TopoisomeraseⅡαGene as a Marker for Prognostic Prediction of Hepatocellular Carcinoma:A Bioinformatics Analysis

Objective To investigate the expression of topoisomeraseⅡα(TOP2α)in hepatocellular carcinoma(HCC)and its role in predicting prognosis of HCC patients.Methods We used HCC-related datasets in UALCAN,HCCDB,and cBioPortal databases to analyze the expression and mutation of TOP2αand its co-expressed genes in HCC tissues.GO function and KEGG pathway enrichment of TOP2αand its co-expressed genes were identified.The TIMER database was used to analyze infiltration levels of immune cells in HCC.The impacts of TOP2αand its co-expression genes and the infiltrated immune cells on the survival of HCC patients were assayed by Kaplan-Meier plotter analysis.Results TOP2αand its co-expression genes were highly expressed in HCC(P<0.001)and detrimental to overall survival of HCC patients(P<0.001).TOP2αand its co-expression genes were mainly involved in cell mitosis and proliferation,and cell cycle pathway(ID:hsa04110,P=0.001945).TOP2αand its co-expression genes were mutated in HCC and the mutations were significantly detrimental to overall survival(P=0.0247)and disease-free survival(P=0.0265)of HCC patients.High TOP2αexpression was positively correlated with the infiltration of B cell(r=0.459,P<0.01),CD8^(+)T cell(r=0.312,P<0.01),CD4^(+)T cell(r=0.370,P<0.01),macrophage(r=0.459,P<0.01),neutrophil(r=0.405,P<0.01),and dendritic cell(r=0.473,P<0.01)in HCC.The CD8^(+)T cell infiltration significantly prolonged the 3-and 5-year survival of HCC patients(all P<0.05),and CD4^(+)T cell infiltration significantly shortened the 3-,5-,and 10-year survival of HCC patients(all P<0.05).Conclusion TOP2αmay be an oncogene,which was associated with poor prognosis of HCC patients and could be used as a biomarker for the prognostic prediction of HCC.

Ki-67及TopoisomeraseⅡ在脑胶质母细胞瘤组织中的表达及其生物学意义

目的探讨人胶质母细胞瘤中Ki-67及TopoisomeraseⅡ（TopoⅡ）之间的相关性及其与胶质母细胞瘤病人预后的关系。方法收集O6-甲基鸟嘌呤-DNA甲基转移酶（MGMT）低表达的胶质母细胞瘤标本60例,应用免疫组化法检测Ki-67和TopoⅡ的表达,研究其相关性。结果在MGMT低表达的胶质母细胞瘤中,Ki-67与TopoⅡ表达呈正相关（γ=0.83,P〈0.05）。对本组标本来源的60例胶质母细胞瘤病人随访12~23个月,其中死亡38例,肿瘤复发46例。结论 Ki-67和TopoⅡ在胶质母细胞瘤中的表达强度相对一致;其表达能客观反映肿瘤细胞的增殖活性和恶性程度,且可能影响胶质母细胞瘤病人的预后。

免疫组化检测大肠癌GST-π、TopoisomeraseⅡ-α表达的临床意义

目的 探讨GST -π、TopoisomeraseⅡ -α蛋白与大肠癌病理学特征之间的关系。方法 分别用鼠抗人TopoisomeraseⅡ -α单克隆抗体和兔抗人GST -π抗体对 6 0例大肠癌石蜡标本进行免疫组化研究。结果 1.GST -π、TopoisomeraseⅡ -α蛋白的表达和肿瘤大小、部位及类型无关 (P >0 .0 5 ) ;但与肿瘤的分化程度、临床分期、淋巴结转移有统计学差异 (P <0 .0 0 1)。 2 .GST -π在癌灶及癌旁组织中的表达意义不同 ,在肿瘤组织中低分化组高表达而在癌旁组织中则低表达 ,二者有统计学差异 (P <0 .0 0 1) ;TopoisomeraseⅡ -α在高分化组的表达高于低分化组 (P <0 .0 0 1)。结论 1.GST -π在瘤组织中的表达强度及在癌旁组织中的表达均与肿瘤的分化及临床分期有关 ,可作为肿瘤预后的指标。 2 .Topoi someraseⅡ -α在肿瘤组织中的表达和其分化、淋巴结转移有关 。

