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Biomedical subjects

Z Yang

Publications and source records attributed to Z Yang.

At least 865 records · Page 48Linked to original sources
PubMed1992

Tumor necrosis factor alpha and interleukin 1 alpha enhance lipopolysaccharide-mediated bovine endothelial cell injury.

Alveolar macrophages (AMs) are important in the host response to aerogenous pulmonary bacterial infections, such as Pasteurella haemolytica-induced pneumonia in cattle. Previous work has shown that AMs enhance P. haemolytica-mediated pulmonary endothelial cell (EC) damage in vitro. The purpose of this study was to determine the mechanism of AM-enhanced EC damage using an in vitro AM-EC coculture system consisting of AMs cultured on culture plate insert membranes and ECs in the underlying chamber. The addition of lipopolysaccharide (LPS) to the culture plate insert chamber resulted in EC damage indicated by 51Cr release, which was enhanced in the presence of AMs. To determine the role of AM-secreted cytokines, recombinant human interleukin 1 alpha (IL-1) or tumor necrosis factor alpha (TNF) was added to ECs simultaneously with varying concentrations of LPS. Although TNF and IL-1 alone had only marginal toxic effects on ECs, the simultaneous treatment of TNF or IL-1 with LPS greatly increased the LPS cytotoxic effect on ECs. In addition, IL-1 receptor antagonist eliminated the IL-1 enhancement of LPS-mediated EC toxicity. These results suggest that macrophage-secreted cytokines synergistically enhance LPS-mediated pulmonary EC damage.

Animals↗
PubMed1992

The diagnostic significance of gastrin measurement of bronchoalveolar lavage fluid for lung cancer.

In this study, determination of gastrin concentration in bronchoalveolar lavage fluid and serum has been detected by radioimmunoassay in 30 cases of lung cancer and 24 cases of non-cancer pulmonary diseases. The results show that the gastrin concentration and its positive rate of lavage fluids from cancer lung are much higher than those from healthy lung and serum in lung cancer patients, and those from serum and both disease and healthy lung in non-cancer pulmonary disease patients (P less than 0.01). The gastrin ratio of lavage fluids from cancer lung to serum is also significantly higher than the ratio of lavage fluid from healthy lung to serum and all the ratios in the non-cancer pulmonary disease group. These results suggest that there is a high gastrin concentration in local tissue of lung cancer, which is signified by the high concentration of gastrin and its high positive rate in lavage fluids from the lung with cancer. Therefore, the gastrin determination in lavage fluids and gastrin ratio of lavage fluids to serum are more reliable in the differential diagnosis of benign from malignant pulmonary diseases than gastrin determination of serum alone.

Adenocarcinoma↗
PubMed1992

Pre- and postoperative sequential study on the serum gastrin level in patients with lung cancer.

Serial changes in serum gastrin level were detected by radioimmunoassay in 58 lung cancer patients before and after operation. In comparing these tests with those of 40 cases of noncancerous thoracic lesions and 151 normal adults, the serum gastrin from lung cancer patients is significantly higher than that of noncancerous thoracic lesions and normal individuals (P less than 0.01). The gastrin level is closely related to stage of cancer, size of primary tumor, presence of lymph node metastasis, and type of histological classification. The serum gastrin was found to decrease gradually after the removal of the tumor and to return to normal on the 14th postoperative day. Those patients whose serum gastrin level can return to normal on the 14th postoperative day will have a good prognosis; if not, their prognosis will be very poor. These results suggest that serum from patients with lung cancer contains a high concentration of gastrin that can help differentiate benign from malignant thoracic lesions and evaluate prognosis of patients with lung cancer. Therefore, the cause of high serum gastrin in patients with lung cancer is likely due to the gastrin-producing property of the lung cancer cells.

Adenocarcinoma↗
PubMed1992

Gastromucosal lesions in rabbits with chronic schistosomiasis.

Upper gastrointestinal hemorrhage is one of the most important complications in portal hypertension secondary to schistosomiasis. Esophageal varices and gastric mucosal lesions are additional sources of bleeding. We studied the histologic and ultrastructural features of gastric mucosa in rabbits with chronic schistosomiasis (n = 10), with normal animals (n = 10) as controls. Our results confirm that in schistosomiasis, the gastric mucosa has characteristic functional and morphological features that may predispose it to the various damaging factors. Mucosal specimens reveal dilated submucosal vein with submucosal edema, ectasia of mucosal capillaries and venules. The mucosal vessels have conspicuous endothelial cells with prominent cytoplasm and numerous tiny projections extending into the vessel lumen. The submucosal venules show morphologic feature of arterialization. There are increased submucosal arteriovenous communications with a reduction in the effective mucosal blood flow. In addition, there are a number of eggs seen in the gastric mucosa of the rabbits with schistosomiasis. The granuloma may cause structural damage to the gastric mucosa. This finding suggests that schistosomiasis may play an important role in gastric lesions.

