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Bridge vortex-induced vibration (VIV) refers to the vertical resonance phenomenon that occurs in a bridge when pulsating wind passes over it and causes vortices to detach. In recent years, VIV events have been observed in numerous long-span bridges, leading to fatigue damage to the bridge structure and posing risks to driving safety. The advancement of technologies such as structural health monitoring (SHM), machine learning, and big data has opened up new research avenues for the intelligent identification of VIV in bridges. Machine learning algorithms can accurately identify the VIV events from historical data accumulated by SHM systems, thus providing an effective method for VIV recognition. Nevertheless, the existing identification methods have limitations, particularly in their applicability to bridges lacking historical VIV data. This study introduces an adaptive VIV recognition method in the main girders of long-span suspension bridges based on Transfer Component Analysis (TCA). The method can accurately identify VIV patterns in real-time or in historical data, even when specific VIV data are not available for the target bridge. The proposed method exhibits suitability for multiple long-span bridges. Experimental validation is performed using the SHM datasets from two long-span suspension bridges. The results show that the proposed VIV identification method can recognize more VIV samples compared to the benchmark model. When using sensor 1 data of bridge B as the source domain to identify the VIV of the L-section of bridge A, the F1 score of the TCA-based method is 0.836, while the F1 score of the benchmark model is 0.165. In the other 11 cases, the F1 score of the proposed model is higher than 0.8, which demonstrates the method's robust generalization capabilities. [ABSTRACT FROM AUTHOR]

Scholars consider the rise of factional politics as key to understanding party politics during the Maoist period (1949–1976). This article conducts a historical inquiry into the factional politics at the Lushan Conference of 1959. It argues that the very concept of factionalism, adopted not only by Mao Zedong but by all the conference participants, including those accused of being faction members, was created in line with a script generated by Mao to resolve the collective action problems facing the party. This script led the participants at the Lushan Conference to reimagine themselves as engaged in factional struggle within the party, suggesting to each of them the roles they should play as part of that imagined struggle. This article challenges the individualist perspective that takes factional exclusion as a strategic means employed by actors to attain personal goals when competing with others and sheds light on the imaginary and performative features of the CCP's central decision-making dynamics. [ABSTRACT FROM AUTHOR]

Protein aggregation has been proved to be a pathological basis accounting for neuronal death caused by either transient global ischemia or oxygen glucose deprivation (OGD), and inhibition of protein aggregation is emerging as a potential strategy of preventing brain damage. Trehalose was found to inhibit protein aggregation caused by neurodegenerative diseases via induction of autophagy, whereas its effect is still elusive on ischemia-induced protein aggregation. In this study, we investigated this issue by using rat model of transient global ischemia and SH-SY5Y model of OGD. We found that pretreatment with trehalose inhibited transient global ischemia-induced neuronal death in the hippocampus CA1 neurons and OGD-induced death in SH-SY5Y cells, which was associated with inhibition of the formation of ubiquitin-labeled protein aggregates and preservation of proteasome activity. In vitro study showed that the protection of trehalose against OGD-induced cell death and protein aggregation in SH-SY5Y cells was reversed when proteasome activity was inhibited by MG-132. Further studies revealed that trehalose prevented OGD-induced reduction of proteasome activity via suppression of both oxidative stress and endoplasmic reticulum stress. Particularly, our results showed that trehalose inhibited OGD-induced autophagy. Therefore, we demonstrated that proteasome dysfunction contributed to protein aggregation caused by ischemic insults and trehalose prevented protein aggregation via preservation of proteasome activity, not via induction of autophagy. [ABSTRACT FROM AUTHOR]

