The laboratory diagnosis of spring-summer infections in Yekaterinburg in the epidemic season for tick-borne encephalitis

The authors propose a comprehensive approach to laboratory diagnosis of seasonal transmissible infections, based on modern methods permitting etiological deciphering of disease. A universal diagnostic algorithm notably accelerated the laboratory diagnosis due to cutting the period between collection of material from a patient and consecutive screening for antibodies to agents of tick-borne encephalitis, Lyme disease, and California encephalitis.     

脾动脉阻断联合射频消融术治疗脾功能亢进的疗效观察

【摘要】 目的 总结脾动脉球囊阻断联合脾脏射频消融术（RFA）治疗肝硬化门静脉高压型脾功能亢进的有效性及经验。方法 在脾动脉球囊阻断状态下对15例脾功能亢进患者行经皮穿刺脾脏RFA,RFA平均时间为（46．4±5．4）min。术后3 d、1周、1个月、3个月和6个月监测血常规,术后1个月复查腹部CTA。结果 1例患者术后出现左侧大量血性胸腔积液,给予止血及胸腔积液引流后好转,其余患者未发生严重并发症。RFA后1个月行腹部CTA检查示RFA毁损范围占脾脏总体积的比率为34．3％～71.8％,平均（56.20±13.09）％。术前血细胞计数示:白细胞为（3.88±1.75）×109/L,红细胞（4.06± 0.37）×1012/L,血小板（48.14±11.33）×109/L。RFA术后1个月复查示:白细胞（5.62±1.61）×109/L,血小板（132.29±33.20）×109/L;与术前相比,血小板和白细胞显著升高（P<0．05）。结论 脾动脉球囊阻断联合RFA治疗肝硬化门静脉高压型脾功能亢进具有较高的安全性,且近期疗效可靠。     

D-STATCOM不平衡负荷补偿电流的优化设计

在介绍不平衡负荷的电纳补偿原理的同时,分析了其不足之处,即在负荷严重不平衡的情况 下,三相补偿装置分担的负荷不均衡,限制了装置的补偿能力,也容易导致一相或两相过流;针对不 平衡负荷补偿的特殊工况,提出了补偿电流优化设计的目标,即三相电流大小均衡。文中给出了补 偿电流优化设计的理论依据和前提条件:首先,通过选择合适的电路连接方式,电流是多样可选择 的;从数学上证明了提出的优化设计目标的合理性,并给出了优化补偿电流的计算方法。通过 MATLAB计算,与传统补偿思路进行了基波电流、电容电压波动等多项指标的比较,证明优化设 计原理在各项指标上部具有明显的优势。PSCAD仿真和10 kVA样机实验结果表明,优化设计原 理可以实现且效果良好。     

ATP-dependent proteolysis in mitochondria. m-AAA protease and PIM1 protease exert overlapping substrate specificities and cooperate with the mtHsp70 system

To analyze protein degradation in mitochondria and the role of molecular chaperone proteins in this process, bovine apocytochrome P450scc was employed as a model protein. When imported into isolated yeast mitochondria, P450scc was mislocalized to the matrix and rapidly degraded. This proteolytic breakdown was mediated by the ATP-dependent PIM1 protease, a Lon-like protease in the mitochondrial matrix, in cooperation with the mtHsp70 system. In addition, a derivative of P450scc was studied to which a heterologous transmembrane region was fused at the amino terminus. This protein became anchored to the inner membrane upon import and was degraded by the membrane-embedded, ATP-dependent m-AAA protease. Again, degradation depended on the mtHsp70 system; it was inhibited at non-permissive temperature in mitochondria carrying temperature-sensitive mutant forms of Ssc1p, Mdj1p, or Mge1p. These results demonstrate overlapping substrate specificities of PIM1 and the m-AAA protease, and they assign a central role to the mtHsp70 system during the degradation of misfolded polypeptides by both proteases.     

A poroelastic model valid in large strains with applications to perfusion in cardiac modeling

This paper is motivated by the modeling of blood flows through the beating myocardium, namely cardiac perfusion. As in other works, perfusion is modeled here as a flow through a poroelastic medium. The main contribution of this study is the derivation of a general poroelastic model valid for a nearly incompressible medium which experiences finite deformations. A numerical procedure is proposed to iteratively solve the porous flow and the nonlinear poroviscoelastic problems. Three-dimensional numerical experiments are presented to illustrate the model. The first test cases consist of typical poroelastic configurations: swelling and complete drainage. Finally, a simulation of cardiac perfusion is presented in an idealized left ventricle embedded with active fibers. Results show the complex temporal and spatial interactions of the muscle and blood, reproducing several key phenomena observed in cardiac perfusion.