血糖信息化管理系统对2型糖尿病患者治疗效果及自我管理能力的影响分析

目的分析血糖信息化管理系统对糖尿病患者的疗效及自我管理能力的影响。方法实施全院血糖管理前,随机选取2016年1月-2016年6月在郑州人民医院治疗的112例2型糖尿病患者为对照组;实施全院血糖管理后,选取2016年7月-2016年12月该院收治的112例手术患者为观察组。对照组患者采用传统床旁血糖仪及血糖管理模式;观察组患者采用全信息化血糖管理模式。对比患者的自我管理能力的改变,检测患者空腹血糖(FPG)、餐后2 h血糖(2 h PG)、三酰甘油(TG)、总胆固醇(TC)及糖化血红蛋白(Hb A1c)等指标进行比较。结果观察组对血糖相关知识的知晓率、血糖达标率及糖化血红蛋白达标率高于对照组(P<0.05)。观察组的自测血糖率、适当运动率、合理饮食率及规范用药率均高于对照组(P<0.05)。观察组的FPG、2 h PG、TC、TG及Hb AIc低于对照组(P<0.05)。结论医院实施全院血糖信息化管理后,方便医护人员获取患者信息,纠正患者不良生活习惯,有效改善患者的血糖指标,提高患者对医院服务的满意度。

Gasless Laparoscopic Surgery plus Abdominal Wall Lifting for Giant Hiatal Hernia——Our Single-center Experience

Giant hiatal hernia（GHH） comprises 5% of hiatal hernia and is associated with significant complications.The traditional operative procedure,no matter transthoracic or transabdomen repair of giant hiatal hernia,is characteristic of more invasion and more complications.Although laparoscopic repair as a minimally invasive surgery is accepted,a part of patients can not tolerate pneumoperitoneum because of combination with cardiopulmonary diseases or severe posterior mediastinal and neck emphesema during operation.The aim of this article was to analyze our experience in gasless laparoscopic repair with abdominal wall lifting to treat the giant hiatal hernia.We performed a retrospective review of patients undergoing gasless laparoscopic repair of GHH with abdominal wall lifting from 2012 to 2015 at our institution.The GHH was defined as greater than one-third of the stomach in the chest.Gasless laparoscopic repair of GHH with abdominal wall lifting was attempted in 27 patients.Mean age was 67 years.The results showed that there were no conversions to open surgery and no intraoperative deaths.The mean duration of operation was 100 min（range：90–130 min）.One-side pleura was injured in 4 cases（14.8%）.The mean postoperative length of stay was 4 days（range：3–7 days）.Median follow-up was 26 months（range：6–38 months）.Transient dysphagia for solid food occurred in three patients（11.1%）,and this symptom disappeared within three months.There was one patient with recurrent hiatal hernia who was reoperated on.Two patients still complained of heartburn three months after surgery.Neither reoperation nor endoscopic treatment due to signs of postoperative esophageal stenosis was required in any patient.Totally,satisfactory outcome was reported in 88.9% patients.It was concluded that the gasless laparoscopic approach with abdominal wall lifting to the repair of GHH is feasible,safe,and effective for the patients who cannot tolerate the pneumoperitoneum.

RASAL2 Deficiency Attenuates Hepatic Steatosis by Promoting Hepatic VLDL Secretion via the AKT/TET1/MTTP Axis

Background and Aims:RAS protein activator like 2(RASAL2)is a newly discovered metabolic regulator involved in energy homeostasis and adipogenesis.However,whether RASAL2 is involved in hepatic lipid metabolism remains undetermined.This study explored the function of RASAL2 and elucidated its potential mechanisms in nonalcoholic fatty liver disease(NAFLD).Methods:NAFLD models were established either by feeding mice a high-fat diet or by incubation of hepatocytes with 1 mM free fatty acids(oleic acid:palmitic acid=2:1).Pathological changes were observed by hematoxylin and eosin staining.Lipid accumulation was assessed by Oil Red O staining,BODIPY493/503 staining,and triglyceride quantification.The in vivo secretion rate of very lowdensity lipoprotein was determined by intravenous injection of tyloxapol.Gene regulation was analyzed by chromatin immunoprecipitation assays and hydroxymethylated DNA immunoprecipitation combined with real-time polymerase chain reaction.Results:RASAL2 deficiency ameliorated hepatic steatosis both in vivo and in vitro.Mechanistically,RASAL2 deficiency upregulated hepatic TET1 expression by activating the AKT signaling pathway and thereby promoted MTTP expression by DNA hydroxymethylation,leading to increased production and secretion of very low-density lipoprotein,which is the major carrier of triglycerides exported from the liver to distal tissues.Conclusions:Our study reports the first evidence that RASAL2 deficiency ameliorates hepatic steatosis by regulating lipid metabolism through the AKT/TET1/MTTP axis.These findings will help understand the pathogenesis of NAFLD and highlight the potency of RASAL2 as a new molecular target for NAFLD.