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Biomedical subjects

H Xu

Publications and source records attributed to H Xu.

At least 739 records · Page 41Linked to original sources

[Analysis of 18 cases of postpartum haemorrhagic shock in pregnancy with virus hepatitis].

In this article, 147 pregnancies with virus hepatitis admitted to our hospital from Dec 1987 to Jun 1991 were studied. The incidences of postpartum haemorrhage and haemorrhagic shock were 36.05% and 12.24% respectively, and were related to the clinical classification of the hepatitis, with a difference of high significance (P less than 0.01). Analysis of the clinical manifestations and results of the blood tests in 18 cases of shock suggested that the main cause of shock was hepatitis resulting in injury of the liver and thus absence of clotting factors increasing postpartum haemorrhage. Therefore, emphases on antenatal care by keeping the women under the monitoring by obstetrician and physician together. Replenishing clotting factors, rectifying clotting defects; preventing acute hepatitis from proceeding to severe hepatitis and pregnancy-induced hypertension are keys to treat antenatal hepatitis. Close intrapartum care and shortening the duration of labor, especially the third stage, are important to reduce postpartum haemorrhagic and prevent occurrence of haemorrhagic shock.

Adult↗

[Plasmid analysis and antibiotic resistance pattern measurement of Shigella in Chengdu].

A total of 81 strains of Shigella isolated from sporadic cases and cases in an outbreak of Shigella sonnei infection was analysed by plasmid profiles and antibiotic resistance patterns. The strains had a high resistance patterns. The strains had a high resistance of ampicillin, tetracycline, trimethoprim-sulfamethoxazole and chloramphenicol; while 97.2% of the strains were susceptible to gentamicin, kanamycin. The results showed that 50% of the strains harbored plasmid patterns within each species, which indicated that many genetically different strains of Shigella were responsible for dysentery epidemics in Chengdu. According to the results of the plasmid analysis and antibiotic resistance pattern measurement made in the outbreak strains, it was clearly seen that most of the strains were similar or fundamentally similar, which suggested that one or two strains with genetical homology were the main causative agent for the outbreak. We think that plasmid profiles and antibiotic resistance patterns are applicable to the identification of the outbreak strains of dysentery as an efficient epidemiologic tool.

Ampicillin Resistance↗

[Isolation and identification of a strain of Pseudomonas SP. producing insoluble glucan hydrolase].

A strain, CIB871, isolated from the natural world can hydrolyze insoluble glucan(IG) produced by S. mutans. This organism has been identified to be a strain of Pseudomonas SP. It grows well at 30 degrees C. The optimum medium for producing insoluble glucan hydrolase (IGase) is composed of 0.3% peptone, 0.03% IG and M1 salt solution (NH4)2 SO4 1mg/ml, MgSO4 50 micrograms/ml, FeCl2 50 micrograms/ml, K2HPO4 0.5mg/ml). The IGase production reached maximum when cultured for 65-70 hours.

Glucans↗

[Improving the method of processing Polygonum cuspidatum Sieb. et Zucc. and Spatholobus suberectus Dunn].

This paper is concerned with a comparison of Polygonum cuspidatum with Spatholobus suberectus in cutting, drying time, products, chief compositions and aqueous extracts. The results showed that fresh cut was better than the customary cut, i. e. re-cut pieces, for the former could not only raise the quality specifications and contents of ingredients of the drinking tablets, but also avoid repeated labour, save energy for drying and eliminate waste of drug materials.

Anthraquinones↗

[A thin layer chromatography densitometric method for the determination of arecoline content in semen Arecae from different producing areas].

A TLC-densitometric method for the determination of arecoline in Semen Arecae (Areca catechu) was established, and arecoline content in three Semen Arecae (Imported, Hainan, Guanzhou) was determined. The method is accurate, sensitive and simple. The recovery is 102.39% and the coefficient of variation of six samplings is 1.95%. The are coline average content in the three Semen Arecae is 0.22%, 0.19%, 0.56% respectively.

Areca↗

Different G proteins mediate the opioid inhibition or enhancement of evoked [5-methionine]enkephalin release.

