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Biomedical subjects

Q Zhou

Publications and source records attributed to Q Zhou.

At least 325 records · Page 18Linked to original sources
PubMed1995

The effects of magnesium deficiency on DNA and lipid synthesis in cultured human umbilical arterial endothelial cells.

This study investigated the effects of magnesium deficiency on thymidine incorporation and lipid synthesis in human umbilical arterial endothelial cells. To study [3H]thymidine incorporation, the cells were exposed for 12 to 96 h to experimental media containing decreasing magnesium concentrations of 237, 118 and 5 microM. A magnesium concentration of 949 microM was used as control. At 48 h of exposure to the experimental media, magnesium was restored to 949 microM in half of the magnesium-deficient cultures. To determine [14C]acetic acid distributions among cholesterol, phospholipid and triglyceride, the cells were treated with decreased magnesium media at the levels mentioned above for 12 to 48 h. The results showed that [3H]thymidine incorporation into DNA was inhibited by magnesium deficiency. The inhibition was augmented correspondingly with decreased magnesium concentrations and increased exposure periods. When magnesium in the medium was enhanced to normal level, incorporation was no longer inhibited. Incorporation of [14C]acetic acid into phospholipid was inhibited, its incorporation into triglyceride was stimulated, but its incorporation into cholesterol was not affected by magnesium deficiency. We suggest (i) that with the restoration of adequate magnesium, the inhibiting effect of magnesium deficiency on thymidine incorporation is reversible; (ii) that magnesium deficiency can result in a redistribution of [14C]acetic acid between phospholipid and triglyceride.

Acetates↗
PubMed1995

Effects of adrenochrome and epinephrine on human arterial endothelial cells in vitro.

The effects of adrenochrome and epinephrine were investigated in cultured human umbilical arterial endothelial cells. The cells were exposed to either adrenochrome or epinephrine at levels of 50 and 200 microM, respectively, up to 24 hrs. At 3, 5, 7 and 24 hrs of the designed harvesting time, [3H]thymidine incorporation, protein content, [3H]cholesterol uptake, prostacyclin production and lipid peroxidation were measured. We found that adrenochrome at a level of 200 microM inhibited [3H]thymidine incorporation, decreased protein content, stimulated [3H]cholesterol uptake, and decreased prostacyclin production after 3, 5, 24 and 5 hrs of exposure, respectively, compared with control. It took 24 hrs however for epinephrine at a level of 200 microM to inhibit [3H]thymidine incorporation and prostacyclin production. When the concentration was reduced to 50 microM, only adrenochrome inhibited [3H]thymidine incorporation after 24 hrs of treatment. Both adrenochrome and epinephrine had no effect on lipid peroxidation. We suggest that atherogenic changes found in severe hypertension may be due to abnormal high concentration of epinephrine, especially oxidized epinephrine, on endothelial cell functions, such as DNA synthesis, cholesterol uptake and prostacyclin production.

Adrenochrome↗
PubMed1995

Extracellular ATP stimulates adenylyl cyclase and phospholipase C through distinct purinoceptors in NG108-15 cells.

In neuroblastoma x glioma hybrid NG108-15 cells, ATP induced a concentration-dependent increase in the intracellular Ca2+ concentration ([Ca2+]i), accompanied by inositol phosphate formation. Under the same conditions, we found a marked increase in cAMP levels produced by ATP at concentrations similar to those required to increase [Ca2+]i. The Ca2+ ionophore A23187 or bradykinin, which evoked inositol phosphate formation and increases in [Ca2+]i, did not increase, and instead slightly decreased, cAMP content, indicating that ATP-induced cAMP accumulation was not due to activation of Ca(2+)-sensitive adenylyl cyclase. The effect of ATP on cAMP production was not dependent on generation of adenosine caused by ATP hydrolysis. Among several P2 purinoceptor agonists, adenosine-5'-O-(3-thio)triphosphate, 5'-adenylylimidodiphosphate, and adenosine-5'-O-(2-thio)diphosphate evoked both cAMP accumulation and Ca2+ mobilization. In contrast, beta,gamma-methylene-ATP selectively elicited cAMP accumulation, whereas 2-methylthio-ATP and UTP induced only Ca2+ mobilization, without affecting cAMP levels. The potent P2x purinoceptor agonist alpha,beta-methylene-ATP did not induce cAMP accumulation or Ca2+ mobilization. The cAMP accumulation induced by ATP was not affected by the P2 receptor antagonist suramin but was inhibited by P1 receptor antagonists such as 8-(p-sulfophenyl)theophylline, 3-isobutyl-1-methylxanthine, and xanthine amine congener. However, the ATP-induced increase in [Ca2+]i was not affected by suramin or xanthine amine congener. Taken together, these results indicate that ATP activates two distinct purinoceptors that are coupled to different signal transduction systems, one being adenylyl cyclase and the other phospholipase C, in NG108-15 cells. Furthermore, pharmacological profiles of the adenylyl cyclase-coupled receptor were quite different from those of any known purinoceptor subtypes, especially in the unusual sensitivity of the receptor to P1 and P2 receptor agonists and antagonists. It is therefore suggested that ATP-induced cAMP accumulation may be mediated by a novel subtype of purinoceptor in NG108-15 cells.

