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Biomedical subjects

X Wu

Publications and source records attributed to X Wu.

At least 649 records · Page 36Linked to original sources
PubMed1998

[Clinical manifestation of AIDS in oral and maxillofacial region (Report of a case)]

The prevalence morbidity of AIDS rises day after day. As the first symptom of this disease usually occurs in maxillofacial region,it must be well attentioned to the dentists. Here introducing a case who was a patient of AIDS. He was first see doctor in july 1995 in our Department, associating with foreign documents, the authors described all kinds of clinic symptoms of AIDS on oral and maxillofacial region in early to late stage.The typical one includes hairy leukoplakia,monilia albicans infection of angular stomatitis and mucous membrane,KS,etc.At last,the authors indicated there are some preventive methods to the disease for the dentists.

Journal Article↗
PubMed1998

[Measuring trace germanium in vegetables with the spectrofluorometric method].

A spectrofluorometric method to measure trace germanium in vegetables was established. Results showed that the detection limit of the method was 0.569 ng/g, the accuracy of determination on the 1 microg Ge content was +/- 3.59%. The content of Ge in vegetables could be calculated from the standard adding method without extraction when using mixed acid digestion.

Calibration↗
PubMed1998

Cytochrome P450 2E1 DraI polymorphisms in lung cancer in minority populations.

Cytochrome P4502E1 (CYP2E1) is involved in the metabolic activation of carcinogenic N-nitrosamines. This study was performed to examine whether CYP2E1 DraI polymorphisms in intron 6 are related to susceptibility to lung cancer and are associated with carcinogenetic exposure. We therefore genotyped CYP2E1 by PCR amplification of peripheral WBC DNA from 126 patients with previously untreated lung cancer (85 African Americans and 41 Mexican Americans) and 193 controls (104 African Americans and 89 Mexican Americans). Mutagen sensitivity was measured with an in vitro assay quantitating bleomycin-induced chromatid breaks in peripheral blood lymphocyte cultures. The CYP2E1 DraI DD genotype was found in 86.5% of all cases and in 74.6% of all controls (P = 0.03), in 78.1% of 41 Mexican-American cases and in 69.6% of their controls (P = 0.70), and in 90.6% of African American cases and in 78.8% of their controls (P = 0.05). The DD genotype was found to be associated with a significantly higher risk of lung cancer overall with an odds ratio (OR) of 2.4 [95% confidence interval (CI), 1.1-5.3]. This risk was significantly elevated for men and for those who had ever smoked [ORs of 3.4 (95% CI, 1.3-8.7) and 2.6 (95% CI, 1.1-6.0), respectively], but not for women and nonsmokers [ORs of 0.7 (95% CI, 0.1-3.8) and 0.9 (95% CI, 0.1-10.6), respectively]. Stratified analysis showed an interaction that seemed greater than multiplicative between cigarette smoking and the CYP2E1 DraI DD genotype. The ORs for the CYP2E1 DraI DD genotype, cigarette smoking, and both risk factors combined were 1.5, 8.5, and 22.7, respectively. The CYP2E1 DraI polymorphism and the CYP2E1 PstI polymorphism in the upstream flanking regions were significantly associated in Mexican Americans but not in African Americans. We therefore conclude that the CYP2E1 DraI polymorphism seems to be associated with lung carcinogenesis. However, a larger study is warranted to evaluate the interactions among CYP2E1 DraI DD genotype, mutagen sensitivity, and cigarette smoking.

Aged↗
PubMed1998

Post-transcriptional induction of p21cip1 protein in condylomata and dysplasias is inversely related to human papillomavirus activities.

Infections of the genital and oral epithelia by human papillomaviruses cause condylomata, papillomas, and squamous intraepithelial neoplasms, some of which can progress to invasive cancers. We describe an induction of p21cip1/WAF1/sdi1 protein in a fraction of the spinous cells in benign lesions and in cervical intraepithelial neoplasia grades I and II. The induction appears to be post-transcriptional and independent of p53. p21cip1 antigen-positive cells were sporadic in cervical intraepithelial neoplasia III and rare and focal in carcinomas. In contrast, p21cip1 protein was below or at the threshold of detection in the differentiated cells of normal squamous epithelia from different body sites despite an up-regulation of p21cip1 RNA. In cervical intraepithelial neoplasias from patients who were also positive for the human immunodeficiency virus, there was an additional increase in p21cip1 RNA in the upper spinous cells without concomitant p21cip1 protein induction. A consistent inverse relationship was observed between the p21cip1 protein induction and abundant human papillomavirus DNA and RNAs. We propose that p21cip1 protein induction is a novel host response that inhibits viral DNA replication and thus prevents elevated viral transcription. This hypothesis can partly account for the heterogeneity and the differentiation-dependent viral activities commonly observed in benign human papillomavirus lesions.

