Polyether Synthesis through Reductive Etherification Reaction Strategy

The reductive etherification reaction (RER) of carbonyl groups (aldehydes or ketones) through silane as a reducing agent together with Bronsted or Lewis acid affords the synthesis of symmetrical and unsymmetrical ethers. This strategy is applied at the macromolecular level for the first time in 1993, and isophthalaldehyde is self-polymerized in the presence of triethylsilane (Et₃SiH)/ tritylperchlorate (TrClO₄) to yield polyethers with low to moderate molecular weights. Next, the polyethers with alternating structures are achieved by reacting isophthalaldehyde with bis(trimethylsilyl) ethers or diols as comonomers using reducing agent silane and Lewis acid. Moreover, in recent years, it is shown that polyether synthesis and post-polymerization modification (PPM) of polymers proceeds smoothly and effectively with the RER strategy in the presence of chlorodimethylsilane (CDMS), which acts as both a reducing agent and a Lewis acid.     

Surgical myectomy versus alcohol septal ablation for obstructive hypertrophic cardiomyopathy: A propensity score–matched cohort

Objectives

In patients with hypertrophic cardiomyopathy, obstruction of the left ventricular outflow tract can be relieved by surgical septal myectomy or alcohol septal ablation, but uncertainty remains regarding long-term results and comparative effectiveness of alcohol septal ablation. This study aims to compare short- and long-term outcomes of the 2 procedures.

Cardiac Implantable Electronic Devices in Patients With Left Ventricular Assist Systems

Recent progress and evolution in device engineering, surgical implantation practices, and periprocedural management have advanced the promise of durable support with left ventricular assist systems (LVAS) in patients with stage D heart failure. With greater uptake of LVAS globally, a growing population of LVAS recipients have pre-existing cardiac implantable electronic devices (CIEDs). Strategies for optimal clinical management of CIEDs in patients with durable LVAS are evolving, and clinicians will increasingly face complex decisions regarding implantation, programming, deactivation, and removal of CIEDs. Traditional decision-making pathways for CIEDs may not apply to LVAS-supported patients, as few patients die of arrhythmic causes and many arrhythmias may be well tolerated. Given limited data, treatment decisions must be individualized and made collaboratively among electrophysiologists, advanced heart failure specialists, and patients and their caregivers. Large, prospective, well-conducted studies are needed to better understand the contemporary utility of CIEDs in patients with newer-generation LVAS.     

A Novel Regulatory Defect in the Branched‐Chain α‐Keto Acid Dehydrogenase Complex Due to a Mutation in the PPM1K Gene Causes a Mild Variant Phenotype of Maple Syrup Urine Disease

This article describes a hitherto unreported involvement of the phosphatase PP2Cm, a recently described member of the branched‐chain α‐keto acid dehydrogenase (BCKDH) complex, in maple syrup urine disease (MSUD). The disease‐causing mutation was identified in a patient with a mild variant phenotype, involving a gene not previously associated with MSUD. SNP array‐based genotyping showed a copy‐neutral homozygous pattern for chromosome 4 compatible with uniparental isodisomy. Mutation analysis of the candidate gene, PPM1K, revealed a homozygous c.417_418delTA change predicted to result in a truncated, unstable protein. No PP2Cm mutant protein was detected in immunocytochemical or Western blot expression analyses. The transient expression of wild‐type PPM1K in PP2Cm‐deficient fibroblasts recovered 35% of normal BCKDH activity. As PP2Cm has been described essential for cell survival, apoptosis and metabolism, the impact of its deficiency on specific metabolic stress variables was evaluated in PP2Cm‐deficient fibroblasts. Increases were seen in ROS levels along with the activation of specific stress‐signaling MAP kinases. Similar to that described for the pyruvate dehydrogenase complex, a defect in the regulation of BCKDH caused the aberrant metabolism of its substrate, contributing to the patient's MSUD phenotype—and perhaps others.     