Background and Purpose: Shikonin was reported to induce necroptosis in leukemia cells, but apoptosis in glioma cell lines. Thus, it is needed to clarify whether shikonin could cause necroptosis in glioma cells and investigate its underlying mechanisms. Methods: Shikonin and rat C6 glioma cell line and Human U87 glioma cell line were used in this study. The cellular viability was assayed by MTT. Flow cytometry with annexin V-FITC and PI double staining was used to analyze cellular death modes. Morphological alterations in C6 glioma cells treated with shikoinin were evaluated by electronic transmission microscopy and fluorescence microscopy with Hoechst 33342 and PI double staining. The level of reactive oxygen species was assessed by using redox-sensitive dye DCFH-DA. The expressional level of necroptosis associated protein RIP-1 was analyzed by western blotting. Results: Shikonin induced cell death in C6 and U87 glioma cells in a dose and time dependent manner. The cell death in C6 and U87 glioma cells could be inhibited by necroptosis inhibitor necrotatin-1, not by pan-caspase inhibitor z-VAD-fmk. Shikonin treated C6 glioma cells presented electron-lucent cytoplasm, loss of plasma membrane integrity and intact nuclear membrane in morphology. The increased ROS level caused by shikonin was attenuated by necrostatin-1 and blocking ROS by anti-oxidant NAC rescued shikonin-induced cell death in both C6 and U87 glioma cells. Moreover, the expressional level of RIP-1 was up-regulated by shikonin in a dose and time dependent manner as well, but NAC suppressed RIP-1 expression. Conclusions: We demonstrated that the cell death caused by shikonin in C6 and U87 glioma cells was mainly via necroptosis. Moreover, not only RIP-1 pathway, but also oxidative stress participated in the activation of shikonin induced necroptosis. [ABSTRACT FROM AUTHOR]

Background and Purpose: Complications due to brain edema and breakdown of blood brain barrier are an important factor affecting the treatment effects of patients with severe carotid stenosis. In this study, we investigated the protective effects of ischemic postconditioning on brain edema and disruption of blood brain barrier via establishing rat model of hypoperfusion due to severe carotid stenosis. Methods: Wistar rat model of hypoperfusion due to severe carotid stenosis was established by binding a stainless microtube to both carotid arteries. Ischemic postconditioning procedure consisted of three cycles of 30 seconds ischemia and 30 seconds reperfusion. Brain edema was evaluated by measuring cerebral water content, and blood brain barrier permeability was assayed by examining cerebral concentration of Evans' Blue (EB) and fluorescein sodium (NaF). ELISA was used to analyze the expression of MMP-9, claudin-5 and occludin. The activity and location of MMP-9 was analyzed by gelatin zymography and in situ zymography, respectively. The distribution of tight junction proteins claudin-5 and occludin was observed by immunohistochemistry. Results: The increased brain water content and cerebral concentration of EB and NaF were suppressed by administration of ischemic postconditioning prior to relief of carotid stenosis. Zymographic studies showed that MMP-9 was mainly located in the cortex and its activity was significantly improved by relief of carotid stenosis and, but the elevated MMP-9 activity was inhibited markedly by ischemic postconditioning. Immunohistochemistry revealed that ischemic postconditioning improved the discontinuous distribution of claudin-5 and occludin. ELISA detected that the expression of up-regulated MMP-9 and down-regulated claudin-5 and occludin caused by carotid relief were all attenuated by ischemic postconditioning. Conclusions: Ischemic postconditioning is an effective method to prevent brain edema and improve BBB permeability and could be used during relief of severe carotid stenosis. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of inhalation of hydrogen gas on cognitive impairment induced by transient cerebral ischemia and its potential mechanism. Methods: Two-vessel occlusion rat model was used to produce 10-minute transient global cerebral ischemia. One hundred and twenty male Wistar rats were randomly divided into sham, sham+H2, ischemia, and ischemia+H2 groups (n=30 each group). Inhalation of 2% hydrogen gas was performed immediately at the end of operation and lasted for 3 hours. Cognitive function of rats was evaluated via Morris water maze. Neuronal damage in the CA1 region was quantified according to their morphological changes revealed by hematoxylin-eosin staining. The levels of oxidative stress products malondialdehyde (MDA) and 8-iso-prostaglandin F2alpha, and the activities of anti-oxidative enzymes catalase and superoxide dismutase were measured to investigate the effects of inhalation of hydrogen gas on oxidative stress. Results: Inhalation of hydrogen gas decreased significantly the average latency of the ischemic rats in finding hidden platform and elongated markedly their retention in the target quadrant. The neuronal density 3.3±2.1 cells/mm in CA1 region of the ischemic rats increased to 21.7±2.6 cells/mm after they were treated with hydrogen gas. Moreover, hydrogen gas made higher levels of MDA and 8-iso-PGF2α in the ischemic rats attenuate to 3.2±0.2, 3.5±0.5, 3.4±0.3 and 26.4±2.3, 28.2±2.6, 26.8±2.1 at reperfusion 4, 24, and 72 hours, respectively (P,0.01 versus ischemia group at each indicated time). By contrast, the activities of superoxide dismutase and catalase damaged by ischemia/reperfusion recovered to 129.7±14.8, 100.5±12.2 and 11.4±0.8, 9.6±1.1 at reperfusion 24 and 72 hours, respectively (P<0.01 versus ischemia group at each indicated time). Conclusion: Inhalation of hydrogen gas could attenuate cognitive impairment in the ischemic rats. This protection is associated with decreased neuronal death in CA1 region and inhibition of oxidative stress. [ABSTRACT FROM AUTHOR]

