LncRNA CEBPA-AS1 alleviates cerebral ischemia-reperfusion injury by sponging miR-340-5p regulating APPL1/LKB1/AMPK pathway.

Long non-coding RNAs (lncRNAs) regulate neurological damage in cerebral ischemia-reperfusion injury (CIRI). This study aimed to investigate the biological roles of lncRNA CEBPA-AS1 in CIRI. Middle cerebral artery occlusion and ischemia-reperfusion injury (MCAO/IR) rat model and oxygen-glucose deprivation and reoxygenation (OGD/R) cell lines were generated; the expression of CEBPA-AS1 was evaluated by qRT-PCR. The effects of CEBPA-AS1 on cell apoptosis and nerve damage were examined. The downstream microRNA (miRNA) and mRNA of CEBPA-AS1 were predicted and verified. We found that overexpression of CEBPA-AS1 could attenuate MCAO/IR-induced nerve damage and neuronal apoptosis in the rat model. Knockdown of CEBPA-AS1 aggravated cell apoptosis and enhanced the production of LDH and MDA in the OGD/R cells. Upon examining the molecular mechanisms, we found that CEBPA-AS1 stimulated APPL1 expression by combining with miR-340-5p, thereby regulating the APPL1/LKB1/AMPK pathway. In the rescue experiments, CEBPA-AS1 overexpression was found to attenuate OGD/R-induced cell apoptosis and MCAO/IR induced nerve damage, while miR-340-5p reversed these effects of CEBPA-AS1. In conclusion, CEBPA-AS1 could decrease CIRI by sponging miR-340-5, regulating the APPL1/LKB1/AMPK pathway.

Assessment of bypass patency using transcranial Doppler sonography: correlations with computerized tomography angiography findings in patients with moyamoya disease.

To explore the utility of transcranial Doppler (TCD) findings when assessing bypass patency in patients with Moyamoya disease (MMD). Computed tomography angiography (CTA) and TCD sonography (TCDS) were performed before and after surgery to evaluate bypass patency. The peak systolic flow velocity (PSV) of the superficial temporal artery (STA) and the pulsatility index (PI) were compared between the groups that achieved patency and not, and receiver operating characteristic (ROC) curve analyses were used to define the TCDS criteria revealing patency. This study included 35 hemispheres (15 women; mean age 47 years) with Moyamoya disease who underwent STA-middle carotid artery bypass in our institution between January 2022 and October 2022. The PSV first increased on postoperative days 4-5 and then decreased on postoperative days 6-7 and 7-8. Patients with transient neurological diseases (TNDs), compared to those without, evidenced a significantly lower PSV value (P < 0.05). Compared with the non-patency group, the PSV was higher (P < 0.001) in the patency group. The cutoff values reflecting patency with good sensitivity and specificity were PSV > 49.00; PSV ratio (postoperative/preoperative) > 1.218; PSV ratio (operation side/contralateral side) > 1.082; and PSV ratio (adjusted) > 1.202. In the patency group, the PSV and PI significantly increased (P < 0.001) and decreased (P < 0.001) respectively. Bypass patency can be noninvasively and accurately evaluated via TCDS, affording an objective basis for assessment of the effect of revascularization surgery on patients with MMD.

Propofol Reduces Inflammatory Brain Injury after Subarachnoid Hemorrhage: Involvement of PI3K/Akt Pathway.

