排序方式: 共有53条查询结果,搜索用时 234 毫秒
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Chalasani SH Chronis N Tsunozaki M Gray JM Ramot D Goodman MB Bargmann CI 《Nature》2007,450(7166):63-70
Although many properties of the nervous system are shared among animals and systems, it is not known whether different neuronal circuits use common strategies to guide behaviour. Here we characterize information processing by Caenorhabditis elegans olfactory neurons (AWC) and interneurons (AIB and AIY) that control food- and odour-evoked behaviours. Using calcium imaging and mutations that affect specific neuronal connections, we show that AWC neurons are activated by odour removal and activate the AIB interneurons through AMPA-type glutamate receptors. The level of calcium in AIB interneurons is elevated for several minutes after odour removal, a neuronal correlate to the prolonged behavioural response to odour withdrawal. The AWC neuron inhibits AIY interneurons through glutamate-gated chloride channels; odour presentation relieves this inhibition and results in activation of AIY interneurons. The opposite regulation of AIY and AIB interneurons generates a coordinated behavioural response. Information processing by this circuit resembles information flow from vertebrate photoreceptors to 'OFF' bipolar and 'ON' bipolar neurons, indicating a conserved or convergent strategy for sensory information processing. 相似文献
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Diola Marina Núñez-Ramírez Aquiles Solís-Soto Javier López-Miranda Benito Pereyra-Alférez Miriam Rutiaga-Quiñónes Luis Medina-Torres Hiram Medrano-Roldán 《矿物冶金与材料学报》2011,18(5):523-526
The iron concentrate from Hercules Mine of Coahuila, Mexico, which mainly contained pyrite and pyrrhotite, was treated by
the bioleaching process using native strain Acidithiobacillus ferrooxidans (A. ferrooxidans) to determine the ability of these bacteria on the leaching of zinc. The native bacteria were isolated from the iron concentrate
of the mine. The bioleaching experiments were carried out in shake flasks to analyze the effects of pH values, pulp density,
and the ferrous sulfate concentration on the bioleaching process. The results obtained by microbial kinetic analyses for the
evaluation of some aspects of zinc leaching show that the native bacteria A. ferrooxidans, which is enriched with a 9K Silverman medium under the optimum conditions of pH 2.0, 20 g/L pulp density, and 40 g/L FeSO4, increases the zinc extraction considerably observed by monitoring during15 d, i.e., the zinc concentration has a decrease of about 95% in the iron concentrate. 相似文献
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Merveille AC Davis EE Becker-Heck A Legendre M Amirav I Bataille G Belmont J Beydon N Billen F Clément A Clercx C Coste A Crosbie R de Blic J Deleuze S Duquesnoy P Escalier D Escudier E Fliegauf M Horvath J Hill K Jorissen M Just J Kispert A Lathrop M Loges NT Marthin JK Momozawa Y Montantin G Nielsen KG Olbrich H Papon JF Rayet I Roger G Schmidts M Tenreiro H Towbin JA Zelenika D Zentgraf H Georges M Lequarré AS Katsanis N Omran H Amselem S 《Nature genetics》2011,43(1):72-78
Primary ciliary dyskinesia (PCD) is an inherited disorder characterized by recurrent infections of the upper and lower respiratory tract, reduced fertility in males and situs inversus in about 50% of affected individuals (Kartagener syndrome). It is caused by motility defects in the respiratory cilia that are responsible for airway clearance, the flagella that propel sperm cells and the nodal monocilia that determine left-right asymmetry. Recessive mutations that cause PCD have been identified in genes encoding components of the outer dynein arms, radial spokes and cytoplasmic pre-assembly factors of axonemal dyneins, but these mutations account for only about 50% of cases of PCD. We exploited the unique properties of dog populations to positionally clone a new PCD gene, CCDC39. We found that loss-of-function mutations in the human ortholog underlie a substantial fraction of PCD cases with axonemal disorganization and abnormal ciliary beating. Functional analyses indicated that CCDC39 localizes to ciliary axonemes and is essential for assembly of inner dynein arms and the dynein regulatory complex. 相似文献