Animals↗
PubMed1992

Enhancement of cellular immune function during cold adaptation of BALB/c inbred mice.

The cell-mediated immune function of cold-adapted BALB/c inbred mice was studied in experiments of splenic lymphocyte blastogenesis, indicated by tritium-labeled deoxythymidine incorporation and SDS-PAGE autoradiography of synthetic proteins in lymphocytes. Male BALB/c inbred mice were randomly divided into two groups: control (living at 25 degrees C) and cold-exposed (living at 2 degrees C). Results are as follows: in contrast with the control group, there was an obvious fluctuation of cell-mediated immune function in the cold-exposed group at initial cold exposure because of transient stress to cold; then cell-mediated immune function gradually recovered to control level. From Day 15, the cell-mediated immune function of the cold-exposed group was remarkably enhanced. On Day 15, the lymphocyte blastogenesis rate was increased by 20.66% (P less than 0.05), which implies the onset of cold adaptation; on Days 21 and 31, the rates increased by 80.15% (P less than 0.05) and 40.36% (P less than 0.05), respectively. Two to six months later, with continuing cold exposure, the murine lymphocyte blastogenesis rate in the cold-exposed group remained higher than that in the control group. The lymphocyte protein synthesis of the cold-exposed group, indicated by tritium-labeled leucine incorporation, apparently increased on Day 15 and the stimulated rate was 101.47% (P less than 0.05). SDS-PAGE autoradiography of synthetic proteins in lymphocytes demonstrated that after 2 weeks of cold exposure, protein bands were enriched in both quantity and quality. These results are identical to the results obtained from lymphocyte blastogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1992

Interferon-gamma response region in the promoter of the class II MHC gene, DPA.

The class II MHC gene DPA is inducible by interferon-gamma (IFN-gamma), whereas the DQB gene is not inducible in most cell types. To investigate the DNA region specifically responsible for inducibility or its lack that may be required (in addition to the elements required for constitutive expression of class II genes), hybrid promoters were constructed between the proximal 5' regions of the DPA promoter up to -148 bp, which is IFN-gamma inducible, and of the DQB promoter up to -160 bp, which is not inducible. As a result of these and previous studies [9, 10], the region of the DPA gene required for its IFN-gamma inducibility was localized to 27 bp between -55 and -81, including the Y-box element and its flanking nucleotides.

Base Sequence↗
PubMed1992

Dietary calcium modifies concentrations of lead and other metals and renal calbindin in rats.

We studied the effects of dietary calcium on kidney, femur, testis, liver, heart and brain concentrations of lead, magnesium, iron, copper, calcium and zinc in rats exposed to lead for 1 y. Renal levels of the 28,000 Da, vitamin D-dependent, calcium-binding protein calbindin-D28K were also measured. Seventy-two weanling male Sprague-Dawley rats were randomly assigned to one of nine treatment groups. Rats were fed diets containing 0.1, 0.5 or 2.5% Ca for 52 wk and were simultaneously given either 0, 50 or 100 mg lead/L in their drinking water. Rats fed the 0.1% Ca diet had organ lead concentrations that were two- to 20-fold greater than the corresponding animals fed 0.5% Ca. Rats fed diets containing 2.5% Ca had the lowest organ lead concentrations. Despite substantial effects of diet Ca on organ lead concentrations, Ca did not significantly influence concentrations of most other divalent metals studied with the exception of kidney calcium and magnesium, testis iron, plasma ionic calcium and magnesium, and several femur metals. Kidney calcium concentrations were lower in rats fed 2.5% Ca diets than in those fed 0.1 or 0.5% Ca diets. For rats not given lead, renal calbindin concentrations were highest in rats fed 0.1% Ca, and lowest in rats fed 2.5% Ca. Lead inhibited an increase in renal calbindin in the rats fed 0.1% Ca, but paradoxically increased renal calbindin levels in animals fed 2.5% Ca.

