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Biomedical subjects

S Yang

Publications and source records attributed to S Yang.

At least 199 records · Page 11Linked to original sources
PubMed2000

Effect of trichloroethylene and its metabolites, dichloroacetic acid and trichloroacetic acid, on the methylation and expression of c-Jun and c-Myc protooncogenes in mouse liver: prevention by methionine.

Trichloroethylene (TCE), dichloroacetic acid (DCA), and trichloroacetic acid (TCA) are environmental contaminants that are carcinogenic in mouse liver. 5-Methylcytosine (5-MeC) in DNA is a mechanism that controls the transcription of mRNA, including the protooncogenes, c-jun and c-myc. We have previously reported that TCE decreased methylation of the c-jun and c-myc genes and increased the level of their mRNAs. Decreased methylation of the protooncogenes could be a result of a deficiency in S-adenosylmethionine (SAM), so that methionine, by increasing the level of SAM, would prevent hypomethylation of the genes. For 5 days, female B6C3F1 mice were administered, daily by oral gavage, either 1000 mg/kg body weight of TCE or 500 mg/kg DCA or TCA. At 30 min after each dose of carcinogen, the mice received, by ip injection, 0-, 30-, 100-, 300-, or 450-mg/kg methionine. Mice were euthanized at 100 min after the last dose of DCA, TCA, or TCE. Decreased methylation in the promoter regions of the c-jun and c-myc genes and increased levels of their mRNA and proteins were found in livers of mice exposed to TCE, DCA, and TCA. Methionine prevented both the decreased methylation and the increased levels of the mRNA and proteins of the two pro-tooncogenes. The prevention by methionine of DCA- TCA-, and TCE-induced DNA hypomethylation supports the hypothesis that these carcinogens act by depleting the availability of SAM. Hence, methionine would prevent DNA hypomethylation by maintaining the level of SAM. Furthermore, the results suggest that the dose of DCA, TCA, or TCE must be sufficient to decrease the level of SAM in order for these carcinogens to be active.

Animals↗
PubMed2000

Effect of trihalomethanes on cell proliferation and DNA methylation in female B6C3F1 mouse liver.

Trihalomethanes (chloroform, bromodichloromethane, chlorodibromomethane, and bromoform) are regulated organic contaminants in chlorinated drinking water. In female B6C3F1 mouse liver, the 4 trihalomethanes have demonstrated carcinogenic activity when administered by oral gavage; however, chloroform was not carcinogenic when administered in drinking water. Female B6C3F1 mice were administered the trihalomethanes for 11 days by gavage at 2 dose levels or in the drinking water at approximately 75% saturation. When administered by gavage, the trihalomethanes were toxic to the liver, increased the liver:body weight (bw) ratio, and increased the proliferating cell nuclear antigen-labeling index (PCNA-LI). Chloroform and bromodichloromethane were the most toxic, and they increased the liver:bw ratio the most, while bromoform and chloroform increased the PCNA-LI the most. When administered in drinking water, the toxicity of the trihalomethanes was similar to their low gavage-dose. Furthermore, only chloroform significantly increased the liver:bw ratio and bromoform and chloroform increased the PCNA-LI. Chloroform and bromodichloromethane decreased the level of 5-methylcytosine in hepatic DNA. Methylation in the promoter region of the c-myc gene was reduced by the trihalomethanes. Chloroform administered by gavage was more efficacious than given in drinking water; the efficacy of the other trihalomethanes did not differ for the 2 routes. Thus, in mouse liver, the trihalomethanes administered by gavage enhanced cell proliferation and decreased the methylation of the c-myc gene, consistent with their carcinogenic activity. Furthermore, the more modest toxicity, enhancement of cell proliferation, and decreased methylation induced by chloroform administered in drinking water correlated with its lack of carcinogenic activity. Hence, the activity of the trihalomethanes was dependent on the rate of delivery, i.e. rapid by oral gavage and more slowly in drinking water.

Animals↗
PubMed2000

Estrogen increases eNOS and NOx release in human coronary artery endothelium.

