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41.
被称为聚能光生伏打效应的技术,既得益于太阳能电池的进步(这种电池可吸收太阳光并将其转化成电能),也得益于将阳光聚集到电池上的反射镜或透镜聚光器(concentrator)系统。不久,这种技术将产生和从电网上获取电力一样便宜的太阳能动力。将太阳光聚集以减小太阳能电池的尺寸,从而降低成本的想法早在几十年前就有了。但重新对这种想法产生兴趣,还是2年前的事情。去年10月,日本电子巨头夏普公司展示了用弗雷斯内尔透镜(用于灯塔上)将太阳光聚集到一种超高效率的太阳能电池上的新系统,其效率大约为传统硅太阳能电池的两倍。其他公司,如美国加利… 相似文献
42.
面对全球气候变暖和能源价格的持续上涨等因素,1年前,当加州议会推出了“加利福尼亚太阳能倡议”计划后,全加州兴起了一股安装家用太阳能发电系统的热潮,并逐渐向周边地区蔓延—— 相似文献
43.
人类把树木用作燃料已经有数千年的历史;然而,现在人们把木材当作燃料,是因一种高新技术而有了新的改变:这就是用木材替代通常用的玉米或甘蔗来制造乙醇——一种生物燃料。政治家和环境保护论者由于各种原因也开始对乙醇产生了兴趣:与石油不同的是,乙醇可以再生, 相似文献
44.
45.
在现代技术器件产生的废料中,热量可能是最有利用价值的东西。但是,对计算机、电子器件、发电设备、汽车以及在炎热天气中倍受煎熬的人来说,过热是一个令人关注的大问题。同时热也是一种很特别的废料,因为它是一种能为更多有用目的服务的能源副产物,也是一种能量形式。如果它能被收集并转化成电能,就可以提高能量效率并可消除过热问题; 相似文献
46.
二向性归一化植被指数:概念及应用 总被引:5,自引:1,他引:5
最近发布的星载法国地表反射的极化与方向性观测仪(POILDER)与美国中分辨率成像光谱仪(MODIS)的地表二向性反射(BRDF)数据产品,其输入数据的大气纠正未能满足定量遥感的需求.提出了二向性归一化植被指数(BiNDVI)的概念,以同时考虑地表反射的二向性与大气程辐射的影响,并用于定义卫星多角度遥感观测值的大气质量指数.用该指数加权迭代反演,能明显改进MODIS-BRDF的数据产品质量. 相似文献
47.
Anthropogenic ocean acidification over the twenty-first century and its impact on calcifying organisms 总被引:15,自引:0,他引:15
Orr JC Fabry VJ Aumont O Bopp L Doney SC Feely RA Gnanadesikan A Gruber N Ishida A Joos F Key RM Lindsay K Maier-Reimer E Matear R Monfray P Mouchet A Najjar RG Plattner GK Rodgers KB Sabine CL Sarmiento JL Schlitzer R Slater RD Totterdell IJ Weirig MF Yamanaka Y Yool A 《Nature》2005,437(7059):681-686
Today's surface ocean is saturated with respect to calcium carbonate, but increasing atmospheric carbon dioxide concentrations are reducing ocean pH and carbonate ion concentrations, and thus the level of calcium carbonate saturation. Experimental evidence suggests that if these trends continue, key marine organisms--such as corals and some plankton--will have difficulty maintaining their external calcium carbonate skeletons. Here we use 13 models of the ocean-carbon cycle to assess calcium carbonate saturation under the IS92a 'business-as-usual' scenario for future emissions of anthropogenic carbon dioxide. In our projections, Southern Ocean surface waters will begin to become undersaturated with respect to aragonite, a metastable form of calcium carbonate, by the year 2050. By 2100, this undersaturation could extend throughout the entire Southern Ocean and into the subarctic Pacific Ocean. When live pteropods were exposed to our predicted level of undersaturation during a two-day shipboard experiment, their aragonite shells showed notable dissolution. Our findings indicate that conditions detrimental to high-latitude ecosystems could develop within decades, not centuries as suggested previously. 相似文献
48.
