利用FY-2C资料对西北太平洋海域云分类的研究

使用2006年8月的31次FY-2C卫星资料进行地理定位研究,发现定位误差小于0.13条扫描线,此精度满足云分类研究需求;在此基础上,使用云分析法和聚类分析法对云进行分类试验,分类结果与FY-2C业务云产品进行对比。结果表明,云分析法确定的云型比业务云产品类型多,并对中低云有很好的识别;而聚类分析结果要优于业务云产品分类结果,在云分布细节上接近实际情况。     

Ti-47Al-1.5Cr-0.5Mn-2.8Nb合金高温力学性能应变速率敏感性及机制分析

在温度1123～1273K和应变速率5×10-5～5×10-3s-1范围内,研究了具有复相组织的Ti-47Al-1.5Cr-0.5Mn-2.8Nb合金拉伸性能的应变速率敏感性.发现提高应变速率或降低温度均可使合金的延伸率下降、强度增加,不同温度下拉伸强度与应变速率对数之间存在线性关系;利用热激活理论不仅解释了这一关系,还获得了应变速率方程,指出控制合金拉伸形变的微观机制是原子扩散过程.形变亚结构透射电镜观察证实该微观机制是位错攀移     

Wnt-beta-catenin signaling initiates taste papilla development

Fungiform taste papillae form a regular array on the dorsal tongue. Taste buds arise from papilla epithelium and, unusually for epithelial derivatives, synapse with neurons, release neurotransmitters and generate receptor and action potentials. Despite the importance of taste as one of our five senses, genetic analyses of taste papilla and bud development are lacking. We demonstrate that Wnt-beta-catenin signaling is activated in developing fungiform placodes and taste bud cells. A dominant stabilizing mutation of epithelial beta-catenin causes massive overproduction of enlarged fungiform papillae and taste buds. Likewise, genetic deletion of epithelial beta-catenin or inhibition of Wnt-beta-catenin signaling by ectopic dickkopf1 (Dkk1) blocks initiation of fungiform papilla morphogenesis. Ectopic papillae are innervated in the stabilizing beta-catenin mutant, whereas ectopic Dkk1 causes absence of lingual epithelial innervation. Thus, Wnt-beta-catenin signaling is critical for fungiform papilla and taste bud development. Altered regulation of this pathway may underlie evolutionary changes in taste papilla patterning.     

Structure of the catalytic domain of human phosphodiesterase 5 with bound drug molecules

Phosphodiesterases (PDEs) are a superfamily of enzymes that degrade the intracellular second messengers cyclic AMP and cyclic GMP. As essential regulators of cyclic nucleotide signalling with diverse physiological functions, PDEs are drug targets for the treatment of various diseases, including heart failure, depression, asthma, inflammation and erectile dysfunction. Of the 12 PDE gene families, cGMP-specific PDE5 carries out the principal cGMP-hydrolysing activity in human corpus cavernosum tissue. It is well known as the target of sildenafil citrate (Viagra) and other similar drugs for the treatment of erectile dysfunction. Despite the pressing need to develop selective PDE inhibitors as therapeutic drugs, only the cAMP-specific PDE4 structures are currently available. Here we present the three-dimensional structures of the catalytic domain (residues 537-860) of human PDE5 complexed with the three drug molecules sildenafil, tadalafil (Cialis) and vardenafil (Levitra). These structures will provide opportunities to design potent and selective PDE inhibitors with improved pharmacological profiles.     

The afterglow of GRB 050709 and the nature of the short-hard gamma-ray bursts

The final chapter in the long-standing mystery of the gamma-ray bursts (GRBs) centres on the origin of the short-hard class of bursts, which are suspected on theoretical grounds to result from the coalescence of neutron-star or black-hole binary systems. Numerous searches for the afterglows of short-hard bursts have been made, galvanized by the revolution in our understanding of long-duration GRBs that followed the discovery in 1997 of their broadband (X-ray, optical and radio) afterglow emission. Here we present the discovery of the X-ray afterglow of a short-hard burst, GRB 050709, whose accurate position allows us to associate it unambiguously with a star-forming galaxy at redshift z = 0.160, and whose optical lightcurve definitively excludes a supernova association. Together with results from three other recent short-hard bursts, this suggests that short-hard bursts release much less energy than the long-duration GRBs. Models requiring young stellar populations, such as magnetars and collapsars, are ruled out, while coalescing degenerate binaries remain the most promising progenitor candidates.     

