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Biomedical subjects

K M Chung

Publications and source records attributed to K M Chung.

32 records · Page 2Linked to original sources
PubMed1997

Hepatitis C virus nonstructural protein 5A contains potential transcriptional activator domains.

Hepatitis C virus (HCV), a major etiologic agent of transfusion associated hepatitis, is a positive, single-stranded RNA virus and is also known to be implicated in liver cirrhosis and hepatocellular carcinoma. Nonstructural protein 5A (NS5A) of HCV contains acidic and proline-rich amino acids in its carboxy-terminal half. These structural features resemble eukaryotic transcription activators. In this report, we show that NS5A functions as a potent transcriptional activator when fused to the yeast (Saccharomyces cerevisiae) GAL4 DNA-binding domain (1-147). The potential transcriptional activator maps to the C-terminal half of NS5A in the yeast cell. Therefore, our data provides the first evidence that NS5A may modulate host cell function at the transcriptional level.

Gene Expression Regulation, Viral↗
PubMed1997

Markers of bone and cementum formation accumulate in tissues regenerated in periodontal defects treated with expanded polytetrafluoroethylene membranes.

Guided tissue regeneration (GTR) is a concept that evolved from the development of membrane-barrier techniques, which allow the repopulation of periodontal wounds by specific cells, resulting in a new attachment apparatus. To help understand the biological mechanisms involved in membrane barrier-led periodontal healing, the present study investigated the macromolecules phenotypic of bone and cementum formation in tissues grown under the GTR barrier by immunolocalization. Periodontal regeneration was initiated by placing barriers on experimentally induced periodontal defects in a Rhesus monkey model. Samples were harvested 6 wk after healing and sections of soft tissues grown under GTR barriers (membrane tissue) were stained with antibodies to bone morphogenetic proteins-2 and 4 (BMP-2, BMP-4), bone morphogenetic protein-7 (OP-1), cementum attachment protein (CAP), osteonectin (OTN) and bone sialoprotein (BSP). Tissues grown in the absence of any barrier device served as a control (control tissue). Membrane periodontal tissues from beneath the ePTFE membrane were comprised of spindle-shaped fibroblast-like cells encased in a dense fibrillar extracellular matrix (ECM). Round-shaped cells aggregated to form nodules. Newly formed hard tissue was conspicuous. A similar, but very disorganized, fiber network was observed in control tissues, but neither nodule formation nor hard tissue was observed. Osteonectin staining was observed in the ECM of membrane tissues and particularly in the area of the connective tissue adjacent to newly formed hard tissue. The dense network of connective tissue fibers was also stained. In control tissues, cells and fiber network had a significantly weaker signal for osteonectin. An intense reaction was observed in membrane tissues stained for BSP, particularly the connective tissue adjacent to the newly formed hard tissue, while the control tissues did not stain for BSP. Cementum attachment protein (CAP) was observed in the connective tissue adjacent to the newly formed hard tissue of the membrane tissues whereas control tissues exhibited no CAP staining. In membrane tissues, BMP-2 and 4 distribution was found to concentrate in nodule areas, in the newly formed hard tissue and in the fiber network, while very faint staining was observed in control sections. The distribution of OP-1 in membrane and control tissues was found to mimic the BMP-2 pattern, but staining was more distributed in hard tissue matrix. When the profile of BMP-2, BMP-4, OP-1, OTN, CAP and BSP staining was analyzed on membrane tissue sections, striking similarities were noted in the connective tissue adjacent to the newly formed hard tissue and in nodular areas. In addition, the localization of BMP-2 and BMP-4 mRNA was investigated in both tissues by in situ hybridization. An intense expression of BMP-2 and 4 transcripts was observed in membrane tissues while control tissues never yielded any positive hybridization signal. The correlation between these histochemical findings strongly suggests that the forming soft tissues under ePTFE membranes contain cells and ECM macromolecules normally associated with bone and cementum.

Alveolar Process↗
PubMed1997

Acute appendicitis---a recent audit of an old problem.

