非酒精性脂肪肝患者血清肿瘤坏死因子-α、脂联素水平与胰岛素抵抗的相关性

目的:探讨非酒精性脂肪肝(NAFLD)患者肿瘤坏死因子-α、脂联素水平与胰岛素抵抗等指标的相互关系.方法:120例NAFLD患者根据空腹血糖水平分为合并2型糖尿病(T2DM)者32例(DFL组),不伴T2DM者88例(FL组),所有NAFLD患者根据B超结果分为轻度、中度、重度3组.测定NAFLD患者及42例健康对照者的体质量指数(BMI)、腰臀比(WHR)、空腹血糖(FPG)、空腹胰岛素(FINS)、肿瘤坏死因子-α(TNF-α)、脂联素(APN)水平;采用稳态模式计算胰岛素抵抗指数(HOMA-IR)、胰岛素敏感性指数(ISI)、反应胰岛β细胞分泌功能的指标(HOMA-IS)等指标.结果:NAFLD患者的FINS,HOMA-IR均显著升高,ISI显著低于NC组(P<0.01);FPG,FINS,ISI,HOMA-IS是IR抵抗的主要相关因素;DFL组的FINS,HOMA-IR较FL组为高,ISI,HOMA-IS较FL组为低,均有显著性差异(P<0.01);NAFLD患者轻、中度两组间HOMA-IR无显著差异(P>0.05),而重度脂肪肝患者的HOMA-IR明显升高(P<0.01).NAFLD患者血清TNF-α显著升高,APN显著降低(P<0.01);APN与TNF-α,IR呈显著负相关,与ISI呈显著正相关;TNF-α是影响APN水平的重要因素;TNF-α与APN,ISI呈显著负相关,与FPG,FINS,IR呈显著正相关,ISI,APN是其主要的影响因素.结论:NAFLD患者普遍存在IR,合并2型糖尿病的NAFLD患者体内胰岛素抵抗现象更为明显;TNF-α与APN呈显著负相关,且均与IR密切相关.APN作为保护性因子而TNF-α作为损害性因子在NAFLD的发生、发展中起着重要作用.     

2型糖尿病非酒精性脂肪性肝病患者血清脂联素及内脂素的变化及其临床意义的研究

目的探讨T2DM合并非酒精性脂肪性肝病(NAFLD)患者血清脂联素(APN)和内脂素的变化及临床意义。方法选取2011年9月至2013年3月于我院就诊的T2DM患者240例,根据中华医学会NAFLD诊断标准将研究对象分为单纯T2DM组148例和T2DM合并NAFLD组92例,另选正常体检者106名(NC组)。根据影像学诊断再将T2DM合并NAFLD组分为轻度亚组33例,中度亚组30例和重度亚组29例,比较各亚组血清APN和内脂素水平。结果 T2DM组和T2DM合并NAFLD组内脂素、BMI、WC、WHR、AST、ALT、FPG、FIns、TG、TC及胰岛素抵抗指数(HOMA-IR)较NC组升高(P<0.05或P<0.01)。T2DM合并NAFLD组血清APN水平较NC组和T2DM组降低(P<0.01),T2DM组较NC组降低(P<0.01)。T2DM合并NAFLD组轻、中、重度亚组HOMA-IR逐渐升高;血清APN水平逐渐降低,且轻、中、重度亚组间比较差异均有统计学意义(P<0.05);血清内脂素水平逐渐升高,但轻度和中度亚组间比较差异无统计学意义(P>0.05)。结论T2DM合并NAFLD患者血清APN较正常人明显降低,且与NAFLD严重程度相关。低脂联素血症可能与NAFLD发生发展有关;内脂素水平随NAFLD严重程度升高,提示可能参与了向脂肪性肝炎及肝脏纤维化的发展。     

