Biomedical subjects

B Cheng

Publications and source records attributed to B Cheng.

At least 73 records · Page 4Linked to original sources

PubMed1996

[An epidemiologic study on the aetiological factors of primary liver cancer in Shunde City of Guangdong province].

In order to investigate the aetiological factors of Primary Liver Cancer (PLC) in Shunde City of Guangdong province, 96 clinically diagnosed PLC patients and 144 matched hospital controls were interviewed and their blood samples were examined for HBV, HCV and other seven indices. Monofactorial and multifactorial analyses were fitted by using Non-conditional Logistic Regression model. The findings confirmed the strong association between HBV infection and PLC. Histories of hepatitis and histories of eating raw fish, shrimp or salt fish were also noticed. The history of alcohol intake might have associated with PLC. The present study did not find associations between PLC and drinking water, histories of blood transfusion and injection- or exposure to insecticides. Antibody of HBV surface antigen seemed to be a protective factor with a relative risk of 0.3064 (0.1647-0.5701). The results showed that the combined effects of HBsAg infection and HCV infection were worthy for further study.

Case-Control Studies↗

PubMed1996

[A study on the change of myocardial neuropeptide Y release induced by electric stimulation and myocardial ischemia in guinea pig heart].

Electrical stimulation of the left stellate ganglion in guinea pig heart evoked a calcium-dependent, exocytotic release of neuropeptide Y (NPY). Stimulation after 10 min of global ischemia (S2), compared with control period stimulation (S1), had no significant effect on the NPY release. The release of NPY produced by the same stimulation after 20 min of ischemia was inhibited to certain extent (S2/S1: 0.72, P < 0.05), whereas the inhibition of NPY release disappeared after 5 min of reperfusion (with a S2/S1 of 1.01). Ischemia alone, without electric stimulation, did not apparently induce NPY release, suggesting that electrical stimulation may induce a calcium-dependent, exocytotic release of NPY. It is further suggested that the inhibition of NPY release may be produced by some metabolites and the abolishment of the inhibition after reperfusion may be due to washout of the metabolites.

Animals↗

PubMed1996

[Surgical treatment of primary epicardial tumors].

Seven cases of primary epicardial tumors of 3200 cardiac operation cases were diagnosed definitely, including benign in 5, malignant in 2. Among them, readical resection was performed in 5 cases, partial resection in 1, and decompression of pericardium in 1. Data of this series were often regarded as tuberculous pericarditis or others incorrectly. UCC, CT and MRI were helpful in diagnosis. The authors emphasize early surgical treatment as soon as possible and using the different methods of operation whether to utilize cardiopulmonary bypass or not according to site, size and characteristics of tumors to resect tumors, if necessary, reconstruction the heart wall to maintain blood follow dynamics. The prognosis of the diseases was related to the pathology and the area of invasion of tumors.

Adolescent↗

PubMed1995

Brain injury and tumor necrosis factors induce calbindin D-28k in astrocytes: evidence for a cytoprotective response.

Calbindin is a 28 kDa calcium-binding protein expressed in restricted neuronal populations in the mammalian brain where it may play a role in protecting neurons against excitotoxic insults. Recent findings indicate that electrical activity and some neurotrophic factors can induce the expression of calbindin in neurons. We now report that brain injury, effected by systemic administration of the excitotoxin kainate or mechanical trauma, induces expression of calbindin in cells of the corpus callosum and subcortical white matter. Immunohistochemical analysis using antibodies to the astrocyte-specific proteins (glial fibrillary acidic protein and S-100 beta) established the identity of calbindin immunoreactive cells as astrocytes. Because brain injury is known to induce the expression of several neurotrophic factors and cytokines, we employed cultures of hippocampal and neocortical astrocytes to test the hypothesis that such factors can induce expression of calbindin in astrocytes. Tumor necrosis factors (TNF alpha and TNF beta), cytokines that are expressed in response to brain injury, induced the expression of calbindin in cultured rat hippocampal and neocortical astrocytes. Two neurotrophic factors, basic fibroblast growth factor and nerve growth factor, did not induce calbindin in astrocytes. TNF-treated, calbindin-expressing astrocytes were resistant to acidosis and calcium ionophore toxicity, suggesting that TNFs and calbindin may serve a cytoprotective role in astrocytes in the injured brain.