精神分裂症患者内隐攻击性对照研究

目的：探讨精神分裂症患者的内隐攻击性,为临床干预提供依据。方法将216例精神分裂症患者设为患者组,112名健康志愿者设为对照组。采用偏好组词法测评两组内隐攻击性,采用暴力攻击行为筛查标准筛查患者组的暴力行为,采用简明精神病量表评定患者的精神症状,冲动性量表、攻击性量表评定患者的冲动攻击性人格特点。结果有暴力攻击行为组简明精神病量表总分、思维障碍、激活性、敌对猜疑及行为紊乱因子分均显著高于无暴力攻击行为组（P＜0．05或0．01）,冲动性量表总分及行动分量表因子分显著高于无暴力攻击行为组（P＜0．01）,攻击性量表总分及各因子分均显著高于无暴力攻击行为组（ P＜0．05或0．01）。患者组与对照组及有暴力攻击行为组与无暴力攻击行为组偏好组词法测评攻击性词及身体攻击性词和语言攻击性词评分比较差异均无显著性（P＞0．05）。结论精神分裂症患者较正常人有更多的暴力攻击行为,其原因是由精神症状及性格缺陷所致。     

Pre-Dilatation Versus No Pre-Dilatation for Implantation of a Self-Expanding Valve in All Comers Undergoing TAVR: The DIRECT Trial

Objectives

The aim of this study was to compare the implantation of a self-expanding valve with or without balloon aortic valvuloplasty (BAV) in an open-label, noninferiority, randomized trial.

何首乌多糖对免疫功能低下小鼠的免疫保护作用

目的:探讨何首乌多糖(PPM)对免疫功能低下小鼠的免疫保护作用。方法:小鼠腹腔注射环磷酰胺建立小鼠免疫功能低下模型后,灌胃PPM 0.4,0.8,1.6 g.kg-1,qd,连续给药10 d,另设模型对照组和正常对照组。采用显微镜观察腹腔巨噬细胞的吞噬百分率、吞噬指数和T淋巴细胞酯酶阳性率;用分光光度测定血清溶血素含量;用3H-TdR掺入法测定脾细胞淋巴细胞增殖率。结果:PPM能显著拮抗环磷酰胺所致免疫功能低下小鼠的免疫器官重量减轻和白细胞数量减少,明显增加小鼠腹腔巨噬细胞的吞噬率及吞噬指数,显著增加血清溶血素含量,且能明显促进T淋巴细胞酯酶阳性率和ConA诱导的脾T淋巴细胞增殖反应。结论:何首乌多糖对免疫功能低小鼠的免疫功能有明显的增强作用。     

Expression of PTEN, PPM1A and P-Smad2 in hepatocellular carcinomas and adjacent liver tissues

AIM: To investigate the expressions of PTEN, PPM1A and P-Smad2 in hepatocellular carcinoma (HCC) and their significance. METHODS: The expressions of PTEN, PPM1A and P-Smad2 in 31 HCC tissues, 25 adjacent liver tissues and 13 non-tumor liver tissues were detected by using Envision immunohistochemical technique. RESULTS: The positive expression (64.52%) and staining intensity (4.19 ± 3.31) of PTEN in the cytoplasm of HCC were significantly lower and weaker than those in the adjacent or non-tumor liver tissues (97.37%, 7.88 ± 0.93; 100%, 7.77 ± 0.93, respectively) (P < 0.05), and its staining intensity in the cytoplasm of HCC, which belongs to Edmondson pathologic grades Ⅱ-Ⅲ and above, was also lower than that of gradeⅠandⅠ-Ⅱ. Furthermore, its location in the nucleus or cytoplasm of liver cells was negatively correlated with the progression of liver disease (r = -0.339, P = 0.002); most of PPM1A might be only expressed in the nucleus of adjacent liver tissues, non-HCC tissues or Edmondson gradeⅠandⅠ-Ⅱ HCC, but it was mainly expressed in the cytoplasm of HCC with Edmondson grade ≥Ⅱ, weakly or negatively expressed in the nucleus (P < 0.05), and its location was negatively correlated with the progression of liver disease (r = -0.45, P = 0.0000). P-Smad2, which was mostly located in the nucleus and cytoplasm of gradeⅠ andⅠ-Ⅱ HCC, surrounding or non-tumor liver tissues, was only in the nucleus of HCC with Edmondson grade Ⅱ and above (P < 0.001), and its location was positively correlated with the disease progression (r = 0.224, P = 0.016). Spearman correlation analysis revealed that P-Smad2 was significantly negatively correlated with PTEN and PPM1A (r = -0.748, P = 0.000; r = -0.366, P = 0.001, respectively); and PTEN and PPM1A were positively correlated with HCC carcinogenesis (r = 0.428, P = 0.000). CONCLUSION: The aberrant location of expression and staining intensity of PTEN, PPM1A and P-Smad2 in HCC and their relationship might have an impact on the pathogenesis of HCC.