Tanshinone Ⅱ A, the major lipophilic component of Danshen, promotes neuronal differentiation through MAPK42/44 mediated pathways

Danshen has been used in stroke treatment for thousands of years in China. However, the underlying mechanism still remains elusive. Neuron loss is the cardinal feature of stroke. Stimulating endogenous neurogene- sis, especially neuronal differentiation, might potentially provide therapeutic effects to these diseases. To interpret Danshen＇ s disease-modifying effects, the effects of tanshinone 11 A （T 11 A）, the major lipophilic component of Danshen, on neuronal differentiation in rat PC12 pheochromocytoma cells and the rat embryonic cortical neural stem cells （NSCs） were observed. PC12 cells and NSCs were incubated with T II A for 7 days. To detect the neu- ronal differentiation, GAP-43 expression was detected by western blots assay and β-tubulin HI expression was de- tected by immunocytochemical staining. Results showed that T Ⅱ A dose-dependently promoted neuronal differentia- tion. T Ⅱ A activated mitogen-activated protein kinase 42/44 （MAPK42/44） and its downstream transcription fac- tor, cAMP response element-binding protein （CREB）. In addition , T Ⅱ A up-regulated the expressions of brain de- rived neurotrophic factor （BDNF） and nerve growth factor （NGF）. The MEK inhibitor and the antagonist to the re- ceptors of NGF and BDNF could partially attenuate the differentiation effects, indicating that MAPK42/44 mediated BDNF and NGF signals were involved in T Ⅱ A＇ s differentiation effects. Caveolin-1 （ CAV-1 ）, the major functional protein of membrane caveolae, plays critical roles in the endocytosis of exogenous materials. CAV1, which was ac-tivated by T Ⅱ A, might help T Ⅱ A transport across cell membrane to initiate its differentiation effects. It was prov- en by the evidences that suppressing the function of caveolin inhibited the differentiation effects of T Ⅱ A. There- fore, it was concluded that T Ⅱ A promoted neuronal differentiation partially through MAPK42/44 mediated B DNF and NEF signals in a caveolae-dependent manner.

Tanshinone ⅡA improves Alzheimer’s disease via RNA nuclearenriched abundant transcript 1/microRNA-291a-3p/member RAS oncogene family Rab22a axis

BACKGROUND Alzheimer’s disease(AD)is a neurodegenerative condition characterized by oxidative stress and neuroinflammation.Tanshinone ⅡA(Tan-ⅡA),a bioactive compound isolated from Salvia miltiorrhiza plants,has shown potential neuroprotective effects;however,the mechanisms underlying such a function remain unclear.AIM To investigate potential Tan-ⅡA neuroprotective effects in AD and to elucidate their underlying mechanisms.METHODS Hematoxylin and eosin staining was utilized to analyze structural brain tissue morphology.To assess changes in oxidative stress and neuroinflammation,we performed enzyme-linked immunosorbent assay and western blotting.Additionally,the effect of Tan-ⅡA on AD cell models was evaluated in vitro using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Genetic changes related to the long non-coding RNA(lncRNA)nuclear-enriched abundant transcript 1(NEAT1)/microRNA(miRNA,miR)-291a-3p/member RAS oncogene family Rab22a axis were assessed through reverse transcription quantitative polymerase chain reaction.RESULTS In vivo,Tan-ⅡA treatment improved neuronal morphology and attenuated oxidative stress and neuroinflammation in the brain tissue of AD mice.In vitro experiments showed that Tan-ⅡA dose-dependently ameliorated the amyloid-beta 1-42-induced reduction of neural stem cell viability,apoptosis,oxidative stress,and neuroinflammation.In this process,the lncRNA NEAT1-a potential therapeutic target-is highly expressed in AD mice and downregulated via Tan-ⅡA treatment.Mechanistically,NEAT1 promotes the transcription and translation of Rab22a via miR-291a-3p,which activates nuclear factor kappa-B(NF-κB)signaling,leading to activation of the pro-apoptotic B-cell lymphoma 2-associated X protein and inhibition of the anti-apoptotic B-cell lymphoma 2 protein,which exacerbates AD.Tan-ⅡA intervention effectively blocked this process by inhibiting the NEAT1/miR-291a-3p/Rab22a axis and NF-κB signaling.CONCLUSION This study demonstrates that Tan-ⅡA exerts neuroprotective effects in AD by modulating the NEAT1/miR-291a-3p/Rab22a/NF-κB signaling pathway,serving as a foundation for the development of innovative approaches for AD therapy.

