Cranedupont7764

Few percentage that present prominent mental disorders, but we must recognize that when projected to the whole the child-adolescent population, there could be a significant number that could be subsidiary of a more specific help. The return to schooling is going to represent another important moment, the repercussions of confinement being of capital importance, especially in terms of addictive behaviors with information and communication technologies. Intervention by professionals trained in childhood and adolescent mental health is a priority to avoid unwanted clinical evolutions or iatrogenesis.Alzheimer's disease (AD) is the most common type of dementia, but it is very difficult to diagnose with certainty, so many AD studies have attempted to find early and relevant diagnostic markers. Regulated upon activation, normal T cell expressed and secreted (RANTES, also known as C-C chemokine ligand) is a chemokine involved in the migration of T cells and other lymphoid cells. Changes in RANTES levels and its expression in blood or in cerebrospinal fluid have been reported in some neurodegenerative diseases, such as Parkinson's disease and multiple sclerosis, but also in metabolic diseases in which inflammation plays a role. The aim of this observational study was to assess RANTES levels in peripheral blood as clinical indicators of AD. Plasma levels of RANTES were investigated in 85 AD patients in a relatively early phase of AD (median 8.5 months after diagnosis; 39 men and 46 women; average age 75.7 years), and in 78 control subjects (24 men and 54 women; average age 66 years). We found much higher plasmipheral marker for early stages of AD. The study was approved by the Ethics Committee of Institute of Endocrinology, Prague, Czech Republic on July 22, 2011.Many blood biomarkers are reportedly helpful for predicting post-stroke cognitive impairment (PSCI), but no biomarkers are widely used in clinical practice. The purpose of this study was to investigate the association between the plasma immunoproteasome and patients' 90-day prognosis after first-ever acute ischemic stroke. In our prospective, single-center study, 259 patients with first-ever acute ischemic stroke were enrolled from the Department of Neurology, Fujian Provincial Hospital, China, from March to September 2014. Of these, 27 patients (10.4%) had unfavorable outcomes as assessed by the Modified Rankin Scale (scores of 3-6). The National Institutes of Health Stroke Scale score on admission, plasma N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) levels, and immunopro-teasome subunit (low molecular mass peptide [LMP]2, LMP5, and LMP7) levels were significantly higher in the unfavorable outcome group than in the favorable outcome group. selleck chemicals To predict unfavorable outcomes, the optimal cutoff points were National Institutes of Health Stroke Scale score > 12, NT-pro-BNP level > 1883.5 pg/mL, and LMP2 level > 841.4 pg/mL. Of the 193 patients that were able to complete the Mini-Mental State Examination at 90 days post-stroke, 66 patients (34.2%) had PSCI. Plasma levels of NT-pro-BNP and LMP2 were higher in patients with PSCI than in those without PSCI. To predict PSCI, the optimal cutoff values were age > 70.5 years and LMP2 level > 630.5 pg/mL. These findings indicate that plasma LMP2 may serve as a new prognostic biomarker of poor outcome and PSCI at 90 days after stroke. This study was approved by the Ethics Committee of Fujian Provincial Hospital, Provincial Clinical Medical College of Fujian Medical University (approval No. K2014-01-003) on January 15, 2014.Alzheimer's disease (AD) is a progressive brain disorder and complex mechanisms are involved in the physiopathology of AD. However, there is data suggesting that inflammation plays a role in its development and progression. Indeed, some non-steroidal anti-inflammatory drugs, such as meloxicam, which act by inhibiting cyclooxygenase-2 (COX-2) have been used as neuroprotective agents in different neurodegenerative disease models. The purpose of this study was to investigate the effects of co-nanoencapsulated curcumin and meloxicam in lipid core nanocapsules (LCN) on cognitive impairment induced by amyloid-beta peptide injection in mice. LCN were prepared by the nanoprecipitation method. Male Swiss mice received a single intracerebroventricular injection of amyloid-beta peptide aggregates (fragment 25-35, 3 nmol/3 μL) or vehicle and were subsequently treated with curcumin-loaded LCN (10 mg/kg) or meloxicam-loaded LCN (5 mg/kg) or meloxicam + curcumin-co-loaded LCN (5 and 10 mg/kg, respectively). Treatments were , 2015.Motor imagery is defined as an act wherein an individual contemplates a mental action of motor execution without apparent action. Mental practice executed by repetitive motor imagery can improve motor performance without simultaneous sensory input or overt output. We aimed to investigate cerebral hemodynamics during motor imagery and motor execution of a self-feeding activity using chopsticks. This study included 21 healthy right-handed volunteers. The self-feeding activity task comprised either motor imagery or motor execution of eating sliced cucumber pickles with chopsticks to examine eight regions of interest pre-supplementary motor area, supplementary motor area, bilateral prefrontal cortex, premotor area, and sensorimotor cortex. The mean oxyhemoglobin levels were detected using near-infrared spectroscopy to reflect cerebral activation. link2 The mean oxyhemoglobin levels during motor execution were significantly higher in the left sensorimotor cortex than in the supplementary motor area and the left premotor area. Moreover, significantly higher oxyhemoglobin levels were detected in the supplementary motor area and the left premotor area during motor imagery, compared to motor execution. link3 Supplementary motor area and premotor area had important roles in the motor imagery of self-feeding activity. Moreover, the activation levels of the