MicroRNA-153对脑膜瘤细胞放疗敏感性的影响

目的探讨micro RNA-153对(mi R-153)对脑膜瘤细胞放疗敏感性的影响及其作用机制。方法采用实时荧光定量聚合酶链反应检测放疗前后脑膜瘤SF3061细胞系中mi R-153的表达变化,用脂质体转染技术将mi R-153 mimics及对照转染至SF3061细胞中,采用MTT法、流式细胞术及克隆形成实验检测放射处理后细胞的放疗敏感性变化。使用Target Scan预测及双荧光素酶报告基因实验验证mi R-153与视网膜母细胞瘤蛋白结合锌指1(RIZ1)的靶向作用,基因敲除RIZ1验证其对脑膜瘤细胞放疗敏感性的影响。结果脑膜瘤细胞经过放疗处理后mi R-153的表达水平降低;mi R-153 mimics提高放疗后细胞的增殖抑制率和凋亡率,降低细胞克隆形成率;Target Scan预测及双荧光素酶报告基因实验证实RIZ1是mi R-153的靶标;转染si-RIZ1增加脑膜瘤细胞的放疗敏感性。结论 mi R-153通过靶向干扰RIZ1的表达,增加脑膜瘤细胞的放疗敏感性。

Electroacupuncture reduces apoptotic index and inhibits p38 mitogen-activated protein kinase signaling pathway in the hippocampus of rats with cerebral ischemia/reperfusion injury

Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemia/reperfusion injury.To further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebral ischemia/reperfusion injury was associated with the p38 mitogen-activated protein kinase（MAPK） signaling pathway.We established rat models of cerebral ischemia/reperfusion injury using the modified Zea-Longa＇s method.At 30 minutes before model establishment,p38 MAPK blocker SB20358 was injected into the left lateral ventricles.At 1.5 hours after model establishment,electroacupuncture was administered at acupoints of Chize（LU5）,Hegu（LI4）,Zusanli（ST36）,and Sanyinjiao（SP6） for 20 minutes in the affected side.Results showed that the combination of EA and SB20358 injection significantly decreased neurologic impairment scores,but no significant differences were determined among different interventional groups.Hematoxylin-eosin staining also showed reduced brain tissue injuries.Compared with the SB20358 group,the cells were regularly arranged,the structures were complete,and the number of viable neurons was higher in the SB20358 ＋ electroacupuncture group.Terminal deoxynucleotidyl transferase（Td T）-mediated d UTP nick-end labeling assay showed a decreased apoptotic index in each group,with a significant decrease in the SB20358 ＋ electroacupuncture group.Immunohistochemistry revealed reduced phosphorylated p38 expression at 3 days in the electroacupuncture group and SB20358 ＋ electroacupuncture group compared with the ischemia/reperfusion group.There was no significant difference in phosphorylated p38 expression between the ischemia/reperfusion group and SB20358 group.These findings confirmed that the electroacupuncture effects on mitigating cerebral ischemia/reperfusion injury are possibly associated with the p38 MAPK signaling pathway.A time period of 3 days could promote the repair of ischemic cerebral nerves.

Electroacupuncture exerts neuroprotective effects on ischemia/reperfusion injury in JNK knockout mice：the underlying mechanism

Simple regulation of c-Jun N-terminal kinase（JNK） or p38 mitogen-activated protein kinase（MAPK） pathways is not enough to trigger cell apoptosis.However,activation of the stress activated pathway（JNK/p38 MAPK） together with inhibition of the growth factor activated extracellular signal-regulated kinase（ERK） pathway can promote cell apoptosis.We hypothesized that inhibition of the JNK or p38 pro-apoptotic pathway and activating the ERK pathway could be the mechanism of anti-apoptosis following cerebral ischemia/reperfusion injury.To investigate the mechanism of the protective effect of electroacupuncture on cerebral ischemia/reperfusion injury in JNK knockout mice,mouse models of cerebral ischemia/reperfusion injury were established by Longa’s method.Electroacupuncture was conducted at acupoints Chize（LU5）,Hegu（LI4）,Sanyinjiao（SP6） and Zusanli（ST36） 1.5 hours after ischemia/reperfusion injury for 20 minutes,once a day.The neurological function was evaluated using neurological deficit scores.The expression of phospho-extracellular signal-regulated kinase（p-ERK） and phospho-p38（p-p38） in JNK knockout mice was detected using double-labeling immunofluorescence and western blot assay.The m RNA expression of ERK and p38 was measured by quantitative real-time polymerase chain reaction.Electroacupuncture improved neurological function,increased the immunoreactivity and relative expression of p-ERK and reduced that of p-p38 in the cerebral cortex and hippocampus on the injured side.Electroacupuncture increased m RNA expression of ERK,but decreased that of p38 in the cerebral cortex and hippocampus on the injured side.In conclusion,electroacupuncture upregulated the protective ERK pathway and inhibited the pro-apoptotic p38 pathway,thereby exerting a neuroprotective effect and improving the neurological function in JNK knockout mice.

