-increasing component. CONCLUSION: When used with SPA arecoline could reduce markedly the doses of the two agents.

Animals↗
PubMed2000

[Studies on metal porphyrins as two-functional mimic of enzyme].

In this study, four metal porphyrins (tetraphenylporphyrinesulfonatoiron, tetraphenylporphyrinesulfon-atocopper, tetraphenylporphyrinesulfonatomanganese, and tetraphenyl porrphyrinesulfonatocobalt) were used as dual function mimicry of superoxide dismutase (SOD) and catalase (CAT). The first function, scavenging O2.-, has been proved by using riboflavine-methionine photoreduction method in the concentration range of 10(-5)-10(-6) mol/L. The second function, scavenging H2O2, has been demonstrated by means of spectrophotometry, and the percentage of decomposing H2O2 increases with the concentration of the imitating compounds. Metal porphyrins, SOD and CAT were measured by the liver homogenate technique of mice and the results showed that they had obvious action of decreasing the lipid peroxidation. Tetraphenylporphyrinesulfonatomanganese was measured by isolated ischemia reperfusion heart of rats. The results indicated that the Mn-TPPS4 could reduce the damages of active oxygen and had evidently protective effects on isolated ischemia-reperfusion mocardium of rats.

Animals↗
PubMed1999

Effects of L-arginine on endothelial and cardiac function in rats with heart failure.

We examined the effects of chronic oral L-arginine treatment on endothelial and cardiovascular function in rats with heart failure induced by coronary artery ligation. Both heart failure and sham-operated rats were treated with either L-arginine in drinking water (12.5 or 50 g/l) or water placebo for 8 weeks following surgery. Plasma L-arginine levels in heart failure rats (153 +/- 11 microM) were lower than sham rats (201 +/- 13 microM, P < 0.05). The lower dose L-arginine treatment improved endothelium-dependent relaxation of isolated aortic rings of heart failure rats, while the higher dose of L-arginine treatment did not. Neither low nor high dose of L-arginine treatment improved hemodynamic parameters in heart failure rats. Thus, chronic oral L-arginine treatment at a dose of 12.5 g/l in drinking water improves endothelium-dependent relaxation, but fails to improve in vivo cardiac function in rats with heart failure.

Animals↗
PubMed1999

Decreased responsiveness of vascular postjunctional alpha1-, alpha2-adrenoceptors and neuropeptide Y1 receptors in rats with heart failure.

Heart failure is associated with increased sympathetic nerve activity. We hypothesized that chronic sympathetic stimulation in heart failure resulted in decreased vascular sympathetic responsiveness. A pithed rat model was employed to evaluate peripheral vascular alpha-adrenoceptor and neuropeptide Y (NPY) receptor responsiveness. Heart failure was induced in Sprague-Dawley rats by coronary artery ligation. Sham operated rats (Sham) served as controls. Two months after this surgical procedure, both heart failure (n = 30) and Sham (n = 30) rats underwent standard pithing procedure. Pressor responses to preganglionic sympathetic nerve stimulation (PNS) and activation of postjunctional alpha1- and alpha2-adrenoceptors as well as Y1 receptors were studied. In response to PNS, cardiac index was similar between heart failure and sham rats (P = n.s.). Mean arterial pressure (MAP) increased in a frequency-dependent fashion after PNS in heart failure rats as well as in control rats. All the agonists used, i.e. the alpha1-adrenoceptor agonist phenylephrine, the alpha2-adrenoceptor agonists clonidine and BHT933 as well as NPY, induced dose-dependent increases in MAP in heart failure and in sham rats. However, in rats with heart failure, the response to all the agonists studied was significantly decreased and the dose response curves were shifted to the right (P < 0.01). We conclude that in vivo vascular response to postjunctional alpha1- and alpha2-adrenoceptors as well as Y1 receptors are decreased in rats with heart failure.

Adrenergic alpha-Agonists↗
PubMed1999

Expression of tissue type and urokinase type plasminogen activators as well as plasminogen activator inhibitor type-1 and type-2 in human and rhesus monkey placenta.