BACKGROUND: Our previous study showed that propofol, one of the widely used anesthetic agents, can attenuate subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) via inhibiting inflammatory and oxidative reaction. However, it is perplexing whether propofol attenuates inflammatory and oxidative reaction through modulating PI3K/Akt pathway. The present study investigated whether PI3K/Akt pathway is involved in propofol's anti-inflammation, antioxidation, and neuroprotection against SAH-induced EBI. MATERIALS AND METHODS: Adult Sprague-Dawley rats underwent SAH and received treatment with propofol or vehicle after 2 and 12 hours of SAH. LY294002 was injected intracerebroventricularly to selectively inhibit PI3K/Akt signaling. Mortality, SAH grading, neurological scores, brain water content, evans blue extravasation, myeloperoxidase, malondialdehyde, superoxide dismutase, and glutathione peroxidase were measured 24 hours after SAH. Immunoreactivity of p-Akt, t-Akt, nuclear factor- kappa B (NF-κB) p65, nuclear factor erythroid-related factor 2 (Nrf2), NAD(P)H:quinone oxidoreductase (NQO1), and cyclooxygenase-2 (COX-2) in rat brain was determined by western blot. Tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) in rat brain were examined by ELISA. RESULTS: Propofol significantly reduces neurological dysfunction, BBB permeability, brain edema, inflammation, and oxidative stress, all of which were reversed by LY294002. Propofol significantly upregulates the immunoreactivity of p-Akt, Nrf2, and NQO1, all of which were abolished by LY294002. Propofol significantly downregulates the overexpression of NF-κB p65, COX-2, TNF-α, and IL-1ß, all of which were inhibited by LY294002. CONCLUSION: These results suggest that propofol attenuates SAH-induced EBI by inhibiting inflammatory reaction and oxidative stress, which might be associated with the activation of PI3K/Akt signaling pathway.

5-LOX Inhibitor Zileuton Reduces Inflammatory Reaction and Ischemic Brain Damage Through the Activation of PI3K/Akt Signaling Pathway.

Previous studies from our laboratories showed that an anti-inflammatory drug, 5-lipoxygenase inhibitor zileuton, attenuates ischemic brain damage via inhibiting inflammatory reaction. However, it was elusive whether zileuton attenuates inflammatory reaction and ischemic brain damage through the modulation of PI3K/Akt signaling pathway. In the present study, we, for the first time, investigated whether PI3K/Akt pathway was involved in zileuton's anti-inflammatory and neuroprotective properties against brain damage following experimental ischemic stroke. Adult male Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO), then received treatment with zileuton or vehicle after the onset of ischemia. LY294002 was injected intracerebroventricularly to inhibit the activation of PI3K/Akt signaling pathway selectively. Neurological deficit scores, cerebral infarct volume, morphological characteristic and cerebral water content were assessed 24 h after cerebral ischemia. The enzymatic activity of myeloperoxidase (MPO) was measured 24 h after cerebral ischemia. Expression of p-Akt, t-Akt and COX-2 in ischemic brain were determined by western blot. NF-κB p65 immuno-positive cells in ischemic brain were detected 24 h after cerebral ischemia. The content of TNF-α in blood was examined by ELISA. 5-LOX inhibitor zileuton significantly reduces neurological deficit scores, cerebral infarct volume, cerebral water content, ischemic neuronal injury and the enzymatic activity of MPO, all of which were abolished by LY294002 administration. Zileuton significantly up-regulates the expression of p-Akt, which was inhibited by LY294002 administration. Zileuton significantly down-regulates the over-expression of NF-κB p65 and COX-2, and attenuates the release of TNF-α, all of which were disminished by LY294002 administration. These results suggest that zileuton attenuates ischemic brain damage by inhibiting inflammatory reaction through the activation of PI3K/Akt signaling pathway.

Propofol reduces inflammatory reaction and ischemic brain damage in cerebral ischemia in rats.

Our previous studies demonstrated that inflammatory reaction and neuronal apoptosis are the most important pathological mechanisms in ischemia-induced brain damage. Propofol has been shown to attenuate ischemic brain damage via inhibiting neuronal apoptosis. The present study was performed to evaluate the effect of propofol on brain damage and inflammatory reaction in rats of focal cerebral ischemia. Sprague-Dawley rats underwent permanent middle cerebral artery occlusion, then received treatment with propofol (10 or 50 mg/kg) or vehicle after 2 h of ischemia. Neurological deficit scores, cerebral infarct size and morphological characteristic were measured 24 h after cerebral ischemia. The enzymatic activity of myeloperoxidase (MPO) was assessed 24 h after cerebral ischemia. Nuclear factor-kappa B (NF-κB) p65 expression in ischemic rat brain was detected by western blot. Cyclooxygenase-2 (COX-2) expression in ischemic rat brain was determined by immunohistochemistry. ELISA was performed to detect the serum concentration of tumor necrosis factor-α (TNF-α). Neurological deficit scores, cerebral infarct size and MPO activity were significantly reduced by propofol administration. Furthermore, expression of NF-κB, COX-2 and TNF-α were attenuated by propofol administration. Our results demonstrated that propofol (10 and 50 mg/kg) reduces inflammatory reaction and brain damage in focal cerebral ischemia in rats. Propofol exerts neuroprotection against ischemic brain damage, which might be associated with the attenuation of inflammatory reaction and the inhibition of inflammatory genes.

