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S Yin

Publications and source records attributed to S Yin.

At least 127 records · Page 7Linked to original sources
PubMed1993

Partial sequence comparison of eight new Chinese strains of hepatitis E virus suggests the genome sequence is relatively stable.

Partial genomic sequences representing 420 nucleotides of a nonstructional region, 480 nucleotides of the putative RNA polymerase region, and 540 nucleotides of the structural region of epidemic-associated Chinese strains of hepatitis E virus (HEV) were obtained by direct sequencing of PCR-amplified DNA. Comparison with previously published HEV sequences showed a clear relatedness of all Chinese strains to each other and to a Pakistani strain (Sar-55). All eight Chinese strains examined had very similar sequences (98.5-99.8% homology) in the regions examined and were much closer to the Pakistani strain (Sar-55) (97.9-98.4% homology) than to the Burmese strain (92.5-93.3% homology). Sequence comparisons of the three genomic regions in the Chinese strains indicated that the RNA polymerase region was much more conserved than the other nonstructural region or the structural region. HEV isolates from three remote geographic regions of China had sequences closely related to each other.

Amino Acid Sequence↗
PubMed1993

Neurochemistry, connectivity and plasticity of small intensely fluorescent (SIF) cells in the rat superior cervical ganglion.

Applying double-labelling immunofluorescence, the peptide content of solitary and clustered small intensely fluorescent (SIF) cells, identified by an antiserum to a selective membrane glycoprotein marker, synaptophysin, was correlated with the presence of catecholamines in the rat superior cervical ganglion. Most of synaptophysin-immunoreactive solitary and clustered SIF cells apparently contained dopamine (indicated by tyrosine hydroxylase-TH) but not noradrenaline (indicated by dopamine-beta-hydroxylase-DBH). Frequently, immunoreactivities for substance P or rarely, neuropeptide Y were colocalized in TH-immunolabeled cells of both types. Immunostaining for vasoactive intestinal polypeptide was found only in solitary SIF cells and was visible in TH-immunoreactive, as well as in TH-nonreactive cells. Very few solitary SIF cells were TH- and DBH-immunoreactive. Solitary and clustered SIF cells, as a rule, were encircled by leu-enkephalin-positive fibres which were also met-enkephalin-arg6-phe7-immunoreactive, indicating proenkephalin as precursor. SIF cells were additionally approached by varicose fibres which contained immunoreactivity for calcitonin gene-related peptide (CGRP) but not for enkephalins. As observed by immuno-electronmicroscopy, fibres that were immunostained for leu-enkephalin or CGRP, deeply invaginated into SIF cell somata. In addition to close membrane appositions, CGRP-immunolabeled fibres exhibited efferent synaptic contacts wih elements of SIF cell clusters. SIF cells were non-reactive to enkephalin-antisera in control ganglia and after transection of the postganglionic nerves (axotomy); but both types exhibited leu-enkephalin in preganglionically transected ganglia (decentralization) in which enkephalin-immunoreactive fibre baskets were absent. Synthesis of enkephalin in SIF cells after decentralization was confirmed by in situ hybridization demonstrating intracytoplasmic proenkephalin messenger-RNA. The findings are indicative for a differential neurochemical equipment of SIF cells in the rat superior cervical ganglion, which mainly is independent to a topographical classification. Moreover, they demonstrate the involvement of two neuropeptides in preganglionic SIF cell innervation. Finally, the observations indicate the capacity of SIF cells for proenkephalin-expression in response to preganglionic denervation.

Animals↗
PubMed1993

N-acetylation phenotype and genotype and risk of bladder cancer in benzidine-exposed workers.