Growth Inhibition and Apoptosis Induction in Human Hepatoma Cells by Tanshinone Ⅱ_A

In order to .study the effect of tanshinone ⅡA on growth and apoptosis in human hepatoma cell line BEL-7402 in vitro, the human hepatoma cell line BEL-7402 was treated with tanshinone ⅡA at various concentrations for 72 h. Growth suppression was evaluated by MTT assay; apoptosis-relat-ed alterations in morphology and biochemistry were ascertained under cytochemical staining (Hoechst 33258), transmission electron microscopy (TEM), and DNA agarose gel electrophoresis. Apoptotic rate was quantified by flow cytometry (FCM). The results showed that Tanshinone ⅡA could inhibit the growth of hepatoma cells in a dose-dependent manner, with IC50 value being 6. 28μg/ml. After treatment with 1-10μg/ml tanshinone ⅡA for 72 h, BEL-7402 cells apoptosis with nuclear chro-matin condensation and fragmentation as well as cell shrinkage and the formation of apoptotic bodies were observed. DNA ladder could be demonstrated on DNA electrophoresis. FCM analysis showed hypodiploid peaks on histogram, and the apoptotic rates at μg/ml concentration for 12 h> 24 h, 36 h, 48 h and 72 h were (2. 32±0. 16)%, (3. 01±0. 35) %, (3. 87±0. 43)%, (6. 73±0. 58)% and (20. 85 ± 1. 74) % respectively, which were all significantly higher than those in the control group (1. 07±0. 13) %. It is concluded that Tanshinone ⅡA could induce human hepatoma cell line BEL-7402 apoptosis, which may be related to the mechanism of growth inhibition.

Changes of c-fos and c-jun mRNA Expression in Angiotensin Ⅱ-induced Cardiomyocyte Hypertrophy and Effects of Sodium Tanshinone ⅡA Sulfonate

The changes of proto-oncogene c-fos and c-jun mRNA expression in angiotensin Ⅱ （AngⅡ）-induced hypertrophy and effects of sodium tanshinone ⅡA sulfonate （STS） in the primary culture of neonatal rat cardiomyocytes were investigated. Twelve neonatal clean grade Wistar rats were selected. The cardiomyocytes were isolated, cultured and divided according to different treatments in the medium. The cardiomyocyte size was determined by phase contrast microscope, and the rate of protein synthesis was measured by [3H]-Leucine incorporation. The c-fos and c-jun mRNA expression in cardiomyocytes was detected by reverse transcription polymerase chain reaction （RT-PCR）. It was found after cardiomyocytes were treated with AngⅡ for 30 min, the c-fos and c-jun mRNA expression in cardiomyocytes was increased significantly （P〈0.01）. After treatment with AngⅡ for 24 h, the rate of protein synthesis in AngⅡ group was significantly increased as compared with control group （P〈0.01）. After treatment with AngⅡ for 7 days, the size of cardiomyocytes in AngⅡ group was increased obviously as compared with control group （P〈0.05）. After pretreatment with STS or Valsartan before AngⅡ treatment, both of them could inhibit the above effects of AngⅡ （P〈0.05 or P〈0.01）. It was suggested that STS could ameliorate AngⅡ-induced cardiomyocyte hy- pertrophy by inhibiting c-fos and c-jun mRNA expression and reducing protein synthesis rate of cardiomyocytes.