The Value of SINO Robot and Angio Render Technology for Stereoelectroencephalography Electrode Implantation in Drug-Resistant Epilepsy.

BACKGROUND: Stereoelectroencephalography (SEEG) electrodes are implanted using a variety of stereotactic technologies to treat refractory epilepsy. The value of the SINO robot for SEEG electrode implantation is not yet defined. The aim of the current study was to assess the value of the SINO robot in conjunction with Angio Render technology for SEEG electrode implantation and to assess its efficacy. METHODS: Between June 2018 and October 2020, 58 patients underwent SEEG electrode implantation to resect or ablate their epileptogenic zone (EZ). The SINO robot and the Angio Render technology was used to guide the electrodes and visualize the individual vasculature in a three-dimensional (3D) fashion. The 3D view functionality was used to increase the safety and accuracy of the electrode implantation, and for reducing the risk of hemorrhage by avoiding blood vessels. RESULTS: In this study, 634 SEEG electrodes were implanted in 58 patients, with a mean of 10.92 (range: 5-18) leads per patient. The mean entry point localization error (EPLE) was 0.94 ± 0.23 mm (range: 0.39-1.63 mm), and the mean target point localization error (TPLE) was 1.49 ± 0.37 mm (range: 0.80-2.78 mm). The mean operating time per lead (MOTPL) was 6. 18 ± 1.80 minutes (range: 3.02-14.61 minutes). The mean depth of electrodes was 56.96 ± 3.62 mm (range: 27.23-124.85 mm). At a follow-up of at least 1 year, in total, 81.57% (47/58) patients achieved an Engel class I seizure freedom. There were two patients with asymptomatic intracerebral hematomas following SEEG electrode placement, with no late complications or mortality in this cohort. CONCLUSIONS: The SINO robot in conjunction with Angio Render technology-in SEEG electrode implantation is safe and accurate in mitigating the risk of intracranial hemorrhage in patients suffering from drug-resistant epilepsy.

Diffusion spectrum imaging based semi-automatic optic radiation tractography for vision preservation in SEEG-guided radiofrequency thermocoagulation.

OBJECTIVE: To assess the efficacy and safety of stereoelectroencephalography (SEEG)-guided radiofrequency thermocoagulation (RFTC), using diffusion spectrum imaging (DSI) tractography to preoperatively delineate the optic radiation (OR) and reduce the risk of visual field defects (VFDs) where the epileptogenic zones (EZs) are located in or close to the eloquent visual areas. METHODS: We prospectively followed up twenty-four consecutive patients (12 males and 12 females) who underwent SEEG-guided RFTC in or near the OR pathway. A distance of ≥ 3.5 mm away from the OR on the targeted electrodes contacts that exhibited relevant ictal onset patterns, IEDs and EES during SEEG recordings, was required as our selection criterion prior to performing RFTC, enough to theoretically prevent VFDs. Using default tracking parameters, the optic radiation was tracked semi-automatically in DSI-studio. RESULTS: There were 12 male and 12 female patients ranging in age from 6 to 57 years, with follow-up period ranging from 6 to 37 months. Nineteen patients responded to RFTC (R+, 79.16 %), and 5 patients did not benefit from RFTC (R-, 20.83 %). The preoperative application of DSI semi-automatic based OR tractography was successful in the protection of the OR in all 24 patients. Three patients experienced a neurologic deficit following RFTC, and five patients had a partial quadrant visual field deficit prior to surgery that did not worsen, and none of the remaining nineteen patients had a quadrant visual field deficit. CONCLUSION: Our study validates the safety and efficacy of SEEG-RFTC as a viable therapeutic approach for epileptic foci situated in or adjacent to the visual eloquent regions. We demonstrate that DSI-based tractography offers superior precision in delineating the OR compared to DTI. We establish that implementing a criterion of a minimum distance of ≥ 3.5 mm in radius from the OR on the targeted electrode contacts prior to conducting RFTC can effectively mitigate the risk of VFDs.

