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Biomedical subjects

J Yuan

Publications and source records attributed to J Yuan.

At least 289 records · Page 16Linked to original sources
PubMed1995

N-Methyl-beta-carboline-3-carboxamide (FG 7142), an anxiogenic agent in airborne particles and cigarette smoke-polluted indoor air.

beta-Carboline-3-carboxylic acid methylamide (FG 7142), an anxiogenic agent, has been measured in airborne particles, automobile-exhaust particles, incinerator ash, smoke condensate of tree leaves and cigarette-smoke-polluted indoor air by high-performance liquid chromatography. This compound has been detected in indoor as well as outdoor air. The source of this compound in indoor air was determined as cigarette smoke, identified from smoking machine studies. This anxiogenic agent was detected in smoke condensate of tree leaves and incinerator ash from garbage burning plants, but not in diesel-exhaust particles. Considering the present results, together with the previous finding that cigarette smoke contains this compound, FG 7142 is likely to be formed through combustion of plants. Our data also suggest that this compound may be widely distributed in the environment.

Journal Article↗
PubMed1995

Effects of drinking pattern on the peak/trough blood concentrations in drinking water studies.

The effects of changes in drinking patterns on the expected peak/trough blood concentrations of test compounds were examined during rodent dosed drinking water studies. They were based on the assumption that the kinetics of the test compound is linear and time-invariant. Results indicate that drinking patterns have minor effects on the expected peak/trough concentrations and the time to reach these concentrations. If a 12-hr light/dark cycle starting at 7.00 is used for all the drinking patterns studied, the peak and trough concentrations will occur in the early morning and late afternoon, respectively. A comparison of the predicted versus experimentally determined pentachlorophenol (PCP) plasma concentrations in a 1-wk rat drinking water study revealed that using a circadian rhythm drinking pattern in the model generated the most satisfactory prediction. Predictions based on a square wave drinking pattern with 90% drinking activities in the night phase were also excellent. Triangular or sinusoidal drinking patterns were least accurate in predictions.

Animals↗
PubMed1995

Molecular control of life and death.

Recent evidence has shown that two of the three key genes in the programmed cell death pathway of Caenorhabditis elegans, ced-9 (a cell death suppressor) and ced-3 (a cell death inducer), encode proteins that share structural and functional similarities with the mammalian proto-oncogene product Bcl-2 and interleukin-1 beta converting enzyme, respectively. These findings reveal key molecules that control life and death decisions in vertebrates.

Animals↗
PubMed1995

Frequent T:A-->G:C transversions in X-irradiated mouse cells.

Ionizing radiation is a known carcinogen and teratogen. However, the point mutations produced by ionizing radiation in mammalian cells have not been fully characterized. Determination of a characteristic spectrum of X-ray-induced mutations in mammalian cells could provide clues to cellular repair processes and could serve as a marker of individual exposure to radiation. Mouse fibroblasts containing in their genome multiple copies of a recoverable lambda phage shuttle vector were used to detect and analyze radiation-induced point mutations in the supF mutation reporter gene. Following fractionated doses of ionizing radiation, a unique mutational spectrum notable for a high proportion of T:A-->G:C transversions (57%) was found. This pattern was distinct from the spectra of UV-induced and spontaneous mutations detected in the same mouse cell assay system (mainly C:G-->T:A transitions). The predominance of T:A-->G:C transversions and the pattern of mutation hot-spots are consistent with a possible role for polymerase beta in the repair of X-ray-damaged DNA. These results may also help to define a distinctive mutational signature of X-ray exposure in mammalian cells.

Animals↗
PubMed1995

Induction of p53 in mouse cells decreases mutagenesis by UV radiation.

The tumor suppressor protein, p53, is proposed to have a critical role in maintaining the integrity of the genetic material. It has been established that p53 induces a cell cycle block in the G1 phase upon cellular DNA damage. Recent evidence also indicates the involvement of p53 directly and indirectly in nucleotide excision repair (NER). We have examined the role of p53 with respect to UV-induced mutagenesis. By gene transfer, we established a mouse fibroblast cell line overexpressing the val135 temperature-sensitive p53 allele. In this line, p53 activity can be modulated through temperature shift, as confirmed by Western blot and by cell cycle analysis. This cell line was also constructed to contain a recoverable lambda phage shuttle vector carrying the supF mutation reporter gene. Induction of p53 was found to enhance the clonogenic survival of the cells following UV-irradiation compared to the p53-deficient parental mouse cell line. The transfectant line also displayed a 4-fold reduction in the frequency of UV-induced mutations as measured in the chromosomally integrated supF reporter gene. Our results are consistent with a p53-induced cell cycle block at G1 allowing cells to repair chromosomal damage before DNA replication. However, our data may also reflect a more direct role of p53 in the repair of UV-induced lesions as suggested by studies showing that p53 can interact directly with repair factors.

