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191.
192.
Schistosomiasis and hydration status: Schistosoma haematobium,but not Schistosoma mansoni increases urine specific gravity among rural Tanzanian women 下载免费PDF全文
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Xie H Patching SG Gallagher MP Litherland GJ Brough AR Venter H Yao SY Ng AM Young JD Herbert RB Henderson PJ Baldwin SA 《Molecular membrane biology》2004,21(5):323-336
NupG from Escherichia coli is the archetype of a family of nucleoside transporters found in several eubacterial groups and has distant homologues in eukaryotes, including man. To facilitate investigation of its molecular mechanism, we developed methods for expressing an oligohistidine-tagged form of NupG both at high levels (>20% of the inner membrane protein) in E. coli and in Xenopus laevis oocytes. In E. coli recombinant NupG transported purine (adenosine) and pyrimidine (uridine) nucleosides with apparent K(m) values of approximately 20-30 microM and transport was energized primarily by the membrane potential component of the proton motive force. Competition experiments in E. coli and measurements of uptake in oocytes confirmed that NupG was a broad-specificity transporter of purine and pyrimidine nucleosides. Importantly, using high-level expression in E. coli and magic-angle spinning cross-polarization solid-state nuclear magnetic resonance, we have for the first time been able directly to measure the binding of the permeant ([1'-(13)C]uridine) to the protein and to assess its relative mobility within the binding site, under non-energized conditions. Purification of over-expressed NupG to near homogeneity by metal chelate affinity chromatography, with retention of transport function in reconstitution assays, was also achieved. Fourier transform infrared and circular dichroism spectroscopy provided further evidence that the purified protein retained its 3D conformation and was predominantly alpha-helical in nature, consistent with a proposed structure containing 12 transmembrane helices. These findings open the way to elucidating the molecular mechanism of transport in this key family of membrane transporters. 相似文献
195.
Young A. J.; Sawka M. N.; Neufer P. D.; Muza S. R.; Askew E. W.; Pandolf K. B. 《Journal of applied physiology》1989,66(4):1809-1816
This investigation studied the importance of muscle glycogen levels for body temperature regulation during cold stress. Physiological responses of eight euglycemic males were measured while they rested in cold (18 degrees C, stirred) water on two separate occasions. The trials followed a 3-day program of diet and exercise manipulation designed to produce either high (HMG) or low (LMG) preimmersion glycogen levels in the muscles of the legs, arms, and upper torso. Preimmersion vastus lateralis muscle glycogen concentrations were lower during the LMG trial (144 +/- 14 mmol glucose/kg dry tissue) than the HMG trial (543 +/- 53 mmol glucose/kg dry tissue). There were no significant differences between the two trials in shivering as reflected by aerobic metabolic rate or in the amount of body cooling as reflected by changes in rectal temperature during the immersions. Postimmersion muscle glycogen levels remained unchanged from preimmersion levels in both trials. Small but significant increases in plasma glucose and lactate concentration occurred during both immersions. Plasma glycerol increased during immersion in the LMG trial but not in the HMG trial. Plasma free fatty acid concentration increased during both immersion trials, but the change was apparent sooner in the LMG immersion. It was concluded that thermoregulatory responses of moderately lean and fatter individuals exposed to cold stress were not impaired by a substantial reduction in the muscle glycogen levels of several major skeletal muscle groups. Furthermore, the data suggest that, depending on the intensity of shivering, other metabolic substrates are available to enable muscle glycogen to be spared. 相似文献
196.
