Prevalence, characteristics, and risk factors of venous thromboembolism in patients with brain tumor undergoing craniotomy: a meta-analysis.

BACKGROUND: Brain tumor patients undergoing craniotomy are significantly associated with the development of venous thromboembolism (VTE), while the contributing factors remains controversial. Our study aimed to investigate the prevalence and risk factors for VTE in postoperational brain tumor patients. METHODS: We searched the PubMed, Embase, Web of Science, Medline, and Cochrane Library databases from their inception to July 2023. Article selection, data extraction, and study quality assessment were performed independently by two reviewers. Publication bias was assessed using Egger's and Begg's tests. Stata 15.0 software was used for data analysis. RESULTS: A total of 25 studies were considered, with a total of 49,620 brain tumor individuals. The pooled prevalence of VTE during hospitalization in postoperational brain tumor patients was 9% [95% CI: (0.08, 0.10)]. Moreover, our results demonstrated that patients with VTE were older than those without VTE [mean difference [MD] = 8.14, 95% CI: (4.97, 11.30)]. The following variables were significantly associated with VTE: prior history of VTE [OR = 7.81, 95% CI: (3.62, 16.88)], congestive heart failure [OR = 2.33, 95% CI: (1.08-5.05)], diabetes [OR = 1.87, 95% CI: (1.12-3.10)], hypertension [OR = 1.27, 95% CI: (1.07-1.50)], steroid use [OR = 1.63, 95% CI: (1.41, 1.88)], high white blood cells counts [MD = 0.32, 95% CI: (0.01, 0.63)], and high fibrinogen levels [MD = 0.19, 95% CI: (0.08, 0.30)]. CONCLUSION: This meta-analysis identified risk factors for postoperational VTE in patients with brain tumor, which can serve as a theoretical foundation for medical staff to manage and treat VTE. TRIAL REGISTRATION: CRD42023357459.

Brain-targeting redox-sensitive micelles for codelivery of TMZ and ß-lapachone for glioblastoma therapy.

Glioblastoma (GBM) is a central nervous system cancer with high incidence and poor survival rates. Enhancing drug penetration of the blood-brain barrier (BBB) and targeting efficacy is crucial for improving treatment outcomes. In this study, we developed a redox-sensitive targeted nano-delivery system (HCA-A2) for temozolomide (TMZ) and ß-lapachone (ß-Lapa). This system used hyaluronic acid (HA) as the hydrophilic group, arachidonic acid (CA) as the hydrophobic group, and angiopep-2 (A2) as the targeting group. Control systems included non-redox sensitive (HDA-A2) and non-targeting (HCA) versions. In vitro, HCA-TMZ-Lapa micelles released 100 % of their payload in a simulated tumor microenvironment within 24 h, compared to 43.97 % under normal conditions. HCA-A2 micelles, internalized via clathrin-mediated endocytosis, showed stronger cytotoxicity and better BBB penetration and cellular uptake than controls. In vivo studies demonstrated superior tumor growth inhibition with HCA-A2 micelles, indicating their potential for GBM treatment.

Ultrafast and Ultralarge Lithium-Ion Storage Enabled by Fluorine-Nitrogen Co-Implanted Carbon Tubes.

As a holy grail in electrochemistry, both high-power and high-energy electrochemical energy storage system (EES) has always been a pursued dream. To simultaneously achieve the "both-high" EES, a rational design of structure and composition for storage materials with characteristics of battery-type and capacitor-type storage is crucial. Herein, fluorine-nitrogen co-implanted carbon tubes (FNCT) have been designed, in which plentiful active sites and expanded interlayer space have been created benefiting from the heteroatom engineering and the fluorine-nitrogen synergistic effect, thus the above two-type storage mechanism can get an optimal balance in the FNCT. The implanted fluorine heteroatoms can not only amplify interlayer spacing, but also induce the transformation of nitrogen configuration from pyrrole nitrogen to pyridine nitrogen, further promoting the activity of the carbon matrix. The extraordinary electrochemical performance as results can be witnessed for FNCT, which exhibit fast lithium-ion storage capability with a high energy density of 119.4 Wh kg-1 at an ultrahigh power density of 107.5 kW kg-1 .