Enhancement effect of cytotoxicity response of silver nanoparticles combined with thermotherapy on C6 rat glioma cells.

The present studies reveal that silver nanoparticles (AgNPs) can induce apoptosis and enhance radio-sensitivity on cancer cells. In this paper, we mainly investigated the effect of AgNPs on rat glioma C6 cells upon the combination treatment of hyperthermia treatment (HTT). AgNPs were synthesized by a polyol process and the mean size was 15 nm. The particles showed dose-dependent cytotoxicity on C6 cells from the experimental data. Besides, we found that heating cells could enhance the contents of cell uptake of AgNPs. From the survival curves, AgNPs showed the ability to enhance thermo-sensitivity on C6 cells. Our results revealed that AgNPs could have a potential application in enhancing effect on HTT induced killing of glioma cells.

Multimodal endovascular treatment for traumatic carotid-cavernous fistula.

OBJECTIVE: To present our experience in treating traumatic carotid-cavernous fistula (TCCF) by multimodal endovascular treatment. METHODS: The management of 28 patients with TCCF between January 2004 and October 2012 in our hospital was retrospectively analyzed. According to imaging charateristics, 24 cases were categorized into Type I, 3 Type II and 1 Type III. Totally 30 endovascular treatments were performed: Type I TCCFs were obliterated via transvenous approach (7/25), or transarterial approach (18/25) including 6 by detachable balloon occlusion, 6 by microcoil embolization, 3 by Hyperglide balloon-assisted coil embolization and 3 by a combination of detachable balloon and coil embolization. Two patients were treated with closure of internal carotid artery (ICA). Type II TCCFs were treated with transvenous embolotherapy (2/3) or carotid artery compression therapy (1/3). The Type III patient underwent detachable balloon embolization. RESULTS: Immediate postoperative angiography showed recovery in 26 cases. One recurrent TCCF was found 2 weeks after detachable balloon embolization, and then re-obliterated by transarterial coils. Reexamination found balloon deflation and fistula recanalization in 1 patient one month after combination of detachable balloons and coil embolization, which was cured by a second treatment via transvenous approach. The immediate angiography revealed residual blood flow in 4 patients. Among them, 2 patients with delayed symptoms at follow-up needed a second treatment, 1 patient recovered after carotid artery compression therapy, and the remaining patient's symptoms disappeared on digital subtraction angiography at five-month follow-up. CT angiography revealed anterior communicating artery aneurysm in the patient who was treated with closure of ICA 4 years later. CONCLUSION: According to results of images, characteristics of the fistula and type of drainage, proper treatment approach and embolic material can maximally heal pathological changes, retain the ipsilateral ICA patency and reduce long-term complications.

Diagnosis of pituitary abscess and treatment via transsphenoidal surgery: experience from 15 cases.