Glioma still remains a major health problem in the world. Celastrol has been proved to be an effective natural proteasome inhibitor and was used for treatment of autoimmune disease, chronic inflammation and neurodegenerative disease. However, its effect on glioma is unclear. In this study, we investigated the therapeutic effects of celastrol on C6 glioma cells. The results demonstrated that celastrol inhibited cell proliferation in a time- and dose-dependent manner, suppressed proteasome chymotrypsin-like activity and induced apoptosis and cell cycle arrest at G2/M phase in C6 cells. Proapoptosis proteins bax and caspase-3 were up-regulated, as well as cell cycle G2/M-related proteins cyclin B1, p21 and p27. Conversely, anti-apoptosis proteins bcl-2 and XIAP and cell cycle regulator cyclin-dependent kinase 2 were down-regulated. Taken together, our data suggest that celastrol can suppress proteasome activity and induce apoptosis and cell cycle arrest in C6 glioma cells, which make it be a potential drug for glioma. [ABSTRACT FROM AUTHOR]

Abstract: We describe a rare scalp malignant peripheral nerve sheath tumor (MPNST) with cranial destruction and intracranial extension in a 52-year-old male with neurofibromatosis type 1 (NF1). The scalp tumor measured 22cm×18cm, with local surface ulceration. Skin examination revealed many café-au-lait spots and small, hard dermal nodules on the trunk. CT scans revealed the scalp tumor to have heterogeneous density with partial destruction of the right parietal cranium; on T1-weighted MRI the scalp tumor displayed heterogeneous hypointensity, whereas on T2-weighted and fluid-attenuated inversion recovery MRI it was hyperintense. The tumor was excised totally and the scalp reconstructed using a skin flap isolated from the lateral aspect of the left thigh. Histological examination confirmed that the tumor was an MPNST. The patient recovered uneventfully and was well at the 6-month follow-up, with no local or other tumor recurrence noted. [ABSTRACT FROM AUTHOR]

Summary: Brain ischemia has been an important risk factor for human being health, there is no effective medicine can be used to protect delayed neuronal injury or death secondary to blood reperfusion following ischemia. Recent discovery shows protein aggregation is an important factor resulting in ischemia-induced neuron death. Therefore, we propose the hypothesis that inhibiting protein aggregation may be an effective way to prevent delayed neuronal death after transient ischemia. At present, in vitro studies show some chemicals such as 4PBA (sodium 4-phenylbutyrate) and trehalose have the features of antagonizing protein aggregation in vitro. Moreover, polyQ-binding peptide (QBP1), geldanamycin, amino acids and amino acid derivatives have been also used in vitro to decrease aggregation and to increase protein stability. Although in vivo and systematical study should be performed to evaluate their effects of anti-protein aggregation, this enlightening us on using them to protect ischemic-induced neuronal death, and find new potential chemicals or methods which could be effective in keeping protein stable and prevent forming aggregates. [Copyright &y& Elsevier]

