μ,δ,κ阿片受体在创伤失血性休克大鼠心血管功能抑制中的作用

目的探讨μ，δ和κ阿片受体与创伤失血性休克大鼠心血管功能抑制的关系。方法用大鼠创伤失血性休克模型，观察创伤失血性休克后大鼠心脏和脑μ，δ和κ阿片受体变化及其与血流动力学指标的变化的关系；观察δ和κ阿片受体特异性拮抗剂对创伤失血性休克大鼠血流动力学指标的影响。结果创伤失血性休克后，大鼠心脏和脑δ和κ阿片受体数目明显升高，亲和力无明显变化，心脏和脑的δ和κ阿片受体数目升高与创伤失血性休克后大鼠血流动力学指标下降呈显著负相关。δ和κ阿片受体特异性拮抗剂可明显逆转创伤失血性休克大鼠血流动力学指标的下降。结论δ和κ阿片受体在创伤失血性休克心血管功能抑制中起重要作用，参与了创伤失血性休克的发病过程     

Traumatic Memories: Empirical Foundations, Forensic and Clinical Implications

This article reviews empirical research on memories for negative personal experiences among adults. It examines basic concepts (including neural underpinnings), theoretical models of the affect-memory relationship, and data from three sources: victims or witnesses to crimes and atrocities, "flashbulb memories" for traumatic events, and laboratory simulations of shocking experiences. Evidence suggests that memories for traumatic experiences contain more central than peripheral detail, are reasonably accurate and well-retained for very long periods, but are not completely indelible. Assertions of eyewitness memory's vulnerability to change through suggestion have overstated the evidence. Forensic and clinical implications are discussed and a plea issued for more study of the memory phenomena that characterize posttraumatic stress disorder (PTSD) and are the focus of trauma survivors' treatment.     

Long-term potentiation deficits and excitability changes following traumatic brain injury

The effects of traumatic brain injury (TBI) on hippocampal long-term potentiation (LTP) and cellular excitability were assessed at postinjury days 2, 7, and 15. TBI was induced using a well-characterized central fluid-percussion model. LTP of the Schaffer collateral/commissural system was assessed in vivo in urethane-anesthetized rats. Significant LTP of the population excitatory postsynaptic potential (EPSP) slope was found only in controls, and no recovery to control levels was observed for any postinjury time point. Four measurement parameters reflecting pyramidal cell discharges (population spike) indicated that TBI significantly increased cellular excitability at postinjury day 2: (1) pretetanus baseline recording showed that TBI reduced population spike threshold and latency; (2) tetanic stimulation (400 Hz) increased population spike amplitudes to a greater degree in injured animals than in control animals; (3) tetanus-induced population spike latency shifts were greater in injured cases; and (4) tetanic stimulation elevated EPSP to spike ratios (E-S potentiation) to a greater degree in injured animals. These parameters returned to control levels, as measured on postinjury days 7 and 15. These results suggest that TBI-induced excitability changes persist at least through 2 days postinjury and involve a differential impairment of mechanisms subserving LTP of synaptic efficacy and mechanisms related to action potential generation     

Traumatic aneurysms of the descending thoracic aorta

From July 1979 to December 1985 we observed 51 patients with traumatic lesions of the descending thoracic aorta. Twenty-nine had acute ruptures, mostly accompanied by multiple injuries, and 27 had to be operated upon immediately. Twenty-two patients (19 males, 3 females) had chronic traumatic aneurysms of the descending thoracic aorta (more than six weeks after trauma). Mean age at the time of trauma was 24 years. Mean age at time of surgery was 36.5 years. Twelve patients were symptomatic. All were treated surgically. At surgery, complete aortic disruption was found in 15 patients and partial rupture in seven. We did not use aortic shunting of any kind, only aortic cross-clamping. Hypertension was controlled by intravenous drug infusion. The ruptured aortic segment was replaced in all cases by prosthetic Dacron graft. There were no operative deaths. One patient (age 77) died 11 weeks after surgery from multiple organ failure. One case of postoperative paraplegia was observed. This patient recovered almost completely from his neurological deficit.     

大鼠液压脑损伤后bax和bcl—XL的表达改变在mRNA和蛋白水平的相关性

目的探讨脑创伤后bax和bcl-XL在mRNA和蛋白水平的变化规律及其与神经细胞凋亡发生、发展的关系.方法在液压脑损伤模型中,应用逆转录聚合酶链反应、免疫组化分别检测大鼠脑创伤后不同时程bax和bcl-xL的表达;采用凋亡原位末端标记、电镜超微结构、DNA凝胶电泳观察脑创伤后细胞凋亡的形态和生化特征.结果伤后6h,bcl-xL.mRNA下调[伤侧半球为对侧的(67.42±7.54)%],bcl-xL蛋白水平下降[伤侧为对侧的(85.85±5.72)%].伤后3d,bcl-xLmRNA和bd-xL蛋白表达分别为对侧的(39.97±3.61)%和(57.50±6.21)%;baxmRNA和bax蛋白分别为对侧半球的(203.95±17.53)%和(189.02±7.23)%.伤后bax/bclxL比率升高比细胞凋亡提前出现,早期由于bcl-xL.的表达下降,后期主要是由于bax的升高所致.结论细胞凋亡及其调节基因的表达间具有一致性;脑创伤对bax和bcl-xL的调节发生在转录水平以前的某一环节.bax/bcl-xL平衡体系的维持或紊乱影响脑创伤后神经细胞生存或死亡.     