T2DM患者血浆内脏脂肪素、瘦素与胰岛素抵抗的相关性研究

目的 探讨2型糖尿病(T2DM)患者血浆内脏脂肪素、瘦素水平与胰岛素抵抗(IR)的相关性.方法 102例T2DM患者和64例正常糖耐量(NGT)对照者,根据BMl分为肥胖组(Ob)和非肥胖(Non-Ob)组,均测定空腹血浆内脏脂肪素、瘦素和相关临床指标,计算胰岛素抵抗指数(HOMA-IR)和腰臀比(WHR).结果 T2DM组与NGT组比较空腹血浆内脏脂肪素和瘦素水平明显升高(t=3.922,P=0.00;t=2.128,P=0.038).相关分析显示T2DM患者空腹血浆内脏脂肪紊与HOMA-IR、WHR、瘦素、HbA<,1> c和TG正相关(r=0.543,P=0.001;r=0.442,P=0.008;r=0.385,P=0.013,r=0.345,P=0.025;r=0.427,P=0.005),瘦素与HOMA-IR、性别、BMI正相关(r=0.578,P<0.01;r=0.547,P<0.01;r=0.607,P<0.01).结论 T2DM患者空腹血浆内脏脂肪素和瘦素水平显著升高,且与IR关系密切.     

糖代谢异常大鼠心肌超微结构改变及TNF-α的表达

目的观察糖代谢异常(糖调节受损和糖尿病)大鼠心肌的超微结构改变及肿瘤坏死因子-α(TNF-α)的表达,揭示糖尿病心肌病(diabetic cardiomyopathy,DC)发生发展的炎性机制。方法30只雄性Wistar大鼠随机分为:正常对照组、胰岛素抵抗组(IR组)和T2DM组。用免疫组化法检测心肌组织中TNF-α的表达,透射电镜观察心肌的超微结构,并测定空腹血糖(FPG)、空腹血清胰岛素(FINS)等生化指标及计算胰岛素敏感指数(ISI)。结果TNF-α在IR组、T2DM组大鼠心肌组织中的阳性表达平均积分光密度值(IDP)显著高于正常对照组(P<0.01);且T2DM组大鼠IDP值显著高于IR组(P<0.01)。IR、T2DM组ISI负值均显著高于正常对照组(P<0.01)。电镜下IR、T2DM组大鼠心肌超微结构发生不同程度的损害。相关分析表明:TNF-α的IDP值与FPG水平、糖化血红蛋白(HbA1c)、甘油三酯(TG)、总胆固醇(TC)呈明显正相关(r=0.905,0.602,0.493,0.430,均P<0.01),与ISI明显呈负相关(r=-0.896,P<0.01),多元逐步回归分析显示FBG、ISI是影响TNF-α水平的重要因素。结论TNF-α的表达与高血糖、胰岛素抵抗(IR)密切相关,且TNF-α作为一种重要的炎症因子可能参与了DC的发病机制。     

2型糖尿病合并非酒精性脂肪肝患者TNF-α与早期大血管病变的关系

将192例2型糖尿病（T2DM）患者分为T2DM合并非酒精性脂肪肝（NAFL）组及T2DM无NAFL组,另设健康对照组。测定血清肿瘤坏死因子α（TNF-α）水平、颈动脉内膜—中层（CIMT）厚度、颈动脉斑块发生率及胰岛素抵抗指数（HOMA-IR）。结果与对照组相比,T2DM组CIMT及颈动脉斑块发生率增加（P〈0.01）;T2DM合并NAFL组则更为显著（P〈0.01）。与对照组相比,T2DM各组随着CIMT增厚,TNF-α和HOMA-IR明显增加（P〈0.01）。TNF-α、HOMA-IR与CIMT呈显著正相关（r=0.548,P〈0.01）。提示T2DM合并NAFL更易出现大血管病变;血清TNF-α通过增加CIMT厚度参与动脉粥样硬化的形成。     

