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Résumé On a étudié la toxicité de tétracycline injectée par voie intraveneuse chez le rat. On a montré qu'il n'y a pas d'ischémie significative du rein après l'administration de tétracycline. On a demontré aussi que la nécrose expérimentale des tabules rénales du rat provoquée par diverses substances chimiques n'est pas augmentée par la tétracycline. 相似文献
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Novel treatment for joint inflammation 总被引:3,自引:0,他引:3
J T Dingle J L Gordon B L Hazleman C G Knight D P Page Thomas N C Phillips I H Shaw F J Fildes J E Oliver G Jones E H Turner J S Lowe 《Nature》1978,271(5643):372-373
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CH Wu C Fallini N Ticozzi PJ Keagle PC Sapp K Piotrowska P Lowe M Koppers D McKenna-Yasek DM Baron JE Kost P Gonzalez-Perez AD Fox J Adams F Taroni C Tiloca AL Leclerc SC Chafe D Mangroo MJ Moore JA Zitzewitz ZS Xu LH van den Berg JD Glass G Siciliano ET Cirulli DB Goldstein F Salachas V Meininger W Rossoll A Ratti C Gellera DA Bosco GJ Bassell V Silani VE Drory RH Brown JE Landers 《Nature》2012,488(7412):499-503
Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disorder resulting from motor neuron death. Approximately 10% of cases are familial (FALS), typically with a dominant inheritance mode. Despite numerous advances in recent years, nearly 50% of FALS cases have unknown genetic aetiology. Here we show that mutations within the profilin 1 (PFN1) gene can cause FALS. PFN1 is crucial for the conversion of monomeric (G)-actin to filamentous (F)-actin. Exome sequencing of two large ALS families showed different mutations within the PFN1 gene. Further sequence analysis identified 4 mutations in 7 out of 274 FALS cases. Cells expressing PFN1 mutants contain ubiquitinated, insoluble aggregates that in many cases contain the ALS-associated protein TDP-43. PFN1 mutants also display decreased bound actin levels and can inhibit axon outgrowth. Furthermore, primary motor neurons expressing mutant PFN1 display smaller growth cones with a reduced F/G-actin ratio. These observations further document that cytoskeletal pathway alterations contribute to ALS pathogenesis. 相似文献
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S Izraeli L A Lowe V L Bertness D J Good D W Dorward I R Kirsch M R Kuehn 《Nature》1999,399(6737):691-694
The establishment of the main body axis and the determination of left-right asymmetry are fundamental aspects of vertebrate embryonic development. A link between these processes has been revealed by the frequent finding of midline defects in humans with left-right anomalies. This association is also seen in a number of mutations in mouse and zebrafish, and in experimentally manipulated Xenopus embryos. However, the severity of laterality defects accompanying abnormal midline development varies, and the molecular basis for this variation is unknown. Here we show that mouse embryos lacking the early-response gene SIL have axial midline defects, a block in midline Sonic hedgehog (Shh) signalling and randomized cardiac looping. Comparison with Shh mutant embryos, which have axial defects but normal cardiac looping, indicates that the consequences of abnormal midline development for left-right patterning depend on the time of onset, duration and severity of disruption of the normal asymmetric patterns of expression of nodal, lefty-2 and Pitx2. 相似文献
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Ovotransferrin with one iron atom 总被引:3,自引:0,他引:3
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