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Biomedical subjects

H P Sheng

Publications and source records attributed to H P Sheng.

At least 19 recordsLinked to original sources
PubMed2001

Protective effect of polysaccharides-enriched fraction from Angelica sinensis on hepatic injury.

A polysaccharides-enriched fraction from the root of Angelica sinensis, which is known for its antiulcer action on the gastrointestinal tract, was isolated and studied for its hepato-protective effect in rodents. Intra-gastric administration of Angelica sinensis polysaccharides-enriched fraction (AP) at the doses of 50 or 75 mg/kg dose-dependently prevented liver toxicity induced by acetaminophen in mice but did not affect the serum acetaminophen concentration. It normalized the rises of serum alanine transferase (ALT) and hepatic nitric oxide synthase (NOS) activities and the decrease of glutathione level in the liver. It also reduced the hepatic malondialdehyde (MDA) concentration. The protective effect was less evident in the carbon tetrachloride (CCl4)-treated animals including mice and rats. In the rat the elevated serum ALT level was unaffected though the MDA level was similarly reduced by the higher dose of AP. In these animals, CCl4 increased the hepatic glutathione level instead while the NOS activity remained unchanged. These findings suggest that the pathogenic mechanisms of both acetaminophen and CCl4 are different. AP is more effective in the protection against liver damage induced by acetaminophen, which is associated with the glutathione depletion and nitric oxide synthase activation in the liver.

Acetaminophen↗
PubMed2001

bcl-2 protects HL-60 cells from apoptosis by stabilizing their intracellular calcium pools.

bcl-2 has been shown to enhance cell survival by inhibiting apoptosis induced under different circumstances. In this study we investigated the effects of bcl-2 overexpression on the homeostasis of subcellular organelles such as ER and mitochondria. In our study, HL-60/bcl-2 and control HL-60/neo cells were obtained by transfection of bcl-2 cDNA or the neomycin-resistant gene, respectively. Apoptosis was evaluated by both DNA fragmentation and flow cytometry qualitatively and quantitatively, and the intracellular calcium by Fura-2/AM. Thapsigargin (TG), a highly specific inhibitor of the ER-associated Ca2+ pump, and Br-A23187, a calcium ionophore, were used in this study. Our results showed that overexpression of bcl-2 significantly blocked TG- and Br-A23187-induced apoptosis in calcium containing buffer. Measurement of intracellular calcium showed that bcl-2 overexpression could reduce sustained elevation of cytosolic Ca2+ induced by these agents. However, in calcium-free medium, bcl-2 overexpression maintained Ca2+ uptake in ER of both TG- and Br-A23187-treated cells. Moreover, the depletion of Ca2+ by EGTA enhanced TG- and Br-A23187-induced apoptosis, and reduced the anti-apoptotic action of bcl-2, suggesting that cytosolic Ca2+ elevation may be required for optimal ER pool refilling. These findings suggest that bcl-2 facilitates and maintains the replenishment of Ca2+ in intracellular stores and, as a result, influences the intracellular calcium, thus protecting the cells from death. In addition, there were no cytochrome c release from mitochondria into the cytosol in TG- and Br-A23187- induced apoptosis, suggesting that cytochrome c release is not a universal phenomenon in the apoptotic process.

Apoptosis↗
PubMed2001

Hepatotoxicity of prenatal and postnatal exposure to nicotine in rat pups.