2型糖尿病合并代谢相关脂肪性肝病患者胎球蛋白A水平与胰岛素抵抗的相关性研究

目的观察T2DM合并代谢相关脂肪性肝病(MAFLD)患者胎球蛋白A(FA)水平,并分析其与IR的相关性。方法选取2018年11月至2020年10月于我院新诊断的单纯T2DM患者(T2DM组)、单纯MAFLD患者(MAFLD组)和T2DM合并MAFLD患者(T2DM+MAFLD组),每组各160例,另选取同期体检健康人群(NC组)160名。检测各组血清FA水平,分析FA与各指标的相关性。结果 T2DM+MAFLD、T2DM、MAFLD及NC组血清FA水平依次降低(P0.05);T2DM+MAFLD组FA水平与BMI(r=0.813,P0.001)、TG(r=0.637,P0.001)、FPG(r=0.583,P0.001)、2 hPG(r=0.681,P0.001)、HbA_1c(r=0.581,P0.001)和胰岛素抵抗指数(HOMA-IR)(r=0.735,P0.001)呈正相关,与HDL-C(r=-0.219,P=0.005)、胰岛素分泌指数(HOMA-IS)(r=-0.693,P0.001)呈负相关。结论血清FA水平升高与HOMA-IR是T2DM合并MAFLD患者的危险因素,HOMA-IS是T2DM合并MAFLD患者的保护因素。     

非酒精性脂肪性肝病患者血清胰腺衍生因子水平及其与胰岛素抵抗的关系

目的探讨血清胰腺衍生因子(pancreatic derived factor,PANDER)在非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)患者中的水平及其在胰岛素抵抗(insulin resistance,IR)相关代谢性疾病的发生、发展及相互影响中的作用。方法选取单纯NAFLD患者30例、单纯2型糖尿病(T2DM)患者28例、NAFLD合并T2DM患者21例、健康对照者15名。收集体格检查资料,测定肝功、血脂、空腹血糖、FINS、血清FFA、血清PANDER、TNF-α及IL-6浓度。应用SPSS 19. 0进行相关统计学分析。结果 (1)NAFLD患者的血清PANDER水平(72. 33±0. 02)μg/L高于健康对照者(67. 80±0. 02)μg/L,低于T2DM患者(73. 80±0. 02)μg/L,但各组间差异无统计学意义(P0. 05)。(2) NAFLD、BMI及TG水平是HOMA-IR的主要预测因子,而血清PANDER未进入回归方程(回归方程=NAFLD×0. 551+BMI×0. 040+TG×0. 260-1. 710)。(3) HOMA-IR及血清FFA是血清PANDER水平的主要影响因素(回归方程=HOMA-IR×0. 191+FFA×0. 050-3. 181),但其与BMI、腹围、ALT、LDL、TG、HOMA-IR、血清TNF-α、血清IL-6尚无线性相关。(4)健康人群中,腹型肥胖(腹围)是NAFLD最重要的危险因素;而T2DM患者中,高TG血症是T2DM合并NAFLD最重要的危险因素;但不论是健康人群或T2DM人群,血清PANDER水平升高都不是NAFLD的危险因素。结论血清PANDER水平升高可能不是影响IR及NAFLD发病的危险因素,但IR是血清PANDER水平的影响因素之一。     

新诊断2型糖尿病患者血清Nesfatin-1、肿瘤坏死因子-α水平与胰岛素抵抗的相关性研究

目的探讨新诊断T2DM患者血清Nesfatin-1、TNF-α水平与IR的关系。方法 ELISA测定新诊断T2DM组(n=64)和体检健康者(NC组,n=41)空腹血清Nesfatin-1、TNF-α水平。同期测定FPG、HbA_1c、TG、TC、FIns等指标,计算BMI、胰岛素抵抗指数(HOMA-IR)、胰岛β细胞功能指数(HOMA-β)及胰岛素敏感指数(ISI)。结果 T2DM组血清Nesfatin-1、TNF-α水平高于NC组。多元线性回归分析发现,影响Nesfatin-1水平最显著的因素为TNF-α、ISI(β=0.005、-6.847,P0.05);影响TNF-α水平最显著的因素为HbA_1c(β=26.652,P0.01)。结论新诊断T2DM血清Nesfatin-1、TNF-α水平升高,并均可能通过胰岛素信号通路影响糖脂代谢,从而参与T2DM及IR的病理过程。     

