A Very Long-term Longitudinal Study on the Evolution and Clinical Outcomes of Persistent Iatrogenic Atrial Septal Defect After Cryoballoon Ablation

Background

Persistent iatrogenic atrial septal defect (iASD) is a common but poorly characterized complication after cryoballoon (CB) pulmonary vein isolation (PVI) procedures. We therefore investigate its prevalence, evolution, risk factors, and clinical outcomes in a prospective longitudinal study.

Results From a Large,Multicenter, Retrospective Analysis On Radium223 Use in Metastatic Castration-resistant Prostate Cancer (mCRPC) in the Triveneto Italian Region

Background

Radium 223 was introduced for metastatic castration-resistant prostate cancer based on the results of a randomized controlled trial showing risk reduction for death and skeletal events. Our aim was to evaluate the outcome of patients receiving radium 223 in a real-world setting.

进展型脑梗死患者miRNA的表达水平及临床意义

目的探讨进展型脑梗死患者微小RNA(miRNA)的表达水平及临床意义。方法回顾性分析2016年7月至2018年7月期间我院收治的138例脑梗死患者病例资料。根据斯堪的那维亚卒中量表(SSS)将其分为对照组(稳定型脑梗死,82例)和观察组(进展型脑梗死,56例)。观察组患者按照高级中枢损伤严重程度评定标准(MESSS)评分为轻度进展(30例)、中度进展(17例)、重度进展(9例)三个亚组。对观察组出院两个月后进行预后随访,并将其分为预后不良组及预后良好组。分析进展型脑梗死患者miRNA的表达水平及临床意义。结果进展型脑梗死患者的miRNA-21、miRNA-223水平均显著高于稳定型脑梗死患者(P 0. 05); miRNA-21、miRNA-223的高表达均是进展型脑梗死的危险因素(P 0. 05),且进展型脑梗死的严重程度与血清miRNA-21、miRNA-223的表达水平均呈正相关(r=0. 834,P=0. 008;r=0. 896,P=0. 001)。预后不良组患者血清miRNA-21、miRNA-223表达水平显著高于预后良好组(P 0. 05);血清miRNA-21、miRNA-223表达水平预测进展型脑梗死预后的AUC面积分别为0. 805、0. 834,并分别得出截断值4. 45 (敏感度77. 14%,特异性82. 28%)、7. 06(敏感度82. 86%,特异性73. 42%)。结论进展型脑梗死患者miRNA-21、miRNA-223呈高表达,且其表达水平与脑梗死严重程度呈正相关,同时对预测进展型脑梗死预后均具有较高的敏感度和特异度,有可能成为一种早期诊断和预测进展型脑梗死生物标志物。     

谷氨酰胺在危重病患者中的应用

目的探讨危重病患者中早期经静脉应用谷氨酰胺（glutamine，Gl）的临床价值。方法42例患者随机分成两组（对照组和Gln组），Gln组进行Gln治疗（100mL／d，共7d）。治疗前后检测患者体质量、白蛋白、谷胱甘肽（GSH）、握力的变化和肠功能不全的发生率。结果体质量两组治疗前后比较差异无显著性（P〉0．05）。白蛋白、握力和GSH Gl治疗后非常显著高于治疗前（P〈0．01）；白蛋白对照组治疗后较治疗前显著增高（P〈0．05），但握力和GSH治疗前后均无显著变化（P〉0.05）；肠功能不全的发生率Gln组为4．8％，显著低于对照组（28．6％，P〈0．05）。结论在危重病患者疾病早期通过静脉途径外源性地补充Gln，有效改善了患者的营养状况；使患者血浆中的GSH水平增高，加强了机体的抗氧化能力；减少了患者肠功能不全的发生率。     

Relaxin down-regulates renal fibroblast function and promotes matrix remodelling in vitro.

BACKGROUND: Renal fibroblasts are important effector cells in tubulointerstitial fibrosis, with experimental antifibrotic strategies focusing on the functional down-regulation of these cells. Several experimental models of fibrosis have provided evidence for the effectiveness of the polypeptide hormone relaxin as a potential antifibrotic agent. This study was conducted to further elucidate the antifibrotic mechanisms of relaxin on renal fibroblasts in vitro. METHODS: Rat cortical fibroblasts were obtained from outgrowth culture of renal tissue isolated from kidneys 3 days post-unilateral ureteric obstruction and constituted 100% of cells studied. A relaxin radio-receptor assay was used to establish binding of relaxin to renal fibroblasts in vitro. Functional studies then examined the effects of H2 relaxin (0, 1, 10 and 100 ng/ml) on fibroblast kinetics, expression of alpha-smooth muscle actin (alpha-SMA), total collagen synthesis, collagenase production and collagen-I lattice contraction. CTGF mRNA expression was also measured by northern analysis. RESULTS: H2 relaxin bound with high affinity to rat renal fibroblasts, but receptor numbers were low. Consistent with its previously reported bimodal effect, transforming growth factor (TGF-beta 1) reduced fibroblast proliferation, an effect abrogated by H2 relaxin. Fibroblasts exposed to H2 relaxin (100 ng/ml) for 24 h demonstrated decreased immunostaining for alpha-SMA and reduced alpha-SMA protein expression compared with controls. There was a trend for a relaxin-mediated reduction in total collagen synthesis and alpha 1(I) mRNA expression with large dose-related increases in collagenase protein expression being observed. TGF-beta 1-stimulated collagen-I lattice contraction was significantly inhibited following co-incubation with 100 ng/ml relaxin. Incremental doses of H2 relaxin had no significant effect on CTGF mRNA expression. CONCLUSIONS: The findings of this study suggest that the antifibrotic effects of relaxin involve down-regulation of fibroblast activity, increase in collagenase synthesis and restructuring of collagen-I lattices, which are consistent with its known physiological role of matrix remodelling. Although there appears to be an interaction between TGF-beta 1 and H2 relaxin, this does not appear to involve a reduction in CTGF mRNA expression.