Chromatinolysis refers to enzymatic degradation of nuclear DNA and is regarded as one of the crucial events leading to cell death. Mixed-lineage kinase domain-like protein (MLKL) has been identified as a key executor of necroptosis, but it remains unclear whether MLKL contributes to necroptosis via regulation of chromatinolysis. In this study, we find that shikonin induces MLKL activation and chromatinolysis in glioma cells in vitro and in vivo, which are accompanied with nuclear translocation of AIF and γ-H2AX formation. In vitro studies reveal that inhibition of MLKL with its specific inhibitor NSA or knockdown of MLKL with siRNA abrogates shikonin-induced glioma cell necroptosis, as well as chromatinolysis. Mechanistically, activated MLKL targets mitochondria and triggers excessive generation of mitochondrial superoxide, which promotes AIF translocation into nucleus via causing mitochondrial depolarization and aggravates γ-H2AX formation via improving intracellular accumulation of ROS. Inhibition of nuclear level of AIF by knockdown of AIF with siRNA or mitigation of γ-H2AX formation by suppressing ROS with antioxidant NAC effectively prevents shikonin-induced chromatinolysis. Then, we found that RIP3 accounts for shikonin-induced activation of MLKL, and activated MLKL reversely up-regulates the protein level of CYLD and promotes the activation of RIP1 and RIP3. Taken together, our data suggest that MLKL contributes to shikonin-induced glioma cell necroptosis via promotion of chromatinolysis, and shikonin induces a positive feedback between MLKL and its upstream signals RIP1 and RIP3. [ABSTRACT FROM AUTHOR]

RSL3 is a type of small molecular compound which can inactivate glutathione peroxidase 4 (GPX4) and induce ferroptosis, but its role in glioma cell death remains unclear. In this study, we found RSL3 inhibited the viabilities of glioma cells and induced glioma cell death in a dose-dependent manner. In vitro studies revealed that RSL3-induced cell death was accompanied with the changes of autophagy-associated protein levels and was alleviated by pretreatment of 3-Methyladenine, bafilomycin A1 and knockdown of ATG5 with siRNA. The ATP and pyruvate content as well as the protein levels of HKII, PFKP, PKM2 were decreased in cells treated by RSL3, indicating that RSL3 induced glycolysis dysfunction in glioma cells. Moreover, supplement of exterior sodium pyruvate, which was a final product of glycolysis, not only inhibited the changes of autophagy-associated protein levels caused by RSL3, but also prevented RSL3-induced cell death. In vivo data suggested that the inhibitory effect of RSL3 on the growth of glioma cells was associated with glycolysis dysfunction and autophagy activation. Taken together, RSL3 induced autophagic cell death in glioma cells via causing glycolysis dysfunction. • RSL3 inhibited glioma cellular viabilities and induced glioma cell death. • RSL3 activated autophagy in glioma cells in vivo and in vitro. • RSL3 induced glycolysis dysfunction in glioma cells in vivo and in vitro. • Supplement of pyruvate prevented RSL3-induced autophagic cell death. [ABSTRACT FROM AUTHOR]

Ferroptosis is a form of programmed cell death decided by iron-dependent lipid peroxidation, but its role in glioma cell death remains unclear. In this study, we found Pseudolaric acid B (PAB) inhibited the viabilities of glioma cells in vitro and in vivo, which was accompanied by abnormal increases of intracellular ferrous iron, H2O2 and lipid peroxidation, as well as depletion of GSH and cysteine. In vitro studies revealed that the lipid peroxidation and the cell death caused by PAB were both inhibited by iron chelator deferoxamine, but exacerbated by supplement of ferric ammonium citrate. Inhibition of lipid peroxidation with ferrostatin-1 or GSH rescued PAB-induced cell death. Morphologically, the cells treated with PAB presented intact membrane, shrunken mitochondria with increased membrane density, and normal-sized nucleus without chromatin condensation. Mechanistically, PAB improved intracellular iron by upregulation of transferrin receptor. The increased iron activated Nox4, which resulted in overproduction of H2O2 and lipid peroxides. Moreover, PAB depleted intracellular GSH via p53-mediated xCT pathway, which further exacerbated accumulation of H2O2 and lipid peroxides. Thus, PAB triggers ferroptosis in glioma cells and is a potential medicine for glioma treatment. [ABSTRACT FROM AUTHOR]

