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Biomedical subjects

B Chen

Publications and source records attributed to B Chen.

At least 469 records · Page 26Linked to original sources
PubMed1993

Smith-Fineman-Myers syndrome: report on a large family.

Smith-Fineman-Myers syndrome is considered an X-linked mental retardation (XLMR) syndrome. Three families have been reported to date. However, none presented a typical pattern of X-linked inheritance. Here we reported on 5 males with Smith-Fineman-Myers syndrome with similar phenotypic expression as in those cases reported previously; they were distributed in 4 sibships of one large maternal kindred. This finding adds strong support to the hypothesis of the Smith-Fineman-Myers syndrome being a rare XLMR syndrome.

Child↗
PubMed1993

Kainate elicits elevated nuclear calcium signals in retinal neurons via calcium-induced calcium release.

Intracellular Ca2+ was imaged in cultured neonatal rat retinal neurons using the Ca(2+)-sensitive dye fluo-3 and confocal scanning laser microscopy. Depolarization via elevation of bath K+ concentration resulted in large cytoplasmic and nuclear Ca2+ signals; responses in the nucleus exceeded those of the cytoplasm. Glutamate or kainate application elicited the same intracellular pattern of elevated Ca2+ signals. Kainate stimulation was blocked by the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and greatly reduced by removing Ca2+ from the bath and adding ethylene glycol-bis (beta-amino-ethyl ether) N,N,N',N'-tetraacetic acid (EGTA). Kainate was equally effective in eliciting Ca2+ signals when bath Na+ was replaced with equimolar concentrations of choline, or in the presence of the NMDA receptor antagonist, 2-amino-5-phosphonovaleric acid (APV). Caffeine treatment significantly reduced the kainate-induced intracellular Ca2+ response. These results suggest that Ca2+ can enter through the kainate receptor of retinal neurons and amplify the Ca2+ signals in the cytoplasm and nucleus by releasing Ca2+ from intracellular stores.

2-Amino-5-phosphonovalerate↗
PubMed1993

Mitotic stability and nuclear inheritance of integrated viral cDNA in engineered hypovirulent strains of the chestnut blight fungus.

Transmissible hypovirulence is a novel form of biological control in which virulence of a fungal pathogen is attenuated by an endogenous RNA virus. The feasibility of engineering hypovirulence was recently demonstrated by transformation of the chestnut blight fungus, Cryphonectria parasitica, with a full-length cDNA copy of a hypovirulence-associated viral RNA. Engineered hypovirulent transformants were found to contain both a chromsomally integrated cDNA copy of the viral genome and a resurrected cytoplasmically replicating double-stranded RNA form. We now report stable maintenance of integrated viral cDNA through repeated rounds of asexual sporulation and passages on host plant tissue. We also demonstrate stable nuclear inheritance of the integrated viral cDNA and resurrection of the cytoplasmic viral double-stranded RNA form in progeny resulting from the mating of an engineered hypovirulent C. parasitica strain and a vegetatively incompatible virulent strain. Mitotic stability of the viral cDNA ensures highly efficient transmission of the hypovirulence phenotype through conidia. Meiotic transmission, a mode not observed for natural hypovirulent strains, introduces virus into ascospore progeny representing a spectrum of vegetative compatibility groups, thereby circumventing barriers to anastomosis-mediated transmission imposed by the fungal vegetative incompatibility system. These transmission properties significantly enhance the potential of engineered hypovirulent C. parasitica strains as effective biocontrol agents.

Ascomycota↗
PubMed1993

Serial spatial filters in vision.

Observers viewing two superimposed laser interference fringes of nearly equal spatial frequency see an illusory grating of low spatial frequency, even when the spatial frequency of the fringes exceeds the resolution limit. This grating is a product of nonlinear distortion within the visual system [MacLeod, Williams and Makous (1992) Vision Research, 32, 347-363]. By separately manipulating the spatial frequencies of the interference fringes and the distortion gratings, we decomposed the contrast sensitivity function into two serial components separated by the nonlinear process. Losses in the optics of the eye were avoided by use of laser interferometry. Spatial summation preceding the nonlinear stage was restricted to the light-collecting area of individual cones and was directly proportional to the diameters of cone inner segments at three retinal eccentricities; this suggests that light is trapped within cones at the level of their inner segments. Even 30 degrees from the fovea, the nonlinear stage precedes the site where separate signals from individual cones are no longer maintained; this leads us to suggest that the nonlinear process lies within the retina. In addition, spatial antagonism precedes the nonlinear stage; this places the nonlinear process at a site following the outer segments of the cones. Dichoptic presentation of the interference fringes failed to produce illusory gratings; that is, the nonlinearities within the binocular pathway do not produce distortions like those produced by the monocular nonlinearity.

Contrast Sensitivity↗
PubMed1993

Dose-dependent ras mutation spectra in N-nitrosodiethylamine induced mouse liver tumors and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone induced mouse lung tumors.

