不同时期COPD患者血清DcR3、Survivin表达水平及临床意义

目的 探讨不同时期慢性阻塞性肺疾病(COPD)患者血清诱饵受体3(DcR3)、凋亡抑制蛋白(Survivin)表达水平及临床意义。方法 选取2018年9月—2019年12月本院收治的92名COPD患者为研究对象,其中稳定型COPD 50例,急性加重期COPD 42例;同期本院健康体检者88例为对照组。测定各组研究对象血清DcR3、Survivin水平及肺功能指标。 与对照组[DcR3(106.54±48.35)pg/mL,Survivin(98.85±26.59)pg/mL]比较,稳定期组和急性加重期组血清DcR3[(395.23±123.85)pg/mL,(1 248.81±213.59)pg/mL]、Survivin [(267.54±84.69)pg/mL,(1 233.95±307.26)pg/mL]水平升高;与稳定期组比较,急性加重期组血清DcR3、Survivin水平升高。与对照组比较,稳定期组和急性加重期组FEV1%、FEV1 /FVC、DLCO%水平降低(P<0.001);与稳定期组比较,急性加重期组FEV1%、FEV1 /FVC、DLCO%水平降低(P<0.001)。随着低氧血症严重程度的增加,COPD患者血清DcR3、Survivin水平逐渐增加(P<0.001)。多因素logistics回归分析显示,高水平DcR3、Survivin、IL-12、hs-CRP为COPD病情的危险因素(P<0.001)。DcR3、Survivin与FEV、FEV1 /FVC呈负相关,与IL-12、TNF-α、hs-CRP呈正相关(P<0.001)。 COPD稳定期、急性加重期患者血清DcR3、Survivin表达水平升高,且DcR3、Survivin与COPD病情严重程度呈正相关。     

Cardioprotective effects of sinomenine in myocardial ischemia/reperfusion injury in a rat model

BackgroundIschemia reperfusion (I/R) play an imperative role in the expansion of cardiovascular disease. Sinomenine (SM) has been exhibited to possess antioxidant, anticancer, anti-inflammatory, antiviral and anticarcinogenic properties. The aim of the study was scrutinized the cardioprotective effect of SM against I/R injury in rat.MethodsRat were randomly divided into normal control (NC), I/R control and I/R + SM (5, 10 and 20 mg/kg), respectively. Ventricular arrhythmias, body weight and heart weight were estimated. Antioxidant, inflammatory cytokines, inflammatory mediators and plasmin system indicator were accessed.ResultsPre-treated SM group rats exhibited the reduction in the duration and incidence of ventricular fibrillation, ventricular ectopic beat (VEB) and ventricular tachycardia along with suppression of arrhythmia score during the ischemia (30 and 120 min). SM treated rats significantly (P < 0.001) altered the level of antioxidant parameters. SM treatment significantly (P < 0.001) repressed the level of creatine kinase MB (CK-MB), creatine kinase (CK) and troponin I (Tnl). SM treated rats significantly (P < 0.001) repressed the tissue factor (TF), thromboxane B2 (TXB2), plasminogen activator inhibitor 1 (PAI-1) and plasma fibrinogen (Fbg) and inflammatory cytokines and inflammatory mediators.ConclusionOur result clearly indicated that SM plays anti-arrhythmia effect in I/R injury in the rats via alteration of oxidative stress and inflammatory reaction.     

Practice developments supporting change implementation in Wellington,New Zealand (NZ) for ‘continuity of care when transitioning complex preterm infants from NICU to home’

The discussion paper will focus on continuity of care relating to previous NZ research, specifically to transitioning complex preterm infants from NICU to home based on parent experiences, and on the practice developments that have occurred, to ensure optimal health outcomes. Previous NZ research discovered parent desire a consistent service delivery for the entire transition journey from NICU and at home.An informative and comprehensive opportunity has occurred for reflective professional practice, evaluation, development and implementation which have transpired in positive change through innovative practice developments and support change implementation in Wellington, NZ. This has resulted in the articulation of a model of care that has both embraced and integrated parental desires for a continuity of care process for complex preterm infants. This has been achieved by having the same Discharge Facilitator/Key Case Manager present within the NICU and external to the NICU for Home-based infants for the entire transition journey.The paper will focus and emphasis additional practice development changes and furthermore, will present a real purpose, for other countries to learn of such practice developments that have exemplified a celebratory success for families of Wellington, NZ.     

How does transfusion-associated graft-versus-host disease compare to hematopoietic cell transplantation-associated graft-versus-host disease?

Transfusion-associated graft-versus-host disease (TA-GVHD) is a rare life-threatening complication of blood transfusion caused by donor T cells that escape rejection by the recipient immune system. These donor T cells drive recipient tissue damage in response to host antigens. On the other hand, GVHD occurring after allogeneic hematopoietic cell transplantation (HCT-GVHD) is also caused by donor T cells, but its pathophysiology is more complex and differs due to the effects of tissue damage caused by pre?HCT conditioning and profound immunosuppression. Both TA-GVHD and HCT-GVHD can be fatal; however, mortality is higher with TA-GVHD due to the paucity of treatment options. Here, we compare and summarize the presentation, diagnosis, pathophysiology, prevention, and treatment of TA-GVHD and HCT-GVHD.