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21.
Szappanos B Kovács K Szamecz B Honti F Costanzo M Baryshnikova A Gelius-Dietrich G Lercher MJ Jelasity M Myers CL Andrews BJ Boone C Oliver SG Pál C Papp B 《Nature genetics》2011,43(7):656-662
Although experimental and theoretical efforts have been applied to globally map genetic interactions, we still do not understand how gene-gene interactions arise from the operation of biomolecular networks. To bridge the gap between empirical and computational studies, we i, quantitatively measured genetic interactions between ~185,000 metabolic gene pairs in Saccharomyces cerevisiae, ii, superposed the data on a detailed systems biology model of metabolism and iii, introduced a machine-learning method to reconcile empirical interaction data with model predictions. We systematically investigated the relative impacts of functional modularity and metabolic flux coupling on the distribution of negative and positive genetic interactions. We also provide a mechanistic explanation for the link between the degree of genetic interaction, pleiotropy and gene dispensability. Last, we show the feasibility of automated metabolic model refinement by correcting misannotations in NAD biosynthesis and confirming them by in vivo experiments. 相似文献
22.
Finberg KE Heeney MM Campagna DR Aydinok Y Pearson HA Hartman KR Mayo MM Samuel SM Strouse JJ Markianos K Andrews NC Fleming MD 《Nature genetics》2008,40(5):569-571
Iron deficiency is usually attributed to chronic blood loss or inadequate dietary intake. Here, we show that iron deficiency anemia refractory to oral iron therapy can be caused by germline mutations in TMPRSS6, which encodes a type II transmembrane serine protease produced by the liver that regulates the expression of the systemic iron regulatory hormone hepcidin. These findings demonstrate that TMPRSS6 is essential for normal systemic iron homeostasis in humans. 相似文献
23.
Ross MT Grafham DV Coffey AJ Scherer S McLay K Muzny D Platzer M Howell GR Burrows C Bird CP Frankish A Lovell FL Howe KL Ashurst JL Fulton RS Sudbrak R Wen G Jones MC Hurles ME Andrews TD Scott CE Searle S Ramser J Whittaker A Deadman R Carter NP Hunt SE Chen R Cree A Gunaratne P Havlak P Hodgson A Metzker ML Richards S Scott G Steffen D Sodergren E Wheeler DA Worley KC Ainscough R Ambrose KD Ansari-Lari MA Aradhya S Ashwell RI Babbage AK Bagguley CL Ballabio A Banerjee R Barker GE Barlow KF 《Nature》2005,434(7031):325-337
The human X chromosome has a unique biology that was shaped by its evolution as the sex chromosome shared by males and females. We have determined 99.3% of the euchromatic sequence of the X chromosome. Our analysis illustrates the autosomal origin of the mammalian sex chromosomes, the stepwise process that led to the progressive loss of recombination between X and Y, and the extent of subsequent degradation of the Y chromosome. LINE1 repeat elements cover one-third of the X chromosome, with a distribution that is consistent with their proposed role as way stations in the process of X-chromosome inactivation. We found 1,098 genes in the sequence, of which 99 encode proteins expressed in testis and in various tumour types. A disproportionately high number of mendelian diseases are documented for the X chromosome. Of this number, 168 have been explained by mutations in 113 X-linked genes, which in many cases were characterized with the aid of the DNA sequence. 相似文献
24.
Nanoscale hydrodynamics: enhanced flow in carbon nanotubes 总被引:3,自引:0,他引:3
Nanoscale structures that could mimic the selective transport and extraordinarily fast flow possible in biological cellular channels would have a wide range of potential applications. Here we show that liquid flow through a membrane composed of an array of aligned carbon nanotubes is four to five orders of magnitude faster than would be predicted from conventional fluid-flow theory. This high fluid velocity results from an almost frictionless interface at the carbon-nanotube wall. 相似文献
25.