ISG15 enhances glioma cell stemness by promoting Oct4 protein stability.

The effects of ISG15 or ISGylation on tumor progression have been widely revealed; however, its roles in glioma progression are largely unknown. This study aims to explore the roles and underlying mechanisms of ISG15 in glioma progression. Here, ISG15 level was found to be upregulated in glioma tissues compared to the paired/unpaired normal tissues, and positively correlated with the level of stemness markers in glioma tissues. Loss of functional experiments indicated that ISG15 positively regulated glioma cell stemness, as evident by the increase of sphere formation ability, ALDH activity, stemness marker expression, and tumor-initiating ability. Further mechanistic studies revealed that ISG15 directly interacted with Oct4 protein, a critical stemness promoter, induced the ISGylation of Oct4 protein, and thus enhanced Oct4 protein stability. Additionally, it was found that Oct4 was ISGylated at lysine 284 (K284), which has been confirmed to be the ubiquitination site of Oct4 protein, and ISG15 knockdown did not degrade K284R mutant Oct4. Furthermore, ISG15 knockdown-induced downregulation of glioma cell stemness was rescued by Oct4 overexpression, but not by K284R mutant Oct4. Altogether, we suggest that ISG15-induced ISGylation of Oct4 protein is essential for glioma cell stemness.

Surgical overreduction and hyperlordotic fusion of C1-C2 joint are associated with cervical sagittal malalignment.

INTRODUCTION: Previous studies have shown that hyperlordotic C1-C2 fusion was related to postoperative subaxial kyphosis. However, most of the patients in these studies were complicated with rheumatoid arthritis (RA). Moreover, no studies have specifically evaluated the relationship between C1-C2 fusion angle and cervical sagittal vertical axis (cSVA), T1 slope or cranial tilt (CRT) after posterior C1-C2 fusion. This study aimed to investigate the cervical sagittal alignment in non-RA patients following posterior C1-C2 fusion and the correlation between C1-C2 fusion angle and postoperative cervical sagittal alignment. MATERIALS AND METHODS: From August 2004 to December 2015, twenty-eight consecutive patients with an average age of 39.2 years (range 6-70 years) who underwent posterior C1-C2 fusion from a single institution were enrolled. The mean follow-up period was 30.7 months (range 12-77 months). Angles of Oc-C1, C1-C2, C2-C3 and C2-C7, cSVA, T1 slope and CRT were measured in lateral cervical radiographs in neutral position before surgery and at the final follow-up. RESULTS: C1-C2 angle significantly increased from 13.6° ± 12.4° to 22.0° ± 8.1° at the final follow-up (P < 0.001). A significant decrease was found both in Oc-C1 and C2-C7 angles from pre-operation to the final follow-up (P < 0.001 and P = 0.011, respectively). Moreover, cSVA and CRT dramatically increased from pre-operation to the final follow-up (P < 0.001). C1-C2 fusion angle was significantly associated with Oc-C1, C2-C7 angle, cSVA and CRT at the final follow-up. A significant correlation was also observed between postoperative change of C1-C2 angle and that of Oc-C1, C2-C7 angle, cSVA and CRT. CONCLUSIONS: Apart from decreased subaxial lordosis, posterior C1-C2 fusion in hyperextension may also lead to kyphotic change of atlanto-occipital alignment and increased tilting forward of the cervical spine. Therefore, intraoperative overreduction of C1-C2 angle and hyperlordotic C1-C2 fusion should be avoided to maintain the physiologic cervical sagittal alignment.

[Characterization of ibeB gene of meningitic Escherichia coli strains in calves from Xinjiang].

