On the structure and funtion of white-tailed prairie dog burrows

The architecture of burrows of the white-tailed prairie dog ( Cynomys leucurus ) is poorly known. For this reason and for comparative purposes, one recenlty active burrow of this species was excavated in southern Montana; the detailed methodology is described. Data were compiled on the dimensions of 29.3 m of excavated passages, and interpretations of several features are discussed. A ""turning bay,"" sleeping quarters, two hibernacula, and a maternity area are described, the last feature for the first time in print. In addition, we report Cynomys using their teeth to dig, also for the first time. Further, an inadvertent remodeling of the burrows is ascribed to normal animal traffic and appears to confirm a prediction based on late Pleistocene fossil burrows in Alberta.     

孤岛油田馆(1+2)地层划分对比与沉积模式

孤岛油田馆(1 2)砂层组属于河流相沉积，其纵向、横向相变迅速，砂体难以大面积追踪，本利用河流结构单元分析法、标准层与辅助标志层控制下的“旋回-厚度”对比法，很好地解决了馆(1 2)地层的划分对比问题，其中馆(1 2)砂层组内辅助标志层的发现为地层的划分对比提供了重要的保证．根据结构单元分析、砂体的岩性特征、粒度特征、河流砂体的空间展布形态以及河流曲率的计算，对馆(1 2)河流沉积的垂向旋回性及沉积模式进行了研究。对比Miall的16种河流分类方案，孤岛油田馆(1 2)砂层组属于细粒曲流河沉积．     

A restricted cell population propagates glioblastoma growth after chemotherapy

Glioblastoma multiforme is the most common primary malignant brain tumour, with a median survival of about one year. This poor prognosis is due to therapeutic resistance and tumour recurrence after surgical removal. Precisely how recurrence occurs is unknown. Using a genetically engineered mouse model of glioma, here we identify a subset of endogenous tumour cells that are the source of new tumour cells after the drug temozolomide (TMZ) is administered to transiently arrest tumour growth. A nestin-ΔTK-IRES-GFP (Nes-ΔTK-GFP) transgene that labels quiescent subventricular zone adult neural stem cells also labels a subset of endogenous glioma tumour cells. On arrest of tumour cell proliferation with TMZ, pulse-chase experiments demonstrate a tumour re-growth cell hierarchy originating with the Nes-ΔTK-GFP transgene subpopulation. Ablation of the GFP+ cells with chronic ganciclovir administration significantly arrested tumour growth, and combined TMZ and ganciclovir treatment impeded tumour development. Thus, a relatively quiescent subset of endogenous glioma cells, with properties similar to those proposed for cancer stem cells, is responsible for sustaining long-term tumour growth through the production of transient populations of highly proliferative cells.     

CPEB and two poly(A) polymerases control miR-122 stability and p53 mRNA translation

Cytoplasmic polyadenylation-induced translation controls germ cell development, neuronal synaptic plasticity and cellular senescence, a tumour-suppressor mechanism that limits the replicative lifespan of cells. The cytoplasmic polyadenylation element binding protein (CPEB) promotes polyadenylation by nucleating a group of factors including defective in germline development 2 (Gld2), a non-canonical poly(A) polymerase, on specific messenger RNA (mRNA) 3' untranslated regions (UTRs). Because CPEB regulation of p53 mRNA polyadenylation/translation is necessary for cellular senescence in primary human diploid fibroblasts, we surmised that Gld2 would be the enzyme responsible for poly(A) addition. Here we show that depletion of Gld2 surprisingly promotes rather than inhibits p53 mRNA polyadenylation/translation, induces premature senescence and enhances the stability of CPEB mRNA. The CPEB 3' UTR contains two miR-122 binding sites, which when deleted, elevate mRNA translation, as does an antagomir of miR-122. Although miR-122 is thought to be liver specific, it is present in primary fibroblasts and destabilized by Gld2 depletion. Gld4, a second non-canonical poly(A) polymerase, was found to regulate p53 mRNA polyadenylation/translation in a CPEB-dependent manner. Thus, translational regulation of p53 mRNA and cellular senescence is coordinated by Gld2/miR-122/CPEB/Gld4.