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Biomedical subjects

B Cheng

Publications and source records attributed to B Cheng.

At least 55 records · Page 3Linked to original sources
PubMed1996

mu-Oxo-bis[(5,10,15,20-tetraphenylporphyrinato)oxomolybdenum(V)].

The crystal structure of a new solvated crystal form of the title complex, [¿Mo(O)(TPP)¿2O].1.5H2O.0.5CH2Cl2 (TPP = C44H28N4), has been determined. The dimeric molecule is in a general position, and the overall structural features are extremely similar to those of the previously reported non-solvated form.

Crystallography, X-Ray↗
PubMed1996

Chloro(5,10,15,20-tetraphenylporphyrinato)manganese(III) with 4/m symmetry.

The crystal structure of [Mn(TPP)Cl] in space group I4/m (where TPP is C44H28N4) has been determined. The unit cell contains two full molecules, with one eighth of a molecule unique. An out-of-plane model for the Mn atom was applied and all non-H atoms were refined anisotropically. The Mn--N distance is 2.002 (3) A, the axial Mn--Cl distance is 2.297 (15) A and the out-of-plane displacement of the Mn atom is 0.16 A. The possibility of a reverse-doming porphyrin core conformation is mentioned briefly.

Crystallography, X-Ray↗
PubMed1996

A scintigraphic study on gastric emptying in patients with non-ulcer dyspepsia.

Solid gastric emptying rates (GER) were determined with scintigraphic techniques in 20 patients with non-ulcer dyspepsia (NUD) and 9 healthy volunteers. GER were significantly decreased in NUD patients compared with controls, especially 45 min (P < 0.05), 60 and 90 min (P < 0.01) and 120 min (P < 0.05) after ingestion. In 13 out of 20 NUD patients who demonstrated lower GER, only 4 cases gave a lower GER at all stages throughout the determination, the other 9 showed their abnormal GER only after 60 min. In 3 cases who received repeated GER studies after cisapride therapy, 2 patients showed symptomatic relief accompanied by GER improvement. It is concluded that gastric emptying delay may be present with a high percentage in patients with non-ulcer dyspepsia. Scintigraphic gastric emptying test is a safe and reliable technique with good reproducibility. It may be helpful in quantitative study about gastric motion disorders.

Adolescent↗
PubMed1996

Estrogens attenuate and corticosterone exacerbates excitotoxicity, oxidative injury, and amyloid beta-peptide toxicity in hippocampal neurons.

Steroid hormones, particularly estrogens and glucocorticoids, may play roles in the pathogenesis of neurodegenerative disorders, but their mechanisms of action are not known. We report that estrogens protect cultured hippocampal neurons against glutamate toxicity, glucose deprivation, FeSO4 toxicity, and amyloid beta-peptide (A beta) toxicity. The toxicity of each insult was significantly attenuated in cultures pretreated for 2 h with 100 nM-10 microM 17 beta-estradiol, estriol, or progesterone. In contrast, corticosterone exacerbated neuronal injury induced by glutamate, FeSO4, and A beta. Several other steroids, including testosterone, aldosterone, and vitamin D, had no effect on neuronal vulnerability to the different insults. The protective actions of estrogens and progesterone were not blocked by actinomycin D or cycloheximide. Lipid peroxidation induced by FeSO4 and A beta was significantly attenuated in neurons and isolated membranes pretreated with estrogens and progesterone, suggesting that these steroids possess antioxidant activities. Estrogens and progesterone also attenuated A beta- and glutamate-induced elevation of intracellular free Ca2+ concentrations. We conclude that estrogens, progesterone, and corticosterone can directly affect neuronal vulnerability to excitotoxic, metabolic, and oxidative insults, suggesting roles for these steroids in several different neurodegenerative disorders.

Amyloid beta-Peptides↗
PubMed1996

Characterization and identification of an adrenal age-related nonpolar fluorescent substance.

The adrenal cortexes of humans and rodents accumulate lipofuscin with age, but the chemical nature of the substance that produces lipofuscin fluorescence in the gland is not known. Analysis of rat adrenal nonpolar lipids revealed a fluorescence profile with increased intensity in the lipids extracted from older animals (23-24 months > 6 months > 6 weeks). The peak occurred at a wavelength of 470 +/- 5 nm(n = 26) when excited at 340 nm. After sucrose density gradient centrifugation, the fluorescent substance was primarily concentrated in subcellular lipid droplets rather than supernatant or particulate. Prolonged stimulation of rats with ACTH for 7 consecutive days caused 14-51% decreases in the fluorescence levels, with a tendency of return to control levels poststimulation regardless of age. In contrast, the nonpolar lipids of mouse adrenal tumor (Y1) cells, which contain no lipofuscin, did not display this fluorescence in the presence or absence of ACTH. The chromatographic characteristics of the substance in a silica gel-60 column resembled those of authentic retinyl palmitate and cholesteryl oleate. Analysis of the substance by HPLC demonstrated at least three prominent peaks, designated XI-3 in order. X1 and X2 were minor peaks; X3 was the major peak. Whereas none of the peaks comigrated with cholesteryl esters, X1 comigrated with authentic retinyl palmitate. Determination of the fatty acid component of the major fluorescent substance X3 by gas-liquid chromatography disclosed stearic acid. Retinyl stearate was, therefore, synthesized. The fluorescent profiles, HPLC retention time and mass spectrometric fragmentation of purified X3 substance were all identical to those of the synthetic compound. In contrast, the rat liver principally accumulated retinyl palmitate with age. Thus, we conclude that 1) the major nonpolar fluorescent substance accumulated in the rat adrenal with age is retinyl stearate, which may be a fluorophore of adrenal lipofuscin; 2) ACTH action may be related to this accumulation; and 3) the type of retinyl ester accumulated in aged animals is organ specific.

Adrenal Cortex↗
PubMed1996

Guide to CMV management.

Explore the source record for details and available documents.

AIDS-Related Opportunistic Infections↗
PubMed1996

Apolipoprotein E is increased in aged rat kidney.

There is growing evidence to indicate that apolipoprotein (apo) E may be associated with age-related disorders and altered longevity in humans. Using rats as a model, we measured apoE in plasma, brain, heart, kidney, liver and spleen in aged (24-25 mo) and younger rats (6-8 mo). The results disclosed that: (a) the plasma concentrations of immunoreactive apoE in aged rats were higher than those in young animals by 70% (P < 0.01); (b) there was no age-related difference of apoE in the brain, heart, liver or spleen; (c) in contrast, the concentrations of apoE in the kidney of aged rats were markedly higher than those of young animals by 490% (P < 0.01). Our data suggest that, in the rat, age-related change in the organ concentrations of apoE is heterogeneous, and the selective increase in the kidney may have physiologic importance which merits further study.

Aging↗
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↗