Objective: To understand the molecular biology information of ibeB gene of meningitic Escherichia coli isolates in calves. Methods: The strain used was isolated from the brain and liver tissue of calves died from Meningitis. It was identified to be an O161-K99-STa pathogenic Escherichia coli strain and named as bovine-EN and bovine-EG. Based on the sequence of ibeB gene of meningitic Escherichia coli K1 RS218 strain in GenBank, a pair of primers was designed and the ibeB gene was cloned from isolates by PCR. Part molecular biology information of ibeB among different strains was compared. Results: The sequence length of isolates ibeB gene was 1500 bp, containing a 1371 bp open reading frame (ORF) encoding 457 amino acids. Bioinformatics analysis showed that the nucleotide and amino acid homology of ibeB gene of bovine-EN strain shared 90.5% and 96.9% identity with Escherichia coli K1 RS218 ibeB gene, respectively, while bovine-EG strain shared 99.4% and 100.0% identity with Escherichia coli K12 respectively. The ibeB gene of bovine-E strains encoded water-soluble protein whose molecular weight was 50.26 kDa and isoelectric point was 6.05. This protein contained a signal peptide A but no transmembrane domain. Subcellular localization of ibeB belonged to the secreted protein, which secretory signal path site (SP) proportion was 0.939. Conclusion: The ibeB gene was cloned from meningitic E. coli isolates and had higher homology and similar biological characteristics with meningitis E. coli K1 RS218ibeB, which belongs to extraintestinal pathogenic Escherichia coli.

Anti-inflammatory effects of curcumin in experimental spinal cord injury in rats.

AIM: Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to play an important role in protection against spinal cord injury (SCI) induced inflammatory response. The objective of this study was to test whether curcumin, a novel Nrf2 activator, can protect the spinal cord against SCI-induced inflammatory damage. METHODS: Adult male Sprague-Dawley rats were subjected to laminectomy at T8-T9 and compression with a vascular clip. The spinal cords spanning the injury site about 0.8 cm were collected for testing. There were three groups: (a) sham group; (b) SCI group; and (c) SCI + curcumin group. We measured Nrf2 and nuclear factor kappa B (NF-κB) binding activities by electrophoretic mobility shift assay, concentrations of tumor necrosis factor-α, interleukin-1ß and interleukin-6 by enzyme-linked immunosorbent assay, hindlimb locomotion function by Basso, Beattie, and Bresnahan rating, spinal cord edema by the wet/dry weight method, and apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling analysis. RESULTS: Induction of the Nrf2 activity by curcumin markedly decreased NF-κB activation and inflammatory cytokines production in the injured spinal cord. Administration of curcumin also significantly ameliorated the secondary spinal cord damage, as shown by decreased severity of locomotion deficit, spinal cord edema, and apoptosis. CONCLUSION: Post-SCI curcumin administration attenuates the inflammatory response in the injured spinal cord, and this may be a mechanism whereby curcumin improves the outcome following SCI.

Curcumin inhibits the increase of labile zinc and the expression of inflammatory cytokines after traumatic spinal cord injury in rats.

BACKGROUND: The present study aimed to investigate the effects of curcumin on the levels of spinal cord labile zinc (Zn) and inflammatory cytokines in rats after traumatic spinal cord injury (SCI). METHODS: Adult male Sprague-Dawley rats were subjected to laminectomy at T8-T9 and compression with a vascular clip. There were three groups: (a) sham group; (b) SCI group; and (c) SCI + curcumin group. We measured spinal labile Zn by N-(6-methoxy-8-quinolinyl)-4-methylbenzenesulfonamide (TSQ) fluorescence staining, inflammatory cytokines such as interleukin 1ß, interleukin-6, and tumor necrosis factor α by enzyme-linked immunosorbent assay, hindlimb locomotion function by Basso, Beattie, and Bresnahan rating, spinal cord edema by wet dry weight method, and apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling analysis. RESULTS: The results showed that SCI caused a significant increase in labile Zn and inflammatory cytokines in the injured rat spinal cord. Treatment with curcumin after SCI markedly downregulated the levels of these agents and ameliorated SCI-induced hindlimb locomotion deficits, spinal cord edema, and apoptosis. CONCLUSIONS: Curcumin treatment attenuates the increase of labile Zn and the expression of inflammatory cytokines in the injured spinal cord, and this may be a mechanism whereby curcumin improves the outcome after SCI.

Chemokine receptor CXCR4 interacts with nuclear receptor Nur77 and promote glioma invasion and progression.