We conducted a retrospective review of all patients who had an appendicectomy performed at the Queen Elizabeth Hospital, Hong Kong, from January 1993 through December 1994. The diagnostic accuracy for true appendicitis was 74%. Nine per cent of patients had other pathologies, which also needed exploration. The diagnostic accuracy in female patients was 66%, compared with 82% for male patients (P<0.0001). Female patients aged between 15 to 40 years were diagnosed accurately 62% of the time, which has significantly lower than the rate for other female patients (P=0.016). the overall morbidity and mortality rates were 9.2% and 3%, respectively. Complicated appendicitis had a higher morbidity rate of 21%, compared with 9% for uncomplicated appendicitis (P<0.0001). Results for patients who were operated on the day of admission were compared with those who were operated on the day after admission. No significant difference in diagnostic accuracy (P=0.46), percentage of complicated appendicitis (P=0.7), and morbidity rate (P=0.8) was found.

Journal Article↗
PubMed1996

Nicotine enhances morphine- and beta-endorphin-induced antinociception at the supraspinal level in the mouse.

The effect of nicotine administered supraspinally on antinociception induced by supraspinally administered opioids was examined in ICR mice. The intracerebroventricular (i.c.v.) injection of nicotine alone at doses from 1 to 12 micrograms produced only a minimal inhibition of the tail-flick response. Morphine (0.2 micrograms), beta-endorphin (0.1 microgram), D-Pen2.5-enkephalin (DPDPE; 0.5 microgram), trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl) cyclohexyl] benzeocetamide (U50, 488H; 6 micrograms) caused only slight inhibition of the tail-flick response. Nicotine dose dependently enhanced inhibition of the tail-flick response induced by i.c.v. administered morphine (0.2 microgram) or beta-endorphin (0.1 microgram). The degree of enhancing effect of nicotine toward beta-endorphin-induced inhibition of the tail-flick response was greater than toward morphine-induced inhibition of the tail-flick response. However, i.c.v. administered nicotine at the same doses was not effective in enhancing the inhibition of the tail-flick response induced by DPDPE (0.5 microgram) or U50, 488H (6 micrograms) administered i.c.v. Our results suggest that stimulation of supraspinal nicotinic receptors may enhance antinociception induced by morphine (a mu-opioid receptor agonist) and beta-endorphin (an epsilon-opioid receptor agonist) administered supraspinally. However, the activation of nicotinic receptors at supraspinal sites may not be involved in enhancing the antinociception induced by DPDPE (a delta-opioid receptor agonist) or U50, 488H (a kappa-opioid receptor agonist) administered supraspinally.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1996

Differential effects of forskolin and phorbol-13-myristate injected intrathecally or intracerebroventricularly on antinociception induced by morphine or beta-endorphin administered intracerebroventricularly in the mouse.

The effects of forskolin or phorbol-13-myristate (PMA) injected intrathecally (i.t.) or intracerebroventricularly (i.c.v.) on the inhibition of the tail-flick and hotplate responses induced by morphine or beta-endorphin administered i.c.v. were studied. Animals pretreated with forskolin (20 micrograms) i.t. for 10 min had an attenuated inhibition of the tail-flick response induced by i.c.v. administered morphine (2 micrograms) or beta-endorphin (1 microgram). However, i.t. pretreatment with PMA (100 ng) was not effective in reducing the inhibition of the tail-flick response induced by morphine or beta-endorphin administered i.c.v. In addition, i.t. pretreatment with either forskolin or PMA did not affect the inhibition of the hotplate response induced by morphine or beta-endorphin administered i.c.v. Forskolin pretreatment i.c.v. for 10 min attenuated the inhibition of the tail-flick and hotplate responses induced by i.c.v. administered morphine or beta-endorphin. However, i.c.v. pretreatment with PMA was not effective in reducing the inhibition of the tail-flick or hotplate responses induced by morphine or beta-endorphin administered i.c.v. Our results suggest that activation of adenylate cyclase located at both spinal and supraspinal sites appears to be involved in antagonizing antinociception induced by morphine and beta-endorphin administered supraspinally. However, spinal or supraspinal protein kinase C may not be involved in antagonizing antinociception induced by morphine or beta-endorphin administered supraspinally.

Adenylyl Cyclases↗
PubMed1996

Prevalence of visual disorders in Chinese schoolchildren.

