The Effects of Exercise Training on Mitochondrial Function in Cardiovascular Diseases: A Systematic Review and Meta-Analysis

Mitochondria dysfunction is implicated in the pathogenesis of cardiovascular diseases (CVD). Exercise training is potentially an effective non-pharmacological strategy to restore mitochondrial health in CVD. However, how exercise modifies mitochondrial functionality is inconclusive. We conducted a systematic review using the PubMed; Scopus and Web of Science databases to investigate the effect of exercise training on mitochondrial function in CVD patients. Search terms included “mitochondria”, “exercise”, “aerobic capacity”, and “cardiovascular disease” in varied combination. The search yielded 821 records for abstract screening, of which 20 articles met the inclusion criteria. We summarized the effect of exercise training on mitochondrial morphology, biogenesis, dynamics, oxidative capacity, antioxidant capacity, and quality. Amongst these parameters, only oxidative capacity was suitable for a meta-analysis, which demonstrated a significant effect size of exercise in improving mitochondrial oxidative capacity in CVD patients (SMD = 4.78; CI = 2.99 to 6.57; p < 0.01), but with high heterogeneity among the studies (I² = 75%, p = 0.003). Notably, aerobic exercise enhanced succinate-involved oxidative phosphorylation. The majority of the results suggested that exercise improves morphology and biogenesis, whereas findings on dynamic, antioxidant capacity, and quality, were inadequate or inconclusive. A further randomized controlled trial is clearly required to explain how exercise modifies the pathway of mitochondrial quantity and quality in CVD patients.     

Opaganib Protects against Radiation Toxicity: Implications for Homeland Security and Antitumor Radiotherapy

Exposure to ionizing radiation (IR) is a lingering threat from accidental or terroristic nuclear events, but is also widely used in cancer therapy. In both cases, host inflammatory responses to IR damage normal tissue causing morbidity and possibly mortality to the victim/patient. Opaganib, a first-in-class inhibitor of sphingolipid metabolism, has broad anti-inflammatory and anticancer activity. Opaganib elevates ceramide and reduces sphingosine 1-phosphate (S1P) in cells, conditions that increase the antitumor efficacy of radiation while concomitantly suppressing inflammatory damage to normal tissue. Therefore, opaganib may suppress toxicity from unintended IR exposure and improve patient response to chemoradiation. To test these hypotheses, we first examined the effects of opaganib on the toxicity and antitumor activity of radiation in mice exposed to total body irradiation (TBI) or IR with partial bone marrow shielding. Oral treatment with opaganib 2 h before TBI shifted the LD₇₅ from 9.5 Gy to 11.5 Gy, and provided substantial protection against gastrointestinal damage associated with suppression of radiation-induced elevations of S1P and TNFα in the small intestines. In the partially shielded model, opaganib provided dose-dependent survival advantages when administered 4 h before or 24 h after radiation exposure, and was particularly effective when given both prior to and following radiation. Relevant to cancer radiotherapy, opaganib decreased the sensitivity of IEC6 (non-transformed mouse intestinal epithelial) cells to radiation, while sensitizing PAN02 cells to in vitro radiation. Next, the in vivo effects of opaganib in combination with radiation were examined in a syngeneic tumor model consisting of C57BL/6 mice bearing xenografts of PAN02 pancreatic cancer cells and a cross-species xenograft model consisting of nude mice bearing xenografts of human FaDu cells. Mice were treated with opaganib and/or IR (plus cisplatin in the case of FaDu tumors). In both tumor models, the optimal suppression of tumor growth was attained by the combination of opaganib with IR (± cisplatin). Overall, opaganib substantially protects normal tissue from radiation damage that may occur through unintended exposure or cancer radiotherapy.     

基于改进的 Sage-Husa 滤波 MEMS陀螺阵列降噪技术研究

为充分挖掘 MEMS 陀螺的性能,提高 MEMS 陀螺在实际应用中的精度,通过搭建四陀螺阵列结合改进的 Sage-Husa 滤 波算法对陀螺阵列的输出信号进行降噪,在不改变陀螺加工工艺和显著提高生产成本的条件下有效提高了 MEMS 陀螺仪的实 际性能。 通过分析 MEMS 陀螺仪的系统误差和随机误差,搭建误差模型,利用传统卡尔曼滤波、移动平均滤波、小波阈值去噪 和改进的 Sage-Husa 滤波算法对单个陀螺和陀螺仪阵列进行降噪处理,实验对比发现改进的 Sage-Husa 滤波算法和陀螺仪阵列 结合后能有效降低陀螺的输出噪声。 利用 Allan 方差分析陀螺仪阵列经过改进的 Sage-Husa 算法滤波后的随机误差,四陀螺阵 列角度随机游走从 0. 40°/ h降低到 0. 03°/ h ,零偏不稳定性从 71. 11°/ h 降低到 5. 83°/ h,有效提高了 MEMS 陀螺在实际应用 中的性能。     

