The “Angiogenic Switch” and Functional Resources in Cyclic Sports Athletes

Regular physical activity in cyclic sports can influence the so-called “angiogenic switch”, which is considered as an imbalance between proangiogenic and anti-angiogenic molecules. Disruption of the synthesis of angiogenic molecules can be caused by local changes in tissues under the influence of excessive physical exertion and its consequences, such as chronic oxidative stress and associated hypoxia, metabolic acidosis, sports injuries, etc. A review of publications on signaling pathways that activate and inhibit angiogenesis in skeletal muscles, myocardium, lung, and nervous tissue under the influence of intense physical activity in cyclic sports. Materials: We searched PubMed, SCOPUS, Web of Science, Google Scholar, Clinical keys, and e-LIBRARY databases for full-text articles published from 2000 to 2020, using keywords and their combinations. Results: An important aspect of adaptation to training loads in cyclic sports is an increase in the number of capillaries in muscle fibers, which improves the metabolism of skeletal muscles and myocardium, as well as nervous and lung tissue. Recent studies have shown that myocardial endothelial cells not only respond to hemodynamic forces and paracrine signals from neighboring cells, but also take an active part in heart remodeling processes, stimulating the growth and contractility of cardiomyocytes or the production of extracellular matrix proteins in myofibroblasts. As myocardial vascularization plays a central role in the transition from adaptive heart hypertrophy to heart failure, further study of the signaling mechanisms involved in the regulation of angiogenesis in the myocardium is important in sports practice. The study of the “angiogenic switch” problem in the cerebrovascular and cardiovascular systems allows us to claim that the formation of new vessels is mediated by a complex interaction of all growth factors. Although the lungs are one of the limiting systems of the body in cyclic sports, their response to high-intensity loads and other environmental stresses is often overlooked. Airway epithelial cells are the predominant source of several growth factors throughout lung organogenesis and appear to be critical for normal alveolarization, rapid alveolar proliferation, and normal vascular development. There are many controversial questions about the role of growth factors in the physiology and pathology of the lungs. The presented review has demonstrated that when doing sports, it is necessary to give a careful consideration to the possible positive and negative effects of growth factors on muscles, myocardium, lung tissue, and brain. Primarily, the “angiogenic switch” is important in aerobic sports (long distance running). Conclusions: Angiogenesis is a physiological process of the formation of new blood capillaries, which play an important role in the functioning of skeletal muscles, myocardium, lung, and nervous tissue in athletes. Violation of the “angiogenic switch” as a balance between proangiogenic and anti-angiogenic molecules can lead to a decrease in the functional resources of the nervous, musculoskeletal, cardiovascular, and respiratory systems in athletes and, as a consequence, to a decrease in sports performance.     

(S)-Reutericyclin: Susceptibility Testing and In Vivo Effect on Murine Fecal Microbiome and Volatile Organic Compounds

We aimed to assess the in vitro antimicrobial activity and the in vivo effect on the murine fecal microbiome and volatile organic compound (VOC) profile of (S)-reutericyclin. The antimicrobial activity of (S)-reutericyclin was tested against Clostridium difficile, Listeria monocytogenes, Escherichia coli, Enterococcus faecium, Staphylococcus aureus, Staphylococcus (S.) epidermidis, Streptococcus agalactiae, Pseudomonas aeruginosa and Propionibacterium acnes. Reutericyclin or water were gavage fed to male BALBc mice for 7 weeks. Thereafter stool samples underwent 16S based microbiome analysis and VOC analysis by gas chromatography mass spectrometry (GC-MS). (S)-reutericyclin inhibited growth of S. epidermidis only. Oral (S)-reutericyclin treatment caused a trend towards reduced alpha diversity. Beta diversity was significantly influenced by reutericyclin. Linear discriminant analysis Effect Size (LEfSe) analysis showed an increase of Streptococcus and Muribaculum as well as a decrease of butyrate producing Ruminoclostridium, Roseburia and Eubacterium in the reutericyclin group. VOC analysis revealed significant increases of pentane and heptane and decreases of 2,3-butanedione and 2-heptanone in reutericyclin animals. The antimicrobial activity of (S)-reutericyclin differs from reports of (R)-reutericyclin with inhibitory effects on a multitude of Gram-positive bacteria reported in the literature. In vivo (S)-reutericyclin treatment led to a microbiome shift towards dysbiosis and distinct alterations of the fecal VOC profile.     

