OBJECTIVE:To investigate the effect of long non-coding RNA (LncRNA) differentiation antagonizing non-protein coding RNA (DANCR) on the immune microenvironment of glioma cells by regulating the miR-656/bone morphogenetic protein receptor type 1A (BMPR1A) axis. METHODS:The expression levels of DANCR, miR-656 and BMPR1A in glioma cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The U87 cells were transfected or co-transfected to form the following groups: sh-DANCR (transfected with sh-DANCR), overexpression (pcDNA 3.1) DANCR (transfected with pcDNA 3.1 DANCR), NC sh (transfected with negative control sh), pcDNA 3.1 (transfected with pcDNA 3.1 vector), sh-DANCR + miR-656 inhibitor (co-transfected with sh-DANCR and miR-656 inhibitor), sh-DANCR + NC inhibitor (co-transfected with sh-DANCR and NC inhibitor), sh-DANCR + pcDNA 3.1 BMPR1A (co-transfected with sh-DANCR and pcDNA 3.1 BMPR1A), and sh-DANCR + pcDNA 3.1 (co-transfected with sh-DANCR and pcDNA 3.1 BMPR1A). The untreated U87 cells were used as the blank group. The proliferation of U87 cells was detected by CCK-8; invasion and migration were detected by Transwell assay; apoptosis was detected by flow cytometry; the expression of DANCR, miR-656, and BMPR1A mRNA in cells was detected by qRT-PCR; the targeting relationship between DANCR and miR-656 was verified by dual-luciferase; and BMPR1A and immune escape factors [programmed death receptor 1 (PD-1) and programmed death-ligand 1 (PD-L1)] were detected by Western blot. RESULTS:The mRNA expressions of DANCR and BMPR1A in U87, A172, LN229 and U251 cells were significantly increased, while the expression of miR-656 was significantly decreased compared with those in NHA cells (P < 0.05). Compared with the blank group and sh-DANCR group, the proliferation rate, invasion, migration number, DANCR, BMPR1A mRNA, BMPR1A, PD-1, PD-L1 expression of U87 cells in the sh-DANCR group were obviously reduced, while the apoptosis rate and miR-656 expression were obviously increased (P < 0.05). Compared with the pcDNA 3.1 group, the proliferation rate, invasion, migration number, DANCR, BMPR1A mRNA, BMPR1A, PD-1, and PD-L1 expression of U87 cells in the pcDNA 3.1 DANCR group were obviously increased, while the apoptosis rate and miR-656 expression were obviously reduced (P < 0.05). Compared with the sh-DANCR +NC inhibitor group, the proliferation rate, invasion, migration number, BMPR1A mRNA, BMPR1A, PD-1, and PD-L1 expression of U87 cells in the sh-DANCR+miR-656 inhibitor group were obviously increased, and the apoptosis rate and miR-656 expression were obviously reduced (P < 0.05), while the expression of DANCR was not obvious (P>0.05). Compared with the sh-DANCR+pcDNA 3.1 group, the proliferation rate, invasion, migration number, BMPR1A mRNA, BMPR1A, PD-1, and PD-L1 expression of U87 cells in the sh-DANCR+pcDNA 3.1 BMPR1A group obviously increased, and the apoptosis rate obviously decreased (P < 0.05), while here was no statistically obvious difference in miR-656 expression and DANCR expression (P>0.05). DANCR and miR-656 had a targeted negative regulatory relationship. CONCLUSION:LncRNA DANCR improves the immune microenvironment of glioma cells and inhibits the malignant behavior development of cancer cells by regulating the miR-656/BMPR1A axis.

