Search PubMed⌕ Search

Biomedical subjects

M L Cheng

Publications and source records attributed to M L Cheng.

At least 19 recordsLinked to original sources
PubMed2001

Development of an SPME/ATR-IR chemical sensor for detection of phenol type compounds in aqueous solutions.

A new method, based on a combination of solid phase micro-extraction (SPME) and attenuated total reflection infrared (ATR-IR) spectroscopy, was developed for the detection of phenols in aqueous solutions. Several types of phenols were studied including phenols attached to methyl, hydroxyl, chlorine and nitro groups, which are environmentally toxic. Because of the polarity of the phenol-type compounds, the performance of six polymers in attracting phenols was investigated. Results indicated that poly(acrylonitrile-co-butadiene) was the most suitable SPME phase among the investigated polymers. To further increase the sensitivity in phenol detection, factors, such as the pH effect, salt effect and thickness of the SPME phase, were investigated. Results indicated that pH values affected the neutral form percentage of the analytes strongly and, hence, affected the detected signals. Due to the acid nature of phenols, phenol detection occurs best in solutions with a low pH value. A two- to three-fold increase in signals was observed after the addition of salt into the solution. The results on the examination of standard curve linearity indicated that the regression coefficients (R2) were higher than 0.996 for four types of phenols. The obtained detection limits for phenols were lower than 200 micrograms L-1 for most of the compounds.

Journal Article↗
PubMed2001

Application of cDNA microarray to the study of arsenic-induced liver diseases in the population of Guizhou, China.

Arsenic is an environmental toxicant and a human carcinogen. Epidemiology studies link human arsenic exposure to various diseases and cancers, including liver diseases and hepatocellular carcinoma. However, the molecular mechanisms for arsenic toxicity and carcinogenicity are poorly understood. To better understand these mechanisms, we used the human cancer cDNA expression array to profile aberrant gene expression in arsenic-exposed populations in Guizhou, China. The selected patients had a history of exposure to environmental arsenic for at least 6-10 years, and had arsenic-induced skin lesions and hepatomegaly. Samples were obtained by liver needle biopsy. Histology showed degenerative liver lesions, such as chronic inflammation, vacuolation, and focal necrosis. The University of North Carolina Hospitals provided normal human liver tissues from surgical resection or rejected transplants. Microarray was performed with total RNA from liver samples, and signal intensities were analyzed with AtlasImage software and normalized with 9 housekeeping genes. Means and SEM were calculated for statistical analysis. Approximately 60 genes (10%) were differentially expressed in arsenic-exposed human livers compared to controls. The differentially expressed genes included those involved in cell-cycle regulation, apoptosis, DNA damage response, and intermediate filaments. The observed gene alterations appear to be reflective of hepatic degenerative lesions seen in the arsenic-exposed patients. This array analysis revealed important patterns of aberrant gene expression occurring with arsenic exposure in human livers. Aberrant expressions of several genes were consistent with the results of array analysis of chronic arsenic-exposed mouse livers and chronic arsenic-transformed rat liver cells. Clearly, a variety of gene expression changes may play an integral role in arsenic hepatotoxicity and possibly carcinogenesis.

Arsenic↗
PubMed2000

Enhanced oxidative stress and accelerated cellular senescence in glucose-6-phosphate dehydrogenase (G6PD)-deficient human fibroblasts.

Glucose-6-phosphate dehydrogenase (G6PD) is involved in the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and the maintenance of the cellular redox balance. The biological effects of G6PD deficiency in nucleated cells were studied using G6PD-deficient human foreskin fibroblasts (HFF). In contrast to that of normal HFF, the doubling time of G6PD-deficient cells increased readily from population doubling level (PDL) 15 to 63. This was accompanied by a significant increase in the percentage of G(1) cells. The slow-down in growth preceded an early entry of these cells into a nondividing state reminiscent of cellular senescence. These cells exhibited a significant increase in level of senescence-associated beta-galactosidase (SA-beta-gal) staining. The importance of G6PD activity in cell growth was corroborated by the finding that ectopic expression of active G6PD in the deficient cells prevented their growth retardation and early onset of senescence. Mechanistically, the enhanced fluorescence in dichlorofluorescin (H(2)DCF)-stained G6PD-deficient cells suggests the possible involvement of reactive oxygen species in senescence. Taken together, our results show that G6PD deficiency predisposes human fibroblasts to retarded growth and accelerated cellular senescence. Moreover, G6PD-deficient HFF provides a useful model system for delineating the effects of redox alterations on cellular processes.

Cell Cycle↗
PubMed2000

Cellular glucose-6-phosphate dehydrogenase (G6PD) status modulates the effects of nitric oxide (NO) on human foreskin fibroblasts.