TopoisomeraseⅡ-α在大肠癌中的表达和临床意义

目的 探讨TopoisomeraseⅡ α蛋白与大肠癌病理学特征之间 ,耐药之间的关系。 方法 分别用鼠抗人TopoisomeraseⅡ α单克隆抗体对 60例大肠癌石蜡标本进行免疫组化研究。 结果 TopoisomeraseⅡ α蛋白及癌旁组织中的表达和性别、肿瘤大小、部位及类型无关 (P >0 .0 5 ) ;但与肿瘤的分化程度、Dukes分期、TMN分期、临床分期、淋巴结转移有统计学差异 (P <0 .0 0 1)。TopoisomeraseⅡ α在高分化组的表达高于低分化组 (P <0 .0 0 1) ,淋巴结转移组表达则低于无淋巴结转移组 (p <0 .0 0 1)。结论 TopoisomeraseⅡ α在肿瘤组织中的表达 ,强度和肠癌生物学特性密切相关 ,与肿瘤的分化及临床分期、淋巴结转移有关 ,可做为衡量恶性程度 ,耐药性及预后的指标之一。

Inhibitory effects of lapachol on rat C6 glioma in vitro and in vivo by targeting DNA topoisomerase Ⅰ and topoisomerase Ⅱ

OBJECTIVE The aim of this study is to investigate the inhibitory effects of lapachol on rat C6 glioma both in vitro and in vivo,as well as the potential mechanisms.METHODS First,the model of C6 glioma in Wistar rats was established and verified by hemotoxylin and eosin staining,immunohistochemical staining and magnetic resonance imaging(MRI).Then different doses of lapachol were gavaged and tumor volumes of the C6 glioma were detected by MRI.The effects of lapachol on C6 cell proliferation,apoptosis and DNA damage were detected by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium(MTS)/phen-azinemethosulfate(PMS)assay,Hoechst33358 staining,AnnexinⅤ-FITC/PI staining,and comet assay.Effects of lapachol on topoisomeraseⅠ(TOPⅠ)and topoisomeraseⅡ(TOPⅡ)activities were detected by TOPⅠand TOPⅡmediated supercoiled p BR322 DNA relaxation assay.Molecular docking was used to predict the interaction of lapachol-TOPⅠand lapachol-TOPⅡ.TOP I and TOPⅡexpression levels in C6 cells were determined by Enzymelinked immunosorbent assay kits and real-time polymerase chain reaction(RT-PCR).RESULTS The rat C6 glioma model was successfully established.High dose lapachol showed significant inhibitory effect on the C6 glioma in Wistar rats(P<0.05).MTS/PMS assay,Hoechst 33258 staining,AnnexinⅤ-FITC/PI staining,and comet assay showed that lapachol could inhibit proliferation,induce apoptosis and DNA damage of C6 cells in dose dependent manners.Lapachol could inhibit the activities of both TOPⅠandⅡ.Molecular docking showed that lapachol-TOPⅠshowed relatively stronger interaction than that of lapachol-TOPⅡ.Enzyme-linked immunosorbent assay and RT-PCR showed that lapachol could inhibit TOPⅡexpression levels,but not TOPⅠexpression levels.CONCLUSION These results showed that lapachol could significantly inhibit C6 glioma both in vivo and in vitro,which might be related with inhibiting TOPⅠand TOPⅡactivities,as wel as TOPⅡexpression.