supplementary motor area and the premotor area during motor execution and motor imagery are likely affected by intentional cognitive processes. Levels of cerebral activation differed in some areas during motor execution and motor imagery of a self-feeding activity. This study was approved by the Ethical Review Committee of Nagasaki University (approval No. 18110801) on December 10, 2018.Spinal cord injury (SCI) is a serious traumatic event to the central nervous system. Studies show that long non-coding RNAs (lncRNAs) play an important role in regulating the inflammatory response in the acute stage of SCI. Here, we investigated a new lncRNA related to spinal cord injury and acute inflammation. We analyzed the expression profile of lncRNAs after SCI, and explored the role of lncRNA Airsci (acute inflammatory response in SCI) on recovery following acute SCI. The rats were divided into the control group, SCI group, and SCI + lncRNA Airsci-siRNA group. The expression of inflammatory factors, including nuclear factor kappa B [NF-κB (p65)], NF-κB inhibitor IκBα and phosphorylated IκBα (p-IκBα), and the p-IκBα/IκBα ratio were examined 1-28 days after SCI in rats by western blot assay. The differential lncRNA expression profile after SCI was assessed by RNA sequencing. The differentially expressed lncRNAs were analyzed by bioinformatics technology. The differentially expressed lncRNA Airsci, which i following SCI, and that inhibiting lncRNA Airsci reduces the inflammatory response through the NF-κB signaling pathway, thereby promoting functional recovery. All experimental procedures and protocols were approved by the approved by the Animal Ethics Committee of Jining Medical University (approval No. JNMC-2020-DW-RM-003) on January 18, 2020.The blood-spinal cord barrier plays a vital role in recovery after spinal cord injury. The neurovascular unit concept emphasizes the relationship between nerves and vessels in the brain, while the effect of the blood-spinal cord barrier on the neurovascular unit is rarely reported in spinal cord injury studies. Mouse models of spinal cord injury were established by heavy object impact and then immediately injected with platelet-derived growth factor (80 μg/kg) at the injury site. Our results showed that after platelet-derived growth factor administration, spinal cord injury, neuronal apoptosis, and blood-spinal cord barrier permeability were reduced, excessive astrocyte proliferation and the autophagy-related apoptosis signaling pathway were inhibited, collagen synthesis was increased, and mouse locomotor function was improved. In vitro, human umbilical vein endothelial cells were established by exposure to 200 μM H2O2. At 2 hours prior to injury, in vitro cell models were treated with 5 ng/mL platelet-derived growth factor. Our results showed that expression of blood-spinal cord barrier-related proteins, including Occludin, Claudin 5, and β-catenin, was significantly decreased and autophagy was significantly reduced. Additionally, the protective effects of platelet-derived growth factor could be reversed by intraperitoneal injection of 80 mg/kg chloroquine, an autophagy inhibitor, for 3 successive days prior to spinal cord injury. Our findings suggest that platelet-derived growth factor can promote endothelial cell repair by regulating autophagy, improve the function of the blood-spinal cord barrier, and promote the recovery of locomotor function post-spinal cord injury. Approval for animal experiments was obtained from the Animal Ethics Committee, Wenzhou Medical University, China (approval No. wydw2018-0043) in July 2018.Melatonin can attenuate cardiac microvascular ischemia/reperfusion injury, but it remains unclear whether melatonin can also ameliorate cerebral microvascular abnormalities. Rat models of Alzheimer's disease were established by six intracerebroventricular injections of amyloid-beta 1-42, administered once every other day. Melatonin (30 mg/kg) was intraperitoneally administered for 13 successive days, with the first dose given 24 hours prior to the first administration of amyloid-beta 1-42. Melatonin ameliorated learning and memory impairments in the Morris water maze test, improved the morphology of microvessels in the cerebral cortex and hippocampus, increased microvessel density, alleviated pathological injuries of cerebral neurons, and decreased the expression of vascular endothelial growth factor and vascular endothelial growth factor receptors 1 and 2. These findings suggest that melatonin can improve microvessel abnormalities in the cerebral cortex and hippocampus by lowering the expression of vascular endothelial growth factor and its receptors, thereby improving the cognitive function of patients with Alzheimer's disease. This study was approved by the Animal Care and Use Committee of Jinzhou Medical University, China (approval No. 2019015) on December 6, 2018.Regenerating functional new neurons in the adult mammalian central nervous system has been proven to be very challenging due to the inability of neurons to divide and repopulate themselves after neuronal loss. Glial cells, on the other hand, can divide and repopulate themselves under injury or diseased conditions. We have previously reported that ectopic expression of NeuroD1 in dividing glial cells can directly convert them into neurons. Here, using astrocytic lineage-tracing reporter mice (Aldh1l1-CreERT2 mice crossing with Ai14 mice), we demonstrate that lineage-traced astrocytes can be successfully converted into NeuN-positive neurons after expressing NeuroD1 through adeno-associated viruses. Retroviral expression of NeuroD1 further confirms that dividing glial cells can be converted into neurons. Importantly, we demonstrate that for in vivo cell conversion study, using a safe level of adeno-associated virus dosage (1010-1012 gc/mL, 1 µL) in the rodent brain is critical to avoid artifacts caused by toxic dosage, such as that used in a recent bioRxiv study (2 × 1013 gc/mL, 1 µL, mouse cortex).