In a previous study, the spectrum of H-ras mutations detected in B6C3F1 mouse liver tumors induced by 5, 50 or 150 mumol/kg body wt of N-nitrosodiethylamine (NDEA) was similar to that in spontaneous B6C3F1 mouse liver tumors, suggesting that activation of the H-ras gene in NDEA-induced mouse liver tumors may not be the direct result of the chemical interaction with the H-ras gene. In the present study, mutations in the H-ras oncogene from B6C3F1 mouse liver tumors induced by 5 or 50 mumol/kg body wt of NDEA were characterized by DNA amplification with polymerase chain reaction (PCR), single-strand conformation of polymorphism (SSCP) and direct sequence analysis. Twenty-one of 66 NDEA-induced B6C3F1 mouse liver tumors contained activated H-ras gene with 2 of 21 having a CG to AT transversion at the first base of codon 61, 17 of 21 having AT to GC transition and 2 of 21 having an AT to TA transversion at the second base of codon 61 in the H-ras gene. The predominant mutation, AT to GC transition (17/21, 81%) is consistent with the formation of O4-ethylthymine adduct, and is distinct from the predominant CG to AT transversion (50%) at the first base of codon 61 detected in H-ras gene from NDEA-induced B6C3F1 mouse liver tumors in a previous study by Stowers et al. Mutations in the K-ras oncogene from 59 A/J mouse lung tumors induced by 0.53 mmol/kg body wt of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were also characterized by using the above mentioned methods. Forty-six of 59 NNK-induced A/J mouse lung tumors contained activated K-ras genes. All 46 (100%) of the activated K-ras gene had GC to AT transitions at the second base of codon 12. The same mutation was observed in 70% (7/10) of the K-ras oncogene from A/J lung tumors induced by 4.8 mmol/kg body wt (given in 21 doses) of NNK. These data suggest that other factors in addition to genotoxic effect might be involved in the induction of rodent tumors by some carcinogens when given at higher doses. Therefore, further studies to compare the dose-dependent differences in the profile of ras mutations induced by chemical carcinogens may help to assess human cancer risk. Mutation(s) in exons 5-8 of the p53 gene was not found in these NDEA-induced mouse liver tumors and NNK-induced mouse lung tumors.

Animals↗
PubMed1993

A common element involved in transcriptional regulation of two DNA alkylation repair genes (MAG and MGT1) of Saccharomyces cerevisiae.

The Saccharomyces cerevisiae MAG gene encodes a 3-methyladenine DNA glycosylase that protects cells from killing by alkylating agents. MAG mRNA levels are induced not only by alkylating agents but also by DNA-damaging agents that do not produce alkylated DNA. We constructed a MAG-lacZ gene fusion to help identify the cis-acting promoter elements involved in regulating MAG expression. Deletion analysis defined the presence of one upstream activating sequence and one upstream repressing sequence (URS) and suggested the presence of a second URS. One of the MAG URS elements matches a decamer consensus sequence present in the promoters of 11 other S. cerevisiae DNA repair and metabolism genes, including the MGT1 gene, which encodes an O6-methylguanine DNA repair methyltransferase. Two proteins of 26 and 39 kDa bind specifically to the MAG and MGT1 URS elements. We suggest that the URS-binding proteins may play an important role in the coordinate regulation of these S. cerevisiae DNA repair genes.

Alkylation↗
PubMed1993

Role of mesenchymal cell death in lung remodeling after injury.

Repair after acute lung injury requires elimination of granulation tissue from the alveolar airspace. We hypothesized that during lung repair, signals capable of inducing the death of the two principal cellular elements of granulation tissue, fibroblasts and endothelial cells, would be present at the air-lung interface. Bronchoalveolar lavage fluid obtained from patients during lung repair induced both fibroblast and endothelial cell death, while fluid obtained at the time of injury or from patient controls did not. The mode of cell death for endothelial cells was apoptosis. Fibroblast death, while morphologically distinct from necrosis, also differed from typical apoptosis. Only proliferating cells were susceptible to the bioactivities in lavage fluid, which were trypsin sensitive and lipid insoluble. Histological examination of lung tissue from patients after lung injury revealed evidence of apoptotic cells within airspace granulation tissue. Our results suggest that cell death induced by peptide(s) present at the air-lung interface may participate in the remodeling process that accompanies tissue repair after injury.

Acute Disease↗
PubMed1993

[Application of RFLP analysis to Duchenne and Becker muscular dystrophy in Shandong Province. I. Carrier detections in females at risk].

There were eight intragenic and two flanking bridge DNA polymorphic markers used in the RFLP analysis in 21 Duchenne and Becker muscular dystrophy selected from nine different districts in Shandong Province. A total number of 173 individuals of the families were accepted for gene tracking and carrier detection, as well as prenatal diagnosis. Based on the frequency of the probe polymorphism tested in our study of 53 unrelated individuals, one to three high polymorphic probes were sequentially used and all families presented the informativeness in RFLP analysis. Some more introgenio probes were supplied for assessment of mutated sites and carrier status with the help of gene phases, if recombinations were found. Our results presented a ratio of 85.45% of carrier detection at risk females with 95% or more reliability, including 17 carriers and 30 non-carriers. It was not able to ascertain the carrier status of 8 females because of DNA absence from key family members. Finally, we proposed a diagnostic procedure for the RFLP analysis to DMD/BMD families.

