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Biomedical subjects

Y Gao

Publications and source records attributed to Y Gao.

At least 271 records · Page 15Linked to original sources
PubMed1998

Role of microtubules in glucose uptake by C6 glioma cells.

Drugs that influence tubulin function were used to investigate the role of microtubules in hexose uptake by C6 glioma cells. In C6 cells, colchicine and vinblastine (which inhibit tubulin polymerization) inhibited radioactive [3H]2-deoxy-D-glucose uptake by about 30%. Paclitaxel (which promotes tubulin polymerization) stimulated hexose uptake by about 25%. To further demonstrate that microtubules play a role in hexose uptake, C6 cells were transfected with GLUT1 cDNA and then challenged with 100 nM paclitaxel. In GLUT1-transfected cells paclitaxel stimulated 2-deoxy-D-glucose uptake by about 35%. To study the role of tubulin in agonist-stimulated hexose uptake, the effect of colchicine on carbachol-induced uptake was next examined. Hexose uptake was increased with carbachol in concentration-dependent manner which was abolished by pretreatment with colchicine. To examine the specificity of the inhibitory effect of colchicine on G protein-mediated signal transduction pathway, the influence of colchicine on insulin (which acts via tyrosine kinase pathway) stimulation of 2-deoxy-D-glucose uptake was investigated. Hexose uptake was increased by insulin in a concentration-dependent manner which was unaffected by pretreatment with colchicine. These results suggest that microtubules are involved in basal and carbachol-stimulated glucose uptake by C6 cells.

Animals↗
PubMed1998

Genetic characterization and heterologous expression of brochocin-C, an antibotulinal, two-peptide bacteriocin produced by Brochothrix campestris ATCC 43754.

Brochocin-C, produced by Brochothrix campestris ATCC 43754, is active against many strains of the closely related meat spoilage organism Brochothrix thermosphacta and a wide range of other gram-positive bacteria, including spores of Clostridium botulinum. Purification of the active compound and genetic characterization of brochocin-C revealed that it is a chromosomally encoded, two-peptide nonlantibiotic bacteriocin. Both peptides of brochocin-C are ribosomally synthesized as prepeptides that are typical of class II bacteriocins. They are cleaved following Gly-Gly cleavage sites to yield the mature peptides, BrcA and BrcB, containing 59 and 43 amino acids, respectively. Fusion of the nucleotides encoding the signal peptide of the bacteriocin divergicin A in front of the structural genes for either BrcA or BrcB allowed independent expression of each component by the general protein secretion pathway. This revealed the two-component nature of brochocin-C and the necessity for both peptides for activity. A 53-amino-acid peptide encoded downstream of brcB functions as the immunity protein (BrcI) for brochocin-C. In addition, the cloned chromosomal fragment revealed open reading frames downstream of brcI, designated brcT and brcD, that encode proteins with homology to ATP-binding cassette translocator and accessory proteins, respectively, involved in the secretion of Gly-Gly-type bacteriocins.

Amino Acid Sequence↗
PubMed1998

Neuronal nitric oxide synthase is expressed in principal cell of collecting duct.

We used the RT-PCR technique and immunocytochemical methods to determine the expression of endothelial nitric oxide synthase (eNOS) or neuronal nitric oxide synthase (nNOS) in the cortical collecting duct (CCD) in rats on high-K+ diet. The microdissected CCDs of the rat kidney were lysed, and RT-PCR was carried out using rat nNOS and eNOS gene-specific primers. Southern analysis showed the presence of mRNA of nNOS but not eNOS in the CCD. The presence of nNOS in the CCD was further confirmed by light microscopy. We used the polyclonal nNOS antibody in immunocytochemical studies of the isolated CCD. We found that immunoreactivity to nNOS was present in the CCD and heterogeneous with positive and negative immunostaining. We performed the immunocytochemical studies in the split-open CCD and found that the immunoreactivity to nNOS was detected only in principal cells but not in intercalated cells. We conclude that nNOS is expressed in the rat CCD in rats on high-K+ diet. The presence of nNOS in the CCD is heterogeneous and mainly located in principal cells.