Estrogen protects against the development of coronary heart disease in women. This study was designed to examine the direct effects of estrogen on nitric oxide release and endothelial nitric oxide synthase (eNOS) expression in cultured human coronary artery endothelial cells (HCAECs). NOx (nitrate, nitrite, and nitric oxide) was measured by the chemiluminescence method. Prolonged treatment (48 h) of the cells with 17beta-estradiol (E2beta), but not 17alpha-estradiol (E2alpha), resulted in a 2.3-fold increase in basal NOx release in HCAECs and an enhanced adenosine triphosphate (ATP)- and calcium ionophore A23187-induced NOx release. The effects of E2beta on endothelial NOx release were blocked by estrogen-receptor antagonist ICI 182,780. E2beta had no effect on basal and ATP-stimulated intracellular Ca2+ concentrations in HCAECs. However, E2beta significantly increased eNOS protein levels, as determined by Western analysis. We conclude that estrogen increases NOx release in HCAECs, which is independent of cytosolic Ca2+ mobilization and is mediated by the upregulation of eNOS.

Adenosine Triphosphate↗
PubMed2000

Canine ehrlichiosis caused simultaneously by Ehrlichia canis and Ehrlichia platys.

To identify the causative agent of canine ehrlichiosis that has occurred in the suburbs of Guangzhou, China, since 1998, the 16S rRNA gene was amplified and sequenced. Two sequences of 1,482 and 1,483 base pairs were obtained and named as Gzh981 and Gzh982, respectively. The level of similarity of these two was 91.50%, and Gzh981 closely resembled the 16S rRNA gene of Ehrlichia canis, whereas Gzh982 resembled Ehrlichia platys. We therefore conclude that E. canis and E. platys together caused recent outbreaks of canine ehrlichiosis in China.

Animals↗
PubMed2000

Localization of cochlear implant electrodes in radiographs.

Multielectrode cochlear implantation is the most effective treatment for profound sensorineural hearing loss. In vivo three-dimensional 3-D localization of cochlear implant electrodes is important for modeling of the electrical field in the cochlea, design of electrode arrays, and may improve speech processor programming for better speech recognition. The prerequisite for 3-D localization of the electrodes is their 2-D localization in x-ray radiographs. In this paper, we develop a practical method to localize the electrodes with high efficiency, accuracy, and reproducibility. In this method, a priori knowledge of the electrodes and their approximate positions are utilized, an intelligent thresholding and segmentation mechanism is embedded, and the electrode center is computed as the weighted geometric center of segmented electrode pixels. Experiments with physical phantoms and human data demonstrate the feasibility and utility of this method. The PC-based program developed for this project is disseminated on the Web.

Cochlear Implants↗
PubMed2000

Partial rescue of the Vif-negative phenotype of mutant human immunodeficiency virus type 1 strains from nonpermissive cells by intravirion reverse transcription.

Virion infectivity factor (Vif) is a protein encoded by human immunodeficiency virus type I (HIV-1) and is essential for viral replication. It appears that Vif functions in the virus-producing cells and affects viral assembly. Viruses with defects in the vif gene (vif-) generated from the "nonpermissive cells" are not able to complete reverse transcription. In previous studies, it was demonstrated that defects in the vif gene also affect endogenous reverse transcription (ERT) when mild detergents were utilized to permeabilize the viral envelope. In this report, we demonstrate that defects in the vif gene have much less of an effect on ERT if detergent is not used. When ERT was driven by addition of deoxyribonucleoside triphosphates (dNTPs) at high concentrations, certain levels of plus-strand viral DNA could also be achieved. Interestingly, if vif- viruses, generated from nonpermissive cells and harboring large quantities of viral DNA generated by ERT, were allowed to infect permissive cells, they could partially bypass the block at intracellular reverse transcription, through which vif- viruses without dNTP treatment could not pass. Consequently, viral infectivity can be partially rescued from the vif- phenotype. Based on our observations, we suggest that vif defects may cause the reverse transcription complex (RT complex) to become sensitive to mild detergent treatments within HIV-1 virions and become unstable in the target cells, such that the process of reverse transcription cannot be efficiently supported. Further dissection of RT complexes of vif- viruses may be key to uncovering the molecular mechanism(s) of Vif in HIV-1 pathogenesis.

DNA, Viral↗
PubMed2000

Gut-derived norepinephrine plays a critical role in producing hepatocellular dysfunction during early sepsis.

