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4篇 您的检索式:作者名="Allan Fernandes"
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1自由衰减模型试验的横摇阻尼评估方法研究(英文)显示文摘The methodology to obtain the non-linear roll damping from decay tests is very old. It has been proposed by Froude in the 19th century and used from then on. Behind it there is a quadratic model [θ│θ│] for the damping and a subsequent equivalent linearization. Probably all model basin in the world follows this approach to assess the damping from a decay test. This is well documented and so is the methods to get the p1-p2 coefficients. This is very general in the sense that in principle,it could be applied to any kind of hull. However,it has become clear that for hull with a flat bottom such as a very large crude carrier (VLCC),this approach may lead to confusing results such as negative p2. Faced with this,the work presents a completely new idea. Avoiding the polynomial approximation,the basic attitude is to devise two regions from the decaying test response. The first,called the large amplitude response region yields a larger damping,probably due to the large bilge keel vortices that are attracted to the hull flat bottom. The second is the small amplitude response region where the vortices are not attracted to the bottom but travels approximately 45o sidewise. These observations has led to a new approach called the bi-linear approach as discussed in the work after analyzing several (many) model test results. In fact,a new modified bi-linear approach is ultimately proposed after the understanding of a transition region instead of a transition angle.Antonio C. FERNANDES Allan C. OLIVEIRA 2009Journal of Marine Science and Application2009,8,2:3
2Quaternary Structure of the Insulin-insulin Receptor Complex显示文摘Robert Z-T Luo Deniel R Beniac Allan Fernandes 1999Science1999,285,10:1
3PLGA nanodepots co-encapsulating prostratin and anti-CD25 enhance primary natural killer cell antiviral and antitumor function显示文摘Natural killer(NK)cells are attractive effector cells of the innate immune system against human immunodeficiency virus(HIV)and cancer.However,NK cell therapies are limited by the fact that target cells evade NK cells,for example,in latent reservoirs(in HIV)or through upregulation of inhibitory signals(in cancer).To address this limitation,we describe a biodegradable nanoparticlebased“priming”approach to enhance the cytotoxic efficacy of peripheral blood mononuclear cell-derived NK cells.We present poly(lactic-co-glycolic acid)(PLGA)nanodepots(NDs)that co-encapsulate prostratin,a latency-reversing agent,and anti-CD25(aCD25),a cell surface binding antibody,to enhance primary NK cell function against HIV and cancer.We utilize a nanoemulsion synthesis scheme to encapsulate both prostratin and aCD25 within the PLGA NDs(termed Pro-aCD25-NDs).Physicochemical characterization studies of the NDs demonstrated that our synthesis scheme resulted in stable and monodisperse Pro-aCD25-NDs.The NDs successfully released both active prostratin and anti-CD25,and with controllable release kinetics.When Pro-aCD25-NDs were administered in an in vitro model of latent HIV and acute T cell leukemia using J-Lat 10.6 cells,the NDs were observed to prime J-Lat cells resulting in significantly increased NK cell-mediated cytotoxicity compared to free prostratin plus anti-CD25,and other controls.These findings demonstrate the feasibility of using our Pro-aCD25-NDs to prime target cells for enhancing the cytotoxicity of NK cells as antiviral or antitumor agents.Elizabeth E.Sweeney Preethi B.Balakrishnan Allison B.Powell Allan Bowen Indra Sarabia Rachel A.Burga R.Brad Jones Alberto Bosque C.Russell Y.Cruz Rohan Fernandes 2020Nano Research2020,13,3:0
4Maternal low protein diet induces persistent expression changes in metabolic genes in male rats显示文摘BACKGROUND Perinatal exposure to a poor nutritional environment predisposes the progeny to the development of metabolic disease at the adult age,both in experimental models and humans.Numerous adaptive responses to maternal protein restriction have been reported in metabolic tissues.However,the expression of glucose/fatty acid metabolism-related genes in adipose tissue and liver needs to be described.AIM To evaluate the metabolic impact of perinatal malnutrition,we determined malnutrition-associated gene expression alterations in liver and adipose tissue.METHODS In the present study,we evaluated the alterations in gene expression of glycolytic/Krebs cycle genes(Pyruvate dehydrogenase kinase 4 and citrate synthase),adipogenic and lipolytic genes and leptin in the adipose tissue of offspring rats at 30 d and 90 d of age exposed to maternal isocaloric low protein(LP)diet throughout gestation and lactation.We also evaluated,in the livers of the same animals,the same set of genes as well as the gene expression of the transcription factors peroxisome proliferator-activated receptor gamma coactivator 1,forkhead box protein O1 and hepatocyte nuclear factor 4 and of gluconeogenic genes.RESULTS In the adipose tissue,we observed a transitory(i.e.,at 30 d)downregulation of pyruvate dehydrogenase kinase 4,citrate synthase and carnitine palmitoyl transferase 1b gene expression.Such transcriptional changes did not persist in adult LP rats(90 d),but we observed a tendency towards a decreased gene expression of leptin(P=0.052).The liver featured some gene expression alterations comparable to the adipose tissue,such as pyruvate dehydrogenase kinase 4 downregulation at 30 d and displayed other tissue-specific changes,including citrate synthase and fatty acid synthase upregulation,but pyruvate kinase downregulation at 30 d in the LP group and carnitine palmitoyl transferase 1b downregulation at 90 d.These gene alterations,together with previously described changes in gene expression in skeletal muscle,may account for the metabolic adaptations in response to maternal LP diet and highlight the occurrence of persistent transcriptional defects in key metabolic genes that may contribute to the development of metabolic alterations during the adult life as a consequence of perinatal malnutrition.CONCLUSION We conclude that perinatal malnutrition relays long-lasting transcriptional alterations in metabolically active organs,i.e.,liver and adipose tissue.Allan de Oliveira Lira JoséLuiz de Brito Alves Mariana Pinheiro Fernandes Diogo Vasconcelos David Filipe Santana João Henrique da Costa-Silva Béatrice Morio Carol Góis Leandro Luciano Pirola 2020World Journal of Diabetes2020,11,5:0
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