BACKGROUND: Glioma is the most common primary brain tumor. It is prone to progress and have high rate of mortality regardless of radiation or chemotherapy due to its invasive growth features. Chemokine and its receptor CXCL12 and CXCR4 play important roles in cancer metastasis. METHODS: In this study, we investigate the role of CXCR4 in the progression of glioma by various molecular technologies, including qRT-PCR, Western blotting, wound closure assay, transwell assay et al. RESULTS: It was found that CXCR4 was overexpressed in glioma tissues. The expression of CXCR4 was correlated with patients' overall survival. Wound closure assay and transwell invasion assay showed that inhibition of CXCR4 significantly reduced the expression of biomarkers related to the formation of invadopodium, leading to decrease the invasion and migration of glioma tumor cells. Knocking down the nuclear receptor Nur77 remarkably decreased CXCR4 expression and reduced glioma cell invasion and migration. The reduction of glioma cell invasion and migration were observed after Nur77 inhibitor treatment. CONCLUSION: Taken together, these results indicated that CXCR4 is critical in promoting glioma migration and invasion. Inhibition of Nur77 reduces CXCR4 related cancer progression.

The application of extracorporeal shock wave therapy on stem cells therapy to treat various diseases.

In the last ten years, stem cell (SC) therapy has been extensively used to treat a range of conditions such as degenerative illnesses, ischemia-related organ dysfunction, diabetes, and neurological disorders. However, the clinical application of these therapies is limited due to the poor survival and differentiation potential of stem cells (SCs). Extracorporeal shock wave therapy (ESWT), as a non-invasive therapy, has shown great application potential in enhancing the proliferation, differentiation, migration, and recruitment of stem cells, offering new possibilities for utilizing ESWT in conjunction with stem cells for the treatment of different systemic conditions. The review provides a detailed overview of the advances in using ESWT with SCs to treat musculoskeletal, cardiovascular, genitourinary, and nervous system conditions, suggesting that ESWT is a promising strategy for enhancing the efficacy of SC therapy for various diseases.

Ketogenic diet time-dependently prevents NAFLD through upregulating the expression of antioxidant protein metallothionein-2.

BACKGROUND & AIMS: The past few decades have witnessed a rapid growth in the prevalence of nonalcoholic fatty liver disease (NAFLD). While the ketogenic diet (KD) is considered for managing NAFLD, the safety and efficacy of the KD on NAFLD has been a controversial topic. Here, we aimed to investigate the effect of KD of different durations on metabolic endpoints in mice with NAFLD and explore the underlying mechanisms. METHODS: NAFLD mice were fed with KD for 1, 2, 4 and 6 weeks, respectively. The blood biochemical indexes (blood lipids, AST, ALT and etc.) and liver fat were measured. The LC-MS/MS based proteomic analysis was performed on liver tissues. Metallothionein-2 (MT2) was knocked down with adeno-associated virus (AAV) or small interfering RNA (siRNA) in NAFLD mice and AML-12 cells, respectively. H&E, BODIPY and ROS staining were performed to examine lipid deposition and oxidative stress. Furthermore, MT2 protein levels, nucleus/cytoplasm distribution and DNA binding activity of peroxisome proliferators-activated receptors α (PPARα) were evaluated. RESULTS: KD feeding for 2 weeks showed the best improvement on NAFLD phenotype. Proteomic analysis revealed that MT2 was a key candidate for different metabolic endpoints of NAFLD affected by different durations of KD feeding. MT2 knockdown in NAFLD mice blocked the effects of 2 weeks of KD feeding on HFD-induced steatosis. In mouse primary hepatocytes and AML-12 cells, MT2 protein levels were induced by ß-hydroxybutyric acid (ß-OHB). MT2 Knockdown blunted the effects of ß-OHB on alleviating PA-induced lipid deposition. Mechanistically, 2 weeks of KD or ß-OHB treatment reduced oxidative stress and upregulated the protein levels of MT2 in nucleus, which subsequently increased its DNA binding activity and PPARα protein expression. CONCLUSIONS: Collectively, these findings indicated that KD feeding prevented NAFLD in a time dependent manner and MT2 is a potential target contributing to KD improvement on steatosis.

APRIL depletion induces cell cycle arrest and apoptosis through blocking TGF-ß1/ERK signaling pathway in human colorectal cancer cells.