Prenatal and postnatal exposure to nicotine have been shown to affect developing tissues in growing animals. Rat pups were exposed to nicotine prenatally and/or postnatally for 10 days by feeding pregnant and lactating rat dams water containing 0, 54, or 108 microM of nicotine. Nicotine exposure did not affect either litter sizes or body weights at birth and at 10 days of age. Exposure to 108 microM of nicotine prenatally increased significantly the incidence of focal necrosis at birth, and the liver damage was still evident at 10 days of age even after the pups were allowed to suckle dams not exposed to any nicotine during the study period. Continuation of nicotine exposure postnatally increased the incidence and severity of focal and confluent necrosis. Postnatal exposure to 108 microM of nicotine to pups not previously exposed also increased the incidence of mild focal and confluent necrosis, although not significantly. Exposure to nicotine prenatally did not affect liver malondialdehyde (MDA) levels at birth. However, liver MDA was significantly lower in rat pups exposed to nicotine prenatally when they were 10 days of age irrespective of whether there were further exposure to nicotine postnatally. Reasons for the late onset of the low MDA levels need further investigation. Postnatal nicotine exposure to either 54 or 108 microM of nicotine to pups not previously exposed fails to affect liver MDA at 10 days of age. The significant decrease in hepatic superoxide dismutase (SOD) levels reflects those of hepatic injury, indicating the possibility of a nicotine-induced downregulation of SOD enzyme production.

Animals↗
PubMed2000

Telomerase activity is not related to apoptosis in leukemic cell lines.

Any deregulation of apoptosis or an escape from cellular senescence will drive the cells to neoplasia. It remains unclear whether there is a direct linkage between apoptosis and telomerase activity particularly in transformed cell lines. In the present study, we investigated the telomerase activities in three leukemic cell lines (HL-60, U937 and K562) after treating these cells with various doses of antitumor drugs, puromycin or actinomycin D (ActD). Our results showed that HL-60 cells underwent apoptosis rapidly when treated with either 20 microg/ml of puromycin or 5 microg/ml of Act D with more than 60% of the cells becoming apoptotic at 6 hrs and almost 100% at 12 hrs. But telomerase activity analyzed by TRAP assay in these apoptotic cells remained unchanged as compared with the untreated control cells suggesting that whether the cells were apoptotic or not, it had no effect on telomerase activity. However, if lower dosages of the drugs were used, that is, 0.5-1.5 microg/ml of puromycin or 0.01-0.5 microg/ml of Act D, a decrease in telomerase activity was observed at 24-48 hrs, and was completely undetectable at 72 hrs. This decrease in telomerase activity was dose- and time-dependent. The suppression of telomerase activity by low doses of these two drugs is probably due to the inhibitory effect of the drugs on protein translation or RNA transcription rather than direct inhibition of the telomerase activity. Flow cytometry analysis of the cell cycle of the drug-treated cells showed that these drugs unselectively induced apoptosis at all phases of the cell cycle and was unrelated to the changes in telomerase activity. Similar results were observed in U937 and K562 cells except that K562 cells underwent apoptosis more slowly than the former two cell lines.

Antimetabolites, Antineoplastic↗
PubMed2000

Perinatal feedings adversely affect lipogenic activities but not glucose handling in adult rats.

The long-term effects of early under- and overfeeding on glucose metabolism and fat cell lipogenesis were studied. Newborn rats were reared in litter sizes of four, 10, and 16 pups. The amount of milk intake per pup varied inversely with litter sizes. A subgroup of pups from each group was studied at age 20 d, whereas another subgroup was weaned to an ad libitum feeding of standard rat chow and studied at 12 wk of age. There were no differences among groups in food intake on the basis of per gram body weight. Overfeeding during suckling resulted in fatter rats at weaning and in the adults. The higher fat contents in the adipose tissues and carcasses were associated with higher fatty acid synthase and lipogenic activities in the adipose tissues at weaning and 12 wk of age. Differences in plasma insulin and glucose levels among groups were observed only in the 20-d-old rats: basal insulin and glucose levels and 30-min postglucose insulin levels were highest in the overnourished and lowest in the undernourished rats. However, by 12 wk of age, there were no significant differences among groups in their basal insulin and glucose levels and after an oral dose of glucose. Our results suggest that overfeeding or underfeeding during the suckling period affects the glucose-insulin axis only temporarily and not permanently, but early overfeeding permanently enhances fatty acid synthase and lipogenic activities in adipose tissues, resulting in fatter adult rats.

