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排序方式: 共有492条查询结果,搜索用时 203 毫秒
401.
Nanog safeguards pluripotency and mediates germline development   总被引:3,自引:0,他引:3  
  相似文献   
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403.
The remains of the scorpion Diplocentrus peloncillensis Francke were found in 7 scats of black bears ( Ursus americanus ) collected in the Sierra de San Luis, Sonora, Mexico. The collection data and previously reported black bear population estimates for the study area suggested that, although scorpions are not a large part of black bear diets in Sonora, feeding on scorpions is not restricted to a single individual or family unit and is apparently a relatively common behavior in the population. Also, the discovery of D. peloncillensis in Sonora represents a new country record.  相似文献   
404.
用新型的6-相步光弹仪,对直径25μm的单玻璃纤维增强环氧树脂复合材料的纤维-树脂相界面微观应力分布进行测试.相步弹性学分析表明纤维末端和纤维断裂处附近的等级条纹级数较高,存在较大的应力集中区域.试样两端加载18.38,25.61和32.53MPa时,纤维末端相界面剪应力最大值分别出现在距纤维末端7,18和33μm处,为26.87,30.22和33.20MPa.纤维断裂处,加载为24.69MPa时,相界面剪应力最大值出现在距纤维断裂25μm处,约30MPa;加载增加到33.09MPa时,高的等级条纹级数区域向远离纤维断裂处延伸,相界面剪应力最大值增加到约36MPa.  相似文献   
405.
General Relativity and the Standard Model often are touted as the most rigorously and extensively confirmed scientific hypotheses of all time. Nonetheless, these theories appear to have consequences that are inconsistent with evidence about phenomena for which, respectively, quantum effects and gravity matter. This paper suggests an explanation for why the theories are not disconfirmed by such evidence. The key to this explanation is an approach to scientific hypotheses that allows their actual content to differ from their apparent content. This approach does not appeal to ceteris-paribus qualifiers or counterfactuals or similarity relations. And it helps to explain why some highly idealized hypotheses are not treated in the way that a thoroughly refuted theory is treated but instead as hypotheses with limited domains of applicability.  相似文献   
406.
Genome-wide association studies (GWAS) have identified ten loci harboring common variants that influence risk of developing colorectal cancer (CRC). To enhance the power to identify additional CRC risk loci, we conducted a meta-analysis of three GWAS from the UK which included a total of 3,334 affected individuals (cases) and 4,628 controls followed by multiple validation analyses including a total of 18,095 cases and 20,197 controls. We identified associations at four new CRC risk loci: 1q41 (rs6691170, odds ratio (OR) = 1.06, P = 9.55 × 10?1? and rs6687758, OR = 1.09, P = 2.27 × 10??, 3q26.2 (rs10936599, OR = 0.93, P = 3.39 × 10??), 12q13.13 (rs11169552, OR = 0.92, P = 1.89 × 10?1? and rs7136702, OR = 1.06, P = 4.02 × 10??) and 20q13.33 (rs4925386, OR = 0.93, P = 1.89 × 10?1?). In addition to identifying new CRC risk loci, this analysis provides evidence that additional CRC-associated variants of similar effect size remain to be discovered.  相似文献   
407.
Numerous types of DNA variation exist, ranging from SNPs to larger structural alterations such as copy number variants (CNVs) and inversions. Alignment of DNA sequence from different sources has been used to identify SNPs and intermediate-sized variants (ISVs). However, only a small proportion of total heterogeneity is characterized, and little is known of the characteristics of most smaller-sized (<50 kb) variants. Here we show that genome assembly comparison is a robust approach for identification of all classes of genetic variation. Through comparison of two human assemblies (Celera's R27c compilation and the Build 35 reference sequence), we identified megabases of sequence (in the form of 13,534 putative non-SNP events) that were absent, inverted or polymorphic in one assembly. Database comparison and laboratory experimentation further demonstrated overlap or validation for 240 variable regions and confirmed >1.5 million SNPs. Some differences were simple insertions and deletions, but in regions containing CNVs, segmental duplication and repetitive DNA, they were more complex. Our results uncover substantial undescribed variation in humans, highlighting the need for comprehensive annotation strategies to fully interpret genome scanning and personalized sequencing projects.  相似文献   
408.
As an organellar network, mitochondria dynamically regulate their organization via opposing fusion and fission pathways to maintain bioenergetic homeostasis and contribute to key cellular pathways. This dynamic balance is directly linked to bioenergetic function: loss of transmembrane potential across the inner membrane (Δψ m) disrupts mitochondrial fission/fusion balance, causing fragmentation of the network. However, the level of Δψ m required for mitochondrial dynamic balance, as well as the relative contributions of fission and fusion pathways, have remained unclear. To explore this, mitochondrial morphology and Δψ m were examined via confocal imaging and tetramethyl rhodamine ester (TMRE) flow cytometry, respectively, in cultured 143B osteosarcoma cells. When normalized to the TMRE value of untreated 143B cells as 100%, both genetic (mtDNA-depleted ρ0) and pharmacological [carbonyl cyanide m-chlorophenyl hydrazone (CCCP)-treated] cell models below 34% TMRE fluorescence were unable to maintain mitochondrial interconnection, correlating with loss of fusion-active long OPA1 isoforms (L-OPA1). Mechanistically, this threshold is maintained by mechanistic coordination of DRP1-mediated fission and OPA1-mediated fusion: cells lacking either DRP1 or the OMA1 metalloprotease were insensitive to loss of Δψ m, instead maintaining an obligately fused morphology. Collectively, these findings demonstrate a mitochondrial ‘tipping point’ threshold mediated by the interaction of Δψ m with both DRP1 and OMA1; moreover, DRP1 appears to be required for effective OPA1 maintenance and processing, consistent with growing evidence for direct interaction of fission and fusion pathways. These results suggest that Δψ m below threshold coordinately activates both DRP1-mediated fission and OMA1 cleavage of OPA1, collapsing mitochondrial dynamic balance, with major implications for a range of signaling pathways and cellular life/death events.  相似文献   
409.
We performed a meta-analysis of five genome-wide association studies to identify common variants influencing colorectal cancer (CRC) risk comprising 8,682 cases and 9,649 controls. Replication analysis was performed in case-control sets totaling 21,096 cases and 19,555 controls. We identified three new CRC risk loci at 6p21 (rs1321311, near CDKN1A; P = 1.14 × 10(-10)), 11q13.4 (rs3824999, intronic to POLD3; P = 3.65 × 10(-10)) and Xp22.2 (rs5934683, near SHROOM2; P = 7.30 × 10(-10)) This brings the number of independent loci associated with CRC risk to 20 and provides further insight into the genetic architecture of inherited susceptibility to CRC.  相似文献   
410.
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