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B Zhang

Publications and source records attributed to B Zhang.

At least 577 records · Page 32Linked to original sources
PubMed1994

Multiple receptors mediate the modulatory effects of serotonergic neurons in a small neural network.

The gastropyloric receptor (GPR) cells are a set of cholinergic/serotonergic mechanosensory neurons that modulate the activity of neural networks in the crab stomatogastric ganglion (STG). Stimulation of these cells evokes a variety of slow modulatory responses in different STG neurons that are mimicked by exogenously applied serotonin (5-HT); these responses include tonic inhibition, tonic excitation and induction of rhythmic bursting. We used pharmacological agonists and antagonists to show that these three classes of modulatory response in the STG neurons are mediated by distinct 5-HT receptor subtypes. GPR stimulation or application of 5-HT or 2-me-5HT (a vertebrate 5-HT3 agonist) inhibited the pyloric constrictor (PY) neurons; these actions were selectively antagonized by gramine. GPR stimulation or application of 5-HT induced rhythmic bursting in the electrically coupled anterior burster (AB) and pyloric dilator (PD) neurons; these effects were antagonized by the 5-HT1c/2 antagonist cinanserin and by atropine at concentrations that do not block muscarinic cholinergic receptors in the crab STG. The 5-HT agonists 5-CT (5-HT1) and alpha-me-5HT (5-HT2) also induced AB/PD bursting, which was blocked by cinanserin, but not by atropine. GPR stimulation or application of 5-HT and 5-CT evoked tonic excitation of the lateral pyloric (LP) neuron. These effects were blocked by cinanserin. Several other 5-HT agonists and nearly all the vertebrate 5-HT antagonists we tested had little or no effect on the crab pyloric 5-HT receptors. These results provide further evidence that the modulatory sensory GPR neuron uses serotonin to evoke multiple modulatory responses via multiple 5-HT receptors. However, the 5-HT receptors in the crab STG neurons are not pharmacologically similar to vertebrate 5-HT receptors.

Animals↗
PubMed1994

[Voice rehabilitation with duck's bill silicone tube after laryngectomy].

The voice rehabilitation of 43 laryngectomized patients were performed with endoscopic tracheoesophageal fistulation for interposition of ducks bill silicone tube from 1986 to 1993. 12 cases were performed from 1986 to 1989. Voice rehabilitated in 7 cases (58.3%). 31 cases were performed from 1989 to 1993, of which 29 cases (93.3%) obtained voice successfully with criconphageal myotomy cricoid chondredomy and test of esophageal speech flowing during operation.

Aged↗
PubMed1994

[The uvulopalatopharyngoplasty operation for obstructive sleep apnea syndrome].

We performed uvulopalatopharyngoplasty operations on 216 patients and conducted 6-month to 2-year follow-ups. 40 patients have had polysomnograms before and after operations. The clinical results showed 50 percent markedly improved, 28 percent somewhat improved, and 22 percent unimproved. The total success rate was 78%. The surgical procedures and polysomnogram methods have been introduced, and the pathogenesis, diagnostic criteria and results were discussed.

Adult↗
PubMed1994

[Chromosome 15 satellite enlargement and hereditary deafness].

The clinical and cytologic examinations in 6 deaf patients from 2 genealogical trees with chromosomal 15 satellite enlargement, karyotype 46, XY(X), PS++(15) are reported. A proband as well as his brother and sister suffered from phenotype with gradual hearing loss at the age of 12 to 13 and big satellite 15 existed in chromatinic karyotype. His father's phenotype was normal, but karyotype was the same as the 3 siblings of the proband, which suggested that the abnormal chromosome may originate from the father. The proband as well as his mother and uncle from family tree 2 may all suffer from dysaudia in both ears without any cause and with rapid exacerbation of the disease and deafness at last, 1 to 2 years after birth. Based on the fact that they had similar clinical phenotype and karyotype, their delayed deaf-mutism may be related to the structural abnormality of chromosome 15. An examination of the proband's grandparents showed that both phenotype and karyotype were normal. The abnormal chromosome from the proband's mother and uncle may originate from a new mutation. Obviously, the proband's abnormal chromosome originates from the mother. It is estimated that such chromosomal structural abnormality may be caused by some hearing genetic effects.

