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Biomedical subjects

B Cheng

Publications and source records attributed to B Cheng.

At least 91 records · Page 5Linked to original sources
PubMed1995

Overtraining following intensified training with normal muscle glycogen.

The purpose of this study was to determine if consumption of appropriate amounts of carbohydrate during a period of increased exercise training would protect the athletes from becoming overtrained. Eight male competitive cyclists were monitored and tested during three training periods: a) normal training (moderate intensity, long duration, 7 d, NORM); b) overtraining (high intensity training, 15 d, OVER); and c) recovery (minimal training, 6 d, REC). Throughout the training 160 g of liquid carbohydrate were consumed within the first 2 h after the daily exercise bout. Mean dietary intake (NORM = 13.7 +/- 1.6, OVER = 14.1 +/- 1.0 MJ.d-1) and carbohydrate percent (NORM = 64.0 +/- 2.1, OVER = 67.4 +/- 2.5%) were not different during the different training periods. Similarly, resting muscle glycogen levels were not different (NORM = 530.9 +/- 42.5, OVER = 571.2 +/- 27.5 mumol.g-1 dry weight). Five criteria were used to determine if overtraining occurred in a subject (decreased maximal workload, maximal heart rate, ratio of maximal lactate to rating of perceived exertion (HLa:RPE), and resting plasma cortisol levels, increased affirmative response to a daily questionnaire). All subjects met at least three of the five criteria and thus were classified as overtrained. Therefore, short-term overtraining may occur even when resting muscle glycogen levels are maintained.

Adult↗
PubMed1995

PDGFs protect hippocampal neurons against energy deprivation and oxidative injury: evidence for induction of antioxidant pathways.

Platelet-derived growth factors (PDGFs) and PDGF receptors are expressed in brain, where their functions are largely unknown. We tested the hypothesis that PDGFs play a role in promoting the survival of neurons exposed to metabolic and oxidative insults. Exposure of rat and mouse hippocampal cell cultures to glucose-deficient medium or the hydroxyl radical-promoting agent FeSO4 resulted in progressive neuronal loss. Pretreatment of cultures with PDGF-AA or PDGF-BB resulted in highly significant attenuation of glucose deprivation- and FeSO4-induced neuronal degeneration. In each injury paradigm the neuroprotective actions of the PDGFs were concentration dependent (3-100 ng/ml). In the case of glucose deprivation, significant protection was seen when cells were exposed to PDGFs prior to, or up to 8 hr following, the onset of glucose deprivation. Pretreatment with PDGFs was required for protection against FeSO4-induced oxidative injury. Western blot and immunocytochemical analyses demonstrated that cultured embryonic hippocampal neurons expressed both PDGF alpha- and beta-receptors. PDGFs induced tyrosine phosphorylation of several proteins including a band at 180 kDa, the molecular weight of PDGF receptors. Induction of peroxide accumulation in neurons by FeSO4 was attenuated in cultures pretreated with PDGFs, suggesting that PDGFs enhanced cellular antioxidant mechanisms. Measurements of anti-oxidant enzyme activities in control and PDGF-treated cultures showed that both PDGF-AA and PDGF-BB increased both catalase and glutathione peroxidase activities, and PDGF-AA also increased superoxide dismutase activities. These findings suggest that PDGFs, which are widely expressed in brain and induced in response to injury, may play roles in protecting neurons against metabolic and oxidative insults.

Animals↗
PubMed1995

[The results of operative treatment of diastematomyelia].

From May 1978 to July 1993, 31 cases of diastematomyelia were treated surgically. There were 7 males and 24 females, 2 to 34 years old. The follow-up period varied from 2 month to 14.4 years. All patients were couplicated by congenital spinal deformity. Three of them had two septums. The results of operative treatment of the 31 cases were: recovery in 10 cases, remarkable effectiveness in 5, effectiveness in 11, noneffectiveness in 5. The effective rate was 84%. The operative indications and key points were also discussed.

Adolescent↗
PubMed1995

[Anatomical study on the Riolan's anastomosis arch].

The Riolan's anastomosis arch is discussed on the basis of colon vessel constructions in 162 operations of the colonic interposition for esophageal substitution, and the materials reported in some journals. The Riolan's arch is not the marginal vessels of the flexura lienalis, because of its lower incidence (< 10%). We believe that the integrity of the arch is not responsible for the blood supply of the colon.