TNF-α和IL-6在非酒精性脂肪性肝病患者血清中的水平及意义

目的:探讨肿瘤坏死因子-α(TNF-α)和白介素-6(IL-6)在非酒精性脂肪性肝病(NAFLD)患者血清中的水平及意义.方法:收集NAFLD组患者57例[包括单纯性脂肪肝21例、非酒精性脂肪性肝炎(NASH)29例肝硬化7例和正常对照组22例.采用ELISA法检测受试者血清TNF-α仅和IL-6水平.同时检查受试者体质量指数、血压、空腹血糖、空腹胰岛素、血脂,用以计算胰岛素抵抗指数(HOMA-IR)和了解合并代谢综合征情况.比较各组间血清TNF-α和IL-6水平的变化,并分析TNF-α、IL-6水平与胰岛素抵抗指数和代谢综合征发生的关系.结果:单纯性脂肪肝、NASH和肝硬化组患者血清TNF-α、IL-6水平均显著高于对照组(P<0.05),其中以NASH组水平最高,且显著高于单纯性脂肪肝和肝硬化组(P<0.05).受试者血清TNF-α、IL-6水平与HOMA-IR均呈显著性正相关(r=608,0.709,均P=0.000).合并代谢综合征的NAFLD患者血清TNF-α、IL-6水平均显著高于不合并代谢综合征的患者(P<0.05).患者血清TNF-α、IL-6水平与是否合并代谢综合征呈显著性相关(r=0.409,P=0.002;r=0.552,P:0.000).结论:TNF-α、IL-6通过诱导胰岛素抵抗对NAFLD疾病的发生发展起重要作用,并有助于NAFLD患者代谢综合征的形成.     

2型糖尿病一级亲属血清脂联素、瘦素及其比值与胰岛素抵抗的相关性研究

目的 研究血清瘦素、脂联素与2型糖尿病(T2DM)一级亲属胰岛素抵抗(IR)相关性,探讨二者在T2DM发病中作用.方法 收集既往无糖耐量异常史的T2DM一级亲属, 分为糖耐量正常(NGT)组174例、空腹血糖受损(IFG)或糖耐量低减(IGT)组55例,及新发T2DM组71例;以其无糖尿病家族史的配偶或亲友中OGTT正常者114例作为正常对照组(NC).酶联免疫法测定上述人群的血清真胰岛素(TI)、瘦素和脂联素水平.用HOMA-IR评价胰岛素抵抗(IR)状态.结果 从NC至NGT、IGT/IFG到DM组,IR进行性加重(HOMA-IR分别为1.3±0.7、1.7±1.5、 2.2±1.4 和3.2±2.8,P＜0.01);血清瘦素水平进行性增高(P＜0.01),瘦素水平与HOMA-IR正相关(r=0.35, P＜0.01);血清脂联素水平进行性降低(分别为20±12、17±11、13±8和10±6mg/L,P＜0.01),与HOMA-IR负相关(r=-0.41,P＜0.01);脂联素/瘦素比值进性行降低,与HOMA-IR负相关(r=-0.53, P＜0.01). 结论 T2DM一级亲属在NGT时即存在瘦素水平升高和脂联素水平明显下降.脂联素/瘦素比值下降趋势与IR和糖调节受损的严重程度密切相关,推测该比值的变化可能是糖尿病一级亲属存在的固有遗传缺陷的一种表现,可能在IR和T2DM的发生发展中起重要作用,因而渴望作为预测T2DM发病的早期观察指标.     