RIP1 and RIP3 are necroptosis initiators, but their roles in regulation of glycolysis remain elusive. In this study, we found shikonin activated RIP1 and RIP3 in glioma cells in vitro and in vivo, which was accompanied with glycolysis suppression. Further investigation revealed that shikonin-induced decreases of glucose-6-phosphate and pyruvate and downregulation of HK II and PKM2 were significantly prevented when RIP1 or RIP3 was pharmacologically inhibited or genetically knocked down with SiRNA. Moreover, shikonin also triggered accumulation of intracellular H2O2 and depletion of GSH and cysteine. Mitigation of intracellular H2O2 via supplement of GSH reversed shikonin-induced glycolysis suppression. The role of intracellular H2O2 in regulation of glycolysis suppression was further confirmed in the cells treated with exogenous H2O2. Notably, inhibition of RIP1 or RIP3 prevented intracellular H2O2 accumulation, which was correlated with preventing shikonin-induced downregulation of x-CT and depletion of GSH and cysteine. In addition, supplement of pyruvate effectively inhibited shikonin- or exogenous H2O2-induced accumulation of intracellular H2O2 and glioma cell death. Taken together, we demonstrated in this study that RIP1 and RIP3 contributed to shikonin-induced glycolysis suppression via increasing intracellular H2O2. [ABSTRACT FROM AUTHOR]

Background: To explore the epidemiology, clinical features, risk indicators, and long-term outcomes of neurological complications caused by veno-arterial extracorporeal membrane oxygenation (V-A ECMO). Methods: We retrospectively analyzed 60 adult patients who underwent V-A ECMO support in our unit from February 2012 to August 2020. These patients were separated into the neurological complications group (NC group) and the non-neurological complications group (nNC group). The differences in basic data and ECMO data between the two groups were compared. The data of long-term neurological prognosis were collected by telephone follow-up. Results: Thirty-nine patients (65.0%) had neurological complications. There were significant differences between the two groups in terms of median age, hypertension, median blood urea nitrogen, median troponin I (TNI), median lactic acid, pre-ECMO percutaneous coronary intervention, continuous renal replacement therapy (CRRT), median Sequential Organ Failure Assessment score, median Acute Physiology and Chronic Health Evaluation II score, median peak inspiratory pressure, median positive end expiratory pressure, and median fresh frozen plasma ( P < 0.05). The median Intensive Care Unit length of stay (ICU LOS), 28-day mortality, median post-ECMO vasoactive inotropic score, non-pulsate perfusion (NP), and median ECMO duration of the NC group were significantly higher than those of the nNC group ( P < 0.05). Furthermore, multiple logistic regression analysis revealed that TNI ( P = 0.043), CRRT ( P = 0.047), and continuous NP > 12 h ( P = 0.043) were independent risk indicators for neurological complications in patients undergoing ECMO. Forty-four patients (73.3%) survived after discharge, and 38 patients (63.3%) had Cerebral Performance Category score of 1-2. And there were significant differences between the two groups in long-term neurological outcomes after discharge for 6 months ( P < 0.05). Conclusion: The incidence of neurological complications was higher in patients undergoing V-A ECMO and was closely related to adverse outcomes (including ICU LOS and 28-day mortality). TNI, CRRT, and continuous NP > 12 h were independent risk indicators for predicting neurological complications in ECMO supporting patients. And the neurological complications of patients during ECMO support had significant adverse effect on long-term surviving and neurological outcomes of patients after discharge for 6 months., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Luo, Gu, Wen, Li, Peng, Zhu, Hu and Xi.)

Oxidative stress, which is characterized by excessive production of reactive oxygen species (ROS), is a common pathway that results in neuronal injury or death due to various types of pathological stress. Although lycopene has been identified as a potent antioxidant, its effect on hydrogen peroxide (H2O2)‑induced neuronal damage remains unclear. In the present study, pretreatment with lycopene was observed to protect SH‑SY5Y neuroblastoma cells against H2O2‑induced death via inhibition of apoptosis resulting from activation of caspase‑3 and translocation of apoptosis inducing factor (AIF) to the nucleus. Furthermore, the over‑produced ROS, as well as the reduced activities of anti‑oxidative enzymes, superoxide dismutase and catalase, were demonstrated to be alleviated by lycopene. Additionally, lycopene counteracted H2O2‑induced mitochondrial dysfunction, which was evidenced by suppression of mitochondrial permeability transition pore opening, attenuation of the decline of the mitochondrial membrane potential, and inhibition of the increase of Bax and decrease of Bcl‑2 levels within the mitochondria. The release of cytochrome c and AIF from the mitochondria was also reduced. These results indicate that lycopene is a potent neuroprotectant against apoptosis, oxidative stress and mitochondrial dysfunction, and could be administered to prevent neuronal injury or death.

