Biomedical subjects

X M Yang

Publications and source records attributed to X M Yang.

At least 91 records · Page 5Linked to original sources

PubMed1990

The involvement of central noradrenergic systems and corticotropin-releasing factor in defensive-withdrawal behavior in rats.

The role of the central noradrenergic systems and corticotropin-releasing factor (CRF) in modulating defensive withdrawal behavior was studied in rats. The apparatus consisted of a small chamber set on one side of a one-meter open field, into which the rat was placed to start the test. When rats were unfamiliar with the apparatus, they displayed species typical defensive withdrawal behavior with long latencies to emerge from and a high proportion of time spent in the small chamber. Intraperitoneal administration of clonidine (0.03 mg/kg), l-propranolol (2.5 micrograms/kg), prazosin (0.1 mg/kg) or chlordiazepoxide (CDP, 5 mg/kg) each significantly decreased the latency to emerge from and the mean time spent in the small chamber (MTIC) and increased the number of chamber entries. When rats were familiar with the apparatus, prior restraint for 20 min significantly increased the latency and MTIC, and decreased the number of chamber entries and rears, but did not alter locomotor activity. Prazosin, clonidine, CDP, l-propranolol and the CRF-antagonist, alpha-helical CRF9-41 (25 micrograms i.c.v.), reversed the restraint-induced increase in the latency and MTIC. CRF (10-100 ng i.c.v.) dose-dependently induced defensive withdrawal behavior in rats familiar with the apparatus; the minimum statistically significant dose was 50 ng. dl-Propranolol (5 mg/kg) and CDP blocked the CRF-induced changes in the latency to emerge and the MTIC; whereas clonidine and prazosin significantly reduced the latency, but had no statistically significant effects on the MTIC. Phenylephrine (25-200 ng i.c.v.) dose-dependently induced defensive withdrawal behavior. This effect of phenylephrine (200 ng) was significantly antagonized by prazosin or alpha-helical CRF9-41 (25 or 50 mg i.c.v.), but not by CDP. Our results suggest that the hyperactivity of the central noradrenergic systems caused by exposure to the novel environment may stimulate the release of CRF, which through some unknown mechanism induces defensive withdrawal behavior in rats. Activation of beta adrenergic receptors may also induce defensive withdrawal.

Animals↗

PubMed1990

Vacuole sign and nodule sign in early peripheral bronchogenic carcinoma. Diagnostic value and pathologic correlation.

We analyzed the radiological and pathological characteristics of 30 peripheral lung masses 1.5-3 cm in diameter. We describe the vacuole and the nodule sign. Retrospective examination of 100 conventional tomograms of peripheral pulmonary masses and comparison with the histological diagnoses allowed us to determine the usefulness of these two signs in differentiating small peripheral bronchogenic carcinomas from tuberculomas.

Adenocarcinoma↗

PubMed1989

Evolutionary expression of the neuronal form of the src protein in the brain.

The protooncogene src encodes two proteins, designated pp60c-src+ and pp60c-src.pp60c-src+ is expressed only in neurons, whereas pp60c-src is expressed in neuronal and nonneuronal cells. pp60c-src+ differs from pp60c-src in that it contains an insert of 6 amino acids. To study the evolutionary conservation of the 6-amino acid insert, the expression of pp60c-src+ in the brain of animals from different classes was assayed by using pp60c-src+-specific antibodies raised against a synthetic peptide corresponding to the insert. pp60c-src+ was detected only in the brain of mammals, birds, and reptiles, but not amphibians and fish, whereas pp60c-src was present in the brain of all animals tested, including lobster (invertebrate). These findings indicate that pp60c-src+ may play a role in events associated with higher brain function, such as neuronal plasticity.

Amino Acid Sequence↗

PubMed1989

Behavioral evidence for the role of noradrenaline in the putative anxiogenic actions of the inverse benzodiazepine receptor agonist methyl-4-ethyl-6,7-dimethoxy-beta-carboline-3-carboxylate.

The role of noradrenaline in the anxiogenic action of the inverse benzodiazepine receptor agonist methyl-4-ethyl-6,7-dimethoxy-beta-carboline-3-carboxylate (DMCM) was assessed in a drug discrimination procedure using yohimbine as the stimulus cue and a conflict procedure using a conditioned behavioral suppression paradigm in rats. The yohimbine cue was antagonized by clonidine (0.03-0.5 mg/kg) and diazepam (0.1-10.0 mg/kg). DMCM (0.1-0.7 mg/kg) only partially substituted for the yohimbine stimulus cue. However, DMCM, in a smaller dose (0.1 mg/kg), significantly shifted the dose-effect curve of the yohimbine cue to the left. This potentiating effect of DMCM on the yohimbine cue was antagonized by Ro 15-1788, a benzodiazepine receptor antagonist, and by the type I benzodiazepine receptor agonist CL218,872. In the conditioned behavioral suppression paradigm, both clonidine (0.03 mg/kg) and diazepam (3 mg/kg) had an anticonflict effect by increasing responses in the conditioned fear period, whereas DMCM (0.1, 0.5 mg/kg) decreased the responses of rats in the conditioned fear period. This proconflict effect of DMCM was antagonized by muscimol (0.5 mg/kg), a type A gamma-aminobutyric acid receptor agonist, Ro 15-1788 (3 mg/kg) and clonidine (0.01 mg/kg). Our results suggest that the depressive effect of DMCM on the function of the gamma-aminobutyric acid-benzodiazepine receptor complex may cause increased noradrenergic activity, which may, in turn, be one of the anxiogenic mechanisms in DMCM.