Administration, Oral↗
PubMed1992

Norepinephrine stimulates immunoreactive (ir) atrial natriuretic peptide (ANP) secretion and pro-ANP mRNA expression from rat hypothalamic neurons in culture: effects of alpha 2-adrenoceptors.

Although ANP or its smaller congeners are produced and secreted from rat hypothalami, the role or roles of neurotransmitter(s) in regulating their release and production from the neurons remains unclear. We report here that norepinephrine or epinephrine (NE/EPI) facilitates irANP secretion and pro-ANP mRNA expression in long term cultures of rat hypothalamic neurons through their effects on alpha 2-adrenoceptors. Hypothalami of 3 day-old Sprague-Dawley rats were removed and digested with collagenase. The dispersed cells were plated on poly-D-lysine coated culture dishes (10(6) cells/well) in Hepes buffered Dulbecco's Modified Eagle Medium supplemented with 8% fetal calf serum. Six days after plating, media were replenished with serum free media and the cultures incubated for 4 more days with vehicle or various doses of NE, EPI, alpha- or beta-adrenoceptor agonists in the presence of absence of antagonists. Culture media were then extracted with C18 Sep-pak and the levels of irANP determined by a well characterised RIA for ANP. NE or EPI treatment significantly increased irANP secretion from the cultures in a dose related manner with ED50 and Emax of approximately 0.2 microM and 1 microM respectively. The stimulation effect of NE was blocked by yohimbine (alpha 2-antagonist), but not prazosin (alpha 1-antagonist) or propranolol (beta-antagonist). Clonidine (alpha 2-agonist), but not phenylephrine (alpha 1-agonist) or isoprenaline (beta-agonist) mimicked the effects of NE or EPI. At the concentration of 0.1 microM, clonidine increased irANP release approximately 3 fold above that of control values (34.7 +/- 3.3; mean +/- SE, n = 4). These changes were accompanied by corresponding increments in the abundance of pro-ANP mRNA in the cultures as examined by a colorimetric Northern blot analysis. Our results indicate that NE or EPI, acting through its alpha 2-adrenoceptors, may modulate the function of ANP neurons in rat hypothalami by regulating the secretion and production of the neuropeptide at the genomic level.

Animals↗
PubMed1992

In vitro evidence for modulation of morphological and functional development of hypothalamic immunoreactive atrial natriuretic peptide neurons by cyclic 3',5'-adenosine monophosphate.

In the hypothalamus of the rat, the precursor of atrial natriuretic peptide (ANP) is produced and processed into its smaller congeners of 3K mol wt species, which are secreted from neurons with cell bodies in the periventricular areas and the paraventricular nuclei of the tissue. Employing long term monolayer cultures of neonatal rat hypothalamic cells, we have identified a small population of cells that stained positive for immunoreactive (ir) ANP. Seventy-two +/- 7% (mean +/- SE; n = 4 per 1000 cells) of the irANP positive cells were colocalized with the staining of neuron-specific enolase; some of the cells possessed multiple neurites and showed irANP staining in the perikarya, in the varicosities along neuronal processes, and at the terminals of long neurites. Over the range of 10(-6)-10(-4) M, forskolin, 3-isobutyl-1-methylxanthine, or 8-bromo-cAMP significantly augmented the total number of irANP-positive cells and those possessing neurites in a dose-related and time-dependent manner. At 10(-4) M, 4 days of forskolin treatment increased the number of irANP-positive neurons 4-fold (P less than 0.01) while tripling that of the cells with long neurites (P less than 0.01). Furthermore, it approximately tripled the number of cells (P less than 0.01) showing positive signals for pro-ANP mRNA, as ascertained by colorimetric in situ hybridization using a 30-basepair antisense oligonucleotide probe labeled with digoxigenin. Consistent with the above observation, forskolin, 3-isobutyl-1-methylxanthine, or 8-bromo-cAMP treatment significantly augmented the total amount of irANP present in the cultures, with an ED50 of forskolin approximating 5 x 10(-5) M. Although treatment with 10(-7) M phorbol 12-myristate 13-acetate approximately doubled the production of irANP in the cultures (P less than 0.05), phorbol 12-myristate 13-acetate had little effect on modulating the number or neurite outgrowth of irANP neurons. Thus, our present findings suggest that protein kinase-A pathways are of greater importance than protein kinase-C pathways in regulating both the functional and morphological development of ANP-producing neurons during the ontogenesis of the rat hypothalamus.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Evidence for atrial natriuretic peptide-(5-28) production by rat placental cytotrophoblasts.