Animals↗
PubMed1995

Glucocorticoids rescue CD4+ T lymphocytes from activation-induced apoptosis triggered by HIV-1: implications for pathogenesis and therapy.

OBJECTIVE: During HIV-1 infection, CD4+ T lymphocytes migrate to immune-reactive lymphoid organs where they are infected by the virus and/or killed by apoptosis on immunoregulatory stimuli--a potential mechanism underlying fatal CD4+ T-cell depletion observed in AIDS. This study seeks to determine the effects of glucocorticoids (GCC) on the activation-induced T-cell apoptosis triggered by HIV-1. METHODS: CD4+ and CD8+ T cells were purified from HIV-negative donor peripheral blood mononuclear cells (PBMC) by positive selection and exposed to HIV-1 (primary isolates). HIV-1-exposed CD4+ and CD8+ T cells as well as PBMC derived from HIV-1-infected patients were cultured with medium alone or anti-CD3 monoclonal antibodies (MAb)/mitogens in the presence or absence of hydrocortisone or prednisolone. Viral infection kinetics were assessed by polymerase chain reaction and viral replication was measured by p24 enzyme-linked immunosorbent assay. Cell survival, apoptosis, T-cell proliferation, blast cell transformation, and interleukin (IL)-2 receptor (CD25) expression were monitored in parallel for each cell population. RESULTS: Fractionated CD4+ T cells acutely infected by HIV-1 underwent apoptotic death on anti-CD3 MAb/mitogen stimulation. This activation-induced apoptotic cell killing was antagonized by pharmacological doses of prednisolone or hydrocortisone added up to 6 h after stimulation. GCC were also found to be capable of inhibiting the accelerated apoptosis in PBMC (including both CD4+ and CD8+ T-cell fractions) from HIV-1-infected patients. This anti-apoptotic action of GCC overbalanced their downregulatory effect on T-cell proliferation, resulting in an overall improvement of CD4+ T-cell survival in patient PBMC. These effects of GCC were abrogated by the anti-GCC RU 486 and were not associated with significant suppression of CD25 expression and IL-2-dependent T-cell blast transformation; moreover, GCC had no impact on viral infection and replication. CONCLUSION: GCC exert a receptor-mediated anti-apoptotic activity in mature T cells through both activation-induced and HIV-1-triggered pathways and could be potent inhibitors of T-cell apoptosis in HIV-1-infected patients.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Expression of apogens and engulfens during programmed cell death in the nervous system of the chick embryo.

Two categories of cell death related to antigens, apogens and engulfens, have been reported to be expressed by apoptotic cells and the cells involved in their engulfment in the immune system, and in mesenchymal tissue in the limb of the chick embryo (ROTTELLO et al., 1994). To determine whether these antigens are also expressed during the process of neuronal death, the distribution of immunoreactivity to both anti-apogen and anti-engulfen antibodies was examined in the spinal cord and the dorsal root ganglia of the chick embryo. Anti-apogen antibodies labeled a sub-population of the profiles of dying cells in regions where cell death was occurring. The extent of labeling by anti-apogens varied from 3% to 70% of the total number of dying profiles depending on the specific antibody used and the neuronal region examined. Immunoreactive labeling by the anti-engulfen antibodies mainly involved large cells that contained debris of dead cells. These results indicate that at least some dying neuronal cells express common antigens that are shared by dying mesenchymal cells during programmed cell death, and that phagocytotic cells of the immune system are involved in the engulfment of neuronal cells that have undergone programmed cell death.

Animals↗
PubMed1995

[The effect of platelet-activating factor antagonists on early bacteria translocation of rat after burn injury].

30% third degree burn model of Wistar rat was used in this experiment. The animals were divided randomly into three groups (normal control, burn, and platelet-activating factor antagonist treatment). After poured E. coli which labelled with acridine orange into intestine, the rats were killed at 6, 12, 24, and 48 hrs postburn, the bacteria in mesentery lymph node (MLN), liver and pulmonary organisms were cultured and counted, also observed by fluorescent microscopy directly. The results showed that, in PAF antagonist (WEB2170) treatment group, the quantity of bacteria in MLN, liver and lung were decreased significantly (P < 0.001). The labelled bacteria in MLN, liver and lung of burn group were 100%, 80.0%, and 50.0% respectively compared with 40.0%, 30.0%, and 20.0% in treatment group. It is suggested that WEB 2170 could protect the intestine from bacteria translocation after burn injury.

Animals↗
PubMed1995

GM1 antibody in Guillain-Barre syndrome after Campylobacter jejuni infection.