Protective Effect of Tanshinone Ⅱ A on Lipopolysaccharide-induced Lung Injury in Rats

Objective To explore the protective effect of tanshinone Ⅱ A on lipopolysaccharide （LPS）-induced lung injury in rats, and possible mechanism. Methods： LPS （O111： B4） was used to produce a rat model of acute lung injury. Sprague-Dawley rats were randomly divided into 3 groups （8 in each group）： the control group, the model group （ALl group）, and the tanshinone Ⅱ A treatment group. Expression of adhesion molecule CD18 on the surface of polymorphonuclear neutrophil （PMNCD18） in venous white blood cells （WBC）, and changes in coagulation-anticoagulant indexes were measured 6 h after injection of LPS or normal saline. Changes in malondialdehyde （MDA） content, wet and dry weight （W/D） ratio and morphometry of pulmonary tissue as well as PMN sequestration in the lung were also measured. Results： （1） When compared with the control group, expression of PMNCD18 and MDA content were enhanced in the ALl group with a hypercoagulable state （all P〈0.01） and an increased W/D ratio （P〈0.05）. Histopathological morphometry in the lung tissue showed higher PMN sequestration, wider alveolar septa; and lower alveolar volume density （Vv） and alveolar surface density （Sv）, showing significant difference （P〈0.01）. （2） When compared with the ALl group, the expression of PMN-CD18, MDA content, and W/D ratio were all lower in Tanshinone Ⅱ A treatment group （P〈0.05） with ameliorated coagulation abnormality （P〈0.01）. Histopathological morphometry in the lung tissue showed a decrease in the PMN sequestration and the width of alveolar septa （both P〈0.01）, and an increase in the Vv and Sv （P〈0.05, P〈0.01）. Conclusion： Tan Ⅱ A plays a protective role in LPS-induced lung injury in rats through improving hypercoagulating state, decreasing PMN-CD18 expression and alleviating migration, reducing lipid peroxidation and alleviating pathological changes.

Growth-inhibiting and Apoptosis-inducing Effects of Tanshinone ⅡA on Human Gastric Carcinoma Cells

To explore the effects of Tanshinone Ⅱ A on the proliferation, apoptosis and gene expression of p53 and bcl-2 in human gastric carcinoma MKN-45 cells. Cell count and MTT assay were used to study the proliferation-inhibiting effect of Tanshinone Ⅱ A on MKN-45 cells. The effect of Tanshinone Ⅱ A on the cell cycle and apoptosis of MKN-45 cells were examined by propidium iodide （PI） staining and flow cytometry. Semi-quantitative RT-PCR was used to further verify the ex- pression of p53 and bcl-2 gene after exposure to Tanshinone Ⅱ A in MKN-45 cells. The results showed that Tanshinone Ⅱ A significantly inhibited the growth and proliferation of MKN-45 cells in a dose- and time-dependent manner （P〈0.05）. Tanshinone Ⅱ A arrested MKN-45 cells in G2/M phase which led to an obvious accumulation of G2/M phase cells while decreased number of Go/G1 phase cells. This resulted in apoptosis of MKN-45 cells and the apoptosis rate was as high as 43.91% after treatment with 2.0 lag/mL Tanshinone Ⅱ A for 96 h. It was also found that Tanshinone Ⅱ A up-regulated expression of p53 gene and down-regulated expression of bcl-2 gene. The cytostatic and antiproliferative effect of Tanshinone Ⅱ A makes it a promising anticancer agent for the treatment of gastric carcinoma.

Sodium Tanshinone Ⅱ A Sulfonate Injection as Adjuvant Treatment for Unstable Angina Pectoris: A Meta-Analysis of 17 Randomized Controlled Trials