Effect of phosphorus on the microstructure and mechanical properties of strip cast carbon steel

有不同的磷和碳内容的碳钢脱衣被使用扔过程的成双的转动长带生产。好谷物和树突结构在 high-P 钢被观察。否定的磷分离在长带演员组 high-P 和 high-C 钢被发现。为有不同的碳内容的钢，在长带的厚度方向的磷分发显然是不同的。这是因为溶质在融化的水池被再分配，磷分离率在不同阶段与软糊糊的地区和磷溶解度的长度被联系。在铁酸盐的溶质能与更低的塑料 propertyies 导致更高的坚硬和力量的磷。

Effect of V and Sn on microstructure and mechanical properties of gray cast iron

The cylinder liner is one of the important parts of a diesel engine.Gray cast iron is the main material for manufacturing cylinder liners due to its good casting performance,convenient processing performance,good wear resistance and low cost.In the present work,the effects of vanadium(V)and tin(Sn)on the microstructure and properties of gray cast iron were studied.Results show that increasing the contents of V and Sn can not only refine the graphite,but also reduce the pearlite lamellar space.The graphite size and lamellar spacing of pearlite are firstly reduced and then increased.Pearlite quantity reaches over 98%after adding V and Sn.Adding V and Sn can promote the precipitation and solid solution strengthening of gray cast iron,so as to improve the mechanical properties.The Brinell hardness reaches the peak of 424 HB at the contents of 0.21wt.%V and 0.06wt.%Sn,and the sample containing 0.11wt.%V and 0.08wt.%Sn shows the highest compressive strength and tensile strength of 1,699 MPa and 515 MPa,respectively.The main strengthening mechanism comes from the solid solution strengthening and fine grain strengthening of V and Sn.

The progress in the verification of key technologies for floating structures near islands and reefs

In 2019 a Scientific Research&Demonstration Platform was deployed near islands and reefs in South China Sea by a joint research group of 7 institutes and universities in China.It is a simplified small model of a two-module semi-submersible-type VLFS.The test on site has continued for more than one and half years since then for long-term observations to validate the developed key technologies for design and behavior predictions of floating structures deployed near islands and reefs.An integrated information system was set up to continuously collect and inspect the data of the encountered waves,structure responses,connector forces,mooring line forces,anti-corrosion status of the platform,the performance efficiencies of a floating breakwater nearby and a wave energy converter attached on the breakwater.In this paper,the status of the on-site measurements and validations of the key technologies are briefly described.

MicroRNA-125b regulates Th17/Treg cell differentiation and is associated with juvenile idiopathic arthritis

Background Juvenile idiopathic arthritis(JIA)is the most common rheumatic disease in childhood driven by aberrant pathways of T-cell activation.T helper 17(Th17)/regulatory T cell(Treg)imbalance plays critical roles in the pathogenesis of arthritis.MicroRNA-125b(miR-125b)was upregulated after the activation of the initial CD4^+T cells,and could regulate the differentiation of CD4^+T cells.However,the effects of miR-125b on Th17/Treg imbalance and differentiation of Th 17/Treg cells remain unknown.Methods In this study,we evaluated the expression of miR-125b in the peripheral blood mononuclear cells(PBMCs)of children with JIA,and the relationship of miR-125b with Th17/Treg imbalance.Then,we used lentivirus vector-mediated overexpression technology to investigate the regulatory function of miR-125b in CD4^+T cells or dendritic cell/CD4^+T co-culture system.Results Decreased miR-125b expression in PBMCs and CD4^+T cells of JIA patients was negatively correlated with the ratio of Th17/Treg cells.It also correlated negatively with retinoic acid receptor-related orphan receptorγt but positively with Forkhead box protein 3 at transcriptional levels.Furthermore,we found that miR-125b overexpression inhibited Th17 cell differentiation,whereas facilitated the differentiation of Treg cells.MiR-125b upregulation led to the decrease of Th 17-secreting cytokines but the increase of the Treg-secreting cytokines.Conclusions Our results demonstrate that miR-125b participated in regulating Thl7/Treg cell differentiation and imbalance in JIA patients.These findings provide novel insight into the critical role of miR-125b in the Th17/Treg imbalance of JIA,and raise the distinct possibility that miR-125b may prove to be a potential therapeutic target for JIA.