Extracorporeal life support in paediatrics

Extracorporeal membrane oxygenation (ECMO) is a life support technique based on modifications of heart-lung bypass technology. It is used to support severe but potentially reversible pulmonary or cardiopulmonary failure. There is increasing use of the technique for neonates and a return of interest in its use for adults. The number of non-neonatal paediatric patients receiving pulmonary support with ECMO worldwide is, however, small, and survival rates average less than 50%. Initial experience in 15 patients aged 3 months to 5 years with a high survival and low morbidity is reported.     

Pathological complications of non-survivors of newborn extracorporeal membrane oxygenation

The pathology was reviewed of the early deaths identified from the first 50 neonates treated with extracorporeal membrane oxygenation (ECMO) during its introduction to the UK. Fifteen neonates died during or shortly after ECMO between August 1989 and June 1992. Data on 12 are presented (three did not have a postmortem examination). The clinical diagnoses at referral for ECMO were as follows: persistent pulmonary hypertension of the newborn (six infants), primary congenital pneumonia (one infant), community acquired pneumonia (two infants), birth asphyxia (one infant), respiratory distress syndrome (one infant), and meconium aspiration syndrome (one infant). In our group, at necropsy, five had significant haemorrhage (three intracranial, one pulmonary, one pericardial and intraventricular). Three of five infants with evidence of haemorrhage also had signs of sepsis. Six infants had evidence at necropsy of systemic sepsis, five showed evidence of severe anoxic brain injury, and four infants had cerebellar haemorrhages. Three infants had evidence of myocardial ischaemia. It is difficult to discriminate between the relative influence of the primary diagnosis, the mode of treatment, and the severity of presentation in the genesis of this pathology. It is likely that the extent and severity of some of the findings represent a pathological progression that would have been interrupted by the death of the patient, had ECMO not been instituted.     

我国胫骨远端骨折经MIPPO与切开复位内固定治疗的系统评价

目的：系统评价我国小切口复位内固定术（MIPPO）与切开复位内固定治疗胫骨远端骨折的疗效与安全性。方法计算机检索中国知网（CNKI：2003年9月-2013年5月）、万方数据库（2003年9月-2013年5月）、维普数据库（2003年9月-2013年5月）,中国生物医学数据库及超星电子图书。手工检索国内近五年来发表于《中华骨科杂志》、《中国矫形外科杂志》及《临床骨科杂志》等各骨科杂志及相关杂志的相关文献。收集所有相关 MIPPO与切开复位内固定治疗胫骨远端骨折的随机对照试验及半随机对照试验,采用 Cochrane协作网提供的软件 RevMan5．0进行系统评价。结果共纳入12篇随机对照试验及半随机对照试验,共733例患者,纳入研究质量评价结果为 B级10篇,C级2篇。系统评价结果显示,与切开复位内固定组相比,MIPPO 组术中失血量少[SMD＝-4．46,95％CI（-5．87,-3．05）,P ＜0．05];骨折愈合时间短[SMD＝-1．54,95％CI（-2．02,-1．06）,P＜0．05];术后优良率高[RR＝1．22,95％CI（1．13,1．32）,P ＜0．05],但两组手术时间比较差异无统计学意义。结论采用 MIPPO术治疗胫骨远端骨折具有明显的优势,值得临床推广。但由于该系统评价尚存在一定的局限性,故需要大量严格的、大样本量的、多中心性的,并且采用正确的随机、盲法、分配隐藏以及对失访与退出的患者进行正确的意向性分析（ITT分析）等文献研究来进一步论证。     

再发性低血糖对幼鼠脑内GLUT1及GLUT3表达的影响

目的观察再发性低血糖后脑内葡萄糖转运蛋白1(glucose transporter 1,GLUT1)及葡萄糖转运蛋白3(GLUT3)表达的变化,从而探讨无症状低血糖的发生机制。方法将80只15日龄野生型小鼠随机分为正常对照组及低血糖组,每组40只。低血糖组给予正规胰岛素腹腔注射3次,每次剂量为5U/kg,对照组注射等体积生理盐水。两组分别在最后1次注射后12、24、48及72 h处死小鼠取脑组织(每组每时间点10只),应用免疫组化方法观察小鼠脑内GLUT1及GLUT3表达的变化。结果低血糖后脑内微血管上GLUT1表达有增加趋势,皮质增加高于海马,72 h皮质GLUT1表达显著高于对照组;低血糖后48、72 h皮质及海马GLUT3表达均显著高于相应对照组。结论再发性低血糖后脑内GLUT1及GLUT3适应性增高,这种适应既能节省神经元的能量代谢,但也能削减神经元对低血糖的反应。     

Neural sensitivity to social rejection is associated with inflammatory responses to social stress

Although stress-induced increases in inflammation have been implicated in several major disorders, including cardiovascular disease and depression, the neurocognitive pathways that underlie inflammatory responses to stress remain largely unknown. To examine these processes, we recruited 124 healthy young adult participants to complete a laboratory-based social stressor while markers of inflammatory activity were obtained from oral fluids. A subset of participants (n = 31) later completed an fMRI session in which their neural responses to social rejection were assessed. As predicted, exposure to the laboratory-based social stressor was associated with significant increases in two markers of inflammatory activity, namely a soluble receptor for tumor necrosis factor-α (sTNFαRII) and interleukin-6 (IL-6). In the neuroimaging subsample, greater increases in sTNFαRII (but not IL-6) were associated with greater activity in the dorsal anterior cingulate cortex and anterior insula, brain regions that have previously been associated with processing rejection-related distress and negative affect. These data thus elucidate a neurocognitive pathway that may be involved in potentiated inflammatory responses to acute social stress. As such, they have implications for understanding how social stressors may promote susceptibility to diseases with an inflammatory component.