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Biomedical subjects

W Xu

Publications and source records attributed to W Xu.

At least 433 records · Page 24Linked to original sources
PubMed1996

[Loss of heterozygosity involving DCC gene in human colorectal cancers is correlated with the metastatic potential].

DCC gene located at chromosome 18q21.3 is an important tumor-supressor gene associated with tumorigenesis and progression, especially in colorectal carcinomas. Adopting Southern blot technique and RFLP analysis, 33 primary Chinese colorectal cancer patients were examined for loss of heterozygosity (LOH) of DCC gene. Among 16 informative cases, 6 (38%) showed allelic deletion. 18q LOH was correlated with lymph node and hepatic metastases (P < 0.05). The results indicate that application of molecular genetics is of value in ascertaining the metastatic potential of colorectal carcinomas.

Adult↗
PubMed1996

Sexually transmitted disease control in China (1949-1994).

This paper summarizes the historical experiences in venereal disease control in China during the 1950s. Venereal diseases had been all but eliminated in the whole country till 1964. However, along with the implementation of open-door policy and economic reform in the 1980s, the social environment was changed to a great extent in this country. Sexually transmitted diseases (STDs) were re-introduced in the Chinese mainland and new foci of infection established themselves in some cities. During the recent 8 years the national STD case-reporting and sentinel surveillance systems have been set up. The results of surveillance show that the annual incidence of STD has been on the increase. The existing factors associated with the increasing incidence of STD mainly are; population movement, increasing affluence in a part of population, the availability of multiple sexual partners (including the prostitution) and asymptomatic STD increased. Finally, the strategies for STD control are discussed in detail.

China↗
PubMed1996

[Chemosensitivity test for head and neck cancers].

The chemosensitivities of 27 fresh specimens of head and neck cancers were tested with MTT assay to study the practicability and accuracy of the assay for the examination of chemosensitivity in head and neck cancer patients. The chemosensitivities among cancers of different primary sites, pathologic types, histological differentiations, DNA ploidies and estrogen receptors were compared in an attempt to evaluate the choice of anticancer drugs for individual chemotherapy. Eight anticancer drugs: Methotroxate (MTX), Mitomycin C (MMC), fluorouracil (5-Fu), Carboplatin (CBDCA), Pingyangmycin (PYM), Homoharringtonine (HHA), Etoposid (VP16) and Vincristine (VCR) were included. The success rate of MTT assay in the present study was 92.6% and the accuracy was relatively high. The sensitivity sequence was PYM > HHA > MTX > CBDCA > MMC > 5-Fu > VCR > VP16, which suggested HHA should be recommended first to the chemotherapy of head and neck cancer. No chemosensitivity differences were found among different primary sites histological differentiations and estrogen receptors. The chemosensitivity of squamous cell carcinoma was significantly higher than that of adenoid cystic carcinoma. The chemosensitivity of aneuploid tumor was significantly higher than that of diploid.

Adult↗
PubMed1996

[Furosemide test for diagnosis of endolymphatic hydrops: a clinical exploration].

Furosemide test (FT) is a clinical method for the diagnosis of endolymphatic hydrops (EH). Immediately preceding i.v. injection of 20 mg furosemide, a caloric test was performed with 50 micromilligrams of water at 30 degrees C. Nystagmography was employed to measure the maximum slow velocity of caloric nystagmus. The test was repeated one hour after the injection. The two sets of data were then compared. An increase beyond 22.97% was defined as positive. The first group was composed of 54 patients of EH as the experimental group, and the second group 54 patients with vertigo of non-EH as control. The positive rates of the two groups were 70.4% and 25.9% respectively. It showed that FT was useful for detecting EH. The percentage of directional preponderance (DP) was obviously descended in the two groups after i.v. furosemide. Descending rate was 77.8% (21/27) in the first group, which had reached the normal value in 9 cases. It was showed that DP was important also for criticizing FT. The hearing of all subjects was not damaged. When the renal function of the subject was normal and not combined with the use of aminoglycoside antibiotics, the dose of FT was not dangerous to the hearing and had few side reactions. The mechanism of dehydration in hydropic labyrinth was presumed to be acute systemic diuresis, but the effect in inner ear was unknown.

Diagnosis, Differential↗
PubMed1996

Effect of anisodine on acute forebrain ischemia-reperfusion damage in rats.

AIM: To study the protective effect of anisodine (Ani) on acute forebrain ischemia-reperfusion injury in rats. METHODS: Both vertebral arteries were occluded by electrocautery. Severe, but transient bilateral cerebral ischemia was produced by clamping both common carotid arteries in rats. Atomic absorption spectrophotometric and spectrophotometric methods were used to determine the contents of calcium and extravasated Evans blue (EB), respectively, remained in forebrain at 60-min recirculation after 30-min ischemia. RESULTS: At 60-min recirculation, the brain calcium contents were increased from 112 +/- 6 micrograms/g brain dry weight in control (sham operation) group to 165 +/- 7 micrograms/g brain dry weight with marked increase of EB extravasation. Ani (2.5 mg.kg-1, i.p.), and scopolamine (Sco, 0.25 mg.kg-1, i.p.) decreased the elevated calcium and extravasated EB contents. CONCLUSION: Ani prevented the brain from ischemia insults through reducing intracellular calcium accumulation resulted from ischemia and reperfusion.