Glioma is a type of tumor derived from glial cells, which is associated with a high level of incidence and mortality. At present, the generation of a fast and efficient method to evaluate the malignancy grade of glioma is required. Cancer stem cells (CSCs) are currently attracting attention in oncological studies; therefore, the present study aimed to investigate novel biomarkers of glioma CSCs, in order to provide new criteria for the grading of glioma. The mRNA expression levels of CD133, (sex determining region Y)-box 2, nestin, vascular endothelial growth factor (VEGF) and phosphoinositide-3-kinase (PI3K) were detected in 15 human samples of high-malignancy glioma and 12 human samples of low-malignancy glioma in vitro . The mRNA expression levels of VEGF and PI3K were higher in the high-malignancy group, as compared with in the low-malignancy group. In conclusion, the mRNA expression levels of VEGF and PI3K in glioma CSCs may be considered a novel criteria for the grading of glioma.

Objective: To examine the effect and underlying mechanism of action of the proteasome inhibitor lactacystin on glioma, in vitro and in vivo., Methods: Rat C6 glioma cells were cultured with or without lactacystin. Cell proliferation, apoptosis and mitochondrial membrane potential were determined. A glioma xenograft model was established in mice and animals were treated with 0, 1 or 5 µg/20 g body weight lactacystin for 7 days. Animals were sacrificed on day 17 after completion of treatment. Apoptosis in tumour tissue was examined by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Levels of B cell lymphoma 2 (Bcl-2), and Bcl2-associated X protein (Bax) protein and mRNA, were determined in C6 cells and tumour tissues., Results: Lactacystin significantly inhibited the proliferation of C6 cells, increased apoptosis and reduced mitochondrial membrane potential in vitro, and suppressed tumour growth in vivo. Lactacystin increased the ratio of Bax to Bcl-2 at the mRNA and protein levels, both in vitro and in vivo., Conclusions: The effects of lactacystin are associated with apoptosis induction. Proteasome inhibition may represent an effective treatment option for glioma.

The effects of early relief of heavy bilateral carotid stenosis and ischemic postconditioning on hippocampus CA1 neurons are still unclear. In this study, we used a rat model to imitate severe bilateral carotid stenosis in humans. The rats were divided into sham group, carotid stenosis group, stenosis relief group and ischemic postconditioning group. Ischemic postconditioning consisted of three cycles of 30 s ischemia and 30 s reperfusion. The cerebral blood flow was measured with a laser Doppler flowmeter. Neuronal death in the CA1 region was observed by hematoxylin-eosin staining, and the number of live neurons was assessed by cell counting under a light microscope. The levels of oxidative products MDA and 8-iso-PGF2α, inflammatory factors IL-1β and TNF-α, and the activities of anti-oxidative enzymes SOD and CAT were assayed by specific enzyme-linked immunosorbent assay (ELISA) kits, respectively. We found that relief of carotid stenosis and ischemic postconditioning could increase cerebral blood flow. When stenosis was relieved, the percentage of live neurons was 66.6% ± 6.2% on day 3 and 62.3% ± 9.8% on day 27, which was significantly higher than 55.5% ± 4.8% in stenosis group. Ischemic postconditioning markedly improved the live neurons to 92.5% ± 6.7% on day 3 and 88.6% ± 9.1% on day 27. Further study showed that, neuronal death caused by relief of stenosis is associated with increased oxidative stress and enhanced inflammatory response, and the protection of ischemic postconditioning is related to inhibition of oxidative stress and suppression of inflammatory response.

Formation of tuberculoma is a rare response of neurotuberculosis in patients regularly and adequately treated with anti-tuberculous drugs. We report a 13-year-old girl with two tuberculomas which formed in the dorsal part of the medulla oblongata during chemotherapy for tuberculous meningitis. The tuberculomas were both removed via a suboccipital midline approach and were demonstrated by pathological findings but the girl died of cardiac arrest that was thought to be caused by postoperative medulla oblongata oedema. In combination with a literature review, we discuss the clinical features and treatment options of brainstem tuberculomas.

