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H Xu

Publications and source records attributed to H Xu.

At least 721 records · Page 40Linked to original sources
PubMed1992

Isolation, characterization, and expression of mouse ICAM-2 complementary and genomic DNA.

Intercellular adhesion molecule-2 (ICAM-2), a cell surface glycoprotein, is a second counter-receptor for lymphocyte function-associated Ag-1 (LFA-1). We report here the isolation and characterization of the cDNA and the gene that encode murine ICAM-2 (Accession numbers X65493 and X65490, respectively). The deduced sequence of the cDNA has 60% amino acid identity with its human counterpart and has the same expression pattern in cells and tissues. Furthermore, COS cells transfected with mouse ICAM-2 complementary and genomic DNA bind to purified human LFA-1, demonstrating the conservation of the function of ICAM-2 as a ligand for LFA-1 and conservation across species of sequences that are critical for binding to human LFA-1. COS cells transfected with the ICAM-2 cDNA do not react with mAb PA3, previously suggested to define ICAM-2 in the mouse. The mouse ICAM-2 gene was isolated and its structural organization determined. The gene is present in a single copy in the mouse genome and contains four exons spanning about 5.0 kb of DNA. The exon/intron architecture correlates to the structural domains of the protein and resembles that of other Ig superfamily members. The gene for ICAM-2, which is constitutively expressed in endothelial cells, has several conserved sequence motifs in its promoter region, including a direct repeat, and lacks transcription factor-binding sites present in the ICAM-1 gene, which is inducible in endothelial cells.

Amino Acid Sequence↗
PubMed1992

Effect of side-chain amide thionation on turnover of beta-lactam substrates by beta-lactamases. Further evidence on the question of side-chain hydrogen-bonding in catalysis.

Two side-chain-thionated beta-lactams, a penicillin and a cephalosporin, have been prepared and found to be not significantly poorer as substrates of typical serine (classes A and C) beta-lactamases than are their oxo analogues. This result is interpreted to mean that any hydrogen-bonding site on these enzymes for the beta-lactam side-chain amide carbonyl group must be flexible and is more likely to be a passive rather than active or essential feature of the active site. Previously, data from crystal structures and site-directed mutagenesis had suggested that the side chain of Asn-132 of class-A beta-lactamases, a component of the conserved SDN loop, forms a hydrogen bond with the side-chain carbonyl of the beta-lactam substrate and may provide significant transition-state stabilization during catalysis. The thionocephalosporin was also equally as good as its oxo analogue as a substrate of the class-B beta-lactamase II of Bacillus cereus and not significantly less effective as an inhibitor of the Streptomyces R61 DD-peptidase; a tight hydrogen-bond donor site for the beta-lactam side-chain amide is apparently not present in these enzymes either.

Amides↗
PubMed1992

Dopamine transporter site-directed mutations differentially alter substrate transport and cocaine binding.

Polar amino acids lying within three hydrophobic regions of the dopamine transporter (DAT) are analogous to those important for ligand recognition by catecholamine receptors. Possible functional significance of these amino acids was examined by expressing DAT cDNAs mutated in these polar residues. Replacement of aspartate at position 79 with alanine, glycine, or glutamate dramatically reduced uptake of [3H]dopamine and the tritium-labeled Parkinsonism-inducing neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and reduced the mutants' affinity for the tritium-labeled cocaine analog (-)-2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane (CFT) without affecting Bmax. Replacement of the serine residues at positions 356 and 359 in the seventh hydrophobic region by alanine or glycine caused reductions in [3H]dopamine and [3H]MPP+ uptake, whereas [3H]CFT binding was less affected. Substitution of two serines in the eighth hydrophobic region yielded wild-type values for [3H]dopamine and [3H]MPP+ uptake and [3H]CFT binding. These results demonstrate that aspartate and serine residues lying within the first and seventh hydrophobic putative transmembrane regions are crucial for DAT function and provide identification of residues differentially important for cocaine binding and for dopamine uptake.

1-Methyl-4-phenylpyridinium↗
PubMed1992

CDC14 of Saccharomyces cerevisiae. Cloning, sequence analysis, and transcription during the cell cycle.