Interplay between interferon-mediated innate immunity and porcine reproductive and respiratory syndrome virus

Innate immunity is the first line of defense against viral infection, and in turn, viruses have evolved to evade host immune surveillance. As a result, viruses may persist in host and develop chronic infections. Type I interferons (IFN-α/β) are among the most potent antiviral cytokines triggered by viral infections. Porcine reproductive and respiratory syndrome (PRRS) is a disease of pigs that is characterized by negligible induction of type I IFNs and viral persistence for an extended period. For IFN production, RIG-I/MDA5 and JAK-STAT pathways are two major signaling pathways, and recent studies indicate that PRRS virus is armed to modulate type I IFN responses during infection. This review describes the viral strategies for modulation of type I IFN responses. At least three non-structural proteins (Nsp1, Nsp2, and Nsp11) and a structural protein (N nucleocapsid protein) have been identified and characterized to play roles in the IFN suppression and NF-κB pathways. Nsp's are early proteins while N is a late protein, suggesting that additional signaling pathways may be involved in addition to the IFN pathway. The understanding of molecular bases for virus-mediated modulation of host innate immune signaling will help us design new generation vaccines and control PRRS.     

Control of intraabdominal hemorrhage and shock: a comparison of fluid resuscitation, MAST, and balloon occlusion

Our study examined the efficacy of four treatment modalities in controlling hemorrhage and achieving hemodynamic stabilization in hemorrhagic shock: intravenous fluid replacement (IV); military antishock trousers used concomitantly with fluids (MAST); balloon occlusion at the level of the diaphragm with concomitant fluid replacement (balloon); and a combination of MAST inflation, balloon occlusion, and fluid resuscitation (MAST and balloon). Twenty-eight mongrel dogs were anesthetized, and the spleen was exposed and completely crushed. The abdomen was closed, and treatment was initiated and continued for four hours or until the dog died. For all conditions the hematocrit dropped during the course of the experiment; balloon occlusion was effective at slowing this drop (P less than .0001), but MAST had no statistically significant effect. Animals with balloons bled more slowly into the abdominal cavity than did animals in the other two groups (P less than .0001). MAST also were effective at slowing the bleeding (P less than .05). Of the balloon and the MAST and balloon dogs, all except one survived the entire four hours; this difference between balloon and nonballoon dogs is significant (P = .002). MAST did not have a statistically significant effect on survival. Perfusion pressure (PP) declined during the course of the experiment, and the balloon was effective at slowing this decline (P less than .0001); none of the other comparisons was statistically significant.     

Disease Pandemics and Major Epidemics Arising From New Encounters between Indigenous Viruses and Introduced Crops

Virus disease pandemics and epidemics that occur in the world’s staple food crops pose a major threat to global food security, especially in developing countries with tropical or subtropical climates. Moreover, this threat is escalating rapidly due to increasing difficulties in controlling virus diseases as climate change accelerates and the need to feed the burgeoning global population escalates. One of the main causes of these pandemics and epidemics is the introduction to a new continent of food crops domesticated elsewhere, and their subsequent invasion by damaging virus diseases they never encountered before. This review focusses on providing historical and up-to-date information about pandemics and major epidemics initiated by spillover of indigenous viruses from infected alternative hosts into introduced crops. This spillover requires new encounters at the managed and natural vegetation interface. The principal virus disease pandemic examples described are two (cassava mosaic, cassava brown streak) that threaten food security in sub-Saharan Africa (SSA), and one (tomato yellow leaf curl) doing so globally. A further example describes a virus disease pandemic threatening a major plantation crop producing a vital food export for West Africa (cacao swollen shoot). Also described are two examples of major virus disease epidemics that threaten SSA’s food security (rice yellow mottle, groundnut rosette). In addition, brief accounts are provided of two major maize virus disease epidemics (maize streak in SSA, maize rough dwarf in Mediterranean and Middle Eastern regions), a major rice disease epidemic (rice hoja blanca in the Americas), and damaging tomato tospovirus and begomovirus disease epidemics of tomato that impair food security in different world regions. For each pandemic or major epidemic, the factors involved in driving its initial emergence, and its subsequent increase in importance and geographical distribution, are explained. Finally, clarification is provided over what needs to be done globally to achieve effective management of severe virus disease pandemics and epidemics initiated by spillover events.     

