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A Fresh New Beginning

    全新的开始意味着挑战,意味着会有不称心和不如意,意味着挫败感扑面而来。要适应的地方还有很多,先把相亲这件事情拎出来好了。某人把签名改称“单身公害”,这分明就是向单身的同志们挑衅嘛。。。不过“公害”终究还是有道理的,比如一放假就到处瞎晃,既不利于社会和谐稳定,又不利于拉动内需;再比如当公害遇到公害,看对眼了那就是办公室恋情,没看对眼也沦落为办公室绯闻,三下五除二总归是定时炸弹一枚。

    被别人问的多了,OK,连咱这样的人都总结出来条条框框了。人家说了,事无巨细,越细越好,省得被打上要求高,看感觉的标签。本来就是五讲四美三热爱教育出来的,抓细节是咱的强项,说细了能唠叨上一天,拿着游标卡尺去比划一下。。。。

“身高165以上,本科以上,别超过120,否则抱不动,也别太瘦,90以下就免了,能持家,没小姐脾气,正当职业,身心健康的一般人就成,说的够具体了吧”

On the cover: Eukaryotic cells rely on aerobic mitochondrial metabolism to generate ATP. Here, Cárdenas et al. (pp. 270–283) demonstrate that constitutive low-level Ca2+ release through endoplasmic reticulum InsP3 receptor release channels (yellow flashes), in close proximity to mitochondria, is essential for mitochondria to produce sufficient ATP and to maintain normal cell bioenergetics. The image is modified from the original artwork of Odra Noel, with her permission (http://www.odranoel.eu).

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In This Issue

Available online 22 July 2010.

Mapping Glycosylation Disease Back to the Starting Line

PAGE 203Congenital disorders of glycosylation (CDGs) are a rare but incurable class of developmental syndromes caused by defects in N-linked protein glycosylation. Cantagrel et al. now report that the steroid 5α-reductase type 3 (SRD5A3) gene is mutated in a new type of human CDG. They show that SRD5A3 is required for the synthesis of a critical glycolipid that donates polysaccharides to proteins during glycosylation. Thus, this study sheds new light on an early step of protein N-glycosylation conserved from yeast to humans while also pinpointing a genetic cause of CDG.

TRF2 Cops a Topological Feel during Replication

PAGE 230

Telomeres are essential for chromosome stability. TRF2, a human DNA-binding protein involved in telomere end protection, and its associated exonuclease Apollo are required for telomere integrity during S phase. Ye et al. now report that TRF2 binds to positively supercoiled DNA during replication and functions in conjunction with Apollo to modulate the amount of topoisomerase 2 needed to release the positive superhelical stress created by fork progression. These findings link telomere end protection with replication via sensing of DNA topology.

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Circumventing RA Resistance in Neuroblastoma

PAGE 218

Retinoic acid (RA) induces differentiation of neuroblastoma cells, but its clinical benefit is variable. Hölzel et al. identify crosstalk between the tumor suppressor NF1 and RA-induced differentiation in neuroblastoma. Loss of NF1 activates RAS-MEK signaling, which in turn represses ZNF423, a critical transcriptional coactivator of the RA receptors. Neuroblastomas with low levels of NF1 and/or ZNF423 fail to respond to RA and have an extremely poor outcome. Inhibition of MEK signaling downstream of NF1 restores responsiveness to RA, suggesting a therapeutic strategy to overcome RA resistance in NF1-deficient neuroblastomas.

Dmc Runs Cold to Hot in Crossovers

PAGE 243

Meiotic crossovers are important for proper homolog segregation and are initiated by DNA double-strand breaks (DSBs). Despite the concentration of DSBs in hotspots, crossovers are distributed relatively uniformly along chromosomes. Hyppa and Smith report that in fission yeast this incongruence is due in large part to the use of the sister chromatid, rather than the homolog, for DSB repair at hotspots. Conversely, the homolog is used in regions with few DSBs, so called cold regions. DSB repair in cold regions requires the meiosis-specific strand-transfer protein Dmc1 that is dispensable at hotspots. Partner choice for repair thereby leads to distributed crossover events.

ER Estate Lawyer

PAGE 256

The endoplasmic reticulum (ER) is a gateway for folding and maturation of virtually all secreted and membrane proteins of the cell. ER cannot be generated de novo and must be inherited by daughter cells. Now Babour et al. find that the functional quality of inherited ER is assured during each round of cell division through an ER surveillance mechanism. Cells lacking this mechanism can only sustain a few further rounds of cell division, indicating a critical need for cells to inherit a functionally sound ER.


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Calcium Supplement Gives an Energy Boost

PAGE 270

Most eukaryotic cells rely on mitochondrial oxidative phosphorylation as their major source of ATP. Here, Cárdenas et al. demonstrate that constitutive Ca2+ release from the ER to mitochondria mediated by the InsP3R channel has an essential role in maintaining normal levels of oxidative phosphorylation. In its absence, cellular ATP levels fall, inducing AMP kinase-dependent autophagy as a survival mechanism. Constitutive mitochondrial uptake of InsP3R-released Ca2+ is required to maintain sufficient mitochondrial NADH production to support respiration.