Several studies in subjects occupationally exposed to arylamine carcinogens have shown increased risks for bladder cancer associated with the slow acetylator phenotype. To follow up these reports, a case-control study of N-acetylation and bladder cancer risk was carried out among subjects occupationally exposed to benzidine, in benzidine dye production and use facilities in China. Thirty-eight bladder cancer cases and 43 controls from these factories were included for study of acetylation phenotype, by dapsone administration, and for polymorphisms in the NAT2 gene, by a polymerase chain reaction (PCR)-based test. In contrast to previous studies, no increase in bladder cancer risk was found for the slow N-acetylation phenotype (OR = 0.3; 95% CI = 0.1-1.3) or for slow N-acetylation-associated double mutations in NAT2 (OR = 0.5; 95% CI = 0.1-1.8). Examination of specific mutations and adjustment for age, weight, city and tobacco use did not alter the results. When examined by level of benzidine exposure in the cases, the bladder cancer risks associated with low (OR = 0.3, 95% CI = 0.0-2.2), medium (OR = 0.7, 95% CI = 0.1-4.5) and high (OR = 0.6, 95% CI = 0.1-3.5) exposure showed no interaction between genotype and benzidine exposure, within the range of exposures experienced by subjects in this study. This study, which is the first to incorporate phenotypic and genotypic analyses, provides evidence that the NAT2-related slow N-acetylation polymorphism is not associated with an increased risk of bladder cancer in workers exposed to benzidine, and may have a protective effect.

Acetylation↗
PubMed1993

Correlation between N-acetyltransferase activity and NAT2 genotype in Chinese males.

Eighty-four healthy Chinese male control subjects derived from an occupation-based case-control study of bladder cancer were evaluated for hepatic N-acetyltransferase activity by dapsone and for NAT2 genotype using allele-specific amplification of peripheral leukocyte DNA by the polymerase chain reaction. Fifty-nine percent of the overall variation in acetylation activity was explained by genotype (p < 0.0001). The remaining variation in acetylation was not associated with dapsone N-hydroxylation activity, age, current smoking status, or weight in the study population, or within any genotype subgroup. Although acetylation activity in the homozygous mutant group did not overlap with the other genotype categories, there was moderate overlap in acetylation between the heterozygous mutant and wildtype groups, and substantial variation in acetylation within them. Considering all subjects with the identical NAT2 genotype as phenotypically similar and all subjects with differing NAT2 genotypes as phenotypically distinct may result in misclassification of metabolic risk factors in epidemiological investigations. As such, it would seem prudent, where possible, to collect both acetylation phenotype and NAT2 genotype data, since the advantages and limitations of these two sources of information complement, and serve to assess the accuracy of each other.

Aged↗
PubMed1993

Hematologic effects of stem cell factor alone and in combination with G-CSF and GM-CSF in vivo and in vitro in rodents.

The intravenous injection of rrSCF causes neutrophilia and lymphocytosis as well as the appearance of immature myeloid cells and occasional blast cells in the circulation. The marrow shows a left-shifted myeloid and erythroid hyperplasia as evidenced by increases in numbers of morphologically recognizable early myeloid and erythroid precursors. A decrease in the number of mature marrow neutrophils is noted, suggesting that the release of marrow neutrophils contributes to the peripheral neutrophilia. After 2 weeks of daily injections of rrSCF, the marrow demonstrates a remarkable mast cell hyperplasia accompanied by erythroid and lymphoid hypoplasia. rrSCF causes mast cells to appear in the circulation and causes a systemic increase in embryonic connective tissue-type mast cells. In vitro long-term culture of mouse marrow cells with rrSCF results in an outgrowth of mast cells. The coinjection of rrSCF and G-CSF for 1 week causes a synergistic increase in mature marrow neutrophils accompanied by a striking decrease in erythroid and lymphoid marrow elements. Spleens demonstrate increased granulopoiesis as well as erythropoiesis as compared to the spleens of rats treated with single growth factors. Splenic extramedullary erythropoiesis may act to compensate for the decrease in marrow erythropoiesis. The coinjection of rrSCF and G-CSF causes an increase in marrow mast cells at the end of 1 week, but the increase is much less than in rats treated with rrSCF alone. The combination of rrSCF and G-CSF causes a synergistic peripheral neutrophilia. In vivo daily administration of SCF plus GM-CSF results in a synergistic increase in marrow neutrophils, but not the striking synergistic increase in circulating neutrophils that is observed after SCF plus G-CSF. Colony-forming assays reveal a synergistic increase in CFU-GMs in the marrow, but not in peripheral blood, after coincubation with SCF plus GM-CSF as opposed to GM-CSF alone, demonstrating anatomic compartmentalization between a more primitive marrow CFU-GM subset and a more mature peripheral blood CFU-GM subset.

