镁离子在治疗心律失常中的研究进展

Mg^2＋是人体内重要的电解质离子，是人体细胞内含量第二丰富的阳离子，具有复杂的调节机制，对维持机体新陈代谢及其他生理功能具有极其重要的作用。目前已发现人体内超过300种酶的作用离不开其参与，其中包括Mg^2＋-K^＋-ATP酶、Ca^2＋-ATP酶等。临床上利用Mg^2＋调节这些酶的活性等特点，将Mg^2＋作为一种预防和治疗心律失常的药物在很多方面运用，但其规范化运用仍有待进一步明确。现将Mg^2＋在心律失常中的运用综述如下。     

老年脓毒症患者临床特征及预后影响因素

 目的 探讨老年脓毒症患者临床特征及影响预后的危险因素。方法 选取2020年7月-2021年9月某三级甲等医院收治的老年脓毒症患者为研究对象，记录患者的临床及实验室资料，根据患者28天预后情况分为存活组和死亡组，比较各临床指标在两组间的差异，应用二元logistic回归分析法分析影响老年脓毒症患者预后的独立危险因素，进一步绘制受试者工作特征（ROC）曲线，评估不同指标预测患者预后的价值。结果 共纳入121例患者，其中74例为脓毒症，47例为脓毒性休克。存活组92例，死亡组29例。与存活组相比，死亡组患者发生脓毒性休克、合并症个数 ≥ 2的比例均较高（P<0.05）；序贯器官衰竭评估（SOFA）评分和急性生理与慢性健康状况评估（APACHEⅡ）评分也较高，白细胞介素6（IL-6）、胱抑素C（Cys-C）、降钙素原（PCT）、凝血酶原时间（PT）和D -二聚体（D -D）表达水平均增高（均P<0.05），而淋巴细胞绝对计数（ALC）和清蛋白（ALB）表达水平降低（均P<0.01）。二元logistic回归分析显示脓毒性休克、SOFA评分、D -D及Cys-C表达水平是影响老年脓毒症患者28天预后的独立危险因素。ROC曲线分析显示SOFA评分（AUC=0.758）、D -D（AUC=0.774）、Cys-C（AUC=0.650）预测患者的预后均有一定的价值（均P<0.01），与单个指标相比，三个指标的联合检测显示出更高的预测价值（AUC=0.882）。结论 发生脓毒性休克、SOFA评分增高、D -D及Cys-C表达水平增加是导致老年脓毒症患者病死率上升的独立危险因素，SOFA评分、D -D和Cys-C的联合检测可进一步提高脓毒症患者预后的预测价值，为临床治疗和预后评估提供参考依据。     

Prophylactic intra-abdominal drainage following colorectal anastomoses. A systematic review and meta-analysis of randomized controlled trials

BackgroundClinically evident Anastomotic Leakage (AL) remains one of the most feared complications after colorectal resections with primary anastomosis. The primary aim of this systematic review and meta-analysis was to determine whether Prophylactic Drainage (PD) after colorectal anastomoses confers any advantage in the prevention and management of AL.MethodsSystematic literature search was performed using MEDLINE, the Cochrane Central Register of Controlled Trials, and EMBASE databases for randomized studies comparing clinical outcomes of patients with Drained (D) or Undrained (UD) colorectal anastomoses performed for any cause.ResultsFour randomized controlled trials comparing D and UD patients undergoing colorectal resections with primary anastomosis were included for quantitative synthesis. In total, 1120 patients were allocated to group D (n = 566) or group UD (n = 554). The clinical AL rate was 8.5% in the D group and 7.6% in the UD group, with no statistically significant difference (P = 0.57). Rates of radiological AL (D: 4.2% versus UD: 5.6%; P = 0.42), mortality (D: 3.6% versus UD: 4.4%; P = 0.63), overall morbidity (D: 16.6% versus UD: 18.6%, P = 0.38), wound infection (D: 5.4% versus UD: 5.3%, P = 0.95), pelvic sepsis (D: 9.7% versus UD: 10.5%, P = 0.75), postoperative bowel obstruction (D: 9.9% versus UD: 6.9%, P = 0.07), and reintervention for abdominal complication (D: 9.1% versus UD: 7.9%, P = 0.48) were equivalent between the two groups.ConclusionsThe present meta-analysis of randomized controlled trials investigating the value of PD following colorectal anastomoses does not support the routine use of prophylactic drains.     

A 16-plex Y-SNP typing system based on allele-specific PCR for the genotyping of Chinese Y-chromosomal haplogroups

Y-chromosomal SNP (Y-SNP), with its stable inheritance and low mutation, can provide Supplementary information in forensic investigation. While commonly used Y-chromosomal STR haplotypes show their limitations, typing of Y-SNP would become a powerful complement. In this study, a 16-plex Y-SNP typing system based on allele-specific PCR (AS-PCR) was developed to discriminate four dominant Y-chromosomal haplogroups (C-M130, D-CTS3946, N-M231, and O-M175) and 12 predominant sub-haplogroups of O-M175 (O1a-M119, O1a1a1a-CTS3265, O1b-M268, O1b1a2-Page59, O2-M122, O2a1-L127.1, O2a1b-F240, O2a1b1a1-CTS5820, O2a2-P201, O2a2b1a1-M177, O2a2b1a1a1a-Y17728, O2a2b1a2-F114). A series of experimental validation studies including sensitivity, species specificity, male-female mixture and inhibition were performed. The discrimination of the typing system was preliminarily proved with a haplogroup diversity of 0.9239. Altogether, the Y-SNP typing system based on AS-PCR should be capable of distinguishing China’s dominant Y-chromosomal haplogroups in a rapid and reliable manner, thus can be employed as a useful complement in forensic casework.     

