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Articles by Qin Wang
Total Records ( 5 ) for Qin Wang
  Zhenzhen Jin , Min Zhang , Aijun Yang , Yafei Shi , Huanfu Niu , Qin Wang , Chunna Yu , Zefeng Wei and Xuenan Wang
  Background and Objective: Ginsenoside Rg1 (GRg1) is the most abundant and active steroid saponin of Panax notoginseng with several pharmaceutical properties. The present study was undertaken to evaluate the effect of ginsenoside Rg1 (GRg1) on ethanol-induced male infertility in rat model. Materials and Methods: Thirty-two male rats were divided into four groups. One group (control) received saline (2 mL/day), while another group was given ethanol (EtOH, 4 g kg–1 b.wt./day). One treatment group received 20 mg GR1 kg–1 b.wt./day, while another treatment group was given 40 mg GR1 kg–1 b.wt./day. Both treatment groups were also given 4 g EtOH kg–1 b.wt./day. All treatment were given orally for 28 days. The significant differences between the groups were determined using one-way ANOVA and data were analyzed using SPSS software followed by Tukey’s test. Results: The weights of epididymis, testis and seminal vesicles, as well as testicular sperm count, viability, motility and serum testosterone levels were significantly elevated (p<0.01) by exposure to GRg1 at each of the two doses (20 and 40 mg kg–1 b.wt./day), when compared to the EtOH-treated groups. The two doses of GRg1 also led to significant (p<0.01) increases in the activities of testicular antioxidant enzymes (SOD, CAT) and the steroidogenic enzymes 3β hydroxy steroid dehydrogenase (3β HSD) and 17β hydroxy steroid dehydrogenase (17β HSD), as well as lower levels of MDA. Histomorphological lesions such as thickening of seminiferous tubules and disintegration of leydig and sertoli cells were ameliorated by both doses of GRg1. However, 40 mg kg–1 GRg1 showed better anti-infertility effect. Conclusion: Co-administration of ethanol and 40 mg kg–1 GRg1 to rats produced anti-infertility effects by suppressing alcohol-induced sperm oxidative stress and testicular toxicity.
  Qiong Huang , Jie Hu , Lin Sun and Qin Wang
  Heat Shock/Stress Proteins (HSPs) are a group of stress proteins which are closely associated with organisms’ adaptability to environment and the heat shock protein 70 is the most conserved and important member. Researchers cloned an hsp70 gene from Tenebrio molitor larvae by PCR and RACE Method and determined the mRNA abundance in the beetle developmental stages by real-time qPCR. The cDNA cloned was 2,282 bp in full length containing a 115 bp 5'untranslated region rich in adenine, a 1,935 bp open reading frame and a 232 bp 3'untranslated regionrich in adenine and thymine. It also had seven repeats of the Heat Shock Element (HSE) nGAAn in its 5'UTR and a 22 bp Poly (A) tail in the 3'UTR. The deduced heat shock protein had a highly conserved N-terminal ATPase domain and a conserved C-terminal peptide-binding domain. The tertiary structure of ATPase domain was made of two large globular subdomains which were separated by a deep cleft and the peptide-binding domain was a sandwich of 2 four-stranded β-sheets with four loops protruding upwards and two α-helices. Real-time qPCR analysis revealed that the hsp70 mRNA expression in T. molitor was characterized by heat-inducible and developmental-regulation features. The results form a basis for further research on structure, function and expression regulation of HSPs from T. molitor as well as to decipher the relationship between HSPs and stress-resistance in the beetle.