This laboratory has previously demonstrated that there is an opiate receptor-mediated, concentration-dependent modulation of the electrically stimulated release of enkephalin from the guinea pig myenteric plexus. Low doses of opioids (nanomolar) enhance release, whereas higher concentrations (10-100 nM) inhibit release. We now demonstrate that the in vivo i.p. administration of the islet-activating protein from pertussis toxin (PTX; 50 micrograms/500 g of body weight) markedly diminishes the potency of mu, delta, or kappa-selective opioids to inhibit the evoked release of enkephalin. In contrast, PTX is without effect on the enhancement of enkephalin release observed after treatment with nanomolar concentrations of the above opioids. Conversely, pretreatment with cholera toxin (CTX; 0.01 nM for 3 hr in vitro) has no effect on the mu, delta, or kappa opioid inhibition of evoked enkephalin release but abolishes the ability of nanomolar concentrations of these agonists to enhance stimulated enkephalin release. These data indicate that different classes of guanine nucleotide-binding proteins (G proteins) appear to mediate the opioid enhancement or inhibition of stimulated enkephalin release. Furthermore, they suggest that a PTX-sensitive G protein (Gi or Go) and a CTX-sensitive G protein (Gs) are integral components of the mechanism that mediates opioid inhibition and opioid enhancement, respectively, of evoked enkephalin release. To our knowledge, this report represents the first demonstration that Gs-coupled opiate receptors (in addition to those that are coupled to Gi) can modulate transmitter release.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Regulation of adhesion of ICAM-1 by the cytoplasmic domain of LFA-1 integrin beta subunit.

Interactions between cytotoxic lymphocytes and their targets require the T cell antigen receptor (TCR) and the integrin lymphocyte function-associated molecule-1 (LFA-1, CD11a/CD18). LFA-1 is not constitutively avid for its counter-receptors, intercellular adhesion molecules (ICAMs)-1 and -2. Cross-linking of the TCR transiently converts LFA-1 to a high avidity state and thus provides a mechanism for regulating cellular adhesion and de-adhesion in an antigen-specific manner. Truncation of the cytoplasmic domain of the beta, but not the alpha, subunit of LFA-1 eliminated binding to ICAM-1 and sensitivity to phorbol esters. Thus, LFA-1 binding to ICAM-1 was found to be regulated by the cytoplasmic domain of the beta subunit of LFA-1.

Amino Acid Sequence↗

Identification of cis and trans-elements involved in the timed control of a Caulobacter flagellar gene.

The genes encoding the structural components of the Caulobacter crescentus flagellum are temporally controlled and their order of expression reflects the sequence of assembly. Transcription of the operon containing the structural gene for the flagellar hook protein occurs at a defined time in the cell cycle, and information necessary for transcription is contained within a region between -81 and -120 base-pairs from the transcription start site. To identify the sequence elements that contribute to the temporal control of hook operon transcription, we constructed deletions and base changes in the 5' region and fused the mutagenized regulatory region to transcription reporter genes. We demonstrate that sequences 3' to the transcription start site do not contribute to temporal control. We confirm that upstream sequences between -81 and -120 base-pairs are necessary for temporal activation, and that transcription also requires sequences at -26 to -46 base-pairs. A specific binding activity for the region between -81 and -122 base-pairs was shown to be temporally controlled, appearing prior to the activation of hook operon transcription. This binding activity was missing from strains containing mutations in flaO and flaW, two genes near the top of the flagellar hierarchy known to be required for hook operon transcription. Thus, the hook operon upstream region contains a sequence element that responds to a temporally controlled trans-acting factor(s), and in concert with a second sequence element causes the timed activation of transcription.

Bacterial Proteins↗

Preliminary ligand binding data for subtypes of the delta opioid receptor in rat brain membranes.

Delta opioid binding sites were assayed using [3H][D-ala2,D-leu5]enkephalin and rat brain membranes depleted of mu binding sites with the site-directed acylating agent, 2-(p-ethoxybenzyl)-1-diethylaminoethyl-5-isothiocyanatobenzimid a zole-HCI. [D-Pen2,D-Pen5]enkephalin (DPDPE), [D-Pen2,L-Pen5]enkephalin, [D-Ala2]deltorphin-I and [D-Ala2]deltorphin-II inhibition curves were characterized by slope factors (Hill coefficients) less than 1. The low slope factor of DPDPE persisted in the presence of 50 microM 5'-guanylyimidodiphosphate in the assay Quantitative analysis of [D-ala2,D-leu5]enkephalin, DPDPE and [D-Ala2]deltorphin-I binding surfaces resolved two binding sites. Whereas [D-ala2,D-leu5]enkephalin had equal affinity for both sites, DPDPE and [D-Ala2]deltorphin-I had high affinity for the high capacity binding site, and low affinity for the low capacity binding site. These data support pharmacological studies demonstrating delta receptor subtypes which mediate antinociception.

