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Biomedical subjects

Q Gu

Publications and source records attributed to Q Gu.

At least 91 records · Page 5Linked to original sources

[Responses of growth hormone and prolactin to L-Dopa in women with polycystic ovarian syndrome].

OBJECTIVE: To evaluate the altered dopaminergic modulation of growth hormone (GH) and prolactin (PRL) in polycystic ovarian syndrome (PCOS). METHODS: Responses of GH and PRL to L-Dopa (L-DA) (500 mg) were observed in two PCOS groups (LH/FSH > or = 3, Group I, n = 15, LH/FSH < 3, Group II, n = 15) and the control (n = 20). RESULTS: Significantly lower GH (P < 0.01) and higher PRL levels (P < 0.05 in group I) in the basal state, and lower responses of GH and PRL to L-DA were found in two PCOS groups as compared with the control. CONCLUSION: The altered basal levels and blunted L-DA evoked responses of GH and PRL suggest a relative decrease of the dopaminergic activity in PCOS patients.

Adult↗

[Prenatal screening for major fetal defects by using of maternal serum markers].

OBJECTIVE: To investigate the effect of second-trimester maternal serum markers AFP, beta-hCG, uE3, for prenatal screening of the fetal defects. METHODS: In 677 women the triple markers were measured. Some factors that may affect the testing such as maternal weight, gestational age, were adjusted on analyzing the result of the testing. Each woman, who underwent the triple screening, will be followed up until her fetus was delivered. RESULTS: Among the women who were screened, 11 patients who presented at least one marker positive were identified as having an abnormal fetus, and the positive rate was 1.6%. While 32 women were confirmed to be false positive with a rate of 4.7%. Another 11 women had fetal demise on second-trimester, which had been proved to be not caused by fetal abnormality. CONCLUSION: Maternal triple serum markers may take as a routine protocol for prenatal screening of the fetal defects.

Adult↗

The tumour-suppressor gene patched encodes a candidate receptor for Sonic hedgehog.

The protein Sonic hedgehog (Shh) controls patterning and growth during vertebrate development. Here we demonstrate that it binds Patched (vPtc), which has been identified as a tumour-suppressor protein in basal cell carcinoma, with high affinity. We show that Ptc can form a physical complex with a newly cloned vertebrate homologue of the Drosophila protein Smoothened (vSmo), and that vSmo is coexpressed with vPtc in many tissues but does not bind Shh directly. These findings, combined with available genetic evidence from Drosophila, support the hypothesis that Ptc is a receptor for Shh, and that vSmo could be a signalling component that is linked to Ptc.

Amino Acid Sequence↗

Nerve growth factor induced modification of presynaptic elements in adult visual cortex in vivo.

Nerve growth factor (NGF) has been shown to play important roles in neuronal survival, growth and differentiation. Recently, we have found that intracortical infusion of NGF into adult cat visual cortex can recreate ocular dominance plasticity, suggesting that NGF is also involved in activity-dependent modification of synaptic connectivity in the adult brain. To further explore the mechanisms of NGF-induced plasticity in adult visual cortex, we studied two presynaptic markers: GAP-43 and synaptophysin. Immunocytochemical staining showed that NGF-treatment of adult visual cortex selectively increased the level of the phosphorylated form of GAP-43, while the total level of GAP-43 was not changed. These results demonstrate that NGF-treatment stimulates phosphorylation processes of GAP-43 in vivo. In addition, NGF-treatment of adult visual cortex increased the level of synaptophysin immunoreactivity. Since the phosphorylated form of GAP-43 is known to be enriched in the membrane skeleton of growth cones and of developing synapses, and the phosphorylation of GAP-43 has been linked with events that underlie synaptic plasticity, and since synaptophysin is a major component of presynaptic vesicles, our results suggest that NGF-treatment of adult visual cortex modulates presynaptic terminals, possibly by inducing axonal sprouting and formation of new synapses, and that these changes may play a role in the NGF-induced functional plasticity.

Animals↗

Selection for genes encoding secreted proteins and receptors.

Extracellular proteins play an essential role in the formation, differentiation, and maintenance of multicellular organisms. Despite that, the systematic identification of genes encoding these proteins has not been possible. We describe here a highly efficient method to isolate genes encoding secreted and membrane-bound proteins by using a single-step selection in yeast. Application of this method, termed signal peptide selection, to various tissues yielded 559 clones that appear to encode known or novel extracellular proteins. These include members of the transforming growth factor and epidermal growth factor protein families, endocrine hormones, tyrosine kinase receptors, serine/threonine kinase receptors, seven transmembrane receptors, cell adhesion molecules, extracellular matrix proteins, plasma proteins, and ion channels. The eventual identification of most, or all, extracellular signaling molecules will advance our understanding of fundamental biological processes and our ability to intervene in disease states.

