Cysteine and glycine-rich protein 2 is crucial for maintaining the malignant phenotypes of gliomas through its action on Notch signalling cascade.

Cysteine and glycine-rich protein 2 (CSRP2) is expressed differently in numerous cancers and plays a key role in carcinogenesis. However, the role of CSRP2 in glioma is unknown. This study sought to determine the expression profile and clinical significance of CSRP2 in glioma and explore its biological functions and mechanisms via lentivirus-mediated CSRP2 silencing experiments. Increased CSRP2 was frequently observed in gliomas, which was associated with clinicopathological characteristics and an unfavourable prognosis. Decreasing CSRP2 led to the suppression of malignant proliferation, metastasis and stemness in glioma cells while causing hypersensitivity to chemotherapeutic drugs. Mechanistic investigations revealed that CSRP2 plays a role in mediating the Notch signalling cascade. Silencing CSRP2 decreased the levels of Notch1, cleaved Notch1, HES1 and HEY1, suppressing the Notch signalling cascade. Reactivation of Notch markedly diminished the tumour-inhibiting effects of CSRP2 silencing on the malignant phenotypes of glioma cells. Notably, CSRP2-silencing glioma cells exhibited reduced potential in the formation of xenografts in nude mice in vivo, which was associated with an impaired Notch signalling cascade. These results showed that CSRP2 is overexpressed in glioma and has a crucial role in sustaining the malignant phenotypes of glioma, suggesting that targeting CSRP2 could be a promising strategy for glioma treatment.

Inhibition of PTPN21 has antitumor effects in glioma by restraining the EGFR/PI3K/AKT pathway.

Protein tyrosine phosphatase non-receptor type 21 (PTPN21) has been recognised as a new tumour-associated protein that is implicated in diverse tumours. However, the correlation between PTPN21 and glioma remains unaddressed. This investigation focused on the relevance of PTPN21 in glioma. The Cancer Genome Atlas (TCGA) analysis identified PTPN21 as being up-regulated in glioma tissue. The elevation of PTP21 in glioma was validated by evaluating clinical specimen. Kaplan-Meier plot analysis revealed that a high PTPN21 level predicted poor survival rate in glioma patient. Silencing of PTPN21 produced remarkable anticancer effects in glioma cells including proliferation inhibition, cell cycle arrest, metastasis suppression and enhanced chemosensitivity. Mechanistic studies uncovered that PTPN21 contributes to mediation of the phosphatidyl-inositole-3 kinase (PI3K)/AKT pathway via the regulation of epidermal growth factor receptor (EGFR). Restraint of EGFR diminished PTPN21 overexpression-induced promoting effect on PI3K/AKT pathway. Reactivation of AKT reversed PTPN21 silencing-evoked antitumor effect. The tumorigenic potential of PTPN21-silenced glioma cells in vivo was markedly compromised. In summary, this study demonstrates that silencing of PTPN21 produces remarkable anticancer effects in glioma by restraining the EGFR/PI3K/AKT pathway.

Isorhynchophylline Relieves Ferroptosis-Induced Nerve Damage after Intracerebral Hemorrhage Via miR-122-5p/TP53/SLC7A11 Pathway.

Isorhynchophylline (IRN), a component of traditional Chinese herb Uncaria rhynchophylla, possesses strong antioxidant activity. Ferroptosis induced by iron overload causes cell oxidative stress after intracerebral hemorrhage (ICH). Therefore, this study aims to explore the effects of IRN on the ferroptosis following ICH. In this study, mouse hippocampal HT-22 cells were treated with ferric ammonium citrate (FAC) alone or together with IRN, and we found IRN reduced the FAC-induced cell damage. Then, cells were treated with IRN following treatment with FAC after transfection with miR-122-5p inhibitor, and the results showed IRN reduced the FAC-induced decrease of miR-122-5p levels and relieved the ferroptosis by detecting ferroptotic marker proteins, iron ion concentration and oxidative stress level; after transfection with miR-122-5p inhibitor, the protective effects of IRN against FAC-induced ferroptosis in these cells were weakened. TP53 (also known as p53) was verified as a target of miR-122-5p by using dual luciferase reporter assay, and restoration of TP53 attenuated the effects of miR-122-5p on ferroptotic marker proteins expression, iron ion concentration and lipid ROS levels, as well as solute carrier family seven member 11 (SLC7A11) mRNA expression. SLC7A11 siRNA reversed the inhibitory effects of IRN on FAC-induced ferroptosis and oxidative stress levels. Subsequently, IRN increased the mNSS score, and decreased brain water content and EB content in ICH model. Moreover, IRN decreased ferroptosis and lipid ROS level, upregulated the expression of miR-122-5p and SLC7A11 mRNA, and inhibited TP53 expression. Our findings reveal that IRN protects neurocyte from ICH-induced ferroptosis via miR-122-5p/TP53/SLC7A11 pathway, which may provide a potential therapeutic mechanism for ICH.