Adipose Tissue↗
PubMed1999

Redistribution of cytochrome c is not an essential requirement in C2-ceramide induced apoptosis in HL-60 cells.

bcl-2 has been shown to enhance cell survival by inhibiting apoptosis. The present study investigates the potential role of bcl-2 on apoptosis in HL-60 cells induced by different agents. HL-60/bcl-2 and control HL-60/neo cells were obtained by transfection of bcl-2 cDNA or the neomycin-resistant gene, respectively. Staurosporine (STS) promoted DNA fragmentation dose-dependently in the 6 h exposure assay while C2-ceramide was relatively slow in the induction of apoptosis (approximately 40% after 24 h) and required higher concentrations (> 20 microM). Caspases inhibitors, Ac-YVAD-cmk (100 microM) and zVAD-fmk (20 microM) had no effect on DNA fragmentation themselves. However, they blocked C2-ceramide-induced caspase-3 cleavage and apoptosis, but not the release of cytochrome c from the mitochondria. In addition, we found that both Ac-YVAD-cmk and zVAD-fmk failed to protect STS-induced apoptosis in HL-60 cells. Overexpression of bcl-2 inhibited STS and C2-ceramide induced cytochrome c redistribution, caspase-3 activation and apoptosis. These results suggest a protective role of bcl-2 in the regulation of apoptosis and cytochrome c release is unlikely to be involved in the final common pathway in apoptosis.

Apoptosis↗
PubMed1998

Lactation increases prolactin receptor expression in spleen and thymus of rats.

Prolactin receptors (PRL-R) are widely expressed on cells of the immune system. During lactation, the increase in serum PRL levels may modify the gene expression of these receptors. Specific PRL binding sites and the expressions of both PRL-R-L and PRL-R-S forms in thymus and spleen of nulliparous control, 10-day postpartum lactating, and 10-day postpartum nonlactating rats were studied. A semi-quantitative RT-PCR technique was used to detect the PRL-R gene transcript in the tissues. Our results showed that specific PRL binding sites and PRL-R-L mRNA and PRL-R-S mRNA were present in the lymphoid tissues with the PRL-R-L mRNA predominant. Lactation markedly increased specific binding sites and PRL-R-L mRNA in both spleen and thymus and only PRL-R-S in spleen. No differences between nulliparous control and postpartum nonlactating rats were observed in any of the parameters measured. The parallel increase in specific PRL binding sites and PRL-R-L mRNA suggests that lactation up-regulates PRL-R expression in lymphoid tissues and may be beneficial to the maternal immune system.

Animals↗
PubMed1998

Lean body mass of well-nourished women is preserved during lactation.

To determine whether the lean body mass of well-nourished women was mobilized to support milk protein output during lactation, the body composition of 10 lactating and 10 nonlactating women was examined longitudinally at 6-wk intervals between 6 and 24 wk postpartum and at 52 wk postpartum, and that of 10 nulliparous women was examined at equivalent intervals, by using clinical anthropometry and whole-body potassium counting. Milk production was determined at 6-wk intervals during the period of exclusive breast-feeding (6-24 wk postpartum) by the test-weighing procedure. Milk composition was determined by chemical analysis. Dietary intakes were determined at 6-wk intervals between 6 and 24 wk postpartum from 3-d food records with use of a nutrient database. Lean body mass was maintained in women who exclusively breast-fed their infants during the first 6 mo postpartum while consuming dietary protein in amounts that exceeded those of their nonlactating counterparts by 55%. The high protein intakes were sustained throughout lactation despite a progressive reduction by 32% of milk protein output. Lean body mass was preserved throughout lactation in well-nourished women, suggesting that the metabolic needs of milk protein production were met solely by higher protein intakes of the lactating women.

Adipose Tissue↗
PubMed1997

Human milk protein does not limit growth of breast-fed infants.

