在科学方面科学同大学的相互影响

许多大学的行政领导人似乎相信,由学校教工进行的研究工作可以通过专利和发明被用来为他们的机构带来巨大的经济收入。国家科学院出版社最近出版的一份报告提供了关于工业同大学相互影响的对比看法。该报告是一份访问17名高级工业职员的谈话总结。将可获利的产品推向市场,这要求一套与创造和普及知识不同的动机、组织和文化。企业也注意到,对花费在研究上的每1美元需要投入10美元用于开发,100美元用于设计和建造工厂。这些活动的许多方面都需要有目的明确的跨学科人员的参与。在许多工业部门,主要的活动在于改善现有产品的质量或加工方法。这往往是通过一点一点的累积起     

矿物燃料之后的能源会怎样?--《没有天燃气的时代》作者古德斯坦访谈录

美国加利福尼亚技术学院物理系教授戴维·古德斯坦(DavidGoodstein)最近出版了他的第6本著作——《没有天燃气的时代》。他在书中指出,21世纪注定会成为文明的一个转折点:在不太遥远的将来,随着矿物燃料的逐渐耗尽,迫使人类社会去开发其他的新能源。该书对许多问题作了一个扼要的评述,并提出了一些解决办法。不久前,《美国科学家》记者戴维·施奈德(DavidSchneider)采访了古德斯坦,就书中提出的某些问题请他作进一步的阐述。     

数字窄播系统:互联网上的多媒体信息发布网络

互联网和数字窄播系统的产生自从人类有了语言和文字 ,就开始了不断的信息交流和沟通 ,从秦始皇利用烽火台传递敌人入侵的信号 ,到西门子公司第一次使用跨海电缆把电文传递到大洋彼岸 ;从古代的帝王君主通过张贴告示颁布法令 ,到现代企业通过报纸、电视、网络等各种媒体做产品的广告宣传 ,人们早已熟悉了各种信息传递的方式。而社会的文明程度越高 ,需要交流的信息就越多 ,信息发布的渠道就越广 ,同时信息传递的速度也越快。正因为如此 ,新世纪的世界将会是一个高度发达的信息化社会 ,一个海量信息飞速传递和交换的世界。正是由于这样大量的…     

征收碳税 还利于民

<正>一方面,劳动力和企业利润是社会经济繁荣的动力,政府从中获取税收;另一方面,资源的耗竭——可能是经济健康发展的最大威胁——却仍未触及税收的调整,这显然是不公平的。当思考如何重建业已受到威胁的经济时,全面征收碳税应该提到议事日程上来。     

汽车工业如何适应人类社会可持续发展——丹尼尔·斯珀林访谈录

汽车是构成人类社会最大的威胁之一，尽管这种看法存在一定争议。”加利福尼亚大学戴维斯分校工程学教授、该校交通研究所首任所长丹尼尔·斯珀林（Danjel SPerljng）在与政策评论家德博拉·戈登（Deborah Gordon）合著的《20亿辆汽车》一书中指出，新技术、燃料、石油和汽车工业的改革以及最新形成的汽车文化，能够造就一个内含集成交通系统的安全、繁荣而有效率的世界。     

Metagenomic and functional analysis of hindgut microbiota of a wood-feeding higher termite

From the standpoints of both basic research and biotechnology, there is considerable interest in reaching a clearer understanding of the diversity of biological mechanisms employed during lignocellulose degradation. Globally, termites are an extremely successful group of wood-degrading organisms and are therefore important both for their roles in carbon turnover in the environment and as potential sources of biochemical catalysts for efforts aimed at converting wood into biofuels. Only recently have data supported any direct role for the symbiotic bacteria in the gut of the termite in cellulose and xylan hydrolysis. Here we use a metagenomic analysis of the bacterial community resident in the hindgut paunch of a wood-feeding 'higher' Nasutitermes species (which do not contain cellulose-fermenting protozoa) to show the presence of a large, diverse set of bacterial genes for cellulose and xylan hydrolysis. Many of these genes were expressed in vivo or had cellulase activity in vitro, and further analyses implicate spirochete and fibrobacter species in gut lignocellulose degradation. New insights into other important symbiotic functions including H2 metabolism, CO2-reductive acetogenesis and N2 fixation are also provided by this first system-wide gene analysis of a microbial community specialized towards plant lignocellulose degradation. Our results underscore how complex even a 1-microl environment can be.     