Objective： To systematically evaluate the effectiveness and safety of Sodium Tanshinone ⅡA Sulfonate Injection（STS） as one adjuvant therapy for treating unstable angina pectoris（UAP）. Methods： Randomized controlled trials（RCTs） of UAP treated by STS were searched in the China National Knowledge Infrastructure Database（CNKI）, VIP Database for Chinese Technical Periodicals（VIP）, Wanfang Database, the Chinese Biomedical Literature Database（CBM）, Web of Science, the Cochrane Library, Embase, and Pub Med, which from inception to January, 2016. The Cochrane Risk Assessment Tool was used to evaluate the methodological quality of the RCTs. The Review Manager 5.3 software was used to conduct the metaanalysis. Results： The results showed that 17 RCTs involving 1,372 patients were included. The meta-analysis indicated that the combined use of STS and Western medicine（WM） in the treatment of UAP can obviously improve the total effective rate [risk ratio（RR）=1.31, 95% confidence interval（CI）（1.24,1.39）, P〈0.0001], and the total effective rate of electrocardiogram [RR=1.43, 95% CI（1.30,1.56）, P〈0.0001], decrease the level of CRP [mean difference（MD）=–3.06, 95%CI（–3.85, –2.27）, P〈0.00001], fibrinogen [MD=–1.03, 95% CI（–1.16, –0.89）, P〈0.00001], and whole blood high shear viscosity [MD=–0.70, 95% CI（–0.92, –0.49）, P〈0.00001]. Additionally, the occurrence of adverse drug reaction of the experimental group was significantly higher than that of the control group [RR=3.57, 95% CI（1.28, 9.94）, P〈0.05]. Conclusions： Compared with WM, the combined use of STS was more effective.

Effects of Tanshinone ⅡA on Transforming Growth Factor β1-Smads Signal Pathway in Renal Interstitial Fibroblasts of Rats

The effects of tanshinone ⅡA （TSN） on transforming growth factor β1 （TGFβ1） signal transduction in renal interstitial fibroblasts of rats were studied in order to investigate its mechanism in prevention of renal interstitial fibrosis. Rat renal fibroblasts of the line NRK/49F were cultured in vitro, stimulated with 5 ng/mL TGFβ1 and pretreated with 10-6, 10-5, 10-4 mol/L TSN respectively. The mRNA levels of fibronectin （FN） were examined by RT-PCR. The protein expression of FN and Smads was detected by Western blot. TGFβ1 induced the expression of FN mRNA and Smads in a time-dependent manner in a certain range. Compared with pre-stimulation, the FN mRNA and protein levels were increased by 1.1 times and 1.5 times respectively （P〈0.01, P〈0.01）, and the protein expression of phosphorylated Smad2/3 （p-Smad2/3） increased by 7 times at the end of TGFβ1 stimulation （P〈0.01）. TSN pretreatment may down-regulate the FN and p-Smad2/3 expression in a dose-dependent manner. 10-6 mol/L TSN pretreatment had no effect on the FN and p-Smad2/3 expression （both P〉0.05）. After pretreatment with 10-5 and 10-4 mol/L TSN, the FN mRNA levels were decreased by 28.1% and 43.8% respectively （P〈0.05, P〈0.01）, the FN protein levels were decreased by 40% and 44% respectively （P〈0.05, P〈0.05）, and the p-Smad2/3 protein expression were decreased by 40% and 65% respectively （P〈0.05, P〈0.01）. The inhibitory effect of TSN on renal interstitial fibrosis may be related to its blocking effect on TGFβ1-Smads signal pathway in renal intersti- tial fibroblasts.