Parthanatos, a cell death mechanism triggered by PARP-1 activation, is implicated in oncogenic processes, yet their role in low-grade gliomas (LGG) remains poorly understood. This research investigates Parthanatos-related miRNAs' prognostic and immunomodulatory potential, alongside their influence on therapeutic outcomes in LGGs. Comprehensive miRNA and mRNA profiles of LGG patients were extracted from TCGA and CGGA databases, integrating clinical parameters to identify Parthanatos-associated miRNAs. IHC data validated the expression levels of Parthanatos-related genes in glioma versus normal brain tissues. Protein–protein interaction networks and Spearman correlation analysis facilitated the identification of key miRNAs. Parthanatos-related miRNA indices (PMI) were screened using Lasso and assessed for their accuracy in predicting prognosis, comparing their associated potential molecular functions and heterogeneity of the immune microenvironment. Drug sensitivity was assessed between different groups and optimal therapeutic agents were predicted. Validate the expression levels of key miRNAs by qPCR. Ninety-one miRNAs significantly associated with Parthanatos were screened, through which a PMI prognosis model of nine miRNAs was constructed. The PMI score was able to independently predict the prognosis of patients with LGG, and the nomogram constructed based on the PMI provided a practical tool for clinical prediction of patient prognosis. The proportion of immune response was lower in patients in the high-risk group, and there were significant differences in drug sensitivity between different risk classes, while drugs such as Fasudil were identified as the most promising therapeutic agents for patients in the high-risk group. Our findings highlight the critical role of Parthanatos-associated miRNAs in the progression and treatment of LGG, offering novel insights into their prognostic value and therapeutic potential.

目的 探讨老年急性脑梗死(ACI)患者卵泡抑素样蛋白 1(FSTL1)、缺氧诱导因子 1α(HIF-1α)与凋亡分子的表达,对功能结局的预测价值.方法 选取 2021 年 6 月至 2022 年 6 月温州市人民医院收治的 220 例老年 ACI患者作为 ACI组,同期 200 例老年健康体检者作为健康组.ACI 患者溶栓治疗后 3 个月日常生活活动能力量表评分≤60 分记为功能结局不良组,>60 分记为功能结局良好组.检测所有入组患者血清 FSTL1、HIF-1α及相关凋亡分子B淋巴细胞瘤 2 基因(Bcl-2)和半胱氨酸天冬氨酸蛋白酶 3(Caspase-3)表达.结果 ACI 组血清 HIF-1α、FSTL1、Caspase-3 表达水平显著高于健康组,Bcl-2 表达水平显著低于健康组(P<0.01).Pearson 相关性分析显示,ACI组血清 HIF-1α、FSTL1 表达水平与 Caspase-3 呈正相关(P<0.01),与 Bcl-2 表达水平呈负相关(P<0.01).多因素 logistic回归分析显示,入院美国国立卫生研究院卒中量表评分(OR=1.933,95%CI:1.008～3.705,P=0.047)、发病至治疗时间(OR=2.038,95%CI:1.335～3.112,P =0.001)、HIF-1α(OR=1.865,95%CI:1.202～2.892,P=0.005)和 FSTL1(OR=2.160,95%CI:1.142～4.084,P=0.018)是影响老年 ACI 患者溶栓治疗后功能结局的独立危险因素.HIF-1α和 FSTL1 联合检测的敏感性(87.9%)和曲线下面积(0.804)显著高于单项检测(P<0.05).结论 HIF-1α、FSTL1 可能通过调节凋亡相关蛋白 Caspase-3、Bcl-2 表达,HIF-1α和FSTL1 与神经损伤相关,对于老年 ACI患者早期溶栓后功能结局具有预测价值.

目的 探讨雌激素、血脂、和肽素(copeptin)及胰岛素样生长因子-1(IGF-1)水平与女性动脉瘤性蛛网膜下腔出血患者预后的相关性分析.方法 选取2017年1月—2019年12月温州市人民医院收治的60例女性动脉瘤性蛛网膜下腔出血患者为研究对象,根据发病后3个月预后情况将其分为预后不良组(24例)与预后良好组(36例).检测两组血清的雌激素、血脂[总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)]、血清copeptin、IGF-1水平,采用logistic回归方程及ROC曲线分析其与临床预后的相关性.结果 预后良好组的年龄、雌激素、血脂TG、血清copeptin及IGF-1水平均优于预后不良组(均P＜0.05);logistic回归结果显示,雌激素缺乏、copeptin过高及IGF-1过低是aSAH预后不良的危险因素(均P＜0.05);ROC曲线分析雌激素、血清copeptin及IGF-1水平预测aSAH患者预后的AUC分别为0.770、0.865、0.739(均P＜0.05).结论 aSAH患者的预后情况与雌激素、IGF-1及copeptin水平异常密切相关,可为临床预后评估及围术期生物学指标监测提供一定参考价值.

