8794 Spring Street
Montague MI 49437
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License #: 012415
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Obstructive sleep apnea, inflammation, and cardiopulmonary disease. - Frontiers in bioscience : a journal and virtual library
Obstructive sleep apnea (OSA) occurs commonly in the U.S. population and is seen in both obese as well as non-obese individuals. OSA is a disease characterized by periodic upper airway collapse during sleep, which then results in either apnea, hypopnea, or both. The disorder leads to a variety of medical complications. Neuropsychiatric complications include daytime somnolence, cognitive dysfunction, and depression. Increased incidence of motor vehicle accidents has been documented in these patients and probably reflects disordered reflex mechanisms or excessive somnolence. More importantly, vascular disorders such as hypertension, stroke, congestive cardiac failure, arrhythmias, and atherosclerosis occur frequently in these patients. The lungs may be affected by pulmonary hypertension and worsening of asthma. Recent data from several laboratories demonstrate that obstructive sleep apnea is characterized by an inflammatory response. Cytokines are elaborated during the hypoxemic episodes leading to inflammatory responses as marked clinically by elevated C-reactive protein (CRP). As elevated CRP levels are considered markers of the acute phase response and characterize progression of vascular injury in coronary artery disease, it is likely that obstructive sleep apnea could lead to worsening of vasculopathy. Moreover, as inflammatory mechanisms regulate bronchial asthma, it is also likely that cytokines and superoxide radicals generated during hypoxemic episodes could exacerbate reactive airway disease. Patients with Cough, Obstructive sleep apnea, Rhinosinusitis, and Esophageal reflux clustered together can be categorized by the acronym, "CORE", syndrome. The purpose of this manuscript is to review the inflammatory responses that occur in patients with obstructive sleep apnea and relate them to the occurrence of cardiopulmonary disease.
Mixed Germ Cell Tumour in a Case of Pure Gonadal Dysgenesis (Swyer Syndrome) - A Case Report. - CureÌ„us
Swyer syndrome or pure gonadal dysgenesis 46, XY is a medical condition associated with 46 XY karyotype and primary amenorrhea in a phenotypic female. In this syndrome, there is an abnormality in testicular differentiation. Patients with disorders in sexual differentiation have an increased risk for development of genital malignancies. A 14-year-old female admitted with abdominal pain was diagnosed to have Swyer syndrome andÂ a pelvic tumor after clinical and laboratory investigations. She underwent surgery, and the histology report revealed a mixed germ cell tumor in a dysgenetic gonad. She recurred three months later and was successfully treated with chemotherapy and a second surgery to remove the differentiated teratoma. The early diagnosis ofÂ patients with Swyer syndrome is important because of the increased risk for the development of malignancy. Early surgical treatment is required. Recurrent and metastatic disease respondÂ well to chemotherapy.
Brain Insulin Signaling is Increased in Insulin-Resistant States and Decreases in FoxOs and PGC-1Î± and Increases in AÎ²1-40.42 and Phospho-Tau May Abet Alzheimer Development. - Diabetes
Increased coexistence of Alzheimer's disease (AD) and type 2 diabetes (T2D) suggests that insulin resistance abets neurodegenerative processes, but linkage mechanisms are obscure. Here, we examined insulin signaling factors in brains of insulin-resistant high-fat-fed mice, ob/ob mice, mice with genetically-impaired muscle glucose transport, and monkeys with diet-dependent long-standing obesity/T2D. In each model, resting/basal activities of insulin-regulated brain protein kinases, Akt and atypical PKC (aPKC), were maximally increased. Moreover, Akt hyperactivation was accompanied by hyperphosphorylation of substrates, GSK3Î², mTOR and forkhead-homeobox O-proteins, FoxO1, FoxO3a, and FoxO4, and decreased PGC-1Î± expression. Akt hyperactivation was confirmed in individual neurons of anterocortical and hippocampal regions that house cognition/memory centers. Remarkably, AÎ²1-40/42 peptide levels were: increased acutely by insulin in normal mice; increased basally in insulin-resistant mice and monkeys; accompanied by diminished amyloid precursor protein in monkeys. Phospho-tau was increased in ob/ob mice and T2D monkeys. Importantly, with correction of hyperinsulinemia by inhibition of hepatic aPKC and improvement in systemic insulin resistance, brain insulin signaling normalized. As FoxOs and PGC-1Î± are essential for memory and long-term neuronal function and regeneration, and, as AÎ²1-40/42 and phospho-tau may increase interneuronal plaques and intraneuronal tangles, presently-observed aberrations in hyperinsulinemic states may participate in linking insulin resistance to AD.Â© 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
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8794 Spring Street Montague, MI 49437
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