陕西省新型结核病防治管理模式实施前后能力建设与诊治效果分析

目的 分析陕西省新型结核病防治管理模式实施前后结核病防治能力建设及诊治效果,为进一步完善我省结核病防控政策和措施提供参考。方法 本研究采用描述性研究,对全省10个地级市、108个县(区)结核病防治能力建设情况,以及患者发现、治疗管理等指标变化情况进行对比分析。能力建设情况以2014年和2017年数据作对比,分别来源于《陕西省“十二五”结核病防治规划》评估和2017年全省结核病防治工作联合大检查。患者发现、治疗管理指标来源于《结核病信息管理系统》,以实施前3年(2012—2014年)与实施后3年(2015—2017年)的数据作对比。运用SPSS 19.0处理数据,率和构成比的比较采用χ ²检验,以P<0.05为差异有统计学意义。 结果 2014年和2017年全省设有结核病定点医院的数量分别为20家和107家,2017年较2014年增加了87家。2014年全省共有结核病防治人员923名,其中疾病预防控制中心(CDC)656名,定点医院267名。2017年全省共有结核病防治人员1200名,其中CDC 403名,定点医院797名;与2014年相比,CDC人员减少了38.57%,定点医院人员增加了198.50%。2014年全省有3个地级市开展了分子生物学耐药检测,5.56%(6/108)的县(区)开展了分子生物学检测,12.04%(13/108)的县(区)开展了痰培养。2017年全省有8个地级市开展了分子生物学耐药检测,49.07%(53/108)的县(区)开展了分子生物学检测,55.56%(60/108)的县(区)开展了痰培养。新型防治模式实施前3年全省初诊查痰率为98.50%(329981/335014),发现肺结核患者63892例(其中结核性胸膜炎患者4089例),发现病原学阳性患者14087例,病原学阳性率为23.56%(14087/59803)。实施后3年全省初诊查痰率为95.00%(312503/328948),发现肺结核患者61583例(其中结核性胸膜炎5295例),病原学阳性患者10588例,病原学阳性率为18.81%(10588/56288)。新型防治模式实施前后初诊查痰率降低(χ ²=6484.178,P=0.000),病原学阳性率降低(χ ²=390.104,P=0.000)。实施前3年因症就诊发现肺结核患者占29.43%(18805/63892),转诊发现患者占43.90%(28047/63892)。实施后3年因症就诊发现肺结核患者占25.38%(15628/61583),转诊发现患者占57.79%(35586/61583)。转型后因症就诊发现患者的构成比下降(χ ²=259.002,P=0.000),转诊发现患者的构成比上升(χ ²=2419.762,P=0.000)。新模式实施前后3年非结核病防治机构报告患者总体到位率分别为93.18%(62177/66726)和89.96%(61323/68169),实施后总体到位率下降(χ ²=453.550,P=0.000)。新模式实施前后患者治疗成功率分别为95.04%(60464/63619)和94.97%(57872/60939),实施前后比较差异无统计学意义(χ ²=0.356,P=0.551)。 结论 我省新型结核病防治管理模式推进顺利,防治能力加强,但部分患者诊治及管理指标有所下滑,实施质量仍需提升。     

dsRNA-Dependent Protein Kinase PKR and its Role in Stress,Signaling and HCV Infection

The double-stranded RNA-dependent protein kinase PKR plays multiple roles in cells, in response to different stress situations. As a member of the interferon (IFN)‑Stimulated Genes, PKR was initially recognized as an actor in the antiviral action of IFN, due to its ability to control translation, through phosphorylation, of the alpha subunit of eukaryotic initiation factor 2 (eIF2α). As such, PKR participates in the generation of stress granules, or autophagy and a number of viruses have designed strategies to inhibit its action. However, PKR deficient mice resist most viral infections, indicating that PKR may play other roles in the cell other than just acting as an antiviral agent. Indeed, PKR regulates several signaling pathways, either as an adapter protein and/or using its kinase activity. Here we review the role of PKR as an eIF2α kinase, its participation in the regulation of the NF-κB, p38MAPK and insulin pathways, and we focus on its role during infection with the hepatitis C virus (HCV). PKR binds the HCV IRES RNA, cooperates with some functions of the HCV core protein and may represent a target for NS5A or E2. Novel data points out for a role of PKR as a pro-HCV agent, both as an adapter protein and as an eIF2α-kinase, and in cooperation with the di-ubiquitin-like protein ISG15. Developing pharmaceutical inhibitors of PKR may help in resolving some viral infections as well as stress-related damages.     

