Personal comorbidities and their subsequent risks for liver,gallbladder and bile duct cancers

Many environmental risk factors for hepatobiliary cancers are known but whether they are associated with specific cancer types is unclear. We present here a novel approach of assessing standardized incidence ratios (SIRs) of previously diagnosed comorbidities for hepatocellular carcinoma (HCC), gallbladder cancer (GBC), cholangiocarcinoma (CCA) and ampullary cancer. The 13 comorbidities included alcohol and nonalcohol related liver disease, chronic obstructive pulmonary disease, gallstone disease, viral and other kinds of hepatitis, infection of bile ducts, hepatic and other autoimmune diseases, obesity and diabetes. Patients were identified from the Swedish Inpatient Register from 1987 to 2018, and their cancers were followed from 1997 onwards. SIRs for HCC were 80 to 100 in men and women diagnosed with hepatitis C virus and they were also >10 in patients diagnosed with hepatitis B virus, other kind of hepatitis, hepatic autoimmune disease and nonalcohol related liver disease. Many of these risks, as well as alcohol related liver disease, were either specific to HCC or were shared with intrahepatic CCA. For GBC, CCA and ampullary cancer infection of bile ducts was the main risk factor. Gallstone disease, nonhepatic autoimmune diseases and diabetes were associated with all hepatobiliary cancers. The limitations of the study include inability to cover some rare risk factors and limited follow-up time. Many of the considered comorbidities are characterized by chronic inflammation and/or overt immune disturbance in autoimmune diseases. The results suggest that local chronic inflammation and a related immune disturbance is the carcinogenic trigger for all these cancers.     

基于全基因组测序的耐碳青霉烯类抗生素鲍曼不动杆菌耐药基因、毒力因子及同源性分析

摘要：目的 通过应用全基因组测序(whole genome sequencing, WGS)技术分析某三级医疗机构耐碳青霉烯类抗生素鲍曼不 动杆菌(carbapenem-resistant Acinetobacter baumannii, CRAB)的耐药基因、毒力因子及同源性。方法 收集该院2020年1月至3月 重症监护病房(Intensive care unit, ICU)、神经外科分离的11株医院感染CRAB菌株，通过二代测序平台进行全基因组测序, 应用 基因组流行病学中心(Center for genomic epidemiology, CGE)ResFinder 4. 0软件分析其耐药基因型，并应用MORPHEUS在线制作 热图，应用毒力因子数据库(virulence factors of pathogenic bacteria, VFDB)VFanalyzer软件筛选毒力因子，应用MLST软件检测菌 株的ST型，应用Kaptive软件检测荚膜型，应用CSI Phylogeny 1. 4软件及FigTree v1. 4. 4软件构建最大似然树(maximum likelihood tree, MLT)以分析其同源性。结果 11株CRAB对亚胺培南、美罗培南、头孢菌素、环丙沙星均呈现耐药，而对阿米卡星、左氧 氟沙星耐药的菌株株数较少。11株CRAB共检测出18种耐药基因，11株同时携带碳青霉烯酶耐药基因blaOXA-23和blaOXA-66，β-内酰 胺酶耐药基因以blaTEM-1D和blaADC-25为主，大部分菌株携带多种外排泵相关耐药基因及抗菌药物修饰酶耐药基因。11株CRAB均携 带多种毒力因子，包括外膜孔蛋白、脂多糖、生物膜、外排泵、磷脂酶和效应蛋白等，如OmpA、Lps、Csu、Pga、Ade、Plc、 Bas、Bau、Ent、Hem、Aba、Bfm、Pbp和Kat等。11株CRAB均为ST2-K22型，同源性分析结果显示C组内同源性关系相近，存 在院内传播的可能。结论 该院CRAB的耐药性、毒力特征复杂多样，同源性分析显示该院存在1种优势克隆株，该克隆株有医 院内传播的风险。     

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.