Mutant frizzled-4 disrupts retinal angiogenesis in familial exudative vitreoretinopathy

Familial exudative vitreoretinopathy (FEVR) is a hereditary ocular disorder characterized by a failure of peripheral retinal vascularization. Loci associated with FEVR map to 11q13-q23 (EVR1; OMIM 133780, ref. 1), Xp11.4 (EVR2; OMIM 305390, ref. 2) and 11p13-12 (EVR3; OMIM 605750, ref. 3). Here we have confirmed linkage to the 11q13-23 locus for autosomal dominant FEVR in one large multigenerational family and refined the disease locus to a genomic region spanning 1.55 Mb. Mutations in FZD4, encoding the putative Wnt receptor frizzled-4, segregated completely with affected individuals in the family and were detected in affected individuals from an additional unrelated family, but not in normal controls. FZD genes encode Wnt receptors, which are implicated in development and carcinogenesis. Injection of wildtype and mutated FZD4 into Xenopus laevis embryos revealed that wildtype, but not mutant, frizzled-4 activated calcium/calmodulin-dependent protein kinase II (CAMKII) and protein kinase C (PKC), components of the Wnt/Ca(2+) signaling pathway. In one of the mutants, altered subcellular trafficking led to defective signaling. These findings support a function for frizzled-4 in retinal angiogenesis and establish the first association between a Wnt receptor and human disease.     

Chondroitinase ABC promotes functional recovery after spinal cord injury

The inability of axons to regenerate after a spinal cord injury in the adult mammalian central nervous system (CNS) can lead to permanent paralysis. At sites of CNS injury, a glial scar develops, containing extracellular matrix molecules including chondroitin sulphate proteoglycans (CSPGs). CSPGs are inhibitory to axon growth in vitro, and regenerating axons stop at CSPG-rich regions in vivo. Removing CSPG glycosaminoglycan (GAG) chains attenuates CSPG inhibitory activity. To test the functional effects of degrading chondroitin sulphate (CS)-GAG after spinal cord injury, we delivered chondroitinase ABC (ChABC) to the lesioned dorsal columns of adult rats. We show that intrathecal treatment with ChABC degraded CS-GAG at the injury site, upregulated a regeneration-associated protein in injured neurons, and promoted regeneration of both ascending sensory projections and descending corticospinal tract axons. ChABC treatment also restored post-synaptic activity below the lesion after electrical stimulation of corticospinal neurons, and promoted functional recovery of locomotor and proprioceptive behaviours. Our results demonstrate that CSPGs are important inhibitory molecules in vivo and suggest that their manipulation will be useful for treatment of human spinal injuries.     

盐碱胁迫对抗碱盐生植物碱地肤生长特性的影响

以天然盐生植物碱地肤为材料,利用人工生态模拟方法对其施加0～400mmol·L^-1的盐胁迫（摩尔比1：1的NaCl和Na2SO4）和碱胁迫（摩尔比1：1的NaHCO3和Na2CO3）．通过测定其相对生长率（RGR）等生理响应指标分析其抗盐、抗碱能力及特点,以期明确其生态定位的生理基础．结果表明：碱地肤不仅具有强抗盐性也具有强抗碱性,在高达400mmol·L^-1的盐胁迫或400mmol·L^-1的碱胁迫下仍能存活并维持一定的生长．低浓度的盐胁迫（80mmol·L^-1）对其生长非但不抑制反而具有刺激作用．从RGR等胁变指标来看,在相同盐浓度下,碱胁迫对碱地肤的胁迫强度大于盐胁迫,碱地肤对碱胁迫所做出的胁变反应均大于对盐胁迫的反应．以此可推断,碱胁迫甚于盐胁迫,碱地肤的抗盐性大于抗碱性．