板块构造启动的时间和机制:理论和经验探索

板块构造是指位于对流地幔圈层之上的岩石圈的水平运动,主要由岩石圈在俯冲带的下沉作用所致.板块构造是一个典型的、非平衡复杂体系的自组系统(selforganizing,far from equilibrium complex system,SOFFECS),其驱动力主要来自热边界层(岩石圈)的反向浮力,同时又受控于变形岩石圈与下覆粘性软流圈地幔的耗散作用.在太阳系内侧5个硅酸质行星中,板块构造仅发育于地球,这表明板块构造是硅酸质行星不太常见的一种热散逸方式.目前还不清楚这种构造活动和热散逸方式在地球上是从何时开始的.所有的硅酸质行星在形成初期可能都经历过一次短暂的岩浆海阶段.行星固结后,静止盖层模式是行星冷却的共同途径,即行星表面形成了一个不易活动的固化盖层,此时内部的热量只能通过拆沉作用、热点火山作用和岩浆浅部侵位等方式进行逃逸.由于地球早期温度较高,通过减压熔融形成的岩石圈结构不同于现代岩石圈,即地球早期岩石圈由厚的洋壳和薄的岩石圈地幔构成.这种岩石圈要产生反向浮力需要非常长的时间,因此地球早期即便有板块构造存在,其规模也比较零星.只有当地球冷却到一定程度,扩张中脊下部减压熔融形成薄的洋壳且大洋岩石圈只需几十个百万年就可以产生反向浮力时,才能形成与现今风格相似的、可持续性的板块构造.板块构造启动时间的认识最终取决于人们对相关地质记录(事件)的研究成果.板块构造的判别依据包括蛇绿岩、蓝片岩、超高压变质带、榴辉岩、被动大陆边缘、转换断层、指示克拉通陆块移动轨迹的古地磁研究以及岩浆岩地球化学和同位素构造判别等等.对地质记录的解释必须综合各方面的信息.本人认为现存的地质事件记录了地球构造随时间演化的过程,即太古代时期构造和岩浆活动剧烈,大约在1.9 Ga时开始出现近似的板块构造,在新元古代才开始出现与现代相似的、可持续的、具有深俯冲和板片拖曳特性的板块构造.     

Assessing climate model projections: State of the art and philosophical reflections

The present paper draws on climate science and the philosophy of science in order to evaluate climate-model-based approaches to assessing climate projections. We analyze the difficulties that arise in such assessment and outline criteria of adequacy for approaches to it. In addition, we offer a critical overview of the approaches used in the IPCC working group one fourth report, including the confidence building, Bayesian and likelihood approaches. Finally, we consider approaches that do not feature in the IPCC reports, including three approaches drawn from the philosophy of science. We find that all available approaches face substantial challenges, with IPCC approaches having as a primary source of difficulty their goal of providing probabilistic assessments.     

Multimeric structures of HLA-G isoforms function through differential binding to LILRB receptors

The non-classical Human leukocyte antigen G (HLA-G) differs from classical HLA class I molecules by its low genetic diversity, a tissue-restricted expression, the existence of seven isoforms, and immuno-inhibitory functions. Most of the known functions of HLA-G concern the membrane-bound HLA-G1 and soluble HLA-G5 isoforms, which present the typical structure of classical HLA class I molecule: a heavy chain of three globular domains α₁–α₂–α₃ non-covalently bound to β-2-microglobulin (B2M) and a peptide. Very little is known of the structural features and functions of other HLA-G isoforms or structural conformations other than B2M-associated HLA-G1 and HLA-G5. In the present work, we studied the capability of all isoforms to form homomultimers, and investigated whether they could bind to, and function through, the known HLA-G receptors LILRB1 and LILRB2. We report that all HLA-G isoforms may form homodimers, demonstrating for the first time the existence of HLA-G4 dimers. We also report that the HLA-G α₁–α₃ structure, which constitutes the extracellular part of HLA-G2 and HLA-G6, binds the LILRB2 receptor but not LILRB1. This is the first report of a receptor for a truncated HLA-G isoform. Following up on this finding, we show that the α₁–α₃-Fc structure coated on agarose beads is tolerogenic and capable of prolonging the survival of skin allografts in B6-mice and in a LILRB2-transgenic mouse model. This study is the first proof of concept that truncated HLA-G isoforms could be used as therapeutic agents.     

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.     

Independent genome-wide scans identify a chromosome 18 quantitative-trait locus influencing dyslexia.