Female↗
PubMed1993

Induction of murine peritoneal macrophage colony-forming cells by peritoneal administration of macrophage inflammatory protein-1 alpha.

Peritoneal injection of thioglycollate medium (TM) to mice results in a dramatic increase in total number of peritoneal macrophages within 48 to 72 hours. Unlike resident macrophages, a fraction (10 to 20%) of these newly arrived young macrophages, designated as macrophage colony-forming cells (M-CFC), are highly proliferative and formed macrophage colonies in vitro in the presence of either macrophage or granulocyte-macrophage colony-stimulating factor (M-CSF or GM-CSF). Using a reverse transcriptase polymerase chain reaction (RT-PCR) technique, peritoneal exudate macrophages (PEM) obtained 2 to 5 days after a single TM injection actively expressed mRNA for recombinant murine macrophage inflammatory protein-1 alpha (rmMIP-1 alpha). Yet none or only a trace amount of mRNA for MIP-1 alpha was detected in normal resident macrophages or PEM obtained 7 days after TM treatment. The effect of rmMIP-1 alpha on the induction of exudate M-CFC was investigated. Multiple intraperitoneal (IP) administration of rmMIP-1 alpha caused a marked increase in the total number of peritoneal M-CFC and macrophages similar to but weaker than the increase in TM-injected mice. The total number of neutrophils, mast cells, and eosinophils also increased, but with different kinetics, following multiple injections of rmMIP-1 alpha. rmMIP-1 alpha alone did not stimulate the proliferation of M-CFC, nor did it potentiate their responsiveness to either rmGM-CSF or recombinant human (rh) M-CSF in vitro. Taken together, our results suggest that MIP-1 alpha released by exudate macrophages is a major chemoattractant responsible for the migration of M-CFC from the circulation to the peritoneal cavity during a TM-induced inflammatory response.

Animals↗
PubMed1992

Priority among air pollution factors for preventing chronic obstructive pulmonary disease in Shanghai.

The problems that city environmental protection planners face are how important the air pollution exposures are in relation to chronic obstructive pulmonary disease (COPD) in local residents and which factor should be controlled most urgently. The purpose of our study is to determine the control priority among ambient sulphur dioxide (SO2) inhalable particulates (IP) and indoor use of coal to prevent COPD in residents of the city. Ambient air pollution is mainly from SO2 and IP(< 10 nm). Indoor air pollution is mainly from the use of coal for heating and/or cooking. Distribution of ambient SO2, and IP concentrations were described using a quartic trend surface simulation. When stratified by two extreme levels of ambient SO2 and IP and types of fuel used indoors, eight local area populations in four communities with different combinations of exposure levels were selected. In each community a local area population mostly using coal and one mostly burning gas was chosen. Chronic obstructive pulmonary diseases (COPD, ICD 490-493) including chronic bronchitis, asthma and emphysema, are a major cause of death in residents of Shanghai. The relationship between the three air pollution factors and their health effects were analyzed at the level of mortality (1978-1987, 232,459 person-years), prevalence of symptoms (12,037 persons) of COPD, lung function and non-specific immunologic function (514 women). The results show that indoor use of coal has stronger associations with health than estimated exposure to ambient SO2 or IP.

Adult↗
PubMed1992

Transforming growth factor-beta 1 bifunctionally regulates murine macrophage proliferation.

Transforming growth factor-beta (TGF-beta) is a family of polypeptide growth factors with multiple functional activities. Recent studies suggest that TGF-beta is a selective inhibitor of hematopoietic cells. In this report, we study the effect of TGF-beta 1 on the proliferation of murine peritoneal exudate macrophages (PEM) in response to purified murine recombinant granulocyte-macrophage colony-stimulating factor (rMuGM-CSF) and human recombinant M-CSF (rHuM-CSF). In mice, PEM and other types of tissue macrophages display multiple types of receptors for CSFs and respond to them, either alone or in combination, to undergo extensive proliferation in vitro. Recombinant human TGF-beta 1 (rHuTGF-beta 1) (0.1 to 1.0 ng/mL) markedly enhanced the growth of PEM in response to rMuGM-CSF but inhibited their responsiveness to rHuM-CSF. Similar effects of rHuTGF-beta 1 were also detected using murine pulmonary alveolar macrophages (PAM) and bone marrow-derived macrophages (BMDM). Receptor binding assays using iodinated rMuGM-CSF and rHuM-CSF showed that rHuTGF-beta 1 treatment greatly enhanced the expression of GM-CSF receptors in PEM, in a time- and dose-dependent manner, suggesting a possible mechanism for the synergistic effect of TGF-beta 1. On the other hand, the expression of M-CSF receptors was not affected by TGF-beta 1 treatment. Analysis by mRNA PCR showed that the synergistic effect of TGF-beta 1 is not due to autocrine CSFs produced by treated cells. Our results suggest that TGF-beta 1 is an important regulator of macrophage proliferation. Depending on the types of CSFs present, TGF-beta 1 may act either as a growth promoter or inhibitor.

Animals↗