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INTRODUCTION: Intracranial aneurysms (IA) are a focal dilatation of the vessel wall, the rupture of these, causes subarachnoid hemorrhage. Until now, endovascular management is the ideal treatment, providing the interventionist a range of options among which the stent and coils embolization stands out because of its occlusion rate. This study presents the results of a retrospective cohort comparing the effectiveness, morbidity, and mortality of IA treatment with laser-cut stent-assisted coils versus braided stents. METHODOLOGY: Retrospective cohort of patients diagnosed with unruptured intracranial aneurysms treated with coil-assisted laser-cut stents or braided stents between January 2014 and December 2021. RESULTS: In total, 138 patients with 147 intracranial aneurysms were analyzed, 91 of them were treated with laser-cut stent and 56 with braided stents. The main antecedent was arterial hypertension (48.55%). In the immediate angiographic control, a Raymond Roy scale (RRO) I was obtained in 86.81% of the patients with laser-cut stents and 87.50% of the patients with braided stents. In the angiographic follow-up at 12 months, an RRO I occlusion rate of 85.19% was reported in both groups. Perioperative complications occur in 16 patients treated with laser-cut stents and 12 patients treated with braided stents. Three patients presented bleeding complications during the 12-month follow-up, of which two correspond to patients treated with braided stents and one with a laser-cut stent. CONCLUSION: Treatment of patients with intracranial aneurysms with laser-cut stents or braided stents and coils is just as safe and effective.
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Epidemiological and experimental evidence recognize a relationship between sleep-wake cycles and adiposity levels, but the mechanisms that link both are not entirely understood. Adipose tissue secretes adiponectin and leptin hormones, mainly involved as indicators of adiposity levels and recently associated to sleep. To understand how two of the main adipose tissue hormones could influence sleep-wake regulation, we evaluated in male rats, the effect of direct administration of adiponectin or leptin in the ventrolateral preoptic nuclei (VLPO), a major area for sleep promotion. The presence of adiponectin (AdipoR1 and AdipoR2) and leptin receptors in VLPO were confirmed by immunohistochemistry. Adiponectin administration increased wakefulness during the rest phase, reduced delta power, and activated wake-promoting neurons, such as the locus coeruleus (LC), tuberomammillary nucleus (TMN) and hypocretin/orexin neurons (OX) within the lateral hypothalamus (LH) and perifornical area (PeF). Conversely, leptin promoted REM and NREM sleep, including increase of delta power during NREM sleep, and induced c-Fos expression in VLPO and melanin concentrating hormone expressing neurons (MCH). In addition, a reduction in wake-promoting neurons activity was found in the TMN, lateral hypothalamus (LH) and perifornical area (PeF), including in the OX neurons. Moreover, leptin administration reduced tyrosine hydroxylase (TH) immunoreactivity in the LC. Our data suggest that adiponectin and leptin act as hormonal mediators between the status of body energy and the regulation of the sleep-wake cycle.
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Temporal coordination of organisms according to the daytime allows a better performance of physiological processes. However, modern lifestyle habits, such as food intake during the rest phase, promote internal desynchronization and compromise homeostasis and health. The hypothalamic suprachiasmatic nucleus (SCN) synchronizes body physiology and behavior with the environmental light-dark cycle by transmitting time information to several integrative hypothalamic nuclei, such as the paraventricular nucleus (PVN), dorsomedial hypothalamic nucleus (DMH) and median preoptic area (MnPO). The SCN receives metabolic information mainly via Neuropeptide Y (NPY) inputs from the intergeniculate nucleus of the thalamus (IGL). Nowadays, there is no evidence of the response of the PVN, DMH and MnPO when the animals are subjected to internal desynchronization by restricting food access to the rest phase of the day. To explore this issue, we compared the circadian activity of the SCN, PVN, DMH and MnPO. In addition, we analyzed the daily activity of the satiety centers of the brainstem, the nucleus of the tractus solitarius (NTS) and area postrema (AP), which send metabolic information to the SCN, directly or via the thalamic intergeniculate leaflet (IGL). For that, male Wistar rats were assigned to three meal protocols: fed during the rest phase (Day Fed); fed during the active phase (Night Fed); free access to food (ad libitum). After 21 d, the daily activity patterns of these nuclei were analyzed by c-Fos immunohistochemistry, as well as NPY immunohistochemistry, in the SCN. The results show that eating during the rest period produces a phase advance in the activity of the SCN, changes the daily activity pattern in the MnPO, NTS and AP and flattens the c-Fos rhythm in the PVN and DMH. Altogether, these results validate previous observations of circadian dysregulation that occurs within the central nervous system when meals are consumed during the rest phase, a behavior that is involved in the metabolic alterations described in the literature.