Animals↗
PubMed1998

Effect of selective phosphodiesterase inhibitors on response of ovine pulmonary arteries to prostaglandin E2.

Several adenosine 3',5'-cyclic monophosphate (cAMP)-hydrolyzing phosphodiesterase isozymes are present in the pulmonary vasculature. The present study was designed to determine the effect of selective inhibitors of phosphodiesterase subtypes on prostaglandin E2 (PGE2)-induced relaxation of isolated fourth-generation pulmonary arteries of newborn lambs. PGE2 and forskolin caused pulmonary arteries to relax and induced an increase in the intracellular cAMP content in the vessels. The relaxation and change in cAMP content were augmented by milrinone and rolipram, inhibitors of phosphodiesterase type 3 (PDE3) and type 4 (PDE4), respectively. The augmentation in relaxation and the increase in cAMP content caused by milrinone plus rolipram was greater than the sum of the responses caused by either of the inhibitors alone. 8-Methoxymethyl-1-methyl-3-(2-methylpropyl)xanthine, an inhibitor of phosphodiesterase type 1, had no effect on relaxation and change in cAMP induced by PGE2 and forskolin. Acetylcholine alone had no effect on cAMP content in the vessels but augmented the relaxation and the increase in cAMP induced by PGE2 and forskolin in arteries with endothelium. This effect was not observed in arteries without endothelium or in arteries with endothelium treated with NG-nitro-L-arginine. These results suggest that PDE3 and PDE4 are the primary enzymes hydrolyzing cAMP of pulmonary arteries of newborn lambs and that an inhibition of both PDE3 and PDE4 would result in a greater effect than that caused by inhibition of either one of the subtype isozymes alone. Furthermore, endothelium-derived nitric oxide may enhance cAMP-mediated relaxation by inhibition of PDE3.

Animals↗
PubMed1998

Developmental change in isoproterenol-mediated relaxation of pulmonary veins of fetal and newborn lambs.

beta-Adrenergic agonists are important regulators of perinatal pulmonary circulation. They cause vasodilation primarily via the adenyl cyclase-adenosine 3',5'-cyclic monophosphate (cAMP) pathway. We examined the responses of isolated fourth-generation pulmonary veins of term fetal (145 +/- 2 days gestation) and newborn (10 +/- 1 days) lambs to isoproterenol, a beta-adrenergic agonist. In vessels preconstricted with U-46619 (a thromboxane A2 analog), isoproterenol induced greater relaxation in pulmonary veins of newborn lambs than in those of fetal lambs. The relaxation was eliminated by propranolol, a beta-adrenergic antagonist. Forskolin, an activator of adenyl cyclase, also caused greater relaxation of veins of newborn than those of fetal lambs. 8-Bromoadenosine 3',5'-cyclic monophosphate, a cell membrane-permeable analog of cAMP, induced a similar relaxation of all vessels. Biochemical studies show that isoproterenol and forskolin induced a greater increase in cAMP content and in adenyl cyclase activity of pulmonary veins in the newborn than in the fetal lamb. These results demonstrate that beta-adrenergic-agonist-mediated relaxation of pulmonary veins increases with maturation. An increase in the activity of adenyl cyclase may contribute to the change.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1998

A single dose of antenatal betamethasone enhances isoprenaline and prostaglandin E2-induced relaxation of preterm ovine pulmonary arteries.