We have cloned, mapped and sequenced the complete CDC14 gene of Saccharomyces cerevisiae and characterized its transcription during the cell cycle. CDC14 was found within a 3.5-kilobase pair XhoI-XbaI fragment of chromosome VI. The DNA sequence reveals an open reading frame capable of encoding a 423-amino acid polypeptide. Protein sequence comparisons through the Prosite, GenBank and EMBL databases allowed us to identify a conserved protein tyrosine phosphatase active site in the encoded CDC14 protein beginning at amino acid 153. Disruption demonstrates that CDC14 is an essential gene. The level of the CDC14 transcript appears to be weakly cell cycle-regulated and has a periodicity which lags approximately 15 min behind histone HTB1 mRNA accumulation levels. DNA sequence analysis has identified a region within the CDC14 promoter which bears a striking resemblance (15 out of 21 base pairs identity) to the cell cycle regulation region of the promoter of the histone H2A1-H2B1 (HTA1-HTB1) gene pair. The cell cycle regulation sequence is responsible for the periodic accumulation and hydroxyurea sensitivity of the histone HTA1-HTB1 message. However, unlike histone mRNA, which is repressed upon hydroxyurea arrest, CDC14 mRNA appears to be unaffected. This suggests that CDC14 and histone genes are regulated by different mechanisms during the cell cycle. Furthermore, superhelical density measurements suggest that CDC14 is not involved in nucleosome assembly.

Amino Acid Sequence↗
PubMed1992

Opioid enhancement of evoked [Met5]enkephalin release requires activation of cholinergic receptors: possible involvement of intracellular calcium.

Previous work from this laboratory has shown that the electrically evoked release of enkephalin from the guinea pig myenteric plexus is regulated by an opiate receptor-mediated, concentration-dependent mechanism. Low concentrations (nanomolar) of opioids enhance release, whereas higher concentrations (10-100 nM) inhibit release. Each opioid effect is mediated by a different guanine nucleotide-binding protein. We now demonstrate that activation of cholinergic receptors in the myenteric plexus is a prerequisite for opioid excitatory effects, but not inhibitory effects, on enkephalin release. Pretreatment with the muscarinic cholinergic receptor antagonist atropine abolishes the opioid facilitation of stimulated enkephalin release but does not alter the inhibition of release that is observed with higher concentrations of opioid agonist. Exposure to the calcium ionophore A23187 overcomes the abolishment of opioid enhancement of enkephalin release produced by cholinergic receptor blockade. In tissue treated with both atropine and A23187, the magnitude of the opioid enhancement of release is indistinguishable from that observed in untreated preparations. This suggests that the lack of stimulation-induced generation of elevated cytosolic calcium is responsible for the abolishment of facilitory opioid effects when cholinergic receptors are blocked. The known coupling of muscarinic receptors to phospholipase C activation and the generation of inositol trisphosphate (which elevates cytosolic calcium) could suggest that this second messenger is critical for the manifestation of opioid facilitation of enkephalin release.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1992

Endogenous opioids accumulate in plasma in a rat model of acute cholestasis.

To obtain data on the degree to which the opioid system is changed in cholestasis, endogenous opioid activity in plasma of rats with acute cholestasis was determined 5 days after bile duct resection. Total plasma opioid activity was determined using a radioreceptor technique that measured the displacement of the opiate receptor ligand [3H]-DAMGO from lysed synaptosomal fractions of normal rat brain. Plasma total opioid activity was threefold greater in bile duct-resected rats than in sham-operated and unoperated controls (P less than or equal to 0.05). Plasma levels of the individual endogenous opioid, methionine-enkephalin, were determined using a sensitive radioimmunoassay, and the specificity of the assay was confirmed using high-performance liquid chromatography. In cholestatic rats, plasma methionine-enkephalin levels were more than six-fold greater than in sham-operated controls (P less than or equal to 0.001) and more than 17-fold greater than in unoperated controls (P less than or equal to 0.001). However, plasma methionine-enkephalin levels accounted for less than 5% of total plasma opioid activity after bile duct resection. Plasma methionine-enkephalin levels in both cholestatic plasma and plasma from sham-operated animals were stable when incubated in vitro despite the presence of undiminished activity of the major enkephalin-degrading enzymes. Thus, protection of methionine-enkephalin from degradation may be a factor contributing to the elevated plasma levels of methionine-enkephalin found in cholestasis. The magnitude of the increase in plasma endogenous opioid activity in bile duct-resected rats provides support for the hypothesis that endogenous opioids contribute to the pathophysiology of cholestasis.

Acute Disease↗
PubMed1992

Increase of plasma IL-6 concentration with age in healthy subjects.

