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  • Author or Editor: Xiu Wang x
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Yu Shuang Tian, Di Zhong, Qing Qing Liu, Xiu Li Zhao, Hong Xue Sun, Jing Jin, Hai Ning Wang and Guo Zhong Li

OBJECTIVE

Ischemic stroke remains a significant cause of death and disability in industrialized nations. Janus tyrosine kinase (JAK) and signal transducer and activator of transcription (STAT) of the JAK2/STAT3 pathway play important roles in the downstream signal pathway regulation of ischemic stroke–related inflammatory neuronal damage. Recently, microRNAs (miRNAs) have emerged as major regulators in cerebral ischemic injury; therefore, the authors aimed to investigate the underlying molecular mechanism between miRNAs and ischemic stroke, which may provide potential therapeutic targets for ischemic stroke.

METHODS

The JAK2- and JAK3-related miRNA (miR-135, miR-216a, and miR-433) expression levels were detected by real-time quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blot analysis in both oxygen-glucose deprivation (OGD)–treated primary cultured neuronal cells and mouse brain with middle cerebral artery occlusion (MCAO)–induced ischemic stroke. The miR-135, miR-216a, and miR-433 were determined by bioinformatics analysis that may target JAK2, and miR-216a was further confirmed by 3′ untranslated region (3′UTR) dual-luciferase assay. The study further detected cell apoptosis, the level of lactate dehydrogenase, and inflammatory mediators (inducible nitric oxide synthase [iNOS], matrix metalloproteinase–9 [MMP-9], tumor necrosis factor–α [TNF-α], and interleukin-1β [IL-1β]) after cells were transfected with miR-NC (miRNA negative control) or miR-216a mimics and subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) damage with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, annexin V–FITC/PI, Western blots, and enzyme-linked immunosorbent assay detection. Furthermore, neurological deficit detection and neurological behavior grading were performed to determine the infarction area and neurological deficits.

RESULTS

JAK2 showed its highest level while miR-216a showed its lowest level at day 1 after ischemic reperfusion. However, miR-135 and miR-433 had no obvious change during the process. The luciferase assay data further confirmed that miR-216a can directly target the 3′UTR of JAK2, and overexpression of miR-216a repressed JAK2 protein levels in OGD/R-treated neuronal cells as well as in the MCAO model ischemic region. In addition, overexpression of miR-216a mitigated cell apoptosis both in vitro and in vivo, which was consistent with the effect of knockdown of JAK2. Furthermore, the study found that miR-216a obviously inhibited the inflammatory mediators after OGD/R, including inflammatory enzymes (iNOS and MMP-9) and cytokines (TNF-α and IL-1β). Upregulating miR-216a levels reduced ischemic infarction and improved neurological deficit.

CONCLUSIONS

These findings suggest that upregulation of miR-216a, which targets JAK2, could induce neuroprotection against ischemic injury in vitro and in vivo, which provides a potential therapeutic target for ischemic stroke.

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Baotian Zhao, Chao Zhang, Xiu Wang, Yao Wang, Chang Liu, Jiajie Mo, Zhong Zheng, Kai Zhang, Xiao-qiu Shao, Wenhan Hu and Jianguo Zhang

Focal cortical dysplasia type II (FCD II) is a common histopathological substrate of epilepsy surgery. Here, the authors propose a sulcus-centered resection strategy for this malformation, provide technical details, and assess the efficacy and safety of this technique. The main purpose of the sulcus-centered resection is to remove the folded gray matter surrounding a dysplastic sulcus, particularly that at the bottom of the sulcus. The authors also retrospectively reviewed the records of 88 consecutive patients with FCD II treated with resective surgery between January 2015 and December 2018. The demographics, clinical characteristics, electrophysiological recordings, neuroimaging studies, histopathological findings, surgical outcomes, and complications were collected. After the exclusion of diffusely distributed and gyrus-based lesions, 71 patients (30 females, 41 males) who had undergone sulcus-centered resection were included in this study. The mean (± standard deviation) age of the cohort was 17.78 ± 10.54 years (38 pediatric patients, 33 adults). Thirty-five lesions (49%) were demonstrated on MRI; 42 patients (59%) underwent stereo-EEG monitoring before resective surgery; and 37 (52%) and 34 (48%) lesions were histopathologically proven to be FCD IIa and IIb, respectively. At a mean follow-up of 3.34 ± 1.17 years, 64 patients (90%) remained seizure free, and 7 (10%) had permanent neurological deficits including motor weakness, sensory deficits, and visual field deficits. The study findings showed that in carefully selected FCD II cases, sulcus-centered resection is an effective and safe surgical strategy.

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Baotian Zhao, Chao Zhang, Xiu Wang, Yao Wang, Jiajie Mo, Zhong Zheng, Lin Ai, Kai Zhang, Jianguo Zhang, Xiao-qiu Shao and Wenhan Hu

OBJECTIVE

The aim of this study was to characterize the clinical and electrophysiological findings of epilepsy originating from the orbitofrontal cortex (OFC) as well as its surgical outcomes.

METHODS

The authors retrospectively reviewed 27 consecutive cases of patients with drug-resistant orbitofrontal epilepsy (OFE) who underwent tailored resective surgery after a detailed presurgical workup. Demographic features, seizure semiology, imaging characteristics, resection site, pathological results, and surgical outcomes were analyzed. Patients were categorized according to semiology. The underlying neural network was further explored through quantitative FDG-PET and ictal stereo-electroencephalography (SEEG) analysis at the group level. FDG-PET studies between the semiology group and the control group were compared using a voxel-based independent t-test. Ictal SEEG was quantified by calculating the energy ratio (ER) of high- and low-frequency bands. An ER comparison between the anterior cingulate cortex (ACC) and the amygdala was performed to differentiate seizure spreading patterns in groups with different semiology.

RESULTS

Scalp electroencephalography (EEG) and MRI were inconclusive to a large extent. Patients were categorized into the following 3 semiology groups: the frontal group (n = 14), which included patients with hyperactive automatisms with agitated movements; the temporal group (n = 11), which included patients with oroalimentary or manual automatisms; and the other group (n = 2), which included patients with none of the abovementioned or indistinguishable manifestations. Patients in the frontal and temporal groups (n = 23) or in the frontal group only (n = 14) demonstrated significant hypometabolism mainly across the ipsilateral OFC, ACC, and anterior insula (AI), while patients in the temporal group (n = 9) had hypometabolism only in the OFC and AI. The ER results (n = 15) suggested distinct propagation pathways that allowed us to differentiate between the frontal and temporal groups. Pathologies included focal cortical dysplasia, dysembryoplastic neuroepithelial tumor, cavernous malformation, glial scar, and nonspecific findings. At a minimum follow-up of 12 months, 19 patients (70.4%) were seizure free, and Engel class II, III, and IV outcomes were observed in 4 patients (14.8%), 3 patients (11.1%), and 1 patient (3.7%), respectively.

CONCLUSIONS

The diagnosis of OFE requires careful presurgical evaluation. Based on their electrophysiological and metabolic evidence, the authors propose that varied semiological patterns could be explained by the extent of involvement of a network that includes at least the OFC, ACC, AI, and temporal lobe. Tailored resections for OFE may lead to a good overall outcome.