Glucose-6-phosphate dehydrogenase (G6PD) plays an important role in cellular redox homeostasis, which is crucial for cell survival. In the present study, we found that G6PD status determines the response of cells exposed to nitric oxide (NO) donor. Treatment with NO donor, sodium nitroprusside (SNP), caused apoptosis in G6PD-deficient human foreskin fibroblasts (HFF1), whereas it was growth stimulatory in the normal counterpart (HFF3). Such effects were abolished by NO scavengers like hemoglobin. Ectopic expression of G6PD in HFF1 cells switched the cellular response to NO from apoptosis to growth stimulation. Experiments with 1H-¿1,2,4ŏxadiazolo¿4, 3-aquinoxalin-1-one and 8-bromo-cGMP showed that the effects of NO on HFF1 and HFF3 cells were independent of cGMP signalling pathway. Intriguingly, trolox prevented the SNP-induced apoptosis in HFF1 cells. These data demonstrate that G6PD plays a critical role in regulation of cell growth and survival.

Apoptosis↗
PubMed1999

Humic acid-mediated oxidative damages to human erythrocytes: a possible mechanism leading to anemia in Blackfoot disease.

Humic acid (HA) has been proposed as a factor that causes Blackfoot disease, an endemic peripheral vascular disease prevailing in the southwest coast of Taiwan. However, the relationship between HA and anemia associated with Blackfoot disease remains unclear. In this study, we showed that HA imposed damages on human red blood cells (RBCs), which were manifested as reduction in deformability of RBCs and hemolysis. At concentrations ranging from 10 to 100 microg/ml, HA caused lipid peroxidation in a dose-dependent manner. Such changes were accompanied by a depletion of glutathione and a reduction in activities of the antioxidant enzymes including catalase, superoxide dismutase, and glucose-6-phosphate dehydrogenase. These results indicate that HA initiates oxidative stress on RBCs and results in their dysfunction. Consistent with our previous findings, the present study supports the notion that HA plays an important role in the pathogenesis of Blackfoot disease.

Anemia↗
PubMed1999

Intracranial nasal dermoid sinus cyst associated with colloid cyst of the third ventricle. Case report and new concepts.

A case of a 16-year-old male with both a nasal dermoid sinus cyst (NDSC) and a third ventricle colloid cyst is presented. The NDSC was excised via a single-stage combined intracranial-extracranial approach and the third ventricle colloid cyst was resected endoscopically. The pathogenetic theories of NDSC and third ventricle colloid cyst are discussed, and an embryological explanation for the simultaneous development of the two lesions in this patient is explored. This case is best classified among congenital developmental malformations in a category we propose to call 'anterior neuropore corridor defects.'

Adolescent↗
PubMed1998

The protective effects of traditional Chinese medicine prescription, han-dan-gan-le, on CCl4-induced liver fibrosis in rats.

Han-Dan-Gan-Le, a Chinese medicine preparation composed of Salvia miltorrhiza, Radix paeoniae, Astragalus membranaceus, Stephania tetrandra, and dried leaves of Ginkgo biloba, has been used successfully to treat human liver fibrosis and cirrhosis for years. This study was designed to examine the mechanisms of the protection. Male Wistar rats were given CCl4 (1.2 ml/kg, 2 times/week), 20% fat diet, and 30% alcohol in drinking water (every other day) for 6 weeks. Han-Dan-Gan-Le (0.5 and 1.0 g/kg, p.o., daily for 6 weeks) was administered to rats simultaneously to examine the protective effects against CCl4-induced liver fibrosis. The experimentally-induced liver fibrosis and other morphological alterations were significantly ameliorated by Han-Dan-Gan-Le. Han-Dan-Gan-Le treatments decreased CCl4-induced hepatic collagen accumulation by more than 50%, and significantly increased urinary excretion of hydroxyproline. The CCl4-induced lipid peroxidation in liver and serum was ameliorated as a result of Han-Dan-Gan-Le treatment, possibly by restoring the activity of superoxide dismutase activity in liver and erythrocytes, In conclusion, Han-Dan-Gan-Le is effective in protecting against liver fibrosis. The mechanisms of the protection appear to be due to its antioxidant properties and the modulation of hepatic collagen metabolism.

Animals↗
PubMed1998

Optimal depth and duration of mild hypothermia in a focal model of transient cerebral ischemia: effects on neurologic outcome, infarct size, apoptosis, and inflammation.