Management of incidental anterior skull base large and giant meningiomas in elderly patients.

INTRODUCTION: The incidence of meningiomas among the elderly is considered to be high, and are at increased risk of severe morbidity and mortality following surgery due to their aging physiology and unexpected comorbidities. This study aimed to evaluate the optimal management strategies of meningiomas in elderly patients. METHODS: We retrospectively analyzed 150 patients with incidental large (≥ 3 cm) and giant (≥ 6 cm) anterior skull base meningiomas from 2009 to 2018. These patients were divided into elderly group (≥ 65 years, n = 70) and younger group (< 65 years, n = 80). Information of patients with regard to their medical records, operative details, relevant imaging, and follow-up data were obtained from their respective electronic medical records. RESULTS: The elderly patients had significantly longer length of hospital stay (15.9 ± 3.5) compared to younger patients (13.6 ± 3.6, P < 0.001). Karnofsky Performance Scale (KPS) at discharge was significantly lower in elderly group when compared to younger group (P = 0.04). However, the KPS at 1-year after surgery was similar between the two groups. In addition, there was no significant difference in the incidence of surgical complications between the two groups. Multivariate regression analysis of postoperative complications revealed blood loss ≥ 800 mL (P = 0.007) and BMI (< 18.5 or ≥ 24, P < 0.001) as risk factors, rather than age. CONCLUSIONS: Surgical resection in elderly patients with incidental anterior skull base large and giant meningiomas is considered to be a safe and effective therapeutic option owing to acceptable mortality, postoperative complications and postoperative clinical outcomes.

Long non-coding RNA MEG3 regulates proliferation, apoptosis, and autophagy and is associated with prognosis in glioma.

PURPOSE: Accumulating evidence indicates that dysregulated long noncoding RNAs (lncRNAs) play critical roles in tumorigenesis and cancer progression. LncRNA-maternally expressed gene 3 (MEG3) has been shown to be involved in the initiation and development of several cancers, including glioma. However, the clinical prognostic value of MEG3 in glioma has not yet been fully elucidated. METHODS: The expression levels of MEG3 were detected in 79 glioma tissues and adjacent normal brain tissues, as well as, glioma cells and normal human astrocytes by qRT-PCR. Kaplan-Meier and Cox regression methods were utilized for the survival analysis. MTT assay, flow cytometry, and immunofluorescence assay were carried out to detect the impact of MEG3 on glioma cell proliferation, apoptosis, and autophagy. RESULT: The current results showed that MEG3 expression was significantly downregulated in glioma tissues and cell line and negatively correlated with WHO grade in glioma patients. Low MEG3 expression was significantly associated with the advanced WHO grade, low Karnofsky performance score (KPS), IDH wild-type, and tumor recurrence. Patients displaying a low expression of MEG3 contributed to poor overall survival. The downregulated level of MEG3, advanced WHO grade, low KPS, IDH wild-type, and tumor recurrence were independent poor prognostic indicators in glioma patients. The in vitro experiments demonstrated that the MEG3 overexpression remarkably suppressed the proliferation while facilitating apoptosis and autophagy in glioma cells. CONCLUSIONS: These findings indicated a critical role of MEG3 in glioma cell proliferation, apoptosis, and autophagy. Also, the gene was found to be significantly associated with the prognosis in glioma patients. Thus, it might provide a new target for predicting prognosis and therapeutic intervention in glioma.