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。

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。

血清α1-抗胰蛋白酶、血管紧张素-Ⅱ与获得性免疫缺陷综合征患者预后的关系

目的探讨血清α1-抗胰蛋白酶(α1-AT)、血管紧张素-Ⅱ(Ang-Ⅱ)与获得性免疫缺陷综合征(AIDS)患者预后的关系。方法将该院2019年5月至2022年5月收治的97例首诊AIDS患者纳入研究作为研究组,另选取同期于该院进行体检的健康者97例作为对照组。根据病历收集患者临床资料。对纳入研究者进行α1-AT、Ang-Ⅱ水平检测,并进行分组比较。对纳入研究的AIDS患者进行为期1年的随访,观察患者预后情况,并比较不同预后患者的α1-AT、Ang-Ⅱ水平。采用单因素及多因素Logistic回归分析影响AIDS患者预后的因素。用受试者工作特征(ROC)曲线分析α1-AT、Ang-Ⅱ水平对患者预后的预测效能。结果研究组血清α1-AT和Ang-Ⅱ水平高于对照组(P<0.05)。AIDS患者1年内的预后不良发生率为23.71%(23/97)。预后不良患者血清α1-AT和Ang-Ⅱ水平高于预后良好患者(P<0.05)。单因素分析显示,预后不良患者C反应蛋白(CRP)水平、淋巴细胞计数水平、合并淋巴瘤者所占比例均高于预后良好患者,清蛋白(ALB)水平低于预后良好患者(P<0.05)。多因素Logistic回归分析显示,合并淋巴瘤(OR=2.087)、高α1-AT水平(OR=2.611)、高Ang-Ⅱ水平(OR=2.138)是影响患者预后的独立危险因素(P<0.05)。ROC曲线分析显示,α1-AT预测AIDS患者预后的曲线下面积(AUC)为0.778,Ang-Ⅱ预测的AUC为0.798,α1-AT联合Ang-Ⅱ预测的AUC为0.918。结论α1-AT和Ang-Ⅱ在AIDS患者血清中水平异常升高,而且与患者预后有关,是影响患者预后的独立危险因素。α1-AT和Ang-Ⅱ联合检测可有效预测患者预后。

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。

掺杂CoFe_(2)O_(4)膨胀石墨对Pb(Ⅱ)的吸附性能

为解决膨胀石墨吸附后回收难的问题,采用柠檬酸基的溶胶-凝胶法将CoFe_(2)O_(4)粒子负载到膨胀石墨中,制备磁性膨胀石墨。利用扫描电子显微镜(SEM)和磁滞回线对样品的微观形貌和磁性能进行表征,研究了膨胀石墨和磁性膨胀石墨对Pb(Ⅱ)吸附性能的影响因素,包括吸附时间、Pb(Ⅱ)初始质量浓度、吸附剂用量和pH值等,并采用吸附动力学和吸附等温线模型对吸附行为及机理进行了分析。结果表明,膨胀石墨和磁性膨胀石墨对Pb(Ⅱ)的最大吸附量分别为95.6、69.8 mg/g,吸附动力学符合二级动力学模型,吸附等温线符合Langmuir模型。掺杂CoFe_(2)O_(4)粒子缩短了膨胀石墨对Pb(Ⅱ)吸附平衡所需的时间,并使最佳吸附pH值向更加中性条件迁移。

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PROMETHEE-Ⅱ的电网科技项目后评估评价方法研究

为满足双碳背景下电网精准投资的迫切需求,面对目前电网科技项目数量的急剧增加,迫切需要构建一个后评价指标体系,以低碳绿色发展、运营效率和经济效益为特点,以便评估电网发展规模和速度、结构和安全性以及效率和效益,进而带动科技项目成果转化率的提高,加快科研项目向市场的推广进程。从组织管理、技术水平、成果应用以及影响力4个方面构建电网科技项目后评估的评价指标体系,应用三角模糊数和变异系数法结合的组合赋权法确定各评价指标的权重,基于PROMETHEE-Ⅱ方法对电网科技项目进行后评估,确定最终的评价结果。以实际案例分析,验证该模型具有可行性。

基于NSGA-Ⅱ的滑油泵叶轮结构优化设计

滑油泵常需要在高空、低压工况下稳定运转,常会出现供油不足、效率降低等问题。为了得到满足设计要求且具有最佳性能的滑油泵,以某直升机用滑油泵叶轮为研究对象,对其结构进行优化设计。选择高空两个典型工况的效率与扬程作为优化目标,利用NSGA-Ⅱ算法对滑油泵叶轮几何参数进行寻优,对优化前后的滑油泵效率、扬程进行对比分析。采用CFD流体仿真及实验方法对优化结果进行对比验证。结果表明:所选优化参数对滑油泵性能有较大影响,优化后的滑油泵叶片位置附近流动更加平稳,高低压区域过渡平缓,能量损失更小,且降低了汽蚀发生的可能性;优化后的滑油泵设计点扬程提高2.6 m,效率提高2.86%。