血管紧张素Ⅱ对大鼠骨髓间充质干细胞棕色脂肪变的抑制作用

背景:骨髓间充质干细胞是脂肪细胞的来源之一,且表达所有肾素血管紧张素系统成分,但血清血管紧张素Ⅱ对骨髓间充质干细胞向棕色脂肪组织分化的影响尚不清楚。目的:观察血管紧张素Ⅱ对骨髓间充质干细胞向棕色脂肪细胞分化的影响,并探究血管紧张素1a型受体敲除对血管紧张素Ⅱ影响骨髓间充质干细胞向棕色脂肪细胞分化的作用及可能机制。方法:分离培养野生型SD大鼠及血管紧张素1a型受体敲除SD大鼠的骨髓间充质干细胞,将其培养至第3代,随机分为4组:野生组,基因敲除组,野生+血管紧张素Ⅱ组,基因敲除+血管紧张素Ⅱ组,在棕色脂肪诱导分化培养基中诱导分化14 d,后2组在每次更换分化培养基的同时加入100 nmol/L血管紧张素Ⅱ进行干预。采用Western blot、qRT-PCR、免疫荧光等方法检测棕色脂肪诱导分化、脂肪分解、β氧化和线粒体生物发生等相关标记物的表达。结果与结论:血管紧张素Ⅱ可抑制骨髓间充质干细胞向棕色脂肪细胞分化,敲除血管紧张素1a型受体基因能够通过促进脂肪分解、增强脂肪酸β氧化、促进线粒体生物发生、增强线粒体功能来改善血管紧张素Ⅱ对骨髓间充质干细胞向棕色脂肪细胞分化的抑制作用。这些发现为肥胖治疗提供了新的研究方向和潜在治疗靶点,揭示了肾素血管紧张素系统在脂肪代谢中的重要作用及其作为治疗目标的潜力。

Inhibitory effects of lapachol on rat C6 glioma in vitro and in vivo by targeting DNA topoisomeraseⅠ and topoisomeraseⅡ

OBJECTIVE Lapachol is a natural naphthoquinone compound that possesses extensive biological activities.The aim of this study is to investigate the inhibitory effects of lapachol on rat C6 glioma both in vitro and in vivo,as well as the potential mechanisms.METHODS The antitumor effect of lapachol was firstly evaluated in the C6 glioma model in Wistar rats.The effects of lapachol on C6 cell proliferation,apoptosis and DNA damage were detected by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium(MTS)/phenazinemethosulfate(PMS)assay,hoechst 33358 staining,annexinⅤ-FITC/PI staining,and comet assay.Effects of lapachol on topoisomerase I(TOP I)and topoisomeraseⅡ(TOPⅡ)activities were detected by TOPⅠand TOPⅡmediated supercoiled p BR322DNA relaxation assays and molecular docking.TOPⅠand TOPⅡexpression levels in C6 cells were also determined.RESULTS High dose lapachol showed significant inhibitory effect on the C6 glioma in Wistar rats(P<0.05).It was showed that lapachol could inhibit proliferation,induce apoptosis and DNA damage of C6 cel s in dose dependent manners.Lapachol could inhibit the activities of both TOPⅠ and Ⅱ.Lapachol-TOPⅠshowed relatively stronger interaction than that of lapachol-TOPⅡin molecular docking study.Also,lapachol could inhibit TOPⅡexpression levels,but not TOPⅠexpression levels.CONCLUSION These results showed that lapachol could significantly inhibit C6 glioma both in vivo and in vitro,which might be related with inhibiting TOPⅠ and TOPⅡ activities,as wel as TOPⅡ expression.

Fitness profiling links topoisomeraseⅡregulation of centromeric integrity to doxorubicin resistance in fission yeast

OBJECTIVE To address the molecular implication of Top2 in the context of its interaction with doxorubicin resistance(DXR)genes.METHODS To perform epistasis analyses of top2 with 63genes representing doxorubicin resistance(DXR)genes in fission yeast.Fission yeast cells with single and double mutants were serial diluted and spotted to plates containing 15-75μg·mL-1 doxorubicin.Plates were scanned after 3and 7d.Cell growth was measured and compared between single mutants and double mutants.Nucleus morphology was performed by staining the cells with 4′,6-diamidino-2-phenylindole(DAPI)to observe chromosome segregation.Reverse transcriptase PCR(RT-PCR)was employed to visualize the changes in transcription level and evaluate the stability of chromatin structure.RESULTS Our findings revealed a subset that synergistically collaborate with Top2 to confer DXR and showed that the chromatin-regulating RSC and SAGA complexes act with Top2 in a cluster that is functionally distinct from the Ino80 complex.In various DXR mutants,doxorubicin hypersensitivity was unexpectedly suppressed by a concomitant top2 mutation.Several DXR proteins showed centromeric localization,and their disruption resulted in centromeric defects and chromosome missegregation.An additional top2 mutation could restore centromeric chromatin integrity,suggesting a counterbalance between Top2 and these DXR factors in conferring doxorubicin resistance.CONCLUSION The findings reported here show a functional interaction between Top2 and factors that confer genomic stability at centromeric chromatin under doxorubicin condition.Overall,this molecular basis for mitotic catastrophe associated with doxorubicin treatment will help to facilitate drug combinatorial usage in Doxorubicin-related chemotherapeutic regimens.

