Short-term mortality in end-stage heart failure patients

ObjectivesThis study is aimed at analyzing the impact of the main factors contributing to short and long-term mortality in patients at final stages of heart failure (HF).SettingPatients attended at any of the 279 primary health care centers belonging to the Institut Català de la Salut, in Catalonia (Spain).ParticipantsPatients with Advanced HF.DesignMulticenter cohort study including 1148 HF patients followed for one-year after reaching New York Heart Association (NYHA) IV.Main measurementsThe primary outcome was all-cause mortality. Multivariate logistic regression models were performed to assess the outcomes at 1, 3, 6, and 12 months.ResultsMean age of patients was 82 (SD 9) years and women represented 61.7%. A total of 135 (11.8%) and 397 (34.6%) patients died three months and one year after inclusion, respectively. Male gender, age, and decreased body mass index were associated with higher mortality at three, six and twelve months. In addition, low systolic blood pressure levels, severe reduction in glomerular filtration, malignancy, and higher doses of loop diuretics were related to higher mortality from 6 to 12 months.The most important risk factor over the whole period was presenting a body mass index lower than 20 kg/m² (three months OR 3.06, 95% CI: 1.58–5.92; six months OR 4.42, 95% CI: 2.08–9.38; and 12 months OR 3.68, 95% CI: 1.76–7.69).ConclusionsWe may conclude that male, age, and decreased body mass index determined higher short-term mortality in NYHA IV. In addition, low systolic blood pressure, reduced glomerular filtration, malignancy, and higher doses of loop diuretics contribute to increasing the risk of mortality at medium and long-term. Such variables are easily measurable and can help to decide the best way to face the most advances stages of the disease.     

两种技术修复肘关节恐怖三联征中外侧副韧带复合体的疗效比较

目的比较穿骨隧道缝合固定和锚钉固定修复肘关节恐怖三联征中外侧副韧带复合体（lateral collateral ligament complex，LCLC）损伤的疗效。方法回顾分析 2012 年 6 月—2018 年 1 月收治的 50 例肘关节恐怖三联征患者临床资料，其中 22 例采用锚钉固定（锚钉组）、28 例采用穿骨隧道缝合固定（穿骨隧道组）修复 LCLC。两组患者性别、年龄、骨折侧别、受伤至入院时间以及冠状突骨折、桡骨头骨折及肘关节恐怖三联征分型等一般资料比较，差异均无统计学意义（P>0.05）。记录并比较两组手术时间、术中出血量、骨折愈合时间以及并发症发生情况，末次随访时 Mayo 肘关节评分系统（MEPS）、关节活动度、Broberg-Morrey 分级。 结果两组患者均顺利完成手术，手术时间及术中出血量比较差异均无统计学意义（P>0.05）。 患者均获随访，穿骨隧道组随访时间为（24.43±6.84）个月，锚钉组为（21.55±6.16）个月，差异无统计学意义（t=1.534，P=0.132）。X 线片复查示，两组冠状突及桡骨头骨折均愈合，愈合时间组间比较差异无统计学意义（P>0.05）。末次随访时，两组肘关节屈伸活动度、旋转活动度、MEPS 评分、Broberg-Morrey 分级比较，差异均无统计学意义（P>0.05）。随访期间患者均无肘关节再脱位或不稳发生，穿骨隧道组并发症发生率为 28.57%（8/28）、锚钉组为 27.27%（6/22），差异无统计学意义（χ²=2.403，P=0.121）。 结论治疗肘关节恐怖三联征时，采用穿骨隧道固定或锚钉固定修复 LCLC 均可获得满意疗效。     

