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排序方式: 共有130条查询结果,搜索用时 187 毫秒
41.
Lawson B Robinson RA Neimanis A Handeland K Isomursu M Agren EO Hamnes IS Tyler KM Chantrey J Hughes LA Pennycott TW Simpson VR John SK Peck KM Toms MP Bennett M Kirkwood JK Cunningham AA 《EcoHealth》2011,8(2):143-153
Finch trichomonosis emerged in Great Britain in 2005 and led to epidemic mortality and a significant population decline of greenfinches, Carduelis chloris and chaffinches, Fringilla coelebs, in the central and western counties of England and Wales in the autumn of 2006. In this article, we show continued epidemic spread of the disease with a pronounced shift in geographical distribution towards eastern England in 2007. This was followed by international spread to southern Fennoscandia where cases were confirmed at multiple sites in the summer of 2008. Sequence data of the ITS1/5.8S/ITS2 ribosomal region and part of the small subunit (SSU) rRNA gene showed no variation between the British and Fennoscandian parasite strains of Trichomonas gallinae. Epidemiological and historical ring return data support bird migration as a plausible mechanism for the observed pattern of disease spread, and suggest the chaffinch as the most likely primary vector. This finding is novel since, although intuitive, confirmed disease spread by migratory birds is very rare and, when it has been recognised, this has generally been for diseases caused by viral pathogens. We believe this to be the first documented case of the spread of a protozoal emerging infectious disease by migrating birds. 相似文献
42.
Hor H Bartesaghi L Kutalik Z Vicário JL de Andrés C Pfister C Lammers GJ Guex N Chrast R Tafti M Peraita-Adrados R 《American journal of human genetics》2011,(3):474-479
Narcolepsy is a rare sleep disorder characterized by excessive daytime sleepiness and cataplexy. Familial narcolepsy accounts for less than 10% of all narcolepsy cases. However, documented multiplex families are very rare and causative mutations have not been identified to date. To identify a causative mutation in familial narcolepsy, we performed linkage analysis in the largest ever reported family, which has 12 affected members, and sequenced coding regions of the genome (exome sequencing) of three affected members with narcolepsy and cataplexy. We successfully mapped a candidate locus on chromosomal region 6p22.1 (LOD score = 3.85) by linkage analysis. Exome sequencing identified a missense mutation in the second exon of MOG within the linkage region. A c.398C>G mutation was present in all affected family members but absent in unaffected members and 775 unrelated control subjects. Transient expression of mutant myelin oligodendrocyte glycoprotein (MOG) in mouse oligodendrocytes showed abnormal subcellular localization, suggesting an altered function of the mutant MOG. MOG has recently been linked to various neuropsychiatric disorders and is considered as a key autoantigen in multiple sclerosis and in its animal model, experimental autoimmune encephalitis. Our finding of a pathogenic MOG mutation highlights a major role for myelin and oligodendrocytes in narcolepsy and further emphasizes glial involvement in neurodegeneration and neurobehavioral disorders. 相似文献
43.
Vic Norris Axel Hunding Francois Kepes Doron Lancet Abraham Minsky Derek Raine Robert Root-Bernstein K. Sriram 《Origins of life and evolution of the biosphere》2007,37(4-5):429-432
Five common assumptions about the first cells are challenged by the pre-biotic ecology model and are replaced by the following
propositions: firstly, early cells were more complex, more varied and had a greater diversity of constituents than modern
cells; secondly, the complexity of a cell is not related to the number of genes it contains, indeed, modern bacteria are as
complex as eukaryotes; thirdly, the unit of early life was an ‘ecosystem’ rather than a ‘cell’; fourthly, the early cell needed
no genes at all; fifthly, early life depended on non-covalent associations and on catalysts that were not confined to specific
reactions. We present here the outlines of a theory that connects findings about modern bacteria with speculations about their
origins.
Presented at the International School of Complexity – 4th Course: Basic Questions on the Origins of Life; “Ettore Majorana”
Foundation and Centre for Scientific Culture, Erice, Italy, 1–6 October 2006. 相似文献
44.
Patricia Ana Vic H. Arcega Chiara Louise P. Cabantac Ronald Allan L. Cruz 《Developing world bioethics》2019,19(3):180-185
Research involving human participants has been conducted in the Philippines since the beginning of the Spanish colonial period. Such studies are expected to adhere to internationally accepted ethical guidelines. This paper discusses trends in clinical research ethics in the Philippines during the American colonial period (1898‐1946). Specifically, studies were assessed on: 1) their observance of ethical protocols, including review; 2) identification of inclusion and exclusion criteria in the selection of participants; 3) use of vulnerable subjects; and 4) practice of the informed consent process. Only the informed consent process had a significant logistic correlation with progression of years. Recruitment of vulnerable groups was common during this period; children and prisoners were the most common participants. Trends in medical ethics in the Philippines reflected those in the United States prior to the publication of the Nuremberg Code, which served as a milestone in the protection of human welfare in clinical research. 相似文献
45.