蒙古额尔登特铜矿的电化学控制浮选研究与实践

以铜钼硫化矿浮选体系中的电化学理论为基础 ,研究了在硫化矿表面发生的 5类典型的阳极氧化反应在处理斑岩铜矿过程中的浮选意义。研究结果表明 :在抑硫混合浮选铜钼过程中关键是控制好第 1、2类阳极反应 ,同时注意到第 3类阳极反应 ;在混合精矿脱硫浮选中应主要控制第 1、4类阳极氧化反应 ;在铜钼分离浮选中要求严格控制第 4、5类阳极氧化反应。本文还介绍了针对额尔登特铜矿石的电化学控制浮选实验室研究和工业试验应用情况     

钴废料中有价元素综合回收的生产实践

针对某含Cu、Zn、Mn、Ni、Cd等元素的难处理含钴废料 ,采用还原浸出、化学除杂、P2 0 4深度除杂、P5 0 7萃取分离镍钴等主要工序的工艺流程生产出草酸钴 ,钴的回收率为 95 6 1%。文中介绍了这一工艺的生产实践和主要的技术经济指标 ,对同类二次钴资源的综合利用有一定的现实意义     

基于信道特征提取的物理层安全密钥生成方法

物理层密钥具有降低密钥分发、更新和维护的难度的特点,针对无线传感器网络中节点传输信息易遭受窃听攻击的问题,基于物理层安全中的"一次一密"理论,提出了一种物理层密钥生成方法,主要包含信道估计、特征提取、密钥生成与协商。在半双工通信模式下,根据信道估计阶段相干时间的长短,对训练序列的长度进行动态调整,提高信道估计的一致性。仿真试验与对比分析结果表明,窃听节点生成密钥与合法节点生成密钥的一致性始终维持在较低水平,降低了遭受窃听攻击的风险。     

结构光非接触式TCF标定方法研究

针对机器人工具坐标系(TCF)标定结果的准确性问题,采用基于结构光的非接触式TCF标定方法对自制串联机器人的TCF进行标定研究及实验。介绍了标定过程中涉及的相关坐标系、标定原理及结构光视觉成像系统,详细推导了TCF标定算法;阐述了TCF标定实验步骤,以Kinova Mico2机器人为研究对象,通过在工具上粘贴"十"字标记,并约束"十"字标记的中心与激光投影点重合后的点在图像中的像素坐标值相同,经过多次定位约束后求取平均值作为标定结果。研究结果表明,基于结构光的非接触式TCF标定方法对工具坐标系的标定结果较为稳定,数据的准确性满足生产的需要。     

色彩传递算法在不同色彩空间中的成像效果研究

为了在红外与可见光图像融合系统中,评价不同色彩传递算法在不同色彩空间中的成像效果,分别在YCbCr色彩空间和lαβ色彩空间中,采用全局色彩传递算法和点对点色彩传递算法分别对一组图像进行效果对比研究,并使用客观评价方法对处理结果进行计算分析,所得到的评价结果与主观评价结果基本一致。经过实验对比,客观评价方法的结果与主观评价方法的结果一致,色彩空间的选择对色彩传递算法的最终效果有显著的影响,在YCbCr空间中,全局色彩传递效果好于点对点色彩传递效果;在lαβ空间中,点对点色彩传递效果好于全局色彩传递效果。     

Cordycepin Inhibits Growth and Metastasis Formation of MDA-MB-231 Xenografts in Nude Mice by Modulating the Hedgehog Pathway

We previously found that cordycepin inhibits the growth and metastasis formation of MDA-MB-231 cells through the Hedgehog pathway but has not validated this in vivo. In this study, we confirmed cordycepin’s anti-triple-negative breast cancer (TNBC) effect in nude mice and documented its mechanism. We found that cordycepin reduced the volume and weight of MDA-MB-231 xenografts and affected the expression of proliferation-, apoptosis-, epithelial–mesenchymal transition-, and matrix metalloproteinase-related proteins without side effects. RNA sequencing screening, pathway enrichment, and the protein network interaction analysis revealed enriched pathways and targets mainly concentrated on the Hedgehog pathway and its core components of SHH and GLI2. This indicates that the Hedgehog pathway plays a central role in the cordycepin-mediated regulation of growth and metastasis formation in TNBC. The database analysis of the Hedgehog pathway markers (SHH, PTCH1, SMO, GLI1, and GLI2) revealed that the Hedgehog pathway is activated in breast cancer tissues, and its high expression is not conducive to a patient’s survival. Finally, we verified that cordycepin effectively inhibited the Hedgehog pathway in TNBC through Western blotting and immunohistochemistry. This study found that cordycepin could regulate the growth and metastasis formation of TNBC through the Hedgehog pathway in vivo, which provides new insights for targeting and treating breast cancer.     

盛事之后——走向可持续发展的奥运场馆建设

本文根据国外现代奥运场馆建设实例提出,面对近期直接目标和长远间接目标的矛盾,奥运场馆建设必须根据举办城市的发展具体情况,确定各种效益的优先关系,在城市整体长远规划基础上,从节约化、续用化、生态化三方面指导奥运建设,落实可持续发展原则。