Comparison of pediatric and adult antibiotic-associated diarrhea and Clostridium difficile infections

Antibiotic-associated diarrhea(AAD) and Clostridum difficile infections(CDI) have been well studied for adult cases, but not as well in the pediatric population. Whether the disease process or response to treatments differs between pediatric and adult patients is an important clinical concern when following global guidelines based largely on adult patients. A systematic review of the literature using databases Pub Med(June 3, 1978-2015) was conducted to compare AAD and CDI in pediatric and adult populations and determine significant differences and similarities that might impact clinical decisions. In general, pediatric AAD and CDI have a more rapid onset of symptoms, a shorter duration of disease and fewer CDI complications(required surgeries and extended hospitalizations) than in adults. Children experience more community-associated CDI and are associated with smaller outbreaks than adult cases of CDI. The ribotype NAP1/027/BI is more common in adults than children. Children and adults share some similar risk factors, but adults have more complex risk factor profiles associated with more co-morbidities, types of disruptive factors and a wider range of exposures to C. difficile in the healthcare environment. The treatment of pediatric and adult AAD is similar(discontinuing or switching the inciting antibiotic), but other treatment strategies for AAD have not been established. Pediatric CDI responds better to metronidazole, while adult CDI responds better to vancomycin. Recurrent CDI is not commonly reported for children. Prevention for both pediatric and adult AAD and CDI relies upon integrated infection control programs, antibiotic stewardship and may include the use of adjunctive probiotics. Clinical presentation of pediatric AAD and CDI are different than adult AAD and CDI symptoms. These differences should be taken into account when rating severity of disease and prescribing antibiotics.     

A comparison of stapled and handsewn anastomoses in patients undergoing resection for Dukes' B and C colorectal cancer

This study was to assess the effect of stapled colorectal anastomoses on local recurrence, disease-free survival, and survival following curative resection for Dukes' B and C adenocarcinoma. Data were derived from two randomized prospective trials of the National Surgical Adjuvant Breast and Bowel Project designed to evaluate the efficacy of adjuvant therapy in colorectal cancer. Of 1111 patients with colonic anastomoses, 255 were stapled mechanically. There were no significant differences in disease-free survival, survival, or local tumor recurrence among patients subjected to stapled or handsewn anastomoses. Of the 181 patients undergoing anterior resection for rectal cancer, 82 anastomoses were fashioned with staples. No significant disadvantage in disease-free survival, survival, or local recurrence could be attributed to use of the mechanical stapling devices. Twelve percent of patients undergoing stapled rectal anastomoses developed a local recurrence as a first sign of treatment failure compared with 19 percent for the handsewn group. No significant differences in the length of distal margins were detectable. The average time on study was 41 months. The use of stapled anastomoses for carcinoma of the colon or rectum is not associated with an adverse effect on long-term outcome. Read at the meeting of the American Society of Colon and Rectal Surgeons, San Diego, California, May 5 to 10, 1985. Supported by USPHS NIH-U10-34212 and an American Cancer Society Grant RC-13.     

Endothelium Infection and Dysregulation by SARS-CoV-2: Evidence and Caveats in COVID-19