It is well documented that a proliferation-inducing ligand (APRIL), a newly found member of tumor necrosis factor superfamily, overexpressed in the majority of malignancies, plays a potential role in the occurrence and development of these tumors. Herein, we demonstrated that APRIL depletion by using RNA interference in human colorectal cancer (CRC) COLO 205 and SW480 cells resulted in cell proliferation inhibition and evoked cell cycle arrest in G0/G1 phase and apoptosis, coupled with decrease in CDK2, Cyclin D1, Bcl-2 expression and an increase of p21 and Bax expression. In addition, the decreased expression of transforming growth factor-ß1 (TGF-ß1) and p-ERK was also showed in siRNA-APRIL transfected COLO 205 and SW480 cells, whereas the protein expression levels of Smad2/3, p-Smad2/3, and ERK were not significantly changed. Taken together, our results indicate that APRIL depletion induces cell cycle arrest and apoptosis partly through blocking noncanonical TGF-ß1/ERK, rather than canonical TGF-ß1/Smad2/3, signaling pathway in CRC cells. Moreover, our study highlights APRIL as a potential molecular target for the therapy of CRC.

Hederagenin suppresses glioma cell biological activities via Nur77 in vitro study.

The aim of this research was to discuss Hederagenin's antitumor effects on glioma by in vitro study. U251 and U87 cell lines were used as research target in our research. In the first step, the different Hed concentrations were treated to U251 and U87 cell lines, and the second step is Nur77 transfection in U251 and U87 with Hed treatment; measuring cell proliferation by MTT and EdU staining; evaluating cell invasion and migration abilities by transwell assay and relative gene and protein expressions by RT-qPCR and WB assay. Compared with NC group, U251 and U87 cell proliferation were significantly depressed with cell apoptosis significantly increasing, and cell invasion and migration abilities were significantly inhibited in Hed-treated groups (p < .05, respectively); however, with Nur77 transfection, the Hed's antitumor effects disappeared. Meanwhile, with Hed supplement, Nur77, PI3K, and AKT gene expressions were significantly downregulated (p < .05, respectively) in Hed-treated groups; and Nur77, p-PI3K, and p-AKT protein expressions were significantly decreased (p < .05, respectively) in Hed-treated groups. Hed had antitumor effects on glioma cell biological activities via Nur77/PI3K/AKT pathway in vitro study.

An intrinsic polymer electrolyte via in situ cross-linked for solid lithium-based batteries with high performance.

Since the introduction of poly(ethylene oxide) (PEO)-based polymer electrolytes more than 50 years, few other real polymer electrolytes with commercial application have emerged. Due to the low ion conductivity at room temperature, the PEO-based electrolytes cannot meet the application requirements. Most of the polymer electrolytes reported in recent years are in fact colloidal/composite electrolytes with plasticizers and fillers, not genuine electrolytes. Herein, we designed and synthesized a cross-linked polymer with a three-dimensional (3D) mesh structure which can dissolve the Li bis(trifluoromethylsulfonyl)imide (LiTFSI) salt better than PEO due to its unique 3D structure and rich oxygen-containing chain segments, thus forming an intrinsic polymer electrolyte (IPE) with ionic conductivity of 0.49 mS cm-1 at room temperature. And it can hinder the migration of large anions (e.g. TFSI-) in the electrolyte and increase the energy barrier to their migration, achieving Li+ migration numbers (tLi+) of up to 0.85. At the same time, IPE has good compatibility with lithium metal cathode and LiFePO4 (LFP) cathode, with stable cycles of more than 2,000 and 700 h in Li//Li symmetric batteries at 0.2 and 0.5 mAh cm-2 current densities, respectively. In addition, the Li/IPE/LFP batteries show the capacity retention >90% after 300 cycles at 0.5 C current density. This polymer electrolyte will be a pragmatic way to achieve commercializing all-solid-state, lithium-based batteries.

Regulating SEI Components of Sodium Anode via Capturing Organic-Molecule Intermediates in Ester-Based Electrolyte.