Adenocarcinoma↗
PubMed1998

Targeted expression of activated erbB-2 to the epidermis of transgenic mice elicits striking developmental abnormalities in the epidermis and hair follicles.

The erbB-2 proto-oncogene belongs to a receptor tyrosine kinase family that includes the epidermal growth factor receptor, erbB-2, erbB-3, and erbB-4. erbB-2 is expressed in basal cells of the squamous epithelia and the outer root sheath of the hair follicles, but its function in epidermal development has not been well studied. To investigate its role in the skin, we created transgenic mice harboring an activated erbB-2 oncogene under the control of the human keratin 14 promoter. The keratin 14 promoter directed its expression to cells in which erbB-2 is normally expressed, whereas the activated receptor gene ensured increased signaling. All transgenic founder mice exhibited extensive and striking skin phenotype, including epidermal hyperplasia, preneoplasia, papilloma, hyperkeratosis, and dyskeratosis. The majority of the hair follicles were replaced by bizarre hyperproliferative intradermal squamous invaginations, whereas the rest of the follicles exhibited severe hyperplasia and disorganization. All but one of the transgenic mice died before or shortly after birth, probably as a consequence of defects in the skin and esophagus. These observations demonstrate that the skin is sensitive to erbB-2 signaling, suggesting an important role for this receptor tyrosine kinase in epidermal growth, differentiation, and hair follicle morphogenesis.

Animals↗
PubMed1998

Mutagen sensitivity as a susceptibility marker for human hepatocellular carcinoma.

Although the pathogenesis of hepatocellular carcinoma (HCC) remains poorly understood, hepatitis B virus and dietary aflatoxin exposures are established etiological factors for this disease. We conducted a pilot study of 28 patients with HCC and 110 healthy controls matched for age, sex, and ethnicity to determine whether constitutional genetic instability, based on the quantification of mutagen-induced chromatid breaks in cultured lymphocytes, modifies an individual's risk of HCC development. The mean numbers of bleomycin-induced breaks per cell for cases and controls were 0.92 and 0.55, respectively (P < 0.0001). For benzo(a)pyrene diol epoxide (BPDE) sensitivity, the values were 0.90 for cases and 0.46 for controls (P < 0.0001). Nearly 68% of the cases but only 27% of the controls exhibited bleomycin sensitivity (i.e., had > or = 0.68 breaks per cell). Eighty % of the case group but only 22% of the control group exhibited BPDE sensitivity (i.e., had > or = 0.58 breaks per cell). On multivariate analyses, both bleomycin sensitivity and BPDE sensitivity were associated with significantly elevated risks for HCC, with odds ratios (95% confidence intervals) of 5.63 (2.30, 13.81) and 14.13 (3.52, 56.68), respectively. For individuals who were sensitive to both assays, the risk was 35.88. A synergistic interaction between the bleomycin sensitivity and BPDE sensitivity in HCC risk was suggested. These preliminary findings suggest that differences in host factors related to the predisposition to chromosome breakage, the capacity for DNA repair, or both may be involved in HCC development by influencing the predisposition of hepatitis B virus integration into human DNA or that the carcinogens induced DNA damage susceptibility. A larger study is needed to confirm these intriguing results.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1998

Allelic deletion analyses of MMAC/PTEN and DMBT1 loci in gliomas: relationship to prognostic significance.

The frequency of loss of heterozygosity (LOH) around MMAC/PTEN and DMBT1 loci and survival analyses based on the LOH status were assessed in 110 patients with different histological groups of gliomas. Twenty-six of the patients had anaplastic oligodendrogliomas, 31 had anaplastic astrocytomas, and 53 had glioblastomas multiforme (GM). At the DMBT1 locus, LOH was observed very frequently in all three histological groups, with no significant difference in the frequency of LOH among the three histological groups. At the MMAC/PTEN locus, patients with GM exhibited a significantly increased frequency of LOH (72%) compared with patients with anaplastic astrocytomas (29%) or anaplastic oligodendrogliomas (31%) (P < 0.0001). Kaplan-Meier survival plots showed that patients with LOH at the MMAC/PTEN locus had a significantly worse prognosis than did patients without LOH at the MMAC/PTEN locus [hazard ratio (LOH versus non-LOH), 2.65; 95% confidence interval (CI), 1.69-4.46; P < 0.0001]. Cox proportional hazards regression analysis, adjusted for age at surgery and histological grades (GM and non-GM), showed that LOH at the MMAC/PTEN locus was a significant predictor of shorter survival [hazard ratio (LOH versus non-LOH), 2.01; 95% CI, 1.1-3.5; P = 0.018). Our analysis failed to indicate a similar association between the frequency of LOH at the DMBT1 locus and patient survival [hazard ratio (LOH versus non-LOH), 2; 95% CI, 0.37-3.13; P = 0.2]. These results suggest that the DMBT1 gene may be involved early in the oncogenesis of gliomas, whereas alterations in the MMAC/PTEN gene may be a late event in the oncogenesis related to progression of gliomas and provide a significant prognostic marker for patient survival.