Adult↗
PubMed1994

Transactivation of the peroxisome proliferator-activated receptor is differentially modulated by hepatocyte nuclear factor-4.

Peroxisome proliferator-activated receptors (PPARs) stimulate the expression of several genes involved in lipid metabolism by binding to specific cis-acting peroxisome proliferator-responsive elements (PPREs) via cooper-ativity with retinoid X receptors. We demonstrate here that hepatocyte nuclear factor-4 (HNF-4), another member of the nuclear hormone receptor superfamily, bound with differing affinities to the PPREs from the genes encoding rat acyl-CoA oxidase and hydratase-dehydrogenase, the first two enzymes of the peroxisomal beta-oxidation pathway. In cotransfection assays, HNF-4 repressed rat PPAR-dependent activation of a reporter gene linked to the acyl-CoA oxidase PPRE, either in the absence or presence of the peroxisome proliferator, Wy-14,643. Rat PPAR-dependent activation of a reporter gene linked to the hydratase-dehydrogenase PPRE was less efficiently repressed by HNF-4 in the absence of Wy-14,643 than was activation from the acyl-CoA oxidase PPRE. However, in the presence of Wy-14,643, HNF-4 functioned cooperatively with PPAR to significantly enhanced induction from the hydratase-dehydrogenase PPRE. These results suggest that the genes encoding the first two enzymes of the peroxisomal beta-oxidation pathway are subject to differential regulation by the interplay of multiple members of the steroid/nuclear hormone receptor superfamily, mitigated in part by the structures of the PPREs and by the presence of activators of PPARs.

Acyl-CoA Oxidase↗
PubMed1994

Chromatin and nucleosome organizations and DNA replication of nucleus reassembled in vitro using purified exogenous DNA and Xenopus egg extracts.

It has been demonstrated in the last ten years that the nuclear reassembly may occur in the cell-free systems from frog egg extracts added with exogenous naked DNA. However, there remains an open question: is the cell-free reassembled nucleus structurally similar to the nucleus in the intact cell? That is, does the cell-free reassembled nucleus contain nucleosomes and chromatin? For this issue, we have designed experiments for identifying the internal structures of the cell-free reassembled nucleus. These experiments show that the nucleus reassembled in vitro also contains chromatin which is composed of typical 10 nm nucleosome fibers of "beads-on-a-string", 30 nm filaments and the next higher-order structures. The digestion experiment with the enzyme micrococcal nuclease has demonstrated that the DNA in the nucleosome of the reconstituted chromatin is about 200 base pairs (bp) in length, of which 165 bp may be in the nucleosome particle, and 35 bp may be in the linker between two particles. Prolonging digestion of the 165-bp particle DNA fragment will yield a 146-bp fragment, which may be wounded in the nucleosome core. Experiments also provide evidence that the chromatin reconstitution in the cell-free reassembled nucleus is a progressive process, and that the nucleus can replicate its DNA. Based on these observations, we suppose that the chromatin of the cell-free reassembled nucleus may be structurally and functionally similar to the chromatin of the intact cells.

Animals↗
PubMed1994

[Gastric motility in patients with spleen-deficiency symptoms].