BACKGROUND: The efficiency with which breast- and formula-fed infants utilize dietary nutrients is likely to provide insight into their relative requirements for the growth process. METHODS: We measured longitudinal changes in growth, body composition, and dietary intakes in breast- and formula-fed infants and estimated the gross efficiency with which dietary nitrogen and energy were used for lean body mass and body fat deposition. Lean body mass and body fat were determined in 10 breast-fed and 10 formula-fed infants at 6-week intervals during the first 24 weeks of life by the 18O dilution technique. Dietary nitrogen and energy intakes were determined from the amount of milk and food consumed and the nutrient content of the feedings. The gross efficiency of nutrient utilization was calculated for each infant from the cumulative dietary intake and the change in body composition with time. RESULTS: Length and weight gains and lean body mass and body fat accretion during the first 24 weeks of life were similar between breast- and formula-fed infants despite significantly higher nitrogen and energy intakes of the formula-fed group. The gross efficiency of dietary nitrogen utilization for lean body mass deposition was almost two-fold lower in formula- than in breast-fed infants, whereas the efficiency of dietary energy utilization for lean body mass and body fat deposition was similar between groups. Despite apparent differences in the efficiency of nitrogen utilization, there was no association between lean body mass deposition and dietary protein intake, implying that human milk protein does not limit growth quantitatively in breast-fed infants. CONCLUSIONS: These differences in nutrient utilization illustrate the biologic adaptability of human infants who are equipped with mechanisms that promote normal growth despite the variability of their nutrient intake.

Body Composition↗
PubMed1996

Severe protein deficiency and repletion alter body and brain composition and organ weights in infant pigs.

Three-wk-old genetically lean or obese pigs were used in two experiments to determine the changes in body composition, visceral organs and brain in response to severe protein deficiency. In Experiment 1, 16 obese pigs were fed an adequate (A, 21% protein, 3% fat) or a protein-deficient (D, 5% protein, 23% fat) diet for 7 wk. One-half of each group was killed at 7 wk, and the remainder of each group was fed the A diet for an additional 8 wk. At 7 wk, pigs fed D contained a higher percentage of fat than those fed A (P < 0.01); after 8-wk of repletion, body composition of the two groups was similar. Duodenum, jejunum, and ileum of the protein-deficient pigs had severely atrophic villi, submucosal edema, and atrophic muscle layers; after 8 wk of repletion, however, microscopic architecture of the gastrointestinal tract was restored to normal. Absolute cerebrum weight at 7 wk, but not after 8 wk repletion, in the pigs fed D were significantly less than in pigs fed A, indicating reduced brain cellularity after 7 wk of protein restriction, but not after 8 wk repletion. In Experiment 2, genetically obese (O, n = 8) and lean (L, n = 8) pigs consumed the A or D diet ad libitum for 10 wk. L and O pigs responded similarly to protein deficiency; D pigs were fatter than A pigs and plasma constituents, bone mineral content, bone mineral density and most organ weights revealed no interactions between diet and genotype. The pig model system used in these experiments enabled the isolation of protein deficiency from infectious disease, parasites and social environmental stimulation that may confound interpretation of human infant malnutrition experiments. The data suggest that genetically controlled body fatness is not a major determinant in the response of the infant pig to severe protein deficiency.

Animals↗
PubMed1994

Case report: failure to thrive in a breast-fed infant is associated with maternal dietary protein and energy restriction.

OBJECTIVE: To determine whether failure to thrive in a breast-fed infant could be attributed to altered milk production or composition from a mother who consumed a self-imposed energy- and protein-restricted diet. DESIGN: We evaluated the changes in growth and body composition, dietary intakes, and milk production and composition in a mother-infant pair throughout the first postpartum year. SETTING: The Children's Nutrition Research Center Metabolic Research Unit. SUBJECTS: A breast-feeding mother-infant pair. MEASURES OF OUTCOME: Body composition was measured by total body electrical conductance, dietary intakes by food records, milk production by the test weighing procedure, and milk composition by proximate analyses. RESULTS: A marked decline in the infant's linear and ponderal growth rates occurred when the mother consumed an energy- (20 kcal.kg-1.d-1) and protein- (0.7 g.kg-1.d-1) restricted diet. The retardation in body weight gain was associated with an arrest of body fat, but not lean body mass, accretion. Maternal milk production showed positive relationships with maternal dietary energy (p < 0.01, r = 0.93) and protein (p < 0.05, r = 0.83) intakes. Milk composition reflected changes consistent with those of weaning rather than a sequela of the mother's diet. CONCLUSIONS: We concluded that failure to thrive in a breast-fed infant could be attributed to reduced milk production in conjunction with maternal dietary energy- and protein-restriction and that an assessment of maternal dietary intakes is essential in an evaluation of the breast-fed infant with failure to thrive.