Animals↗

PubMed1995

Diaqua(5,10,15,20-tetraphenylporphinato)iron(III) Perchlorate, [Fe(C44H28N4)(H2O)2]ClO4.

The crystal structure of a new crystal form of [Fe(TPP)(H2O)2]ClO4 has been determined. The asymmetric unit contains one molecule in a general position and a half molecule with required inversion symmetry. The two independent molecules have almost identical average values for the equatorial Fe-Np bond lengths [2.029 (4) and 2.028 (6) A], and the axial Fe-O bond lengths are 2.140 (2) and 2.121 (3) A for molecule 1 (in a general position) and 2.126 (2) A for molecule 2 (in a special position). A brief comparison of the core structure and hydrogen-bonding environment of this molecule with two other crystal forms is described.

Crystallography, X-Ray↗

PubMed1995

(2,3,7,8,12,13,17,18-Octaethylporphinato)perchloratomanganese(III).

The crystal structure of [Mn(OEP)(OClO3)] (where OEP = C36H44N4) has been determined. The axial Mn-O bond length is 2.183 (2) A and the equatorial Mn-Np bond lengths have an average value of 2.000 (5) A. The molecules form weak dimers in the solid state with interring distances of 3.49 A and a lateral shift of 3.27 A. The compound is found to be isomorphous with the iron derivative [Fe(OEP)(OClO3)]. A brief comparison of the structural parameters for the two molecules is given.

Chemical Phenomena↗

PubMed1995

Aging in rats is associated with an increase in adrenal apolipoprotein E.

Extrahepatic tissues including the adrenal cortex are capable of synthesizing apolipoprotein E (apoE). Locally synthesized apoE is believed to affect cellular uptake, transport and redistribution of cholesterol within that organ. We and another laboratory have previously reported that the adrenal cortex of aged rats has an elevated cholesteryl ester content. The aim of this work was to investigate whether this elevation is accompanied by increased adrenal apoE levels in aged rats. A Western blotting technique with polyclonal goat anti-human-apoE antiserum was employed as a probe for studies. The results showed that: (a) anti-human-apoE antiserum not only detected apoE in human plasma and adrenal homogenate, but also cross-reacted with a protein (or proteins) resembling apoE in rat plasma and adrenal homogenate (or supernatant) with a molecular weight of 34,000-36,000; (b) rat adrenal apoE concentration (per unit weight of protein) increased with age; (c) the increase did not result from blood trapped in the gland, because after organ perfusion the adrenal of aged rats persistently exhibited 58% more apoE than that of young animals. In conclusion, rat adrenal apoE concentration appears to increase with age. Whether this increase mechanistically causes the accumulation of cholesteryl esters in the aged rat adrenal remains to be investigated.

Adrenal Cortex↗

PubMed1995

Basic fibroblast growth factor selectively increases AMPA-receptor subunit GluR1 protein level and differentially modulates Ca2+ responses to AMPA and NMDA in hippocampal neurons.

The excitatory neurotransmitter glutamate is believed to play important roles in development, synaptic plasticity, and neurodegenerative conditions. Recent studies have shown that neurotrophic factors can modulate neuronal excitability and survival and neurite outgrowth responses to glutamate, but the mechanisms are unknown. The present study tested the hypothesis that neurotrophic factors modulate responses to glutamate by affecting the expression of specific glutamate-receptor proteins. Exposure of cultured embryonic rat hippocampal cells to basic fibroblast growth factor (bFGF) resulted in a concentration-dependent increase in levels of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)-receptor subunit GluR1 protein as determined by western blot, dot-blot, and immunocytochemical analyses. In contrast, bFGF did not alter levels of GluP2/3, GluR4, or the NMDA-receptor subunit NR1. Nerve growth factor did not affect GluR1 levels. Calcium-imaging studies revealed that elevation of [Ca2+]i, resulting from selective AMPA-receptor activation, was enhanced in bFGF-pretreated neurons. On the other hand, [Ca2+]i responses to NMDA-receptor activation were suppressed in bFGF-treated neurons, consistent with previous studies showing that bFGF can protect neurons against NMDA toxicity. Moreover, neurons pretreated with bFGF were relatively resistant to the toxicities of glutamate and AMPA, both of which were shown to be mediated by NMDA receptors. These data suggest that differential regulation of the expression of specific glutamate-receptor subunits may be an important mechanism whereby neurotrophic factors modulate activity-dependent neuronal plasticity and vulnerability to excitotoxicity.

Animals↗

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