Clinical analysis and treatment of symptomatic intracranial hemorrhage after deep brain stimulation surgery.

BACKGROUND: Symptomatic intracranial hemorrhage (ICH) may lead to permanent neurological disability of patients and has impeded the extensive clinical application of deep brain stimulation (DBS). The present study was conducted to discuss the incidence, prevention, and treatment of symptomatic ICH after DBS surgery. METHODS: From January 2009 to December 2014, 396 patients underwent DBS with a total of 691 implanted leads. In all, 10 patients had symptomatic ICH. We analyzed these cases' clinical characteristics, including comorbid diagnoses and coagulation profile. We described the onset of ICH, imaging features, clinical manifestations, treatment, neurological impairment, and outcome of DBS. RESULTS: Of the 10 patients with symptomatic ICH, 2 had hypertension. Three cases of ICH occurred within 12 h of the procedure; four cases within 24 h. Five experienced grand mal seizures concurrently with hemorrhage. Unilateral frontal lobe hemorrhage occurred in all cases. In seven cases, hematomas occurred around the electrodes. Some hematomas were not well-circumscribed and had perihematomal edema. Conservative therapy was administered to 8 patients, and 2 patients underwent craniotomy and hematoma evacuation. All electrodes were successfully preserved. Neurological dysfunction in all patients gradually improved. Nine patients ultimately experienced effective symptom relief of Parkinson's disease with DBS. CONCLUSIONS: Symptomatic ICH should be identified as soon as possible after implantation surgery and treated effectively to limit neurological deficit and preserve DBS leads.

Inhibitory effects of low decibel infrasound on the cardiac fibroblasts and the involved mechanism.

INTRODUCTION: Infrasound is a mechanical vibration wave with frequency between 0.0001 and 20 Hz. It has been established that infrasound of 120 dB or stronger is dangerous to humans. However, the biological effects of low decibel infrasound are largely unknown. The purpose of this study was to investigate the effects of low decibel infrasound on the cardiac fibroblasts. MATERIALS AND METHODS: The cardiac fibroblasts were isolated and cultured from Sprague-Dawley rats. The cultured cells were assigned into the following four groups: control group, angiotensin II (Ang II) group, infrasound group, and Ang II+infrasound group. The cell proliferation and collagen synthesis rates were evaluated by means of [3H]-thymidine and [3H]-proline incorporation, respectively. The levels of TGF-ß were determined by enzyme-linked immunosorbent assay. Moreover, RNAi approaches were used for the analysis of the biological functions of miR-29a, and the phosphorylation status of Smad3 was detected using western blotting analysis. RESULTS: The results showed that low decibel infrasound significantly alleviated Ang II-induced enhancement of cell proliferation and collagen synthesis. DISCUSSION: Compared with the control, Ang II markedly decreased the expression of miR-29a levels and increased the secretion of TGF-ß and phosphorylation of Smad3, which was partly reversed by the treatment with low decibel infrasound. Importantly, knockdown of miR-29a diminished the effects of infrasound on the cardiac fibroblasts. In conclusion, low decibel infrasound inhibits Ang II-stimulated cardiac fibroblasts via miR-29a targeting TGF-ß/Smad3 signaling.

Antioxidant catalase rescues against high fat diet-induced cardiac dysfunction via an IKKß-AMPK-dependent regulation of autophagy.