The ongoing pandemic of coronavirus disease 2019 (COVID-19) caused by the acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) poses a persistent threat to global public health. Although primarily a respiratory illness, extrapulmonary manifestations of COVID-19 include gastrointestinal, cardiovascular, renal and neurological diseases. Recent studies suggest that dysfunction of the endothelium during COVID-19 may exacerbate these deleterious events by inciting inflammatory and microvascular thrombotic processes. Although controversial, there is evidence that SARS-CoV-2 may infect endothelial cells by binding to the angiotensin-converting enzyme 2 (ACE2) cellular receptor using the viral Spike protein. In this review, we explore current insights into the relationship between SARS-CoV-2 infection, endothelial dysfunction due to ACE2 downregulation, and deleterious pulmonary and extra-pulmonary immunothrombotic complications in severe COVID-19. We also discuss preclinical and clinical development of therapeutic agents targeting SARS-CoV-2-mediated endothelial dysfunction. Finally, we present evidence of SARS-CoV-2 replication in primary human lung and cardiac microvascular endothelial cells. Accordingly, in striving to understand the parameters that lead to severe disease in COVID-19 patients, it is important to consider how direct infection of endothelial cells by SARS-CoV-2 may contribute to this process.     

Crohn's disease and growth deficiency in children and adolescents

Nutritional concerns, linear growth deficiency, and delayed puberty are currently detected in up to 85% of patients with Crohn’s disease (CD) diagnosed at childhood. To provide advice on how to assess and manage nutritional concerns in these patients, a Medline search was conducted using “pediatric inflammatory bowel disease”, “pediatric Crohn’s disease”, “linear growth”, “pubertal growth”, “bone health”, and “vitamin D” as key words. Clinical trials, systematic reviews, and meta-analyses published between 2008 and 2013 were selected to produce this narrative review. Studies referring to earlier periods were also considered if the data was relevant to our review. Although current treatment strategies for CD that include anti-tumor necrosis factor-α therapy have been shown to improve patients’ growth rate, linear growth deficiencies are still common. In pediatric CD patients, prolonged diagnostic delay, high initial activity index, and stricturing/penetrating type of behavior may cause growth deficiencies (in weight and height) and delayed puberty, with several studies reporting that these patients may not reach an optimal bone mass. Glucocorticoids and inflammation inhibit bone formation, though their impact on skeletal modeling remains unclear. Long-term control of active inflammation and an adequate intake of nutrients are both fundamental in promoting normal puberty. Recent evidence suggests that recombinant growth factor therapy is effective in improving short-term linear growth in selected patients, but is of limited benefit for ameliorating mucosal disease and reducing clinical disease activity. The authors conclude that an intense initial treatment (taking a “top-down” approach, with the early introduction of immunomodulatory treatment) may be justified to induce and maintain remission so that the growth of children with CD can catch up, ideally before puberty. Exclusive enteral nutrition has a key role in inducing remission and improving patients’ nutritional status.     

Prevalence and factors associated with hypertension among school children and adolescents in urban and semi‐urban areas in Cameroon

Few data to date exist on pediatric hypertension (PH) prevalence and risk factors in semi‐urban areas in Cameroon, and they are believed to be the same as urban areas. These data are needed to design targeted preventive strategies and contribute to reducing the burden of PH in Cameroon and countries with equivalent standards of care. The authors conducted a cross‐sectional study, from November, 2017 to June, 2018, in primary and secondary schools, from semi‐urban (Bamboutos, West Region) and urban (Mfoundi, Center Region) settings in Cameroon, including children and adolescent aged between 3 and 19 years, recruited on a stratified probability sampling. PH was defined according to the American Academy of Pediatrics 2017. Overall, 1001 and 842 participants were, respectively, included in urban and semi‐urban areas. The overall average age was 13.9 ± 4.03 years, and two‐thirds were girls. Overweight and obesity were more prevalent in urban area (overweight: 17.1%; obesity: 5.9%), compared to semi‐urban (overweight: 1.1% and obesity: 0.8%) (p < .001). The prevalence of hypertension was higher in urban (12%) than semi‐urban areas (8.6%) (p = .01). We have identified as factors associated with PH: age > 14 years (OR = 3.18 [1.6; 6.2]) and secondary level of education (OR = 2.5 [1.2; 5.5]) in urban areas; family history of hypertension (OR 1.93 [1.1; 3.4] in semi‐urban areas. PH prevalence is higher in urban than semi‐urban areas, and the associated factors are not the same. Policies to address hypertension in the pediatric population must be targeted and tailored to the different population profiles.