Search PubMed⌕ Search

Biomedical subjects

Y Dong

Publications and source records attributed to Y Dong.

At least 307 records · Page 17Linked to original sources
PubMed1989

[The clinical significance of anti-RNP antibody].

67 cases of anti-RNP antibody were reported in different patients with connective tissue disease. The high titre of anti-RNP antibody not only presents in patients with mixed connective tissue disease (MCTD), but also in individual patient with systemic lupus erythematosus (SLE). Anti-RNP antibody is usually associated with clinical manifestation of raynauds phenomena, myositis, and sclerodactyly. The clinical significance of anti-RNP antibody and the diagnosis about MCTD were discussed in this article.

Autoantibodies↗
PubMed1988

Localization of glucocorticoid receptor mRNA in the male rat brain by in situ hybridization.

The localization and distribution of mRNA encoding the glucocorticoid receptor (GR) was investigated in tissue sections of the adult male rat brain by in situ hybridization and RNA blot analysis. GR mRNA levels were measured by quantitative autoradiography with 35S- and 32P-labeled RNA probes, respectively. Strong labeling was observed within the pyramidal nerve cells of the CA1 and CA2 areas of the hippocampal formation, in the granular cells of the dentate gyrus, in the parvocellular nerve cells of the paraventricular hypothalamic nucleus, and in the cells of the arcuate nucleus, especially the parvocellular part. Moderate labeling of a large number of nerve cells was observed within layers II, III, and VI of the neocortex and in many thalamic nuclei, especially the anterior and ventral nuclear groups as well as several midline nuclei. Within the cerebellar cortex, strong labeling was observed all over the granular layer. In the lower brainstem, strong labeling was found within the entire locus coeruleus and within the mesencephalic raphe nuclei rich in noradrenaline and 5-hydroxytryptamine cell bodies, respectively. A close correlation was found between the distribution of GR mRNA and the distribution of previously described GR immunoreactivity. These studies open the possibility of obtaining additional information on in vivo regulation of GR synthesis and how the brain may alter its sensitivity to circulating glucocorticoids.

Animals↗
PubMed1988

Regulation of gene expression of class I alcohol dehydrogenase by glucocorticoids.

The effect of glucocorticoids on gene expression of rat class I alcohol dehydrogenase (ADH; alcohol:NAD+ oxidoreductase, EC 1.1.1.1) was investigated. A cDNA clone for the beta-subunit of human ADH (ADH2) was used to analyze class I ADH mRNA levels in rat hepatoma cells, which are known to contain a functional glucocorticoid receptor. RNA gel blot analysis of total cellular RNA isolated from these cells showed hybridization of the human ADH2 cDNA probe to a single approximately equal to 1500-base RNA species. Treatment of the cells with dexamethasone (0.1 nM to 1 microM) caused a dose-dependent increase in total cellular class I ADH mRNA levels by a factor of 2-4. Maximal levels were reached within 18-24 hr of treatment. This effect was reversible following withdrawal of dexamethasone. The glucocorticoid induction of class I ADH mRNA does not seem to require ongoing protein synthesis since treatment of the cells with cycloheximide did not affect the increase in class I ADH mRNA levels by dexamethasone. The human ADH2 gene contains both upstream and within the coding region sequence motifs that display homology with response elements of genes positively regulated by glucocorticoids. These data suggest a receptor-mediated transcriptional enhancement of the ADH2 gene as the mechanism of regulation. However, analysis of RNA decay in cells treated with actinomycin D indicates that the dexamethasone-induced increase in class I ADH mRNA might, at least in part, be due to enhanced ADH mRNA stability.

Alcohol Dehydrogenase↗
PubMed1988

Regulation of glucocorticoid receptor expression: evidence for transcriptional and posttranslational mechanisms.

The mechanism of ligand-induced (homologous) down-regulation of the glucocorticoid receptor (GR) has been studied. Dexamethasone caused a down-regulation of the levels of GR mRNA and protein both in hepatoma tissue culture cells and rat liver in vivo. The decrease in the level of rat liver GR mRNA was due to a reduced transcription rate of the GR gene, as assessed by nuclear run-on transcription experiments. The half-life of GR mRNA in hepatoma tissue culture cells was determined to be approximately 4.5 h and was unaffected by dexamethasone. In addition to the transcriptional regulation of GR gene expression, a dexamethasone-dependent posttranslational modification in the rate of GR protein turnover was observed. In the absence of dexamethasone, GR protein half life was approximately 25 h whereas it decreased to approximately 11 h in the presence of hormone. Down-regulation of GR protein occurred with a 6- to 24-h delay as compared to the decline in GR mRNA. This is most likely due to the differences in half-lives of GR mRNA and protein, respectively. Our results suggest that auto-regulation of GR by its cognate ligand is complex and occurs at both transcriptional and posttranslational levels.