OBJECTIVE: Pituitary abscess is an often misdiagnosed, rare clinical disorder. To improve diagnostic accuracy and the efficacy of surgical and antibiotic therapy for patients with pituitary abscess, herein, we retrospectively reviewed 15 patients who presented with pituitary abscesses from 2005 to 2022. DESIGN: Retrospective study. PATIENTS: Fifteen patients underwent transsphenoidal surgery and received antibiotic treatment. MEASUREMENTS: Complete details regarding medical history, clinical manifestations, laboratory examinations, imaging studies, and treatment strategies were obtained for all patients. RESULTS: Most patients presented with hypopituitarism and headaches, while some presented with fever, visual disturbances, and diabetes insipidus (DI). Abscesses showed significant annular enhancement post gadolinium injection. In most patients, pituitary abscess can be cured via microscopic or endoscopic drainage of the abscess followed by antibiotic treatment. Complete cure of pituitary abscess was observed in nine patients, with six cases of prolonged hypopituitarism and only one case of recurrence. Long-term hormone replacement therapy was effective in the postoperative management of hypopituitarism. CONCLUSIONS: The typical manifestations of pituitary abscess include hypopituitarism and headaches; the presence of an enhanced ring at the edge of the mass on contrast-enhanced magnetic resonance images (MRI) is highly suggestive of pituitary abscess. We recommend antibiotic treatment for 4-6 weeks postoperatively, based on the results of bacterial cultures or metagenomic next-generation sequencing (mNGS).

Cordycepin improves sensitivity to temozolomide in glioblastoma cells by down-regulating MYC.

PURPOSE: Glioblastoma is one of the malignant tumors with poor prognosis and no effective treatment is available at present. METHODS: To study the effect of cordycepin combined with temozolomide on glioblastoma, we explored the effect of the combination based on network pharmacology and biological verification. RESULTS: It was found that the drug combination significantly inhibited the cell growth, proliferation, migration and invasion of LN-229 cells. Drug combination inhibited epithelial-mesenchymal transition (EMT) by up-regulating the expression of E-cadherin and suppressing the expression of N-cadherin, Zeb1 and Twist1. Through network pharmacology, we further explored the molecular mechanism of drug combination against glioblastoma, and 36 drug-disease common targets were screened. The GO biological process analysis included 44 items (P < 0.01), which mainly involved the regulation of apoptosis, cell proliferation, cell migration, etc. The enrichment analysis of KEGG pathways included 28 pathways (P < 0.05), and the first four pathways were "MicroRNA in cancer, Proteoglycans in cancer, Pathways in cancer and PI3K-AKT signaling pathway". We detected the expression of important genes in the pathways and PPI network, and the results showed that the drug combination down-regulated NFKB1, MYC, MMP-9, MCL1, CTNNB1, and up-regulated PDCD4. CONCLUSION: Cordycepin combined with temozolomide may down-regulate MYC through "MicroRNA in cancer, Proteoglycans in cancer, Pathways in cancer and PI3K-AKT signaling pathway", which in turn regulate the expression of MCL1, CTNNB1, MMP9, PDCD4, thus regulating cell proliferation, migration and apoptosis in glioblastoma.

GLP-1R knockdown abrogates the protective effects of liraglutide on ischaemic stroke via inhibition of M2 polarisation and activation of NLRP3 inflammasome by reducing Nrf2 activation.

Liraglutide has been recently discovered to penetrate the blood-brain barrier to exert neuroprotective effects. However, relevant mechanisms of the protective effects of liraglutide on ischaemic stroke remain to be elucidated. This study examined the mechanism of GLP-1R in regulating the protective effect of liraglutide against ischaemic stroke. Middle cerebral artery occlusion (MCAO) male Sprague-Dawley rat model with/without GLP-1R or Nrf2 knockdown was established and subjected to liraglutide treatment. Then neurological deficit and brain oedema of rats was evaluated and brain tissues were subjected to TTC, Nissl, TUNEL and immunofluorescence staining. Rat primary microglial cells firstly underwent lipopolysaccharide (LPS) treatment, then GLP-1R or Nrf2 knockdown treatment, and finally Liraglutide treatment to research the NLRP3 activation. As a result, Liraglutide protected rats' brain tissues after MCAO, which attenuated brain oedema, infarct volume, neurological deficit score, neuronal apoptosis and Iba1 expression but enhanced live neurons. However, GLP-1R knockdown abrogated these protective effects of liraglutide on MCAO rats. According to in vitro experiments, Liraglutide promoted M2 polarisation, activated Nrf2 and inhibited NLRP3 activation in LPS-induced microglial cells, but GLP-1R or Nrf2 knockdown reversed these effects of Liraglutide on LPS-induced microglial cells. Further, Nrf2 knockdown counteracted the protection of liraglutide on MCAO rats, whereas sulforaphane (agonist of Nrf2) counteracted the effect of Nrf2 knockdown on liraglutide-treated MCAO rats. Collectively, GLP-1R knockdown abrogated the protection of liraglutide on MCAO rats by activating NLRP3 via inactivating Nrf2.

