首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   5篇
  免费   0篇
  2019年   1篇
  2018年   1篇
  2015年   1篇
  2012年   1篇
  2005年   1篇
排序方式: 共有5条查询结果,搜索用时 15 毫秒
1
1.
Topography should create spatial variation in water and nutrients and play an especially important role in the ecology of water-limited systems. We use stable isotopes to discern how plants respond both to ecological gradients associated with elevation and to neighboring legumes on a south-facing slope in the semi-arid, historically grazed steppe of northern Mongolia. Out of three target species, Potentilla acaulis, Potentilla sericea, and Festuca lenensis, when >30 cm from a legume, all showed a decrease in leaf δ15N with increasing elevation. This, together with measures of soil δ15N, suggests greater N processing at the moister, more productive, lower elevation, and more N fixation at the upper elevation, where cover of legumes and lichens and plant-available nitrate were greater. Total soil N was greater at the lower elevation, but not lichen biomass or root colonization by AMF. Leaf δ13C values for P. acaulis and F. lenensis are consistent with increasing water stress with elevation; δ13C values indicated the greatest intrinsic water use efficiency for P. sericea, which is more abundant at the upper elevation. Nearby legumes (<10 cm) moderate the effect of elevation on leaf δ15N, confirming legumes’ meaningful input of N, and affect leaf δ13C for two species, suggesting an influence on the efficiency of carbon fixation. Variation in leaf %N and %C as a function of elevation and proximity to a legume differs among species. Apparently, most N input is at upper elevations, pointing to the possible importance of grazers, in addition to hydrological processes, as transporters of N throughout this landscape.  相似文献   
2.
Histone deacetylases (HDACs) play vital roles in the pathophysiology of heart failure, which is associated with mitochondrial dysfunction. Tumor necrosis factor-α (TNF-α) contributes to the genesis of heart failure and impairs mitochondria. This study evaluated the role of HDACs in TNF-α-induced mitochondrial dysfunction and investigated their therapeutic potential and underlying mechanisms. We measured mitochondrial oxygen consumption rate (OCR) and ATP production using Seahorse XF24 extracellular flux analyzer and bioluminescent assay in control and TNF-α (10 ng/ml, 24 h)-treated HL-1 cells with or without HDAC inhibition. TNF-α increased Class I and II (but not Class IIa) HDAC activities (assessed by Luminescent) with enhanced expressions of Class I (HDAC1, HDAC2, HDAC3, and HDAC8) but not Class IIb HDAC (HDAC6 and HDAC10) proteins in HL-1 cells. TNF-α induced mitochondrial dysfunction with impaired basal, ATP-linked, and maximal respiration, decreased cellular ATP synthesis, and increased mitochondrial superoxide production (measured by MitoSOX red fluorescence), which were rescued by inhibiting HDACs with MPT0E014 (1 μM, a Class I and IIb inhibitor), or MS-275 (1 μM, a Class I inhibitor). MPT0E014 reduced TNF-α-decreased complex I and II enzyme (but not III or IV) activities (by enzyme activity microplate assays). Our results suggest that Class I HDAC actions contribute to TNF-α-induced mitochondrial dysfunction in cardiomyocytes with altered complex I and II enzyme regulation. HDAC inhibition improves dysfunctional mitochondrial bioenergetics with attenuation of TNF-α-induced oxidative stress, suggesting the therapeutic potential of HDAC inhibition in cardiac dysfunction.  相似文献   
3.
Tumour necrosis factor (TNF)‐α induces cardiac metabolic disorder and mitochondrial dysfunction. Hydrogen sulphide (H2S) contains anti‐inflammatory and biological effects in cardiomyocytes. This study investigated whether H2S modulates TNF‐α‐dysregulated mitochondrial function and metabolism in cardiomyocytes. HL‐1 cells were incubated with TNF‐α (25 ng/mL) with or without sodium hydrosulphide (NaHS, 0.1 mmol/L) for 24 hours. Cardiac peroxisome proliferator‐activated receptor (PPAR) isoforms, pro‐inflammatory cytokines, receptor for advanced glycation end products (RAGE) and fatty acid metabolism were evaluated through Western blotting. The mitochondrial oxygen consumption rate and adenosine triphosphate (ATP) production were investigated using Seahorse XF24 extracellular flux analyzer and bioluminescence assay. Fluorescence intensity using 2′, 7′‐dichlorodihydrofluorescein diacetate was used to evaluate mitochondrial oxidative stress. NaHS attenuated the impaired basal and maximal respiration, ATP production and ATP synthesis and enhanced mitochondrial oxidative stress in TNF‐α‐treated HL‐1 cells. TNF‐α‐treated HL‐1 cells exhibited lower expression of PPAR‐α, PPAR‐δ, phosphorylated 5′ adenosine monophosphate‐activated protein kinase‐α2, phosphorylated acetyl CoA carboxylase, carnitine palmitoyltransferase‐1, PPAR‐γ coactivator 1‐α and diacylglycerol acyltransferase 1 protein, but higher expression of PPAR‐γ, interleukin‐6 and RAGE protein than control or combined NaHS and TNF‐α‐treated HL‐1 cells. NaHS modulates the effects of TNF‐α on mitochondria and the cardiometabolic system, suggesting its therapeutic potential for inflammation‐induced cardiac dysfunction.  相似文献   
4.
用mtDNA D-环序列探讨蒙古和中国绵羊的起源及遗传多样性   总被引:16,自引:0,他引:16  
为了在分子水平上探讨绵羊的起源,对中国和蒙古共20个绵羊群体、314只绵羊mtDNA D-环的部分序列进行了测定,结果表明:中国绵羊和蒙古绵羊mtDNA D-环区的部分序列中A、T、G、C含量没有明显的差别;蒙古绵羊的多态位点数(28.85%)略高于中国绵羊(24.22%);中国绵羊群体的单倍型多样度在青海藏羊、甘肃藏羊、甘肃高山细毛羊、青海细:色羊、甘南藏羊、小尾寒羊和滩羊群体中较高,但在湖羊和岷县黑裘皮羊中较低;蒙古绵羊的单倍型多样度在Bayad和Baidrag群体中最高,但在Gobi—Altai群体中最低。从总体上看,蒙古绵羊的遗传多样性要略高于中国绵羊,例如单倍犁比例的平均值为86.06%(142/185):78.83%(108/137),单倍型多样度(Hd)的甲均值为0.976:0.936,核苷酸多样度(Pi(π))的平均值为0.036:0.034,平均核苷酸差异数(k)的平均值为23.50:22.48~217个中国和蒙古绵羊的单倍型序列的系统发生分析表明,中国和蒙古绵羊均有3个母系起源,被定义为A、B和C3类主要的单倍型。其中A类单倍型在所有中国绵羊群体及绝大多数蒙古绵羊群体(9/11)中占优势,平均比例为58.73%;B类单倍型居中,为24.88%;C类单倍型最少,仅为16.59%。进一步从GenBank获得的91个绵羊D-环区的序列与中国和蒙古绵羊D-环区的单倍型的进行网络关系分析,发现欧洲摩弗仑羊(European mouflon,O.musimon)与中国和蒙古绵羊具有较近的亲缘关系,但没有发现塬羊(Argali.O.ammon)、盘羊(0.rignei bochariensis)和东方盘羊(0.ammon nigrimontana)对中国和蒙古绵羊起源有贡献的证据。  相似文献   
5.
1
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号