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。

基于NSGA-Ⅱ的复合材料防撞梁碰撞损伤多目标优化

为在设计时考虑低速碰撞损伤对碳纤维复合材料(CFRP)防撞梁力学性能的影响,发展了改进Hashin失效准则的VUSDFLD子程序来判定低速碰撞时CFRP防撞梁7个方向的损伤程度,采用壳单元模拟了复合材料的力学性能,建立了CFRP防撞梁低速碰撞有限元显式动力学模型。采用该方法对相同实验条件下的复合材料层合板低速冲击剩余强度进行了计算,并将计算结果与实验结果进行了对比,仿真结果与实验结果吻合较好。在此基础上,以复合材料防撞梁铺层厚度和铺层角度为设计变量,将复合材料防撞梁的质量和低速冲击时产生的损伤单元数作为优化目标,建立了CFRP防撞梁低速碰撞损伤动力学多目标优化模型,采用基于Pareto策略改进的NSGA-Ⅱ非支配排序遗传算法对其进行多目标优化求解。优化后,CFRP防撞梁质量由1.02 kg降为0.76 kg,减重率为25%;损伤单元数由30238个降为23206个,损伤降低率为23%。结果表明,所发展基于Hashin失效准则的VUSDFLD子程序和对CFRP防撞梁低速碰撞损伤多目标优化是行之有效的,为复合材料防撞梁结构的优化设计提供了参考。

双相Ⅰ型障碍和双相Ⅱ型患者人口学和临床特征的比较

目的:比较双相Ⅰ型障碍和双相Ⅱ型障碍患者的人口学特征、临床特征、治疗特征和生理指标。方法:选取符合美国精神障碍诊断与统计手册第5版(DSM-5)双相障碍的患者381例,其中Ⅰ型302例(79.27%),Ⅱ型74例(19.42%),其他特定及相关障碍5例(1.31%)。用自编临床资料访谈表收集人口学资料及临床特征数据。采用多因素logistic回归和多重线性回归分析方法进行因素分析。结果:与双相II型障碍相比,双相I型障碍患者更容易伴有精神病性特征(OR=5.75,95%CI:2.82~11.76),病程更长,接受重复经颅磁刺激治疗较多(OR=3.09,95%CI:1.02~9.35),尿酸、总胆固醇、高密度脂蛋白浓度更高,汉族更常见(OR=11.50,95%CI:1.76~75.30)、受教育程度更低(OR=10.22,95%CI:1.16~89.77),更少有精神病家族史(OR=2.34,95%CI:1.01~5.42)。结论:双相Ⅰ型障碍和双相Ⅱ型障碍的人口学特征、临床特征、治疗情况和生理指标有差异,可为探讨双相障碍的发病机制提供线索。

温升作用下CRTSⅡ型板宽窄接缝受力及损伤分析

为研究宽窄接缝在温升作用下的受力和损伤,根据混凝土塑性损伤理论和内聚力理论,建立考虑新旧混凝土界面的宽窄接缝细部的有限元模型;计算不同温升条件下的宽窄接缝应力和损伤因子,并分析宽窄接缝强度和窄接缝宽度的影响.研究结果表明:窄接缝挤碎是一种渐变受压损伤,宽、窄接缝交界处断裂是一种脆性受拉损伤;与宽、窄接缝交界处断裂相比,窄接缝挤碎对结构受力影响更大;宽窄接缝尺寸不均匀导致宽、窄接缝交界处垂向受拉,这是宽窄接缝产生损伤的主要原因;提高宽窄接缝的混凝土强度可有效降低垂向拉应力和受拉损伤,但对纵向应力和受压损伤影响较小;为改善受力并降低损伤,建议宽窄接缝混凝土与轨道板等强,并且宽窄接缝上下等宽.