Highly reversible sodium metal anodes are still regarded as a stubborn hurdle in ester-based electrolytes due to the issue of uncontrollable dendrites and incredibly unstable interphase. Evidently, a strong protective film on sodium is decisive, while the quality of the protective film is mainly determined by its components. However, it is challenging to actively adjust the expected components. This work can regulate the solid electrolyte interphase (SEI) components by introducing a functional electrolyte additive (2-chloro-1,3-dimethylimidazoline hexafluorophosphate (CDIH, namely CDI+ +PF6 - )) into FEC/PC ester-based electrolyte. Specifically, the chloride element in the CDI+ can easily react to form a NaF/NaCl-rich SEI together with the decomposition products of FEC; then the CDI+ without chlorine as a gripper to capture the organic-molecule intermediates generated during FEC decomposition to greatly reduce the content of unstable organic components in SEI, which can be confirmed by molecular dynamic simulation and experiment. Eventually, a highly reversible Na deposition behavior can be delivered. As expected, under the action of CDIH additives, the Na||Na symmetrical cell performs an excellent long-term cycling (>800 h, 0.5 mA cm-2 -0.5 mAh cm-2 ) and rate performance (0.5-4 mA cm-2 ). Furthermore, the Na||PB full cell exhibits the outstanding electrochemical performance with small polarization.

Characteristics of TP53 germline variants and their correlations with Li-Fraumeni syndrome or Li-Fraumeni-like syndrome in Chinese tumor patients.

Li-Fraumeni syndrome (LFS), a rare autosomal-dominant inheritance condition, is associated with a family cancer history as well as pathogenic/likely-pathogenic TP53 germline variants (P/LP TP53 GV). The current clinical methods for detecting LFS are limited. Here, we retrospectively investigate P/LP TP53 GV among Chinese cancer patients by next-generation sequencing and evaluate its relationship with a family cancer history. A total of 270 out of 19,226 cancer patients have TP53 GV, including 53 patients with P/LP TP53 GV. Patients with P/LP TP53 GV are mainly found in male with glioma, lung cancer or sarcoma. The median age of diagnosis for P/LP TP53 GV patients is significantly lower than that of non-P/LP TP53 GV patients (31-years vs. 53-years; P < 0.01). One LFS patient and 3 Li-Fraumeni-like syndrome (LFL) patients are among the 26 followed-up P/LP TP53 GV patients. Among 25 types of P/LP TP53 GV, the highest variant frequencies occurred at codon 175 and 248. p.M237I, p.R158H, p.C238Y and p.C275R, are firstly identified among the Chinese LFS/LFL patients. This study reports the (P/LP) TP53 GV characteristics of Chinese pan-cancer patients. These findings suggest analyzing the P/LP TP53 GV in cancer patients is an effective strategy for identifying cancer predisposition syndrome.

Chitinase-3 like-protein-1 promotes glioma progression via the NF-κB signaling pathway and tumor microenvironment reprogramming.

Background: Chitinase-3-like protein 1 (CHI3L1) is overexpressed in various types of tumors, especially in glioma, and contributes to tumor progression. However, the definite role of CHI3L1 and involved pathway in glioma progression are not completely understood. Methods: CHI3L1 expression in human gliomas and its association with patient survival was determined using enzyme-linked immunosorbent assay, western blot, immunohistochemistry, and public databases. Single-cell RNA-seq was used to characterize the landscape of tumor and myeloid cells. Human proteome microarray assay was applied to identify the binding partners of CHI3L1. Protein-protein interactions were analyzed by co-immunoprecipitation and cellular co-localization. The roles of CHI3L1 in glioma proliferation and invasion were investigated in tumor cell lines by gain- and loss- of function, as well as in vivo animal experiments. Results: CHI3L1 was up-regulated in all disease stages of glioma, which was closely related with tumor survival, growth, and invasion. CHI3L1 was primarily expressed in glioma cells, followed by neutrophils. Moreover, glioma cells with high expression of CHI3L1 were significantly enriched in NF-κB pathway. Pseudo-time trajectory analysis revealed a gradual transition from CHI3L1low to CHI3L1high glioma cells, along with the NF-κB pathway gradually reversed from inhibition to activation. Intriguingly, CHI3L1 binds to actinin alpha 4 (ACTN4) and NFKB1, and enhances the NF-κB signaling pathway by promoting the NF-κB subunit nuclear translocation in glioma cells. Further, CHI3L1 were released into the tumor microenvironment (TME) and interacted with CD44 expressed on tumor-associated macrophages to activate AKT pathway, thereby contributing to M2 macrophage polarization. In addition, CHI3L1 positively correlated to the expression of immune checkpoints, such as CD274 (PD-L1) and HAVCR2 (LAG3), which then remodeled the TME to an immunosuppressive phenotype. Conclusion: Our research revealed that CHI3L1 facilitated NF-κB pathway activation within glioma cells and reprogramed the TME, thereby serving as a promising therapeutic target for glioma.

