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Background: The ketogenic diet (KD) is a proven therapy for refractory epilepsy. Although the anti-seizure properties of this diet are understood to a certain extent, the exploration of its neuroprotective effects and underlying mechanisms is still in its infancy. Tissue acidosis is a common feature of epileptogenic foci. Interestingly, the activation of acid-sensing ion channel 1a (ASIC1a), which mediates Ca2+-dependent neuronal injury during acidosis, has been found to be inhibited by ketone bodies in vitro. This prompted us to investigate whether the neuroprotective effects induced by the KD occur via ASIC1a and interconnected downstream mechanisms in a rat model of temporal lobe epilepsy. Methods: Male Sprague-Dawley rats were fed either the KD or a normal diet for four weeks after undergoing pilocarpine-induced status epilepticus (SE). The effects of KD on epileptogenesis, cognitive impairment and hippocampal neuron injury in the epileptic rats were subsequently evaluated by video electroencephalogram, Morris water maze test and Nissl staining, respectively. The expression of ASIC1a and cleaved caspase-3 in the hippocampus were determined using Western blot analysis during the chronic period following SE. Moreover, the intracellular Ca2+ concentration, mitochondrial membrane potential (MMP), mitochondrial reactive oxygen species (mROS) and cell apoptosis of hippocampal cells were detected by flow cytometry. Results: We found that the KD treatment strongly attenuated the spontaneous recurrent seizures, ameliorated learning and memory impairments and prevented hippocampal neuronal injury and apoptosis. The KD was also shown to inhibit the upregulation of ASIC1a and the ensuing intracellular Ca2+ overload in the hippocampus of the epileptic rats. Furthermore, the seizure-induced structure disruption of neuronal mitochondria, loss of MMP and accumulation of mROS were reversed by the KD treatment, suggesting that it has protective effects on mitochondria. Finally, the activation of caspase-3 was also inhibited by the KD. Conclusion: These findings indicate that the KD suppresses mitochondria-mediated apoptosis possibly by regulating ASIC1a to exert neuroprotective effects. This may provide a mechanistic explanation of the therapeutic effects of KD. [ABSTRACT FROM AUTHOR]

Objective: To report the first case series of robotic single-site (RSS) surgery via the da Vinci Si Surgical System for mature cyst teratoma cystectomy in China.Materials and Methods: The study was devised as a retrospective study in a single medical center. Five patients with mature cyst teratomas requested a minimally invasive surgical treatment. These patients were treated with RSS surgery for mature cyst teratoma between January 2014 and January 2015. RSS mature cyst teratoma cystectomies were performed with the da Vinci single-site platform in the Hainan branch of PLA General Hospital. Data regarding patient characteristics, surgical approach, and perioperative clinical outcomes were collected and analyzed in a retrospective study.Results: All RSS procedures were completed successfully in the five patients. No instrument failure was noted during the procedures. The median operating time was 65 minutes (range 45-100 minutes). The median docking time was 20 minutes (range 18-28 minutes). No instrument failure was noted during any surgical procedures. The median blood loss was 30 mL (range 10-70 mL). No patient had massive intraoperative bleeding nor required a transfusion. No extra trocar was placed during the surgery. None of the patients had bladder or rectal injury. The median length of stay in hospital was 2.8 days. All patients were followed up until 6 months postoperatively, and no surgical complication occurred.Conclusion: RSS mature cyst teratoma cystectomy using the wristed semirigid instrumentation is feasible. Randomized controlled trials with a larger number of patients and longer postoperative follow-up should be conducted to further evaluate the effect of this therapeutic strategy. [ABSTRACT FROM AUTHOR]