Amino Acid Sequence↗

17 beta-Estradiol potentiates kainate-induced currents via activation of the cAMP cascade.

Evidence for nongenomic actions of steroids is now coming from a variety of fields of steroid research. Mechanisms of steroid action are being studied with regard to the membrane receptors and the activation of second messengers. The present study investigated the mechanism for the rapid effect of estrogen on acutely dissociated hippocampal CA1 neurons by using the whole-cell, voltage-clamp recording. Under the perforated patch configuration, 17 beta-estradiol potentiated kainate-induced currents in 38% of tested neurons. The potentiation was stereospecific, rapid in onset, and reversible after the removal of the steroid. Dose-response curves show that the potentiation by 17 beta-estradiol was evident at a concentration as low as 10 nM and saturated at 10 microM. 17 beta-Estradiol did not affect the kinetics (i.e., affinity and cooperativity) and reversal potential of kainate-induced currents. This suggests that the potentiation did not result from direct interaction with kainate receptors nor the activation of ion channels other than kainate receptor-channels. The potentiation by 17 beta-estradiol was similar to the enhancement of kainate-induced currents evoked by 8-bromo-cAMP, and was modulated by an inhibitor of phosphodiesterase (IBMX). The estrogen potentiation was blocked by a specific blocker of PKA (Rp-cAMPS). Under standard recording configuration, the effect was significantly affected by intracellular perfusing with GDP-beta-S or GTP-gamma-S. The data suggest that the potentiation of kainate-induced currents by 17-beta-estradiol was likely a G-protein(s) coupled, cAMP-dependent phosphorylation event. By involvement of this non-genomic mechanism, estrogen may play a role in the modulation of excitatory synaptic transmission in the hippocampus.

8-Bromo Cyclic Adenosine Monophosphate↗

P/O ratios reassessed: mitochondrial P/O ratios consistently exceed 1.5 with succinate and 2.5 with NAD-linked substrates.

The efficiency of ATP synthesis coupled to cell respiration, commonly referred to as the P/O ratio, has been the subject of extensive studies for more that 50 years. The general conclusion from these studies is that respiring mitochondria can convert external ADP to ATP at a maximal P/O ratio of 3 for NAD-linked substrates and 2 for succinate. However, in recent years the validity of these "integral" values has been questioned on both mechanistic and thermodynamic grounds, and a mechanistic P/O ratio of 2.5 for NAD-linked substrates and 1.5 for succinate have been concluded on the basis of experiments with isolated mitochondria. These values have been widely adopted in the scientific literature, including several recent textbooks. In this paper we report that under optimal conditions with respect to preparation and assay procedures, the P/O ratios obtained with isolated rat liver mitochondria consistently exceed 2.5 with NAD-linked substrates and 1.5 with succinate. These results, although not excluding "nonintegral" P/O ratios due to various energy-dissipating side reactions, warrant caution in accepting the reported lower values and, in general, in referring to mechanistic considerations unless the underlying molecular mechanisms are understood.

Adenosine Diphosphate↗

Multicopy suppressors of prc mutant Escherichia coli include two HtrA (DegP) protease homologs (HhoAB), DksA, and a truncated R1pA.

We have isolated three multicopy suppressors of the conditional lethal phenotype of a prc (tsp) null strain of Escherichia coli. One of these suppressors included two novel putative protease genes in tandem that map to 3400 kb or 72.5 centisomes on the chromosome. We propose the names hhoA and hhoB, for htrA homolog, to denote that these genes encode proteins that are 58 and 35% identical, respectively, to the HtrA (DegP) serine protease and 36% identical to each other. The HhoA and HhoB proteins are predicted to be 455 and 355 amino acids, respectively, in length. The mature HhoA protein is periplasmic in location, and amino-terminal sequencing shows that it arises following cleavage of a 27-amino-acid signal peptide. Searches of the protein and DNA databases reveal a rapidly growing family of homologous genes in a variety of other bacteria, including several which are required for virulence in their host. Deletion of the hhoAB genes shows that they are not required for viability at high temperatures like the homologous htrA but grow more slowly than wild-type strains. A second multicopy prc suppressor is the dksA (dnaK suppressor) gene, which is also a multicopy suppressor of defects in the heat shock genes dnaK, dnaJ, and grpE. The dksA gene was independently isolated as a multicopy suppressor of a mukB mutation, which is required for chromosomal partitioning. A third dosage-dependent prc suppressor includes a truncated rare lipoprotein A (rlpA) gene.