Autophagy, a conservative degradation process for long-lived and damaged proteins, participates in a variety of biological processes including obesity. However, the precise mechanism of action behind obesity-induced changes in autophagy still remains elusive. This study was designed to examine the role of the antioxidant catalase in high fat diet-induced changes in cardiac geometry and function as well as the underlying mechanism of action involved with a focus on autophagy. Wild-type (WT) and transgenic mice with cardiac overexpression of catalase were fed low or high fat diet for 20 weeks prior to assessment of myocardial geometry and function. High fat diet intake triggered obesity, hyperinsulinemia, and hypertriglyceridemia, the effects of which were unaffected by catalase transgene. Myocardial geometry and function were compromised with fat diet intake as manifested by cardiac hypertrophy, enlarged left ventricular end systolic and diastolic diameters, fractional shortening, cardiomyocyte contractile capacity and intracellular Ca²âº mishandling, the effects of which were ameliorated by catalase. High fat diet intake promoted reactive oxygen species production and suppressed autophagy in the heart, the effects of which were attenuated by catalase. High fat diet intake dampened phosphorylation of inhibitor kappa B kinase ß(IKKß), AMP-activated protein kinase (AMPK) and tuberous sclerosis 2 (TSC2) while promoting phosphorylation of mTOR, the effects of which were ablated by catalase. In vitro study revealed that palmitic acid compromised cardiomyocyte autophagy and contractile function in a manner reminiscent of fat diet intake, the effect of which was significantly alleviated by inhibition of IKKß, activation of AMPK and induction of autophagy. Taken together, our data revealed that the antioxidant catalase counteracts against high fat diet-induced cardiac geometric and functional anomalies possibly via an IKKß-AMPK-dependent restoration of myocardial autophagy. This article is part of a Special Issue entitled: Autophagy and protein quality control in cardiometabolic diseases.

Gas1 up-regulation is inducible and contributes to cell apoptosis in reactive astrocytes in the substantia nigra of LPS and MPTP models.

BACKGROUND: Reactive astrogliosis is a remarkable pathogenetic hallmark of the brains of Parkinson's disease (PD) patients, but its progressive fate and regulation mechanisms are poorly understood. In this study, growth arrest specific 1 (Gas1), a tumor growth suppressor oncogene, was identified as a novel modulator of the cell apoptosis of reactive astrocytes in primary culture and the injured substantia nigra. METHODS: Animal models and cell cultures were utilized in the present study. Lipopolysaccharide (LPS)- and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated animal models were used to detect Gas1 expression in the brain via immunohistochemistry and western blot. Cell cultures were performed to analyze Gas1 functions in the viability and apoptosis of reactive astrocytes and SH-SY5Y cells by double labeling, CCK-8, LDH, TUNEL, flow cytometry, and siRNA knockdown methods. RESULTS: Gas1 expressions were significantly elevated in the majority of the reactive astrocytes of the brains with LPS or MPTP insults. In the injured substantia nigras, GFAP-positive astrocytes exhibited higher levels of cleaved caspase-3. In cell culture, the up-regulated Gas1 expression induced apoptosis of reactive astrocytes that were insulted by LPS in combination with interferon-γ and tumor necrosis factor-a. This effect was confirmed through siRNA knockdown of Gas1 gene expression. Finally and interestingly, the potential underlying signaling pathways were evidently related to an increase in the Bax/Bcl-2 ratio, the abundant generation of reactive oxygen species and the activation of cleaved caspase-3. CONCLUSIONS: This study demonstrated that the up-regulation of inducible Gas1 contributed to the apoptosis of reactive astrocytes in the injured nigra. Gas1 signaling may function as a novel regulator of astrogliosis and is thus a potential intervention target for inflammatory events in PD conditions.

Current status and research progress of minimally invasive treatment of glioma.

Glioma has a high malignant degree and poor prognosis, which seriously affects the prognosis of patients. Traditional treatment methods mainly include craniotomy tumor resection, postoperative radiotherapy and chemotherapy. Although above methods have achieved remarkable curative effect, they still have certain limitations and adverse reactions. With the introduction of the concept of minimally invasive surgery and its clinical application as well as the development and progress of imaging technology, minimally invasive treatment of glioma has become a research hotspot in the field of neuromedicine, including photothermal treatment, photodynamic therapy, laser-induced thermal theraphy and TT-Fields of tumor. These therapeutic methods possess the advantages of precision, minimally invasive, quick recovery and significant curative effect, and have been widely used in clinical practice. The purpose of this review is to introduce the progress of minimally invasive treatment of glioma in recent years and the achievements and prospects for the future.

Progress in the application of ultrasound in glioma surgery.