Adipose Tissue↗
PubMed1993

Pre-term infant volume measurements by acoustic plethysmography.

An acoustic plethysmograph has been developed to provide routine total body volume measurements of pre-term (1.5-3.0 kg) infants. It operates near 50 Hz and is excited by band-limited 25 Hz span noise. Excitation, measurement, analysis, and environment are computer controlled for greater accuracy, speed, and objectivity in volume determinations. Performance tests produced volume measurements with a mean per cent error (+/- SD) of 0.77 +/- 0.66% for two phantoms with volumes of 2880 and 2130 cm3. Ten, one-minute volume measurements were obtained for 14 infants over a 20 to 30 min period. Their mean density was 1.061 +/- 0.028 g cm-3 and their weight ranged from 1294 to 2025 g.

Body Composition↗
PubMed1993

Pitfalls of body fat assessments in premature infants by anthropometry.

Subcutaneous fat mass (SFM) and total fat mass (TFM) were estimated in 16 preterm infants at 8 +/- 2 days postnatal age. SFM was estimated from anthropometric measurements: 5 skinfold thicknesses, 5 body circumferences, and regional body lengths. TFM was estimated from total body water measurements using dilution of isotopic water, H2(18)O. The proportion of TFM that was SFM decreased with an increase in TFM. In infants with less than 100 g of TFM (5% body weight), 74% of TFM is in the subcutaneous layer compared with only 35% in infants with higher TFM (more than 100 g). Subscapular skinfold thickness is the best predictor of TFM (r = 0.78). Additional skinfold thickness measurements (triceps, biceps, supra-iliac and thigh) do not improve the predictability of TFM by the subscapular skinfold thickness. We conclude that measurement of subscapular skinfold thickness is an appropriate choice for estimating fat deposition in preterm infants, particularly in field studies and in developing countries.

Adipose Tissue↗
PubMed1992

Neonatal genetically lean and obese pigs respond differently to dietary cholesterol.

The impact of cholesterol exposure in early life on later cholesterol metabolism is not clearly understood. Sixteen newborn genetically lean and obese pigs were fed 0 or 5.0 g cholesterol/kg diet (0 or 0.5%) (liquid diets for 12 d, dry diets thereafter) for 33 d, after which they were all fed 10.0 g cholesterol/kg diet (1.0%) for 23 d. All animals were killed on d 56 and whole-body protein, fat and water were determined on the ground carcass. Dietary cholesterol had no consistent effect on growth rates or body composition. Mean fat content of lean pigs was 15.1% compared with 22.7% for obese pigs; corresponding values were 14.8 and 14.4% for protein and 65.5 and 58.3% for water. Concentrations of plasma total cholesterol, HDL cholesterol and apolipoproteins B and A-1 were increased by 0.5% dietary cholesterol in obese but not in lean piglets, although dietary cholesterol caused HDL and LDL size distribution profiles to shift toward larger-sized components in both strains. Plasma total cholesterol and apolipoprotein B concentrations rose two- to eightfold in all groups after the 1% cholesterol diet was consumed; these changes were accompanied by shifts in LDL and HDL size distribution profiles towards larger-sized components. With 1.0% cholesterol in the diet of all groups, HDL cholesterol concentration increased by approximately 50% in both groups of lean pigs and in obese pigs previously fed cholesterol, but did not increase further in obese pigs previously fed 0.5% cholesterol. The magnitude of the hypercholesterolemic response in lean pigs was blunted by previous exposure to 0.5% dietary cholesterol, but the response was accentuated in obese animals that had been previously exposed to 0.5% dietary cholesterol. These data provide evidence that genetic differences between obese and lean pigs affect their serum lipoprotein responses to high cholesterol intake.