目的 探讨微RNA(microRNA,miR)-138-5p对胶质瘤细胞增殖、侵袭的调控机制.方法 体外培养人胶质瘤U251细胞,采用随机数字表法将其分为对照组(n=6)、miR-NC组(n=6)、miR-138-5p组(n=6)、miR-138-5p+pc-NC组(n=6)、miR-138-5p+pc-细胞分裂周期5样(cell division cycle 5-like,CDC5L)组(n=6).采用实时荧光定量PCR(real-time quantitative PCR,RT-qPCR)检测细胞中miR-138-5p、CDC5L mRNA水平,检测细胞增殖活力、细胞周期和细胞凋亡以及细胞侵袭能力,检测细胞中CDC5L和侵袭相关蛋白表达.结果 miR-138-5p的过表达可下调CDC5L mRNA和蛋白水平,降低胶质瘤细胞增殖活力和侵袭能力,并诱导G2/M期细胞周期停滞,促进细胞凋亡,降低N-钙粘蛋白、波形蛋白水平,升高E-钙粘蛋白水平,差异均有统计学意义(P<0.05);上调CDC5L表达可明显逆转过表达miR-138-5p对胶质瘤细胞恶性生物学行为的影响(P<0.05);与miR-NC和CDC5L-WT质粒共转染比较,miR-138-5p mimic和CDC5L-WT质粒共转染的细胞中荧光素酶活性降低,差异有统计学意义(P<0.05).结论 过表达miR-138-5p可能通过靶向下调CDC5L,抑制胶质瘤细胞增殖和侵袭.

目的 分析神经生长抑制因子A(Nogo-A)、高迁移率蛋白-1(HMGB-1)、Adropin蛋白对脑出血的诊断价值.方法 选取2018年5月-2020年5月浙江省温州市人民医院收治的脑出血患者51例为脑出血组,另选取同时期在该院体检的体检健康者50例为健康对照组,采用酶联免疫吸附法检测Nogo-A、HMGB-1、Adropin表达水平,分析Nogo-A、HMGB-1、Adropin水平对脑出血的诊断价值.结果 与健康对照组相比,脑出血组Nogo-A、HMGB-1表达量较高,Adropin表达量较低,差异有统计学意义(P<0.05).血清Nogo-A、HMGB-1、Adropin诊断脑出血的ROC曲线下面积(AUC)分别为0.761(95％CI:0.883～1.00,P<0.01),0.844(95％CI:0.816～0.985,P<0.01),0.892(95％CI:0.869～0.984,P<0.01),三者联合诊断的AUC为0.944(95％CI:0.883～1.964,P<0.01).结论 Nogo-A、HMGB-1在脑出血患者血清中表达升高,Adropin蛋白在脑出血患者血清中表达降低,对脑出血具有一定的诊断价值,其中三项联合对脑出血的诊断价值较高.

目的 本研究探讨了二甲双胍对胶质瘤细胞替莫唑胺(TMZ)化疗敏感度的影响以及分子机制研究.方法 TMZ联合二甲双胍药物处理胶质瘤细胞,qRT-PCR及Western blot法检测蛋白表达;细胞免疫荧光检测HIF-1α 细胞定位和表达;葡萄糖和乳酸检测试剂盒检测葡萄糖消耗量和乳酸释放量;Annexin V-FITC/PI染色检测细胞凋亡;CCK8测定IC50检测胶质瘤细胞TMZ化疗敏感度;mTOR激动剂联合TMZ和二甲双胍处理胶质瘤细胞,检测化疗敏感度变化.结果 TMZ单独处理能够促进HIF-1α表达,并且研究发现下调HIF-1α表达使得糖酵解活性降低,PD-L1表达下调.同时,TMZ联合二甲双胍处理使得胶质瘤细胞HIF-1α表达下调,糖酵解活性降低,PD-L1表达下调,并且促进了细胞凋亡,TMZ的IC50值变小.此外,mTOR激动剂(MHY1485)减弱了二甲双胍对胶质瘤细胞TMZ化疗敏感度的增强作用.结论 本研究阐明了二甲双胍通过调节糖酵解活性增强了胶质瘤细胞对TMZ的化疗敏感度,为提升胶质瘤现有治疗药物敏感度、寻找新的有效干预策略提供了科学依据.