The present study demonstrated that plasma IL-6 concentration was higher in older subjects than in younger ones and significantly in the male group (P = 0.02); Spearman rank correlation showed that plasma IL-6 concentration was positively correlated with age (r = 0.28, N = 55, P < 0.05); there was a highly significant correlation between the concentrations in plasma IL-6 and IL-1 alpha (r = 0.51, N = 52, P < 0.001). These findings suggest the possibility that age-related changes of plasma IL-6 and IL-1 alpha may provide a pathological basis for the susceptibility to such illness as commonly occurs in elderly people, especially Alzheimer's disease as the two interleukins can induce the production of alpha 1-antichymotrypsin and beta-amyloid protein precursor.

Adult↗
PubMed1992

Central mu-opioid receptors are down-regulated in a rat model of cholestasis.

Ameliorations of the pruritus of cholestasis by opioid antagonists are consistent with this form of pruritus being centrally mediated by the opioid system. To determine whether the central opioid system is altered in cholestasis, the specific binding of a selective mu-opioid receptor ligand, 3H-DAMGO, to mu-opioid receptors was studied in rats with acute cholestasis due to bile duct resection. Using whole brain membranes and subcellular mitochondrial-synaptosomal fractions the density of mu-receptor sites was 30% (p less than 0.01) and 22% (p = 0.03) less in bile-duct-resected rats than in sham-resected rats. Using membranes from individual brain regions specific binding of 3H-DAMGO was reduced by 43-53% in the cerebral cortex, hippocampus and caudate nucleus of bile-duct-resected rats. Thus mu-opioid receptors in the brain are down-regulated in a classical model of cholestasis. This alteration of the central opioid system could be a consequence of increased exposure of opioid receptors to endogenous opioids in cholestasis and may reflect an important mechanism in the pathogenesis of the pruritus of cholestasis.

Animals↗
PubMed1992

Increased survival rate in patients with massive burns.

A review of 113 patients with massive burns treated in our centre from 1970 to 1989 is presented. There were 57 adults patients with massive burns (> or = 50 per cent TBSA) in 1980-89 who were compared with 56 patients with similar massive burns in the period between 1970 and 1979. The results show a significant improvement (P < 0.01) in survival rate of the more recent patients. The increased survival rate is attributed to improvements in the early treatment of inhalation injury, sepsis and multiorgan failure.

Adolescent↗
PubMed1992

Human blood dendritic cells exhibit a distinct T-cell-stimulating mechanism and differentiation pattern.

In this study, the mechanisms underlying stimulation of T-cell proliferation by human blood dendritic cells (BDC) and their differentiation have been defined with a panel of monoclonal antibodies (MoAbs). It was found that the MoAbs against LFA-1 (CD11a), CD11c, LFA-3 (CD58), ICAM-1 (CD54) or HLA-DR could significantly suppress T-cell proliferation in an allogeneic mixed lymphocyte reaction (P < 0.05), while being unable to inhibit clustering of BDC with T cells. Addition of anti-CD18 or CD45 MoAbs increased the size of clusters after 18 h of culture, but had no effect on the proliferation of T cells (P < 0.05). The suppressive effect of the MoAbs may be viewed not as an inhibition of contact between BDC and T cells, but rather as a blocking of co-stimulatory signals for T-cell activation, which are mediated by interaction of the adhesion molecules. After depleting the BDC preparations of monocytes, we used a double staining in FACS analysis to demonstrate that BDC do not express specific T (CD3), B (CD20 and CD21) and myeloid cell markers (CD11b, CD13 and CD14), but abundant class II antigens. This pattern remained unaltered after 8 days of culture in the presence of 100 U/ml GM-CSF, although a threefold increase of HLA-DQ and ICAM-1 molecules on the cultured cells was observed.

Antibodies, Monoclonal↗
PubMed1992

Identification of a new set of cell cycle-regulatory genes that regulate S-phase transcription of histone genes in Saccharomyces cerevisiae.

Histone mRNA synthesis is tightly regulated to S phase of the yeast Saccharomyces cerevisiae cell cycle as a result of transcriptional and posttranscriptional controls. Moreover, histone gene transcription decreases rapidly if DNA replication is inhibited by hydroxyurea or if cells are arrested in G1 by the mating pheromone alpha-factor. To identify the transcriptional controls responsible for cycle-specific histone mRNA synthesis, we have developed a selection for mutations which disrupt this process. Using this approach, we have isolated five mutants (hpc1, hpc2, hpc3, hpc4, and hpc5) in which cell cycle regulation of histone gene transcription is altered. All of these mutations are recessive and belong to separate complementation groups. Of these, only one (hpc1) falls in one of the three complementation groups identified previously by other means (M. A. Osley and D. Lycan, Mol. Cell. Biol. 7:4204-4210, 1987), indicating that at least seven different genes are involved in the cell cycle-specific regulation of histone gene transcription. hpc4 is unique in that derepression occurs only in the presence of hydroxyurea but not alpha-factor, suggesting that at least one of the regulatory factors is specific to histone gene transcription after DNA replication is blocked. One of the hpc mutations (hpc2) suppresses delta insertion mutations in the HIS4 and LYS2 loci. This effect allowed the cloning and sequence analysis of HPC2, which encodes a 67.5-kDa, highly charged basic protein.

