What Can We Learn from FGF-2 Isoform-Specific Mouse Mutants? Differential Insights into FGF-2 Physiology In Vivo

Fibroblast growth factor 2 (FGF-2), ubiquitously expressed in humans and mice, is functionally involved in cell growth, migration and maturation in vitro and in vivo. Based on the same mRNA, an 18-kilo Dalton (kDa) FGF-2 isoform named FGF-2 low molecular weight (FGF-2LMW) isoform is translated in humans and rodents. Additionally, two larger isoforms weighing 21 and 22 kDa also exist, summarized as the FGF-2 high molecular weight (FGF-2HMW) isoform. Meanwhile, the human FGF-2HMW comprises a 22, 23, 24 and 34 kDa protein. Independent studies verified a specific intracellular localization, mode of action and tissue-specific spatiotemporal expression of the FGF-2 isoforms, increasing the complexity of their physiological and pathophysiological roles. In order to analyze their spectrum of effects, FGF-2LMW knock out (ko) and FGF-2HMWko mice have been generated, as well as mice specifically overexpressing either FGF-2LMW or FGF-2HMW. So far, the development and functionality of the cardiovascular system, bone formation and regeneration as well as their impact on the central nervous system including disease models of neurodegeneration, have been examined. This review provides a summary of the studies characterizing the in vivo effects modulated by the FGF-2 isoforms and, thus, offers a comprehensive overview of its actions in the aforementioned organ systems.     

镍钛合金心血管支架电解抛光流场仿真及试验研究

针对不同转速对电解抛光镍钛合金心血管支架流场分布的影响特点,利用ANSYS软件对电解抛光心血管支架过程中电解液的流速分布进行了仿真,分析了电解液速度场及涡流场对电解抛光心血管支架去除机理的影响规律,并通过试验验证了其仿真结果的正确性。结果表明：随着转速的增加,速度场分布均匀,涡流变化小,电解液更新及时,电解产物可及时排出,加工精度提高,抛光后的心血管支架表面完整性好；但当转速过高时,涡流分布区域明显增大,较多气体析出,导致速度场分布不均匀且不连续,加工精度低,抛光后的心血管支架表面完整性差。     

Visceral Obesity and Its Shared Role in Cancer and Cardiovascular Disease: A Scoping Review of the Pathophysiology and Pharmacological Treatments

The association between obesity, cancer and cardiovascular disease (CVD) has been demonstrated in animal and epidemiological studies. However, the specific role of visceral obesity on cancer and CVD remains unclear. Visceral adipose tissue (VAT) is a complex and metabolically active tissue, that can produce different adipokines and hormones, responsible for endocrine-metabolic comorbidities. This review explores the potential mechanisms related to VAT that may also be involved in cancer and CVD. In addition, we discuss the shared pharmacological treatments which may reduce the risk of both diseases. This review highlights that chronic inflammation, molecular aspects, metabolic syndrome, secretion of hormones and adiponectin associated to VAT may have synergistic effects and should be further studied in relation to cancer and CVD. Reductions in abdominal and visceral adiposity improve insulin sensitivity, lipid profile and cytokines, which consequently reduce the risk of CVD and some cancers. Several medications have shown to reduce visceral and/or subcutaneous fat. Further research is needed to investigate the pathophysiological mechanisms by which visceral obesity may cause both cancer and CVD. The role of visceral fat in cancer and CVD is an important area to advance. Public health policies to increase public awareness about VAT’s role and ways to manage or prevent it are needed.     

The Potential of Probiotics in the Prevention and Treatment of Atherosclerosis

Atherosclerosis, the underlying cause of cardiovascular diseases such as myocardial infarction, cerebrovascular accident, and peripheral vascular disease, is the leading cause of global mortality. Current therapies against atherosclerosis, which mostly target the dyslipidemia associated with the disease, have considerable residual risk for cardiovascular disease together with various side effects. In addition, the outcomes from clinical trials on many promising pharmaceutical agents against atherosclerosis (e.g., low‐dose methotrexate, inhibitors against cholesteryl ester transfer protein) have been disappointing. Nutraceuticals such as probiotic bacteria have, therefore, generated substantial recent interest for the prevention of atherosclerosis and potentially as add‐ons with current pharmaceutical drugs. This review will discuss the current understanding of the anti‐atherogenic actions of probiotics from preclinical and clinical studies together with their potential underlying mechanisms of action.     

液压支架快速撤除技术研究应用

新汶矿业集团经过探索和实践,研究运用了差异互补式全掩护支护技术、掩护支架自牵引联动装置工艺、矿车运输、滑移运输多用轨道、自动找正装车平台、液控调整装置等新技术、新工艺,做到了液压支架综合流程快速回撤,实现了高效化、连贯化安全回撤,取得了良好的经济效益。     

高效液相色谱-氢化物发生原子荧光光谱法测定食品中多形态硒含量

目的 探究急性心肌梗死(AMI)患者经皮冠状动脉介入术(PCI)后血清成纤维细胞生长因子21(FGF-21)、髓过氧化物酶(MPO)水平与预后的关系。方法 选择2016年1月至2018年12月在我院接受PCI术治疗的108例AMI患者作为研究对象。根据随访过程中是否发生主要不良心血管事件(MACE),病人分为预后不良组(25例)和预后良好组(83例)。采用酶联免疫吸附法检测受试者血清FGF-21水平,采用胶体金免疫层析法检测受试者血清MPO水平。分析FGF-21、MPO与AMI患者PCI术后MACE发生的关系及诊断MACE发生的效能。结果 预后不良组血清FGF-21、MPO水平均高于预后良好组,差异均有统计学意义(P＜0.05)。FGF-21＋MPO诊断AMI患者PCI术后MACE发生的ROC曲线下面积(AUC)为0.860,高于FGF-21、MPO单独诊断AMI患者PCI术后MACE发生的AUC。FGF-21＞140.41 ng/L和FGF-21≤140.41 ng/L的患者,MACE发生率分别为39.58%和10.00%,差异有统计学意义(P＜0.001)。MPO＞419.42 μg/L和MPO≤419.42 μg/L的患者,MACE发生率分别为35.00%和8.33%,差异有统计学意义(P＝0.001)。Cox单因素及Cox多因素分析显示FGF-21、MPO与AMI患者PCI术后MACE发生密切相关(均P＜0.05)。结论 AMI患者PCI术后血清FGF-21、MPO水平与预后有关。高水平的FGF-21、MPO与MACE发生密切相关。     

The Role of Cell Cycle Regulators in Cell Survival—Dual Functions of Cyclin-Dependent Kinase 20 and p21Cip1/Waf1

The mammalian cell cycle is important in controlling normal cell proliferation and the development of various diseases. Cell cycle checkpoints are well regulated by both activators and inhibitors to avoid cell growth disorder and cancerogenesis. Cyclin dependent kinase 20 (CDK20) and p21^Cip1/Waf1 are widely recognized as key regulators of cell cycle checkpoints controlling cell proliferation/growth and involving in developing multiple cancers. Emerging evidence demonstrates that these two cell cycle regulators also play an essential role in promoting cell survival independent of the cell cycle, particularly in those cells with a limited capability of proliferation, such as cardiomyocytes. These findings bring new insights into understanding cytoprotection in these tissues. Here, we summarize the new progress of the studies on these two molecules in regulating cell cycle/growth, and their new roles in cell survival by inhibiting various cell death mechanisms. We also outline their potential implications in cancerogenesis and protection in heart diseases. This information renews the knowledge in molecular natures and cellular functions of these regulators, leading to a better understanding of the pathogenesis of the associated diseases and the discovery of new therapeutic strategies.