Background: Malignant gliomas are the most prevalent malignancy of the brain. However, there was still lack of sensitive and accurate biomarkers for gliomas. Objective: To explore the mechanisms underlying glioma progression and identify novel diagnostic and prognostic markers for glioma. Methods: By analyzing TCGA dataset, whole-genome genes expression levels were evaluated in 19 different types of human cancers. A protein-protein interacting network was constructed to reveal the potential roles of these glioma special genes. KEGG and GO analysis revealed the potential effect of these genes. Results: We identified 698 gliomas specially expressed genes by analyzing TCGA dataset. A protein-protein interacting network was constructed to reveal the potential roles of these glioma special genes. KEGG and GO analysis showed gliomas specially expressed genes were involved in regulating neuroactive ligand-receptor interaction, retrograde endocannabinoid signaling, Glutamatergic synapse, chemical synaptic transmission, nervous system development, central nervous system development, and learning. Of note, GRIA1, GNAO1, GRIN1, CACNA1A, CAMK2A, and SYP were identified to be down-regulated and associated with poor prognosis in gliomas. Conclusion: GRIA1, GNAO1, GRIN1, CACNA1A, CAMK2A, and SYP were identified to be down-regulated and associated with poor prognosis in gliomas. We thought this study will provide novel biomarkers for gliomas.

目的 探究分析胶质瘤患者术后伴随癫痫的临床特征及组织中高迁移率族蛋白B1(high mobility group box protein B1,HMGB1)的表达情况.方法 选择温州市人民医院2013年1月-2017年6月收治的101例胶质瘤术后痫性再发的患者,并选择同期该院收治的胶质瘤未发癫痫的患者70例、无肿瘤仅发癫痫的患者70例以及进行颅内减压手术的患者50例.比较胶质瘤并癫痫患者的临床病理因素对HMGB1表达的影响,比较4组患者的HMGB1表达情况,分析胶质瘤病理级别、癫痫的存在与否与胶质瘤组织中HMGB1表达的影响.结果 胶质瘤并癫痫组患者致痫灶组织中HMGB1的表达与患者的性别、年龄和致痫灶所处位置差异无统计学意义(均P＞0.05);患者致痫灶组织中HMGB1的表达与患者的胶质瘤病理级别、癫痫持续时间和发作频率有明显相关性,差异具有统计学意义(均P ＜0.05).胶质瘤并癫痫组的HMGB1阳性表达量高于胶质瘤非癫痫组、无肿瘤癫痫组的HMGB1阳性表达量.对胶质瘤并癫痫组和胶质瘤非癫痫组不同病理级别的HMGB1的表达,低病理级别组中,胶质瘤并癫痫组患者的HMGB1表达量更高,差异有统计学意义(P＜0.05);高病理级别组中,胶质瘤并癫痫组患者的HMGB1表达量与胶质瘤非癫痫组相比,差异无统计学意义(P＞0.05).结论 胶质瘤术后伴随痫性患者的胶质瘤组织中HMGB1表达量高,并与患者的病理级别、癫痫持续时间和发作频率有关,HMGB1的高表达可能与癫痫发作有关,具有临床研究价值.