基于Cre-loxP重组酶系统构建肺泡Ⅱ型上皮细胞特异性敲除SENP1基因小鼠

背景:前期在体外成功构建了SENP1基因沉默的人肺泡上皮细胞系,在细胞水平上研究了SENP1在高氧性肺损伤中的作用。目的:基于Cre-loxP重组酶系统构建肺泡Ⅱ型上皮细胞特异性敲除SENP1基因小鼠模型。方法:将SENP1^(flox/-)小鼠自交得到SENP1^(flox/flox)和SENP1^(flox/-)小鼠;将Sftpc-Cre^(+/+)小鼠与野生型小鼠交配获得更多的Sftpc-Cre^(+/-)小鼠。将Sftpc-Cre^(+/+)或子代Sftpc-Cre^(+/-)小鼠与SENP1^(flox/-)或子代SENP1^(flox/flox)小鼠进行杂交,获得SENP1^(flox/-)Sftpc-Cre^(+/-)双杂合小鼠。将SENP1^(flox/-)Sftpc-Cre^(+/-)小鼠与SENP1^(flox/flox)小鼠杂交,获得SENP1^(flox/flox)Sftpc-Cre^(+/-)小鼠。剪鼠尾提取基因组DNA,行PCR扩增,扩增产物经琼脂糖凝胶电泳确定小鼠基因型。取SENP1^(flox/flox)和SENP1^(flox/flox)Sftpc-Cre^(+/-)小鼠肺组织行免疫荧光双标实验及Western blot以验证SENP1敲除效果;取SENP1^(flox/flox)和SENP1^(flox/flox)Sftpc-Cre^(+/-)小鼠心、肝、肺、肾组织行苏木精-伊红染色以观察两组小鼠各脏器的组织形态。结果与结论:琼脂糖凝胶电泳正确筛选出SENP1^(flox/flox)Sftpc-Cre^(+/-)小鼠。免疫荧光双标实验显示,与SENP1^(flox/flox)小鼠相比,SENP1^(flox/flox)Sftpc-Cre^(+/-)小鼠肺组织中SENP1的平均荧光强度降低(P<0.01),且SENP1和Sftpc未见明显共定位(P<0.01)。Western blot结果显示,与SENP1^(flox/flox)小鼠相比,SENP1^(flox/flox)Sftpc-Cre^(+/-)小鼠肺组织中SENP1蛋白表达降低(P<0.001)。苏木精-伊红染色结果显示SENP1^(flox/flox)和SENP1^(flox/flox)Sftpc-Cre^(+/-)小鼠的心、肝、肺和肾脏组织形态无明显改变。该研究利用Cre-loxP重组酶系统成功构建了肺泡Ⅱ型上皮细胞特异性敲除SENP1基因小鼠,为后续研究SENP1基因在以肺泡Ⅱ型上皮细胞为主要损伤细胞的肺疾病如支气管肺发育不良、特发性肺纤维化中的作用提供了良好的工具。