Agglutinins↗
PubMed1998

Glucose does not stimulate apoprotein B secretion from HepG2 cells because of insufficient stimulation of triglyceride synthesis.

We have previously demonstrated a close relationship between oleic acid (OA)-stimulated triglyceride (TG) synthesis and apolipoprotein B (apoB) secretion in HepG2 cells. However, other investigators studying the association between glucose-stimulated TG synthesis and apoB secretion have reported variable results. The present study was carried out to answer the question: does TG derived from glucose have different effects on apoB secretion from HepG2 cells compared to TG derived from oleate? We observed that incubations of HepG2 cells for as long as 48 h in 30 mm glucose did not increase apoB secretion. We then demonstrated that the failure of glucose to stimulate apoB secretion from HepG2 cells results from insufficient stimulation of TG synthesis by glucose. Thus, incorporation of [3H]glycerol into [3H]TG in the presence of 30 mm glucose for up till 48 h was not increased compared to basal conditions. The inability of glucose to stimulate TG synthesis was also evidenced by the inability of both 8 -h and 24 -h incubations with 30 mm glucose to increase cell TG mass; similar incubations with OA increased TG mass 50-100%. Additional studies demonstrated that glucose conversion to either glycerol or fatty acids was minimal; this accounted for the lack of stimulation of TG synthesis. We conclude that in HepG2 cells, availability of high glucose levels in the media for as long as 48 h does not stimulate triglyceride synthesis, and that this is the basis for the failure of glucose to stimulate apoB secretion.

Apolipoproteins B↗
PubMed1998

Multiple subtypes of serotonin receptors are expressed in rat sensory neurons in culture.

[3H]5-HT revealed the presence of serotonin receptors in cultured rat sensory neurons. [3H]5-CT binding was inhibited by cyanopindolol with an IC50 of 0.87 +/- 0.30 nM, suggesting the expression of the 5-HT1B receptor in these neurons. The presence of 5-HT1B receptors was confirmed by the displacement of [125I]Iodocyanopindolol binding by cyanopindolol with an IC50 of 2.43 +/- 0.81 nM. 5-HT1B receptors are the predominant type of serotonin receptors labeled by [3H]5-HT in cultured DRG neurons, representing approximately 60% of the specific [3H]5-HT binding sites. In addition, 5-HT1D and 5-HT2A receptor binding was also found in these neurons. RT-PCR analysis of RNA isolated from embryonic sensory neurons in culture confirmed the expression of 5-HT1B, 5-HT1D and 5-HT2A receptor mRNA. It also demonstrated the presence of 5-HT1F, 5-HT2C, 5-HT3, 5-HT4, 5-HT5A and 5-HT5B receptor mRNA and the absence of 5-HT1A, 5-HT1E, 5-HT2B, 5-HT6 and 5-HT7 mRNA. The identification of multiple subtypes of serotonin receptors expressed in cultured embryonic sensory neurons suggests that DRG neuronal cultures may be an excellent model to examine the direct effects of serotonin on the activity of these sensory neurons.

Animals↗
PubMed1997

Evidence that a viral replicase protein is involved in the disassembly of tobacco mosaic virus particles in vivo.

Tobacco mosaic virus (TMV) particles have been shown to undergo bidirectional disassembly when they are introduced into host cells. Approximately three-quarters of the genomic RNA (i.e., the 126-kDa and 183-kDa protein ORFs) is first uncoated in the 5'-to-3' direction and the process is then completed by removal of coat protein molecules in the 3'-to-5' direction. An effort was made to determine whether the 126-kDa protein or the 183-kDa protein, both of which are involved in replication of the viral RNA, is required for the second part of the disassembly reaction. It was shown that progeny negative-strand viral RNA begins to be produced in inoculated cells at about the same time that 3'-to-5' disassembly is initiated thus suggesting that the two processes may be coupled. Particles containing mutant forms of the viral RNA in which large sections of the 126-kDa and 183-kDa protein ORFs were missing were not disassembled in the 3'-to-5' direction when they were introduced into cells. However, they were disassembled when the inoculum contained purified TMV RNA from which, presumably, the two functional proteins could be translated Particles containing mutants of the RNA from which a few codons had been deleted in or near conserved regions in the 126-kDa protein ORF also did not undergo 3'-to-5' disassembly unless mixed with wild type viral RNA prior to inoculation. These results suggest that the 126-kDa and/or 183-kDa protein plays a role in the completion of disassembly of TMV particles at the onset of the infection process.