Amino Acid Sequence↗

[Analysis of complications following laparoscopic surgery].

OBJECTIVE: To analysis the causes, management and prevention of complications following gynecological laparoscopic surgery. METHOD: We analysed retrospectively the clinical data of 22 cases with complications following laparoscopic surgery performed from Sep 1992 to May 1994. RESULTS: The overall incidence of operative complications was 6.29% (22/350). Among them, 9 cases (including pneumoderma 6 and pneumo-omentum 3) were related to inappropriate CO2 insufflation. The other 10 cases were associated with bleeding, i.e. vessel injury 4 cases, hypodermal ecohymosis 5, and bleeding from the sutured site 1. The remaining 3 were omental or intestinal hernia of the incisional sites. One out of the 22 cases were turned to laparotomy. The outcomes of this group were all good. CONCLUSIONS: The occurrence of these complications was related to the doctors experiences and skills. Therefore, well-training and practice should be emphasized in order to avoid these complications.

Adolescent↗

Effect of verapamil on Ca2+ influx and CVB3-RNA replication in cultured neonatal rat heart cells infected with CVB3.

The effect of verapamil on Ca2+ influx across the myocardial plasma membrane and coxsackie virus B3 (CVB3) -RNA replication in cultured neonatal rat heart cells infected with CVB3 was investigated. It was found that the Ca2+ influx could be inhibited significantly (P < 0.01) by verapamil (1 mumol/L) after infection of heart cells for 48 h. However, when the cultured heart cells infected with CVB3 and treated with verapamil (1 mumol/L and 10 nmol/L) at the same time for 48 h, the amounts of CVB3-RNA in myocytes were significantly higher than that in infected control group (P < 0.05). These phenomena suggest that the increase of Ca2+ influx of cultured heart cells infected with CVB3 could be inhibited by some calcium antagonists, e.g. verapamil at the early stage. On the other hand, verapamil might accelerate viral replication in myocardium. Thus, although verapamil could be beneficial for decreasing the secondary Ca2+ damages and improve the myocardial electric activity, it isn't a sensible choice for therapy in early stage of virus infection with cardiac symptoms.

Animals↗

Cloning and expression of a second photoreceptor-specific membrane retina guanylyl cyclase (RetGC), RetGC-2.

One of the membrane guanylyl cyclases (GCs), RetGC, is expressed predominantly in photoreceptors. No extracellular ligand has been described for RetGC, but it is sensitive to activation by a soluble 24-kDa protein (p24) and is inhibited by Ca2+. This enzyme is, therefore, thought to play a role in resynthesizing cGMP for photoreceptor recovery or adaptation. By screening a human retinal cDNA library at low stringency with the cytoplasmic domains from four cyclases, we cloned cDNAs encoding a membrane CG that is most closely related to RetGC. We have named this GC RetGC-2, and now term the initially described RetGC RetGC-1. By in situ hybridization, mRNA encoding RetGC-2 is found only in the outer nuclear layer and inner segments of photoreceptor cells. By using synthetic peptide antiserum specific for each RetGC subtype, RetGC-2 can be distinguished from RetGC-1 as a slightly smaller protein in immunoblots of bovine rod outer segments. Membrane GC activity of recombinant RetGC-2 expressed in human embryonic kidney 293 cells is stimulated by the activator p24 and is inhibited by Ca2+ with an EC50 value of 50-100 nM. Our data reveal a previously unappreciated diversity of photoreceptor GCs.

Amino Acid Sequence↗

Involvement of serotonin in developmental plasticity of kitten visual cortex.