Objective To detect the expressions of high mobility group box-1,nuclear factor-kB(NF-kB)in tumor tissues of glioma patients and analyze the correlation of HMGB1 and NF-kB expressions with tumor pathology. Methods A total of 76 patients who undertook glioma resection were selected as observation group,and 20 patients who undertook intracranial decompression were selected as control group during September 2013 to September 2017. The expressions of HMGB1 and NF-kB were detected by SP immunohistochemistry(SP)and analyzed by combining clinical factors and postoperative tumor pathology to investigate the relationship between the expression levels of HMGB1 and NF-kB and the pathology of glioma. Results The positive expression rates of HMGB1 and NF-kB in glioma tissues of the observation group were both higher than those of the control group(P<0.05). The expression levels of HMGB1 and NF-kB in glioma tissues were observed in the observation group. The pathological grade of the tumor was related(P<0.05). Expression levels of HMGB1 and NF-kB in glioma tissue of the trial group were related with pathological grade of glioma(P<0.05). In the observation group,HMGB1 expression level was positively correlated with NF-kB expression level(r=0.316,P<0.05). Conclusion HMGB1 and NF-kB are significantly higher in glioma tumor specimens than normal tissues,and the expression of HMGB1 and NF-kB is correlated with tumor pathological grade,suggests that may be closely related to the occurrence and pathology of glioma.

Emerging evidences show RNA back-splicing produces a new type of noncoding RNA, namely circular RNA (circRNA). Many reports demonstrate that circRNA circHIPK3 exerts oncogenic or anti-tumor roles in different cancers, such as ovarian cancer, bladder cancer, osteosarcoma, colorectal cancer and liver cancer. However, no study about circHIPK3 function in glioma exists until today. In this study, we showed that circHIPK3 was upregulated in glioma tissues. Elevated level of circHIPK3 was linked to poor prognosis. Functional investigation indicated that circHIPK3 promotes glioma cell proliferation and invasion, and tumor propagation in vivo. Furthermore, miR-654 was identified as a target of circHIPK3 while IGF2BP3 was targeted by miR-654. CircHIPK3 could promote IGF2BP3 expression via interacting with miR-654 in glioma cells. Finally, CCK8 and transwell assays illustrated that IGF2BP3 overexpression could reverse the effects of IGF2BP3 depletion. Altogether, our findings demonstrated that circHIPK3 contributes to glioma progression through targeting miR-654 from IGF2BP3 and implies circHIPK3 might be a potential target for glioma therapy.

目的 探讨超声多普勒(Carotid artery Doppler ultrasound,CDU)在评价颈动脉血管重建术后再狭窄中的意义.方法 选取行颈动脉内膜剥脱术(Carotid endarterectomy,CEA)和颈动脉支架置入术(Carotid artery stenting,CAS)的患者75例共95支血管.于术后12个月行颈动脉多普勒超声和数字减影血管造影(Digital Subtrac-tion Angiography,DSA),以DSA诊断为金标准,观察不同狭窄程度患者CDU指标差异,评估CDU指标在判断不同狭窄程度血管中的ROC曲线下面积,比较CDU指标评价不同狭窄程度血管的诊断效能.结果 (1)术后12个月DSA检查显示,70支血管无明显狭窄或轻度狭窄(狭窄程度<50％),16支血管中度狭窄(狭窄程度50～79％),9支血管重度狭窄(狭窄程度≥80％);与狭窄程度<50％血管相比,狭窄程度50％～79％和≥80％血管的颈动脉内径(t=9.877,16.109,P=0.000,0.000)显著缩小,PSV(t=8.466,13.571,P=0.000,0.000)、EDV(t=8.136,20.914,P=0.000,0.000)、PSVICA/PSVCCA(P=5.801,12.602;P=0.000,0.000)显著升高;(2)预测再狭窄程度50％～79％的CDU各指标ROC曲线下面积分别为PSV(0.992)、EDV(0.899)、PSVICA/PSVCCA(0.892),PSV预测再狭窄50％～79％的ROC曲线下面积明显高于EDV和PSVICA/PSVCCA,PSV的最佳截点为210cm/s;预测再狭窄程度≥80％的CDU各指标ROC曲线下面积分别为PSV(0.984)、EDV(0.812)和PSVICA/PSVCCA(0.924),PSV预测再狭窄≥80％的ROC曲线下面积明显高于EDV和PSVICA/PSVCCA,PSV的最佳截点为285cm/s;(3)以ROC曲线得出的最佳截点为界值,PSV在评价再狭窄程度≥50％和≥80％时的诊断准确率、灵敏度和阳性预测值均明显高于EDV和PSVICA/PSVCCA.结论 超声多普勒能够有效评价CAS和CEA术后颈动脉再狭窄程度,其中PSV≥210cm/s和285cm/s可作为再狭窄≥50％和≥80％的参考指标.