Adenosine↗
PubMed1995

[Synthesis and antifertility activity of a-nor-5 alpha-androstane derivatives].

In order to study the relationship between the structure of A-nor-5 alpha-androstane derivatives and their antifertility activity, we designed and synthesized 16 A-nor-5 alpha-androstane compounds through several reaction steps with dehydroepiandrosterone acetate as a starting material. Their structures were confirmed by IR, 1HNMR, MS, elemental analyses, etc. Preliminary pharmacological tests showed that compounds 8, 9, 10 and 16 possess antiimplantation activity to some extent (2.5 mg.kg-1, administered po, gave 67-75% antiimplantation rate). Other compounds showed low activity. The possible relationship between compound structures and their activities is analysed briefly.

Animals↗
PubMed1995

[Recurrent meningitis and spontaneous cerebrospinal fluid otorrhea].

Five children with recurrent meningitis were surgically confirmed to have vestibular fistula and spontaneous cerebrospinal fluid (CSF) otorrhea. The vestibular fistulas were successfully repaired under general anaesthesia. No complications were found after follow-up for 3-8 years. The etiology of CSF otorhinorrhea, location of fistulas, diagnosis and treatment of spontaneous vestibular CSF otorrhea were discussed.

Cerebrospinal Fluid Otorrhea↗
PubMed1994

Changes in p53 and cyclin D1 protein levels and cell proliferation in different stages of human esophageal and gastric-cardia carcinogenesis.

The objective of this study was to quantify the changes in p53 and cyclin D1 protein levels in different stages of human esophageal and gastric cardia carcinogenesis in a high-risk population in Henan, China. Immunoreactivity of p53, cyclin D1 and proliferating-cell nuclear antigen (PCNA) was observed in the cell nuclei of esophageal and gastric cardia biopsies. The number of p53-immunostaining-positive cells was low in normal epithelia, slightly increased in basal-cell hyperplasia (BCH), markedly increased in dysplasia (DYS) (10-fold), and further increased in squamous-cell carcinoma (SCC) (40-fold). This pattern of change was similar to that of cell proliferation as indicated by PCNA immunostaining. On the other hand, the number of cyclin D1-immunostaining-positive cells did not increase from BCH to DYS, although a slight increase from DYS to SCC was noted. In the gastric cardia, again, the pattern of change of p53-positive cells in different stages of lesions paralleled the pattern of cell proliferation. The number of p53-positive cells was very low, much lower than that of PCNA-positive cells, in normal, chronic superficial gastritis (CSG) and chronic atrophic gastritis (CAG); therefore, the increase of p53-positive cells from CAG to DYS was more dramatic (100-fold). From DYS to adenocarcinoma (AC), the p53-positive and the PCNA-positive cells increased 4-fold. On the other hand, the number of cyclin D1-positive cells did not increase in pre-cancerous lesions, but increased slightly in AC. This study demonstrates that p53 protein accumulation increased with the progression of pre-cancerous lesions, especially in the genesis of dysplasia, both in the esophagus and in the gastric cardia. Our approach of quantitative immunohistochemistry sheds light on the mechanisms of genesis of esophageal and gastric-cardia cancers, which frequently occur together in many high-incidence areas.

Adenocarcinoma↗
PubMed1994

p53 tumor suppressor gene mutation in early esophageal precancerous lesions and carcinoma among high-risk populations in Henan, China.