By using a method for synchronously-detecting gastric myoelectric activity and intraluminal pressure and a radioimmunoassay of plasmic motilin, gastric motility, plasmic level of motilin and their relationship in 12 normal individuals and in the patients with a variety of Spleen-Deficiency (SD) Syndromes, i.e. 12 SD with Cold type (H type), 7 SD with Stomach-Yin-Deficiency type(I type), 38 SD with Heat type (R type) and 6 SD with Liver-Qi-Stagnation type (U Type) were investigated. The results showed: degree of myoelectric dysrhythmia and rate of electro-mechanical decouple in all patients (except for I type) were much higher than those in the normals (P < 0.01 or P < 0.05); both mean frequency and amplitude of contraction in the patients were decreased; percentage of contractive action in the patients (except for I type) was lower than that in the normals (P < 0.05); plasmic level of motilin in the patients (except for I type) had a tendency to increase and had a linear correlation to degree of myoelectric dysrhythmia (r = 0.33, P < 0.01). It was suggested that some significant disorders of gastric motility exist in different SD patients and there might be an intrinsic cause effect relationship among increased plasmic motilin, myoelectric dysrhythmia and abnormal mechanical motion. The similar changes suggested that there is pathophysiological mechanism of SD syndrome. Furthermore, this synchronously-detecting method was useful to discover intrinsic relationship between gastric myoelectric activity and mechanical motion.

Adult↗
PubMed1994

[Fetal umbilical artery velocity waveforms to predict the outcome in high risk pregnancy and its correlation with placental pathology].

Pulsed-wave Doppler ultrasound was used to measure the umbilical artery flow velocity S/D ratio in 101 high risk pregnancies. S/D ratio represented the ratio of maximum systolic velocity (S) to minimum diastolic velocity (D), The result of performing the receiver operating curve demonstrated that the cut off point of 2.8 had the best predictive value with sensitivity 0.706, specificity 0.976, accuracy 0.92 and false positive value 0.024. The abnormal pregnancy outcomes of S/D > 2.8 were obviously higher than of S/D < 2.8 (P < 0.01). In order to investigate the correlation of S/D ratio and placental pathology, 29 pregnant women were divided into 3 groups: (1) 10 normal pregnancies with S/D < 2.8; (2) 9 high risk pregnancies with S/D < 2.8; (3) 10 high risk pregnancies with S/D > 2.8. The result of placental pathological examination showed that the mean number of small muscular arteries of the tertiary stem villi per 100 microscope low power field (LPF) was less in the high risk pregnancy with S/D > 2.8 group (2.15 +/- 0.16 than in the other two groups (4.84 +/- 1.6, 4.17 +/- 1.4, respectively) (P < 0.01). Our study suggested that the umbilical artery Doppler was a useful screening tool for identifying the abnormal outcomes in high risk pregnancies and its main placental pathological finding was the obliteration of small muscular arteries in the tertiary stem villi.

Blood Flow Velocity↗
PubMed1994

Selective coexpression of insulin receptor-related receptor (IRR) and TRK in NGF-sensitive neurons.

The insulin receptor-related receptor (IRR) has recently been identified as a member of the insulin receptor tyrosine kinase family; however, its endogenous ligand and biological function are still unknown. In contrast to the very widespread pattern of expression of the homologous insulin and IGF-I receptors, IRR demonstrates a very restricted cellular distribution. Using in situ hybridization and immunohistochemistry, we now show that the expression of this receptor is selectively concentrated in a subset of neurons where its appearance is closely associated with that of the NGF receptor TRK. IRR and TRK demonstrate synchronized patterns of coexpression in neural crest-derived sensory and sympathetic neurons and in non-neural crest basal forebrain and striatal neurons. Both appear early in the embryonic development of dorsal root and trigeminal neurons and somewhat later, near the time of birth, in sympathetic neurons. Expression of both IRR and TRK appears perinatally in basal forebrain neurons, reaching maximal levels about postnatal day 20. This association is highly selective, since TRK mRNA is not detected anywhere in the developing nervous system in the absence of coordinate IRR expression, and the same is true for IRR expression with respect to TRK. In the adult rat, the majority of TRK-positive sensory neurons still express IRR mRNA, and coexpression in sympathetic and forebrain neurons continues without evidence of diminution. These findings are consistent with a functional linkage of the IRR and TRK receptors in NGF-sensitive neurons.

Animals↗
PubMed1994

Stimulation of HIV replication in mononuclear phagocytes by leukemia inhibitory factor.

