原特提斯的消減極性:西昆侖128公里巖體的啟示

The Yirba (128 km) pluton is an early Paleozoic dioritic intrusion of western Kunlun orogenic belt, northwest China as an important element when reconstructing the evolution history of this belt. Due to the scarcity of field data and methodological difference in studying this pluton, however, no consensus for its age, source and tectonic setting has been adopted. In this paper, we present new geochronological and geochemical data for the Yirba pluton, aiming to better understand its age, source, and hence the early Paleozoic tectonic evolutionary history of western Kunlun. U-Pb data by single grain zircon analyses suggest that the Yirba pluton was emplaced 471 ± 5 Ma ago and contains ca. 490 Ma zircon grains inherited from source, or captured in the magma chamber. The pluton is enriched in Al 2 O 3 (15.7% ∼ 18.4%), Sr (470 ∼ 864 μg/g) and other LILEs (large ion lithosphile elements), but relatively depleted in HFSE (high field strength elements and HREE), with LREE-enriched patterns and low to medium europium anomalies (δEu = ∼ 0.7), showing typical characteristics of I-type, volcanic arc granitoids. Although its relatively high Al 2 O 3, Sr and low MgO contents make it resemble adakite, its relatively high Yb (1.92 ∼ 2.88 μg/g), Y (19.4 ∼ 34.0 μg/g) contents, low Sr/Y (24.2 ∼ 37.0) , Zr/Sm (7.3 ∼ 21) and relatively high initial Sr isotope ratios (0.7075 ∼ 0.7091) do not support a subducting slab origin. Its Nd model ages (1.06 ∼ 1.35 Ga) indicate a juvenile source, while its O isotope compositions (+5.7‰ ∼ + 7.4‰) and Sr-O isotope relationship preclude significant involvement of sialic materials. The major, trace, REE and Nd-Sr-O isotope compositions strongly suggest that the Yirba pluton was formed by partial melting of mafic lower crust in a southward growing, active continental margin environment. The existence of volcanic arc granitoids in the south margin of the North Kunlun terrane suggests that the subduction polarity of the Proto-Tethys was northward.128公里巖體是西昆侖造山帶中一個早古生代的花崗閃長巖體,長期以來一直是研究西昆侖構造演化的重要參考依據。然而由于區域地質資料的不足和研究手段的不同,對該巖體的形成年代、源區性質以及構造背景等方面還存在著不同的認識。本文試圖通過地質年代學和地球化學方面的研究,明確128公里巖體的成巖時代和構造背景,進而制約西昆侖的早古生代構造演化。單顆粒鋯石的U-Pb定年結果表明128公里巖體形成于471±5 Ma并含有可能形成于早期巖漿房或繼承自源區的490 Ma左右的鋯石。128公里巖體富Al_2O_3(15.7％～18.4％),Sr(470～864μg/g)和大離子親石元素但相對虧損 高場強元素,相對富集輕稀土且具有低到中等的負銪異常(δEu=～0.7),顯示出典型的Ⅰ型弧花崗巖特征。盡管其富集Al_2O_3、Sr、相對低的MgO含量和Y/Yb比值使其非常類似于埃達克巖,但其相對高的Yb(1.92～2.88μg/g)、Y(19.4～34.0μg/g)含量,低的Sr/Y(24.2～37.0)和Zr/Sm(7.3～21)比值以及相對高的初始Sr同位素組成(0.7075～0.7091)排除了消減板塊在石榴石穩定區發生部分熔融的可能性。低的氧同位素组成( + 5.7％～7.4％) 以及Sr-O 同位素关系表明该岩体并非形成于地慢来源的岩泉与变质围岩间的同化混染。高的稀土含量、明显的稀土分馏以及相对高的Sr 同位素组成表明12 8 公里岩体不大可能形成于受陆源物质影响较小的大洋岛弧, 而更可能形成于活动大陆边缘环境中基性地壳物质的部分熔融。北昆仑地体的南缘存在火山弧型花岗岩的事实表明, 原特提斯的消减方向应当是向北的。published_or_final_versio

Mapping Dynamic Histone Acetylation Patterns to Gene Expression in Nanog-depleted Murine Embryonic Stem Cells