Amino Acid Sequence↗

RTI-4614-4: an analog of (+)-cis-3-methylfentanyl with a 27,000-fold binding selectivity for mu versus delta opioid binding sites.

The objective of this study was to determine the binding affinities of (+/-)-cis-N-[1-(2-hydroxy-2-phenylethyl)-3-methyl-4-piperidyl]- N-phenylpropanamide-HCI (RTI-4614-4), which is an analog of (+)-cis-3-methylfentanyl for opioid receptor subtypes. The Ki values (nM) of this agent for opioid receptor subtypes were as follows: mu (0.0055), delta (148), kappa 1 (84.8), kappa 2a (2275), and kappa 2b (22.3). The selectivity of this agent for the mu binding site was 27,000 vs. the delta binding site, 15,400 vs. the kappa 1 binding site, 413,700 vs the kappa 2a and 4,054 vs the kappa 2b binding site. In contrast, two other fentanyl analogs, N-(2-(4-methylpyridinyl))-N-(1-phenethyl-4-piperidinyl) 2-furamide and N-(2-pyrazinyl)-N-(1-phenethyl-4-piperdinyl)2-furamide had considerably higher Ki values at, and were less selective for, the mu binding site. Since RTI-4614-4 is composed of a mixture of four stereoisomers, the resolution of these isomers should permit identification of an extremely potent and selective agent for the opioid mu receptor.

Animals↗

(+)-cis-3-methylfentanyl and its analogs bind pseudoirreversibly to the mu opioid binding site: evidence for pseudoallosteric modulation.

Previous studies demonstrated that preincubation of membranes from the brain of the rat with 1 microM (+)-cis-3-methylfentanyl produced a wash-resistant inhibition of mu receptor binding. The present study was designed to: (1) determine the mechanism by which (+)-cis-3-methylfentanyl produced a wash-resistant inhibition of mu receptor binding, and (2) to generate a structure-activity study, using wash-resistant inhibition as the end-point. Pretreatment of membranes with 500 nM (+)-cis-3-methylfentanyl increased the Kd of binding sites for [3H]ohmefentanyl, without altering the Bmax. The increase in the Kd was only partially due to the presence of residual drug and was accompanied by an increase in the dissociation rate of the binding of [3H]ohmefentanyl. Therefore, pretreatment of membranes with (+)-cis-3-methylfentanyl resulted in a lower affinity interaction of [3H]ohmefentanyl with the mu binding site, consistent with a model postulating pseudoallosteric modulation of mu binding sites by (+)-cis-3-methylfentanyl and its analogs. The rank order of potencies for wash-resistant inhibition of the binding of [3H]6 beta-fluoro-6-desoxyoxymorphone or [3H]ohmefentanyl, was lofentanil greater than (+)-cis-3-methylfentanyl greater than ohmefentanyl greater than sufentanil. All other opioids tested (1 microM morphine, 1 microM naloxone, 1 microM fentanyl, 1 microM (+)-cyclazocine, 1 microM (-)-cis-3-methylfentanyl) did not act as wash-resistant inhibitors of mu binding sites. Although the pseudoirreversible IC50 of these agents did not correlate with their ED50 values for producing antinociception, after intravenous administration, the authors speculate that this property, termed "pseudoirreversible inhibition", might contribute to the extraordinary potency of (+)-cis-3-methylfentanyl and its analogs as antinociceptive agents.

Allosteric Regulation↗

IL-4 decreases the expression of the monocyte differentiation marker CD14, paralleled by an increasing accessory potency.