White blood cell count to mean platelet volume ratio (WMR), a combination of both WBC and mean platelet volume, has been reported as a novel and promising prognostic marker in patients with non-ST elevation acute coronary syndrome and ST-segment elevation myocardial infarction. We speculated that WMR, a combination of two inflammatory marker (WBC and mean platelet volume), may be a novel inflammatory marker. Since the presence of inflammation plays an important role in the pathogenesis of myasthenia gravis (MG), we aimed to evaluate diagnostic information of admission WMR and the relationship between admission WMR and disease disability and progression in patients with MG. Venous blood was drawn and hematological parameters were obtained from 373 individuals comprising 185 patients with MG and 188 healthy controls (HC). We confirmed that admission WMR in MG patients were significantly higher than those in the HC group. We also found that WMR has the highest area under ROC curve (AUC 0.733, 95% CI, 0.685 to 0.778) and WMR has the highest discriminative ability for differentiating MG patients from healthy controls. Moreover, the relative increase in the mean WMR of the patients with MG were observed to be positively correlated with the degree of disease disability expressed by the MGFA clinical classification (r = 0.234, P = 0.001). Multiple regression analysis suggested that WMR was independently associated with the degree of disease disability performed by the MGFA scores after adjustment by CRP, PLR. In conclusion, we evidenced that WMR could be considered as a novel inflammatory marker in patients with MG. Furthermore, we demonstrated that WMR was positively correlated with disability in patients with MG.

BACKGROUND Neural stem cells are reported to exist in the hippocampus of adult mammals and are important sources of neurons for repair. The Notch1 signaling pathway is considered as one of the important regulators of neural stem cells, but its role in adult brains is unclear. We aimed to describe the role of Notch1 signaling in the adult rat hippocampus after traumatic brain injury. MATERIAL AND METHODS The model rats were randomly divided into 4 groups as follows: sham, sham-TBI, sham-Ad-TBI, and NICD-Ad-TBI. We used adenovirus-mediated gene transfection to upregulate endogenous NICD in vivo. Firstly, a TBI rat model was constructed with lateral fluid percussion. Then, the hippocampus was collected to detect the expression of Notch1 markers and stem cell markers (DCX) by Western blot analysis, immunohistochemistry, and immunofluorescence. The prognosis after TBI treatment was evaluated by the Morris Water Maze test. RESULTS First, we found the expression of NICD in vivo was significantly increased by adenovirus-mediated gene transfection as assessed by Notch1 immunofluorescence and Western blot analysis. Second, enhancing NICD stimulated the regeneration of neural stem cells in the DG of the adult rat brain following traumatic brain injury, as evaluated by DCX and NeuN double-staining. Furthermore, Notch1 signaling activation can promote behavioral improvement after traumatic brain injury, including spatial learning and memory capacity. CONCLUSIONS Our findings suggest that targeted regulation of Notch1 signaling may have a useful effect on stem cell transformation. Notch1 signaling may have a potential brain-protection effect, which may result from neurogenesis.

