FCGR3A V(176) polymorphism for systemic lupus erythematosus susceptibility in Mexican population

The objective of this study is to establish whether there is an association between the presence of FCGR3A V(176) polymorphism with SLE or its manifestations. We included 94 patients according to the 1982 ACR criteria as well as 98 controls matched by age and gender. The 11 ACR diagnostic criteria were analyzed on the clinical files. The polymorphism FCGR3A V(176) was determined by direct sequencing. There was not an association between the polymorphism FCGR3A V(176) with SLE or its main manifestations. The allelic frequency for F(176) was: 0.80 and 0.72 in cases and controls, respectively (P?=?0.09, IC95%: 0.42?C1.07); and the genotypic frequency in the group of cases was: 0.65 for homozygotes F(176)/F(176), 0.30 for heterozygotes and 0.05 for the homozygotes V(176)/V(176), while for the control group it was 0.53, 0.39 and 0.08, respectively. The polymorphism FCGR3A V(176) is not associated with SLE or any of its manifestations in patients with SLE from the West of Mexico.     

Melatonin enhances neural stem cell differentiation and engraftment by increasing mitochondrial function

Neural stem cells (NSCs) are regarded as a promising therapeutic approach to protecting and restoring damaged neurons in neurodegenerative diseases (NDs) such as Parkinson's disease and Alzheimer's disease (PD and AD, respectively). However, new research suggests that NSC differentiation is required to make this strategy effective. Several studies have demonstrated that melatonin increases mature neuronal markers, which reflects NSC differentiation into neurons. Nevertheless, the possible involvement of mitochondria in the effects of melatonin during NSC differentiation has not yet been fully established. We therefore tested the impact of melatonin on NSC proliferation and differentiation in an attempt to determine whether these actions depend on modulating mitochondrial activity. We measured proliferation and differentiation markers, mitochondrial structural and functional parameters as well as oxidative stress indicators and also evaluated cell transplant engraftment. This enabled us to show that melatonin (25 μM) induces NSC differentiation into oligodendrocytes and neurons. These effects depend on increased mitochondrial mass/DNA/complexes, mitochondrial respiration, and membrane potential as well as ATP synthesis in NSCs. It is also interesting to note that melatonin prevented oxidative stress caused by high levels of mitochondrial activity. Finally, we found that melatonin enriches NSC engraftment in the ND mouse model following transplantation. We concluded that a combined therapy involving transplantation of NSCs pretreated with pharmacological doses of melatonin could efficiently restore neuronal cell populations in PD and AD mouse models depending on mitochondrial activity promotion.     

Obstructive Sleep Apnea Syndrome (OSAS). Review of the literature

Obstructive sleep apnea and hypopnea syndrome is characterized by repeated airway collapse during sleep. The li-terature describes multiple causes of the disease. The main cause is a reduction of the expansion forces of the pharyngeal dilator muscles, as in situations of genioglossal muscle dysfunction, and discoordination between the inspiratory activity of the muscle and respiratory effort, which play an important role in progression of the disease. Other described causes are soft tissue disorders, such as macroglossia or tonsillar hypertrophy, and skeletal structural alterations such as micrognathia and retrognathia. The syndrome is also more frequent in obese people, where the accumulation of fat in the neck region produces narrowing of the pharyngeal airway, thereby diminishing the passage of air. This review focuses on the pathogenesis, epidemiology, main features and diagnosis of the disease, and on its main forms of treatment. Key words:Sleep apnea, obstructive sleep apnea, sleep apnea syndrome, obstructive sleep apnea syndrome.