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The trackway of a swimming theropod (ichnogenus Characichnos) is reported from the Lower Cretaceous Feitianshan Formation of Sichuan, China. These swim tracks help confirm that non-avian theropods were capable of forging moderately deep bodies of water. The trackway occurs on the same surface as a typical walking trackway of a sauropod (ichnogenus Brontopodus). Both occurrences are the first reported from the Cretaceous of Sichuan, and the swim tracks are the first well-preserved example of a Characichnos trackway from China. Additionally, a theropod walking trackway and several ornithopod walking trackways (similar to the ichnogenus Caririchnium) occur in the same horizon. The ornithopod trackways show a parallel orientation, suggesting gregarious behavior of the trackmakers, which may have been iguanodontiforms and/or hadrosauriforms. The co-occurrence of theropod swim tracks and theropod walking tracks suggests a fluctuation of water depth within a distinct time span.  相似文献   
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翼龙是已知的、最早飞上天际的脊椎动物,目前已经发现了成千上万件化石,代表着这一大家族从晚三叠世到晚白垩世在全球范围内的蓬勃发展史.自2004年甘肃盐锅峡地区首次报道翼龙足迹以来,中国陆续发现了一批翼龙足迹化石,绝大多数的足迹点都保存了翼龙的前后足迹.2013年,我们在盐锅峡地区发现了至少20个翼龙前足迹的凸型足迹,而没有发现任何后足迹,这些足迹可归于一个单独翼龙遗迹属——Pteraichnus.这是中国第一次发现由前足迹主导的翼龙足迹组合,这可能反映了翼龙前后足迹在同等保存条件下的不同深度.更重要的是,盐锅峡的这批翼龙足迹与当地发现的大量虫迹相关,一些足迹甚至就保存在虫迹面上,这些虫迹包括Cochlichnus,Spongeliomorpha和Paleophycus,因此推断这批翼龙造迹者很可能以这些无脊椎动物造迹者为食.  相似文献   
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Charcot-Marie-Tooth disease (CMT) is the most common inherited neuromuscular disease and is characterized by considerable clinical and genetic heterogeneity. We previously reported a Russian family with autosomal dominant axonal CMT and assigned the locus underlying the disease (CMT2F; OMIM 606595) to chromosome 7q11-q21 (ref. 2). Here we report a missense mutation in the gene encoding 27-kDa small heat-shock protein B1 (HSPB1, also called HSP27) that segregates in the family with CMT2F. Screening for mutations in HSPB1 in 301 individuals with CMT and 115 individuals with distal hereditary motor neuropathies (distal HMNs) confirmed the previously observed mutation and identified four additional missense mutations. We observed the additional HSPB1 mutations in four families with distal HMN and in one individual with CMT neuropathy. Four mutations are located in the Hsp20-alpha-crystallin domain, and one mutation is in the C-terminal part of the HSP27 protein. Neuronal cells transfected with mutated HSPB1 were less viable than cells expressing the wild-type protein. Cotransfection of neurofilament light chain (NEFL) and mutant HSPB1 resulted in altered neurofilament assembly in cells devoid of cytoplasmic intermediate filaments.  相似文献   
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