Capsid↗
PubMed1997

Aqueous oxygen: a highly O2-supersaturated infusate for regional correction of hypoxemia and production of hyperoxemia.

BACKGROUND: High levels of hyperoxemia may have utility in the treatment of regional tissue ischemia, but current methods for its implementation are impractical. A catheter-based method for infusion of O2, dissolved in a crystalloid solution at extremely high concentrations, ie, 1 to 3 mL O2/g (aqueous oxygen [AO]), into blood without bubble nucleation was recently developed for the potential hyperoxemic treatment of regional tissue ischemia. METHODS AND RESULTS: To test the hypotheses that hypoxemia is correctable and that hyperoxemia can be produced locally by AO infusion, normal saline equilibrated with O2 at 3 MPa (30 bar; 1 mL O2/g) was delivered into arterial blood in two different animal models. In 15 New Zealand White rabbits with systemic hypoxemia, AO was infused into the midabdominal aorta at 1 g/min. Mean distal arterial PO2 increased to 236+/-113 and 593+/-114 mm Hg on 1-hour periods of air and O2 breathing, respectively, from a baseline of 70+/-10 mm Hg (P<.01). In contrast, infusion of ordinary normal saline in a control group (n=7) had no effect on arterial PO2. No differences between groups (P>.05) in temporal changes in blood counts and chemistries were identified. In 10 dogs, low coronary blood flow in the circumflex artery was delivered with a roller pump through the central channel of an occluding balloon catheter. Hypoxemic, normoxemic, and AO-induced hyperoxemic blood perfusates (mean PO2, 52+/-4, 111+/-22, and 504+/-72 mm Hg, respectively) were infused for 3-minute periods in a randomized sequence. Short-axis two-dimensional echocardiography demonstrated a significant decrease (P<.05) in left ventricular ejection fraction compared with baseline physiological values with low-flow hypoxemic and normoxemic perfusion but not with low-flow hyperoxemic perfusion. CONCLUSIONS: Intra-arterial AO infusion was effective in these models for regional correction of hypoxemia and production of hyperoxemia.

Animals↗
PubMed1997

Cloning of two candidate tumor suppressor genes within a 10 kb region on chromosome 13q14, frequently deleted in chronic lymphocytic leukemia.

Previous studies have indicated the presence of a putative tumor suppressor gene on chromosome 13q14, commonly deleted in patients with B-cell chronic lymphocytic leukemia (B-CLL). We have previously defined a minimally deleted region of 130 kb centromeric to the marker D13S272, and constructed a PAC and cosmid contig encompassing this area. In the present study we have made a detailed restriction and transcriptional map of the region of interest. Using these tools we have screened a panel of 206 primary CLL clones and three cell lines. In five CLL cases we found limited deletions defining the region of interest to an area of no more than 10 kb. Two adjacent genes, termed Leu1 and Leu2 (leukemia-associated gene 1 and 2), were mapped to the minimally deleted region, with several patients showing deletion borders within these genes. The Leu1 and Leu2 genes show little homology to previously published genes at the nucleotide and expected translated amino acid sequence level. Mutational analysis of the Leu1 and 2 genes in 170 CLL samples revealed no small intragenic mutations or point mutations. However, in all cases of 13q14 loss examined, the first exon of both genes, which are only 300 bp apart, were deleted. We conclude that the Leu1 and Leu2 genes are strong candidates as tumor suppressor gene(s) involved in B-CLL leukemogenesis.

Amino Acid Sequence↗
PubMed1997

Transforming growth factor beta 1 transduced mouse prostate reconstitutions: II. Induction of apoptosis by doxazosin.