Beta-adrenergic agonists and prostaglandin E2 (PGE2) play an important role in perinatal pulmonary circulation. We have determined the effect of antenatal glucocorticoid treatment on isoprenaline- and PGE2-mediated relaxation of pulmonary arteries of newborn preterm lambs. Ovine fetuses (121 days of gestation; term = 150 days) received a single intramuscular dose of betamethasone (0.5 mg/kg) or saline. Fifteen hours after the injection, the lambs were delivered, ventilated for 3 h, and sacrificed. The fourth-generation pulmonary arteries were dissected and cut into rings for study. In endothelin-1-preconstricted vessels, isoprenaline, PGE2, and forskolin (an activator of adenylyl cyclase) induced greater relaxations of pulmonary arteries of betamethasone-treated lambs than those of controls. 8-Bromo-cyclic adenosine monophosphate, a cell membrane permeable analogue of cyclic adenosine monophosphate, caused similar relaxation of all vessels. When stimulated with isoprenaline and PGE2, the adenylyl cyclase activity of crude membrane preparations of pulmonary arteries treated with betamethasone was greater than that of controls. These results show that single-dose antenatal betamethasone treatment enhances relaxation of pulmonary arteries of preterm lambs induced by isoprenaline and PGE2 and that an enhanced adenylyl cyclase activity contributes to the effect of betamethasone on pulmonary arteries of preterm lambs.

Adenylyl Cyclases↗
PubMed1998

Mechanisms of downregulation of transfected E-cadherin cDNA during formation of invasive tumors in syngeneic mice.

Loss of E-cadherin expression has been observed both in experimental tumors and in human cancers and is related to invasiveness and poor differentiation. The E-cadherin-negative mouse mesenchymal tumor cell line MO4 was transfected with several plasmids expressing mouse E-cadherin cDNA. These plasmids differed from each other by the extent of E-cadherin-specific 3' untranslated region (UTR) sequences and by the use of different constitutive promoters. Transfectants were isolated that expressed functional E-cadherin in a homogeneous way. In syngeneic mice, such MO4-Ecad transfectants invariably produced malignant fibrosarcoma-like tumors, which were completely E-cadherin-negative at the protein level. Northern blotting revealed that E-cadherin mRNA expression was downregulated in some but not all MO4-Ecad tumors. Downregulation was caused by mRNA instability triggered by particular 3' UTR sequences. This in vivo downregulation of E-cadherin in malignant MO4-Ecad tumors turned out to be reversible and is likely to be mediated by host factors to be further identified.

Animals↗
PubMed1998

Heterogeneity in endothelium-derived nitric oxide-mediated relaxation of different sized pulmonary arteries of newborn lambs.

Endothelium-derived nitric oxide (EDNO) plays a pivotal role in regulating pulmonary circulation. To determine whether there is a heterogeneity in EDNO-mediated responses of different sized pulmonary vessels, we studied small and large isolated pulmonary arteries of newborn lambs (diameter, 0.4-0.7 and 1.5-2.5 mm, respectively). The isometric tension of vessel rings were recorded while suspended in organ chambers filled with modified Krebs-Ringer bicarbonate solution (95% O2-5% CO2, 37 degrees C). In vessels preconstricted with norepinephrine, acetylcholine and bradykinin induced a greater relaxation of small pulmonary arteries than of large pulmonary arteries. Acetylcholine, bradykinin, and nitric oxide also induced a greater increase in cGMP content in small arteries than in large ones. The responses to acetylcholine and bradykinin were endothelium-dependent and inhibited by nitro-L-arginine, an inhibitor of nitric oxide synthase. In vessels without endothelium, the response to nitric oxide was inhibited by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, an inhibitor of soluble guanylate cyclase. The activity of soluble guanylyl cyclase of small arteries was greater than that of large arteries under basal conditions and after stimulation with S-nitroso-N-acetylpenicillamine, a nitric oxide donor. These results demonstrate that heterogeneity exists in EDNO-mediated relaxation of small and large pulmonary arteries in newborn lambs. A difference in the soluble guanylate cyclase activity of vascular smooth muscle may have contributed to this phenomenon.

Acetylcholine↗
PubMed1998

Evaluation of a safety educational programme for the prevention of pesticide poisoning.