Ilizarov 跖骨延长治疗糖尿病足溃疡并跖骨头慢性骨髓炎

目的探讨清创后一期 Ilizarov 跖骨延长治疗糖尿病足溃疡并跖骨头慢性骨髓炎的临床疗效。方法2015 年 1 月—2018 年 10 月，应用清创后一期 Ilizarov 跖骨延长治疗糖尿病足溃疡并跖骨头慢性骨髓炎患者 8 例（9 足、11 个部位）。其中男 3 例（4 足、5 个部位），女 5 例（5 足、6 个部位）；年龄 44～65 岁，平均 57.5 岁。糖尿病足分级：Wagner 3 级 6 例（7 足）、4 级 2 例（2 足）。左足 4 例，右足 3 例；双足 1 例。慢性骨髓炎病程 1～5 年，平均 3.1 年。骨髓炎部位：第 1 跖骨头 3 足，第 3 跖骨头 1 足，第 4 跖骨头 1 足，第 5 跖骨头 6 足。其中 2 例为同一足合并 2 个部位慢性骨髓炎。记录跖骨延长长度及时间、佩戴外固定架时间，计算外固定架带架指数；观察足部溃疡及骨延长段愈合情况，记录愈合时间，计算骨延长段愈合指数。末次随访时，按照美国矫形足踝协会（AOFAS）评分标准评定足部功能。结果患者术后获随访 9～26 个月，平均 15.0 个月。除骨延长期间发生针道感染外，治疗期间均无皮肤坏死以及血管、神经损伤等并发症发生。跖骨延长长度 12～35 mm，平均 20.5 mm；跖骨延长时间 21～84 d，平均 57.8 d。佩戴外固定架时间 10.4～21.1 周，平均 14.6 周；外固定架带架指数为 42.9～59.2 d/cm，平均 54.3 d/cm。患者足部溃疡均愈合，愈合时间 19～70 d，平均 30.5 d；随访期间溃疡均无复发。X 线片复查示骨延长段均达骨性愈合，愈合指数为 37～51 d/cm，平均 42.5 d/cm。末次随访时，踝关节 AOFAS 评分为 87～95 分，平均 91.7 分；获优 5 足、良 4 足，优良率 100%。结论清创后按照 Ilizarov 张力-应力法则行一期跖骨延长，能促进糖尿病足溃疡愈合、重建跖骨长度、保留跖骨负重功能，是治疗糖尿病足溃疡并跖骨头慢性骨髓炎的一种有效方法。     

miR-200、 miR -155及血管新生因子与复发性流产的相关性分析

目的 研究miR-200、miR-155及血管新生因子与原因不明复发性流产(unexplained recurrent spontaneousabortion,URSA)的相关性分析。 方法 选择2015年3月—2018年1月在青岛市妇女儿童医院妇产科就诊的URSA患者作为URSA组、要求终止妊娠的正常早孕患者作为对照组,检测绒毛组织中微小RNA(microRNA, miR)miR-200、miR-155、血管内皮生长因子(vascular endothelial growth factor,VEGF)、可溶性FMS样酪氨酸激酶1(soluble FMS like tyrosine kinase-1,sFlt-1)的表达量及血清中VEGF、sFlt-1的含量,对miR-200、miR-155靶向结合VEGF、sFlt-1进行生物信息学分析。 结果 URSA组的绒毛组织中miR-200(1.78±0.32 vs. 0.91±0.15)、sFlt-1(1.87±0.35 vs. 1.06±0.21)的相对表达量及血清中sFlt-1的含量[(12.39±2.31)ng/ml vs. (6.51±0.95)ng/ml]均高于对照组,差异有统计学意义(均P<0.05)。绒毛组织中miR-155相对表达量(0.60±0.10 vs. 0.93±0.16)、VEGF mRNA相对表达量(0.59±0.09 vs. 1.02±0.16)及蛋白表达量(0.62±0.07 vs. 1.04±0.18)、血清中VEGF的含量[(601.25±94.39)ng/ml vs. (935.12±132.47)ng/ml]低于对照组,差异有统计学意义(均P<0.05);URSA组患者绒毛组织中miR-200的表达量与血清中VEGF的含量、绒毛组织中VEGF的表达量均呈负相关,绒毛组织中miR-155的表达量与血清中sFlt-1的含量和绒毛组织中sFlt-1的表达量均呈负相关;miR-200、miR-155分别靶向结合VEGF、sFlt-1基因的3’UTR。 结论 miR-200表达增多、miR-155表达减少与URSA发生有关,miR-200靶向VEGF、miR-155靶向sFlt-1是介导该过程的可能机制。     