Animals↗
PubMed1995

Analysis of interleukin-2-dependent signal transduction through the Shc/Grb2 adapter pathway. Interleukin-2-dependent mitogenesis does not require Shc phosphorylation or receptor association.

The interleukin (IL)-2 receptor system has previously been shown to signal through the association and tyrosine phosphorylation of Shc. This study demonstrates that the IL-2 receptor beta (IL-2R beta) chain is the critical receptor component required to mediate this effect. The use of IL-2R beta chain deletion mutants transfected into a Ba/F3 murine cell model describes a requirement for the IL-2R beta "acid-rich" domain between amino acids 315 and 384 for Shc tyrosine phosphorylation and receptor association. COS cell co-transfection studies of IL-2R beta chain constructs containing point mutations of tyrosine to phenylalanine along with the tyrosine kinase Jak-1 and a hemagglutinin-tagged Shc revealed that the motif surrounding phosphorylated tyrosine 338 within the acid-rich domain of the IL-2R beta is a binding site for Shc. Deletion of this domain has previously been shown to abrogate the ability of IL-2 to activate Ras but does not affect IL-2-dependent mitogenesis in the presence of serum. Proliferation assays of Ba/F3 cells containing IL-2R beta chain deletion mutants in serum-free medium with or without insulin shows that deletion of the acid-rich domain does not affect IL-2-driven mitogenesis regardless of the culture conditions. This study thus defines the critical domain within the IL-2R beta chain required to mediate Shc binding and Shc tyrosine phosphorylation and further shows that Shc binding and phosphorylation are not required for IL-2-dependent mitogenesis. Neither serum nor insulin is required to supplement the loss of induction of the Shc adapter or Ras pathways, which therefore suggests a novel mechanism for mitogenic signal transduction mediated by this hematopoietin receptor.

Adaptor Proteins, Signal Transducing↗
PubMed1995

Human glucose phosphate isomerase: exon mapping and gene structure.

The structure of the gene for human glucose phosphate isomerase (GPI) has been determined. Three GPI clones were isolated from a human genomic library by using a full-length GPI cDNA probe and were characterized. Oligonucleotides based on the known cDNA sequence were used as primers in amplification and sequence analyses. This led to the identification of the exon-intron junctions. By this approach, 18 exons and 17 introns have been identified. The exons range in size from 44 to 431 nucleotides. The intronic sequences surrounding the exons provide useful information for the identification of mutations that give rise to human GPI deficiency associated with chronic hemolytic anemia.

Amino Acid Sequence↗
PubMed1995

Oxygen sensors based on luminescence quenching: interactions of pyrene with the polymer supports.

Oxygen quenching of pyrene has been studied in a diverse series of polymers. Most measurements were made using homo- or copolymers containing a poly(dimethylsiloxane) region. Systematic variations in the polymer properties have been made in order to delineate the structural features important for satisfactory use as supports for oxygen sensors. In particular, quenching behavior was examined as a function of the type and amount of copolymer cross-linkers; these were added to produce domains of different polarity and rigidity that would segregate the sensor molecule. A domain model (Xu, W.; et al. Anal. Chem. 1994, 66, 4133-4141) was used to explain the variations in oxygen-quenching properties as a function of additives and cross-linkers. The relative affinity of the different domains for the pyrene and the efficacy of the domains for oxygen quenching controls the overall behavior of the sensing response.

Electrodes↗
PubMed1995

Growth signal transduction by the human interleukin-2 receptor requires cytoplasmic tyrosines of the beta chain and non-tyrosine residues of the gamma c chain.

