婴猴麻疹38例临床分析

麻疹病毒是副粘病毒科麻疹病毒属成员之一,主要通过呼吸道传播,其传染性强,人群发病率很高,主要常发于婴幼儿及儿童[1].国外有报道人源麻疹病毒和狗的犬温热病毒可引起捕获猕猴麻疹病毒感染的暴发[2-4],并表现为与人相似的临床症状和病理表现[5-6].目前,国内还未有猕猴麻疹暴发的病例报道.本中心2008年1月至3月共有38例8月龄~15月龄的腹泻猕猴诊断为麻疹,经过及时确诊,有效治疗,临床效果很好的.分析如下.

Si_(0.75)Ge_(0.25)虚衬底上应变补偿Si/Si_(0.62)Ge_(0.38)量子阱发光

由于Si/SiGe异质结构的带阶差主要发生在价带,为实现高效率的发光,本文从理论上设计了在硅基Si_(1-x) Ge_x虚衬底上外延应变补偿的Si/S_(1-y) Ge_y(y>x)量子阱的能带结构,将量子阱对电子的限制势垒提高到100meV以上.在实验上,采用300℃生长的Ge量子点插入层,制备出薄的SiGe驰豫缓冲层(虚衬底),表面Ge组份达到0.25,表面粗糙度小于2nm,驰豫度接近100%.在我们制备的SiGe缓冲层上外延了应变补偿SiGe/Si多量子阱结构,并初步研究了其发光特性.

Megiston agathon (Pl. Ap. 38 a) – Sedno życia i filozoficznego wyzwania Sokratesa

We suggest a certain minimal approach to the historical Socrates on the basis of Plato’s Apology. This text makes it possible to reconstruct the authentic charge and the defense line of Socrates, as well as his motivation and the quintessence of his philosophical challenge. The most important thing is what the philosopher says in the face of his death sentence: that the greatest good for a man is to live an examined life focusing on virtues and ethical values. Unfortunately, the preponderance of studies, even the most recent ones, fail to recognize the philosopher’s provocative challenge, whilst it is not only a crucial motif in the Socratic examining (ἐξετάζειν), i.e. testing the interlocutors’ knowledge by means of irony, elenchos and aporia, but also an inspiration for his direct and indirect followers in seeking virtues and the greatest good.

Practice links [Issue 38, June 2010]

Practice Links is a free e-publication for practitioners working in Irish social services, voluntary and nongovernmental sectors. Practice Links was created to enable practitioners to keep up-to-date with new publications, electronic resources and conference opportunities. Issue 38 contains the text for a proposed constitutional amendment on children’s rights

Yeast screens identify the RNA polymerase II CTD and SPT5 as relevant targets of BRCA1 interaction.

BRCA1 has been implicated in numerous DNA repair pathways that maintain genome integrity, however the function responsible for its tumor suppressor activity in breast cancer remains obscure. To identify the most highly conserved of the many BRCA1 functions, we screened the evolutionarily distant eukaryote Saccharomyces cerevisiae for mutants that suppressed the G1 checkpoint arrest and lethality induced following heterologous BRCA1 expression. A genome-wide screen in the diploid deletion collection combined with a screen of ionizing radiation sensitive gene deletions identified mutants that permit growth in the presence of BRCA1. These genes delineate a metabolic mRNA pathway that temporally links transcription elongation (SPT4, SPT5, CTK1, DEF1) to nucleopore-mediated mRNA export (ASM4, MLP1, MLP2, NUP2, NUP53, NUP120, NUP133, NUP170, NUP188, POM34) and cytoplasmic mRNA decay at P-bodies (CCR4, DHH1). Strikingly, BRCA1 interacted with the phosphorylated RNA polymerase II (RNAPII) carboxy terminal domain (P-CTD), phosphorylated in the pattern specified by the CTDK-I kinase, to induce DEF1-dependent cleavage and accumulation of a RNAPII fragment containing the P-CTD. Significantly, breast cancer associated BRCT domain defects in BRCA1 that suppressed P-CTD cleavage and lethality in yeast also suppressed the physical interaction of BRCA1 with human SPT5 in breast epithelial cells, thus confirming SPT5 as a relevant target of BRCA1 interaction. Furthermore, enhanced P-CTD cleavage was observed in both yeast and human breast cells following UV-irradiation indicating a conserved eukaryotic damage response. Moreover, P-CTD cleavage in breast epithelial cells was BRCA1-dependent since damage-induced P-CTD cleavage was only observed in the mutant BRCA1 cell line HCC1937 following ectopic expression of wild type BRCA1. Finally, BRCA1, SPT5 and hyperphosphorylated RPB1 form a complex that was rapidly degraded following MMS treatment in wild type but not BRCA1 mutant breast cells. These results extend the mechanistic links between BRCA1 and transcriptional consequences in response to DNA damage and suggest an important role for RNAPII P-CTD cleavage in BRCA1-mediated cancer suppression.