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Neonatal hypoxic-ischemic encephalopathy (HIE) is a hypoxic-ischemic brain injury caused by hypoxia after perinatal asphyxia in neonates, and one of the major causes of neonatal death, lifelong neurological disability and cognitive dysfunction. Although the mechanisms of HIE are complex and still unclear, it generally holds that HIE has a relationship with acute inflammatory reaction and is regulated by multiple cytokines and neuromodulators. Presently, therapeutic hypothermia, in the light of the lower mortality and improvement of prognosis, becomes a standard of care in many medical institutes, but there are still neonates dead or disabled after treatment. Therefore, it is necessary to use hypothermia in combination with other new adjuvant therapies (such as anti-inflammatory cytokine) to improve the prognosis of neonatal HIE. Besides, glutamate receptor antagonist, calcium channel blockers, erythropoietin, and nerve growth factors also have certain therapeutic effects on neonatal HIE. Therefore, this review mainly focused on the mechanisms and treatments of HIE. Based on this, we hold that the future studies should concentrate on how to attenuate early brain injury and to improve the growth and differentiation of neuronal cells and non-neuronal cells, which is of great signifcance to prolong the therapeutic window of neuroprotection, promote long-term neural restoration and improve the prognosis.

Objective: To study the degree of trauma and levator ani muscle contraction function after pelvic floor reconstruction and traditional surgical treatment of pelvic organ prolapse. Methods: Patients with III-IV pelvic organ prolapse who received surgical treatment in our hospital between May 2011 and October 2015 were randomly divided into observation group who received vaginal hysterectomy combined with pelvic floor reconstruction and control group who received vaginal hysterectomy combined with colporrhaphy, and then the degree of trauma, urodynamics and levator ani muscle contraction function were compared between two groups of patients. Results: Operating time, intraoperative blood loss as well as serum CRP, IL-1β, TNF-α, Ins, NE and E content were not significantly different between two groups (P>0.05); 2 weeks after operation, maximum bladder volume and QMax of observation group were significantly higher than those of control group, PdetQMax, PdetMax and PVR were significantly lower than those of control group (P0.05), LAT under Valsalva maneuver was significantly more than that of control group while LHS under Valsalva maneuver was significantly less than that of control group (P

Major depressive disorder has become one of the most serious neuropsychiatric disorders worldwide. However, currently available antidepressants used in clinical practice are ineffective for a substantial proportion of patients and always have side effects. Besides being a lipid-regulating agent, gemfibrozil is an agonist of peroxisome proliferator-activated receptor-α (PPAR-α). We investigated the antidepressant effects of gemfibrozil on C57BL/6J mice using the forced swim test (FST) and tail suspension test (TST), as well as the chronic unpredictable mild stress (CUMS) model of depression. The changes in brain-derived neurotrophic factor (BDNF) signaling cascade in the brain after CUMS and gemfibrozil treatment were further assessed. Pharmacological inhibitors and lentivirus-expressed short hairpin RNA (shRNA) were also used to clarify the antidepressant mechanisms of gemfibrozil. Gemfibrozil exhibited significant antidepressant actions in the FST and TST without affecting the locomotor activity of mice. Chronic gemfibrozil administration fully reversed CUMS-induced depressive-like behaviors in the FST, TST and sucrose preference test. Gemfibrozil treatment also restored CUMS-induced inhibition of the hippocampal BDNF signaling pathway. Blocking PPAR-α and BDNF but not the serotonergic system abolished the antidepressant effects of gemfibrozil on mice. Gemfibrozil produced antidepressant effects in mice by promoting the hippocampal BDNF system.

To evaluate the impact of labor epidural analgesia on maternal–fetal safety outcomes in a signal Chinese academic medical center. A single-intervention impact study was conducted at The Second Affiliated Hospital, Wenzhou Medical University. The study period was divided into three phases: (1) baseline phase: from January 1 and June 30, 2009 when no analgesic method was routinely employed during labor; (2) phase-in period: the epidural analgesia was implemented 8 a.m.–5 p.m. during weekdays; and (3) the post—No Pain Labor N’Delivery phase when the labor epidural was applied 24 h a day, 7 days a week, from June 1, 2010 and June 30, 2011. The maternal–fetal safety outcomes of delivery were compared between the different periods. There were 15,415 deliveries with 42.3% of nulliparous parturients in the 31-month study period. As the primary outcomes, the labor epidural analgesia rate increased from 0 to 57%, the vaginal delivery rate increased, and cesarean delivery rate decreased by 3.5% after full implementation. As the secondary outcomes, the rate of episiotomy and severe perineal injury after the implementation periods were significant decreased. The rate of postpartum oxytocin administration was decreased by 17.8%. No significant difference between the baseline and implementation periods was found in the rate of postpartum hemorrhage, Apgar scores less than 7 at both 1 and 5 min, 7-day mortality, and the overall neonatal intensive care unit admission rate. Implementation of labor epidural analgesia increased the vaginal delivery rate and use of labor epidural analgesia is safe to parturients and fetus.

Cognitive deficits are core symptoms of schizophrenia, but effective treatments are still lacking. Previous studies have reported that the brain-derived neurotrophic factor (BDNF) signaling is closely involved in learning and memory. Monosialotetrahexosylganglioside (GM1) is a ganglioside with wide-ranging pharmacologic effects that enhances the BDNF signaling cascade. This study aimed to assess the effects of GM1 on schizophrenia-related cognitive impairments. A brief disruption of N-methyl-D-aspartate receptors with MK801 was used to generate the animal model for cognitive deficits in schizophrenia. It was found that MK801-treated mice showed significant deficits in memory ability compared with control mice in different behavior tests, and this was accompanied by decreased hippocampal BDNF signaling pathway. Consecutive administration of GM1 fully restored the MK801-induced cognitive deficits and the impaired BDNF signaling in the hippocampus. Furthermore, a BDNF system inhibitor abolished the effects of GM1 in the MK801 model. Taken together, our results show that GM1 could reverse the MK801-induced cognitive deficits, suggesting a potential usefulness of GM1 in treating the schizophrenia-related cognitive impairments.