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Cambon-Thomsen A Thorisson GA Mabile L Andrieu S Bertier G Boeckhout M Cambon-Thomsen A Carpenter J Dagher G Dalgleish R Deschênes M di Donato JH Filocamo M Goldberg M Hewitt R Hofman P Kauffmann F Leitsalu L Lomba I Mabile L Melegh B Metspalu A Miranda L Napolitani F Oestergaard MZ Parodi B Pasterk M Reiche A Rial-Sebbag E Rivalle G Rochaix P Susbielle G Tarasova L Thomsen M Thorisson GA Zawati MH Zins M;BRIF workshop group 《Nature genetics》2011,43(6):503-504
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Legend naturalism and scientific progress: An essay on Philip Kitcher's : The advancement of science
Philip Kitcher's The Advancement of Science sets out, programmatically, a new naturalistic view of science as a process of building consensus practices. Detailed historical case studies—centrally, the Darwinian revolutio—are intended to support this view. I argue that Kitcher's expositions in fact support a more conservative view, that I dub ‘Legend Naturalism’. Using four historical examples which increasingly challenge Kitcher's discussions, I show that neither Legend Naturalism, nor the less conservative programmatic view, gives an adequate account of scientific progress. I argue for a naturalism that is more informed by psychology and a normative account that is both more social and less realist than the views articulated in The Advancement of Science. 相似文献
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Mechanosensory transduction in touch receptor neurons is believed to be mediated by DEG/ENaC (degenerin/epithelial Na+ channel) proteins in nematodes and mammals. In the nematode Caenorhabditis elegans, gain-of-function mutations in the degenerin genes mec-4 and mec-10 (denoted mec-4(d) and mec-10(d), respectively) cause degeneration of the touch cells. This phenotype is completely suppressed by mutation in a third gene, mec-6 (refs 3, 4), that is needed for touch sensitivity. This last gene is also required for the function of other degenerins. Here we show that mec-6 encodes a single-pass membrane-spanning protein with limited similarity to paraoxonases, which are implicated in human coronary heart disease. This gene is expressed in muscle cells and in many neurons, including the six touch receptor neurons. MEC-6 increases amiloride-sensitive Na+ currents produced by MEC-4(d)/MEC-10(d) by approximately 30-fold, and functions synergistically with MEC-2 (a stomatin-like protein that regulates MEC-4(d)/MEC-10(d) channel activity) to increase the currents by 200-fold. MEC-6 physically interacts with all three channel proteins. In vivo, MEC-6 co-localizes with MEC-4, and is required for punctate MEC-4 expression along touch-neuron processes. We propose that MEC-6 is a part of the degenerin channel complex that may mediate mechanotransduction in touch cells. 相似文献
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Jones JM Datta P Srinivasula SM Ji W Gupta S Zhang Z Davies E Hajnóczky G Saunders TL Van Keuren ML Fernandes-Alnemri T Meisler MH Alnemri ES 《Nature》2003,425(6959):721-727
The mouse mutant mnd2 (motor neuron degeneration 2) exhibits muscle wasting, neurodegeneration, involution of the spleen and thymus, and death by 40 days of age. Degeneration of striatal neurons, with astrogliosis and microglia activation, begins at around 3 weeks of age, and other neurons are affected at later stages. Here we have identified the mnd2 mutation as the missense mutation Ser276Cys in the protease domain of the nuclear-encoded mitochondrial serine protease Omi (also known as HtrA2 or Prss25). Protease activity of Omi is greatly reduced in tissues of mnd2 mice but is restored in mice rescued by a bacterial artificial chromosome transgene containing the wild-type Omi gene. Deletion of the PDZ domain partially restores protease activity to the inactive recombinant Omi protein carrying the Ser276Cys mutation, suggesting that the mutation impairs substrate access or binding to the active site pocket. Loss of Omi protease activity increases the susceptibility of mitochondria to induction of the permeability transition, and increases the sensitivity of mouse embryonic fibroblasts to stress-induced cell death. The neurodegeneration and juvenile lethality in mnd2 mice result from this defect in mitochondrial Omi protease. 相似文献