Developmental dyslexia is defined as a specific and significant impairment in reading ability that cannot be explained by deficits in intelligence, learning opportunity, motivation or sensory acuity. It is one of the most frequently diagnosed disorders in childhood, representing a major educational and social problem. It is well established that dyslexia is a significantly heritable trait with a neurobiological basis. The etiological mechanisms remain elusive, however, despite being the focus of intensive multidisciplinary research. All attempts to map quantitative-trait loci (QTLs) influencing dyslexia susceptibility have targeted specific chromosomal regions, so that inferences regarding genetic etiology have been made on the basis of very limited information. Here we present the first two complete QTL-based genome-wide scans for this trait, in large samples of families from the United Kingdom and United States. Using single-point analysis, linkage to marker D18S53 was independently identified as being one of the most significant results of the genome in each scan (P< or =0.0004 for single word-reading ability in each family sample). Multipoint analysis gave increased evidence of 18p11.2 linkage for single-word reading, yielding top empirical P values of 0.00001 (UK) and 0.0004 (US). Measures related to phonological and orthographic processing also showed linkage at this locus. We replicated linkage to 18p11.2 in a third independent sample of families (from the UK), in which the strongest evidence came from a phoneme-awareness measure (most significant P value=0.00004). A combined analysis of all UK families confirmed that this newly discovered 18p QTL is probably a general risk factor for dyslexia, influencing several reading-related processes. This is the first report of QTL-based genome-wide scanning for a human cognitive trait.     

Mechanism of urea nitrogen binding by proposed oxidized starch gastrointestinal absorbents.

By use of 14-C label it was demonstrated that apparent binding of urea N to polyaldehyde starch was probably preceeded by hydrolysis to ammonium ion. Thus direct urea binding was not the mechanism through which ingested polyaldehyde starch might increase fecal N excretion in uremic patients.     

Prediction from the regression model with two‐way error components

In this paper we extend the Baillie and Baltagi ( 1999 ) paper (Prediction from the regression model with one‐way error components. In Analysis of Panels and Limited Dependent Variables Models, Hsiao C, Lahiri K, Lee LF, Pesaran H (eds). Cambridge University Press, Cambridge, UK). In particular, we derive six predictors for the two‐way error components model, as well as their associated asymptotic mean squared error (AMSE) of multi‐step prediction. In addition, we also provide both theoretical and simulation evidence as to the relative efficiency of our six alternative predictors. The adequacy of the prediction AMSE formula is also investigated by the use of Monte Carlo methods which indicate that the ordinary optimal predictors perform well for various accuracy criteria. Copyright © 2010 John Wiley & Sons, Ltd.     

Effects of Douglas-fir beetle (Coleoptera: Scolytidae) infestations on forest overstory and understory conditions in western Wyoming

Douglas-fir beetle ( Dendroctonus pseudotsugae Hopk.) infestations frequently result from disturbance events that create large volumes of weakened Douglas-fir trees, Pseudotsuga menziesii (Mirb.) Franco. Previous research has focused on determining susceptibility of forest stands to Douglas-fir beetle and predicting the amount of tree mortality from Douglas-fir beetle infestations following disturbance events. Little work has been done on consequent changes in the forest overstory and understory. In the early 1990s, populations of Douglas-fir beetle increased in fire-scorched trees, subsequently infesting undamaged neighboring stands in the Rocky Mountains of western Wyoming, USA. In 1999 transect sampling and 25 pairs of previously infested and uninfested plots were used to quantify changes in forest stand conditions and ensuing responses in the understory caused by Douglas-fir beetle infestations. Significant effects of the Douglas-fir beetle infestation comprised 3 general categories: (1) overstory effects: basal area was reduced by 40%-70%, average tree diameter decreased by 8%-40%, and the Douglas-fir component of the overstory decreased by more than 12%; (2) regeneration effects: conifer seedling regeneration increased nearly fourfold in infested plots and 90% of the regeneration was Douglas-fir; (3) understory effects: understory vegetation (forbs, grass, and shrubs) had a threefold increase in infested compared with uninfested plots. In addition, basal area of Douglas-fir killed by the Douglas-fir beetle was significantly correlated with initial Douglas-fir basal area and percentage of Douglas-fir, but not with stand density index, tree diameter, or trees per hectare. Significant inverse relationships also were found between post-infestation basal area and abundance of forbs, grass, and shrubs, and understory height. Thus, we found that Douglas-fir beetle infestations cause significant short-term effects in both the overstory and understory and contribute to an altered mosaic in forest structure.