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991.
Genetic Fine‐Mapping and Identification of Candidate Genes and Variants for Adiposity Traits in Outbred Rats 下载免费PDF全文
Gregory R. Keele Jeremy W. Prokop Hong He Katie Holl John Littrell Aaron Deal Sanja Francic Leilei Cui Daniel M. Gatti Karl W. Broman Michael Tschannen Shirng‐Wern Tsaih Maie Zagloul Yunjung Kim Brittany Baur Joseph Fox Melanie Robinson Shawn Levy Michael J. Flister Richard Mott Leah C. Solberg Woods 《Obesity (Silver Spring, Md.)》2018,26(1):213-222
992.
993.
2012~2013年每年的4~7月,在陕西神木县红碱淖(39°04'21″~39°04'43″N,109°53'12″~109°53'40″E)对白喉林莺(Sylvia curruca)的繁殖生态进行了研究。结果表明,白喉林莺4月末迁来繁殖,5月初开始营巢于油蒿(Artemisia ordosia)、臭柏(Sabina vulgaris)和沙棘(Hippophae rhamnoides)灌丛中,巢口向上呈深杯状,巢由柳絮、枯枝和干草编织而成。对33个巢的参数进行了测量,巢外径(9.62±0.227)cm,巢内径(5.21±0.084)cm,巢深(5.05±0.160)cm,巢高(9.03±0.185)cm,巢距地面高度(24.91±1.084)cm,巢约位于植株高度的1/3处(由下而上)。营巢成功率为77.1%(n=35),窝卵数4~5枚(n=27),卵重(7.49±0.021)g,卵长径(17.27±0.057)mm,卵短径(12.86±0.080)mm(n=130)。孵化期为11~13 d,孵化率为93.1%,雏鸟出飞为90.9%。雏鸟的形态参数生长符合Logistic曲线方程拟合。植被高度、植被盖度和单株植物冠径是制约白喉林莺巢址选择的主要因素,同时恶劣天气和人为干扰是影响繁殖成效的主要原因。 相似文献
994.
Calvin Pan Yurong Gu Wei Zhang Yubao Zheng Liang Peng Hong Deng Youming Chen Lubiao Chen Sui Chen Min Zhang Zhiliang Gao 《PloS one》2012,7(11)
Background
High serum levels of lipopolysaccharide (LPS) with LPS-MD-2/TLR4 complex activated NF-kb and cytokine cause hepatic necrosis in animal models. We investigated the dynamic changes of LPS levels in patients with acute on chronic hepatitis B liver failure (ACHBLF).Methods
We enrolled ACHBLF patients for a 12-week study. Patients’ LPS levels were measured along with 10 healthy controls. Patients on supportive care and recovered without intervention(s) were analyzed. Patients’ LPS levels during the disease progression phase, peak phase, and remission phase were compared with healthy controls.Results
Among 30 patients enrolled, 25 who received interventions or expired during the study period were excluded from the analysis, five patients on supportive care who completed the study were analyzed. Significant abnormal distributions of LPS levels were observed in patients in different phases (0.0168±0.0101 in progression phase; 0.0960±0.0680 in peak phase; 0.0249±0.0365 in remission phase; and 0.0201±0.0146 in controls; respectively, p<0.05). The highest level of LPS was in the peak phase and significantly elevated when compared to controls (0.0201±0.0146 vs. 0.0960±0.0680, p = 0.007). There were no statistically significant differences in LPS levels between healthy controls and subjects in the progression phase or remission phase. Dynamic changes of LPS were correlated with MELD-Na in the progression phase (p = 0.01, R = 0.876) and in the peak phase (p = 0.000, R = −1.00).Conclusions
Significant abnormal distributions of LPS levels were observed in ACHBLF with the highest level in the peak phase. The dynamic changes of LPS were correlated with disease severity and suggested LPS causing secondary hepatic injury. 相似文献995.
In previous studies, we have shown that the inactivation of the adenosine A2A receptor exacerbates chronic cerebral hypoperfusion-induced white matter lesions (WMLs) by enhancing neuroinflammatory responses. However, the molecular mechanism underlying the effect of the adenosine A2A receptor remains unknown. Recent studies have demonstrated that cystatin F, a potent endogenous cysteine protease inhibitor, is selectively expressed in immune cells in association with inflammatory demyelination in central nervous system diseases. To understand the expression of cystatin F and its potential role in the effect of A2A receptor on WMLs induced through chronic cerebral hypoperfusion, we investigated cystatin F expression in the WMLs of A2A receptor gene knockout mice, the littermate wild-type mice and wild-type mice treated daily with the A2A receptor agonist or both CGS21680 and A2A receptor antagonist CGS21680 after chronic cerebral hypoperfusion. The results of quantitative-PCR and western blot analysis revealed that cystatin F mRNA and protein expression were significantly up-regulated in the WMLs after chronic cerebral hypoperfusion. In addition, cystatin F expression in the corpus callosum was significantly increased in A2A receptor gene knockout mice and markedly decreased in mice treated with SCH58261 on both the mRNA and protein levels. Additionally, CGS21680 counteracted the attenuation of cystatin F expression produced by SCH58261 after chronic cerebral hypoperfusion. Moreover, double immunofluorescence staining revealed that cystatin F was co-localized with the activated microglia marker CD11b. In conclusion, the cystatin F expression in the activated microglia is closely associated with the effect of the A2A receptors, which may be related to the neuroinflammatory responses occurring during the pathological process. CGS21680相似文献
996.