Erythropoietin administration modulates pulmonary Nrf2 signaling pathway after traumatic brain injury in mice.

BACKGROUND: In our previous studies, antioxidant transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway has been shown to play an important role in protecting traumatic brain injury (TBI)-induced acute lung injury (ALI). This study was designed to explore whether recombinant human erythropoietin (rhEPO) administration modulates pulmonary Nrf2 signaling pathway in a murine TBI model. METHODS: Closed head injury was made by Hall's weight-dropping method. The rhEPO was administered at a dose of 5,000 IU/kg 30 minutes after TBI. Pulmonary capillary permeability, wet or dry weight ratio, apoptosis, Nrf2 and its downstream cytoprotective enzymes including NAD(P)H:quinone oxidoreductase 1, and glutathione S-transferase were investigated at 24 hours after TBI. RESULTS: We found that treatment with rhEPO markedly ameliorated TBI-induced ALI, as characterized by decreased pulmonary capillary permeability, wet or dry weight ratio, and alveolar cells apoptosis. Administration of rhEPO also significantly upregulated the mRNA expressions and activities of Nrf2 signaling pathway-related agents, including Nrf2, NAD(P)H:quinone oxidoreductase 1, and glutathione S-transferase. CONCLUSIONS: The results of this study suggest that post-TBI rhEPO administration may induce Nrf2-mediated cytoprotective response in the lung, and this may be a mechanism whereby rhEPO reduces TBI-induced ALI.

Effects of tert-butylhydroquinone on intestinal inflammatory response and apoptosis following traumatic brain injury in mice.

Traumatic brain injury (TBI) can induce intestinal inflammatory response and mucosal injury. Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to prevent oxidative stress and inflammatory response in gut after TBI. The objective of this study was to test whether tert-butylhydroquinone (tBHQ), an Nrf2 inducer, can protect against TBI-induced intestinal inflammatory response and mucosal injury in mice. Adult male ICR mice were randomly divided into three groups: (1) sham + vehicle group, (2) TBI + vehicle group, and (3) TBI + tBHQ group (n = 12 per group). Closed head injury was adopted using Hall's weight-dropping method. Intestinal mucosa apoptosis and inflammatory-related factors, such as nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), were investigated at 24 h after TBI. As a result, we found that oral treatment with 1% tBHQ prior to TBI for one week markedly decreased NF-κB activation, inflammatory cytokines production, and ICAM-1 expression in the gut. Administration of tBHQ also significantly attenuated TBI-induced intestinal mucosal apoptosis. The results of the present study suggest that tBHQ administration could suppress the intestinal inflammation and reduce the mucosal damage following TBI.

Intracranial solitary fibrous tumor mimicking meningioma: A case report.

RATIONALE: Solitary fibrous tumor is a rare mesenchymal tumor. This case report describes the diagnosis and treatment of this tumor. PATIENT CONCERNS: A 31-year-old patient presented with epileptic seizure and headache 1 day prior to the visit and showed transient right limb hemiplegia for 6 hours that was resolved after intravenous infusion of mannitol. DIAGNOSES: Based on imaging, the provisional diagnosis was meningioma. Postsurgical histopathological diagnosis confirmed solitary fibrous tumor. INTERVENTIONS: The lesion was totally excised. The patient improved remarkably after the operation, without any signs of associated limb movement disorder. No epileptic seizure was observed or reported after the operation. OUTCOMES: Postoperation computed tomography (CT) scans showed no obvious residual tumor. The patient was followed up every 3 months for a total of 1 year following the operation, during which time the patient did not complain of headache or seizure. LESSONS: The manifestation of solitary fibrous tumor (SFT) through imaging methods has certain specific findings,butimmunohistochemistry is still very important for confirming the diagnosis.