Animals↗
PubMed1993

Effect of acupuncture and point-injection treatment on immunologic function in rheumatoid arthritis.

The results of treatment of 54 cases of rheumatoid arthritis (RA) by warm needling (WN) and point-injection (PI) with Zhuifengsu are reported. Good clinical results were observed with an effective rate of 100%. At the same time, changes in cellular and humoral immunity and other parameters in peripheral blood were noted before and after treatment. The NK activity and IL-2 value in RA patients were found to be lower than those of normal individuals; both increased after treatment (P < 0.01). This suggests that the WN and PI with Zhuifengsu exert a regulatory effect on the cellular immunological function.

Acupuncture Points↗
PubMed1993

Intratracheal administration of endotoxin and cytokines. IV. The soluble tumor necrosis factor receptor type I inhibits acute inflammation.

Endotoxin lipopolysaccharide (LPS) administered intratracheally to rats causes pulmonary tumor necrosis factor alpha (TNF) and interleukin-1 (IL-1) production and results in acute broncho-alveolar neutrophilic inflammation. In the present study, the recombinant human TNF soluble receptor type I (sTNFrI) co-injected intratracheally with LPS is shown to inhibit significantly (P < 0.0001) the number of neutrophils in bronchoalveolar lavage specimens at 6 hours as compared to intratracheal injection of LPS alone. The sTNFrI was at least as effective as the recombinant human IL-1 receptor antagonist (IL-1ra) as an inhibitor of acute inflammation. Inhibition of LPS-induced acute inflammation by the combination of sTNFrI and IL-1ra was not significantly more than the inhibition afforded by sTNFrI alone. Intratracheal co-injection of sTNFrI with LPS unexpectedly increased TNF levels in BAL specimens, perhaps by changing the normal catabolism of TNF. On the other hand, co-injection of sTNFrI and LPS decreased IL-6 levels in BAL fluid, most likely by interfering with the induction of IL-6 by TNF. The sTNFrI may prove to be an important pharmacological down-regulator of acute inflammation.

Acute Disease↗
PubMed1992

Endotoxin-induced cytokine gene expression in vivo. IV. Expression of interleukin-1 alpha/beta and interleukin-1 receptor antagonist mRNA during endotoxemia and during endotoxin-initiated local acute inflammation.

After the intravenous (IV) injection of endotoxin, (lipopolysaccharide [LPS]), in the rat, interleukin-1 alpha/beta (IL-1 alpha/beta) mRNA expression peaks at 1 hour in whole organ RNA preparations of the lung, liver, spleen, and bowel. Interleukin-1 receptor antagonist (IL-1ra) mRNA peaks at 2 to 4 hours, consistent with the hypothesis that IL-1ra acts as an endogenous negative feedback mechanism to downregulate the proinflammatory effects of IL-1. After the intratracheal (IT) injection of LPS, however, IL-1 and IL-1ra mRNA levels in whole lung peak at 6 hours, concurrent with the maximum influx of neutrophils (PMNs) into the bronchoalveolar space. To address the cellular source of IL-1 and IL-1ra mRNA in the lung during acute pneumonitis, mRNA levels were studied in bronchoalveolar lavage (BAL) macrophages incubated with LPS in vitro for 6 hours as compared with BAL cells (95% PMNs) obtained 6 hours after IT injection of LPS. A much greater expression of IL-1 and IL-1ra mRNA was observed in PMN-rich BAL cells obtained after IT injection of LPS, suggesting that PMNs contribute substantially to IL-1 and IL-1ra mRNA expression. Fractionation of alveolar macrophage-enriched and PMN-enriched subpopulations from the BAL cells obtained at 6 hours after IT injection of LPS confirmed that neutrophils are a source of IL-1 and IL-1ra mRNA. The difference in the kinetics of IL-1 and IL-1ra mRNA expression in whole lung RNA preparations after IV and IT injections of LPS is due to the contribution of PMNs that appear in the lung in large numbers after IT injection. Finally, human peripheral blood PMNs were found to express IL-1ra mRNA and protein after in vitro incubation with LPS. PMNs may contribute to the up- and downregulation of their own accumulation by expressing both IL-1 and IL-1ra.