Objective: High dose fluorescein sodium has been utilized for fluorescence-guided tumor resection with conflicting reports on the efficacy of this procedure. The aim of this study was to reevaluate the utility and clinical limitations of using fluorescein sodium for the treatment and resection of glioma brain tumors., Methods: Patients diagnosed with glioma were divided into two groups with a total of 22 patients enrolled in the study: 1) the study group (n=10), patients that received intravenous injection of fluorescein sodium and 2) the control group (n=12), patients that did not receive injections during surgical resection. Quality of life was evaluated according to Karnofsky Performance Scale (KPS) score and neurological status. Fluorescein sodium was intravenously injected at a dose of 15-20mg/kg of body weight. Glioma resection was evaluated preoperative and postoperatively with enhanced Magnetic Resonance Imaging (MRI)., Results: Significant differences in the gross total resection (GTR) rates were observed between the two patient groups (Fisher's Exact Test p=0.047). Progressive free survival was significantly longer in the study group (Student's T-Test p=0.033) as well as in the GTR group (Student's T-Test p=0.0001) compared to the control and non-GTR groups, respectively. Three patients in the study group and four patients in the control group had transient neurological deterioration. One patient in the control group had permanent hemiplegia., Conclusion: The intraoperative utility of using fluorescein sodium can significantly increase the GTR rate without obvious deterioration. In addition, we find that it is better to apply the fluorescein sodium in the cases with BBB (blood-brain barrier) disruption, which had been enhanced in preoperative MRI.

Intracranial dermoid cysts with hemorrhage are fairly rare. Herein, we reported a 28-year-old female patient with a cerebellar dermoid cyst, which was found accidently on neuro-imaging after head trauma. MR scanning revealed that the lesion was located within the cerebellar vermis and was measured 3.5cm×3.9cm×3.0cm, with hyper-intensity on T1WI and hypo-intensity on T2WI. However, on CT imaging, it showed hyper-dense signals. It was removed completely via midline sub-occipital approach under surgical microscope. Histological examination proved it was a dermoid cyst with internal hemorrhage. In combination with literature review, we discussed the factors that might be responsible for the hemorrhage within dermoid cysts.

Cerebral hyperperfusion syndrome is a serious complication of revascularization after carotid endarterectomy, extracranial-intracranial bypass surgery, or stent placement. The mechanisms underlying cerebral hyper-perfusion syndrome are mainly ascribed to the dysfunction of cerebral auto-regulation to blood flow and injury of the endothelia in blood vessels. Although blood pressure control is often used to prevent cerebral hyper-perfusion after revascularization, cases of cerebral hyperperfusion are still reported in the literature. Current animal studies have shown that ischemic post-conditioning has protective effects on brain tissue, and further studies also showed that it had positive effects on human brachial artery and heart. Therefore, we propose the hypothesis that ischemic post-conditioning could be used to prevent cerebral hyperperfusion syndrome following revascularization. Although the mechanism of ischemic post-conditioning and its clinical application should be further investigated, it has shown its potential effectiveness as a feasible method for prevention of cerebral hyperperfusion syndrome.

A 50-year-old male presented with a recurrent epidermoid cyst with malignant transformation into squamous cell carcinoma. The patient was first hospitalized for intermittent seizures in 2000. Computed tomography (CT) showed a hypodense lesion with enhanced capsule but no peripheral edema in the right temporal lobe. Craniotomy was performed and the lesion was completely removed. The histological diagnosis was epidermoid cyst. Six years later, the patient experienced blurred vision and hemiparesis in the left extremities. CT showed a hyperdense mass with peripheral edema in the right temporal lobe. Repeat CT 2 months later revealed a larger mass. The recurrent lesion was removed, and the histological diagnosis was squamous cell carcinoma. Intracranial epidermoid cyst is a benign tumor which often appears hypodense on CT, so change to hyperdensity in the recurrent tumor may indicate malignant transformation.

Objective: To describe the transvenous catheterization technique for the treatment of cavernous sinus dural arteriovenous fistulas (CSdAVFs), including its indications, complications and efficacy., Methods: Eight patients with symptomatic CSdAVFs were treated by endovascular embolization with platinum coils, via the inferior petrosal sinus (IPS) in 6 patients, and via the Sylvian vein after surgical exposure in other 2 patients., Results: Complete angiographic resolution of the fistula was obtained in six patients immediately after the procedures, and a complete resolution of symptoms and signs was achieved in all patients. The residual fistulas in two patients disappeared completely in the follow-up angiography., Conclusion: Transvenous embolization is a useful and safe approach in the management of CSdAVFs.