Animals↗
PubMed1992

Extracellular volume estimation from ratios of bromide to chloride in urine or saliva.

Use of either urine or saliva samples to estimate extracellular water volume was investigated in 10 men using nonradioactive bromide (Br) and in seven newborn piglets using radioactive Br (82Br) and chloride (36Cl). The relation to Br to Cl concentrations in urine enabled an estimation of Br dilution volume from human urine (267 +/- 42 ml/kg, mean +/- SD) that was not significantly different (P = 1.0) from the Br dilution volume calculated from plasma Br concentration (268 +/- 20 ml/kg). Although the Br dilution volume estimated from saliva was not different from that of plasma, the error in the estimates of Br dilution volume from saliva was too large (mean difference, -36 +/- 64 ml/kg) to make its use practical. The data from piglets showed good agreement between 82Br and 36Cl dilution volumes calculated from 4-hr plasma samples (356 +/- 14 ml/kg and 347 +2- 12 ml/kg; P greater than 0.1) and between 82Br dilution volumes calculated from urine 82Br:36Cl and plasma 82Br (360 +/- 31 ml/kg and 356 +/- 14 ml/kg; P greater than 0.1). Extracellular water volume can be estimated in both adult and young animals using the Br dilution volume calculated from urine samples. It requires (i) two urine collections: one before and one 4 to 8 hr after administration of Br; (ii) a measurement or estimate of plasma Cl concentration; and (iii) a correction factor that describes the relationship of the ratio of Br to Cl in urine to that ratio in plasma.

Adult↗
PubMed1991

Calcium and phosphorus deficiencies affect mineral distribution in neonatal miniature piglets.

Current efforts to monitor the mineral status of preterm infants fed human milk may not provide sufficient information on the distribution of body minerals. To investigate the body distribution of calcium and phosphorus during various degrees of mineral deficiency, neonatal miniature piglets were raised for 2 wk on diets differing only in calcium and phosphorus. Groups A, B, and C were fed 100%, 60%, and 20%, respectively, of the recommended amounts of calcium and phosphorus that, when adjusted for rates of growth, approximated the range of dietary intakes of preterm infants. Group C manifested biochemical and body-composition evidence of mineral deficiency when compared with group A: lower serum phosphorus; higher serum alkaline phosphatase activity; less fat-free tissue, calcium, and phosphorus in tibiae, vertebrae, and whole carcasses. Neonatal miniature piglets are useful for studying mineral deposition during mineral deficiency in preterm infants.

Alkaline Phosphatase↗
PubMed1991

A comparison of chloride, bromide, and sucrose dilution volumes in neonatal pigs.

Use of 36Cl, 82Br, and [3H]sucrose to estimate extracellular water volume was evaluated in 14 piglets (7-14 days old). 36Cl and 82Br were distributed in approximately the same volume, but a period of 5-6 hr after injection was required to reach equilibrium in the neonatal pig. Dilution volumes calculated before equilibration (2-5 hr) for 36Cl (326 +/- 11 ml/kg) and 82Br (328 +/- 13 ml/kg) were different from equilibration (6-8 hr) phase volumes (356 +/- 13 ml/kg and 355 +/- 13 ml/kg, respectively; P less than 0.001). A 3-hr sample estimated the same volume distribution calculated by extrapolation of the 6- to 8-hr period because of the relationship between the two slopes of the plasma clearance curves. After the 82Br and 36Cl had achieved equilibration, each was distributed in a volume equivalent to total body chloride space (362 +/- 29 ml/kg) measured by neutron activation; no statistical differences were found (P = 0.6). The early equilibration phase measured a 10% smaller, faster exchangeable fraction of total body Cl. Sucrose dilution volume (332 +/- 19 ml/kg) required multiple plasma samples for extrapolation and measured a dilution volume 7% smaller (P less than 0.05) than total body chloride space.

Animals↗