To understand whether p53 gene mutation is an early or late event in esophageal carcinogenesis, biopsy samples of esophageal epithelium from symptom-free subjects in a high incidence area, Huixian county of Henan Province, China, were analyzed. Mutations in exons 5, 6, 7, and 8 of p53 were analyzed by single-strand conformation polymorphism analysis and DNA sequencing. Among the 37 biopsy samples showing accumulation of p53 protein in immunohistochemical staining, missense mutations of p53 gene were detected in 1 of 3 samples with normal epithelia, 3 of 23 samples with basal cell hyperplasia, and 4 of 11 samples with dysplasia. All mutations occurred at exon 5 with 3 at codon 175, 2 at codon 176, and 1 each at codons 159, 135, and codon 132. Of the 8 mutations, there were 3 G to A transitions and 3 G to T transversions. To understand the mutation spectrum and possible causative factors of esophageal cancer in this area, surgically resected human primary esophageal carcinomas from Linxian county were analyzed for p53 gene mutations in exons 5, 6, 7, and 8. Mutations were detected in 16 of 29 samples (55%). Twelve samples contained different missense point mutations, with 75% transitions (7 G to A and 2 A to G) and 25% transversions (2 G to T and 1 G to C). Most of the mutations were located at either exon 5 or exon 7. A deletion and an insertion of nucleotides leading to frame-shift mutations were detected in each of two other samples. The results demonstrate that p53 protein accumulation and gene mutation may occur at very early stages of esophageal carcinogenesis. In carcinomas, there was a higher frequency of p53 gene mutations, which accounts for most of the cases with p53 protein accumulation.

Adult↗
PubMed1994

GM3 directly inhibits tyrosine phosphorylation and de-N-acetyl-GM3 directly enhances serine phosphorylation of epidermal growth factor receptor, independently of receptor-receptor interaction.

GM3 ganglioside (II3NeuAcLacCer) inhibits epidermal growth factor (EGF)-dependent receptor autophosphorylation and cell growth (Bremer, E.G., Schlessinger, J., and Hakomori, S. (1986) J. Biol. Chem. 261, 2434-2440), whereas de-N-acetyl-GM3 (deNAcGM3; II3NeuNH2Lac-Cer) promotes these processes (Hanai, N., Dohi, T., Nores, G. A., and Hakomori, S. (1988) J. Biol. Chem. 263, 6296-6301). Receptor-receptor interaction has been proposed as an essential initial mechanism for EGF-dependent activation of EGF receptor kinase (EGF-RK) (Schlessinger, J. (1988) Trends Biochem. Sci. 13, 443-447). We studied the effects of GM3 and deNAcGM3 on EGF-RK function and EGF-R dimerization, and observed that (i) EGF-dependent in vitro and in vivo (in situ) phosphorylation of A431 cells at both monomeric and dimeric forms of EGF-R was inhibited in a dose-dependent manner by GM3, but unaffected by GM1. (ii) Quantities of both forms of EGF-R remained constant regardless of addition of various quantities of GM3 or GM1, as revealed by blotting with antibodies directed to the C-terminal region of EGF-R, or by cell surface 125I-labeling followed by immunoprecipitation. (iii) DeNacGM3 in the absence as well as in the presence of a minimal quantity of detergent significantly enhanced EGF-R phosphorylation, particularly Ser phosphorylation. (iv) DeNAcGM3 was detected in a large variety of actively growing tumor cells. Findings i and ii above indicate that GM3 directly inhibits EGF-dependent Tyr phosphorylation but does not affect receptor-receptor interaction. Findings iii and iv suggest that deNAcGM3 strongly promotes serine phosphorylation (in addition to Tyr phosphorylation) of EGF-R and may function as a second messenger in the process of cell growth stimulation.

Animals↗
PubMed1994

Vasoinhibitory action of KT2-734, an antihypertensive agent, in isolated rat aorta.

In rat aorta, KT2-734 inhibited contractile responses to 5-hydroxytryptamine (5-HT) and KCl. KT2-734 inhibited the relaxing effect of verapamil, but not nifedipine. Similarly, verapamil, but not nifedipine, inhibited the vasorelaxing effect of KT2-734. KT2-734 relaxation was inhibited by endothelium removal but not by atropine and propranolol. Methylene blue, a guanylyl cyclase inhibitor, and NG-monomethyl arginine also inhibited the relaxation both in the presence and absence of endothelium. In the absence of endothelium, KT2-734 potentiated the relaxation induced by L-arginine, nitroglycerin and isoproterenol. In addition, M & B 22,948, a cGMP phosphodiesterase inhibitor, and theophylline inhibited and potentiated, respectively, KT2-734-induced relaxation. However, methylene blue inhibited the potentiation of isoproterenol relaxation by KT2-734 and that of KT2-734-relaxation by theophylline. KT2-734 caused increases in the level of cGMP without significantly affecting the cAMP level. These results suggest that KT2-734 may cause endothelium-independent relaxation mainly due to inhibition of cGMP-phosphodiesterase.