This study examined the effects of leukemia inhibitory factor (LIF) on human immunodeficiency virus (HIV) replication in mononuclear phagocytes (MNP). LIF induced a dose-dependent increase in p24 antigen production in the chronically infected promonocytic cell line U1. The magnitude and time kinetics of the LIF effects were similar to interleukin 1 (IL-1), IL-6, and tumor necrosis factor (TNF), other cytokines known to induce HIV replication in this cell line. To characterize mechanisms responsible for these LIF effects, levels of HIV mRNA, activation of the DNA binding protein nuclear factor (NF)-kB, signal transduction pathways, and potential interactions with other cytokines were analyzed. LIF increased steady-state levels of HIV mRNA at 2.0, 4.3, and 9.2 kB. This was detectable by 24 h and persisted until 72 h. The DNA binding protein NF-kB is a central mediator in cytokine activation of HIV transcription. NF-kB levels were higher in unstimulated U1 cells as compared to the parent cell line U937. In both cell lines LIF increased NF-kB activity. Induction of NF-kB and HIV replication by cytokines are at least in part dependent on reactive oxygen intermediates. The oxygen radical scavenger N-acetyl-L-cysteine, but not an inhibitor of nitric oxide synthase, inhibited LIF-induced HIV replication. LIF induces the production of other cytokines in monocytes but its effects on HIV replication were not inhibited by antibodies to IL-1, TNF, or IL-6. These results identify LIF as a stimulus of HIV replication.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcysteine↗
PubMed1993

Protein tyrosine kinase activation is required for lipopolysaccharide induction of cytokines in human blood monocytes.

Bacterial LPS induce production of cytokines such as IL-1, IL-6, and TNF in mononuclear phagocytes, and this represents a central component in the pathogenesis of septic shock syndrome. However, the mechanisms by which LPS activates these cells to express cytokines are not completely characterized. The present study addressed the role of different protein kinases in the LPS induction of cytokines. It is shown that LPS induced a 12- to 16-fold increase in IL-1 beta, IL-6, and TNF-alpha mRNA levels, and this was completely or more than 80% blocked by the protein tyrosine kinase specific inhibitors herbimycin A and genistein at the concentrations of 1.7 and 37 microM, respectively. Protein kinase C inhibition by staurosporine reduced LPS induction of TNF-alpha, whereas it had no effects on IL-6 and IL-1 beta. Inhibition of protein kinase A by H89 reduced IL-6 mRNA levels but did not detectably change IL-1 beta or TNF-alpha mRNA levels. In contrast, LPS did not increase leukemia inhibitory factor mRNA, which was constitutively expressed and not significantly reduced by these inhibitors. In addition to cytokine mRNA levels, LPS-induced IL-6 protein synthesis and IL-6 bioactivity were also reduced to baseline levels by the PTK inhibitors herbimycin A and genistein. Both PTK inhibitors also reduced the LPS activation of nuclear factor-kappa B (NF-kappa B), which is a transcription factor involved in the expression of cytokine genes such as IL-6 and TNF-alpha. The activation of NF-kappa B was also reduced by H89, whereas staurosporine had no effect on this response. In summary, these findings suggest that protein kinase C and protein kinase A appear to have selective effects in the LPS induction of cytokines, whereas PTK is required for LPS induction of a broad spectrum of cytokines and NF-kappa B activation in monocytes.

Base Sequence↗
PubMed1993

Chicken ovalbumin upstream promoter transcription factor (COUP-TF) binds to a peroxisome proliferator-responsive element and antagonizes peroxisome proliferator-mediated signaling.