Lim JE Jin O Bennett C Morgan K Wang F Trenor CC Fleming MD Andrews NC 《Nature genetics》2005,37(11):1270-1273
Hemoglobin deficit (hbd) mice carry a spontaneous mutation that impairs erythroid iron assimilation but does not cause other defects. Normal delivery of iron to developing erythroid precursors is highly dependent on the transferrin cycle. Through genetic mapping and complementation experiments, we show that the hbd mutation is an in-frame deletion of a conserved exon of the mouse gene Sec15l1, encoding one of two Sec15 proteins implicated in the mammalian exocyst complex. Sec15l1 is linked to the transferrin cycle through its interaction with Rab11, a GTPase involved in vesicular trafficking. We propose that inactivation of Sec15l1 alters recycling of transferrin cycle endosomes and increases the release of transferrin receptor exocytic vesicles. This in turn decreases erythroid iron uptake. Determining the molecular basis of the hbd phenotype provides new insight into the intricate mechanisms necessary for normal erythroid iron uptake and the function of a mammalian exocyst protein. 相似文献
26.
A one-hit model of cell death in inherited neuronal degenerations 总被引:18,自引:0,他引:18
Clarke G Collins RA Leavitt BR Andrews DF Hayden MR Lumsden CJ McInnes RR 《Nature》2000,406(6792):195-199
In genetic disorders associated with premature neuronal death, symptoms may not appear for years or decades. This delay in clinical onset is often assumed to reflect the occurrence of age-dependent cumulative damage. For example, it has been suggested that oxidative stress disrupts metabolism in neurological degenerative disorders by the cumulative damage of essential macromolecules. A prediction of the cumulative damage hypothesis is that the probability of cell death will increase over time. Here we show in contrast that the kinetics of neuronal death in 12 models of photoreceptor degeneration, hippocampal neurons undergoing excitotoxic cell death, a mouse model of cerebellar degeneration and Parkinson's and Huntington's diseases are all exponential and better explained by mathematical models in which the risk of cell death remains constant or decreases exponentially with age. These kinetics argue against the cumulative damage hypothesis; instead, the time of death of any neuron is random. Our findings are most simply accommodated by a 'one-hit' biochemical model in which mutation imposes a mutant steady state on the neuron and a single event randomly initiates cell death. This model appears to be common to many forms of neurodegeneration and has implications for therapeutic strategies. 相似文献
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29.
E. J. Andrews 《Cellular and molecular life sciences : CMLS》1973,29(6):715-716
Résumé La testostérone, administrée de facon chronique à des souris femelles provoque und diminution statistiquement significative de l'index juxtaglomérulaire. Les femelles traitées par la progestérone ou les souris mâles et femelles des groupes contrôlés ne présentent aucune variation. Ces constatations sont discutées en relation avec l'effet de la testostérone sur le flux sanguin rénal, la pression de perfusion glomérulaire et la secrétion d'aldostérone, de rénine et d'érythropoiétine.
This study was supported by Grant No. RR00469 from The National Institutes of Health, U.S.P.H.S. 相似文献
This study was supported by Grant No. RR00469 from The National Institutes of Health, U.S.P.H.S. 相似文献
30.
Tripling the capacity of wireless communications using electromagnetic polarization 总被引:15,自引:0,他引:15
Wireless communications are a fundamental part of modern information infrastructure. But wireless bandwidth is costly, prompting a close examination of the data channels available using electromagnetic waves. Classically, radio communications have relied on one channel per frequency, although it is well understood that the two polarization states of planar waves allow two distinct information channels; techniques such as 'polarization diversity' already take advantage of this. Recent work has shown that environments with scattering, such as urban areas or indoors, also possess independent spatial channels that can be used to enhance capacity greatly. In either case, the relevant signal processing techniques come under the heading of 'multiple-input/multiple-output' communications, because multiple antennae are required to access the polarization or spatial channels. Here we show that, in a scattering environment, an extra factor of three in channel capacity can be obtained, relative to the conventional limit using dual-polarized radio signals. The extra capacity arises because there are six distinguishable electric and magnetic states of polarization at a given point, rather than two as is usually assumed. 相似文献