Animals↗

PubMed1989

[Effect of clonidine on the schedule-controlled performance action of two benzodiazepine receptor agonists].

Effect of clonidine, a presynaptic adrenoceptor agonist, on the schedule-controlled performance action of two benzodiazepine receptor agonists was assessed in rats in a fixed-ratio (FR6) procedure. Diazepam (0.03 approximately 1.0 mg/kg), an agonist of both type I and II benzodiazepine receptors, decreased the FR performance in a dose-dependent manner. Clonidine (10 micrograms/kg) significantly potentiated the action of diazepam when the dose of diazepam was increased to 0.1 mg/kg. However, clonidine did not show any potentiating effect on the mild depressive action of CL 218,872, a special agonist of type I benzodiazepine receptor until its dose was increased to 10 mg/kg. The Potentiating effect of clonidine on the depressive action of diazepam was significantly antagonized by yohimbine. Bicuculline (3.0 mg/kg) significantly antagonized the depressive action of diazepam (1.0 mg/kg). Our results suggest that the depressive action of benzodiazepines on the function of central noradrenaline system may be one of the benzodiazepine sedative mechanisms, which may be related to the type II benzodiazepine receptors.

Animals↗

PubMed1989

[Effects of diazepam on the rat open field behavior and high K+ induced release of monoamine neurotransmitters from brain slices].

Acute i. p injection of diazepam (3 mg/kg) significantly decreased the open field behaviors (locomotion and rearing) of rats. However, when diazepam (3 mg/kg) was given ip daily for 15 consecutive days, no depressive effect on the open field behaviors was observed. After the open field observation, rats were immediately decapitated and brain slices of cortex, hippocampus, amygdala and brain stem were stimulated by high K+ (65 mmol/L) to cause the release of noradrenaline (NA), dopamine (DA) and serotonin (5-HT). Diazepam (9 mumol/Ls) significantly depressed the release of monoamine neurotransmitters caused by high K+, which were antagonized by Ro 15-1788 (5 mumol/L) in vitro. Acute administration of diazepam (ip 3 mg/kg) also significantly depressed the release of monoamine neurotransmitters caused by high K+ from all regions observed. However, hippocampus showed tolerance to the depressive effects of diazepam on the releases of NA and DA, and amygdala only on the release of DA, caused by high K+, when given ip chronically (3 mg/kg, 15 d). Our results suggest that the depressive effect of benzodiazepines on the release caused by anxiogenic factors of catecholamine in the hippocampus, front cortex and amygdala regions may be one of the mechanisms of sedative and anxiolytic actions of benzodiazepines.

Animals↗

PubMed1989

[Use of double McAb sandwich ELISA to detect circulating antigen of Toxoplasma in infected rabbits].

This paper reports on the cumulative positive frequencies of circulating antigen (CAg) detected in the sera of rabbits infected with Toxoplasma by using double-McAb sandwich ELISA. The positive frequencies of rabbits with heavy and medium infection in the incubation period are 30.8% and 11.1%. Those with medium infection in acute, subacute and early chronic period are 86.1% and 76.7%, 43.3% and 32.0% with light infection. The positive rates of CAg in rabbits of medium and light infection rose progressively in acute period, but declined in subacute and early chronic period. Cross reaction with schistosomiasis and coccidiosis was all negative. This method of high specificity, sensitivity and duplication possesses certain value in the diagnosis of acute or active Toxoplasma infection and may be useful for the diagnosis in the early period.

Animals↗

PubMed1989

Antibodies detecting abnormalities of the retinoblastoma susceptibility gene product (pp110RB) in osteosarcomas and synovial sarcomas.

The retinoblastoma (RB) susceptibility gene is one member of a putative "cancer suppressor gene" family in which loss of gene function is associated with tumor formation. Using antibodies generated against a trypE-RB fusion protein, we previously identified a nuclear phosphoprotein, pp110RB, as the RB gene product. Here we describe three additional polyclonal antibodies that were generated to separate epitopes of pp110RB with three synthetic peptides deduced from the RB cDNA sequence. All four antibodies could specifically recognize the same phosphoprotein in human cells. This protein was phosphorylated on serine and threonine, but not tyrosine, residues. RB homologous proteins with molecular masses of 105-128 kD were detected in other vertebrates, such as monkey, rodent, and chicken, by at least two antibodies, indicating evolutionary conservation of the RB gene. These antibodies were specific and sensitive for monitoring RB gene inactivation as demonstrated by screening several osteosarcoma and synovial sarcoma cell lines. Of nine cell lines examined, three expressed no immunoprecipitable normal RB protein. DNA rearrangement and abnormal RB mRNA were detected in two of these three cell lines, whereas RB protein was absent from one synovial sarcoma cell line in which normal-sized RB mRNA was clearly present. Therefore, direct immunoprecipitation of RB protein can reveal RB gene mutations that are undetectable by DNA and mRNA analysis. These results further support a crucial role for the RB gene in the oncogenesis of some mesenchymal tumors.