Animals↗
PubMed1992

[Isolation and identification of a strain of Pseudomonas SP. producing insoluble glucan hydrolase].

A strain, CIB871, isolated from the natural world can hydrolyze insoluble glucan(IG) produced by S. mutans. This organism has been identified to be a strain of Pseudomonas SP. It grows well at 30 degrees C. The optimum medium for producing insoluble glucan hydrolase (IGase) is composed of 0.3% peptone, 0.03% IG and M1 salt solution (NH4)2 SO4 1mg/ml, MgSO4 50 micrograms/ml, FeCl2 50 micrograms/ml, K2HPO4 0.5mg/ml). The IGase production reached maximum when cultured for 65-70 hours.

Glucans↗
PubMed1991

Hematologic effects of stem cell factor in vivo and in vitro in rodents.

Recombinant rat stem cell factor (rrSCF) administered to rats as a single intravenous injection causes a dose-dependent neutrophilia and lymphocytosis as well as the appearance of immature myeloid cells and occasional blast cells in the circulation. Neutrophilia begins at 2 hours, peaks at 4 to 6 hours, and subsides between 12 and 24 hours. Lymphocytosis occurs at 0.5 hours and has subsided by 2 hours. rrSCF-induced neutrophilia and lymphocytosis are abrogated by boiling, demonstrating that endotoxin-contamination of the rrSCF preparation is not responsible for the observed hematologic effects. The bone marrow at 6 hours after injection of rrSCF shows a left-shifted myeloid and erythroid hyperplasia as evidenced by significant increases in the absolute numbers of morphologically recognizable early myeloid and erythroid precursors. A concurrent decrease in the absolute numbers of mature marrow neutrophils is noted, suggesting that the release of marrow neutrophils contributes to the peripheral neutrophilia. After 2 weeks of daily injections of rrSCF, bone marrow smears demonstrate a remarkable mast cell hyperplasia accompanied by a decrease in total marrow cellularity and by a striking erythroid and lymphoid hypoplasia. rrSCF also causes mast cells to appear in the circulation and causes a systemic increase in embryonic connective tissue-type, but not mucosal-type, mast cells. In vitro long-term culture of lineage-depleted mouse bone marrow cells with rrSCF results in an almost pure outgrowth of mast cells.

Animals↗
PubMed1991

Specific binding and internalization of monoclonal antibody HI98-daunorubicin conjugate by human leukemic cells (HL60).

McAb-HI98 has been proved to bind specifically to HL60 cells. In this study, we further observed the specific binding of HI98-Daunorubicin (DNR) conjugate to HL60 cells, the transmembranal transport of HI98-DNR and the process of internalization by immunoelectron microscopy. After HL60 cells were incubated with HI98-DNR-Au, gold particles were first found on the surface membranes of HL60 cells, and then inside the cells. Internalization was found to occur through the formation of endocytic vesicles. Results indicate that the immunoconjugate selectively binds to target cells and enters the cells specifically and rapidly, thus enhancing intracellular drug concentration.