Schisandrin B Protects against Ischemic Brain Damage by Regulating PI3K/AKT Signaling in Rats.

OBJECTIVE: To explore the effect and mechanism of schisandrin B (Sch B) in the treatment of cerebral ischemia in rats. METHODS: The cerebral ischemia models were induced by middle cerebral artery occlusion (MCAO) and reperfusion. Sprague-Dawley rats were divided into 6 groups using a random number table, including sham, MCAO, MCAO+Sch B (50 mg/kg), MCAO+Sch B (100 mg/kg), MCAO+Sch B (100 mg/kg)+LY294002, and MCAO+Sch B (100 mg/kg)+wortmannin groups. The effects of Sch B on pathological indicators, including neurological deficit scores, cerebral infarct volume, and brain edema, were subsequently studied. Tissue apoptosis was identified by terminal transferase-mediated dUTP nick end-labeling (TUNEL) staining. The protein expressions involved in apoptosis, inflammation response and oxidative stress were examined by immunofluorescent staining, biochemical analysis and Western blot analysis, respectively. The effect of Sch B on phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling was also explored. RESULTS: Sch B treatment decreased neurological deficit scores, cerebral water content, and infarct volume in MCAO rats (P<0.05 or P<0.01). Neuronal nuclei and TUNEL staining indicated that Sch B also reduced apoptosis in brain tissues, as well as the Bax/Bcl-2 ratio and caspase-3 expression (P<0.01). Sch B regulated the production of myeloperoxidase, malondialdehyde, nitric oxide and superoxide dismutase, as well as the release of cytokine interleukin (IL)-1 ß and IL-18, in MCAO rats (P<0.05 or P<0.01). Sch B promoted the phosphorylation of PI3K and AKT. Blocking the PI3K/AKT signaling pathway with LY294002 or wortmannin reduced the protective effect of Sch B against cerebral ischemia (P<0.05 or P<0.01). CONCLUSIONS: Sch B reduced apoptosis, inflammatory response, and oxidative stress of MCAO rats by modulating the PI3K/AKT pathway. Sch B had a potential for treating cerebral ischemia.

Clinical features, surgical treatment, and long-term outcomes of moyamoya disease in a single institution of Fujian, Southeast China: A retrospective study.

At present, detailed demographic and clinical data of moyamoya disease (MMD) in the population of Southeast China are lacking. Therefore, this study aimed to evaluate the epidemiological and clinical features of MMD in Southeast China. Our cohort included 170 patients diagnosed with MMD over the preceding 5 years. Clinical characteristics were obtained through a retrospective chart review, while follow-up information and outcomes were obtained through clinical visits and imaging. The median age at symptom onset was 49 years (range 4-73), with a peak in the age distribution observed at 41 to 60 years. The female-to-male ratio was 1.125 (90/80), and the ratio of the ischemic type to the hemorrhagic type was 2.33 (119/50). The most common initial symptom was an ischemic event. The 5-year Kaplan-Meier risk of stroke was 4.9% for all patients treated with surgical revascularization. Of all patients, 83.9% were able to live independently with no significant disability, and 89.8% showed improved cerebral hemodynamics. Our study provided detailed demographic and clinical data on Southeastern Chinese patients with MMD, which was consistent with findings in other parts of China. Raising clinical awareness of MMD in primary hospitals is important to facilitate early diagnosis and timely treatment of MMD patients.

Schisandrin B Inhibits NLRP3 Inflammasome Pathway and Attenuates Early Brain Injury in Rats of Subarachnoid Hemorrhage.