Embryonic stem cells (ESC) have the potential to self-renew indefinitely and to differentiate into any of the three germ layers. The molecular mechanisms for self-renewal, maintenance of pluripotency and lineage specification are poorly understood, but recent results point to a key role for epigenetic mechanisms. In this study, we focus on quantifying the impact of histone 3 acetylation (H3K9,14ac) on gene expression in murine embryonic stem cells. We analyze genome-wide histone acetylation patterns and gene expression profiles measured over the first five days of cell differentiation triggered by silencing Nanog, a key transcription factor in ESC regulation. We explore the temporal and spatial dynamics of histone acetylation data and its correlation with gene expression using supervised and unsupervised statistical models. On a genome-wide scale, changes in acetylation are significantly correlated to changes in mRNA expression and, surprisingly, this coherence increases over time. We quantify the predictive power of histone acetylation for gene expression changes in a balanced cross-validation procedure. In an in-depth study we focus on genes central to the regulatory network of Mouse ESC, including those identified in a recent genome-wide RNAi screen and in the PluriNet, a computationally derived stem cell signature. We find that compared to the rest of the genome, ESC-specific genes show significantly more acetylation signal and a much stronger decrease in acetylation over time, which is often not reflected in an concordant expression change. These results shed light on the complexity of the relationship between histone acetylation and gene expression and are a step forward to dissect the multilayer regulatory mechanisms that determine stem cell fate.Comment: accepted at PLoS Computational Biolog

Notch signaling during human T cell development

Notch signaling is critical during multiple stages of T cell development in both mouse and human. Evidence has emerged in recent years that this pathway might regulate T-lineage differentiation differently between both species. Here, we review our current understanding of how Notch signaling is activated and used during human T cell development. First, we set the stage by describing the developmental steps that make up human T cell development before describing the expression profiles of Notch receptors, ligands, and target genes during this process. To delineate stage-specific roles for Notch signaling during human T cell development, we subsequently try to interpret the functional Notch studies that have been performed in light of these expression profiles and compare this to its suggested role in the mouse

Disparities and risks of sexually transmissible infections among men who have sex with men in China: a meta-analysis and data synthesis.

BACKGROUND: Sexually transmitted infections (STIs), including Hepatitis B and C virus, are emerging public health risks in China, especially among men who have sex with men (MSM). This study aims to assess the magnitude and risks of STIs among Chinese MSM. METHODS: Chinese and English peer-reviewed articles were searched in five electronic databases from January 2000 to February 2013. Pooled prevalence estimates for each STI infection were calculated using meta-analysis. Infection risks of STIs in MSM, HIV-positive MSM and male sex workers (MSW) were obtained. This review followed the PRISMA guidelines and was registered in PROSPERO. RESULTS: Eighty-eight articles (11 in English and 77 in Chinese) investigating 35,203 MSM in 28 provinces were included in this review. The prevalence levels of STIs among MSM were 6.3% (95% CI: 3.5-11.0%) for chlamydia, 1.5% (0.7-2.9%) for genital wart, 1.9% (1.3-2.7%) for gonorrhoea, 8.9% (7.8-10.2%) for hepatitis B (HBV), 1.2% (1.0-1.6%) for hepatitis C (HCV), 66.3% (57.4-74.1%) for human papillomavirus (HPV), 10.6% (6.2-17.6%) for herpes simplex virus (HSV-2) and 4.3% (3.2-5.8%) for Ureaplasma urealyticum. HIV-positive MSM have consistently higher odds of all these infections than the broader MSM population. As a subgroup of MSM, MSW were 2.5 (1.4-4.7), 5.7 (2.7-12.3), and 2.2 (1.4-3.7) times more likely to be infected with chlamydia, gonorrhoea and HCV than the broader MSM population, respectively. CONCLUSION: Prevalence levels of STIs among MSW were significantly higher than the broader MSM population. Co-infection of HIV and STIs were prevalent among Chinese MSM. Integration of HIV and STIs healthcare and surveillance systems is essential in providing effective HIV/STIs preventive measures and treatments. TRIAL REGISTRATION: PROSPERO NO: CRD42013003721

lincRNAs act in the circuitry controlling pluripotency and differentiation

Although thousands of large intergenic non-coding RNAs (lincRNAs) have been identified in mammals, few have been functionally characterized, leading to debate about their biological role. To address this, we performed loss-of-function studies on most lincRNAs expressed in mouse embryonic stem (ES) cells and characterized the effects on gene expression. Here we show that knockdown of lincRNAs has major consequences on gene expression patterns, comparable to knockdown of well-known ES cell regulators. Notably, lincRNAs primarily affect gene expression in trans. Knockdown of dozens of lincRNAs causes either exit from the pluripotent state or upregulation of lineage commitment programs. We integrate lincRNAs into the molecular circuitry of ES cells and show that lincRNA genes are regulated by key transcription factors and that lincRNA transcripts bind to multiple chromatin regulatory proteins to affect shared gene expression programs. Together, the results demonstrate that lincRNAs have key roles in the circuitry controlling ES cell state.Broad InstituteHarvard UniversityNational Human Genome Research Institute (U.S.)Merkin Family Foundation for Stem Cell Researc