Molecular Mechanisms of the Deregulation of Muscle Contraction Induced by the R90P Mutation in Tpm3.12 and the Weakening of This Effect by BDM and W7

Point mutations in the genes encoding the skeletal muscle isoforms of tropomyosin can cause a range of muscle diseases. The amino acid substitution of Arg for Pro residue in the 90th position (R90P) in γ-tropomyosin (Tpm3.12) is associated with congenital fiber type disproportion and muscle weakness. The molecular mechanisms underlying muscle dysfunction in this disease remain unclear. Here, we observed that this mutation causes an abnormally high Ca²⁺-sensitivity of myofilaments in vitro and in muscle fibers. To determine the critical conformational changes that myosin, actin, and tropomyosin undergo during the ATPase cycle and the alterations in these changes caused by R90P replacement in Tpm3.12, we used polarized fluorimetry. It was shown that the R90P mutation inhibits the ability of tropomyosin to shift towards the outer domains of actin, which is accompanied by the almost complete depression of troponin’s ability to switch actin monomers off and to reduce the amount of the myosin heads weakly bound to F-actin at a low Ca²⁺. These changes in the behavior of tropomyosin and the troponin–tropomyosin complex, as well as in the balance of strongly and weakly bound myosin heads in the ATPase cycle may underlie the occurrence of both abnormally high Ca²⁺-sensitivity and muscle weakness. BDM, an inhibitor of myosin ATPase activity, and W7, a troponin C antagonist, restore the ability of tropomyosin for Ca²⁺-dependent movement and the ability of the troponin–tropomyosin complex to switch actin monomers off, demonstrating a weakening of the damaging effect of the R90P mutation on muscle contractility.     

Investigation of the Anti-Methicillin-Resistant Staphylococcus aureus Activity of (+)-Tanikolide- and (+)-Malyngolide-Based Analogues Prepared by Asymmetric Synthesis

Herein, we report antibacterial and antifungal evaluation of a series of previously prepared (+)-tanikolide analogues. One analogue, (4S,6S)-4-methyltanikolide, displayed promising anti-methicillin-resistant Staphylococcus aureus activity with a MIC of 12.5 µg/mL. Based on the antimicrobial properties of the structurally related (−)-malyngolide, two further analogues (4S,6S)-4-methylmalyngolide and (4R,6S)-4-methylmalyngolide bearing a shortened n-nonyl alkyl side chain were prepared in the present study using a ZrCl₄-catalysed deprotection/cyclisation as the key step in their asymmetric synthesis. When these were tested for activity against anti-methicillin-resistant Staphylococcus aureus, the MIC increased to 50 µg/mL.     

DMFC阳极催化剂用GRQD-NiCo2O4复合物的制备与电催化活性分析

采用水热法制备GRQD-NiCo₂O₄复合物,利用XRD、SEM及TEM分析其微结构,并探讨其作为DMFC阳极催化剂使用时的电化学性能。微结构分析表明所得GRQD-NiCo₂O₄复合物皆为具NiCo₂O₄单一相的尖晶石结构,且GRQD质量浓度高于0.25 g/mL后表面形貌将转变GRQD与NiCo₂O₄相互结合的状态。电化学分析表明添加GRQD可有效增强NiCo₂O₄的导电性并提升其电化学稳定性,其中GRQD质量浓度为0.25 g/mL时所得样品经500次循环测试后电流密度约为77.5 A/g,与循环5次后相比其电流密度剩余量最大（约为69.7%）,该样品作为DMFC阳极催化剂使用时性价比最佳。     

