To investigate the neurepretoctive effect of the aqueous extract of dried fruits of lycium barbarum(LBA)OH the hereditary retihal dystrophy of the Royal CoUege of Surgeon(RCS)rats,a total of 24 postnatal RCS mrs were randomly and equally divided into two groups.control group(CG)and experimental group(EG),respectively.EG rats were fed with 1 mg/kg LBA daily 10 days postpartum,and CG rats were fed normally.CG and EG RCS rats were executed at postnatal 25,35 and 50 days.Then photoreceptor cells necrosis and apoptosis Wag assessed by HE staining,and TUNEL detection.The expression of Cagpage-2 protein Wag detected in retina by immunohistochemistry.The results showed that comparing with RCS rata in the CG,25 and 35 days postpartum,the positive expression of TUNEL in RCS rats in the EG obviously reduced(P＜0.05);25 and 50 days postpartum,Caspage-2 positive ceils were seen in both ganglion cell layer and inner nuclear layer in both CG and EG rats.The positive expression of Caspage-2 Wag less$een 25 days postpartum in EG rats than CG rats(P＜0.05).The present results suggest that LBA hag neuroprotecdve effects on the early stage of retinal degeneration of the hereditary retinal dystrophy RCS rats by inhibiting apoptosis,resulting more photoreceptors preserved.Cagpage-2 protein may contribute to the retinal degeneration and LBA might protect apoptotic ueuron$by inhibiting the expression of Cagpage-2.

Objective To investigate the influence of ropivacaine with isodosage on heart rate variability (HRV ) following interscalene brachial plexus block under ultrasound guidance. Methods Forty-five ASA grade Ⅰ patients (28 males,1 7 females,aged 18-50 years)scheduled for upper limb fracture internal fixation removal were randomized into group R1 (0.375% ropivacaine 40ml),group R2(0.5% ropivacaine 30ml)and group R3 (0.75% ropivacaine 20 ml),1 5 in each group.Changes in HRV,such as LF,HF,LF/HF,SDNN,RMSSD,PNN50% were evaluated with dynamic electrocardiogram.The degree and duration of sensory and motor block were recorded 30 min after drug injection.Results The anesthetic effect and maintaining time had no significant difference among the groups.The incidence rate of Horner syndrome had no significant difference among groups,group R1 was 26.7%,group R2 20% and group R3 20%.LF(30 min after drug injection)in both group R2 and group R3 were significantly decreased compared with that before drug injection, and the decreased degree of LF had significant difference among the three groups.SDNN(30 min after drug injection)in group R2 and PNN50% in group R3 were significantly decreased compared with that before drug injection.The time required for LF,the most obvious changeable HRV parameter, returning to the pre injection level was (876.2 +43.7)min for group R1,(798.8 + 61.5 )min for group R2, group R3 (712.2 + 45.7 ) min, the difference between the three groups was not statistically significant.Conclusion ISBPB can affect the stability of the cardiovascular autonomic ac-tivities by reducing the cardiac sympathetic nerve function and increasing parasympathetic nerve func-tion,possibly through blockade of stellate ganglion or branches of vagus nerve.Along with the in-crease of the dose of anesthetic,the influence on HRV is greater.

Abstract Teen E sports and their negative impact should not be underestimated. The effects of gaming, as an emerging sport, should be examined to determine whether it plays an active role in contributing to the onset of adolescent depression. Therefore, this study outlines the development status of E sports, analyzes the influence of E sports on adolescent depression, and highlights the hidden concerns that E sports pose for the mental health development of adolescents. While taking into account the advantages of E sports and exercise intervention programs, an emphasis should be placed on the prevention of depression, and feasible suggestions and countermeasures should be put forward to promote E sports, while at the same time safeguarding the healthy and orderly development of adolescent mental health.

Research on the mechanisms of depression is currently a focus of the field of neuroscience.The degeneration of brain plasticity(e.g.,decrease in volume,structural degradation,and functional disorder of the hippocampus,PFC,and CG)leads to depression.Exercise is an important means of improving the symptoms of depression.Current research confirms the importance of improving the volume,structure,and function of the hippocampus,PFC,and CG,in this process,but related research has focused solely on changes to the volume of certain brain regions or connectivity functions.Thus,we lack a comprehensive understanding of the antidepressant mechanisms that improve brain plasticity with exercise.Therefore,this study aimed to explore the roles of brain plasticity in the occurrence of depression and improvements to depression through exercise,promoting a more comprehensive understanding the role of brain plasticity in depression.We also provide new ideas for exercise intervention in depression.

Oral potentially malignant disorders (OPMDs) are precursors of oral squamous cell carcinoma (OSCC). Deregulated cellular energy metabolism is a critical hallmark of cancer cells. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α) plays vital role in mitochondrial energy metabolism. However, the molecular mechanism of PGC1α on OPMDs progression is less unclear. Therefore, we investigated the effects of knockdown PGC1α on human dysplastic oral keratinocytes (DOKs) comprehensively, including cell proliferation, cell cycle, apoptosis, xenograft tumor, mitochondrial DNA (mtDNA), mitochondrial electron transport chain complexes (ETC), reactive oxygen species (ROS), oxygen consumption rate (OCR), extracellular acidification rate (ECAR), and glucose uptake. We found that knockdown PGC1α significantly inhibited the proliferation of DOKs in vitro and tumor growth in vivo, induced S-phase arrest, and suppressed PI3K/Akt signaling pathway without affecting cell apoptosis. Mechanistically, downregulated of PGC1α decreased mtDNA, ETC, and OCR, while enhancing ROS, glucose uptake, ECAR, and glycolysis by regulating lactate dehydrogenase A (LDHA). Moreover, SR18292 (an inhibitor of PGC1α) induced oxidative phosphorylation dysfunction of DOKs and declined DOK xenograft tumor progression. Thus, our work suggests that PGC1α plays a crucial role in cell proliferation by reprograming energy metabolism and interfering with energy metabolism, acting as a potential therapeutic target for OPMDs.
Humans ; Carcinoma, Squamous Cell/metabolism* ; Cell Proliferation ; DNA, Mitochondrial ; Energy Metabolism ; Glucose ; Mouth Neoplasms/metabolism* ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism* ; Phosphatidylinositol 3-Kinases ; Reactive Oxygen Species