芍药苷对血管紧张素Ⅱ诱导心肌成纤维细胞纤维化的保护作用

背景:研究表明芍药苷对肝、肾等器官纤维化具有改善作用,尤其是在肝纤维化中表现出突出优势,但芍药苷对于血管紧张素Ⅱ诱导的心肌纤维化的保护作用尚不明确。目的:探讨芍药苷对血管紧张素Ⅱ诱导的心肌成纤维细胞的保护作用及分子机制。方法:在分离培养的SD大鼠乳鼠心肌成纤维细胞中加入血管紧张素Ⅱ(1μmol/L)干预48 h作为模型组;芍药苷低、高剂量组给予不同剂量的芍药苷(50,100μmol/L)预处理2 h,再用血管紧张素Ⅱ处理48 h;SIRT1抑制剂组先用10μmol/L SIRT1抑制剂EX527处理2 h,再用100μmol/L芍药苷处理2 h,最后用血管紧张素Ⅱ处理48 h。采用CCK-8法检测细胞活力,Transwell检测细胞迁移能力,用DHA荧光探针检测细胞内活性氧水平,用试剂盒检测氧化应激标志物水平,Western blot检测纤维化相关基因的蛋白表达,qRT-PCR检测细胞外基质和纤维化相关基因的mRNA表达。结果与结论:①与对照组相比,血管紧张素Ⅱ干预后心肌成纤维细胞的增殖、迁移能力明显提高,细胞内活性氧和丙二醛水平升高,超氧化物歧化酶和过氧化氢酶活性降低,α-平滑肌肌动蛋白、Ⅰ型胶原蛋白、Ⅲ型胶原蛋白、纤维连接蛋白、结缔组织生长因子、基质金属蛋白酶9的mRNA表达增加;与模型组相比,芍药苷剂量依赖性抑制上述效应改变(P<0.01);②与模型组相比,芍药苷剂量依赖性上调SIRT1的蛋白表达(P<0.001);③与芍药苷高剂量组相比,SIRT1抑制剂组细胞迁移数量、α-平滑肌肌动蛋白、Ⅰ型胶原蛋白、Ⅲ型胶原蛋白表达水平显著增加(P<0.01)。结果表明,芍药苷可能通过上调SIRT1的表达,有效减轻了血管紧张素Ⅱ诱导的心肌成纤维细胞纤维化改变,剂量依赖性地抑制了心肌成纤维细胞氧化应激和细胞外基质沉积,对于心肌成纤维细胞纤维化具有保护作用。

尼莫地平对癫痫大鼠海马Ca^(2+)浓度及Ca^(2+)/钙调蛋白依赖性蛋白激酶Ⅱ_α表达的影响

目的探讨尼莫地平(nimodipin,NIM)对戊四氮(pentylenetetrazol,PTZ)点燃癫痫大鼠空间学习记忆能力及海马细胞内游离Ca2+浓度([Ca2+]i)、Ca2+/钙调蛋白依赖性蛋白激酶Ⅱα(calcium/calmodulin-dependent protein kinaseⅡα,CaMKⅡα)蛋白表达的影响。方法将动物分为正常对照组、PTZ组和NIM+PTZ组,采用PTZ慢性点燃癫痫模型,应用Mor-ris水迷宫观察各组大鼠空间学习记忆能力,运用流式细胞仪检测海马细胞内[Ca2+]i变化,Western blot方法测定CaMKⅡα蛋白的表达。结果PTZ组大鼠空间学习记忆能力受损,其海马细胞内[Ca2+]i明显升高(P<0.05),CaMKⅡα蛋白水平较正常对照组减少(P<0.05);与PTZ组比较,NIM+PTZ组大鼠空间学习记忆能力好转,其海马细胞内[Ca2+]i下降(P<0.05),CaMKⅡα蛋白水平升高(P<0.05)。结论PTZ点燃癫痫大鼠海马存在钙超载及CaMKⅡα的表达异常,由此引起大鼠空间学习记忆能力受损;NIM可以降低细胞内[Ca2+]i,提高CaMKⅡα的表达,改善癫痫大鼠的学习记忆能力。

Amplatzer动脉导管封堵器-Ⅱ治疗伴发主动脉窦脱垂室间隔缺损患儿效果分析

目的探讨Amplatzer动脉导管封堵器(ADO)-Ⅱ治疗伴发主动脉窦脱垂室间隔缺损(VSD)患儿的效果。方法回顾性收集2018年1月至2022年9月于湖南省儿童医院住院治疗的94例伴发主动脉窦脱垂VSD患儿临床资料。其中男60例,女34例,年龄为(4.7±3.1)岁;主动脉窦轻中度脱垂83例,VSD为(4.12±0.97)mm,重度脱垂11例,VSD为(4.95±0.51)mm;VSD类型为膜周部54例,嵴内以上40例。分析VSD大小、主动脉窦脱垂程度与ADO-Ⅱ选择的关系,以及术后中期主动脉瓣反流、残余漏变化,明确ADO-Ⅱ对此类患儿的适用性。结果术后中期最终存留主动脉瓣轻度反流6例,多发于使用4-4 mm、5-4 mm型ADO-Ⅱ封堵器;残余漏10例,主要发生于使用5-4 mm、6-4 mm型封堵器。结论ADO-Ⅱ封堵器在置入形态良好状况下,适用于VSD<6 mm伴主动脉窦脱垂患儿。术后有一定的残余漏和主动脉脉瓣反流发生,但能满足介入治疗要求。