Molecular mechanism of anaerobic ammonium oxidation

Two distinct microbial processes, denitrification and anaerobic ammonium oxidation (anammox), are responsible for the release of fixed nitrogen as dinitrogen gas (N(2)) to the atmosphere. Denitrification has been studied for over 100 years and its intermediates and enzymes are well known. Even though anammox is a key biogeochemical process of equal importance, its molecular mechanism is unknown, but it was proposed to proceed through hydrazine (N(2)H(4)). Here we show that N(2)H(4) is produced from the anammox substrates ammonium and nitrite and that nitric oxide (NO) is the direct precursor of N(2)H(4). We resolved the genes and proteins central to anammox metabolism and purified the key enzymes that catalyse N(2)H(4) synthesis and its oxidation to N(2). These results present a new biochemical reaction forging an N-N bond and fill a lacuna in our understanding of the biochemical synthesis of the N(2) in the atmosphere. Furthermore, they reinforce the role of nitric oxide in the evolution of the nitrogen cycle.     

Mutations in the gene encoding the basal body protein RPGRIP1L, a nephrocystin-4 interactor, cause Joubert syndrome

Protein-protein interaction analyses have uncovered a ciliary and basal body protein network that, when disrupted, can result in nephronophthisis (NPHP), Leber congenital amaurosis, Senior-L?ken syndrome (SLSN) or Joubert syndrome (JBTS). However, details of the molecular mechanisms underlying these disorders remain poorly understood. RPGRIP1-like protein (RPGRIP1L) is a homolog of RPGRIP1 (RPGR-interacting protein 1), a ciliary protein defective in Leber congenital amaurosis. We show that RPGRIP1L interacts with nephrocystin-4 and that mutations in the gene encoding nephrocystin-4 (NPHP4) that are known to cause SLSN disrupt this interaction. RPGRIP1L is ubiquitously expressed, and its protein product localizes to basal bodies. Therefore, we analyzed RPGRIP1L as a candidate gene for JBTS and identified loss-of-function mutations in three families with typical JBTS, including the characteristic mid-hindbrain malformation. This work identifies RPGRIP1L as a gene responsible for JBTS and establishes a central role for cilia and basal bodies in the pathophysiology of this disorder.     

Mutations in ISPD cause Walker-Warburg syndrome and defective glycosylation of α-dystroglycan

Walker-Warburg syndrome (WWS) is an autosomal recessive multisystem disorder characterized by complex eye and brain abnormalities with congenital muscular dystrophy (CMD) and aberrant a-dystroglycan glycosylation. Here we report mutations in the ISPD gene (encoding isoprenoid synthase domain containing) as the second most common cause of WWS. Bacterial IspD is a nucleotidyl transferase belonging to a large glycosyltransferase family, but the role of the orthologous protein in chordates is obscure to date, as this phylum does not have the corresponding non-mevalonate isoprenoid biosynthesis pathway. Knockdown of ispd in zebrafish recapitulates the human WWS phenotype with hydrocephalus, reduced eye size, muscle degeneration and hypoglycosylated a-dystroglycan. These results implicate ISPD in a-dystroglycan glycosylation in maintaining sarcolemma integrity in vertebrates.     

Loss-of-function mutations in TGFB2 cause a syndromic presentation of thoracic aortic aneurysm

Loeys-Dietz syndrome (LDS) associates with a tissue signature for high transforming growth factor (TGF)-β signaling but is often caused by heterozygous mutations in genes encoding positive effectors of TGF-β signaling, including either subunit of the TGF-β receptor or SMAD3, thereby engendering controversy regarding the mechanism of disease. Here, we report heterozygous mutations or deletions in the gene encoding the TGF-β2 ligand for a phenotype within the LDS spectrum and show upregulation of TGF-β signaling in aortic tissue from affected individuals. Furthermore, haploinsufficient Tgfb2(+/-) mice have aortic root aneurysm and biochemical evidence of increased canonical and noncanonical TGF-β signaling. Mice that harbor both a mutant Marfan syndrome (MFS) allele (Fbn1(C1039G/+)) and Tgfb2 haploinsufficiency show increased TGF-β signaling and phenotypic worsening in association with normalization of TGF-β2 expression and high expression of TGF-β1. Taken together, these data support the hypothesis that compensatory autocrine and/or paracrine events contribute to the pathogenesis of TGF-β-mediated vasculopathies.