Amino Acid Sequence↗
PubMed1992

[Analysis of active ingredients in wuren liguid].

The active ingredients and their relative concentration in Wuren liquid were analyzed by GC/MS. It has been found that there are concentrative antimicrobiological ingredients in the liquid such as phenols, benzoic acids, fatty acids, and so on. The results have confirmed the effectiveness of Wuren liquid in disinfection, germ-killing and treatment of skin diseases.

Anti-Infective Agents↗
PubMed1992

[Pathogenesis of traumatic proliferative vitreoretinopathy].

Proliferative vitreoretinopathy is the main cause of loss of vision following posterior penetrating eye injury. Clinically, it can range from macular epiretinal membrane to total retinal detachment and phthisis bulbi. To gain more knowledge of its pathogenesis, the author performed morphologic studies using a primate model and also studied the distribution of fibronectin in 13 enucleated patient eyes using immunofluorescent histochemical techniques. Results indicate this disease process represents an overstimulated response to retinal injury. Posterior vitreous detachment at the level of internal limiting membrane appears to be a predisposing factor. During the active phase of the disease process, there is selective increase of fibronectin in the choroid. This increase is not merely due to the passive leakage of plasma caused by the injury, but the choroid itself produces cellular fibronectin. Fibronectin is known to enhance wound healing and may be an important factor in the pathogenesis of proliferative vitreoretinopathy.

Animals↗
PubMed1992

[Evaluation of long-term efficacy on plasma-derived hepatitis B vaccine].

From April 1986 to May 1990, 265 pupils aged 5 to 9 years in Xian suburbs were studied to evaluate long-term efficacy of plasma-derived hepatitis B vaccine made in China. Anti-HBs titers in vaccine group reached the highest at twelfth month after the first injection and decreased afterwards. The positive rate of anti-HBs decreased slow, but geometric mean titers of anti-HBs fell sharply. Compared with placebo group, the differences were all significant. The peak anti-HBs titers and the response time positively correlated with the persistence of anti-HBs. 4 years observation showed that protection rate of hepatitis B vaccine against HBV infection was 80%. Protection rate was 100% if HBsAg was only considered.

Child↗
PubMed1992

Detection of the tumor marker D-galactose-beta-(1-->3)-N-acetyl-D-galactosamine in colonic cancer and precancer.

The enzyme D-galactose oxidase (GO) oxidizes the carbon-6 position of the hydroxyl groups of galactose-N-acetyl galactosamine, which are commonly present in colon cancer cells and in rectal mucin of patients with colon cancer. We have studied the marker disaccharide galactose and N-acetylgalactosamine on tissue sections by the GO-Schiff reagent in normal, preneoplastic, and neoplastic human colorectal epithelial and compared it with peanut agglutinin reactivity. Fifty-seven (81.4%) of 70 carcinomas, 83.3% (10/12) of precancerous lesions, 50% (10/20) of the mucosa remote from cancer, and 58.1% (25/43) of the mucosa immediately adjacent to cancer showed a positive reaction with GO-Schiff, but the normal control mucosa was nonreactive. The GO-Schiff reagent showed an intense reactivity with mucinous adenocarcinomas and poorly differentiated adenocarcinomas. An intense reactivity was also seen in the intracellular mucus of abnormal dilated crypts (polyps, five of five cases; colitis, four of seven cases; and remote mucosa, 10 of 20 cases). Comparison of peanut agglutinin and GO-Schiff reactivity showed that the nonmucinous (glandular) adenocarcinomas less frequently reacted with the GO-Schiff sequence. Our results showed that the carbohydrate moiety detected by the two techniques may not necessarily be the same, warranting further biochemical analysis. Meanwhile, the data suggested that, like peanut agglutinin, the GO-Schiff sequence has the potential to identify the tumor marker either at the tissue level or by a mucin test for screening colorectal cancer or precancer.

Adenocarcinoma↗