The causal factors of pesticide poisoning in spraymen usually include sloppy handling, leakage of sprayers and a lack of personal protection, as well as of a knowledge about pesticide toxicity. This paper outlines the results of a safety educational programme to prevent pesticide poisoning among Chinese village spraymen in 1991 and 1992. The programme consisted of two parts: an interview of 3,286 trained subjects who were surveyed before and after the education courses, and a survey on the prevalence of pesticide poisoning among spraymen in 10 villages in 1991 and 1992, respectively. The results showed a general improvement in the knowledge about pesticide toxicity and safe use among the surveyed subjects. The prevalence of pesticide poisoning among the surveyed spraymen decreased from 1.05% in 1991 to 0.25% in 1992. Moreover, a 68.2% reduction of pesticide poisoning cases was observed in 10 villages in 1992. The success of the safety educational programme proved that education is an effective measure for preventing pesticide poisoning.

Adult↗
PubMed1998

[Effects of carbon disulfide on neurotransmitter and its metabolites in rats].

OBJECTIVE: In order to study the mechanism of neurotoxic effects of carbon disulfide (CS2) on animal behavior. METHODS: Changes in monoamine transmitter, amino acid transmitter and their metabolites in brain tissues were observed in rats exposed to CS2 at levels of 0, 1,200 and 2,400 mg/m3 respectively, for two months, with high performance liquid chromatography. RESULTS: Indicated that exposure to CS2 could cause decrease in 3-methoxy-4-hydroxy mandelic acid (VMA), increase in 3,4-dioxybenzoic acid, a metabolite of dopamine, and high vanillic acid in rat straitum, decrease in excitatory amino acids and their metabolites (glutamine, aspartic acid and asparagine), with a certain relationship between contents of VMA, aspartic acid and asparagine and changes in neurobehavior. CONCLUSION: Disturbance of neurotransmitter metabolism plays an important role in neurotoxic effects of CS2.

Animals↗
PubMed1998

A clinical trial of tang shen ning for treatment of diabetic nephropathy.

This paper reports the clinical trial of Tang Shen Ning ([symbol: see text], TSN) for treating diabetic nephropathy (incipient and clinical, as divided by Mogensen). The results showed that the total effective rate in treatment group (TSN + western medicine) was 90.0%, and that in the control group (simply with western medicine), 56.7%. TSN plays important roles in decreasing proteinuria and improving renal functions.

Adult↗
PubMed1998

[Failure of mifepristone induced interruption of pregnancy: point mutation at genetic codon 722 in human progesterone receptor gene].

OBJECTIVE: To detect the point mutation of hormone binding domain (HBD) of human progesterone receptor (hPR) gene by molecular biological methods in women with insensitivity to mifepristone. METHODS: 26 women in 5 hospitals were consented in the study. 16 women were as study group: continuing pregnancy in 11 and missed abortion in 5. 10 women with successful abortion were as control group. Decidual tissue was collected in each woman and RNA was extracted from it and purified. Reverse transcription-polymerase chain reaction (RT-PCR), single strand conformation polymorphism(SSCP) and restriction enzyme reaction were performed. All women were followed up. RESULT: No point mutation of HBD of hPR gene was detected in control group except one with point mutation in trace. Point mutation of HBD of hPR gene was detected in 7 of women with continuing pregnancy. Mifepristone was administrated in midluteal phase in two of these women and no vaginal bleeding was observed. No mutation of hPR gene in the other women with continuing pregnancy. Three women had pregnancy again in 6 months and had successful abortion. The other one administrated mifepristion in midluteal phase and had second vaginal bleeding. No point mutation of hPR gene was detected in women with missed abortion. CONCLUSION: There is point mutation of HBD of hPR gene in women with insensitivity to mifepristone, and women with point mutation of hPR gene detected by molecular biological methods are really insensitive to mifepristone.

Abortifacient Agents, Steroidal↗
PubMed1998

[Free fatty acids promoting PTP1B expression in rat skeletal muscle and hepatic cells].

