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Multicentre research of hospitalised people together with sports- and also pastime cycling-related upsetting brain injury throughout Hong Kong.
Mitochondria are dynamic organelles, which serve various purposes, including but not limited to the production of ATP and various metabolites, buffering ions, acting as a signaling hub, etc. In recent years, mitochondria are being seen as the central regulators of cellular growth, development, and death. Since neurons are highly specialized cells with a heavy metabolic demand, it is not surprising that neurons are one of the most mitochondria-rich cells in an animal. At synapses, mitochondrial function and dynamics is tightly regulated by synaptic calcium. Calcium influx during synaptic activity causes increased mitochondrial calcium influx leading to an increased ATP production as well as buffering of synaptic calcium. While increased ATP production is required during synaptic transmission, calcium buffering by mitochondria is crucial to prevent faulty neurotransmission and excitotoxicity. Interestingly, mitochondrial calcium also regulates the mobility of mitochondria within synapses causing mitochondria to halt at the synapse during synaptic transmission. In this review, we summarize the various roles of mitochondrial calcium at the synapse.
To compare quality of surgical steps in pediatric cataract surgery performed by pediatric ophthalmology fellows in various stages of training by applying the International Councilof Ophthalmology-Ophthalmology Surgical Competency Assessment Rubric (ICO-OSCAR).

Two experienced pediatric ophthalmologists analyzed video recordings of fellows performing pediatric cataract surgery at our institution between August 2019 and March 2020; fellows were scored according to the ICO-OSCAR with respect to the six key surgical step, namely, (1) wound construction, (2) anterior capsulorrhexis, (3) irrigation and aspiration, (4) intraocular lens implantation, (5) primary posterior capsulotomy (PPC)/anterior vitrectomy (AV), and (6) wound suturing. Cohen's kappa was used for inter-rater agreement. Fellows were categorized by months of training as stage 1 (first 6months), stage 2 (7-18months), and stage 3 (19-24months).

We analyzed 79 procedures performed by 11 pediatric ophthalmology fellows. The inter-rater agreement ranged from 85% to 96%; κ ranged from 0.64 to 0.91. Fellows in stages 2 and 3 of their training required less time and demonstrated superior technical proficiency in PPC and AV compared with fellows in stage 1 (median score, 4 vs 3).

Objective scoring of cataract surgeries performed by fellows at various stages of training highlighted the steep learning curve for PPC and AV and confirmed that execution improves with experience.
Objective scoring of cataract surgeries performed by fellows at various stages of training highlighted the steep learning curve for PPC and AV and confirmed that execution improves with experience.Refractive surgery has been performed under general anesthesia on pediatric and neurobehaviorally challenged adults without reported loss of vision or serious complications. Persistent epithelial defect (PED) is a rare complication of photorefractive keratectomy (PRK) in the general refractive surgery population. We report a case of PED following PRK under general anesthesia for high myopia in a man with autism and ocular history of juvenile open-angle glaucoma and dry eye syndrome.Anesthesia and surgery are associated with perioperative neurocognitive disorders (PND). Dexmedetomidine is known to improve PND in rats; however, little is known about the mechanisms. Male Sprague-Dawley rats were subjected to resection of the hepatic apex under propofol anesthesia to clinically mimic human abdominal surgery. The rats were divided into four groups control group (C), anesthesia group (A), model group (M), and model + dex group (D). Cognitive function was evaluated with the Morris water maze (MWM). Neuronal morphology was observed with H&E staining, Nissl's staining and immunohistochemistry. Transcriptome analysis and quantitative real-time PCR were performed to investigate functional mitochondrial mRNA changes in the hippocampus. Protein levels were measured by Western blotting at 1, 3, and 7 days after surgery. Surgery-induced cognitive decline lasted for three days, but not seven days after surgery in the M group; however, rats in the D group were significantly improved by dexmedetomidine. Adavosertib No significant differences in the number of neurons were observed between the groups after surgery. Rats from the M group showed significantly greater expression levels of Iba-1 and GFAP compared with the C group and the D group. Rats in the M group demonstrated increased Surf1 and Cytochrome c expression on days 1 and 3, but not day 7; similar changes were not induced in rats in the D group. Dexmedetomidine appears to reverse surgery-induced behavior, mitigate the higher density of Iba-1 and GFAP, and downregulate the expression of Surf1 and Cytochrome c protein in the hippocampus of rats in a PND model.Autism spectrum disorder (ASD) is a widespread, complex and serious neurodevelopmental disorder. Complex genetic and environmental factors are thought to contribute to the development of ASD. Genome-wide association analysis has identified multiple autism-related genes. Mutation of the phosphatase and tensin homolog (Pten) is closely related to autism and accounts for 5-17% of cases of autism. However, the detailed mechanism is still unclear. Recently, mitochondrial dysfunction was tightly associated with ASD pathogenesis, such as developmental degeneration, learning and various behavioral disorders. The mitochondrial DNA (mtDNA) copy number in children with autism is also significantly increased. The correlation between Pten and mitochondrial dysfunction in autism is still unknown. In this study, we examined how Pten regulates mitochondrial biogenesis through the AKT/GSK-3β/PGC-1α signaling pathways. We found that PTEN could dephosphorylate AKT to inhibit its activity, leading to decreased GSK3β phosphorylation. This decrease in GSK3β phosphorylation, which could activate itself, increased PGC-1α phosphorylation to promote its degradation and then regulated mitochondrial biogenesis by NRF-1 and TFAM downstream of PGC-1α. In the Valproic acid (VPA) induced autism mouse model, the PTEN protein level was significantly decreased while PGC-1α and COX IV levels were increased in the hippocampus and cortex. Our data suggest that there is a correlation between PTEN and mitochondrial dysfunction and this correlation may be a potential mechanism of ASD.
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