Animals↗
PubMed1994

Effect of octreotide on dynamic excretion of bile in Chinese acromegalic patients assessed by [99mTc]EHIDA hepatobiliary scan.

We used [99mTc]EHIDA hepatobiliary scintigraphy to determine whether both hepatic bile secretion and gallbladder contractility are suppressed in acromegalic patients receiving long-term treatment with the somatostatin analogue octreotide. We studied three groups of patients: group 1, untreated patients; group 2, average dose of octreotide 500 +/- 100 micrograms/day for 33 +/- 4 months; and group 3, 1000 +/- 200 micrograms/day for 33 +/- 4 months. Images were taken at specified time intervals during the 120-min period following injection of EHIDA. After a single injection of octreotide, group 1 patients demonstrated delayed visualization of the radioisotope in the liver, gallbladder, and duodenum. At the end of long-term treatment, group 2 patients showed a delay in appearance of maximal radioactivity in the gallbladder. Two weeks following discontinuation of octreotide, this parameter had decreased significantly (P < 0.001). In group 3, visualization of the liver, gallbladder, and duodenum were prolonged, with delayed visualization of the gallbladder persisting two weeks after withdrawal (P < 0.005). These results indicate that gallbladder contractility is decreased after a single injection of octreotide and that during chronic octreotide therapy the rate of bile secretion is reduced. Impaired gallbladder contractility normalizes more rapidly after discontinuation of octreotide in patients receiving low doses of the analog.

Acromegaly↗
PubMed1994

Alcohols potentiate ion current mediated by recombinant 5-HT3RA receptors expressed in a mammalian cell line.

The effect of acute exposure to alcohols on ion current mediated by recombinant 5-HT3RA receptors transiently expressed in human embryonic kidney 293 cells was investigated. Cells transfected with 5-HT3RA cDNA expressed receptors with pharmacological and functional properties similar to those of native 5-HT3 receptors. Potentiation of receptor-mediated cation current was observed in the presence of ethanol (10-100 mM), butanol (0.1-20 mM), isopentanol (0.01-25 mM) and trichloroethanol (0.5-25 mM). Potentiation increased in a concentration-dependent manner until saturation was achieved for all alcohols tested. The maximal efficacies of potentiation differed among the alcohols with isopentanol > butanol = trichloroethanol > ethanol. Potentiation by butanol and isopentanol appeared to show acute tolerance such that the percent increase in current amplitude was largest upon the first of a series of alcohol applications and decreased during subsequent applications. The effect of ethanol was variable with potentiation occurring in 74% of cells examined, but not in the remaining cells. These observations indicate that the potentiating action of alcohols is similar in recombinant receptors to that previously observed in neuroblastoma cells and neurons expressing native receptors. These findings indicate that this recombinant system is suitable for studying the molecular basis of alcohol actions on the 5-HT3 receptor.

Alcohols↗
PubMed1994

Factors affecting electrofusion of 2-cell mouse embryos.

Parameters of electrofusion of 2-cell mouse embryos were optimized for application as a model for nuclear transplantation. There was considerable lysis of embryos with M(2) as the medium for fusion; however, 100% fusion (n = 58) was obtained with a single 0.31-kv / cm, 1280-musec pulse. With mannitol and sucrose solutions as the medium, a wide range of field strengths (0.31-1.41 kv / cm for 0.26 M sucrose solution and 0.31 to 2.04 kv / cm for 0.3 M mannitol solution) and durations of the electrical pulse (10-1280 musec) resulted in high rates of fusion (often 100%). Likewise, osmolarity of sucrose and mannitol solutions did not affect the rate of fusion using a 0.47-kv / cm pulse. With a field strength of 2.04 kv / cm, the proportion of embryos that fused in mannitol solution increased (P<0.05) and the proportion that were lysed decreased (P<0.05) as osmolarity increased. Both fused (162 642 , 25%) and control embryos (32 72 , 44%) continued to develop in culture for 48 h, after which they began to compact. Fused embryos were only at the 4-cell stage by this time, while control embryos were at the 8-cell stage. Optimal pulse durations are plotted for field strengths between 0.31 and 1.41 kv / cm with 0.26 M sucrose as fusion medium.

Journal Article↗
PubMed1994

Optical sensors for monitoring and control of plant growth systems.

Optical chemical sensors have been developed for monitoring several parameters relevant to plant growth systems. These sensors utilize porous polymer and porous glass as the sensing element, and optical fiber input/output lines connected to a custom optoelectronic interface. Present in the sensing element are immobilized colorimetric indicators, which react with the analyte to be sensed. This reaction results in a change in the optical properties of the sensor. These sensors are particularly suited to in-situ monitoring of nutrient solution parameters and atmospheric trace contaminants in life support and plant growth systems. Sensors for monitoring pH, ammonia, and ethylene will be discussed.