OBJECTIVE: To determine whether that free fatty acids (FFAs) impair glucose metabolism is associated with altered insulin signaling system. METHODS: After skeletal muscle and hepatic cells were incubated with palmitate (0.25 mmol/L) or oleate (0.125 mmol/L) for 6, 12 or 24 hours, the protein abundance of SH-PTP2 and PTP1B was assessed by western blot. RESULTS: SH-PTP2 protein levels showed no significant change in both fatty acids treated muscle and hepatic cells at all time points. The PTP1B was significantly elevated in both liver and muscle cells incubated with FFAs at 6, 12 and 24 hours. CONCLUSIONS: FFAs promote the expression of PTP1B in rat skeletal muscle and liver cells, and the elevated PTP1B may mediate the insulin resistance induced by FFAs.

Animals↗
PubMed1998

Growth regulation of ovarian cancer cell line HO-8910 by transforming growth factor beta 1 in vitro.

OBJECTIVE: To further understand the role of growth regulation of human ovarian cancer cells by transforming growth factor (TGF) beta 1. METHODS: The cell proliferation, cAMP synthesis, gene expression, and induction of programmed cell death (PCD) in human epithelial ovarian cancer cell line HO-8910 cells exposed to TGF beta 1 in vitro were studied. RESULTS: TGF beta 1 inhibited cell growth and DNA synthesis, and induced G0/G1 arrest in cell cycle. It could also trigger PCD in cells. This induction of PCD may occur within G0/G1 phase. Meanwhile, the assay also showed that TGF beta 1 could inhibit the mRNA expression of c-myc, EGFR and TGF beta 1 genes in cells. CONCLUSIONS: TGF beta 1 can not only act as an autocrine to inhibit cell proliferation, but also trigger PCD in HO-8910 cells. These functions may be fulfilled through some specific signal transduction pathways.

Apoptosis↗
PubMed1998

[The study of platelet function in patients with chronic pulmonary heart disease].

OBJECTIVE: To study the platelet function in patients with chronic pulmonary heart disease. METHOD: Subjects were divided into three groups (cor pulmonale exacerbation, cor pulmonale remission stage and normal control). Platelet adhesion rate (PAdT), platelet aggregation rate(PAgT), alpha-granule membrane protein (GMP-140) and glycoproteinII were measured by radioimmunoassay, flow cytometry and other methods. RESULT: In cor pulmonale exacerbation, the values of PAdT, PAgT, GMP-140 and GPII were31% +/- 16%, 14% +/- 8%, 190 +/- 49 molecule/platelet and 145% +/- 36% respectively. In cor pulmonale remission stage, the values were 33% +/- 13%, 38% +/- 16%, 178 +/- 33 molecule/platelet and 137% +/- 48% respectively. These findings showed that the values of PAdT, GMP-140 and GPII in cor pulmonale exacerbation were markedly increased, whereas PAgT was significantly reduced. However, PAdT, PAgT, GMP-140 and GPII in remission stage were all higher than that of normal group. CONCLUSION: In vivo platelet activation is indeed present in patients with chronic pulmonary heart disease.

Aged↗
PubMed1998

[Neurotoxicity of antibody against motoneuron on cultured rat cortical neurons].

OBJECTIVE: In order to determine the role of antibody against motoneuron in the process of neuronal death. METHODS: Cultured rat cortical neurons growing in serum-free medium, were employed to observe the effects of antibody against motoneuron (anti-SMN) on the survival of these cultured neurons. RESULTS: (1) Exposure of the cultures in serum-free medium to anti-SMN with dilution of 1:50 results in death of 31%-41% of neurons for 24 hours incubation, 50%-67% for 48 hours and above 90% after 72 hours. The neurotoxicity induced by anti-SMN was accompanied by concentration-dependent release of lactate dehydrogenase into the culture medium. Cultures exposed to normal rat IgG as controls exhibited no such sign. (2) The cultured neurons exposed to anti-SMN (1:200) expressed markedly higher levels of immunoreactive Calbindin-D28k especially after 48 hours incubation with it. There was a reduction in the number of acetylcholinesterase-positive neurons compared to the normal control. CONCLUSIONS: The anti-SMN could directly initiate the process of cortical neuronal death and this effect was independent of complement. The alteration of Calbindin-D28k immunoreactivity implied that calcium may be involved in the neurotoxicity induced by anti-SMN.

Acetylcholinesterase↗