基于改进NSGA-Ⅱ算法的间歇采油制度优化

对于低渗透率油井,采用间歇采油制度能有效避免空抽磨损,并减少电能消耗量。为此通过分析沉没度和地层流压随抽油机井生产时间变化的规律,从系统节能的角度出发,建立以采油总产量最大、能耗最低为目标的间歇采油制度多目标优化模型。引入NSGA-Ⅱ并改进该算法对间歇采油制度多目标优化模型求解,运用改进算法得到的Pareto最优解的多样性和收敛性,合理优化抽油机的最优停机时间,最大效率地提升采油效率的同时,最小化电能消耗量。试验结果表明,基于Pareto多目标遗传算法的间歇采油机制优化具有明显的优势,在优化系统效率的同时能够有效减少电能消耗。研究结果可为油井间歇采油机制的改进和优化提供有力的技术支持。

基于改进NSGA-Ⅱ的纤维缠绕落纱点轨迹采样特征权重优化

针对基于空间特征曲线特征函数的纤维缠绕落纱点轨迹采样算法无法自动选择特征权重的问题,建立以特征权重为变量,以得到采样点线性插值生成曲线与原曲线的MAE,RMSE为目标函数的双目标优化模型。提出基于改进NSGA-Ⅱ算法的双目标优化求解方法以优化特征权重。实例验证表明,与传统NSGA-Ⅱ算法相比,改进NSGA-Ⅱ算法求得Pareto解集的MAE,RMSE平均下降了0.002和0.105,算法选取特征权重的MAE,RMSE比特征权重为(0.1,0.3)的MAE,RMSE分别降低了约12.9%和8.5%,比特征权重为(0.9,0.1)的MAE,RMSE分别降低了约20.6%和11.4%,有效地提高了落纱点轨迹采样的精度。

基于改进NSGA-Ⅱ算法的梯级水库多目标优化调度

针对在时间步长较小、计算时段数目较多时,传统智能优化算法在求解梯级水库联合优化调度问题上效率低甚至无可行解的问题,提出了一种改进NSGA-Ⅱ算法。该算法基于NSGA-Ⅱ算法框架,引入参考目标值、潜力目标值、偏移度以及变异引导算子来优化种群进化过程,强化迭代中的种群质量,使获得的解集更加接近真实的Pareto前沿。福建省金溪流域梯级水库多目标优化调度实例验证结果表明,改进NSGA-Ⅱ算法相对其他算法运算效率更高,优化结果更好,具有较好的实用性。

股骨近端防旋髓内钉-Ⅱ治疗31-A3型股骨转子间骨折扩髓与否的有限元分析

背景:针对股骨转子间骨折是否需要扩髓的问题尚有争议,一些人认为不扩髓缩短手术时间、减少出血、降低高龄患者术中风险,但此举是否会降低髓内钉支撑效果,尚无依据。另一些人认为扩髓可选择直径更粗的髓内钉,获得更好的力学支撑,但基础研究显示此方法存在脂肪栓塞、破坏骨质(尤其高龄骨质疏松患者)等风险。目的:通过有限元分析股骨近端防旋髓内钉-Ⅱ治疗31-A3型股骨转子间骨折时扩髓与不扩髓的力学分布特点。方法:纳入一名健康志愿者,CT扫描其股骨获取DICOM格式文件,顺序导入Mimics、Geomagic Wrap、SolidWorks、Hypermesh、Ansys软件处理文件,得到A3.1型、A3.2型及A3.3型股骨转子间骨折模型,分别与9,11 mm直径、170 mm长度的股骨近端防旋髓内钉-Ⅱ进行装配,赋予材料属性,设定各接触面相互作用关系及定义载荷及边界条件,之后进行求解。观察不同模型中股骨应力分布、内固定应力分布、股骨位移及内固定位移情况。结果与结论:①各型骨折采用扩髓髓内钉固定时股骨应力均小于非扩髓髓内钉固定,A3.3型骨折股骨最大应力值大于A3.1型和A3.2型;②各型骨折采用扩髓髓内钉固定时内固定应力均大于非扩髓髓内钉固定,A3.3型骨折内固定最大应力值大于A3.1型;③扩髓与非扩髓对股骨及内固定位移影响较小,应力影响较大;④提示采用扩髓髓内钉固定可使股骨应力减小,内固定整体承担应力增大,远端锁钉承担应力减小;与非扩髓髓内钉固定相比,采用扩髓髓内钉固定可能会提供更好的治疗效果。

