Cryptomare magmatism 4.35 Gyr ago recorded in lunar meteorite Kalahari 009

The origin and evolution of the Moon remain controversial, with one of the most important questions for lunar evolution being the timing and duration of basaltic (mare) magmatism. Here we report the result of ion microprobe U-Pb dating of phosphates in a lunar meteorite, Kalahari 009, which is classified as a very-low-Ti mare-basalt breccia. In situ analyses of five phosphate grains, associated with basaltic clasts, give an age of 4.35 +/- 0.15 billion years. These ancient phosphate ages are thought to represent the crystallization ages of parental basalt magma, making Kalahari 009 one of the oldest known mare basalts. We suggest that mare basalt volcanism on the Moon started as early as 4.35 Gyr ago, relatively soon after its formation and differentiation, and preceding the bulk of lunar volcanism which ensued after the late heavy bombardment around 3.8-3.9 Gyr (refs 7 and 8). Considering the extremely low abundances of incompatible elements such as thorium and the rare earth elements in Kalahari 009 (ref. 9) and recent remote-sensing observations illustrating that the cryptomaria tend to be of very-low-Ti basalt type, we conclude that Kalahari 009 is our first sample of a very-low-Ti cryptomare from the Moon.     

Mutations in genes encoding ribonuclease H2 subunits cause Aicardi-Goutières syndrome and mimic congenital viral brain infection

Aicardi-Goutières syndrome (AGS) is an autosomal recessive neurological disorder, the clinical and immunological features of which parallel those of congenital viral infection. Here we define the composition of the human ribonuclease H2 enzyme complex and show that AGS can result from mutations in the genes encoding any one of its three subunits. Our findings demonstrate a role for ribonuclease H in human neurological disease and suggest an unanticipated relationship between ribonuclease H2 and the antiviral immune response that warrants further investigation.     

Common variation at 3p22.1 and 7p15.3 influences multiple myeloma risk

To identify risk variants for multiple myeloma, we conducted a genome-wide association study of 1,675 individuals with multiple myeloma and 5,903 control subjects. We identified risk loci for multiple myeloma at 3p22.1 (rs1052501 in ULK4; odds ratio (OR) = 1.32; P = 7.47 × 10(-9)) and 7p15.3 (rs4487645, OR = 1.38; P = 3.33 × 10(-15)). In addition, we observed a promising association at 2p23.3 (rs6746082, OR = 1.29; P = 1.22 × 10(-7)). Our study identifies new genomic regions associated with multiple myeloma risk that may lead to new etiological insights.     

基于压缩感知过程的语音增强

压缩感知(compressive sensing,CS)是一种基于信号稀疏性的采样方法,可以有效提取信号中所包含的信息。该文提出了一种基于CS过程的语音增强新算法。算法利用语音在离散余弦变换(discrete cosine transform,DCT)域下的稀疏性,采用Hadamard矩阵对带噪语音进行压缩测量,通过改进的正交匹配跟踪(orthogonal matching pursuit,OMP)算法恢复语音信号,实现语音增强。与经典谱减法和子空间算法进行实验对比分析,结果表明:该算法在降噪性能上优于经典谱减法和子空间算法。     

Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans

Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendants. The histone H3 lysine 4 trimethylation (H3K4me3) complex, composed of ASH-2, WDR-5 and the histone methyltransferase SET-2, regulates Caenorhabditis elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5 or SET-2 in the parental generation extend the lifespan of descendants up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendants. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendants.     

VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche

The cellular and molecular mechanisms by which a tumour cell undergoes metastasis to a predetermined location are largely unknown. Here we demonstrate that bone marrow-derived haematopoietic progenitor cells that express vascular endothelial growth factor receptor 1 (VEGFR1; also known as Flt1) home to tumour-specific pre-metastatic sites and form cellular clusters before the arrival of tumour cells. Preventing VEGFR1 function using antibodies or by the removal of VEGFR1(+) cells from the bone marrow of wild-type mice abrogates the formation of these pre-metastatic clusters and prevents tumour metastasis, whereas reconstitution with selected Id3 (inhibitor of differentiation 3)-competent VEGFR1+ cells establishes cluster formation and tumour metastasis in Id3 knockout mice. We also show that VEGFR1+ cells express VLA-4 (also known as integrin alpha4beta1), and that tumour-specific growth factors upregulate fibronectin--a VLA-4 ligand--in resident fibroblasts, providing a permissive niche for incoming tumour cells. Conditioned media obtained from distinct tumour types with unique patterns of metastatic spread redirected fibronectin expression and cluster formation, thereby transforming the metastatic profile. These findings demonstrate a requirement for VEGFR1+ haematopoietic progenitors in the regulation of metastasis, and suggest that expression patterns of fibronectin and VEGFR1+VLA-4+ clusters dictate organ-specific tumour spread.