Vic Norris Ghislain Gangwe Nana Jean-Nicolas Audinot 《Theorie in den Biowissenschaften》2014,133(1):47-61
Fundamental, unresolved questions in biology include how a bacterium generates coherent phenotypes, how a population of bacteria generates a coherent set of such phenotypes, how the cell cycle is regulated and how life arose. To try to help answer these questions, we have developed the concepts of hyperstructures, competitive coherence and life on the scales of equilibria. Hyperstructures are large assemblies of macromolecules that perform functions. Competitive coherence describes the way in which organisations such as cells select a subset of their constituents to be active in determining their behaviour; this selection results from a competition between a process that is responsible for a historical coherence and another process responsible for coherence with the current environment. Life on the scales of equilibria describes how bacteria depend on the cell cycle to negotiate phenotype space and, in particular, to satisfy the conflicting constraints of having to grow in favourable conditions so as to reproduce yet not grow in hostile conditions so as to survive. Both competitive coherence and life on the scales deal with the problem of reconciling conflicting constraints. Here, we bring together these concepts in the common framework of hyperstructures and make predictions that may be tested using a learning program, Coco, and secondary ion mass spectrometry. 相似文献
46.
H Ruffner J Sprunger O Charlat J Leighton-Davies B Grosshans A Salathe S Zietzling V Beck M Therier A Isken Y Xie Y Zhang H Hao X Shi D Liu Q Song I Clay G Hintzen J Tchorz LC Bouchez G Michaud P Finan VE Myer T Bouwmeester J Porter M Hild F Bassilana CN Parker F Cong 《PloS one》2012,7(7):e40976
The Wnt/β-catenin signaling pathbway controls many important biological processes. R-Spondin (RSPO) proteins are a family of secreted molecules that strongly potentiate Wnt/β-catenin signaling, however, the molecular mechanism of RSPO action is not yet fully understood. We performed an unbiased siRNA screen to identify molecules specifically required for RSPO, but not Wnt, induced β-catenin signaling. From this screen, we identified LGR4, then an orphan G protein-coupled receptor (GPCR), as the cognate receptor of RSPO. Depletion of LGR4 completely abolished RSPO-induced β-catenin signaling. The loss of LGR4 could be compensated by overexpression of LGR5, suggesting that LGR4 and LGR5 are functional homologs. We further demonstrated that RSPO binds to the extracellular domain of LGR4 and LGR5, and that overexpression of LGR4 strongly sensitizes cells to RSPO-activated β-catenin signaling. Supporting the physiological significance of RSPO-LGR4 interaction, Lgr4-/- crypt cultures failed to grow in RSPO-containing intestinal crypt culture medium. No coupling between LGR4 and heterotrimeric G proteins could be detected in RSPO-treated cells, suggesting that LGR4 mediates RSPO signaling through a novel mechanism. Identification of LGR4 and its relative LGR5, an adult stem cell marker, as the receptors of RSPO will facilitate the further characterization of these receptor/ligand pairs in regenerative medicine applications. 相似文献
47.
Marcelo A. Mori Vicência Micheline Sales Fabiana Louise Motta Raphael Gomes Fonseca Natalia Alenina Dioze Guadagnini Ines Schadock Elton Dias Silva Hugo A. M. Torres Edson Lucas dos Santos Charlles Heldan Castro Vania D’Almeida Sandra Andreotti Amanda Baron Campa?a Rogério A. L. Sertié Mario J. A. Saad Fabio Bessa Lima Michael Bader Jo?o Bosco Pesquero 《PloS one》2012,7(9)
Background
Kinins participate in the pathophysiology of obesity and type 2 diabetes by mechanisms which are not fully understood. Kinin B1 receptor knockout mice (B1 −/−) are leaner and exhibit improved insulin sensitivity.Methodology/Principal Findings
Here we show that kinin B1 receptors in adipocytes play a role in controlling whole body insulin action and glucose homeostasis. Adipocytes isolated from mouse white adipose tissue (WAT) constitutively express kinin B1 receptors. In these cells, treatment with the B1 receptor agonist des-Arg9-bradykinin improved insulin signaling, GLUT4 translocation, and glucose uptake. Adipocytes from B1 −/− mice showed reduced GLUT4 expression and impaired glucose uptake at both basal and insulin-stimulated states. To investigate the consequences of these phenomena to whole body metabolism, we generated mice where the expression of the kinin B1 receptor was limited to cells of the adipose tissue (aP2-B1/B1 −/−). Similarly to B1 −/− mice, aP2-B1/B1 −/− mice were leaner than wild type controls. However, exclusive expression of the kinin B1 receptor in adipose tissue completely rescued the improved systemic insulin sensitivity phenotype of B1 −/− mice. Adipose tissue gene expression analysis also revealed that genes involved in insulin signaling were significantly affected by the presence of the kinin B1 receptor in adipose tissue. In agreement, GLUT4 expression and glucose uptake were increased in fat tissue of aP2-B1/B1 −/− when compared to B1 −/− mice. When subjected to high fat diet, aP2-B1/B1 −/− mice gained more weight than B1 −/− littermates, becoming as obese as the wild types.Conclusions/Significance
Thus, kinin B1 receptor participates in the modulation of insulin action in adipocytes, contributing to systemic insulin sensitivity and predisposition to obesity. 相似文献48.
49.
50.
What is biological complexity? How many sorts exist? Are there levels of complexity? How are they related to one another? How is complexity related to the emergence of new phenotypes? To try to get to grips with these questions, we consider the archetype of a complex biological system, Escherichia coli. We take the position that E. coli has been selected to survive adverse conditions and to grow in favourable ones and that many other complex systems undergo similar selection. We invoke the concept of hyperstructures which constitute a level of organisation intermediate between macromolecules and cells. We also invoke a new concept, competitive coherence, to describe how phenotypes are created by a competition between maintaining a consistent story over time and creating a response that is coherent with respect to both internal and external conditions. We suggest how these concepts lead to parameters suitable for describing the rich form of complexity termed hypercomplexity and we propose a relationship between competitive coherence and emergence. 相似文献