BACKGROUND AND PURPOSE: Mild hypothermia is possibly the single most effective method of cerebroprotection developed to date. However, many questions regarding mild hypothermia remain to be addressed before its potential implementation in the treatment of human stroke. Here we report the results of 2 studies designed to determine the optimal depth and duration of mild hypothermia in focal stroke and its effects on infarct size, neurological outcome, programmed cell death, and inflammation. METHODS: Rats underwent a 2-hour occlusion of the left middle cerebral artery. In the first study (I) animals were kept (intraischemically) at either 37 degreesC (n=8), 33 degreesC (n=8), or 30 degreesC (n=8). Study II consisted of 4 groups: (1) controls (37 degreesC, n=10), (2) 30 minutes of hypothermia started at ischemic onset (33 degreesC, n=9), (3)1 hour (33 degreesC, n=8), and (4) 2 hours (33 degreesC, n=8). Brain temperature was measured by a thermocouple probe placed in the contralateral cortex. After suture removal, all animals were rewarmed and reperfused for 22 hours (I) or 70 hours (II). RESULTS: Mild hypothermia to 33 degreesC or 30 degreesC was neuroprotective (17+/-7% and 27+/-6%, respectively) relative to controls (53+/-8%, P<0.02), but 33 degreesC was better tolerated and recovery from anesthesia was faster. The neurological score of hypothermic animals was significantly better than that of controls (I & II) at both 24 and 72 hours postischemia except for the 30-minute group (II), which showed no improvement. In Study II, 2 hours of hypothermia reduced injury by 59%, 1 hour reduced injury by 84% whereas 30 minutes did not reduce injury. Normalized for infarct size, 2 hours of mild hypothermia decreased neutrophil accumulation by 57% whereas both 1 hour and 30 minutes had no effect. At 72 hours, 1 and 2 hours of mild hypothermia decreased transferase dUTP nick-end labeling (TUNEL) staining by 78% and 99%, respectively, and 30 minutes of hypothermia had no effect. CONCLUSIONS: Intraischemic mild hypothermia must be maintained for 1 to 2 hours to obtain optimal neuroprotection against ischemic cell death due to necrosis and apoptosis.

Animals↗
PubMed1997

[The clinical study on treatment of hepatic fibrosis of hepatitis B by IFN-alpha 1 and Chinese medical preparation].

OBJECTIVE: To find the effective method of curing hepatic fibrosis of hepatitis B. METHODS: Using interferon alpha 1 and Chinese medical preparation to treat patients with hepatic fibrosis of hepatitis B and the comprehensive indexes, including levels of laminin, precollagen type III and hyaluronic acid, liver puncture, ultrasonographic and fiber-gastroscopic examination were observed before and after treatment. RESULTS: After 3 months of treatment, the fibrotic indexes lowered obviously, in comparing with those before treatment, the difference was significant (P < 0.001). Liver biopsy, B-type ultrasonographic and fiber-gastroscopic examination proved that the hepatofibrosis was improved. The hepato-fibrotic indexes, blood albumin and globulin level were re-examined after 6 months, results showed that the difference between the IFN-effective group and the IFN-ineffective group was significant, P < 0.001. CONCLUSIONS: Beneficial effect might be obtained by using IFN-alpha 1 to suppress the replication of hepatitis B virus and Chinese medical preparation to treat hepatic fibrosis.

Adult↗
PubMed1995

Changes of protein kinase C subspecies in staphylococcal enterotoxin-B-induced thymocyte apoptosis.

Our previous studies demonstrated that intravenous administration of staphylococcal enterotoxin B (SEB) to BALB/c mice resulted in thymocyte apoptosis. In the present study, we evaluated the role of protein kinase C (PKC) in thymocyte apoptosis induced by SEB. Our results showed that the level of protein phosphorylation in the thymocytes was reduced after the in vivo SEB treatment for 24 h. The activity of classical PKC subspecies was decreased in both cytosolic and membrane fractions of thymocytes following SEB administration. The lowest level of PKC activity was reached by 24 and 48 h, then was recovered gradually after 72 h. Furthermore, the mRNA expression of PKC-beta and, to a much less extent, PKC-alpha, but not PKC-sigma, in thymocytes was reduced by SEB. The decrease of mRNA level of PKC-beta showed good correlation with the pattern of PKC activity. These results provide direct evidence showing the changes in PKC subspecies mRNA expression during the process of apoptosis.

Animals↗
PubMed1992

Distribution of specific apolipoproteins determined by immunoblotting of baboon lipoproteins resolved by polyacrylamide gradient gel electrophoresis.

A method for the quantitative assessment of apolipoprotein distributions among baboon serum lipoproteins is described. The method combines the precise and reproducible separation of lipoproteins by polyacrylamide gradient gel electrophoresis with the specificity of immunoblotting. The method permits the measurement of distributions for any apolipoprotein for which there are antibodies available. Radioactive secondary antibodies are used to expose X-ray film, and distributions are determined by densitometry. Absorbance is linearly related to both antigen and antibody concentrations. The method is reproducible, with the mean coefficient of variation calculated to be 0.118, and has a high repeatability (r2 = 0.97). The immunoblotting method can be employed to measure the fine details of lipoprotein phenotypes as they are influenced by genotype and environment.