OBJECTIVE: To determine whether Schisandrin B (Sch B) attenuates early brain injury (EBI) in rats with subarachnoid hemorrhage (SAH). METHODS: Sprague-Dawley rats were divided into sham (sham operation), SAH, SAH+vehicle, and SAH+Sch B groups using a random number table. Rats underwent SAH by endovascular perforation and received Sch B (100 mg/kg) or normal saline after 2 and 12 h of SAH. SAH grading, neurological scores, brain water content, Evan's blue extravasation, and terminal transferase-mediated dUTP nick end-labeling (TUNEL) staining were carried out 24 h after SAH. Immunofluorescent staining was performed to detect the expressions of ionized calcium binding adapter molecule 1 (Iba-1) and myeloperoxidase (MPO) in the rat brain, while the expressions of B-cell lymphoma 2 (Bcl-2), Bax, Caspase-3, nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis-associated specklike protein containing the caspase-1 activator domain (ASC), Caspase-1, interleukin (IL)-1ß, and IL-18 in the rat brains were detected by Western blot. RESULTS: Compared with the SAH group, Sch B significantly improved the neurological function, reduced brain water content, Evan's blue content, and apoptotic cells number in the brain of rats (P<0.05 or P<0.01). Moreover, Sch B decreased SAH-induced expressions of Iba-1 and MPO (P<0.01). SAH caused the elevated expressions of Bax, Caspase-3, NLRP3, ASC, Caspase-1, IL-1ß, and IL-18 in the rat brain (P<0.01), all of which were inhibited by Sch B (P<0.01). In addition, Sch B increased the Bcl-2 expression (P<0.01). CONCLUSION: Sch B attenuated SAH-induced EBI, which might be associated with the inhibition of neuroinflammation, neuronal apoptosis, and the NLRP3 inflammatory signaling pathway.

Molecular diagnosis and treatment of meningiomas: an expert consensus (2022).

ABSTRACT: Meningiomas are the most common primary intracranial neoplasm with diverse pathological types and complicated clinical manifestations. The fifth edition of the WHO Classification of Tumors of the Central Nervous System (WHO CNS5), published in 2021, introduces major changes that advance the role of molecular diagnostics in meningiomas. To follow the revision of WHO CNS5, this expert consensus statement was formed jointly by the Group of Neuro-Oncology, Society of Neurosurgery, Chinese Medical Association together with neuropathologists and evidence-based experts. The consensus provides reference points to integrate key biomarkers into stratification and clinical decision making for meningioma patients. REGISTRATION: Practice guideline REgistration for transPAREncy (PREPARE), IPGRP-2022CN234.

Effect of baicalin on matrix metalloproteinase-9 expression and blood-brain barrier permeability following focal cerebral ischemia in rats.

Focal cerebral ischemia results in an increased expression of matrix metalloproteinase-9 (MMP-9), which induces vasogenic brain edema via disrupting the blood-brain barrier (BBB) integrity. Recent studies from our laboratory showed that baicalin reduces ischemic brain damage by inhibiting inflammatory reaction and neuronal apoptosis in a rat model of focal cerebral ischemia. In the present study, we first explored the effect of baicalin on the neuronal damage, brain edema and BBB permeability, then further investigated its potential mechanisms. Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (MCAO). Baicalin was administrated by intraperitoneally injected twice at 2 and 12 h after the onset of MCAO. Neuronal damage, brain edema and BBB permeability were measured 24 h following MCAO. Expression of MMP-9 protein and mRNA were determined by western blot and RT-PCR, respectively. Expression of tight junction protein (TJP) occludin was detected by western blot. Neuronal damage, brain edema and BBB permeability were significantly reduced by baicalin administration following focal cerebral ischemia. Elevated expression of MMP-9 protein and mRNA were significantly down-regulated by baicalin administration. In addition, MCAO caused the decreased expression of occludin, which was significantly up-regulated by baicalin administration. Our study suggested that baicalin reduces MCAO-induced neuronal damage, brain edema and BBB permeability, which might be associated with the inhibition of MMP-9 expression and MMP-9-mediated occludin degradation.

