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71.
Ton Loontjens Bart Plum 《复旦学报(自然科学版)》2007,(5)
1 Results The objective was to make hyperbranched (HB) polyurethane brushes with reactive end groups, to coat biomedical devices and to enable the introduction of various functionalities that are needed to fulfill biomedical tasks.Biomedical materials should fulfill at least three requirements: (1) good mechanical properties, (2) good biocompatibility and (3) provided with functionalities to perform the required tasks. Since polyurethanes are able to fulfill the first 2 requirements we focused in this w... 相似文献
72.
Baker DJ Wijshake T Tchkonia T LeBrasseur NK Childs BG van de Sluis B Kirkland JL van Deursen JM 《Nature》2011,479(7372):232-236
Advanced age is the main risk factor for most chronic diseases and functional deficits in humans, but the fundamental mechanisms that drive ageing remain largely unknown, impeding the development of interventions that might delay or prevent age-related disorders and maximize healthy lifespan. Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells. Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16(Ink4a), to design a novel transgene, INK-ATTAC, for inducible elimination of p16(Ink4a)-positive senescent cells upon administration of a drug. Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16(Ink4a)-positive senescent cells upon drug treatment. In tissues--such as adipose tissue, skeletal muscle and eye--in which p16(Ink4a) contributes to the acquisition of age-related pathologies, life-long removal of p16(Ink4a)-expressing cells delayed onset of these phenotypes. Furthermore, late-life clearance attenuated progression of already established age-related disorders. These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan. 相似文献
73.
This paper deals with the FEEDBACK VERTEX SET problem on undirected graphs, which asks for the existence of a vertex set of bounded size that intersects all cycles. Due it is theoretical and practical importance,the problem has been the subject of intensive study. Motivated by the parameter ecology program we attempt to classify the parameterized and kernelization complexity of FEEDBACK VERTEX SET for a wide range of parameters.We survey known results and present several new complexity classifications. For example, we prove that FEEDBACK VERTEX SET is fixed-parameter tractable parameterized by the vertex-deletion distance to a chordal graph. We also prove that the problem admits a polynomial kernel when parameterized by the vertex-deletion distance to a pseudo forest, a graph in which every connected component has at most one cycle. In contrast, we prove that a slightly smaller parameterization does not allow for a polynomial kernel unless NP coNP=poly and the polynomial-time hierarchy collapses. 相似文献
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