BACKGROUND: To study the possible relationship between adrenergic activities and the pathogenesis of benign prostatic hyperplasia (BPH), we tested the effect of doxazosin, an alpha 1-adrenoceptor antagonist, on prostatic growth in vivo using a mouse model for BPH. METHODS: The mouse prostate reconstitution (MPR) model system with retroviral (BabeTGF-beta 1Neo) transduction of transforming growth factor beta 1 (TGF-beta 1) was used to induce focally hyperplastic BPH-like lesions and increase the number of catecholaminergic neurons. The mice were treated with daily intraperitoneal injections of doxazosin (3 mg/kg). RESULTS: Doxazosin caused a significant reduction in the wet weight of BabeTGF-beta 1-infected MPRs. The percent of PCNA-positive epithelial cells was similar in the doxazosin-treated and water only, control groups. There was a significant increase in the number of epithelial cells undergoing programmed cell death, apoptosis, in the doxazosin group (apoptotic index = 4.7 for doxazosin group vs. 3.1 for control group, P < 0.05). The doxazosin-induced apoptosis was more apparent in TGF-beta 1 transduced MPRs than BAG alpha control MPRs, and was not seen in the prostates of the adult male mice into which the MPRs were engrafted. CONCLUSIONS: Our data demonstrate a novel and potentially important biological activity of doxazosin in vivo in this mouse model of BPH.

Adrenergic alpha-Antagonists↗
PubMed1997

Molecular mechanism of base excision repair of uracil-containing DNA in yeast cell-free extracts.

Base excision repair (BER) constitutes a ubiquitous excision repair mechanism, which is responsible for the removal of multiple types of damaged and inappropriate bases in DNA. We have employed a yeast cell-free system to examine the biochemical mechanism of the BER pathway in lower eukaryotes. Using uracil-containing DNA as a model substrate, we demonstrate that yeast BER requires Apn1 protein, an Escherichia coli endonuclease IV homolog. In extracts of an apn1 deletion mutant, the 5'-incision at AP (apurinic/apyrimidinic) sites is not detectable, supporting the notion that yeast contains only one major 5'-AP endonuclease. The processing of the 5'-deoxyribose phosphate moieties was found to be a rate-limiting step. During BER of uracil-containing DNA, repair patch sizes of 1-5 nucleotides were detected, with single nucleotide repair patches predominant.

Cell-Free System↗
PubMed1997

The degradation of apolipoprotein B100 is mediated by the ubiquitin-proteasome pathway and involves heat shock protein 70.

Apolipoprotein B (apoB) is the major protein component of atherogenic lipoproteins of hepatic origin. In HepG2 cells, the standard cell culture model of human hepatic lipoprotein metabolism, there is a limited availability of core lipids in the endoplasmic reticulum for association with nascent apoB. Under these conditions, apoB is partially translocated, interacts with cytosolic Hsp70, and undergoes rapid degradation. We show that increasing the expression of Hsp70 in HepG2 cells promotes apoB degradation. In addition, apoB is polyubiquitinated and its degradation both normally and after Hsp70 induction is blocked by inhibitors of the proteasome. The apoB that accumulates after proteasome inhibition is endoplasmic reticulum-associated and can be assembled into lipoproteins and secreted if new lipid synthesis is stimulated. Thus, apoB is the first example of a wild-type mammalian protein whose secretion is regulated by degradation in the cytosol via the ubiquitin-proteasome pathway. Furthermore, targeting of this secretory protein to the proteasome is regulated by the molecular chaperone Hsp70 and the availability of apoB's lipid-ligands.

Apolipoprotein B-100↗
PubMed1997

Functional RT and IN incorporated into HIV-1 particles independently of the Gag/Pol precursor protein.

The expression and incorporation of retroviral enzymes into virions in the form of Gag/Pol precursor polyproteins is believed to be important for the assembly of infectious viral particles. HIV-1 encodes a 160 kDa Gag/Pol precursor that includes Gag, protease (PR), reverse transcriptase (RT) and integrase (IN). We have developed the use of HIV accessory proteins (Vpr and Vpx) as vehicles to incorporate protein of both viral and non-viral origin into virions by expression in trans as heterologous fusion proteins (Wu et al., 1995, 1996a). To analyze the role of Gag/Pol in the formation of infectious virions, we incorporated RT and IN into HIV-1 particles in trans, as fusion partners of viral protein R (Vpr). Virions derived from an RT and IN minus proviral clone were infectious and replicated through a complete cycle of infection when RT and IN proteins were provided in trans. These results demonstrate that functional RT and IN proteins can be provided in trans, and that their expression and incorporation into virions as components of Gag/Pol are not required for the formation of infectious virions. Thus, for the first time, we have demonstrated for a human pathogenic retrovirus that processes of assembly and the function of critical viral enzymes can be unlinked. This finding will provide unique opportunities to explore retroviral RT/IN function and the role of Gag/Pol in the formation of infectious virions in the context of a replicating virus (in vivo).

Blotting, Western↗