Cheon H Rho YH Choi SJ Lee YH Song GG Sohn J Won NH Ji JD 《Journal of immunology (Baltimore, Md. : 1950)》2006,177(2):1092-1100
In inflamed joints of rheumatoid arthritis, PGE(2) is highly expressed, and IL-10 and IL-6 are also abundant. PGE(2) is a well-known activator of the cAMP signaling pathway, and there is functional cross-talk between cAMP signaling and the Jak-STAT signaling pathway. In this study, we evaluated the modulating effect of PGE(2) on STAT signaling and its biological function induced by IL-10 and IL-6, and elucidated its mechanism in THP-1 cells. STAT phosphorylation was determined by Western blot, and gene expression was analyzed using real-time PCR. Pretreatment with PGE(2) significantly augmented IL-10-induced STAT3 and STAT1 phosphorylation, as well as suppressors of cytokine signaling 3 (SOCS3) and IL-1R antagonist gene expression. In contrast, PGE(2) suppressed IL-6-induced phosphorylation of STAT3 and STAT1. These PGE(2)-induced modulating effects were largely reversed by actinomycin D. Pretreatment with dibutyryl cAMP augmented IL-10-induced, but did not change IL-6-induced STAT3 phosphorylation. Misoprostol, an EP2/3/4 agonist, and butaprost, an EP2 agonist, augmented IL-10-induced STAT3 phosphorylation and SOCS3 gene expression, but sulprostone, an EP1/3 agonist, had no effect. H89, a protein kinase A inhibitor, and LY294002, a PI3K inhibitor, diminished PGE(2)-mediated augmentation of IL-10-induced STAT3 phosphorylation. In this study, we found that PGE(2) selectively regulates cytokine signaling via increased intracellular cAMP levels and de novo gene expression, and these modulating effects may be mediated through EP2 or EP4 receptors. PGE(2) may modulate immune responses by alteration of cytokine signaling in THP-1 cells. 相似文献
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Jang Hye Jin Choi Ji Yeon Kim Kangjoon Yong Seung Hyun Kim Yeon Wook Kim Song Yee Kim Eun Young Jung Ji Ye Kang Young Ae Park Moo Suk Kim Young Sam Cho Young-Jae Lee Sang Hoon 《Respiratory research》2021,22(1):1-9
IL-35 subunit EBI3 is up-regulated in pulmonary fibrosis tissues. In this study, we investigated the pathological role of EBI3 in pulmonary fibrosis and dissected the underlying molecular mechanism. Bleomycin-induced pulmonary fibrosis mouse model was established, and samples were performed gene expression analyses through RNAseq, qRT-PCR and Western blot. Wild type and EBI3 knockout mice were exposed to bleomycin to investigate the pathological role of IL-35, via lung function and gene expression analyses. Primary lung epithelial cells were used to dissect the regulatory mechanism of EBI3 on STAT1/STAT4 and STAT3. IL-35 was elevated in both human and mouse with pulmonary fibrosis. EBI3 knockdown aggravated the symptoms of pulmonary fibrosis in mice. EBI3 deficiency enhanced the expressions of fibrotic and extracellular matrix-associated genes. Mechanistically, IL-35 activated STAT1 and STAT4, which in turn suppressed DNA enrichment of STAT3 and inhibited the fibrosis process. IL-35 might be one of the potential therapeutic targets for bleomycin-induced pulmonary fibrosis. 相似文献
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200.
Oikawa H Tun Z Young DR Ozawa H Yamazaki K Tanaka E Honda K 《Biochemical and biophysical research communications》2002,297(2):341-345
Hypervariable segments of mitochondrial DNA (mtDNA) (HV1 and HV2) were analyzed in Klinefelter's syndrome and compared to normal population data. One pair of samples consisting of a Japanese mother and affected son with Klinefelter's syndrome (involved in a criminal case), and seven unrelated DNA samples from Caucasian Klinefelter males (two involved in criminal cases and five diagnosed) were collected in Japan and the United States. The diagnosis of Klinefelter's syndrome was established previously by multiplex XY-STR typing detecting two X alleles and one Y allele in the samples. Haplotype analysis of the mtDNA sequence in Klinefelter males was found to be identical, unique, and specific, as it was not found in the normal population. Astonishingly, family data exhibited that the haplotype of the mtDNA in the son was apparently different from the mother's, suggesting that the mtDNA of Klinefelter male would not be inherited from mother to son. Our data indicate that possible interaction of the sex chromosome and the mtDNA exists, and suggests that the specific mtDNA haplotype could cause the abnormal cell to fertilize and reproduce itself. 相似文献