Amino Acid Sequence↗

PubMed1989

[Studies on hyperglycophilic yeast causing gaseous fermentation of sweetened condensed milk].

This report studied on a hyperglycophilic yeast isolated from sweetened condensed milk in Shandong province. It can fermented glucose, sucrose and raffinose; and can assimilate glucose, sucrose and raffinose as its sole carbon source. According to the morphology, physiology and habitat, it was identified to be Candida lactiscondensi (Hammer) Meyer et Yarrow, one of the synonym is Torulopsis lactiscondensi (Hammer) Lodder et Kreger-van Rij (1952). Detailed description was given in this report.

Animals↗

PubMed1988

Behavioral evidence for the role of noradrenaline in putative anxiolytic and sedative effects of benzodiazepines.

The effects of clonidine on the antianxiety and sedation of benzodiazepines (BZD) were assessed respectively in rats trained in a two-lever diazepam cue discrimination procedure and in single-lever fixed-ratio (FR) water-reinforced performance. Clonidine (10-60 micrograms/kg) significantly shifted to the left the dose-effect curves of diazepam in the discrimination paradigm. This treatment also shifted generalization dose-effect curves of the diazepam cue to chlordiazepoxide and CL 218,872 to the left in the drug discrimination procedure. The diazepam cue was antagonized in a dose-related manner by Ro 15-1788, but not by bicuculline. Clonidine also potentiated the rate-decreasing effects of diazepam on the FR schedule when the dose of diazepam was increased to 0.3 mg/kg, but not the milder rate-decreasing effect of CL 218,872 until the dose of CL 218,872 was increased to 10 mg/kg. The potentiating effects of clonidine on the stimulus control and depression of diazepam were antagonized by yohimbine. Yohimbine (1.0 mg/kg) also significantly shifted the dose-effect curve of diazepam cue to the right. Bicuculline (3 mg/kg) completely antagonized the rate-decreasing effect of diazepam (1 mg/kg), but significantly potentiated the rate-suppressant effect of clonidine (10 micrograms/kg). These results suggest that the central noradrenaline (NA) system may be involved not only in the antianxiety, but also the sadative action of BZD. The nature of NA involvement in relation to the different subtypes of BZD receptors requires further exploration.

Animals↗

PubMed1988

Methylenetetrahydrofolate dehydrogenases in normal and transformed mammalian cells.

Transformed mammalian cells express both the usual NADP-dependent trifunctional methylenetetrahydrofolate dehydrogenase-cyclohydrolase-synthetase as well as the bifunctional NAD-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase. Antisera to these proteins do not crossreact, and Western blots of cell extracts indicate that there is no inactive form of the NAD-dependent enzyme in normal tissues. Immunofluorescence studies suggest a cytosolic location for the NAD-dependent enzyme, although sequence homology seen in the N-terminal 10 residues indicates a closer relationship with the mitochondrial form of the yeast NADP dependent trifunctional enzyme.

Aminohydrolases↗

PubMed1988

Specific kinase activity and phosphorylation state of pp60c-src from neuroblastomas and fibroblasts.

Several tumor lines of neuronal origin were assayed for the presence of two forms of pp60c-src, designated pp60 and pp60+. To determine the specific kinase activity of pp60 and pp60+, an enzymatic analysis was carried out with neuroblastoma LA-N-5, containing a high level of pp60+, neuroblastoma SK-N-SH, containing a low level of pp60+, fibroblast FSD, containing pp60 but no pp60+, and Rous sarcoma virus transformed 3T3 cells, SR-3T3, containing pp60v-src. Km values for Mg2+-ATP of approximately 21, 8, 17 and 13 microM were determined for pp60src kinase from LA-N-5, SK-N-SH, FSD and SR-3T3 respectively, using enolase as a substrate. The Vmax values for pp60c-src kinase from LA-N-5, SK-N-SH and FSD were similar. The Vmax value of pp60v-src was about 50-fold higher. Thirteen distinct phosphopeptides were found in tryptic digests from pp60 and pp60+ labeled in vivo with [32P]. The presence of one phosphopeptide, derived from the N-terminus, correlated with the level of pp60+ in neuroblastoma cells, but a small amount of this peptide was also detected in fibroblasts. Only phosphoserine was detected in the N-terminus of pp60 and pp60+. Our data strongly suggest that the six extra amino acids, present in pp60+ but not in pp60, do not significantly alter the specific kinase activity of pp60+, but might influence its phosphorylation state.

Animals↗

PubMed1988