Adlayer structure of TCNQ molecules on Cu(111): Anin situ STM study

In situ electrochemical scanning tunneling microscopy (STM) was employed to examine tetracyano- quinodimethane (TCNQ) layer adsorbed on Cu(111) electrode surface in 0.1 mol/L HClO₄ solution. The TCNQ molecules are found to form highly-ordered long range adlayer with a (4×4) symmetry. Each TCNQ molecule is adsorbed on Cu(111) surface in flat-lying orientation. The molecules are preferentially aligned with their long axes in the [121] direction. A structural model is proposed for the adlayer.     

25例帕金森病的临床与病理学特征

目的:研究帕金森病(PD)的临床和病理学特征及与路易体痴呆(DLB)病理学的关系。方法:对25例PD的临床和病理学特征进行研究。结果:在25例中5例为伴痴呆的帕金森病(PDD),初发症状为震颤11例,步行障碍6例,运动迟缓4例及吞咽困难1例。16例(69.9%)出现了视幻觉,24例(96%)对左旋多巴有反应,15例(65%)死于肺炎,3例死于肠梗阻。按DLB的病理学分类,25例中新皮质型5例,边缘型6例,脑干优势型14例。结论:本组PD的病理学特点主要是DLB的脑干优势型改变。PDD的病理类型是DLB的新皮质型和边缘型。病理上诊断为PD的患者,在临床上有很高的左旋多巴的反应率,晚期患者多数死于肺炎并发症。     

Sequence- and target-independent angiogenesis suppression by siRNA via TLR3

Clinical trials of small interfering RNA (siRNA) targeting vascular endothelial growth factor-A (VEGFA) or its receptor VEGFR1 (also called FLT1), in patients with blinding choroidal neovascularization (CNV) from age-related macular degeneration, are premised on gene silencing by means of intracellular RNA interference (RNAi). We show instead that CNV inhibition is a siRNA-class effect: 21-nucleotide or longer siRNAs targeting non-mammalian genes, non-expressed genes, non-genomic sequences, pro- and anti-angiogenic genes, and RNAi-incompetent siRNAs all suppressed CNV in mice comparably to siRNAs targeting Vegfa or Vegfr1 without off-target RNAi or interferon-alpha/beta activation. Non-targeted (against non-mammalian genes) and targeted (against Vegfa or Vegfr1) siRNA suppressed CNV via cell-surface toll-like receptor 3 (TLR3), its adaptor TRIF, and induction of interferon-gamma and interleukin-12. Non-targeted siRNA suppressed dermal neovascularization in mice as effectively as Vegfa siRNA. siRNA-induced inhibition of neovascularization required a minimum length of 21 nucleotides, a bridging necessity in a modelled 2:1 TLR3-RNA complex. Choroidal endothelial cells from people expressing the TLR3 coding variant 412FF were refractory to extracellular siRNA-induced cytotoxicity, facilitating individualized pharmacogenetic therapy. Multiple human endothelial cell types expressed surface TLR3, indicating that generic siRNAs might treat angiogenic disorders that affect 8% of the world's population, and that siRNAs might induce unanticipated vascular or immune effects.