Antibodies, Monoclonal↗
PubMed1991

Intratracheal injection of endotoxin and cytokines. II. Interleukin-6 and transforming growth factor beta inhibit acute inflammation.

The nature of the endogenous mediators that down-regulate and curtail the exodus of neutrophils into local acute inflammatory sites is unknown. In the present report, interleukin-6 (IL-6) and transforming growth factor beta (TGF beta), members of a family of macrophage-derived proteins known as cytokines, are shown to inhibit significantly the acute neutrophilic exodus caused by an intratracheal injection of endotoxin (LPS), a proinflammatory component of the cell walls of gram-negative bacteria. Transforming growth factor beta (10 micrograms) and IL-6 (10 micrograms) coinjected intratracheally with LPS (10 micrograms) each inhibited the number of neutrophils in 6-hour bronchoalveolar lavage (BAL) specimens by approximately 50%. The intratracheal coinjection of IL-6, TGF beta, and LPS inhibited the LPS-induced neutrophilic inflammatory exodus by nearly 75%. Interleukin-6 also is shown to be endogenously upregulated within the lung after intratracheal challenge with endotoxin, providing evidence that IL-6 may represent an endogenous negative feedback mechanism to inhibit endotoxin-initiated cytokine-mediated acute inflammation. Interleukin-6 and TGF beta both strongly inhibited the quantity of TNF-alpha recovered in the BAL fluid of LPS-challenged rats, suggesting that downregulation of LPS-induced TNF-alpha production within the lung represents one mechanism whereby IL-6 and TGF beta exert an antiinflammatory action. Interleukin-6 and TGF beta represent novel pharmacologic and, probably, endogenous inhibitors of acute inflammation.

Acute Disease↗
PubMed1990

neu oncogene protein and epidermal growth factor receptor are independently expressed in benign and malignant breast tissues.

The neu oncogene protein, p185, and epidermal growth factor receptor (EGFR) were localized immunohistochemically in benign and malignant human breast tissues using monoclonal antibodies. Both benign and malignant epithelial cells were positive for these oncogene proteins in acetone-postfixed frozen sections. Stromal cells were negative for p185, but occasionally positive for EGFR. Myoepithelial cells were consistently positive for EGFR, and p185 was localized predominantly in duct-lining cells, where the basolateral plasma membrane was the normal expression site of both substances. Paraformaldehyde-prefixed frozen sections were less sensitive for antigen demonstration. Based on the intensity of immunoreactivity, 11 of 37 acetone-postfixed breast carcinomas (30%) were judged neu overexpressors, while none of 24 benign tissues overexpressed neu. Epidermal growth factor receptor was demonstrated in 18 of 36 acetone-postfixed cancer tissues (50%) and was overexpressed in three (8%). At the cellular level, heterogenous expression of p185 and EGFR was occasionally observed in both benign and malignant tissues, and a single case of cancer overexpressing both neu and EGFR showed reciprocal patterns of staining, indicating their independent expression. In some carcinomas, EGFR was localized only in stromal cells. Our findings confirmed mutually independent expression of the two closely related protooncogenes in benign and malignant breast tissues.

Biomarkers, Tumor↗
PubMed1990

Strategies for the analysis of oncogene overexpression. Studies of the neu oncogene in breast carcinoma.