To evaluate the possible role for receptor-based tyrosine phosphorylation in growth signaling induced by interleukin-2 (IL-2), a series of substitution tyrosine mutants of the IL-2 receptor beta and gamma c chains was prepared and analyzed. Concurrent mutation of all six of the cytoplasmic tyrosines present in the beta chain markedly inhibited IL-2-induced growth signaling in both pro-B and T cell lines. Growth signaling in a pro-B cell line was substantially reconstituted when either of the two distal tyrosines (Tyr-392, Tyr-510) was selectively restored in the tyrosine-negative beta mutant, whereas reconstitution of the proximal tyrosines (Tyr-338, Tyr-355, Tyr-358, Tyr-361) did not restore this signaling function. Furthermore, at least one of the two cytoplasmic tyrosines that is required for beta chain function was found to serve as a phosphate acceptor site upon induction with IL-2. Studies employing a chimeric receptor system revealed that tyrosine residues of the beta chain likewise were important for growth signaling in T cells. In contrast, although the gamma c subunits is a target for tyrosine phosphorylation in vivo, concurrent substitution of all four cytoplasmic tyrosines of this chain produced no significant effect on growth signaling by chimeric IL-2 receptors. However, deletion of either the Box 1, Box 2, or intervening (V-Box) regions of gamma c abrogated receptor function. Therefore, tyrosine residues of beta but not of gamma c appear to play a pivotal role in regulating growth signal transduction through the IL-2 receptor, either by influencing cytoplasmic domain folding or by serving as sites for phosphorylation and subsequent association with signaling intermediates. These findings thus highlight a fundamental difference in the structural requirements for IL-2R beta and gamma c in receptor-mediated signal transduction.

Amino Acid Sequence↗
PubMed1995

Signaling through the interleukin 2 receptor beta chain activates a STAT-5-like DNA-binding activity.

To explore the possible involvement of STAT factors ("signal transducers and activators of transcription") in the interleukin 2 receptor (IL-2R) signaling cascade, murine HT-2 cells expressing chimeric receptors composed of the extracellular domain of the erythropoietin receptor fused to the cytoplasmic domains of the IL-2R beta or -gamma c chains were prepared. Erythropoietin or IL-2 activation of these cells resulted in rapid nuclear expression of a DNA-binding activity that reacted with select STAT response elements. Based on reactivity with specific anti-STAT antibodies, this DNA-binding activity was identified as a murine homologue of STAT-5. Induction of nuclear expression of this STAT-5-like factor was blocked by the addition of herbimycin A, a tyrosine kinase inhibitor, but not by rapamycin, an immunophilin-binding antagonist of IL-2-induced proliferation. The IL-2R beta chain appeared critical for IL-2-induced activation of STAT-5, since a mutant beta chain lacking all cytoplasmic tyrosine residues was incapable of inducing this DNA binding. In contrast, a gamma c mutant lacking all of its cytoplasmic tyrosine residues proved fully competent for the induction of STAT-5. Physical binding of STAT-5 to functionally important tyrosine residues within IL-2R beta was supported by the finding that phosphorylated, but not nonphosphorylated, peptides corresponding to sequences spanning Y392 and Y510 of the IL-2R beta tail specifically inhibited STAT-5 DNA binding.

Amino Acid Sequence↗
PubMed1995

Molecular genetic analysis of the duplication of human inducible nitric oxide synthase (NOS2) sequences.

In previous studies, we found multiple copies of inducible nitric oxide synthase gene (NOS2)-like sequences in the human genome and mapped them to the pericentric region of chromosome 17. Here, we describe the cloning and sequencing of exon22 regions from three of these NOS2-like sequences. We have also mapped another NOS2-like sequence to human chromosome 14. Since there are multiple NOS2-like sequences present in the human genome, we have also carried out Zoo Blot hybridisation analysis using a NOS2 cDNA probe. Our data suggest that duplication of NOS2-like sequences occurred very recently in primate evolution.

Amino Acid Oxidoreductases↗
PubMed1995

Uroporphyrinogen-III synthase: molecular cloning, nucleotide sequence, expression of a mouse full-length cDNA, and its localization on mouse chromosome 7.

Uroporphyrinogen-III synthase (URO-S; EC 4.2.1.75), the fourth enzyme in the heme biosynthetic pathway, is responsible for the conversion of hydroxymethylbilane to the cyclic tetrapyrrole, uroporphyrinogen III. The deficient activity of URO-S is the enzymatic defect in congenital erythropoietic porphyria (CEP), an autosomal recessive disorder. For the generation of a mouse model of CEP, the human URO-S cDNA was used to screen 2 x 10(6) recombinants from a mouse adult liver cDNA library. Ten positive clones were isolated, and dideoxy sequencing of the entire 1.6-kb insert of clone pmUROS-1 revealed 5' and 3' untranslated sequences of 144 and 623 bp, respectively, and an open reading frame of 798 bp encoding a 265-amino-acid polypeptide with a predicted molecular mass of 28,501 Da. The mouse and human coding sequences had 80.5 and 77.8% nucleotide and amino acid identity, respectively. The authenticity of the mouse cDNA was established by expression of the active monomeric enzyme in Escherichia coli. In addition, the analysis of two multilocus genetic crosses localized the mouse gene on chromosome 7, consistent with the mapping of the human gene to a position of conserved synteny on chromosome 10. The isolation, expression, and chromosomal mapping of this full-length cDNA should facilitate studies of the structure and organization of the mouse genomic sequence and the development of a mouse model of CEP for characterization of the disease pathogenesis and evaluation of gene therapy.

Amino Acid Sequence↗