Atrial natriuretic peptide (ANP), a 28-amino acid peptide, is produced and secreted by cardiac atriocytes to modulate cardiovascular and renal functions. We report here the production of ANP-(5-28) and its 15K mol wt (M(r)) presumptive precursors by cytotrophoblasts of rat placentae. Placental tissues were collected from Sprague-Dawley fetal rats on days 12, 16, 18, and 20 of gestation and acid extracted for immunoreactive (ir) ANP assay. The contents of placental irANP increased over the course of fetal growth, with the highest amount (mean +/- SE, 1083 +/- 125 pg/tissue; n = 7) found near term. Sephadex G-50 gel chromatographic profiles of the placental extract revealed a major peak of irANP coeluted with the 3K M(r) of synthetic rat (r) ANP-(1-28) and a minor peak in the position consistent with that of 15K M(r). HPLC analysis of the 3K M(r) species showed a single peak of immunoreactivity, which eluted with a retention time similar to that of rANP-(5-28). In placental sections, irANP and pro-ANP mRNA were localized by immunoperoxidase staining and colorimetric in situ hybridization in a subpopulation of placental cytotrophoblasts, but not in syncytiotrophoblasts or chorionic cells. Northern blot analysis showed a single band of pro-ANP mRNA in rat placental tissues similar in size to that found in the heart (approximately 0.85 kilobases), with the highest level of pro-ANP mRNA signal detected in the placentae of 16-day gestation fetuses. Our findings suggest that ANP is expressed and produced by a small population of rat placental cytotrophoblasts and that the 15K M(r) precursor peptide is extensively processed into the N-terminal-truncated form of ANP-(5-28) in the tissue.

Animals↗
PubMed1992

Plasticity of adrenoceptor responsiveness on irANP secretion and pro-ANP mRNA expression in hypothalamic neuron cultures: modulation by dexamethasone.

Atrial Natriuretic Peptide (ANP) or its smaller congeners are produced and secreted from the rat hypothalamus. Whereas immunoreactive (ir)ANP secretion and proANP mRNA expression in hypothalamic cell cultures of neonatal rats were augmented by norepinephrine acting through its alpha 2-adrenoceptors (AR), in the perifusion studies of adult hypothalamic fragments beta-AR was involved in the upregulation of irANP release. Here, we report that dexamethasone (DM) modulates irANP secretion and pro-ANP mRNA expression from hypothalamic neurons in culture by switching the adrenoceptor responsiveness of the cells from alpha 2- to that of beta-AR. In long term cultures of hypothalamic cells, treatment with clonidine (alpha 2-AR agonist) increased irANP secretion in a dose related manner. This effect of clonidine was abolished by DM, a glucocorticoid which by itself had little effect on the basal release of irANP. In contrast, isoprenaline, a beta-AR agonist which was ineffective when applied alone, enhanced irANP secretion from hypothalamic cultures in the presence of DM. Concurrent incubation of DM (5 nM) and isoprenaline (10 microM) augmented irANP release approximately 3 fold above that of cultures treated with DM alone (22.6 +/- 2.2; mean +/- SE, n = 4). However, phenylephrine, an alpha 1-AR agonist alone or in the presence of DM failed to stimulate irANP release. These immunoassay findings were accompanied by corresponding changes in the abundance of pro-ANP mRNA in the cultures as examined by colorimetric Northern blot analysis employing a 30 mer oligonucleotide probe corresponding to the first 10 amino acid sequence of rANP1-28. We conclude from the above observations that glucocorticoids modulate irANP secretion and pro-ANP mRNA expression in hypothalamic neurons by altering the responsiveness of the cells from alpha 2-AR to that of beta-AR.

Animals↗
PubMed1992

cis and trans regulation of tissue-specific transcription.

Analysis of both the cis-regulatory sequences which control globin gene switching as well as the trans-acting factors which bind to these sequences to elicit a differential, developmentally regulated response has lent insight into the general mechanisms responsible for tissue-specific gene regulation. We show here that the chicken adult beta-globin gene promoter sequences are intimately involved in competitive interaction with the beta/epsilon-globin enhancer to regulate differentially epsilon- versus beta-globin gene transcription. Secondly, we show that the family of GATA transcription factors directs gene regulation in a variety of discrete cell types, and describe potential cellular target genes for each member of the GATA factor family, as well as potential mechanisms whereby multiple GATA factors expressed in a single cell might be used to elicit differential transcriptional activities.