Nussbaum JM Schilling S Cynis H Silva A Swanson E Wangsanut T Tayler K Wiltgen B Hatami A Rönicke R Reymann K Hutter-Paier B Alexandru A Jagla W Graubner S Glabe CG Demuth HU Bloom GS 《Nature》2012,485(7400):651-655
Extracellular plaques of amyloid-β and intraneuronal neurofibrillary tangles made from tau are the histopathological signatures of Alzheimer's disease. Plaques comprise amyloid-β fibrils that assemble from monomeric and oligomeric intermediates, and are prognostic indicators of Alzheimer's disease. Despite the importance of plaques to Alzheimer's disease, oligomers are considered to be the principal toxic forms of amyloid-β. Interestingly, many adverse responses to amyloid-β, such as cytotoxicity, microtubule loss, impaired memory and learning, and neuritic degeneration, are greatly amplified by tau expression. Amino-terminally truncated, pyroglutamylated (pE) forms of amyloid-β are strongly associated with Alzheimer's disease, are more toxic than amyloid-β, residues 1-42 (Aβ(1-42)) and Aβ(1-40), and have been proposed as initiators of Alzheimer's disease pathogenesis. Here we report a mechanism by which pE-Aβ may trigger Alzheimer's disease. Aβ(3(pE)-42) co-oligomerizes with excess Aβ(1-42) to form metastable low-n oligomers (LNOs) that are structurally distinct and far more cytotoxic to cultured neurons than comparable LNOs made from Aβ(1-42) alone. Tau is required for cytotoxicity, and LNOs comprising 5% Aβ(3(pE)-42) plus 95% Aβ(1-42) (5% pE-Aβ) seed new cytotoxic LNOs through multiple serial dilutions into Aβ(1-42) monomers in the absence of additional Aβ(3(pE)-42). LNOs isolated from human Alzheimer's disease brain contained Aβ(3(pE)-42), and enhanced Aβ(3(pE)-42) formation in mice triggered neuron loss and gliosis at 3 months, but not in a tau-null background. We conclude that Aβ(3(pE)-42) confers tau-dependent neuronal death and causes template-induced misfolding of Aβ(1-42) into structurally distinct LNOs that propagate by a prion-like mechanism. Our results raise the possibility that Aβ(3(pE)-42) acts similarly at a primary step in Alzheimer's disease pathogenesis. 相似文献
49.
Bone marrow cells regenerate infarcted myocardium 总被引:455,自引:0,他引:455
Orlic D Kajstura J Chimenti S Jakoniuk I Anderson SM Li B Pickel J McKay R Nadal-Ginard B Bodine DM Leri A Anversa P 《Nature》2001,410(6829):701-705
Myocardial infarction leads to loss of tissue and impairment of cardiac performance. The remaining myocytes are unable to reconstitute the necrotic tissue, and the post-infarcted heart deteriorates with time. Injury to a target organ is sensed by distant stem cells, which migrate to the site of damage and undergo alternate stem cell differentiation; these events promote structural and functional repair. This high degree of stem cell plasticity prompted us to test whether dead myocardium could be restored by transplanting bone marrow cells in infarcted mice. We sorted lineage-negative (Lin-) bone marrow cells from transgenic mice expressing enhanced green fluorescent protein by fluorescence-activated cell sorting on the basis of c-kit expression. Shortly after coronary ligation, Lin- c-kitPOS cells were injected in the contracting wall bordering the infarct. Here we report that newly formed myocardium occupied 68% of the infarcted portion of the ventricle 9 days after transplanting the bone marrow cells. The developing tissue comprised proliferating myocytes and vascular structures. Our studies indicate that locally delivered bone marrow cells can generate de novo myocardium, ameliorating the outcome of coronary artery disease. 相似文献
50.
RNAi-mediated gene silencing in non-human primates 总被引:2,自引:0,他引:2
Zimmermann TS Lee AC Akinc A Bramlage B Bumcrot D Fedoruk MN Harborth J Heyes JA Jeffs LB John M Judge AD Lam K McClintock K Nechev LV Palmer LR Racie T Röhl I Seiffert S Shanmugam S Sood V Soutschek J Toudjarska I Wheat AJ Yaworski E Zedalis W Koteliansky V Manoharan M Vornlocher HP MacLachlan I 《Nature》2006,441(7089):111-114
The opportunity to harness the RNA interference (RNAi) pathway to silence disease-causing genes holds great promise for the development of therapeutics directed against targets that are otherwise not addressable with current medicines. Although there are numerous examples of in vivo silencing of target genes after local delivery of small interfering RNAs (siRNAs), there remain only a few reports of RNAi-mediated silencing in response to systemic delivery of siRNA, and there are no reports of systemic efficacy in non-rodent species. Here we show that siRNAs, when delivered systemically in a liposomal formulation, can silence the disease target apolipoprotein B (ApoB) in non-human primates. APOB-specific siRNAs were encapsulated in stable nucleic acid lipid particles (SNALP) and administered by intravenous injection to cynomolgus monkeys at doses of 1 or 2.5 mg kg(-1). A single siRNA injection resulted in dose-dependent silencing of APOB messenger RNA expression in the liver 48 h after administration, with maximal silencing of >90%. This silencing effect occurred as a result of APOB mRNA cleavage at precisely the site predicted for the RNAi mechanism. Significant reductions in ApoB protein, serum cholesterol and low-density lipoprotein levels were observed as early as 24 h after treatment and lasted for 11 days at the highest siRNA dose, thus demonstrating an immediate, potent and lasting biological effect of siRNA treatment. Our findings show clinically relevant RNAi-mediated gene silencing in non-human primates, supporting RNAi therapeutics as a potential new class of drugs. 相似文献