Peroxisome proliferators form a family of diverse xenobiotic compounds that includes hypolipidemic agents, herbicides, and plasticizers. These compounds activate transcription of a subset of nuclear genes including those encoding peroxisomal fatty acid beta-oxidation enzymes, whose elevated activities can lead to hepatocarcinogenesis. Induction of the genes encoding fatty acyl-CoA oxidase and hydratase-dehydrogenase, the first and second enzymes of the pathway, is mediated by peroxisome proliferator-activated nuclear receptors (PPARs) that bind to upstream responsive elements (PPREs) through heterodimerization with retinoid X receptors. We demonstrate that the chicken ovalbumin upstream promoter transcription factor 1 (COUP-TF1), another member of the nuclear hormone receptor superfamily, binds to the hydratase-dehydrogenase PPRE in vitro and in vivo and antagonizes PPAR-dependent signaling. These data suggest that members of the COUP-TF family play a role in modulating receptor-mediated activation of peroxisome proliferator-responsive genes.

Animals↗
PubMed1993

Diverse peroxisome proliferator-activated receptors bind to the peroxisome proliferator-responsive elements of the rat hydratase/dehydrogenase and fatty acyl-CoA oxidase genes but differentially induce expression.

The ability of peroxisome proliferator-activated receptors (PPARs) to induce expression of a reporter gene linked to a peroxisome proliferator-responsive element (PPRE) from either the rat enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase gene or acyl-CoA oxidase [acyl-CoA:oxygen 2-oxidoreductase, EC 1.3.3.6] gene was examined by transient transfection assays in COS cells. Mouse and rat PPARs, as well as Xenopus PPAR alpha (xPPAR alpha) could induce expression of a reporter gene linked to the hydratase/dehydrogenase PPRE in the presence of the peroxisome proliferators ciprofibrate or Wy-14,643, whereas xPPAR beta and xPPAR gamma were ineffective. A similar induction of expression of a reporter gene linked to the acyl-CoA oxidase PPRE was observed with all PPARs except xPPAR beta. Extracts from cells transfected with PPAR-encoding genes contained factors that bound to both PPREs. In vitro synthesized PPARs could interact weakly with both PPREs; however, binding of each PPAR to both PPREs was significantly increased by the addition of COS cell nuclear extracts, demonstrating that efficient PPAR/DNA binding requires auxiliary cofactors. One cofactor was identified as the 9-cis-retinoic acid receptor, RXR alpha (retinoid X receptor alpha). Cooperative DNA binding and heteromerization between RXR alpha and each of the PPARs could be seen with both PPREs. Our results demonstrate that PPAR/PPRE binding and cooperativity with RXR alpha (and other cofactors) are obligatory but not necessarily sufficient for peroxisome proliferator-dependent transcription induction and that distinct PPREs can selectively mediate induction by particular PPARs.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1993

Characterization of protein-DNA interactions within the peroxisome proliferator-responsive element of the rat hydratase-dehydrogenase gene.

A peroxisome proliferator-responsive element is located in the 5'-flanking region of the gene encoding rat hydratase-dehydrogenase, the second enzyme of the peroxisomal beta-oxidation pathway. DNase I footprint analysis with nuclear extracts from proliferator-responsive rat H4IIEC3 cells revealed two protected regions within the 196-base pair peroxisome proliferator-responsive element. Both regions contained multiple copies of a motif related to the consensus steroid hormone receptor binding half-site TGACCT, suggesting that peroxisome proliferator-dependent activation of this gene is mediated via peroxisome proliferator-activated receptors. Region II contains three TGACCT-like motifs in a direct repeat array. An oligonucleotide corresponding to this region was sufficient to confer responsiveness to the peroxisome proliferator ciprofibrate onto a heterologous promoter, as determined by transient transfection assays. Gel retardation assays demonstrated that nuclear factors bound to the hydratase-dehydrogenase oligonucleotide. Mutation of a single G residue within the second repeat motif abolished factor binding and consequently the ability of the element to respond to ciprofibrate, directly demonstrating that factor binding is necessary for peroxisome proliferator responsiveness. These results are discussed in the context of our current understanding of the mechanism of the coordinated transcriptional induction of the genes encoding peroxisomal beta-oxidation enzymes by peroxisome proliferators.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1993

The M.AluI DNA-(cytosine C5)-methyltransferase has an unusually large, partially dispensable, variable region.