SOX2 Co-Occupies Distal Enhancer Elements with Distinct POU Factors in ESCs and NPCs to Specify Cell State

SOX2 is a master regulator of both pluripotent embryonic stem cells (ESCs) and multipotent neural progenitor cells (NPCs); however, we currently lack a detailed understanding of how SOX2 controls these distinct stem cell populations. Here we show by genome-wide analysis that, while SOX2 bound to a distinct set of gene promoters in ESCs and NPCs, the majority of regions coincided with unique distal enhancer elements, important cis-acting regulators of tissue-specific gene expression programs. Notably, SOX2 bound the same consensus DNA motif in both cell types, suggesting that additional factors contribute to target specificity. We found that, similar to its association with OCT4 (Pou5f1) in ESCs, the related POU family member BRN2 (Pou3f2) co-occupied a large set of putative distal enhancers with SOX2 in NPCs. Forced expression of BRN2 in ESCs led to functional recruitment of SOX2 to a subset of NPC-specific targets and to precocious differentiation toward a neural-like state. Further analysis of the bound sequences revealed differences in the distances of SOX and POU peaks in the two cell types and identified motifs for additional transcription factors. Together, these data suggest that SOX2 controls a larger network of genes than previously anticipated through binding of distal enhancers and that transitions in POU partner factors may control tissue-specific transcriptional programs. Our findings have important implications for understanding lineage specification and somatic cell reprogramming, where SOX2, OCT4, and BRN2 have been shown to be key factors

Determination of the number of J/ψ events with J/ψ → inclusive decays

postprin

Higher-order multipole amplitude measurement in ψ ′→γχ c2

Using 106×106 ψ ′ events collected with the BESIII detector at the BEPCII storage ring, the higher-order multipole amplitudes in the radiative transition ψ ′→γχ c2→γπ +π -/γK +K - are measured. A fit to the χ c2 production and decay angular distributions yields M2=0.046±0. 010±0.013 and E3=0.015±0.008±0.018, where the first errors are statistical and the second systematic. Here M2 denotes the normalized magnetic quadrupole amplitude and E3 the normalized electric octupole amplitude. This measurement shows evidence for the existence of the M2 signal with 4.4σ statistical significance and is consistent with the charm quark having no anomalous magnetic moment. © 2011 American Physical Society.published_or_final_versio

Evidence for direct CP violation in B-0 -> K+pi(-) decays

We report evidence for direct CP violation in the decay B-0-->K(+)pi(-) with 253 fb(-1) of data collected with the Belle detector at the KEKB e(+)e(-) collider. Using 275x10(6) B(B) over bar pairs we observe a B-->K(+/-)pi(-/+) signal with 2140+/-53 events. The measured CP violating asymmetry is A(CP)(K(+)pi(-))=-0.101+/-0.025(stat)+/-0.005(syst), corresponding to a significance of 3.9sigma including systematics. We also search for CP violation in the decays B+-->K(+)pi(0) and B+-->pi(+)pi(0). The measured CP violating asymmetries are A(CP)(K(+)pi(0))=0.04+/-0.05(stat)+/-0.02(syst) and A(CP)(pi(+)pi(0))=-0.02+/-0.10(stat)+/-0.01(syst), corresponding to the intervals -0.05< A(CP)(K(+)pi(0))<0.13 and -0.18< A(CP)(pi(+)pi(0))<0.14 at 90% confidence level

Multifaceted roles of GSK-3 and Wnt/β-catenin in hematopoiesis and leukemogenesis: opportunities for therapeutic intervention

Glycogen synthase kinase-3 (GSK-3) is well documented to participate in a complex array of critical cellular processes. It was initially identified in rat skeletal muscle as a serine/threonine kinase that phosphorylated and inactivated glycogen synthase. This versatile protein is involved in numerous signaling pathways that influence metabolism, embryogenesis, differentiation, migration, cell cycle progression and survival. Recently, GSK-3 has been implicated in leukemia stem cell pathophysiology and may be an appropriate target for its eradication. In this review, we will discuss the roles that GSK-3 plays in hematopoiesis and leukemogenesis as how this pivotal kinase can interact with multiple signaling pathways such as: Wnt/β-catenin, phosphoinositide 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/Akt/mammalian target of rapamycin (mTOR), Ras/Raf/MEK/extracellular signal-regulated kinase (ERK), Notch and others. Moreover, we will discuss how targeting GSK-3 and these other pathways can improve leukemia therapy and may overcome therapeutic resistance. In summary, GSK-3 is a crucial regulatory kinase interacting with multiple pathways to control various physiological processes, as well as leukemia stem cells, leukemia progression and therapeutic resistance. GSK-3 and Wnt are clearly intriguing therapeutic targets