IL-4 has been found to affect the phenotype and a variety of functions of human monocytes and macrophages and has been discussed as a monocyte activating protein along with other cytokines, such as IL-1 and IL-6. In this study we compared the effects of the cytokines IL-1, IL-6, IL-4, and a combination of IL-1 and IL-6 on the expression of the CD14 antigen, the FcIIIg receptor molecule CD16 and the MHC-class II molecules HLA-DR and HLA-DP. These molecules represent characteristic monocyte surface markers. Furthermore, the CD14 molecule has been described as a surface antigen of high in vivo relevance representing an indirect receptor for LPS. We further analyzed the effect of IL-4 on monocytes and macrophages with respect to their accessory function to initiate T-lymphocyte proliferation. Human peripheral blood monocytes strongly express the antigen CD14 and maintain it as a stable surface molecule during their differentiation to macrophages. Flow cytometry analysis of cultured monocytes demonstrated that cells incubated in the presence of IL-4, but not IL-1 and/or IL-6 revealed a reduced expression of the CD14 antigen in a dose- and time-dependent manner. After 3 days IL-4 treated cells were virtually CD14-negative. At the same time the expression of the CD16 antigen (FcRIIIg) was also strongly reduced, whereas the treatment with IL-4 led to an increased expression of MHC class II antigens such as HLA-DR and HLA-DP. The spontaneous low expression of HLA-DQ antigen on monocytes was not affected by any of the cytokines. Functionally, IL-4 treated CD14-negative monocytes exhibited a more than 2-fold higher activity to stimulate an accessory cell-dependent T cell proliferation. This was found in a mitogenic assay and in MLC when compared to monocytes cultured in the absence of IL-4. These observations provide further evidence that IL-4 is a major modulator of monocyte surface antigen expression. Moreover, IL-4 has an enhancer-effect on monocytes as accessory cells and therefore may be of considerable importance as a regulatory factor during monocyte development to accessory cells. Inasmuch as the CD14 molecule functions as a receptor for LPS-binding protein, our results suggest that IL-4 might also play an important regulatory role in processes initiated by bacterial lipopolysaccharides during inflammation and sepsis.

Antigen-Presenting Cells↗

Bilateral visual loss after severe burns in a child.

A girl who sustained severe burns was admitted to the hospital 16 h postburn. The patient developed sudden visual loss on day 15 postburn. She responded to treatment with significant return of visual acuity by 5 weeks after injury at the time of discharge from hospital.

Blindness↗

Isolation and developmental expression of Bcp1, an anther-specific cDNA clone in Brassica campestris.

Differential screening of a mature Brassica campestris pollen cDNA library has identified five cDNA clones that represent transcripts expressed exclusively, or at elevated levels, in pollen. We show here that the expression of one of these, clone Bcp1, is tissue specific and temporally regulated. The gene is activated during microspore development, as detected by in situ hybridization. Expression is enhanced at the time of pollen maturation and during pollen germination. In situ hybridization has also shown that Bcp 1 is activated in the tapetal cells in early anther development and continues to be expressed until tapetal dissolution. Homologous transcripts are present in pollen of other taxa of Brassicaceae including Arabidopsis, but not in pollen of any other families tested.

Amino Acid Sequence↗

Inhibition of Ty1 transposition by mating pheromones in Saccharomyces cerevisiae.

The Ty1 elements in the yeast Saccharomyces cerevisiae are a family of retrotransposons which transpose via a process similar to that of retroviral replication. We report here that the Ty1 transposition process can be blocked posttranscriptionally by treatment of cells with mating pheromones. When haploid yeast cells are treated with appropriate mating pheromones, the transposition frequency of a marked Ty1 element driven by the GAL1 promoter is greatly diminished. Ty1 viruslike particles (VLPs), the putative intermediates for transposition, can be isolated from mating pheromone-treated cells. These VLPs accumulate to normal levels but are aberrant in that they produce very few reverse transcripts of Ty1 RNA both in vivo and in vitro and contain subnormal amounts of p90-TYB and related proteins. In addition, a TYA phosphoprotein product accumulates in treated cells, and some species of TYB proteins have decreased stability. We also show that decreased transposition in mating pheromone-treated cells is not a consequence of simply blocking cell division, since Ty1 transposes at a nearly normal rate in yeast cells arrested in G2 by the drug nocodazole.

DNA Transposable Elements↗

Differentiation of human monocytes into CD14 negative accessory cells: do dendritic cells derive from the monocytic lineage?

Human peripheral-blood monocytes, when cultured in the absence of serum, are prevented to differentiate to macrophages (M phi). Instead, they develop into accessory cells which by various properties resemble dendritic cells. Signals that control development either into M phi or monocyte-derived accessory cells (m-AC) have been investigated by us. By applying such triggers, m-AC phenotypes and functions approached those known from lymphoid dendritic cells. Only the monocyte marker CD14, which is absent from dendritic cells, remained positive on m-AC as a last indicator of the monocytic origin of the cells. We now report that this most stable marker of the monocyte/M phi lineage can completely be down-regulated by combining tissue culture techniques with the inductive property of interleukin-4. Evidence has also been obtained by us that the conversion of monocytes into both m-AC and M phi represents a true differentiation, as demonstrated by the expression of the nuclear marker lamin A/C.

Antigen-Presenting Cells↗