Fecal culture of Campylobacter jejuni was prepared by the method of Skirrow, and serum class specific antibodies (IgG, IgM and IgA) to Campylobacter jejuni and serum class specific antibodies (IgG IgM) to GM1 were prepared with solid phase enzyme linked immunasorbent assay in 16 cases of Guillain-Barre syndrome (GBS), 32 controls with other neurological diseases (disease controls) and 90 normal controls. The results showed that the incidence of Campylobacter jejuni infection, especially recent infections, in the group with Guillain-Barre syndrome was much higher than that in the two control groups, and that the positive rate of GM1 antibody was also much higher in the GBS group than in the two control groups. The results suggest that Campylobacter jejuni infection may be one of the important precipitating factors of Guillain-Barre syndrome and play an important role in the epidemiological pattern of Guillain-Barre syndrome in China. It damages the myelin of peripheral nerves through induction of GM1 antibody production.

Adult↗
PubMed1995

[An experimental study of the expression and localization of tumor necrosis factor mRNA in liver of rats with severe burn].

In situ hybridization was used to study the expression and localization of tumor necrosis factor (TNF) mRNA in liver of rats after burn. The results showed that the Kupffer cells expressed TNF mRNA in normal rats. After burn, the number of positive expression cells increased quickly, the expression reached max-mum at 6h postburn, and there were no significantly different with normal at 24h postburn. The dynamic changes of number of TNF mRNA producing cells was similar to that of the portal plasma endotoxin level. Kupffer cells located in sinusoid surrounding portal vein expressed TNF mRNA especially at 6h-12h postburn. Also the sinusoid endothlial cells and infiltrative inflammation cells surrounding portal vein were the TNF mRNA-producing cells, this changes appeared significantly at 12-24h postburn. The results suggested that the endotoxin originated from gut may be the principal stimulator for expression of TNF mRNA. The expression of endothlial cells and neutrophils suggested that these cells had been activated. So the endothlium, neutrophils and Kupffer cell play an important role in the pathogenesis of the endotoxin-induced live injury.

Animals↗
PubMed1994

SecA homolog in protein transport within chloroplasts: evidence for endosymbiont-derived sorting.

The SecA protein is an essential, azide-sensitive component of the bacterial protein translocation machinery. A SecA protein homolog (CPSecA) now identified in pea chloroplasts was purified to homogeneity. CPSecA supported protein transport into thylakoids, the chloroplast internal membrane network, in an azide-sensitive fashion. Only one of three pathways for protein transport into thylakoids uses the CPSecA mechanism. The use of a bacteria-homologous mechanism in intrachloroplast protein transport provides evidence for conservative sorting of proteins within chloroplasts.

Adenosine Triphosphatases↗
PubMed1994

Changes in composition and distribution of LDL subspecies in hypertriglyceridemic and hypercholesterolemic patients during gemfibrozil therapy.

The effect of gemfibrozil (GEM) on composition and distribution of LDL subspecies in 10 hypertriglyceridemic (HTG) patients with triglyceride (TG) levels of 300-750 mg/dl and low density lipoprotein cholesterol (LDL-C) < 160 mg/dl, and 8 hypercholesterolemic (HC) patients with LDL-C > or = 190 mg/dl and TG < 200 mg/dl was investigated. Patients were randomized in a double-blind, crossover design to 12 week periods of placebo and 1200 mg/day GEM with an intervening washout period. All 7 LDL subspecies in the density range of 1.029 to 1.063 g/ml in the HTG group contained more TG (P < 0.01) and less free cholesterol (P < 0.05), while the proportion of cholesterol ester was lower only in LDL subspecies 1 to 3 (P < 0.05) as compared to the HC group. In HTG patients, GEM increased the proportion of cholesterol ester (P < 0.05) in all subfractions, while the proportion of free cholesterol was increased and TG was decreased in LDL subspecies 1 to 4 only (P < 0.05). GEM decreased the LDL subspecies score from 4.8 +/- 0.7 to 4.2 +/- 0.5, and the major LDL subclass density from 1.048 +/- 0.006 to 1.043 +/- 0.002 g/ml (P < 0.01) in HTG patients. GEM decreased TG levels to mean of 228 +/- 52 mg/dl in HTG patients, but there was no change in LDL phenotype. No significant changes in composition and distribution of LDL subspecies were noted in HC patients with GEM. We conclude that GEM significantly altered the composition and distribution of LDL subspecies with a shift from small dense LDL particles to large, less dense particles in HTG patients.

Adult↗
PubMed1994

Ich-1, an Ice/ced-3-related gene, encodes both positive and negative regulators of programmed cell death.