Animals↗
PubMed1992

Chronic cyclosporine therapy impairs endothelium-dependent relaxation in the renal artery of the rat.

Cyclosporine is an immunosuppressive substance that causes structural and functional alterations in endothelial cells. To examine the effects of chronic cyclosporine therapy on endothelial function, Wistar Kyoto rats received daily s.c. injections of saline, cyclosporine solvent, or cyclosporine (15, 30, or 50 mg/kg) for up to 2 wk. Blood pressure remained unchanged in all groups. Segments of the renal artery were suspended in organ chambers filled with physiological salt solution, and isometric tension was recorded. In rats treated with 30 or 50 mg/kg/day of cyclosporine, endothelium-dependent relaxations to acetylcholine of the renal artery were significantly impaired when compared with vessels obtained from rats injected with saline or solvent. The reduced acetylcholine-induced relaxation of cyclosporine-treated vessels was improved by preincubation of the preparations with the cyclooxygenase inhibitor indomethacin. Endothelium-independent relaxations in response to sodium nitroprusside were unimpaired in renal artery rings after 1 wk of cyclosporine but were reduced after 2 wk of treatment with 30 mg/kg/day. Contractions of the renal artery in response to norepinephrine and serotonin were not altered by cyclosporine. Thus, (1) high-dose cyclosporine therapy impairs endothelium-dependent relaxations in the renal artery of the rat; (2) an endothelium-derived cyclooxygenase product reduces the effects of endothelium-derived relaxing factor in cyclosporine-treated rats; and (3) chronic cyclosporine treatment slightly impairs vascular smooth muscle relaxation, whereas vascular contractility remains unaltered.

Acetylcholine↗
PubMed1992

Endothelin-induced vasoconstriction and calcium antagonists.

Endothelial cells can produce contracting factors; endothelin, a 21-amino acid peptide, is one of the most potent of these factors, which can control local vascular tone. The peptide is formed from its precursor, big endothelin, via the activity of the endothelin converting enzyme. The basal production of the peptide is stimulated by epinephrine, angiotensin II, arginine vasopressin, transforming growth factor beta, thrombin, interleukin-1 and the calcium ionophore A23187. In vascular smooth muscle cells, endothelin binds to its specific receptor (ETA-receptor and possibly ETB-receptor) which activate phospholipase C and lead to the formation of inositol trisphosphate, diacylglycerol and increased intracellular calcium levels. In certain blood vessels, the endothelin receptor is linked to voltage-operated calcium channels via a Gi-protein. This linkage may explain why calcium antagonists inhibit endothelin-induced contractions in certain, but not other blood vessels. In large conduit arteries, such as the human internal mammary artery, endothelin-induced contractions are primarily mediated by release of intracellular calcium and hence, calcium antagonists do not markedly affect the response. In contrast, in the human forearm circulation, calcium antagonists of different classes do prevent endothelin-induced contractions. Similarly, in mesenteric resistance arteries of the rat, calcium antagonists can reverse endothelin-induced contraction suggesting that calcium antagonists are particularly potent in inhibiting endothelin-induced contraction in resistance arteries, where peripheral vascular resistance and hence, blood pressure is regulated.

Animals↗
PubMed1992

[Nucleotide frequency analysis of bacteriophage phi X174 genome].

Detailed analysis was carried out on the nucleotide frequencies in the genome of bacteriophage phi X174. In coding regions the distribution of four nucleotides at the three codon sites was highly non-random, and the patterns were conspicuously similar among the genes, implying that it might be a feature of the genome. An index c, which was based on the chi 2 statistics of the site by base 3 x 4 table, was introduced to reveal he extra information embedded in the coding region, and also to discriminate between coding and non-coding open reading frames. Doublet deviation analysis showed that deviation patterns were not significantly related to the codon sites in coding regions, and were also very similar in different genes. Possible mechanisms of such similarity are discussed.

Bacteriophage phi X 174↗
PubMed1992

An epidemiological survey of deformities and disabilities among 14257 leprosy patients in 11 counties.

This study was planned and conducted in 11 counties in Yangzhou Prefecture, which had formerly had a high prevalence of leprosy. Out of 14257 leprosy patients, 8122 (56.97%) with permanent deformities and disabilities were found. The disability rate was much higher among patients with multibacillary (MB) leprosy (81.15%) than among those with paucibacillary (PB) leprosy (53.04%). The statistical data involving the patients and the types of deformities and disabilities are presented in this paper, and the influences of various host factors and disease factors are discussed.

Adolescent↗