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Urces. Therefore, we entertained the hypothesis that either limited or chronic low-level exposures to nitrosamines account for the observed shifts in morbidity and mortality from insulin resistance diseases. Moreover, given the clear role of high dietary fat intake as a mediator of obesity, T2DM, or cognitive impairment, we proposed that the combined effects of HFD and NDEA exposure may act addit
Cer. Clin Cancer Res. 2009;15(17):5308?6. 80. Degterev A, Yuan J. Expansion and evolution of cell death programmes. Nat Rev Mol Cell Biol. 2008;9(5):378?0. 81. Shen HM, Codogno P. Autophagy is a survival force via suppression of necrotic cell death. Exp Cell Res. 2012;318(11):1304?. 82. Munoz-Gamez JA, Rodriguez-Vargas JM, Quiles-Perez R, Aguilar-Quesada R, Martin-Oliva D, de Murcia G, et al. PAR
Ould reduce cases of lenses' falling off.Some patients, (7.1 ) made optometric consultations on account of their lost spectacles with consequential visual discomfort. In a population-based study of spectacles use in southern India, as many as 19.6 of people using spectacles had lost the pairs and could not afford to buy another pairs [21]. The patients should be counselled on how to take good ca
Ysiol Cell Physiol. 2012;302(2):C383?91. 68. Sachdev U, Cui X, Hong G, Namkoong S, Karlsson JM, Baty CJ, et al. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. J Vasc Surg. 2012;55(1):180?1.Yang et al. Cell Bioscience (2015) 5:Page 10 of69. Kang R, Livesey KM, Zeh HJ, Loze MT, Tang D. HMGB1: a
Enile plaques of Alzheimer's disease. Acta Neuropathol 1990, 79(5):486-493.Tong et al. BMC Endocrine Disorders 2010, 10:4 http://www.biomedcentral.com/1472-6823/10/Page 15 of71. Baloyannis SJ: Dendritic pathology in Alzheimer's disease. J Neurol Sci 2009, 283(1-2):153-157. 72. Baloyannis SJ, Manolidis SL, Manolidis LS: Synaptic alterations in the vestibulocerebellar system in Alzheimer's disease
S, could result in cytoskeletal collapse and synaptic disconnection. Alternatively, the finding could reflect neuronal loss associated with neurodegeneration. The reduced levels of ChAT reflect deficits in acetylcholine homeostasis that contribute to cognitive impairment with neurodegeneration [101,102]. Correspondingly, in preliminary studies, we detected evidence of significant spatial learning
Ysiol Cell Physiol. 2012;302(2):C383?91. 68. Sachdev U, Cui X, Hong G, Namkoong S, Karlsson JM, Baty CJ, et al. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. J Vasc Surg. 2012;55(1):180?1.Yang et al. Cell Bioscience (2015) 5:Page 10 of69. Kang R, Livesey KM, Zeh HJ, Loze MT, Tang D. HMGB1: a
S, could result in cytoskeletal collapse and synaptic disconnection. Alternatively, the finding could reflect neuronal loss associated with neurodegeneration. The reduced levels of ChAT reflect deficits in acetylcholine homeostasis that contribute to cognitive impairment with neurodegeneration [101,102]. Correspondingly, in preliminary studies, we detected evidence of significant spatial learning
Enile plaques of Alzheimer's disease. Acta Neuropathol 1990, 79(5):486-493.Tong et al. BMC Endocrine Disorders 2010, 10:4 http://www.biomedcentral.com/1472-6823/10/Page 15 of71. Baloyannis SJ: Dendritic pathology in Alzheimer's disease. J Neurol Sci 2009, 283(1-2):153-157. 72. Baloyannis SJ, Manolidis SL, Manolidis LS: Synaptic alterations in the vestibulocerebellar system in Alzheimer's disease
Ki M, Kitagaki H, Yamaji S, Sakamoto S, Matsuda K, Mori E: Reduction of cerebellar glucose metabolism in advanced Alzheimer's disease. J Nucl Med 1997, 38(6):925-928. 58. Larner AJ: The cerebellum in Alzheimer's disease. Dement Geriatr Cogn Disord 1997, 8(4):203-209. 59. Wegiel J, Wisniewski HM, Dziewiatkowski J, Badmajew E, Tarnawski M, Reisberg B, Mlodzik B, De Leon MJ, Miller DC: Cerebellar at
Induced neutrophil survival is mediated by HIF-1alpha-dependent NF-kappaB activity. J Exp Med. 2005;201(1):105?5. 89. Mihalache CC, Yousefi S, Conus S, Villiger PM, Schneider EM, Simon HU. Inflammation-associated autophagy-related programmed necrotic death of human neutrophils characterized by organelle fusion events. J Immunol. 2011;186(11):6532?2. 90. Naldini A, Morena E, Pucci A, Miglietta D,
E formation of DNA and protein adducts [105-107] that can serve as persistent sources of oxidative stress, and cause further DNA damage and protein dysfunction. Recently, we demonstrated a role for ceramidemediated neurodegeneration in a model of diet-induced obesity with T2DM [45], and showed that in vitro ceramide exposure causes neurodegeneration with impairments in neuronal viability, energy
F vehicle or NDEA (N = 12/group) on alternate days beginning on P3. From P21 (weaning), rats were fed with high fat (60 of calories) or low fat (5 of calories) diets for 8 weeks, after which they were sacrificed to harvest cerebella for histopathological and immunohistochemical staining studies. Cerebella were preserved in Histofix and paraffin-embedded sections (8 microns) were stained with (A
He cerebellum and brain stem in Down's syndrome and Alzheimer's disease: a light microscopical analysis. Acta Neuropathol 1993, 85(5):542-552. 83. Tong M, de la Monte SM: Mechanisms of ceramide-mediated neurodegeneration. J Alzheimers Dis 2009, 16(4):705-714. 84. Hietanen E, Bartsch H, Ahotupa M, Bereziat JC, Bussacchini-Griot V, Cabral JR, Camus AM, Laitinen M, Wild H: Mechanisms of fat-related

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