Although plasma norepinephrine (NE) increases and hepatocellular function is depressed during early sepsis, it is unknown whether gut is a significant source of NE and, if so, whether gut-derived NE helps produce hepatocellular dysfunction. We subjected rats to sepsis by cecal ligation and puncture (CLP), and 2 h later (i.e., early sepsis) portal and systemic blood samples were collected and plasma levels of NE were assayed. Other rats were enterectomized before CLP. Hepatocellular function was assessed with an in vivo indocyanine green (ICG) clearance technique, systemic levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 were determined, and the effect of NE on hepatic ICG clearance capacity was assessed in an isolated, perfused liver preparation. Portal levels of NE were significantly higher than systemic levels at 2 h after CLP. Prior enterectomy reduced NE levels in septic animals. Thus gut appears to be the major source of NE release during sepsis. Enterectomy before sepsis also attenuated hepatocellular dysfunction and downregulated TNF-alpha, IL-1beta, and IL-6. Perfusion of the isolated livers with 20 nM NE (similar to that observed in sepsis) significantly reduced ICG clearance capacity. These results suggest that gut-derived NE plays a significant role in hepatocellular dysfunction and upregulating inflammatory cytokines. Modulation of NE release and/or hepatic responsiveness to NE should provide a novel approach for maintaining hepatocellular function in sepsis.

Animals↗
PubMed2000

Cyclophosphamide prevents systemic keratinocyte growth factor-induced up-regulation of surfactant protein A after allogeneic transplant in mice.

We reported that systemic keratinocyte growth factor (KGF) given before bone marrow transplantation (BMT) prevents allogeneic T cell-dependent lung inflammation assessed on Day 7 post-BMT, but the antiinflammatory effects of KGF were impaired in mice injected with both T cells and conditioning regimen of cyclophosphamide (Cy). Intratracheal KGF is known to stimulate the expression of surfactant protein A (SP-A), an oxidant-sensitive T cell immunomodulator produced by alveolar type II cells. We hypothesized that systemic KGF up-regulates SP-A after allogeneic BMT, and the addition of Cy may interfere with the ability of KGF to enhance SP-A production. The subcutaneous administration of recombinant human KGF (5 mg/kg on Days -6, -5, and -4 pre-BMT) increased SP-A protein and mRNA in allogeneic T cell-recipient irradiated mice measured on Day 7 post-BMT. In contrast, the same KGF treatment in irradiated mice given T cells and Cy failed to up-regulate SP-A mRNA and protein expression. In mixed lymphocyte reaction experiments designed to simulate the in vivo model, the addition of human SP-A (5-50 microg) to alloactivated T cells suppressed the production of interleukin-2 in a dose-dependent fashion. We conclude that the systemic pre-BMT injection of KGF in recipients of allogeneic T cells up-regulates SP-A, which may contribute to the early antiinflammatory effects of KGF. The protective KGF-mediated SP-A production is abolished in mice given alloreactive T cells plus Cy.

Animals↗
PubMed2000

The aryl hydrocarbon receptor, a basic helix-loop-helix transcription factor of the PAS gene family, is required for normal ovarian germ cell dynamics in the mouse.

The aryl hydrocarbon receptor (AhR), so-designated based on the ability of the protein to bind with and be activated by polycyclic aromatic hydrocarbons (PAH) and related halogenated hydrocarbons, is part of an emerging family of ligand-activated transcriptional regulators that are distinct from the steroid-thyroid hormone receptor superfamily. Once bound by ligand, the AhR interacts with the AhR nuclear translocator (ARNT) protein to form the aryl hydrocarbon receptor complex (AHRC). Both subunits of the AHRC contain sequences corresponding to basic helix-loop-helix domains, a motif that is shared by a number of other dimeric transcription factors. Although the natural ligand(s) for the AhR remains to be elucidated, to date over fifteen genes, including enzymes, growth factors and other transcription factors, have been identified as potential targets for transcriptional regulation by the chemically-activated AHRC. In the ovary, PAH exposure is known to cause destruction of oocytes within immature follicles, implying that one function of the AhR is to mediate cell death signaling in the female germ line. To assess this possibility, we explored AhR expression patterns in the murine ovary, and then determined the impact of AhR-deficiency (gene knockout) on female germ cell dynamics. Immunohistochemical analysis of ovaries of wild-type female mice indicated that AhR protein was abundantly and exclusively expressed in oocytes and granulosa cells of follicles at all stages of development. Histomorphometric analysis of serial ovarian sections revealed a two-fold higher number of primordial follicles in Ahr-null versus wild-type females at day 4 postpartum. This phenotype likely results from a cell-intrinsic death defect in the developing germ line since AhR-deficiency attenuated the magnitude of oocyte apoptosis in fetal ovaries cultured without hormonal support for 72 h. We propose that the AhR, activated by an as yet unknown endogenous ligand(s), serves to regulate the size of the oocyte reserve endowed at birth by affecting germ cell death during female gametogenesis.

Animals↗
PubMed2000

Infection of immunosuppressed C57BL/6N adult mice with a single oocyst of Cryptosporidium parvum.