We report here the isolation and characterization of Ich-1, a gene related to the C. elegans cell death gene ced-3 and the mammalian homolog of ced-3, interleukin-1 beta-converting enzyme (ICE). Alternative splicing results in two distinct Ich-1 mRNA species. One mRNA species encodes a protein product of 435 amino acids (ICH-1L) that is homologous to both the P20 and P10 subunits of ICE (27% identity) and the entire CED-3 protein (28% identity). The other mRNA encodes a 312 amino acid truncated version of ICH-1L protein (ICH-1S). Overexpression of IchL induces programmed cell death, suggesting that Ich-1 is also a mammalian programmed cell death gene. More interestingly, overexpression of the Ich-1S suppresses Rat-1 cell death induced by serum deprivation. These observations suggest that Ich-1 plays an important role in both positive and negative regulation of programmed cell death in vertebrate animals.

Alternative Splicing↗
PubMed1994

Expression of a specific marker of avian programmed cell death in both apoptosis and necrosis.

Apoptosis and necrosis are two types of cell death with different morphologic features. We report here the isolation of a monoclonal antibody, BV2, that specifically recognizes cells undergoing developmental programmed cell death in different tissues of the chicken and zebra-finch embryos. The antigen recognized by BV2 monoclonal antibody is detected in vitro in primary chicken embryonic fibroblasts induced to die by actinomycin D, as well as fibroblasts induced to die by chemical anoxia. The expression of this specific antigen during necrosis appears to require active protein synthesis. These findings provide evidence that cells from different embryonic tissues undergoing programmed cell death during vertebrate development express similar antigens and indicate that apoptosis and necrosis may share similar biochemical features.

Animals↗
PubMed1994

Stimulation of the human intercellular adhesion molecule-1 promoter by interleukin-6 and interferon-gamma involves binding of distinct factors to a palindromic response element.

Intercellular adhesion molecule-1 (ICAM-1) is a transmembrane glycoprotein that promotes adhesion in immunological and inflammatory reactions. ICAM-1 is expressed on cells of many lineages and is induced by interleukin-6 (IL-6) and interferon-gamma (IFN-gamma). Functional analysis of ICAM-1 promoter-luciferase constructs in HepG2 cells enabled us to identify a region between -110 and -37 mediating IL-6 and IFN-gamma responsiveness and containing a palindromic IL-6/IFN-gamma response element (pIRE). Site-directed mutagenesis of key nucleotides in the ICAM-1 pIRE abolished the effect of both IL-6 and IFN-gamma stimulation, while this pIRE element was sufficient to confer IL-6 and IFN-gamma responsiveness to a heterologous promoter. We further show by gel retardation analysis that distinct nuclear factors induced by both IL-6 or IFN-gamma specifically bind to this pIRE. Furthermore, treatment with IL-6 results in the formation of multiple complexes while IFN-gamma induces a single binding complex, both in HepG2 and monocytic U937 cells. Differentiation of U937 cells by exposure to 12-O-tetradecanoyl phorbol-13-acetate abolishes response to IL-6 but not IFN-gamma. Supershift data utilizing the ICAM-1 pIRE revealed that IFN-gamma and IL-6 both induce a factor antigenically related to IFN-gamma activation factor. We further provide data suggesting that IL-6 additionally activates an ICAM-1 pIRE binding factor related to the previously described acute-phase response factor in disparate cell types. We therefore conclude that the activation of these related nuclear factors by IL-6 and IFN-gamma is important in the regulation of ICAM-1 gene expression.

Base Sequence↗
PubMed1994

Defective assembly of membrane proteins in erythroid precursors of beta-thalassemic mice.

beta-Thalassemic mice provide a useful model for studying the pathophysiology of human beta-thalassemia in that one can perform experiments that are difficult to perform in humans. The ease of access to beta-thalassemic mouse marrow provided the opportunity to explore the cause of the ineffective erythropoiesis that characterizes severe beta-thalassemia in mouse and man. We hypothesized that the accumulation of excess alpha-globin might interfere with the normal assembly of red blood cell (RBC) membrane proteins, thus contributing to the severe intramedullary lysis. Femoral marrow was obtained from normal and beta-thalassemic mice, and RBC precursors were purified (> 90%) by panning and harvesting CD45- cells. The assembly of RBC membrane proteins was assessed by observing immunofluorescence patterns obtained on fixed permeabilized precursors using rabbit polyclonal antibodies directed against human spectrin, and band 4.1, and murine band 3. The distribution of the proteins was shown with a fluorescein-tagged goat antirabbit antibody. In contrast to normal mice, about 30% of intermediate and late stage erythroblasts in beta-thalassemic mice appear abnormal. Neither spectrin nor band 4.1 formed crisp rim fluorescence in these erythroid precursors of thalassemic mice, whereas assembly of band 3 appeared normal. Therefore, the assembly of membrane skeletal proteins is abnormal in murine beta-thalassemic erythroid precursors perhaps because of the deposition of unmatched alpha-globin chains.

Animals↗