Office 11先睹为快

King Cheese 作为当今最具有影响力的软件开发公司,微软不仅凭借Windows占据了桌面操作系统的大半江山,而且还有着Office这样统领办公系统的垄断家族。面对着这样的软件霸主,很多厂商推出了各种版本的Linux和StarOffice、OpenOffice等产品与之抗衡,也让微软深深地感受到巨大的压力。俗话说“兵来将挡”,微软公司也不失时机地亮出它的杀手锏,Office 11就是专门针对办公系统量身定制的一款最新产品。那么,Office 11最大的改进在哪里?对于普通用户而言增加了哪些实用功能呢?就让我们透过日前发布的Betal版来窥其一二。     

The insecticidal potential of venom peptides

Pest insect species are a burden to humans as they destroy crops and serve as vectors for a wide range of diseases including malaria and dengue. Chemical insecticides are currently the dominant approach for combating these pests. However, the de-registration of key classes of chemical insecticides due to their perceived ecological and human health risks in combination with the development of insecticide resistance in many pest insect populations has created an urgent need for improved methods of insect pest control. The venoms of arthropod predators such as spiders and scorpions are a promising source of novel insecticidal peptides that often have different modes of action to extant chemical insecticides. These peptides have been optimized via a prey–predator arms race spanning hundreds of millions of years to target specific types of insect ion channels and receptors. Here we review the current literature on insecticidal venom peptides, with a particular focus on their structural and pharmacological diversity, and discuss their potential for deployment as insecticides.     

CCDC103 mutations cause primary ciliary dyskinesia by disrupting assembly of ciliary dynein arms

Cilia are essential for fertilization, respiratory clearance, cerebrospinal fluid circulation and establishing laterality. Cilia motility defects cause primary ciliary dyskinesia (PCD, MIM244400), a disorder affecting 1:15,000-30,000 births. Cilia motility requires the assembly of multisubunit dynein arms that drive ciliary bending. Despite progress in understanding the genetic basis of PCD, mutations remain to be identified for several PCD-linked loci. Here we show that the zebrafish cilia paralysis mutant schmalhans (smh(tn222)) encodes the coiled-coil domain containing 103 protein (Ccdc103), a foxj1a-regulated gene product. Screening 146 unrelated PCD families identified individuals in six families with reduced outer dynein arms who carried mutations in CCDC103. Dynein arm assembly in smh mutant zebrafish was rescued by wild-type but not mutant human CCDC103. Chlamydomonas Ccdc103/Pr46b functions as a tightly bound, axoneme-associated protein. These results identify Ccdc103 as a dynein arm attachment factor that causes primary ciliary dyskinesia when mutated.     

Mutations in the gene encoding filamin B disrupt vertebral segmentation, joint formation and skeletogenesis

The filamins are cytoplasmic proteins that regulate the structure and activity of the cytoskeleton by cross-linking actin into three-dimensional networks, linking the cell membrane to the cytoskeleton and serving as scaffolds on which intracellular signaling and protein trafficking pathways are organized (reviewed in refs. 1,2). We identified mutations in the gene encoding filamin B in four human skeletal disorders. We found homozygosity or compound heterozygosity with respect to stop-codon mutations in autosomal recessive spondylocarpotarsal syndrome (SCT, OMIM 272460) and missense mutations in individuals with autosomal dominant Larsen syndrome (OMIM 150250) and the perinatal lethal atelosteogenesis I and III phenotypes (AOI, OMIM 108720; AOIII, OMIM 108721). We found that filamin B is expressed in human growth plate chondrocytes and in the developing vertebral bodies in the mouse. These data indicate an unexpected role in vertebral segmentation, joint formation and endochondral ossification for this ubiquitously expressed cytoskeletal protein.     

Mutations in SEC63 cause autosomal dominant polycystic liver disease

Mutations in PRKCSH, encoding the beta-subunit of glucosidase II, an N-linked glycan-processing enzyme in the endoplasmic reticulum (ER), cause autosomal dominant polycystic liver disease. We found that mutations in SEC63, encoding a component of the protein translocation machinery in the ER, also cause this disease. These findings are suggestive of a role for cotranslational protein-processing pathways in maintaining epithelial luminal structure and implicate noncilial ER proteins in human polycystic disease.     

Functional annotation of a full-length mouse cDNA collection

The RIKEN Mouse Gene Encyclopaedia Project, a systematic approach to determining the full coding potential of the mouse genome, involves collection and sequencing of full-length complementary DNAs and physical mapping of the corresponding genes to the mouse genome. We organized an international functional annotation meeting (FANTOM) to annotate the first 21,076 cDNAs to be analysed in this project. Here we describe the first RIKEN clone collection, which is one of the largest described for any organism. Analysis of these cDNAs extends known gene families and identifies new ones.     

Reduction of soil carbon formation by tropospheric ozone under increased carbon dioxide levels

In the Northern Hemisphere, ozone levels in the troposphere have increased by 35 per cent over the past century, with detrimental impacts on forest and agricultural productivity, even when forest productivity has been stimulated by increased carbon dioxide levels. In addition to reducing productivity, increased tropospheric ozone levels could alter terrestrial carbon cycling by lowering the quantity and quality of carbon inputs to soils. However, the influence of elevated ozone levels on soil carbon formation and decomposition are unknown. Here we examine the effects of elevated ozone levels on the formation rates of total and decay-resistant acid-insoluble soil carbon under conditions of elevated carbon dioxide levels in experimental aspen (Populus tremuloides) stands and mixed aspen-birch (Betula papyrifera) stands. With ambient concentrations of ozone and carbon dioxide both raised by 50 per cent, we find that the formation rates of total and acid-insoluble soil carbon are reduced by 50 per cent relative to the amounts entering the soil when the forests were exposed to increased carbon dioxide alone. Our results suggest that, in a world with elevated atmospheric carbon dioxide concentrations, global-scale reductions in plant productivity due to elevated ozone levels will also lower soil carbon formation rates significantly.