低成本钢尾渣-矿渣基矿山充填料的优化开发

 为实现多固废协同利用、降低充填成本,在矿渣基全粒级细尾砂胶结充填料基础上,以流动性和抗压强度为表征,利用热闷钢渣磁选尾渣(钢尾渣)替代部分矿渣作为胶凝材料,脱硫灰和水泥熟料替代部分专用添加剂作为外加剂,采用正交试验探寻掺量规律,优化固体填充料配比,开发钢尾渣-矿渣基软性矿山充填料,并研究了外加剂与胶材比、灰砂比等因素的影响。对比分析了矿渣基准组、钢尾渣-矿渣基准组(B1)、强度最优外加剂组分钢尾渣-矿渣组(B7)等3组充填料的微观形貌及XRD图谱以探究其水化机理。结果表明,钢尾渣替代矿渣量增加、外加剂与胶材比减小,充填料浆流动性改善,但充填体抗压强度下降。强度正交试验结果表明,钢尾渣掺量大小决定强度低高,脱硫灰掺量宜高于水泥熟料。进一步调整外加剂组分配比,在灰砂比为1∶6、钢尾渣替代矿渣为20%条件下,找出B7组外加剂组分为脱硫灰、水泥熟料分别替代30%、20%专用添加剂,B7组料浆扩展度为143 mm,充填体形貌为富铁绿泥石胶结假方体钙硅灰石,28 d抗压强度达2.13 MPa,较基准组低0.19 MPa,较B1提高0.26 MPa。该替代方案满足现场充填C2级强度的要求,改善流动性并显著降低了充填成本。优化的外加剂组分配比在灰砂比为1∶4条件下同样具有强度优化作用,但较灰砂比为1∶6条件下低。     

Ni2+、Cu2+、Zn2+对氧化亚铁硫杆菌氧化 活性影响

为研究金属离子对氧化亚铁硫杆菌（Acidithiobacillus ferrooxidans,At.f）氧化活性的影响,通过测定经初步驯化的At.f菌在不同初始pH下的生长活性,开展不同浓度梯度的Ni2+、Cu2+、Zn2+及三种金属离子共存时对At.f菌的氧化活性影响的试验。结果表明,当初始pH为1.8时,At.f菌生长活性最好,且低浓度的Ni2+、Zn2+对At.f菌氧化活性影响较小,对两种金属离子的耐受浓度均在20 g/L以上;而该细菌对Cu2+比较敏感,当Cu2+浓度为2.5 g/L时,菌株的生长活性明显下降,特别是10 g/L时,对At.f菌的氧化能力有显著的抑制作用。三种金属离子同时存在时对At.f菌氧化活性的影响大于单一金属离子,当三种金属离子的浓度均为2.5 g/L时,在48小时内对At.f菌的氧化能力有显著的抑制作用,当三种金属离子的浓度均为5 g/L时,80小时时菌株对Fe2+的氧化率极低,说明At.f菌需要经过多种金属离子共存驯化培养后才能更好地运用于多金属复杂矿物的处理。     

KINETICS OF LIQUID PENETRATING INTO GRAIN BOUNDARY

ＫＩＮＥＴＩＣＳＯＦＬＩＱＵＩＤＰＥＮＥＴＲＡＴＩＮＧＩＮＴＯＧＲＡＩＮＢＯＵＮＤＡＲＹ￥Ｃｈｅｎ，Ｋａｎｇｈｕａ；Ｈｕａｎｇ，Ｂａｉｙｕｎ（ＰｏｗｄｅｒＭｅｔａｌｌｕｒｇｙＲｅｓｅａｒｃｈｉｎｓｔｉｔｕｔｅ，ＣｅｎｔｒａｌＳｏｕｔｈＵｎｉｖｅｒｓｉ...     

学术自由与学术规范

学术自由是学术形成与发展的必要条件，已有的学术规范又为新的学术提供了对象与基础。二者对学术具有同样重要的意义。学术是自由探索与遵循规范的矛盾与辩证统一。     

螺旋藻多糖铁配合物制备、抗氧化及淋巴细胞增殖活性分析

以三氯化铁为原料,通过络合反应,对螺旋藻多糖(SP)进行结构修饰,制得有机铁化合物〔螺旋藻多糖铁(Ⅲ)配合物SP-Fe(Ⅲ)〕。采用FTIR、DSC、TGA、XRD和SEM对其结构进行了表征,采用DPPH(1,1-二苯基-2-三硝基苯肼)自由基法、羟自由基法等5种方法和MTT(四唑盐)法分析了SP和SP-Fe(Ⅲ)的抗氧化活性和淋巴细胞增殖活性的影响。制备的SP-Fe(Ⅲ)中Fe(Ⅲ)质量分数为16.42%±1.17%。采用5轴蛛网图对SP-Fe(Ⅲ)的抗氧化活性进行了综合评价。结果表明,SP-Fe(Ⅲ)相比SP具有较高的抗氧化活性。在模拟人工胃液消化后,随着消化时间的延长,在pH=6.8的人工肠液中释放出的Fe(Ⅲ)质量分数达到83.64%;在31.25×10–3 g/L的质量浓度下,与SP相比,SP-Fe(Ⅲ)配合物对淋巴细胞增殖提高了44.35%。