Arteries↗
PubMed1995

[Comparative study on pharmacological effects of various species of Pueraria].

Through comparative studies on the acute toxicity of four species of Pueraria, it was found that the toxicity of P. peduncularis was the highest, followed by P. lobata and P. omeiensis, and that of P. thomsonii was the lowest. The inhibitory effects of P. lobata, P. omeiensis and puerarin on the fever induced by 2,4-dinitrophenol in rats were very fast and significant, maintaining for about 8 hours, while the effect of P. thomsonii is relatively weak. As for influence upon the degrees of myocardiac ischemia induced by pituitrin, P. omeiensis appeared to be the most potent, and P. thomsonii the least one, while P. lobata and puerarin were intermediate between the above two. Summarily, the antipyretic and anti-myocardiac ischemia effects of P. lobata and P. omeiensis are stronger than those of P. thomsonii, and puerarin is one of their effective components.

2,4-Dinitrophenol↗
PubMed1994

Neurotrophin-4/5 protects hippocampal and cortical neurons against energy deprivation- and excitatory amino acid-induced injury.

Neurotrophin-4/5 (NT-4/5) is a recently discovered member of the neurotrophin family of neurotrophic factors which includes NGF, BDNF and NT-3. NT-4/5 is expressed in the brain where its function is unknown. We have found that NT-4/5 can protect cultured embryonic rat hippocampal and cortical neurons against glucose deprivation-induced injury. Significant protection was observed with NT-4/5 concentrations from 100-1000 ng/ml, with a dose-response curve similar to that of BDNF. Neuronal vulnerability to glutamate toxicity was significantly reduced in cultures pretreated with NT-4/5. Moreover, neurons pretreated with NT-4/5 were more resistant to toxicity induced by calcium ionophore A23187, demonstrating that NT-4/5 increases neuronal resistance to calcium-mediated injury. These data indicate that, as with other neurotrophins, NT-4/5 may serve a neuroprotective function in the brain.

Animals↗
PubMed1994

NT-3 and BDNF protect CNS neurons against metabolic/excitotoxic insults.

Neurotrophin-3 (NT-3) and brain-derived neurotrophic factor (BDNF) were recently shown to have biological activity in central neurons. In the present study, NT-3 and BDNF attenuated glucose deprivation-induced neuronal damage dose-dependently in rat hippocampal, septal and cortical cultures. Direct measurements of intraneuronal free calcium levels ([Ca2+]i) and manipulations of calcium influx demonstrated that NT-3 and BDNF each prevented the elevation of [Ca2+]i that mediated glucose deprivation-induced injury. Studies in cultures depleted of glia indicated a direct action of NT-3 and BDNF on neurons. Neurons pretreated with NT-3 or BDNF for 24 hr were more resistant to glutamate neurotoxicity, and showed attenuated [Ca2+]i responses to glutamate. TrkB (BDNF receptor) and trkC (NT-3 receptor) proteins were present in hippocampal, cortical and septal cultures where they were localized to neuronal cell bodies and neurites. The data demonstrate that NT-3 and BDNF can protect neurons against metabolic and excitotoxic insults, and suggest that these neurotrophins may serve [Ca2+]i-stabilizing and neuroprotective functions in the brain.

Animals↗
PubMed1994

Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis.

Emerging data indicate that neurotrophic factors and cytokines utilize similar signal transduction mechanisms. Although neurotrophic factors can protect CNS neurons against a variety of insults, the role of cytokines in the injury response is unclear. We now report that TNF beta and TNF alpha (1-100 ng/ml) can protect cultured embryonic rat hippocampal, septal, and cortical neurons against glucose deprivation-induced injury and excitatory amino acid toxicity. The elevation of intracellular calcium concentration ([Ca2+]i) induced by glucose deprivation, glutamate, NMDA, or AMPA was attenuated in neurons pretreated with TNF beta. The mechanism whereby TNFs stabilize [Ca2+]i may involve regulation of the expression of proteins involved in maintaining [Ca2+]i homeostasis, since both TNF beta and TNF alpha caused a 4- to 8-fold increase in the number of neurons expressing the calcium-binding protein calbindin-D28k. These data suggest a neuroprotective role for TNFs in the brain's response to injury.

Animals↗