Brain glioma, which is highly invasive and has a poor prognosis, is the most common primary intracranial tumor. Several studies have verified that the extent of resection is a considerable prognostic factor for achieving the best results in neurosurgical oncology. To obtain gross total resection (GTR), neurosurgery relies heavily on generating continuous, real-time, intraoperative glioma descriptions based on image guidance. Given the limitations of existing devices, it is imperative to develop a real-time image-guided resection technique to offer reliable functional and anatomical information during surgery. At present, the application of intraoperative ultrasound (IOUS) has been indicated to enhance resection rates and maximize brain function preservation. IOUS, which is promising due to its lower cost, minimal operational flow interruptions, and lack of radiation exposure, can enable real-time localization and precise tumor size and form descriptions while assisting in discriminating residual tumors and solving brain tissue shifts. Moreover, the application of new advancements in ultrasound technology, such as contrast-enhanced ultrasound (CEUS), three-dimensional ultrasound (3DUS), noninvasive ultrasound (NUS), and ultrasound elastography (UE), could assist in achieving GTR in glioma surgery. This article reviews the advantages and disadvantages of IOUS in glioma surgery.

Remifentanil protects liver against ischemia/reperfusion injury through activation of anti-apoptotic pathways.

BACKGROUND: Remifentanil protects against ischemia/reperfusion (I/R)-induced organ injury, although its underlying mechanism remains elusive. This study was designed to examine the protective effect of remifentanil preconditioning, if any, against hepatic I/R injury in rats and the underlying mechanism involved. MATERIALS AND METHODS: Adult Sprague-Dawley rats were randomly divided into sham operation (S group), ischemia/reperfusion (I/R group), and remifentanil preconditioning (R group) groups. Rats in the I/R group were subjected to a partial (70%) hepatic ischemia for 45 min, followed by 1 h, 3 h, and 6 h of reperfusion. Rats in the R group received venous injection of remifentanil (2 µg/kg/min) from 30 min prior to hepatic ischemia to the end of ischemia. Hepatic morphology and apoptosis were examined. Markers of liver damage, oxidative stress, and inflammation were evaluated. Mitochondrial function was assessed using mitochondrial membrane potential and appearance of mitochondrial swelling. RESULTS: Compared with the S group, rats in the I/R group displayed a massive degenerative death in liver tissues and significantly enhanced cell apoptosis. Remifentanil preconditioning significantly reduced I/R-induced hepatocyte apoptosis. In addition, remifentanil protected against I/R-induced mitochondrial swelling and loss of membrane potential. Remifentanil preconditioning inhibited I/R-induced increases in tumor necrosis factor α, intercellular adhesion molecule 1, and nuclear factor κB p65 levels in liver tissues. Remifentanil preconditioning also inhibited the loss in superoxide dismutase and rise in malondialdehyde levels in liver tissues going through I/R injury. CONCLUSIONS: Our data revealed that remifentanil preconditioning may turn on multiple cellular pathways in hepatocytes to protect the liver from I/R injury by alleviating hepatic apoptosis.

Long-term changes in the personality and psychopathological profile of opiate addicts after nucleus accumbens ablative surgery are associated with treatment outcome.