The present study was designed to determine the minimum number of Cryptosporidium parvum oocysts capable of producing patent infections in immunosuppressed C57BL/6N adult mice. Sixty-four female mice were divided into 6 groups of 8 mice each, except group 1 that contained 24 mice. Mice in groups 1-3 were immunosuppressed with dexamethasone and inoculated with 1, 5, and 10 oocysts per mouse, respectively. The accuracy of the inoculum size was microscopically confirmed. Mice in groups 4-6 served as controls: they received either only oocyst inoculation (group 4), or immunosuppression (group 5), or no treatments (group 6). Fecal oocyst shedding was monitored daily for each mouse using an indirect immunofluorescent assay. Parasite colonization in the terminal ileum of each mouse was evaluated histologically. Four of 24 mice in group 1 developed patent infections, with a prepatent period of approximately 6 days. All mice in groups 2 and 3 developed patent infections, with prepatent periods ranging from 4 to 7 days. Mice in groups 4-6 remained uninfected. Parasite colonization was observed in the terminal ilea of all mice in groups 1-3 that shed fecal oocysts. The present study experimentally demonstrates that a single viable oocyst can induce patent C. parvum infections in immunosuppressed C57BL/6N adult mice and indicates that this mouse model could be used for the parasite genotype or isolate cloning.

Animals↗
PubMed2000

2-year observation of attachment loss in a rural Chinese population.

BACKGROUND: Risk indicators for periodontitis seem to vary with study population. The purpose of this study was to determine whether risk indicators of additional attachment loss differ between generations of Chinese villagers in a rural area of China over a 2-year period. METHODS: The study population consisted of 310 subjects aged 15 to 44. In each subject, 2 quadrants from either the upper or lower jaw were randomly selected and 6 sites on each tooth were examined. Clinical parameters included plaque scoring system (PSS), calculus index (CI), probing depth (PD), attachment level (AL), and sulcus bleeding index (SBI). The second examination was done 2 years after the first. RESULTS: In the 15- to 24-year-old age group, mean PSS, CI, and SBI were significantly higher in subjects with additional attachment loss > or =3 mm (AL+) than in those without attachment loss (AL-). In the 25- to 34-year-old age group, mean PD was significantly higher in AL+ than in AL-, and mean PD and AL were significantly higher in AL+ than in AL- in the 35- to 44-year-old age group. Although the number of subjects with AL+ increased with age, the mean number of sites with AL+ per subject did not differ by generation. In addition, smokers tended to exhibit attachment loss more often than non-smokers. CONCLUSIONS: The present results suggest that the clinical parameters associated with attachment loss differ between generations and that gingival inflammation is likely associated with the onset of periodontitis more strongly than progression of periodontitis, whereas PD and/or AL are associated with the progression of periodontitis.

Adolescent↗
PubMed2000

Molecular cloning of canine and feline flt3 ligand reveals high degree of similarity to the human and mouse homologue but uniquely long cytoplasmic domain.

The cDNAs encoding canine and feline flt3 ligand (FL) have been isolated from libraries constructed from canine or feline peripheral blood mononuclear cells and sequenced. A full-length canine FL cDNA encodes a polypeptide of 294 amino acids that shares 52.8% and 71.0% identity with the mouse and human FL protein, respectively. While the feline FL cDNA encodes a polypeptide of 291 amino acids that shares 54.1% and 70.2% identity with the mouse and human FL protein, respectively. The canine and feline FL proteins share 82.8% identity at amino acid level. Besides those encoding the full-length FL protein, several alternatively spliced forms of canine FL transcripts were also isolated. The canine and feline FL proteins have longer cytoplasmic domain than their mouse and human homologue.

Alternative Splicing↗
PubMed2000

Evaluation of safe food-handling instructions on raw meat and poultry products.

Every year in the United States, millions of people become ill, thousands of people die, and substantial economic costs are incurred from foodborne diseases. As a measure to prevent foodborne diseases, since July 1994, the U.S. Department of Agriculture has required that safe food-handling labels be placed on retail packages of raw or partially cooked meat and poultry products. Through selected states' Behavioral Risk Factor Surveillance System (BRFSS) interviews, survey data were collected to determine the proportion of adults aware of the label and adults who reported changing their raw meat-handling practices because of the label. Fifty-one percent of the 14,262 respondents reported that they had seen the label. Of these, 79% remembered reading the label, and 37% of persons who reported that they had seen and read the label reported changing their raw meat preparation methods because of the label. Women were more likely than men to have read the label, as were persons who are at least 30 years of age compared to younger adults (P < 0.05). Both label awareness and risky food-handling behaviors increased with education and income, suggesting that safe food-handling labels have limited influence on consumer practices. Our results also suggest that the labels might be more effective in discouraging cross-contamination than in promoting thorough cooking practices. We suggest that the label is only one component among many food safety education programs that are needed to inform consumers about proper food-handling and preparation practices and to motivate persons who have risky food-handling and preparation behaviors to change these behaviors.