Current updates in management of extremity injuries in polytrauma

Injury-related morbidity and mortality have been one of the most common causes of loss in productivity across all geographic distributions. It remains to be a global concern despite a continual improvement in regional and national safety policies. The establishment of trauma care systems and advancements in diagnostics and management have improved the overall survival of severely injured. A better understanding of the physiopathological and immunological responses to injury led to a significant shift in trauma care from “Early Total Care” to “Damage Control Orthopedics.” While most of these algorithms were tailored to the philosophy of “life before limb,” the impact of improper fracture management on disability and societal loss is increasingly being recognized. Recently, “Early Appropriate Care” of extremities has gained importance; however, its implementation is influenced by regional health care policies, available resources, and expertise and varies between low and high-income countries. A review of the literature was performed using PubMed, Embase, Web of Science, and Scopus databases on articles published from 1990 to 2020 using the Mesh terms “Polytrauma,” “Multiple Trauma,” and “Fractures.” This review aims to consolidate on guidelines and available evidence in the management of extremity injuries in a polytraumatized patient to achieve better clinical outcomes of these severely injured.     

创伤性脑损伤患者脑脊液中嗜中性白细胞碱性磷酸酶-1的表达及意义

目的探讨炎性体蛋白嗜中性白细胞碱性磷酸酶-1(NALP-1)在创伤性脑损伤患者脑脊液中表达水平及其与预后相关性。方法选取2017年2月至2018年9月来自首都医科大学附属北京同仁医院的120例创伤性脑损伤患者,选取同期健康体检者30例作为对照组,采用免疫印迹化学发光法检测研究对象脑脊液中炎性体蛋白NALP-1表达水平,根据格拉斯哥预后评分(GOS)将创伤性脑损伤患者分为预后良好组(GOS>3分)和预后不良组(GOS≤3分)。χ²检验和t检验分析预后良好组和预后不良组NALP-1和临床资料差异,采用多因素Logistic回归模型分析创伤性脑损伤后患者预后影响因素。结果创伤性脑损伤患者脑脊液中NALP-1表达(1.64±0.52)高于对照组(0.94±0.28,t=7.108,P<0.05),差异有统计学意义。NALP-1高表达组急性生理与慢性健康状况评分Ⅱ(APACHEⅡ)得分(26.4±5.4)分、脑挫伤比例(76.62%)、蛛网膜下腔出血比例(77.27%)高于低表达组[(22.3±4.5)分、23.38%、22.73%],差异有统计学意义(χ²/t=4.135、9.586、7.424,P<0.05)。年龄[比值比(OR):2.175,95%可信区间(CI):1.167~8.767,P<0.05]、蛛网膜下腔出血(OR:1.241,95%CI:1.101~3.794,P<0.05)、NALP-1(OR:2.841,95%CI:1.675~10.717,P<0.05)、纤维蛋白原水平(OR:1.215,95%CI:1.056~3.627,P<0.05)、APACHEⅡ得分(OR:1.615,95%CI:1.314~5.485,P<0.05)是预后不良独立影响因素,差异均有统计学意义。结论创伤性脑损伤脑脊液中NALP-1表达增加,且表达量升高与预后不良相关。     

车祸致颅脑损伤患者家属心理健康状况与社会支持相关性研究

目的 了解车祸致颅脑损伤患者家属的心理健康状况和社会支持状况,探讨其相关性。方法 采用自编一般资料调查表、症状自评量表（SCL - 90）和社会支持量表（SSRS）,对225名到精神专科医院就诊的车祸致颅脑损伤患者家属进行问卷调查。结果 车祸致颅脑损伤患家属的SCL - 90总分为（178.45±82.56）分, SCL - 90总分、阳性项目数和9个因子分均显著高于肿瘤患者家属和全国常模(P＜0.05)。社会支持总分为（38.52±8.23）分,社会支持水平与家属的心理健康状况呈显著的负相关（r = - 0.416, P＜0.05）。多元线性回归分析显示,社会支持总分可以负向预测家属的心理健康状况（β = - 0.399,P＜0.05）。结论 车祸致颅脑损伤患者家属的心理问题发生率较高,应从个人、家庭和社会层面为家属提供社会支持资源。     

外伤性晶状体脱位继发性青光眼的治疗分析

目的 探讨外伤性晶状本脱位继发性青光眼的治疗方法。方法 药物保守治疗１８例,单纯小梁切除７例,单纯晶状体摘出１４例,晶状体摘出联合小梁切除７例。结果 ４６例中２例在局部滴用噻吗心安后,眼压控制在２１ｍｍＨｇ以下。治疗后矫正视力和前相比差异有显著性。结论 外伤性晶状体脱位继发性青光眼的治疗关键是尽早地用药物或手术方法缓解瞳孔阻滞,房角损伤≥２个象限者加用滤过性手术。