| 1 | 抗生素耐药性环境中产生和转移的人类健康风险评估(HHRA)显示文摘[背景]直到最近,人们才明确环境能影响抗生素耐药性风险对临床结果的影响,但迄今为止,很少有文献记录正式评估这些风险的方法。[目标]我们研究可能的方法,并试图确定人类健康风险评估(HHRA)的研究需求,这项评估注重环境在抗生素耐药性病原体所致的抗生素治疗失败中所起的作用。[方法]作者参加了2012年3月4—8日在加拿大魁北克省举行的研讨会,定义抗生素耐药性风险与人类健康环境评估的范围和目标。我们专注于环境中耐药性产生'热点区域'的关键要素,(与食品无关的)暴露评估以及剂量反应,以描述风险特征,从而改善抗生素耐药性管理的方案。[讨论]识别传统风险评估中有助于评估环境中抗生素耐药性的各个新方面。包括:a)解释附加的选择压力对环境耐药基因组的作用,即随着时间的推移,促使抗生素耐药性细菌(ARB)产生;b)在相关的环境组成部分的'热点区域'中识别和描述水平基因转移(HGT)率;c)针对不同健康结局和途径的ARB剂量修改传统的剂量反应方法。[结论]我们建议将抗生素耐药性产生造成的环境影响纳入所有涉及ARB的HHRA过程之中。由于可用的数据有限,一种多标准决策分析方法将有助于进行环境中抗生素耐药性的HHRA,并使风险管理者了解环境抗生素耐药性。 | Nicholas J.Ashbolt Alejandro Amézquita Thomas Backhaus Peter Borriello Kristian K.Brandt Peter Collignon Anja Coors Rita Finley William H.Gaze Thomas Heberer John R.Lawrence D.G.Joakim Larsson Scott A.McEwen James J.Ryan Jens Schnfeld Peter Silley Jason R.Snape Christel Van den Eede Edward Topp 王晓宇 张伊人 操仪 | 2014 | 环境与职业医学2014，31，2： | 3 |
| 2 | 减少向环境中释放抗生素和抗生素耐药基因的管理措施显示文摘[背景]全球越来越关注污染土壤、水环境对抗生素耐药性产生和蔓延的作用。[目的]本研究的目的是确定那些可以减少抗生素和抗生素耐药性经环境途径传播影响因素的管理措施,以最终达到延长抗生素使用寿命的目标。此外还研究了实施这些措施的激励和阻碍因素。[方法]着重研究有关农业源头限制,生活、医院和工业废水处理,以及水产养殖三方面的管理措施。[讨论]我们确定了若干措施,如养份管理、径流控制和基础设施升级。凡适当处,可提供世界不同地区的典型实例。研究还强调了监测和验证管理策略有效性的重要性。最后,介绍了一则瑞典的案例研究,展示了通过沟通来发动利益相关方参与和促进行动的重要作用。[结论]在许多情况下,可以花费很少或根本不花费成本来减少抗生素和抗生素耐药性细菌的环境释放。一些管理措施与现有的政策和目标协同作用。预期的效益是延长现有和未来的抗生素使用寿命。虽然往往难以量化所降低的风险,但是全球抗生素耐药性相关发病率和死亡率加速增长,这一情况的严重程度强烈表明采取行动的必要性。 | Amy Pruden D.G.Joakim Larsson Alejandro Amézquita Peter Collignon Kristian K.Brandt David W.Graham James M.Lazorchak Satoru Suzuki Peter Silley Jason R.Snape Edward Topp Tong Zhang Yong-Guan Zhu 何蓉 汪源 张伊人 金泰廙 | 2014 | 环境与职业医学2014，31，1： | 1 |
| 10 | Minocycline fails to improve neurologic and histologic outcome after ventricular fibrillation cardiac arrest in rats显示文摘BACKGROUND Prolonged cardiac arrest(CA)produces extensive neuronal death and microglial proliferation and activation resulting in neuro-cognitive disabilities.Among other potential mechanisms,microglia have been implicated as triggers of neuronal death after hypoxic-ischemic insults.Minocycline is neuroprotective in some brain ischemia models,either by blunting the microglial response or by a direct effect on neurons.AIM To improve survival,attenuate neurologic deficits,neuroinflammation,and histological damage after ventricular fibrillation(VF)CA in rats.METHODS Adult male isoflurane-anesthetized rats were subjected to 6 min VF CA followed by 2 min resuscitation including chest compression,epinephrine,bicarbonate,and defibrillation.After return of spontaneous circulation(ROSC),rats were randomized to two groups:(1)Minocycline 90 mg/kg intraperitoneally(i.p.)at 15 min ROSC,followed by 22.5 mg/kg i.p.every 12 h for 72 h;and(2)Controls,receiving the same volume of vehicle(phosphate-buffered saline).The rats were kept normothermic during the postoperative course.Neurologic injury was assessed daily using Overall Performance Category(OPC;1=normal,5=dead)and Neurologic Deficit Score(NDS;0%=normal,100%=dead).Rats were sacrificed at 72 h.Neuronal degeneration(Fluoro-Jade C staining)and microglia proliferation(anti-Iba-1 staining)were quantified in four selectively vulnerable brain regions(hippocampus,striatum,cerebellum,cortex)by three independent reviewers masked to the group assignment.RESULTS In the minocycline group,8 out of 14 rats survived to 72 h compared to 8 out of 19 rats in the control group(P=0.46).The degree of neurologic deficit at 72 h[median,(interquartile range)]was not different between survivors in minocycline vs controls:OPC 1.5(1-2.75)vs 2(1.25-3),P=0.442;NDS 12(2-20)vs 17(7-51),P=0.328)or between all studied rats.The number of degenerating neurons(minocycline vs controls,mean±SEM:Hippocampus 58±8 vs 76±8;striatum 121±43 vs 153±32;cerebellum 20±7 vs 22±8;cortex 0±0 vs 0±0)or proliferating microglia(hippocampus 157±15 vs 193 cortex 0±0 vs 0±0;16;striatum 150±22 vs 161±23;cerebellum 20±7 vs 22±8;cortex 26±6 vs 31±7)was not different between groups in any region(all P>0.05).Numerically,there were approximately 20%less degenerating neurons and proliferating microglia in the hippocampus and striatum in the minocycline group,with a consistent pattern of histological damage across the individual regions of interest.CONCLUSION Minocycline did not improve survival and failed to confer substantial benefits on neurologic function,neuronal loss or microglial proliferation across multiple brain regions in our model of rat VF CA. | Andreas Janata Ingrid AM Magnet Kristin L Schreiber Caleb D Wilson Jason P Stezoski Keri Janesko-Feldman Patrick M Kochanek Tomas Drabek | 2019 | World Journal of Critical Care Medicine2019，8，7： | 0 |
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