Chronic subdural hematoma associated with sylvian arachnoid cyst in juvenile athletes: report of two cases and literature review.

The association of chronic subdural hematoma (CSDH) and arachnoid cyst (AC) is uncommon. We reported 2 juvenile athletes with CSDH associated with AC which occurred in their daily sports activities and reviewed the literature. Both of them were treated surgically, with satisfactory outcome. AC is a common predisposing factor in young patients with CSDH. The complication of intracranial bleeding is an indication for surgical management. Though there are still controversies in the treatment of asymptomatic AC, it is the consensus that the patients with AC should avoid violent sports so as to reduce the incidence of intracranial hemorrhage resulted from head injuries.

Posttraumatic hydrocephalus associated with decompressive cranial defect in severe brain-injured patients.

OBJECTIVE: To investigate the occurrence of posttraumatic hydrocephalus (PTH) in severe brain- injured patients who underwent decompressive craniectomy (DC) and to discuss the management. METHODS: A total of 389 patients suffering from severe head trauma between January 2004 and May 2010 were enrolled in this study. Clinical data were analyzed retrospectively. Of them, 149 patients who underwent DC were divided into two groups according to the presence of PTH: hydrocephalus group and nonhydrocephalus group. Clinical factors including preoperative Glasgow Coma Score (GCS), bilateral or unilateral decompression, and duraplasty in DC were assessed by single factor analysis to determine its relationship with the occurrence of PTH. RESULTS: Of the 149 patients undergoing DC, 25 (16.8%) developed PTH; while 23 developed PTH (9.6%) among the rest 240 patients without DC. Preoperative GCS, bilateral or unilateral decompression, duraplasty in DC were significantly associated with the development of PTH. Ventriculoperitoneal shunt was performed on 23 of 25 patients with PTH after DC. Frontal horn was preferred for the placement of the catheter. Sixteen of them were operated upon via frontal approach and 7 via occipital approach. After shunt surgery, both radiological and clinical improvements were confirmed in 19 patients. Radiological improvement was found in 2 patients. One patient died eventually of severe pneumonia. Shunt-related infection occurred in 1 patient, which led to the removal of the catheter. CONCLUSIONS: It is demonstrated that the occurrence of PTH is high in patients with large decompressive skull defect. Patients with low GCS and bilateral decompression tend to develop PTH after DC. Duraplasty in DC might facilitate reducing the occurrence of PTH. Patients with PTH concomitant skull defect should be managed deliberately to restore the anatomical and physiological integrity so as to facilitate the neurological resuscitation.

Accuracy and Feasibility Analysis of SEEG Electrode Implantation using the VarioGuide Frameless Navigation System in Patients with Drug-Resistant Epilepsy.

OBJECTIVE: The objective of the study was to evaluate the feasibility and accuracy of frameless stereoelectroencephalography (SEEG) electrode implantation in patients with drug-resistant epilepsy using the VarioGuide system. METHODS: The VarioGuide frameless navigation system was used to implant SEEG electrodes in patients with medically drug-resistant epilepsy. Demographic data, surgery duration, number of electrodes, and complications were retrospectively analyzed. Accuracy was compared by measuring the distance between the planned and actual electrode positions as determined by postoperative computed tomography images. RESULTS: A total of 141 SEEG electrodes were implanted in 19 patients from May 2015 to December 2018 with an average of 7.42 (range: 4-10) leads per patient. The average entry point localization error (EPLE) was 1.96 ± 0.47 mm (range: 0.32-3.29) and average target point localization error (TPLE) was 2.47 ± 0.79 mm (range: 0.72-4.83). The average operating time per lead (OTPL) was 14.16 ± 2.68 minutes (range: 8.64-21.58). No complications occurred. CONCLUSION: The VarioGuide frameless navigation system can be an effective method for SEEG electrode implantation in patients with drug-resistant epilepsy, particularly when the electrodes are concentrated in a relatively small region and the number of implanted electrodes is small.