枣庄市砂姜黑土的改良利用途径初探

砂姜黑土是一种具有“黑土层”和“砂姜层”的暗色土壤 ,在枣庄市沿运滨湖地带广泛分布。由于受土壤环境因素及其内在性质的影响 ,农业生产长期处于低而不稳状态 ,为本市主要的中低产土类之一。本文拟对砂姜黑土的改良利用途径进行研究 ,有助于提高砂姜黑土的肥力水平 ,实现本市农业生产的可持续发展     

人地关系协调发展的途径探讨

人类文明是在人类认识、利用、改造和适应自然的过程中不断演进的。人地关系是人类生存与发展的基本关系。追求人地关系的和谐是实现社会经济持续稳定协调发展的基本原则和根本保证，也是人类文明的共同价值选择和最终归宿。如何实现人地关系的协调，则是当前人地关系研究中的核心所在。     

2010年新西兰M_S7.1级地震地表潜热异常

通过分析2010年9月3日新西兰地震前后3个月的NCEP/NCAR Reanalysis SLHF资料,发现8月1日紧邻震中东北侧出现了孤立的小斑状SLHF异常高值区,幅度约160W/m2.从历史数据分析、背景像元对比、时间序列小波变换等多方面,综合分析了该异常的时空特征.通过排除风速和云的影响,确认导致该次SLHF局部异常的关键因素应是局部地表增温.结合GPS位移数据及构造环境分析,推测此次异常的形成原因可能是深部高温高压区的热物质沿板块俯冲带扩容区上涌,引起震中东北侧、北岛中部及南岛西南部的地热区局部增温,进而改变了该区的地气比湿差,导致SLHF局部增加.     

A giant Ordovician anomalocaridid

Anomalocaridids, giant lightly sclerotized invertebrate predators, occur in a number of exceptionally preserved early and middle Cambrian (542-501?million years ago) biotas and have come to symbolize the unfamiliar morphologies displayed by stem organisms in faunas of the Burgess Shale type. They are characterized by a pair of anterior, segmented appendages, a circlet of plates around the mouth, and an elongate segmented trunk lacking true tergites with a pair of flexible lateral lobes per segment. Disarticulated body parts, such as the anterior appendages and oral circlet, had been assigned to a range of taxonomic groups--but the discovery of complete specimens from the middle Cambrian Burgess Shale showed that these disparate elements all belong to a single kind of animal. Phylogenetic analyses support a position of anomalocaridids in the arthropod stem, as a sister group to the euarthropods. The anomalocaridids were the largest animals in Cambrian communities. The youngest unequivocal examples occur in the middle Cambrian Marjum Formation of Utah but an arthropod retaining some anomalocaridid characteristics is present in the Devonian of Germany. Here we report the post-Cambrian occurrence of anomalocaridids, from the Early Ordovician (488-472?million years ago) Fezouata Biota in southeastern Morocco, including specimens larger than any in Cambrian biotas. These giant animals were an important element of some marine communities for about 30?million years longer than previously realized. The Moroccan specimens confirm the presence of a dorsal array of flexible blades attached to a transverse rachis on the trunk segments; these blades probably functioned as gills.     

Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma

Follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL) are the two most common non-Hodgkin lymphomas (NHLs). Here we sequenced tumour and matched normal DNA from 13 DLBCL cases and one FL case to identify genes with mutations in B-cell NHL. We analysed RNA-seq data from these and another 113 NHLs to identify genes with candidate mutations, and then re-sequenced tumour and matched normal DNA from these cases to confirm 109 genes with multiple somatic mutations. Genes with roles in histone modification were frequent targets of somatic mutation. For example, 32% of DLBCL and 89% of FL cases had somatic mutations in MLL2, which encodes a histone methyltransferase, and 11.4% and 13.4% of DLBCL and FL cases, respectively, had mutations in MEF2B, a calcium-regulated gene that cooperates with CREBBP and EP300 in acetylating histones. Our analysis suggests a previously unappreciated disruption of chromatin biology in lymphomagenesis.     

Structure and function of an irreversible agonist-β(2) adrenoceptor complex

G-protein-coupled receptors (GPCRs) are eukaryotic integral membrane proteins that modulate biological function by initiating cellular signalling in response to chemically diverse agonists. Despite recent progress in the structural biology of GPCRs, the molecular basis for agonist binding and allosteric modulation of these proteins is poorly understood. Structural knowledge of agonist-bound states is essential for deciphering the mechanism of receptor activation, and for structure-guided design and optimization of ligands. However, the crystallization of agonist-bound GPCRs has been hampered by modest affinities and rapid off-rates of available agonists. Using the inactive structure of the human β(2) adrenergic receptor (β(2)AR) as a guide, we designed a β(2)AR agonist that can be covalently tethered to a specific site on the receptor through a disulphide bond. The covalent β(2)AR-agonist complex forms efficiently, and is capable of activating a heterotrimeric G protein. We crystallized a covalent agonist-bound β(2)AR-T4L fusion protein in lipid bilayers through the use of the lipidic mesophase method, and determined its structure at 3.5?? resolution. A comparison to the inactive structure and an antibody-stabilized active structure (companion paper) shows how binding events at both the extracellular and intracellular surfaces are required to stabilize an active conformation of the receptor. The structures are in agreement with long-timescale (up to 30?μs) molecular dynamics simulations showing that an agonist-bound active conformation spontaneously relaxes to an inactive-like conformation in the absence of a G protein or stabilizing antibody.     

Targeted gene correction of α1-antitrypsin deficiency in induced pluripotent stem cells

Human induced pluripotent stem cells (iPSCs) represent a unique opportunity for regenerative medicine because they offer the prospect of generating unlimited quantities of cells for autologous transplantation, with potential application in treatments for a broad range of disorders. However, the use of human iPSCs in the context of genetically inherited human disease will require the correction of disease-causing mutations in a manner that is fully compatible with clinical applications. The methods currently available, such as homologous recombination, lack the necessary efficiency and also leave residual sequences in the targeted genome. Therefore, the development of new approaches to edit the mammalian genome is a prerequisite to delivering the clinical promise of human iPSCs. Here we show that a combination of zinc finger nucleases (ZFNs) and piggyBac technology in human iPSCs can achieve biallelic correction of a point mutation (Glu342Lys) in the α(1)-antitrypsin (A1AT, also known as SERPINA1) gene that is responsible for α(1)-antitrypsin deficiency. Genetic correction of human iPSCs restored the structure and function of A1AT in subsequently derived liver cells in vitro and in vivo. This approach is significantly more efficient than any other gene-targeting technology that is currently available and crucially prevents contamination of the host genome with residual non-human sequences. Our results provide the first proof of principle, to our knowledge, for the potential of combining human iPSCs with genetic correction to generate clinically relevant cells for autologous cell-based therapies.