Ammonia↗
PubMed1994

Vasoinhibitory effects of NC 1005 and NC 1006, new synthesized antiarrhythmic agents, in isolated rat aorta.

1. NC 1005 and NC 1006 (3 x 10(-6) M-10(-4) M) inhibited the contractions induced by phenylephrine (PE) and KCl in isolated rat aortas with or without endothelium. 2. In a Ca(2+)-free medium containing EGTA and nifedipine, NC 1005 and NC 1006 inhibited PE-response and a subsequent response to Ca2+ in the presence of PE. 3. NC 1005 and NC 1006 also caused relaxations of endothelium-removed aortas precontracted with PE. 4. The relaxations induced by NC 1005 and NC 1006 were potentiated by amiloride, zaprinast and theophylline but not by increasing the external Na+ concentration. 5. Methylene blue and ouabain slightly potentiated NC 1005-relaxation, but not NC 1006-relaxation. 6. Glyburide, apamine and nifedipine had no effect on the relaxations. 7. NC 1005 and NC 1006 potentiated the relaxation induced by nitroglycerin (NG) without affecting isoproterenol-relaxation. 8. In the presence of forskolin, NC 1005 and NC 1006 failed to potentiate NG-relaxation. 9. These results suggest that the vasoinhibitory effects of NC 1005 and NC 1006 may be due to an increase in the level of cAMP.

Aniline Compounds↗
PubMed1994

Inhibitory effect of sodium nitroprusside on the relaxing action of isoproterenol in isolated rat urinary bladder.

1. Isoproterenol caused relaxation of rat detrusor muscles contracted by electrical stimulations. Sodium nitroprusside (SNP) and methylene blue inhibited the relaxation induced by isoproterenol without affecting forskolin-induced relaxation. 2. In the presence of theophylline, zaprinast still potentiated isoproterenol-relaxation. In the presence of butoxamine, a selective beta 2-adrenoceptor inhibitor, but not metoprolol, a selective beta 1-adrenoceptor inhibitor, SNP still inhibited isoproterenol-relaxation. 3. SNP inhibited the relaxation to dobutamine, a beta 1-adrenoceptor agonist but not that to terbutaline, a beta 2-adrenoceptor agonist. The relaxation to dobutamine was also inhibited by methylene blue. Further, in the presence of theophylline, zaprinast still potentiated dobutamine-relaxation. 4. Isoproterenol increased tissue level of cGMP, which was inhibited by propranolol. 5. These results suggest a possibility that, in rat detrusor muscles, isoproterenol causes relaxation due to increases in the level of both cAMP and cGMP.

Animals↗
PubMed1994

IR circular dichroism of turns in small peptides.

The observation of circular dichroism (CD) in vibrational transitions in the infrared spectral region offers new possibilities for the determination of peptide solution conformation. Infrared or vibrational CD (VCD) is a particularly sensitive probe for the conformation of various peptide turns. Results of small linear and cyclic peptides containing beta- or gamma-turns are reported.

Amino Acid Sequence↗
PubMed1994

Possible mechanisms of vasoinhibitory effects of mequitazine, an antiallergic agent, on the contractions of isolated rat aorta induced by K+, phenylephrine, 5-hydroxytryptamine, and Ca2+.

Mequitazine, 10-(3-quinuclidinylmethyl) phenothiazine, inhibited contractile responses to KCl, phenylephrine (PE), 5-hydroxytryptamine (5-HT), and Ca2+ in rat aorta. Indomethacin or removal of endothelium did not affect the inhibitory effect of mequitazine on the responses to PE. In Ca(2+)-free medium containing EGTA and nifedipine, mequitazine inhibited both residual response to PE and subsequent response to Ca2+ in the presence of PE. Mequitazine potentiated the relaxation to nitroglycerin (NTG) and isoproterenol. In the presence of forskolin, mequitazine did not cause further potentiation of NTG relaxation. Mequitazine relaxation was slightly inhibited by nifedipine and was potentiated by theophylline. The relaxation was not affected by zaprinast, methylene blue, W-7, propranolol, cimetidine, glyburide, or tetraethylammonium. Tissue level of cyclic AMP in rat aorta was increased by mequitazine. These results suggests that mequitazine may inhibit voltage-operated Ca2+ channels (VOC) and increases the level of cyclic AMP.

Animals↗