28 results match your criteria: "and Saitama Medical University[Affiliation]"
Cell Death Dis
August 2014
1] Rashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Department of Psychiatry and Behavioral Neurosciences, Morsani College of Medicine, University of South Florida, Tampa, FL, USA [2] James A. Haley Veterans' Hospital, Tampa, FL, USA.
Alzheimer's disease (AD), a progressive neurodegenerative disorder that is the most common cause of dementia in the elderly, is characterized by the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles, as well as a progressive loss of synapses and neurons in the brain. The major pertinacious component of amyloid plaques is Aβ, a variably sized peptide derived from the integral membrane protein amyloid precursor protein (APP). The Aβ region of APP locates partly within its ecto- and trans-membrane domains.
View Article and Find Full Text PDFFront Aging Neurosci
August 2014
Research and Development Service, Department of Veterans Affairs, Bay Pines VA Healthcare System Bay Pines, FL, USA ; Center of Research in Biomedical Sciences, Universidad Autónoma de Chile Santiago, Chile ; Research Service, Department of Veterans Affairs, Tampa VA Healthcare System Tampa, FL, USA ; Department of Molecular Medicine, Morsani College of Medicine, University of South Florida Tampa, FL, USA.
Alzheimer's disease (AD) is associated with cognitive and non-cognitive symptoms for which there are currently no effective therapies. We have previously reported that cotinine, a natural product obtained from tobacco leaves, prevented memory loss and diminished amyloid-β (Aβ) plaque pathology in transgenic 6799 mice (Tg6799 mice) when treated prior to the development of the pathology. We have also shown that cotinine reduces depressive-like behavior in normal and chronically stressed C57BL/6 mice.
View Article and Find Full Text PDFAnn Thorac Cardiovasc Surg
June 2010
Department of Pediatric Cardiac Surgery, Saitama International Medical Center, and Saitama Medical University, Hidaka-shi, Saitama, Japan.
Postoperative cardiopulmonary bypass (CPB)-induced lung dysfunction still remains as a serious complication that could lead to life-threatening problems. CPB is associated with a whole-body inflammatory response. The contact of blood components with the artificial surface of the bypass circuit causes activation of complements, upregulation of cytokines and adhesion molecules, and induction of oxygen-free radicals.
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