We performed a vision screening of 1883 Chinese schoolchildren from 4 schools around Kuala Lumpur in June 1990. The group contained 1083-males and 800 females. Visual acuity, refractive error, oculomotor balance, and axial length were measured. The prevalence of myopia in Chinese schoolchildren was found to be 37% in the 6- to 12-year age group and 50% in the 13- to 18-year age group. Approximately 63% of the sample had unaided visual acuity of 6/6 or better and 24% had unaided acuity of 6/12 or worse. Six hundred twenty-five students (33%) failed the vision screening test and were referred for further examinations. The group which failed the vision screening test and had the highest rate of referral (46%) was the 11- to 12-year-old age group. The most common visual disorder was uncorrected myopia, accounting for 38% of the referrals (235 students). Only 26% of the sample were wearing a spectacle correction.

Adolescent↗
PubMed1995

Molecular and cellular biology research in periodontal regeneration and its clinical implication.

The mechanisms by which new periodontium is established on root surfaces previously exposed by periodontal disease have been an area of active research interest. Recently, histological examination of periodontal regeneration has revealed a complex process orchestrated by temporo-spatial specific cell-matrix interactions. Advances in cell and molecular biology techniques have provided invaluable tools to investigate the cascade of events occurring during periodontal regeneration. This paper will provide an overview of current understanding of the cellular and molecular aspects of periodontal repair and regeneration and its implication in applied research resulting in clinical application.

Extracellular Matrix↗
PubMed1994

Effects of intrathecal or intracerebroventricular pretreatment with pertussis toxin on antinociception induced by beta-endorphin or morphine administered intracerebroventricularly in mice.

We have previously demonstrated that beta-endorphin and morphine, when administered supraspinally, produce antinociception by activating different descending pain inhibitory systems in both rats and mice. However, the signal transduction mechanisms involved in the descending pain-inhibitory systems that are activated by beta-endorphin and morphine administered intracerebroventricularly (i.c.v.) have not been characterized. Therefore, in the present study, the effects of intrathecal (i.t.) and i.c.v. pretreatments with pertussis toxin (PTX) on antinociception induced by beta-endorphin or by morphine administered i.c.v. were studied in ICR mice. Antinociception was assessed by the tail-flick assay and by the hot-plate assay. Intrathecal pretreatment with PTX (0.5 microgram) for 6 days effectively reduced the inhibition of the tail-flick response induced by beta-endorphin (1 microgram) or by morphine (1 microgram) administered i.c.v. However, i.t. pretreatment with PTX was not effective in reducing the inhibition of the hot-plate response induced by beta-endorphin or by morphine administered i.c.v. Intracerebroventricular pretreatment with PTX (0.5 microgram) for 6 days effectively reduced the inhibition of the tail-flick and hot-plate responses induced by morphine (1 microgram), but not that induced by beta-endorphin (1 microgram), administered i.c.v. Our results suggest that there are PTX-sensitive G proteins coupled to the spinal descending pain inhibitory systems that are activated by beta-endorphin and morphine administered i.c.v. At a supraspinal level, i.c.v. morphine- but not beta-endorphin-induced antinociception is mediated by PTX-sensitive G proteins.

Analgesics↗
PubMed1994

Clinical implications of cellular biologic advances in periodontal regeneration.

It is known that periodontal tissues retain the ability to regenerate; however, current therapies fail in achieving predictable and consistent regeneration. Cell and molecular biology research in periodontal regeneration hold great promise in providing improved understanding of this complex phenomenon and direct us towards new possibilities of future clinical application. This paper reviews both the cells and extracellular matrix of the periodontal ligament in addition to the cell-to-matrix and cell-to-cell interaction involved in periodontal regeneration. Results of recent studies have suggested that periodontal regeneration recapitulates the process of morphogenesis, histogenesis, and cytodifferentiation, as well as cell field migration that occurs during development of the periodontium. A small population of purported periodontal stem cells is believed to be responsible for maintaining homeostasis in the periodontal ligament. This cell, which may have its origin in late periodontal mesenchyme of the dental papilla, is advocated as a tripotential cell capable of differentiating into cementoblast, osteoblast, and periodontal fibroblast. The clinical implication of advances made in cell and molecular biology research in periodontal regeneration may include future use of biomolecules in periodontal regeneration may include future use of biomolecules to improve the regenerative healing process and use of bioactive degradable membrane barriers in guided tissue regeneration as well as seeding of periodontal stem cells into periodontal defects. If the current trend continues, clinicians can look forward to seeing periodontal wound healing being substantially enhanced to achieve predictable periodontal regeneration.