Genetic Testing in Inherited Arrhythmias: Approach,Limitations, and Challenges

Genetic testing is playing an ever-expanding role in cardiovascular care and is becoming part of the “toolkit” for the cardiovascular clinician. In patients with inherited arrhythmias, genetic testing can confirm a suspected diagnosis, establish a diagnosis in unexplained cases, and help facilitate cascade family screening. Many inherited arrhythmia syndromes are monogenic diseases arising from a single pathogenic variant involved in the structure and function of cardiac ion channels or structural proteins. As such, “arrhythmia gene panels” will often cast a wide net for such heritable diseases. However, challenges may arise when genetic testing results are ambiguous, or when genetic testing results (genotype) and clinical phenotypes do not match. In cases of “genotype-phenotype matching,” genetic results complement the clinical phenotype and genetic testing can be used in diagnosis, family screening, and occasionally prognostication. It becomes more challenging when genetic results are negative or noncontributory and “contradict” the clinical phenotype. “Genotype mismatches” can also occur when genotype-positive patients have no clinical phenotype, or when genetic testing results point towards a completely different disease than the clinical phenotype. We discuss an approach to genetic testing and review the challenges that may arise when interpreting genetic testing results. Genetic testing has opened a wealth of opportunities in the diagnosis, management, and cascade screening of inherited arrhythmia syndromes, but has also opened a “Pandora’s box” of challenges. Genetic results should be interpreted with caution and in a multidisciplinary clinic, with support from genetic counsellors and an expert with a focused interest in cardiovascular genetics.     

Interventions for prevention and treatment of tobacco smoking in school-aged children and adolescents: A systematic review and meta-analysis

ObjectivesTo determine the effectiveness of primary health care relevant interventions to prevent and treat tobacco smoking in school-aged children and adolescents.MethodsThis systematic review considered studies included in a prior review. We adapted and updated the search to April 2015. Titles, abstracts and full-text articles were reviewed in duplicate; data extraction and quality assessments were performed by one reviewer and verified by another. Meta-analyses and pre-specified sub-group analyses were performed when possible. PROSPERO #CRD42015019051.ResultsAfter screening 2118 records, we included nine randomized controlled trials. The mostly moderate quality evidence suggested targeted behavioral interventions can prevent smoking and assist with cessation. Meta-analysis showed intervention participants were 18% less likely to report having initiated smoking at the end of intervention relative to controls (Risk Ratio 0.82; 95% confidence interval 0.72, 0.94); the absolute effect is 1.92% for smoking initiation, Number Needed to Treat is 52 (95% confidence interval 33, 161). For cessation, meta-analysis showed intervention participants were 34% more likely to report having quit smoking at the end of intervention relative to controls (Risk Ratio 1.34; 95% confidence interval 1.05, 1.69); the absolute effect is 7.98% for cessation, Number Needed to Treat is 13 (95% confidence interval 6, 77). Treatment harms were not mentioned in the literature and no data were available to assess long-term effectiveness.ConclusionPrimary care relevant behavioral interventions improve smoking outcomes for children and youth. The evidence on key components is limited by heterogeneity in methodology and intervention strategy. Future trials should target tailored prevention or treatment approaches, establish uniform definition and measurement of smoking, isolate optimal intervention components, and include long-term follow-up.     

ROS act as an upstream signal to mediate cadmium-induced mitophagy in mouse brain

As a well known generator of reactive oxygen species (ROS), cadmium (Cd) is found to be an effective inducer of mitophagy in mouse kidney and liver cells. Here, we aim to elucidate whether Cd can also initiate mitophagy in mouse brain and what role ROS play in this process. Our results showed that Cd caused overproduction of ROS. Meanwhile, Cd induced mitophagy, as indicated by the collapse of mitochondrial membrane potential (MMP), formation of mitophagosomes, increases of PINK1 level and LC3-II/LC3-I ratio and decrease of mitochondrial mass. Scavenging of ROS by N-acetyl-l-cysteine (NAC) or acetyl-l-carnitine (ALC) rescued MMP and mitochondrial mass, and squelched PINK1 level, mitochondrial accumulation of Parkin and LC3-II/LC3-I ratio, suggesting that ROS were associated with Cd-induced mitophagy. Cyclosporine A (CsA), an inhibitor of mitophagy, blocked Cd-induced mitophagy and PINK1/Parkin pathway but failed to suppress ROS increase, revealing that ROS are the causes rather than the results of Cd-induced mitophagy. In conclusion, this study suggested that ROS functioned on the upstream of PINK1/Parkin pathway to mediate Cd-induced mitophagy.