During a critical period of postnatal development, neuronal connections in the kitten visual cortex are susceptible to experience-dependent modifications. These modifications are facilitated by the neuromodulators noradrenaline and acetylcholine. To address the question of whether serotonin (5-hydroxytryptamine; 5-HT), the other major neuromodulator in the cerebral cortex, also plays a role in developmental plasticity, we investigated whether interference with serotoninergic transmission in the kitten visual cortex affects ocular dominance (OD) plasticity. The serotonin neurotoxin 5,7-dihydroxytryptamine or the serotonin receptor blockers ketanserin and methysergide were infused into the visual cortex of kittens undergoing monocular deprivation. We found that both methods of disrupting serotoninergic transmission reduced OD plasticity. However, to be effective, the receptor blockers ketanserin and methysergide had to be applied in combination, suggesting that coactivation of serotonin receptor subtypes of both the 5-HT1 and 5-HT2 families have a permissive function in OD plasticity. Since activation of 5-HT2 receptors stimulates phosphoinositide hydrolysis, our data suggest that second messengers from the phospholipid pathway may play an important role in developmental plasticity of visual cortex.

5,7-Dihydroxytryptamine↗

Molecular cloning of a ligand for the EPH-related receptor protein-tyrosine kinase Htk.

Htk is a receptor protein-tyrosine kinase that is related to the EPH subfamily of tyrosine kinases. The receptor has a wide tissue distribution including expression in several myeloid hematopoietic cell lines. Using an Htk-Fc fusion protein, a protein ligand for this receptor was expression cloned from the murine kidney mesangial cell line SV40MES 13. The Htk ligand cDNA encodes a transmembrane protein of 336 amino acids. Binding competition experiments demonstrated a Kd of 535 pM for binding of Htk-Fc to the Htk ligand. Incubation of 3T3 cells expressing Htk with COS-7 cells expressing the ligand resulted in tyrosine phosphorylation of Htk. The ligand, like its receptor, is widely expressed and may function in a variety of tissues. However, we localized hematopoietic expression of Htk to the monocytic lineage, suggesting that the ligand may play a role in differentiation and/or proliferation of these cells.

3T3 Cells↗

Race-ethnicity and determinants of intracranial atherosclerotic cerebral infarction. The Northern Manhattan Stroke Study.

BACKGROUND AND PURPOSE: The aim of this investigation was to determine the importance of race as a determinant of intracranial atherosclerotic stroke in a community-based stroke sample. METHODS: Residents from northern Manhattan over age 39 years hospitalized for acute ischemic stroke (n = 438, black 35%, Hispanic 46%, white 19%) were prospectively evaluated. Index ischemic strokes were classified as atherosclerotic (17%), lacunar (30%), cardioembolic (21%), cryptogenic (31%), and other (1%). Atherosclerotic infarcts were subdivided into extracranial (9%) and intracranial (8%) atherosclerosis. RESULTS: The proportion of extracranial atherosclerotic stroke was similar among the three race-ethnic groups, while intracranial atherosclerosis was more frequent in blacks and Hispanics. The unadjusted odds ratio for nonwhites (blacks and Hispanics combined) was 0.8 (confidence interval [CI], 0.4 to 1.8) for extracranial and 7.8 (CI, 1.04 to 57.7) for intracranial atherosclerosis. Patients with intracranial disease were significantly younger and had an increased frequency of hypercholesterolemia and insulin-dependent diabetes compared with those with nonatherosclerotic disease. The odds ratio for the association of nonwhite race-ethnicity and intracranial atherosclerosis was reduced to 5.2 (CI, 0.7 to 40) after controlling for age and to 4.4 (CI, 0.6 to 35) after controlling for age, education, insulin-dependent diabetes, and hypercholesterolemia. CONCLUSIONS: The greater prevalence of diabetes and hypercholesterolemia among blacks and Hispanics from northern Manhattan accounted for much of the increased frequency of intracranial atherosclerotic stroke. Further control of these risk factors could reduce the frequency of this stroke subtype and minimize the disparities among different race-ethnic groups.

Adult↗

[Hepatic artery chemotherapy-embolization and biological response modifiers for late hepatic carcinoma].

Since 1989, 63 cases of far-advanced cases of primary hepatic carcinoma were treated by alternating courses of hepatic artery infusion chemotherapy-embolization (HAIE) and biotherapy. For chemotherapy, mitomycin C, epiadriamycin (with lipiodol) and 5-Fu were used. Biotherapy consisted of systemic administration of gamma-interferon, interleukin 2 and transfer factor. Forty-four patients with late hepatic carcinoma were treated with HAIE alone, HAIE plus biotherapy resulted in more marked reduction in tumor size and serum AFP level as compared to that in the HAIE-treated patients. The 1- and 2-year survival rates of the two groups were 50.8% and 22% versus 40.9% and 6.8%, respectively.

Adult↗