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Pathogen Effectors Surf into Host Cells on PI3P

PAGE 284

Pathogens of plants and animals produce effector proteins that enter the cytoplasm of host cells to suppress host defenses and enable disease. Now Kale et al. show that effectors of plant pathogens bind cell surface phosphatidylinositol-3-phosphate (PI3P) in order to enter host cells via lipid microdomain-mediated endocytosis. Surprisingly, PI3P was also found on human cells where it could mediate effector entry, suggesting that human and animal pathogens might exploit the same effector entry mechanism. PI3P inhibitors blocked entry into plant and human cells, suggesting new therapeutic strategies against eukaryotic pathogens.

Boning Up on Glucose Homeostasis

PAGE 296 and PAGE 309

Osteocalcin is an osteoblast-derived hormone that promotes insulin secretion and regulates fat deposition. Whether insulin in turn affects osteocalcin activity has been unclear. Now two studies by Fulzele et al. and Ferron et al. demonstrate that insulin signaling in osteoblasts is necessary for whole-body glucose homeostasis and bone resorption via regulation of osteocalcin activity. The authors propose the existence of a bone-pancreas endocrine loop through which insulin signaling in the osteoblast integrates bone remodeling and energy metabolism.

Sirtuin Regulates APP Cleavage

PAGE 320

A hallmark of Alzheimer’s disease (AD) is the accumulation of plaques containing Aβ peptides. The production of Aβ peptides is avoided by cleavage of APP by the α- and γ-secretases. Here Donmez et al. show that production of Aβ peptides in a mouse model of AD is reduced by overexpressing the NAD-dependent deacetylase SIRT1 in brain and is increased by removing SIRT1. SIRT1 activates the gene encoding the α-secretase, ADAM10. These findings indicate that SIRT1 activation may be a viable strategy to combat AD.


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    有消息称这款超低价平板是针对麻省理工学院推出百元美金电脑的抗议,因为对于印度而言,那样的售价仍然偏高,印度当局认为这款平板更符合当地的学童需求,据称该产品将以20美金的售价销售给学生,未来甚至会低于10美金。而消息的来源居然是印度人力资源发展部,一个官方的政府机构。据称该产品将基于Linux,虽然价格便宜,但却采用了飞思卡尔基于ARM9架构的i.MX233处理器,具备2GB的内存容量和WiFi上网的功能,开启PDF,甚至看Youtube视频都没问题。

硬件配置:

  • 处理器:飞思卡尔基于ARM9的i.MX233处理器,5美元
  • 闪存:3美元
  • 无线模块:支持802.11b/g标准的WiFi,4美元
  • 其他零散元件:3美元
  • 显示屏:7寸800×480分辨率液晶屏,15美元
HTC手机评测   Archos产品评测   MP4数码评测   笔记本比价

    由于Vodafone定制的Samsung LiMo系统手机在市场上表现不好,未被主流市场接受,Vodafone已经官方宣布放弃LiMo系统手机,转而专注于360服务的开发上。虽然三星i8320(Vodafone 360 H1)和i6410(Vodafone 360 M1)目前在国内水货市场备受追捧,但这显然是“出口转内销”的结果。另一个坏消息是,Vodafone在放弃LiMo系统的同时,也放弃了定制Vodafone 360 H2的计划(三星i8330),从而宣告了H2胎死腹中。

    之前,摩托罗拉在09年抛弃了LiMo基金会,三星也忙于开发自家的bada系统,而现在Vodafone的离开正式宣布:LiMo系统已死!未来也不会有LiMo的官方应用程序发布了(其实从来都没有过-_-!)。对于国内i8320的用户来说,移植Android系统是他们将i8320智能化的唯一出路了。不过既然不会再有下一部LiMo手机,整个LiMo的用户群将更加小众,为LiMo手机移植Android系统的开发将越发举步维艰。。。

HTC手机评测   Archos产品评测   MP4数码评测   笔记本比价

2010年香港大学排名榜

    香港专业教育网每年根据大学入学收生成绩结果、研究成功申请率与拨款额、研究作品成果表现、院校教师学生人数比率、图书和电子资源收藏量等5项数据,进行排名。第十二届香港最佳大学排名榜7月26日揭晓,香港大学蝉联第一名,其校长徐立之也在最佳校长排名中高踞榜首。排名一至八名的学校依次为:

  1. 香港大学
  2. 香港中文大学
  3. 香港科技大学
  4. 香港理工大学
  5. 香港城市大学
  6. 香港浸会大学
  7. 香港教育学院
  8. 岭南大学

    在两个月前国际高等教育研究机构Quacquarelli Symonds(QS)最新公布的亚洲大学排名榜中,香港大学同样排名第一,香港科技大学、香港中文大学位列第二及第四位,显示港校水平广受认同。
 
    香港大学各项调查结果均占首位,在“民意榜”上亦以平均分(8.19)与中文大学(7.55)及科技大学(7.37)拉远距离,说明这是一所可以代表香港在国际上争取更高学术地位的大学。科技大学与中文大学在研究成功申请率与拨款额上均较2009年表现更佳。港校对研究上的重视,可以为香港在国际学术地位竞争上获得更佳的成绩。
 
    此外,在校长排名上,港大校长徐立之今年在“民意榜”、“学界榜”上均以高分名列首位。时美真表示,除本身实力外,也许原因是其他大学校长正在“送旧迎新”的过渡期,公众对新校长需要有一段时间去认识。

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