Liu HY Collins QF Moukdar F Zhuo D Han J Hong T Collins S Cao W 《The Journal of biological chemistry》2008,283(18):12056-12063
In this study, we tested the hypothesis that human neutrophil alpha-defensins (HNPs) inhibit hepatic glucose production through a signaling pathway distinct from insulin. The effect of HNP-1 on fasting blood glucose levels and the expression of hepatic gluconeogenic genes was first examined. Using hyperinsulinemic-euglycemic clamps, we determined the effect of HNP-1 on endogenous glucose production, hepatic expression of key gluconeogenic genes and glucose uptake in skeletal muscle in Zucker diabetic fatty rats. In isolated primary hepatocytes, we studied the effect of HNP-1 and -2 on glucose production, expression of gluconeogenic genes, and phosphorylation of Akt, c-Src, and FoxO1. Our results show that HNP-1 reduced blood glucose levels of both normal mice and Zucker diabetic fatty rats predominantly through suppression of hepatic glucose production. HNPs inhibited glycogenolysis and gluconeogenesis in isolated hepatocytes. HNPs also suppressed expression of key gluconeogenic genes including phosphoenoylpyruvate carboxyl kinase and glucose-6-phosphatase. To investigate the mechanism, we found that HNPs stimulated phosphorylation of Akt and FoxO1 without activating IRS1. Nevertheless, HNPs activated c-Src. Blockade of c-Src activity with either a chemical inhibitor PP2 or an alternative inhibitor CSK prevented the inhibitory effect of HNPs on gluconeogenesis. Together, our results support the hypothesis that HNPs can suppress hepatic glucose production through an intracellular mechanism distinct from the classical insulin signaling pathway. 相似文献
997.
Schafer FQ Wang HP Kelley EE Cueno KL Martin SM Buettner GR 《Biological chemistry》2002,383(3-4):671-681
Singlet oxygen initiates lipid peroxidation via a nonfree radical mechanism by reacting directly with unsaturated lipids to form lipid hydroperoxides (LOOHs). These LOOHs can initiate free radical chain reactions leading to membrane leakage and cell death. Here we compare the ability and mechanism by which three small-molecule membrane antioxidants (beta-carotene, alpha-tocopherol and nitric oxide) inhibit lipid peroxidation in membranes. We demonstrate that beta-carotene provides protection against singlet oxygen-mediated lipid peroxidation, but does not slow free radical-mediated lipid peroxidation. Alpha-Tocopherol does not protect cells from singlet oxygen, but does inhibit free radical formation in cell membranes. Nitric oxide provides no direct protection against singlet oxygen exposure, but is an exceptional chain-breaking antioxidant as evident from its ability to blunt oxygen consumption during free radical-mediated lipid peroxidation. These three small-molecule antioxidants appear to have complementary mechanisms for the protection of cell membranes from detrimental oxidations. 相似文献
998.
We treated the glutamine binding protein with diethyl pyrocarbonate (DEPC) and N-bromosuccinimide (NBS) to modify respectively the sole histidine and tryptophan residues and examined the effect of these modifications on the ability of the binding protein to bind glutamine as well as the ability to restore glutamine transport in membrane vesicles of Escherichia coli. Under the conditions used, both DEPC and NBS markedly inhibited the ability to restore glutamine transport in vesicles without any significant effect on glutamine binding. Moreover, saturating quantities of glutamine had no protective effect on the inactivation of the binding protein by DEPC or NBS. Fluorometric measurement and amino acid analysis indicate that the inactivation of the binding protein in restoring vesicle transport by NBS can be attributed to the oxidation of a single tryptophan residue. Similar analysis and the inability of hydroxylamine to reverse the effect of DEPC indicate that the effects of DEPC can probably be attributed to alterations of the sole histidine and/or one or more lysine residues of the binding protein. We conclude that the glutamine binding protein possesses at least two largely nonoverlapping functional domains, one responsible for glutamine binding and the other for the interaction with the other components of the glutamine transport system. 相似文献
999.
1000.
Wei‐Guang Wang Zhao‐Yuan Wu Rui Chen Hai‐Zhou Li Hong‐Mei Li Yuan‐Dan Li Rong‐Tao Li Huai‐Rong Luo 《化学与生物多样性》2013,10(6):1061-1071
Four highly acylated diterpenoids, designated as pierisformotoxins A–D ( 1 – 4 , resp.), along with 26 known compounds, were isolated from the flowers of Pieris formosa. Among them, pierisformotoxins A and B ( 1 and 2 , resp.) were new highly acylated grayanane diterpenoids, of which the five‐membered ring A has undergone an oxidative cleavage between C(3) and C(4), followed by lactonization, to give rise to a five‐membered lactone ring between C(3) and C(5), differing from the previously reported grayanane diterpenoids with a 5/7/6/5 ring system. Results of the cAMP‐regulation‐activity assay showed that pierisformotoxin C ( 3 ) at 10 μM (inhibitory ratio (IR): 10.1%) or 2 μM (9.8%), and pierisformotoxin B ( 2 ) at 50 μM (13.9%) significantly decreased the cAMP level in N1E‐115 neuroblastoma cells (p<0.05). 相似文献