The DNA methyltransferase of the AluI restriction-modification system, from Arthrobacter luteus, converts cytosine to 5-methylcytosine in the sequence AGCT. The gene for this methyltransferase, aluIM, was cloned into Escherichia coli and sequenced. A 525-codon open reading frame was found, consistent with deletion evidence, and the deduced amino acid sequence revealed all ten conserved regions common to 5-methylcytosine methyltransferases. The aluIM sequence predicts a protein of M(r) 59.0k, in agreement with the observed M(r), making M.AluI the largest known methyltransferase from a type II restriction-modification system. M.AluI also contains the largest known variable region of any monospecific DNA methyltransferase, larger than that of most multispecific methyltransferases. In other DNA methyltransferases the variable region has been implicated as the sequence-specific target recognition domain. An in-frame deletion that removes a third of this putative target-recognition region leaves the Alu I methyltransferase still fully active.

Amino Acid Sequence↗
PubMed1993

Retinoic acid inhibits interleukin-1-induced cytokine synthesis in human monocytes.

Retinoids are pluripotent morphogens whose effects on gene expression are mediated through specific intracellular receptors. They have certain anti-inflammatory effects in vivo, the basis of which is not clearly understood. To characterize mechanisms involved with potential anti-inflammatory actions of retinoids, we studied the effects of retinoic acid (RA) on cytokine production in human peripheral blood monocytes. RA differentially modulated the expression of interleukin-1 beta (IL-1 beta), IL-6, and IL-8 mRNAs depending on the inducing stimulus. While phorbol myristate acetate-induced IL-1 beta and IL-8 mRNA expression was increased by RA (IL-6 could not be induced by this pathway in monocytes), IL-1 beta-induced expression of IL-1 beta and IL-8 was markedly reduced and IL-6 gene expression was almost completely suppressed. Lipopolysaccharide (LPS)-induced cytokine synthesis was only slightly reduced and this required a longer preincubation (> 72 h) of monocytes with RA. IL-1-induced de novo synthesis of IL-6 protein and secretion of biologically active IL-6 were also inhibited by RA. The inhibition pattern of RA was different from that of dexamethasone, which inhibited both IL-1 and LPS effects. In summary, our data show that RA regulates monocyte cytokine expression selectively in response to the particular stimuli. Inhibition of IL-1 beta-induced cytokine expression provides a mechanism that can explain some of the anti-inflammatory effects of RA.

Base Sequence↗
PubMed1993

Dextran's antithrombotic properties in small arteries are not altered by low-molecular-weight heparin or the fibrinolytic inhibitor tranexamic acid: an experimental study.

In two separate blind, randomized studies, 48 rabbits were divided into five groups. Three treated groups received dextran 70 (0.51 g/kg) as a single injection, dextran 70 combined with low molecular-weight heparin (LMWH) (560 IU/kg as anti-FXa and 140 IU/kg as APTT in 3 hr), and dextran 70 plus tranexamic acid (14 mg/kg) following severe arterial trauma (arteriotomy/intimectomy). Two control groups received the same amount of saline. The bleeding times from the arteriotomy were recorded, and patency rates and the weight of thrombotic materials were registered 2 hr after reperfusion of the trauma region. The bleeding times in three treated groups, all including dextran, were significantly prolonged compared to the control groups (P < 0.05 or 0.01). The patency rates of treated groups, which were 100% (18/18 vessels patent) in the dextran-treated group, 90% (18/20 vessels patent) in the dextran+LMWH group and 95% 19/20 vessels patent) in dextran+tranexamic acid group, were significantly higher than those of their control groups (55-67% patent vessels) (p < 0.05 or 0.01). The mean weights of thrombotic materials were significantly reduced in the treated groups compared to the corresponding control groups (p < 0.01). In conclusion, dextran 70 in an ordinary dose exerted such a profound antithrombotic effect (100% patency) in small traumatized arteries that the addition of a high dose of LMWH could not further improve patency rates or decrease thrombotic materials but did not prolong vessel bleeding times compared to the single dextran treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