Cell Communication↗
PubMed1990

Clinical evaluation of a biodegradable collagen membrane in guided tissue regeneration.

A bio-resorbable type I collagen membrane was investigated as a barrier for guided tissue regeneration. Ten human subjects with at least one pair of contralateral periodontal lesions with probing pocket depths of greater than or equal to 5 mm and radiographic evidence of greater than or equal to 40% bone loss were included. Each patient underwent contralateral surgical flap procedures. A collagen barrier was adapted to the tooth in the experimental defect and the flap replaced and sutured. The controls consisted of the same procedure without the placement of the barrier. Standardized measurements of change in probing attachment levels and fill of intrabony defects were obtained at the time of surgery and 1 year later at the time of surgical re-entry. The differences in change of probing attachment levels and amount of bone fill between individual test and control sites were compared utilizing the student's t-test for paired samples. The mean probing attachment gain in the test sites was 0.56 +/- 0.57 mm, and there was a mean probing attachment loss of 0.71 +/- 0.91 mm in the control sites (P less than 0.01). The gain of bone in test lesions was 1.16 +/- 0.95 mm, while no gain was observed in the control lesions (P less than 0.01). The results of this study demonstrated that sites treated with a collagen barrier comprised of cross-linked bovine Type I collagen exhibited significantly better healing as compared to control sites over the 1-year period of the study.

Adult↗
PubMedDate not supplied

Supraspinal NMDA and non-NMDA receptors are differentially involved in the production of antinociception by morphine and beta-endorphin administered intracerebroventricularly in the formalin pain model.

Our previous studies have demonstrated that supraspinal glutamate receptors are differentially involved in the antinociception induced by morphine and beta-endorphin given intracerebroventricularly (i.c.v.) in the tail-flick and hot-plate tests. The formalin pain test was used in the present study. Injection of mice with formalin solution (2%, 10 microl) into the hindpaw intraplantarly produced the first (0-5 min) and second (20-40 min) phases of formalin responses. The formalin responses in the both phases were attenuated dose-dependently by morphine (0.125-1 microg) or beta-endorphin (0.125-1 microg) administered i.c.v. 5 min before. The antinociceptive effect of morphine was slightly more potent in the second phase whereas the effect of beta-endorphin was more pronounced in the first phase. MK-801 (0.1-1 microg), a non-competitive NMDA receptor antagonist, and CNQX (0.05-0.5 microg), a non-NMDA antagonist, given i.c.v., produced antinociceptive effect in the both phases, but only in a partial manner. Both MK-801 (0.05 microg) and CNQX (0.01 microg), at the dose which had no intrinsic effect, reversed the antinociceptive effect of beta-endorphin (1 microg) observed during the second, but not the first, phase partially but significantly. However, the antinociceptive effect of morphine (1 microg) was not affected by the same dose of MK-801 or CNQX given i.c.v. Our results indicate that, at the supraspinal level, both NMDA and non-NMDA receptors are involved in the production of antinociception induced by supraspinally administered beta-endorphin, but not morphine, in the formalin pain model.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMedDate not supplied

Pretreatment with cholera or pertussis toxin differentially modulates morphine- and beta-endorphin-induced antinociception in the mouse formalin test.

The present study was designed to examine the possible involvement of supraspinal CTX- and PTX-sensitive G-proteins in an opioid-induced antinociception in the formalin test. Morphine (1 microg) and beta-endorphin (1 microg) given i.c.v. displayed near-maximal inhibitory effects against the formalin response in the first (0-5 min) and the second (20-40 min) phases. CTX (0.1-0.5 microg) pretreated i.c.v. produced antinociceptive effects in both phases of the formalin responses. Its effect was more pronounced in the first phase. However, PTX (0.05-0.5 microg) injected i.c.v produced the antinociceptive effect only in the first, but not the second, phase. Both CTX (0.5 microg) and PTX (0.5 microg), at the dose which had no intrinsic effect, significantly reversed the beta-endorphin-induced antinociceptive effect observed during the second, but not the first, phase. However, the antinociceptive effect by morphine failed to be affected by the same dose of treatment with CTX or PTX. Our results indicate that, at the supraspinal level, CTX- and PTX-sensitive G-proteins appear to be involved in the modulation of antinociception induced by supraspinally administered beta-endorphin, but not morphine, in the formalin pain model.

Analgesics, Opioid↗