Animals↗
PubMed1988

Method for quantitating cholesterol in subfractions of serum lipoproteins separated by gradient gel electrophoresis.

Extensive heterogeneity in particle size distribution of serum lipoproteins of baboons was resolved by a procedure that combined Sudan black B prestaining, polyacrylamide gradient gel electrophoresis (GGE), and quantitative densitometry. Each densitometric scan represented a continuous distribution of the relative amount of cholesterol in a serum sample, as a function of the lipoprotein particle size. For analytical purposes, each scan was divided into 12 fractions, representing 12 particle size ranges. The relationship between the estimated cholesterol concentrations in the summed GGE/densitometric fractions corresponding to very low-density lipoproteins (VLDL) + low-density lipoproteins (LDL) and those corresponding to high-density lipoproteins (HDL) and concentrations measured by the heparin-Mn2+ precipitation/enzymatic procedure was linear over a broad range. However, a systematic overestimation of HDL cholesterol concentration and an underestimation of VLDL + LDL cholesterol concentration was apparent. Therefore, correction factors were developed for adjusting the estimates of VLDL + LDL and HDL cholesterol concentrations obtained by the GGE/densitometric method. This analytical method is rapid, repeatable, economical, and useful for genetic and dietary research in which cholesterol concentrations in multiple particle size ranges of lipoproteins must be measured in large numbers of samples. It also is adaptable to immunoblotting procedures for detecting the distribution of specific apolipoproteins among the size-resolved lipoproteins.

Centrifugation, Density Gradient↗
PubMed1988

Functional response of healthy and diseased glomeruli to a large, protein-rich meal.

Differential solute clearances and hormone assays were used to characterize the effect of a large, protein-rich meal (1.5 g/kg) on glomerular function in 12 healthy volunteers (group I) and 12 patients with chronic glomerular disease (group II). Changes from baseline during 3 h after the meal included an elevation of plasma osmolality, progressive urinary concentration, and increasingly positive fluid balance. Plasma renin activity and arginine vasopressin levels (measured in group II only) increased significantly. Nevertheless, the rate of peak postmeal renal plasma flow became elevated by 13 and 33% in groups I and II, respectively. Corresponding peak increases in postmeal glomerular filtration rate exceeded baseline by 10 and 16%. In the proteinuric subjects of group II the fractional clearances of albumin, IgG and uncharged dextrans in the radius interval 36-54 A, declined significantly after the meal. A similar depression of the fractional dextran-clearance profile was observed also in group I. Applying the fractional clearances of relatively permeant dextrans (radii less than or equal to 44 A) to a model of hindered solute transport through an isoporous membrane, we estimate that transmembrane hydraulic pressure difference increased by 12% in group I and by between 0 to 12% in group II after protein ingestion. We conclude (i) that oral protein ingestion increases glomerular ultrafiltration pressure and rate in both normal and diseased glomeruli, (ii) that this hemodynamic response may be mediated in part by the glomerulopressor hormones angiotensin II and arginine vasopressin, and (iii) that the foregoing hemodynamic changes exert no acute adverse effect on glomerular barrier size-selectivity.

Adult↗
PubMed1987

Detecting genetic effects on lipoprotein phenotypes in baboons: a review of methods and preliminary findings.

Statistical methods for detecting the contribution of major genes to quantitative phenotypes have been widely applied in human family studies. Some of these methods are reviewed, and their application to analysis of an animal model for a human disease is described. Analysis of lipoprotein concentrations in pedigreed baboons provides evidence for genetic effects on specific lipoprotein components that have been associated with reduced susceptibility to atherosclerosis in humans.

Animals↗
PubMed1987

Pregnancy-associated esterase in sera of baboons.

Baboon serum samples were resolved by starch gel electrophoresis and polyacrylamide gradient gel electrophoresis and stained with naphthol substrates for esterase activity. An esterase that hydrolyzed alpha-naphthyl butyrate in preference to alpha-naphthyl acetate was found in very high activities in some individuals but not others. It migrated just cathodal of the albumin band in starch gels. In polyacrylamide gradient gels, it co-migrated with albumin and had an apparent molecular weight of approximately 65,000 daltons. Electrophoretic analysis by gel electrophoresis of random serum samples from male and female baboons indicated that this esterase was present only in the sera of pregnant baboons. Further investigation of serial samples collected from carefully monitored baboons confirmed that the amount of activity of this esterase was correlated with stage of pregnancy. Therefore, it was named pregnancy esterase (PE). PE was detectable by gel electrophoresis and chromogenic staining techniques as early as day 30 of pregnancy; its activity gradually increased with progressive pregnancy and reached maximum activity near full term (182 days). Soon after parturition, the activity of PE decreased rapidly and was not detected in maternal sera by day 14 postpartum. No evidence of PE was detected in sera of pregnant humans.

Animals↗