miR-122 Inhibits Hepatocarcinoma Cell Progression by Targeting LMNB2

In the present study, we investigated the role of miR-122 in hepatocarcinoma progression and explored the mechanism. In hepatocarcinoma tissues and cells, we used qRT-PCR to validate the miR-122 expression level. Next, we used colony formation by crystal violet staining assay to compare cell proliferation ability, and we used scratch test or Transwell assay to compare cell migration or invasion ability. We then conducted bioinformatics or luciferase reporter gene assay to prove the regulation effect of miR-122 on lamin B2 (LMNB2), and the biological function of LMNB2 was analyzed. We used nude mouse tumorigenicity assay to test the inhibition effect of miR-122 ASO therapy against hepatocarcinoma. miR-122 was reduced in hepatocarcinoma tissues compared to the paracarcinoma tissues, which was relatively low or high in hepatocarcinoma cell line SMMC7721 or Hep3B, and overexpressed miR-122 inhibited proliferation, migration, and invasion in hepatocarcinoma cells. Additionally, some reports showed that LMNB2 was regulated by miR-122, which inhibited the expression of LMNB2. Moreover, LMNB2 functioned to promote cell proliferation, migration, and invasion. We could achieve the inhibition of hepatocarcinoma using miR-122 therapy through decreasing LMNB2 expression in vivo. Our data indicated that miR-122 could inhibit hepatocellular carcinoma cell progression by targeting LMNB2 and as a therapeutic target for hepatocarcinoma treatment.     

Knockdown of PVT1 inhibits IL-1β-induced injury in chondrocytes by regulating miR-27b-3p/TRAF3 axis

Long noncoding RNA plasmacytoma variant translocation 1 (PVT1) has been identified to implicate in the progression of osteoarthritis (OA). However, the mechanism underlying PVT1 in OA development remains largely unknown. This study aimed to investigate the effect of PVT1 on interleukin-1 beta (IL-1β)-induced injury in chondrocytes and explore potential mechanism. The cartilage tissues from 25 OA patients and normal controls were collected. Human transformed chondrocytes C28/I2 were stimulated by IL-1β. The levels of PVT1, microRNA (miR)-27b-3p, and tumor necrosis factor receptor-associated factor 3 (TRAF3) were detected by quantitative real-time polymerase chain reaction or western blot. IL-1β-induced injury was investigated by cell viability, apoptosis, autophagy and inflammatory response using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, flow cytometry, western blot and enzyme linked immunosorbent assay, respectively. The target association between miR-27b-3p and PVT1 or TRAF3 was explored by luciferase reporter, RNA immunoprecipitation and RNA pull-down assays. We found that PVT1 expression was enhanced in OA patients and IL-1β-treated C28/I2 cells. Silence of PVT1 promoted cell viability and autophagy but suppressed apoptosis and inflammatory response in IL-1β-treated C28/I2 cells. miR-27b-3p was confirmed as a target of PVT1 and its deficiency reversed the suppressive effect of PVT1 knockdown on IL-1β-induced injury. TRAF3 was a target of miR-27b-3p and attenuated the effect of miR-27b-3p on IL-1β-induced injury in C28/I2 cells. Moreover, TRAF3 expression was positively regulated by PVT1 via sponging miR-27b-3p. Collectively, knockdown of PVT1 increased cell viability and autophagy but inhibited apoptosis and inflammatory response in chondrocytes treated by IL-1β via up-regulating miR-27b-3p and down-regulating TRAF3.