Animals↗
PubMed1987

Mechanisms of regulation of rat ovarian 7,12-dimethylbenz[a]anthracene hydroxylase.

The mechanisms of regulation of ovarian 7,12-dimethylbenz[a]anthracene (DMBA) hydroxylase were investigated with respect to hormonal requirements and effects of the antiestrogen tamoxifen and known inducers of cytochrome P-450. The DMBA hydroxylase is increased endogenously about 3-fold in the proestrus phase as compared to the metestrus/diestrus phases (M. Bengtsson and J. Rydstrom, Science, 219 (1983) 1437-1438). A similar effect was caused by the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) whereas pregnant mare's serum gonadotropin (PMSG) brought about a 3-7-fold increase, suggesting that the estrus cycle-dependence of the DMBA hydroxylase was due directly or indirectly to gonadotropins. In contrast, differentiation of granulosa/theca cells to corpus luteum cells after ovulation, caused by administration of human chorionic gonadotropin (hCG), led to a marked decrease in activity. The activity was not specific for DMBA since substitution of this hydrocarbon for benzo[a]pyrene (BP) as substrate gave similar results. A possible role of estrogens in this context was investigated by the administration of tamoxifen simultaneous with gonadotropin treatment, which caused a partial inhibition of the hydroxylase activity. Both estradiol and 3-methyl-cholanthrene (MC) increased DMBA hydroxylase but the effects of these agents were not additive. In contrast, the effects of estradiol and MC were partially additive to that of gonadotropin. On the basis of these results, it is proposed that the rat ovary contains one or several aryl hydrocarbon hydroxylases located in the granulosa/theca cells which are regulated by estrogens, MC and beta-naphthoflavone (BNF) and that the role of gonadotropins is to proliferate granulosa/theca cells.

Animals↗
PubMed1987

45Ca uptake and the actions of Bay K 8644 on aortic strips from rabbits with perinephritis hypertension.

Uptake of 45Ca was measured in rings of thoracic aorta from rabbits with hypertension, induced by cellophane perinephritis (Page hypertension: one-kidney, one wrap). Basal 45Ca uptake was increased significantly in the hypertensive group (sham: 100 +/- 3, hypertensive: 133 +/- 11 nmol/g wet weight, n = 6). 45Ca uptake was increased by KCl (30 mmol/l), norepinephrine (50 nmol/l) and Bay K 8644 (14 or 56 nmol/l) by the following amounts: 152, 15, 28 and 36%, respectively. Stimulated 45Ca uptake was less in hypertensive animals for all agonists. The augmenting effect of Bay K 8644 on 45Ca uptake, stimulated by norepinephrine or by KCl, was also reduced in hypertension. It is concluded that in hypertension there are alterations in the Ca regulatory process and in the properties of the Ca channel in arterial muscle.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

A microbiologic and clinical study of placental inflammation at term.

This study describes the relationships between histologically evident inflammation of the placenta, membranes, and umbilical cords, and correlates these lesions with clinical outcome and with amniotic fluid and amniotic membrane cultures in pregnancies at risk for clinical infection. The overall frequency of inflammation in 123 placentas was 85.45%. There were good interrelationships between inflammatory lesions at various sites. Membrane infiltrates of 3+ were seen in 90.9% of intra-amniotic infection cases, but in only 18.4% of asymptomatic patients (P less than .001). Conversely, 76.9% of patients with 3+ inflammation had intra-amniotic infection, whereas only 7% with lesser degrees of inflammation had intra-amniotic infection. Inflammation of any degree (1-3+) had a low specificity (28%) for febrile maternal outcome. Bacteria were recovered in 117 (95.1%) of the amniotic fluids. The grade of histologic lesions was associated with total colony count of bacteria in amniotic fluid (P less than .05) and with high-virulence bacteria in amniotic fluid (P less than .05), and Mycoplasma hominis in amniotic fluid (P less than .05). Bacteria were found in 67.6% and mycoplasmas in 18.6% of amniotic membrane cultures. Chlamydia trachomatis was not recovered in any of 35 amniotic membrane cultures. No significant correlation was seen between organisms in the amniotic membrane and histologic inflammation. Thus, positive amniotic fluid culture results are associated with histologic inflammation, and may cause the inflammatory response. A logistic regression model revealed that predictors of histologic inflammation include maternal diagnosis, amniotic fluid colony count, and M hominis in amniotic fluid.

Adult↗