OBJECTIVE: To investigate the long-term outcome and changes of the personality and psychopathological profile of opiate addicts after bilateral stereotactic nucleus accumbens (NAc) ablative surgery. METHODS: 60 patients were followed up for 5 years and abstinent status and adverse events were evaluated. NAc lesion volumes and locations were obtained by postoperative MRI scans. The Chinese version of the Eysenck Personality Questionnaire (EPQ-RSC), the Symptom Checklist-90-Revised (SCL-90-R), the Beck Depression Inventory (BDI), the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) and the World Health Organization's Quality of Life Questionnaire - Brief Version (WHOQOL-BREF) were administered to the patients before and 5 years after the stereotactic surgery. RESULTS: The total abstinence rate of all patients in their 5th postoperative year was 47.4%. The abstinent patients had a significantly larger lesion volume than the relapsed ones, but a larger lesion volume also increased the risk of adverse events. 5 years after surgery, the abstinent patients showed significant decreases on the Psychoticism (EPQ-P) and Neuroticism (EPQ-N) scores by EPQ-RSC, a significant decline on the Global Severity Index and the subscores in all 10 dimensions by SCL-90-R, significant decreases on the BDI and Y-BOCS scores, and significant improvements on the scores of all domains by WHOQOL-BREF, while for the relapsed patients, only the subscores of obsessive-compulsive by SCL-90-R and the Y-BOCS scores significantly decreased. Postoperative analysis revealed that the abstinent patients had a significantly better score than the relapsed ones by various instruments, and NAc lesion volumes and locations did not correlate with the outcome of any of these instruments. CONCLUSION: The bilateral ablation of NAc by stereotactic neurosurgery was a feasible method for alleviating psychological dependence on opiate drugs and preventing a relapse. Long-term follow-up suggested that surgery can improve the personality and psychopathological profile of opiate addicts with a trend towards normal levels, provided persistent abstinence can be maintained; relapse, on the other hand, may ruin this effect.

Global Research Activities on Micro(nano)plastic Toxicity to Earthworms.

Micro(nano)plastics are emerging contaminants that have been shown to cause various ecotoxicological effects on soil biota. Earthworms, as engineers of the ecosystem, play a fundamental role in soil ecosystem processes and have been used as model species in ecotoxicological studies. Research that evaluates micro(nano)plastic toxicity to earthworms has increased greatly over the last decade; however, only few studies have been conducted to highlight the current knowledge and evolving trends of this topic. This study aims to visualize the research status and knowledge structure of the relevant literature. Bibliometrics and visualization analyses were conducted using co-citations, cooperation networks and cluster analysis. The results showed that micro(nano)plastic toxicity to earthworms is an emerging and increasingly popular topic, with 78 articles published from 2013 to 2022, the majority of which were published in the last two years. The most prolific publications and journals involved in this topic were also identified. In addition, the diversity of cooperative relationships among different countries and institutions confirmed the evolution of this research field, in which China contributed substantially. The high-frequency keywords were then determined using co-occurrence analysis, and were identified as exposure, bioaccumulation, soil, pollution, toxicity, oxidative stress, heavy metal, microplastic, Eisenia foetida and community. Moreover, a total of eight clusters were obtained based on topic knowledge clustering, and these included the following themes: plastic pollution, ingestion, combined effects and the biological endpoints of earthworms and toxic mechanisms. This study provides an overview and knowledge structure of micro(nano)plastic toxicity to earthworms so that future researchers can identify their research topics and potential collaborators.

Protective effect of hydrogen sulfide is mediated by negative regulation of epigenetic histone acetylation in Parkinson's disease.

Introduction: Derangements in monoaminergic transmission in the substantia nigra with disturbed signaling in the hypothalamic-pituitary-adrenal axis are the major characteristics of Parkinson's disease (PD). It has been reported that the administration of hydrogen sulfide (H2S) is in practice to treat PD because of its redundant nature in regulating various neuronal signals. Hence, the current investigation was performed to evaluate the hypothesis that H2S might exert protective action via the inhibition of epigenetic histone acetylation. Material and methods: To test this notion, 6-hydroxydopamine (6-OHDA) was used to induce PD and sodium hydrogen sulfide (SHS) was used as a H2S donor and tubastatin A (TSA) was tested in an in vivo rat model to delineate the signaling mechanism. Results: Induction of PD in rats demonstrated elevated oxidative stress with an evidenced decrease in antioxidant enzymes, while elevated pro-inflammatory cytokines and inflammatory mediators were observed in the striatum of PD rats compared to controls. On the other hand, elevated (p < 0.01) levels of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), mRNA transcript of HDAC-2, -3, -4, -6 and total histone deacetylase (HDAC) were found with reduced levels of histone acetyltransferase (HAT) in the brain tissues of PD induced rats. Conclusions: Diversely, H2S exposure reversed these alterations with reduced HDAC activity. Further, PD rats treated with HDAC inhibitor showed a dramatic upsurge in the level of tyrosine hydroxylase, with a decreased level of glial fibrillary acidic protein, α-synuclein, tumor necrosis factor α, and other cytokines. Thus the results of the study suggest that H2S exerts protection via inhibition of HDAC.