  Kai ZHANG , Xiao-Niu XU and Qin WANG
  Nitrogen cycling has been poorly characterized in urban ecosystems. An in-situ buried bag incubation technique was used to quantify net rates of N mineralization and nitrification in soils of two urban sites, a street greening belt and a university campus, and a suburban site, a forest park, in Hefei, East China. The average concentration of extractable NO3 in the surface soil (0–10 cm) was significantly higher at the urban sites than the suburban park site, whereas extractable NH+4 concentration was significantly higher at the suburban park site than the urban sites. The forest park soil had greater potential N mineralization (148.1 μg N cm−3) than the soils from the campus (138.3 μg N cm−3)and street (99.8 μg N cm−3). The net mineralization rates varied between 1.63 and 2.69 μg N cm−3 d−1 and net nitrification rates between 0.82 and 1.02 μg N cm−3 d−1 at the suburban forest park site, but the rates varied from 1.27 to 2.41 μg N cm−3 d−1 and from 1.07 to 1.49 μg N cm−3 d−1, respectively, at the urban campus site. Both net mineralization and nitrification rates were lower during dry seasons. Results from regression analysis indicated that net N mineralization was significantly and positively correlated with soil moisture and soil C/N ratio, and was negatively correlated with soil pH. Relative nitrification was, however, significantly and negatively correlated with soil moisture and soil C/N ratio, and was positively correlated with soil pH. Mean relative nitrification was 0.763, indicating the dominance of nitrate cycling relative to ammonium cycling at the urban sites. The urban soils had the great potential for N losses compared to the suburban soils.
  Jianmin Xu , Yunjia Chen , Roujian Lu , Christopher Cottingham , Kai Jiao and Qin Wang
  Spinophilin plays critical roles in regulating trafficking and signaling of the α2-adrenergic receptor (AR) both in vitro and in vivo (Wang, Q., Zhao, J., Brady, A. E., Feng, J., Allen, P. B., Lefkowitz, R. J., Greengard, P., and Limbird, L. E. (2004) Science 304, 1940–1944). In the present study, we demonstrate that protein kinase A (PKA) phosphorylation of spinophilin modulates the spinophilin-α2AAR interaction to regulate α2AAR internalization. Activation of PKA by forskolin abolishes the agonist-enhanced interaction between spinophilin and the α2AAR, and this event can be blocked by Ser → Ala mutations at the PKA phosphorylation sites of spinophilin. In addition, a Ser → Asp mutation that mimics the phosphorylated state at the PKA phosphorylation site Ser-177, which is located within the α2AAR binding region of spinophilin, is sufficient to block the spinophilin-α2AAR interaction in intact cells. In cells expressing mutant spinophilin carrying the S177D mutation, agonist-induced internalization of the α2AAR is accelerated and enhanced, as revealed by both intact cell enzyme-linked immunosorbent assay and quantitative immunofluorescent studies. Furthermore, activation of PKA by forskolin enhances agonist-induced internalization of the α2AAR in cells expressing wild type spinophilin, but not in cells lacking spinophilin or expressing the spinophilin mutant Sp177D. These results strongly support that PKA phosphorylation of spinophilin is functionally relevant in regulating α2AAR trafficking. Therefore, modulation of spinophilin-receptor interaction through phosphorylation of spinophilin may represent a novel mechanism whereby PKA regulates G protein-coupled receptor trafficking.
  Baldwin C. Mak , Qin Wang , Carol Laschinger , Wilson Lee , David Ron , Heather P. Harding , Randal J. Kaufman , Donalyn Scheuner , Richard C. Austin and Christopher A. McCulloch
  Induction of apoptosis by tensile forces is an important determinant of connective tissue destruction in osteoarthritis and periodontal diseases. We examined the role of molecular components of the unfolded protein response in force-induced apoptosis. Magnetic fields were used to apply tensile force through integrins to cultured fibroblasts bound with collagen-coated magnetite beads. Tensile force induced caspase 3 cleavage, DNA fragmentation, depolarization of mitochondria, and induction of CHOP10, all indicative of activation of apoptosis. Immunoblotting, immunocytochemistry, and release of Ca2+ from the endoplasmic reticulum showed evidence for both physical and functional associations between bound beads and the endoplasmic reticulum. Force-induced apoptosis was not detected in PERK null cells, but reconstitution of wild-type PERK in PERK null cells restored the apoptotic response. Force-induced apoptosis did not require PKR, GCN2, eIF2α, or CHOP10. Furthermore, force more than 24 h did not activate other initiators of the unfolded protein response including IRE-1 and ATF6. However, force-induced activation of caspase 3 was dependent on caspase 9 but was independent of mitochondria. We conclude that force-induced apoptosis depends on a novel function of PERK that occurs in addition to its canonical role in the unfolded protein response.
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