Adolescent↗
PubMed2000

Prevalence of high-risk food consumption and food-handling practices among adults: a multistate survey, 1996 to 1997. The Foodnet Working Group.

Risk factors for foodborne diseases include consumption of high-risk foods and unsanitary food-handling practices; however, little is known about the prevalence of these risk factors in the general population. A survey was done in five FoodNet sites (California, Connecticut, Georgia, Minnesota, Oregon) to determine the prevalence of these risk factors in the population. A total of 7,493 adults were interviewed by telephone between 1 July 1996 and 30 June 1997. Results showed that 1.5% drank raw milk, 1.9% ate raw shellfish, 18% ate runny egg, 30% preferred pink hamburger, 93% said they almost always washed their cutting board after cutting raw chicken, and 93% said they almost always washed their hands after handling raw meat or poultry, during 5 days before interview. The results differed by state and demographic group. Consumption of raw shellfish (3.2%) and undercooked hamburger (43%) were more common in Connecticut than other states. Raw milk consumption was more common among people who lived on a farm (8.6%) compared with people who lived in a city or urban area (1.1%). Preference for undercooked hamburger was more common among men (35%), young adults (18 to 25 years, 33%), people with college education (38%), and among people with household income of more than $100,000/year (49%). African-Americans were less likely to prefer undercooked hamburger compared to other racial groups (10% versus 30%). Young adults compared to older adults were less likely to wash their hands after handling raw chicken (88% versus 95%), and men washed their hands less often than women (89% versus 97%). Although there were statistical differences between demographic groups, they are insufficient to warrant targeted educational programs.

Adult↗
PubMed2000

Superoxide generation and tyrosine kinase.

NADPH oxidase is a multi-subunit enzyme complex responsible for superoxide generation in many cells, for example, B-lymphocytes and osteoclasts. NADPH oxidase is localized on the cell surface and generates superoxide extracellularly. After synthesis, components of this oxidase are transported to the cell membrane where the functional NADPH oxidase complex is assembled. The mechanism by which the membrane-bound components are transported to the cell surface of osteoclasts remains unclear. In this study, we examined the role of tyrosine kinase activity in the transport of NADPH oxidase components. When B-lymphocytes and osteoclasts were treated with herbimycin A, a specific inhibitor of tyrosine kinase, superoxide production was significantly decreased. The amount of p91, the catalytic subunit of NADPH oxidase, was decreased in the cellular membrane of herbimycin A treated cells compared to untreated controls. Similar results were obtained for the movement of a regulatory subunit of the NADPH oxidase complex, p47, in B-lymphocytes. Thus, inhibition of tyrosine kinase decreases superoxide production by disrupting the translocation of the NADPH oxidase complex.

Animals↗
PubMed2000

[High resolution time-frequency analysis method for extracting the sleep spindles].

In this paper, a new method for the auto-detection sleep spindle is presented. The method is based on the Discrete Gabor Spectrogram (DGS), a high resolution time-frequency analysis. Sleep EEG5 were processed and the spindles were accurately detected. By, this method the accuracy of auto-detection almost approched the level of visulal detection. Auto-detection of sleep spindles could release the expert from reading long term sleep EEG and provide useful information for sleep studies.

Adult↗
PubMed2000

Evaluation of the Space Collaboration System: its history, image quality and effectiveness for joint case conference.

A joint case-conference was conducted between the Departments of Radiology at Nagoya and Kobe Universities using the Space Collaboration System (SCS), which connects 39 national universities and institutes by communication satellite. In the conference, both sides presented cases using medical images such as those from CT, MRI, and DSA, and the cases were discussed between participants at the two universities. After the final conference, we distributed a questionnaire to solicit responses from the 43 participating radiologists on the quality of the transferred images and their overall impression of the conference. The responses showed that the CT, MRI, and DSA images were clear enough to allow discussion, whereas the plain X-ray images were not. Hence from the standpoint of image quality, the SCS may be unsuited for medical image diagnosis, but useful for presentation of case images in joint conferences and seminars.

Evaluation Studies as Topic↗