红外高光谱大气探测仪(FY-3E/HIRAS-Ⅱ)在轨数据非线性校正方法

风云三号E星(FY-3E)搭载的高光谱大气探测仪(HIRAS-Ⅱ)能够实现大气的垂直探测,具有高光谱、高灵敏度、高精度的特点。仪器在轨之后由于仪器衰减和环境变化的原因产生非线性响应,影响在轨定标精度。针对非线性响应的问题,提出了一种基于带内光谱的非线性校正方法。首先基于带外低频光谱的非线性特征求解非线性校正系数,将此系数作为初值输入到辐射定标模型中,以星上测量的黑体带内光谱与理想光谱的偏差为目标函数,通过迭代优化非线性校正系数。通过辐射定标实验得出,校正后的黑体亮温偏差明显低于未校正和基于带外光谱的校正方法。将HIRAS-Ⅱ的观测数据与IASI进行交叉比对并计算平均亮温偏差和偏差绝对值,经过带内校正法非线性校正后的亮温平均偏差为-0.13 K,优于带外校正方法。

醋酸戈舍瑞林联合反加屈螺酮炔雌醇片(Ⅱ)辅助手术治疗对子宫内膜异位症患者血清性激素水平和术后复发的影响

目的探讨醋酸戈舍瑞林联合反加屈螺酮炔雌醇片(Ⅱ)辅助手术治疗对子宫内膜异位症(EMS)患者血清性激素水平和术后复发的影响。方法选取2020年1月至2022年1月于青岛市市立医院就诊的104例EMS患者作为研究对象,随机分为对照组(n=52)和联合组(n=52)。对照组采用醋酸戈舍瑞林治疗,联合组采用醋酸戈舍瑞林联合反加屈螺酮炔雌醇片(Ⅱ)治疗。比较两组患者治疗前后雌二醇(E_(2))、黄体生成素(LH)、卵泡刺激素(FSH)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平及临床疗效,随访12个月期间疾病复发与妊娠情况,以及治疗期间安全性情况。结果治疗后,与对照组比较,联合组总有效率更高(P<0.05);两组治疗后E_(2)、LH、FSH水平均下降,但联合组治疗后比对照组高(P<0.05);两组治疗后IL-6和TNF-α水平均下降(P<0.05),两组间比较,差异无统计学意义(P>0.05);随访12个月期间,与对照组比较,联合组复发率更低,妊娠率更高(P<0.05);治疗期间,与对照组比较,联合组不良反应发生率更低(P<0.05)。结论醋酸戈舍瑞林联合反加屈螺酮炔雌醇片(Ⅱ)治疗EMS,可以提升治疗效果,改善性激素水平,降低疾病复发率和副作用发生率,提高妊娠率。

隐形矫治器矫治Ⅱ类错[牙合]畸形对颞下颌关节相关角度、间隙变化值的影响

目的 探讨隐形矫治器矫治Ⅱ类错[牙合]畸形对颞下颌关节的影响。方法 选取Ⅱ类错[牙合]畸形患者70例,采用信封法将患者分为观察组(n=35)和对照组(n=35),观察组给予隐形矫治器矫治,对照组给予自锁托槽矫治器矫治。观察两组颞下颌关节相关角度、间隙变化值等。结果 观察组矫治前后上中切牙长轴与前颅底平面相交的下内角(U1-SN)变化值、上中切牙长轴与鼻根点-上牙槽座点连线交角(U1-NA)变化值分别为(11.05±1.01)°和(4.75±0.76)°,明显高于对照组(P <0.05);观察组矫治前后上颌中切牙、上颌侧切牙、下颌中切牙、下颌侧切牙变化值分别为(0.51±0.21)、(0.40±0.15)、(0.40±0.13)、(0.20±0.05)mm,明显低于对照组(P <0.05);观察组矫治前后菌斑指数(PLI)、牙龈指数(GI)和探诊深度(PD)变化值分别为(0.44±0.19)分、(0.41±0.13)分、(0.38±0.10)mm,明显低于对照组(P <0.05)。结论 隐形矫治器矫治Ⅱ类错[牙合]畸形有较好的应用价值,有利于患者颞下颌关节改善。