Associations between personality changes and nucleus accumbens ablation in opioid addicts.

AIM: It has been reported that nucleus accumbens (NAc) lesions can help to prevent relapse in opioid addicts. This article aimed to investigate associations between personality changes and NAc lesions. METHODS: The surgery group consisted of 78 patients who had received bilateral stereotactic lesions of the NAc to treat opioid addiction. Seventy two non-surgery opioid addicts were appropriately paired with the patients of the surgery group as the non-surgery group. All participants were interviewed in person and received urine tests, naloxone provocative tests and hair tests to determine the prevalence of relapse. Eysenck personality questionnaire (EPQ) and the health survey questionnaire (SF-36) were employed to assess personality and functional health, respectively. RESULTS: In the surgery group, 30 participants relapsed, and the non-relapse rate was 61.5% (48/78). Compared with the Chinese normative data, the neuroticism (N) and psychoticism (P) dimensions of the EPQ in the non-surgery group were significantly higher, whereas the lie (L) dimension was significantly lower. There was no significant difference in all dimensions of the EPQ between the surgery group and the Chinese normative data. The N dimension in the relapse group and the L dimension in the surgery group were significantly lower than those of the non-surgery group. The P dimension in the relapse group was significantly higher than that of the non-relapse group. The extraversion (E) dimension was relatively stable between these groups. CONCLUSION: Although the influence of other factors cannot be excluded, it is apparent that surgically induced NAc lesions are associated with lower P and N dimensions for opioid addicts, and a higher P dimension is associated with a tendency to relapse.

Anti-human Glioma Cancer Potentials of Neobavaisoflavone as Natural Antioxidant Compound and Its Inhibition Profiles for Acetylcholinesterase and Butyrylcholinesterase Enzymes with Molecular Modeling and Spin Density Distributions Studies.

In this study, the carcinogenic potential of Neobavaisoflavone as a natural antioxidant compound and the inhibitory profiles of acetylcholinesterase and butyrylcholinesterase were investigated by molecular modeling and spin density distribution studies. To evaluate the antioxidant properties of neobavaisoflavone, DPPH test was performed in the presence of butyl hydroxytoluene as a control. Neobavaisoflavone cell viability was low compared to normal human glioma cancer cell lines, namely LN-229, U-87 and A-172 cell lines, without any effect of cytotoxicity on normal cell line. Neobavaisoflavone inhibited half of DPPH at 125 µg/mL. The best effects of Neobavaisoflavone antihypertensive glioma against the above cell lines were in the LN-229 cell line. In addition, the significant anti-cancer potential of human glioma Neobavaisoflavone against the popular human glioma cancer cell lines is related in this study. IC50 values were calculated by Neobavaisoflavone diagrams, 63.87 nM for AChE and 112.98 nM for BuChE, % Activity- [Inhibitor]. According to the above results, Neobavaisoflavone can be used to treat a variety of human glioma cancers in humans. In addition, molecular modeling calculations were performed to compare the biochemical activities of the Neobavaisoflavone molecule with enzymes. After molecular insertion calculations, ADME/T analysis was performed to investigate the properties of the neobavaisoflavone molecule, which will be used as a drug in the future. Then, different parameters for the antioxidant activity of the neobavaisoflavone molecule were calculated.

The protective effects of inosine against chemical hypoxia on cultured rat oligodendrocytes.