Background: Pituitary apoplexy is a rare disease caused by a sudden hemorrhage into or infarction of the pituitary gland. Its optimal management remains controversial. The aim of this study was to compare the outcomes of surgical and non-surgical treatments for pituitary apoplexy.Methods: A systematic literature search was performed of MedLine, EmBase, the Cochrane Library, and the Web of Science for articles published between January 1992 and September 2014. Studies of the outcomes in consecutive patients that compared surgical intervention with non-surgical treatment for pituitary apoplexy were included.Results: Six studies met the inclusion criteria. As compared to the non-surgically treated patients, surgically treated patients had a significantly higher rate of recovery of ocular palsy and visual field (both P < 0.05). However, there was no significant difference in the recovery of visual acuity and pituitary function (P > 0.05) between the two groups.Conclusions: The findings of our study suggest that surgical intervention should be advocated for pituitary apoplexy patients with visual field defects and ocular palsy. (C) 2016 Elsevier B.V. All rights reserved.

Glioma is a malignant tumor that affects all kinds of people all over the world. It demonstrates remarkable infiltrative and invasive features. The high expression of interleukin-13 receptor subunit alpha-2 (IL-13Rα2) reportedly plays a pivotal role in some cancers. However, whether IL-13Rα2 contributes to glioma remains unknown. This study demonstrates that IL-13Rα2 is significantly up-regulated in human glioma tissue samples. It is also associated with late stages of disease progression and diminished survival in glioma patients. Gain- and loss-of-function studies demonstrate that IL-13Rα2 promotes the growth, migration, and invasion of glioma cells. In addition, mechanistic investigations show that IL-13Rα2 activates Scr, phosphatidylinositol 3 kinase (PI3K), Akt, and mTOR. Also, restraining Scr in glioma cells attenuates the activation of Scr/PI3K/Akt/mTOR pathway by IL-13Rα2, whereas the silencing of Scr markedly rescues the pro-invasive effect of IL-13Rα2. In conclusion, our results suggest that the high expression of IL-13Rα2 is significantly associated with the growth and metastasis of human glioma cells via the Scr/PI3K/Akt/mTOR pathway, while IL-13Rα2 may be a potential therapeutic target for glioma treatment.

Objective: By detecting Notch 1 signaling pathway proteins Jagged 1 and Hes 1 in light of heavy colsed craniocerebral injury. The role of Notch 1 signaling pathways in traumatic brain injury was explore and the new direction of treatment for closed craniocerebral injury was provide.Methods: Use lateral lfuid per-cussion method to make the light, medium and heavy closed craniocerebral trauma models. Groups of rats after 24 h of neurologic deifcits were evaluated through the nervous system disease severity score (NSS), then use immunohistochemistry and Western blot methods were used to detect Notch 1 signaling pathway downstream factors Jagged 1 and Hes 1.Results: The NSS score difference among the TBI groups was statistically signiifcant (P<0.05), the brain contusion was heavier, the neurologic deifcits were more obvious, which means the model was established successfully. Immunohistochemistry and Western blot showed that in brain contusion the expres-sion of Hes 1 and Jagged 1 levels were signiifcantly higher than that the control group (P<0.05), and increased with the degree of brain injury, the expression of the proteins was increased.Conclusion: Notch 1 signaling path-way may be involved in the development process of craniocerebral injury, and may become the new target for therapy after traumatic brain injury.

Objective: To study the protective effect of hydrogen on renal injury induced by type 1 dibetes in mice and explore the possible mechanism.Methods: Sixty healthy male ICR mice were randomly divided into control group (A), diabetic group (B) and diabetes hydrogen water intervention group (C). Diabetes were induced by intraperitoneal injection of streptozotocin 150 mg/kg. Group C were injected saturated hydrogen-rich water 5 mL/kg and group B were injected with equal normal saline every day for 8 weeks in mice models of type 1 dibetes. The blood was collected from the tail vein and blood glucose was measured. Renal injury were identiifed by hematoxylin and eosin (HE) staining. Expression of Nox4 and HO-1 were identiifed by immuno-histochemical staining.Results: Expression of Nox4 in Group C was signiifcantly lower than that in group B, expression of HO-1 in Group C was signiifcantly higher than that in group B. Blood glucose in Group B and C were higher than that in Group A, but there was no difference between the two groups. Kidney HE staining did not show signiifcant lesions.Conclusion: Hydrogen-rich water can reduce oxidative stress in renal tissue of dia-betic mice.