The distribution of mRNAs and antigens of tissue type (t) and urokinase type (u) plasminogen activators (PA) plus their corresponding inhibitors, type-1 (PAI-1) and type-2 (PAI-2) were studied in human and rhesus monkey placentae by in situ hybridisation and immunocytochemistry. Specific monkey cRNA and antibodies against human tPA, uPA, PAI-1 and PAI-2 were used as probes. The following results were obtained. (1) All the molecules tPA, uPA, PAI-1 and PAI-2 and their mRNAs were identified in the majority of the extravillous cytotrophoblast cells of the decidual layer between Rohr's and Nitabuch's striae and in cytotrophoblast cells of the chorionic plate, basal plate, intercotyledonary septae and cytotrophoblast cells of the chorionic villous tree. (2) Expression of uPA and PAI-2 was noted in villous trophoblast whereas tPA and PAI-1 were mainly concentrated where detachment from maternal tissue occurs. (3) No expression of tPA, uPA, PAI-1 and PAI-2 was observed in the basal plate endometrial stromal cells, chorionic plate connective tissue cells, septal endometrial stromal cells or villous core mesenchyme. (4) The distribution of probes observed following in situ hybridisation is generally consistent with the immunofluorescence pattern of the corresponding antigens and no significant interspecies differences were noted. It is possible that both decidual and extravillous trophoblast cells of placentae of human and rhesus monkey are capable of producing tPA, uPA, PAI-1 and PAI-2 to differing extents. Coordinated expression of these genes in the tissue may play an essential role in the maintenance of normal placentation and parturition. The differences in distribution we observed are consistent with the suggestion that coordinated expression of tPA and its inhibitor PAI-1 may play a key role in fibrinolytic activity in the early stages of placentation and separation of placenta from maternal tissue at term. On the other hand, uPA with its inhibitor PAI-2 appears mainly to play a role in degradation of trophoblast cell-associated extracellular matrix, and thus may be of greatest importance during early stages of placentation.

Animals↗
PubMed1999

Expression of the steroidogenic acute regulatory protein and luteinizing hormone receptor and their regulation by tumor necrosis factor alpha in rat corpora lutea.

Expression of both mRNA and protein of the steroidogenic acute regulatory protein (StAR), in correlation with progesterone (P) production and LH receptor (LHR) mRNA expression, was studied in the corpora lutea (CL) of gonadotropin-induced-pseudopregnant and pregnant rats at various stages of CL development. Immature female rats, 21-22 days old, were injected s.c. with 20 IU eCG to stimulate follicle growth and then with 20 IU hCG 48 h later to induce ovulation. The ovaries were removed at various stages of CL development; either CL were isolated and snap frozen for total RNA analysis, or whole ovaries were fixed in Bouin's fluid for paraffin sectioning. The results of in situ hybridization, immunohistochemistry, and Northern blotting showed that the increase in StAR mRNA and protein expression was well correlated with the increase in serum P concentration. StAR expression was restricted to the luteal cells or theca cells in antral follicles. Both StAR mRNA and protein in the CL of pseudopregnant rats increased steadily on Day 1 and Day 4, reached highest levels on Day 4, and then dropped sharply on Day 8 when luteolysis takes place. LHR mRNA content was high on Day 1 but dropped significantly on Day 2. LHR mRNA increased to high levels on Day 4 and 8 and then declined on Day 12. StAR mRNA and protein levels in the CL of pregnant rats were high during early luteal development (Day 2, 4), increased even further on Day 9, and decreased on Day 13 when luteolysis takes place. It is therefore suggested that the expression of StAR coincides well with the capacity of P production in the CL and that StAR expression can be used as a functional "marker" of CL development. To study the possible effect of cytokines on StAR expression, pseudopregnant rats on Day 5 were injected s.c. with 10 IU hCG plus 20 microg prolactin (PRL), with or without 500 IU tumor necrosis factor alpha (TNFalpha) 30 min later. TNFalpha significantly inhibited hCG/PRL-induced StAR and LHR mRNA expression at 1 and 3 h post-TNFalpha. It is suggested that the luteolytic effect of TNFalpha may be mediated by its direct inhibition on StAR expression or by an indirect decrease in LHR expression.

Animals↗