Objective : Although prophylactic antiepileptic drug (AED) use in patients with aneurysmal subarachnoid hemorrhage (SAH) is a common practice, lack of uniform definitions and guidelines for seizures and AEDs rendered this prescription more habitual instead of evidence-based manner. We herein evaluated the incidence and predictive factors of seizure and complications about AED use. Methods : From July 1999 to June 2007, data of a total of 547 patients with aneurysmal SAH who underwent operative treatments were reviewed. For these, the incidence and risk factors of seizures and epilepsy were assessed, in addition to complications of AEDs. Results : Eighty-three patients (15.2%) had at least one seizure following SAH. Forty-three patients (7.9%) had onset seizures, 34 (6.2%) had perioperative seizures, and 17 (3.1%) had late epilepsy. Younger age (< 40 years), poor clinical grade, thick hemorrhage, acute hydrocephalus, and rebleeding were related to the occurrence of onset seizures. Cortical infarction and thick hemorrhage were independent risk factors for the occurrence of late epilepsy. Onset seizures were not predictive of late epilepsy. Moreover, adverse drug effects were identified in 128 patients (23.4%) with AEDs. Conclusion : Perioperative seizures are not significant predictors for late epilepsy. Instead, initial amount of SAH and surgery-induced cortical damage should be seriously considered as risk factors for late epilepsy. Because AEDs can not prevent early postoperative seizures (< 1 week) and potentially cause unexpected side effects, long-term use should be readjusted in high-risk patients.

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Introduction: Patients may experience problems, including severe adhesion during skull restoration procedures performed after decompressive craniectomy. Cranioplasty is currently the only solution for these adverse outcomes, although there is no established consensus on optimal surgical timing. Here, we study the efficacy and safety of early cranioplasty performed within 1 month after first surgical decompression. Methods: In this study, we retrospectively enrolled 30 patients during a 30-month period. Serial brain computed tomographic scans were obtained to demonstrate relief of brain swelling. During the operative procedure, the efficacy of early cranioplasty was assessed by measuring elapsed operating time, dissection time, and blood loss. Fifteen patients were selected for the control group, all of whom had undergone cranioplasty performed more than 3 months after first decompression. Results: All primary causes for craniectomy were traumatic in enrolled patients. The mean interval for cranioplasty was 28.6 days after first operation. When compared with the control group, the mean time for dissection was much shorter (15.3 min, P G 0.0001) and estimated blood loss was much smaller (336.67 mL, P G 0.0001) in the early cranioplasty group. No patients experienced surgeryrelated complications during the 6-month follow-up period. Conclusions: Early cranioplasty provides satisfactory securing dissection plane during operative procedures compared with later cranioplasty, without causing additional complications including infection, subdural hygroma, and brain parenchymal damage, in selected cases.

BackgroundThe pathology of Parkinson's disease (PD) is characterized by the degeneration of the nigrostriatal dopaminergic pathway, as well as the formation of intraneuronal inclusions known as Lewy bodies and Lewy neurites in the substantia nigra. Accumulations of nitrated α-synuclein are demonstrated in the signature inclusions of Parkinson's disease. However, whether the nitration of α-synuclein is relevant to the pathogenesis of PD is unknown.Methodology/Principal FindingsIn this study, effect of nitrated α-synuclein to dopaminergic (DA) neurons was determined by delivering nitrated recombinant TAT-α-synuclein intracellular. We provide evidence to show that the nitrated α-synuclein was toxic to cultured dopaminergic SHSY-5Y neurons and primary mesencephalic DA neurons to a much greater degree than unnitrated α-synuclein. Moreover, we show that administration of nitrated α-synuclein to the substantia nigra pars compacta of rats caused severe reductions in the number of DA neurons therein, and led to the down-regulation of D2R in the striatum in vivo. Furthermore, when administered to the substantia nigra of rats, nitrated α-synuclein caused PD-like motor dysfunctions, such as reduced locomotion and motor asymmetry, however unmodified α-synuclein had significantly less severe behavioral effects.Conclusions/SignificanceOur results provide evidence that α-synuclein, principally in its nitrated form, induce DA neuron death and may be a major factor in the etiology of PD.

Compound K (20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol, CK), an intestinal bacterial metabolite of panaxoside, has been shown to inhibit tumour growth in a variety of tumours. However, the mechanisms involved are largely unknown. We use human gastric carcinoma cell lines BGC823, SGC7901 and human gastric carcinoma xenograft in nude mice as models to study the mechanisms of CK in gastric cancers. We found that CK significantly inhibits the viabilities of BGC823 and SGC7901 cells in dose- and time-dependent manners. CK-induced BGC823 and SGC7901 cells apoptosis and cell cycle arrest in G2 phase by up-regulation of p21 and down-regulation of cdc2 and cyclin B1. Further studies show that CK induces apoptosis in BGC823 and SGC7901 cells mainly through mitochondria-mediated internal pathway, and that CK induces the translocation of nuclear Bid to mitochondria. Finally, we found that CK effectively inhibited the tumour formation of SGC7901 cells in nude mice. Our studies show that CK can inhibit the viabilities and induce apoptosis of human gastric carcinoma cells via Bid-mediated mitochondrial pathway.