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Glioma is the most common type of primary brain malignancy with high morbidity and mortality, but little is known about its pathological mechanisms. Kinesin family member 11 (KIF11) is a key driver of malignancy in glioblastoma, a grade IV glioma, but its involvement in glioma chemoresistance remains to be determined. We accessed the TCGA open datasets, collected glioma tumor tissue samples, and analyzed the expression of KIF11 in glioma patients. Meanwhile, the correlation between KIF11 and survival outcomes was determined by the Kaplan-Meier analysis. The role of KIF11 in glioma tumor cell function was assessed in an in vitro knockdown and overexpressing system. Here, we found that KIF11 was upregulated in glioma tumors and negatively correlated with overall survival outcomes via analyzing the open datasets. KIF11 was negatively correlated with TP53 expression. Furthermore, KIF11 promoted the stemness in glioma cells, accompanied by increased cell proliferation and chemoresistance. Mechanistically, we found that KIF11 promoted cell cycle progression via upregulating cyclin expression.

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BACKGROUND: Traumatic brain injury (TBI) has been a serious public health issue. Clinically, there is an urgent need for agents to ameliorate the neuroinflammation and oxidative stress induced by TBI. Our previous research has demonstrated that quercetin could protect the neurological function. However, the detailed mechanism underlying this process remains poorly understood. OBJECTIVE: This research was designed to investigate the mechanisms of quercetin to protect the cortical neurons. METHODS: A modified weight-drop device was used for the TBI model. 5, 20 or 50 mg/kg quercetin was injected intraperitoneally to rats at 0.5, 12 and 24 h post TBI. Rats were sacrificed three days post injury and their cerebral cortex was obtained from the injured side. The rats were randomly assigned into three groups of equal number: TBI and quercetin group, TBI group, and Sham group. The brain water content was calculated to estimate the brain damage induced by TBI. Immunohistochemical and Western blot assays were utilized to investigate the neurobehavioral status. Enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction were performed to evaluate the inflammatory responses. The cortical oxidative stress was measured by estimating the activities of malondialdehyde, superoxide dismutase, catalase and glutathione-Px. Western blot was utilized to evaluate the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1). RESULTS: Quercetin attenuated the brain edema and microgliosis in TBI rats. Quercetin treatment attenuated cortical inflammatory responses and oxidative stress induced by TBI insults. Quercetin treatment activated the cortical Nrf2/HO-1 pathway in TBI rats. CONCLUSIONS: Quercetin ameliorated the TBI-induced neuroinflammation and oxidative stress in the cortex through activating the Nrf2/HO-1 pathway.

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BACKGROUND: Traumatic brain injury (TBI) has ranked as one of the leading causes of disability and death in the world. The neuroinflammation mediated by signal transducer and activator of transcription 3 (STAT3) signaling during the progression of TBI leads to long-term neurodegeneration. Ring finger protein 6 (RNF-6) is an E3 ubiquitin ligase and can regulate the activity of STAT3 signaling pathway by targeting its inhibitors. However, the mechanism underlying this process in TBI remains poorly understood. METHODS: In this research, cortical impact injury was used to construct the TBI rat model. Western blot assay was performed to evaluate the protein levels of RNF6, Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1), and STAT3/pSTAT3. QRT-PCR assay was performed to assess the RNA levels of RNF6 and other cytokines. The neural function of TBI rats was estimated by modified Neurological Severity Scores test. RESULTS: The expression of RNF-6 was up-regulated in the brain tissues of TBI rats. Down-regulation of RNF6 alleviated the symptoms and improved the neural recovery postinjury in TBI rats. Inhibition of RNF6 suppressed the cerebral inflammation by up-regulating the protein level of SHP-1 and down-regulating the phosphorylation level of STAT3. CONCLUSION: Inhibition of RNF6 alleviated TBI by suppressing the STAT3 signaling in TBI rats.

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Hollow PtCo nanosphere electrocatalyst-supported multi-walled carbon nanotubes (MWCNTs) were prepared at room temperature in a homogeneous solution employing cobalt metal nanoparticles as sacrificial templates. The structure and elemental composition of the resulting hollow PtCo/MWCNT composites were characterized by transmission electron microscopy (TEM), X-ray diffraction (XRD), and energy dispersive X-ray spectroscopy (EDS). The hollow PtCo/MWCNT electrocatalysts demonstrated enhanced electrocatalytic activity toward methanol oxidation compared with carbon nanotube-supported solid PtCo nanoparticles and commercial E-TEK Pt/C (20 wt.%Pt) catalysts.

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We demonstrate the use of molecular monolayers to enhance the nucleation of electrocatalytically active platinum (Pt) nanoparticles onto multi-walled carbon nanotubes (MWCNTs). The MWCNT is embedded within the 1,4-benzenediamine shell (NH(2)-MWCNT) with large amounts of amino groups outside on the nanotube surfaces. Subsequent deposition of platinum nanoparticles led to high densities of 2 to 5 nm diameter platinum nanocrystals uniformly deposited along the length of the MWCNTs (Pt/NH(2)-MWCNTs). The structure and nature of the resulting Pt/NH(2)-MWCNTs composites were characterized by transmission electron microscopy and X-ray diffraction. Electrochemical measurements show that the molecular monolayers do not impede redox behavior of the electrode, and measurements of the electrocatalytic oxidation of methanol show very high catalytic efficiency compared with commercial E-TEK Pt/C (20 wt%) catalysts, which is crucial for anode electrocatalysis in direct methanol fuel cells.

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