The development of a consistent strategy for the analysis of oncogene expression at the cellular level is essential for understanding the roles of these genes in the development and progression of human neoplasia. Detection of the neu oncogene products in breast carcinoma was selected as a model for analysis of oncogene expression. Fifty-two primary human breast carcinomas were evaluated by quantitation of neu DNA amplification and mRNA expression and by localization of neu mRNA and protein (p 185) at the cellular level by in situ hybridization (ISH) and immunohistochemistry (IHC). The specificity and sensitivity of the molecular and immunologic probes for neu were established with the use of genetically engineered cell lines that overexpressed either neu or epidermal growth factor receptor (EGFR). Twenty-nine percent of breast carcinomas demonstrated neu DNA amplification and mRNA overexpression, and there was close correlation between the level of neu mRNA expression and detection of neu gene products by ISH and IHC. Thirty-two percent of carcinomas demonstrated neu mRNA overexpression by ISH. The immunohistochemical method using TA1 monoclonal antibody for p185 was exquisitely sensitive in acetone-fixed frozen sections and provided an excellent approach for judging overexpression as confirmed by the various molecular analyses. All areas of nonmalignant breast epithelium stained weakly, and a wide range of staining intensity was observed in malignant breast epithelium, with 31% of carcinomas judged to be p185 overexpressors. Heterogeneous expression of p185 was seen in some carcinomas. This study provides a strategic approach for the evaluation of oncogene expression in human tumors.

Antibodies, Monoclonal↗
PubMed1990

[Purging of leukemic cells from mouse marrow and tumor suspensions with lysosomotropic agent N-dodecyl morpholine].

The lysosomotropic agent N-dodecyl morpholine (NDM) showed a marked killing of mice leukemic cells in vitro: 100% killing of L7811 leukemic cells (10(6) cells/ml) at a concentration of 15 micrograms/ml. Bone marrow of 615 mice containing 5% L7811 leukemic cells was treated with NDM and then infused into normal 615 mice. Mean survival times (MST) were 16.3 +/- 1.78 days and 15.8 +/- 2.32 days for control group and solvent group respectively, while the MST of groups treated with NDM were more than 40 days. When the marrow was infused into lethally irradiated mice, those mice receiving NDM-purged marrow died of radiation disease instead of leukemia. But when the number of marrow cells infused was increased to 2 x 10(6) cells/mouse, the mice survived for significantly longer times than did control group mice or those of the group infused with 10(6) cells/mouse.

Animals↗
PubMed1990

Treatment of 910 cases of atrophic gastritis with wei you decoction.

In treatment of 910 cases of chronic atrophic gastritis with Wei You Decoction, the overall effective rate was 96.9%. The disease was considered as due to deficiency of vital energy with stagnation of cold, and therefore treatment was to invigorate blood circulation. The Wei You Decoction had functions of replenishing vital energy, warming the middle burner, invigorating blood circulation, and resolving stasis, thus reversing the morbid process in the gastric mucosa. It was nontoxic, and the side-effects were minimal. The therapeutic effect was prompt and persistent. No malignant change was observed after taking the drug.

Adult↗
PubMed1990

Tumor necrosis factor exerts dose-dependent effects on erythropoiesis and myelopoiesis in vivo.

Recombinant human tumor necrosis factor alpha (TNF) administered i.v. to Lewis rats as a daily low dose for 1 week induces an erythroid hyperplasia of late normoblasts. Although the erythroid marrow compartment is hyperplastic, the morphology of the normoblasts is dysplastic and there is no accompanying increase in circulating red blood cells, suggesting a state of ineffective erythropoiesis. TNF administered on the same daily schedule as a high dose induces an erythroid hypoplasia of late normoblasts and a peripheral anemia with decreases in the hematocrit and hemoglobin. A tremendous myeloid hyperplasia is noted in rats treated with high-dose TNF, and the mechanism of the erythroid anemia may be in part due to the increase in neutrophils. In support of the hypothesis that the erythroid anemia may be partly myelophthisic in nature, a decrease in marrow lymphocytes was also noted. On the other hand, the dysplastic morphology of the late erythroid precursors in rats treated with low-dose TNF would also be consistent with a destructive effect of TNF on erythroid precursors as a mechanism of TNF-related anemia. In light of the in vitro inhibitory effects of TNF on erythropoiesis and myelopoiesis as reported by previous investigators, the erythroid and myeloid hyperplasia noted in vivo most likely represent indirect effects.

Anemia↗