Inosine is a purine nucleoside and is considered protective to neural cells including neurons and astrocytes against hypoxic injury. However, whether oligodendrocytes (OLs) could also be protected from hypoxia by inosine is not known. Here we investigated the effects of inosine on primarily cultured rat OLs injured by rotenone-mediated chemical hypoxia, and the mechanisms of the effects using ATP assay, MTT assay, PI-Hoechst staining, TUNEL, and immunocytochemistry. Results showed that rotenone exposure for 24 h caused cell death and impaired viability in both immature and mature OLs, while pretreatment of 10 mM inosine 30 min before rotenone administration significantly reduced cell death and improved the viability of OLs. The same concentration of inosine given 120 min after rotenone exposure also improved viability of injured mature OLs. Immunocytochemistry for nitrotyrosine and cellular ATP content examination indicated that inosine may protect OLs by providing ATP and scavenging peroxynitrite for cells. In addition, immature OLs were more susceptible to hypoxia than mature OLs; and at the similar degree of injury, inosine protected immature and mature OLs differently. Quantitative real-time PCR revealed that expression of adenosine receptors was different between these two stages of OLs. These data suggest that inosine protect OLs from hypoxic injury as an antioxidant and ATP provider, and the protective effects of inosine on OLs vary with cell differentiation, possibly due to the adenosine receptors expression profile. As OLs form myelin in the central nervous system, inosine could be used as a promising drug to treat demyelination-involved disorders.

Senescence marker protein 30 confers neuroprotection in oxygen-glucose deprivation/reoxygenation-injured neurons through modulation of Keap1/Nrf2 signaling: Role of SMP30 in OGD/R-induced neuronal injury.

Senescence marker protein 30 (SMP30) is a senescence marker molecule and identified as a calcium regulatory protein. Currently, SMP30 has emerged as a cytoprotective protein in a wide range of cell types. However, the role of SMP30 in regulating neuronal survival during cerebral ischemia/reperfusion injury remains unclear. In the present study, we aimed to investigate the biological function and regulatory mechanism of SMP30 on neuronal survival using a cellular model induced by oxygen-glucose deprivation/reoxygenation (OGD/R). The results showed that SMP30 expression was significantly decreased by OGD/R exposure in neurons. Functional experiments demonstrated that SMP30 overexpression significantly rescued the decreased cell viability and attenuated the apoptosis and reactive oxygen species generation in OGD/R-exposed neurons. By contrast, SMP30 knockdown exhibited the opposite effect. Mechanism research revealed that SMP30 overexpression contributed to the activation of nuclear factor erythroid 2-related factor (Nrf2)/antioxidant response element (ARE) signaling associated with downregulation of Kelch-like ECH-associated protein (Keap1). Keap1 overexpression or Nrf2 silencing significantly reversed SMP30-mediated neuroprotection against OGD/R-induced injury. Overall, these findings demonstrate that SMP30 overexpression protects neurons from OGD/R-induced apoptosis and oxidative stress by enhancing Nrf2/ARE antioxidant signaling via inhibition of Keap1. These data highlight the importance of the SMP30/Keap1/Nrf2/ARE signaling axis in regulating neuronal survival during cerebral ischemia/reperfusion injury.

Clinical Value of 3D-Printed Navigation Technology Combined with Neuroendoscopy for Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is the most common form of hemorrhagic stroke with high morbidity and mortality. Rapid and massive bleeding may compress the brain tissue, causing space-occupying and pathological effects, such as reduced local cerebral blood flow, acidosis, and inflammatory and immune responses. Although the development of minimally invasive technique provides a new option for the treatment of ICH, their application is limited due to the difficulty in achieving accurate puncture localization under the guidance of the marks on CT. We selected 30 patients treated with neuroendoscopic surgery guided by 3D-printed navigation technology (experimental group) and 30 patients treated with neuroendoscopic surgery guided by hand-painted on the patient's body surface according to the marks on CT (control group). Our results showed that patients in the experimental group had a lower number of intraoperative punctures, shorter operation time, less intraoperative blood loss, higher hematoma clearance rate, and smaller volume of perihematomal edema than the patients in the control group. Moreover, patients in the experimental group had higher Glasgow Coma Scale score at discharge, shorter postoperative hospitalization time and ICU stay, and a lower rate of postoperative complications, despite the lack of statistically significant differences. In addition, no statistically significant differences were observed in mortality and Glasgow Outcome Scale score between the two groups. In conclusion, 3D-printed navigation technology used for the neuroendoscopic hematoma removal is a more reliable and less invasive approach in the treatment of ICH. This technique has great application prospects and deserves promotion in the future clinical practice.