Posttraumatic stress disorder and quality of life: Extension of findings to veterans of the wars in Iraq and Afghanistan

The wars in Iraq and Afghanistan—Operation Iraqi Freedom and Operation Enduring Freedom, or OEF/OIF—have created unique conditions for promoting the development of psychological difficulties such as posttraumatic stress disorder (PTSD). PTSD is an important outcome because it can affect quality of life, impairing psychosocial and occupational functioning and overall well-being. The literature on PTSD and quality of life in OEF/OIF Veterans is at an early stage, but the consistency of the evidence is striking. Our review indicates that the findings on PTSD and quality of life in OEF/OIF veterans are comparable to findings obtained from other war cohorts and from nonveterans as well. Even though the duration of PTSD in OEF/OIF Veterans is much shorter than in Vietnam Veterans, for example, those with PTSD in both cohorts are likely to experience poorer functioning and lower objective living conditions and satisfaction. The review ends with discussion of the implications of the evidence for research and clinical practice.     

Military-related PTSD and intimate relationships: From description to theory-driven research and intervention development

Military operations in Iraq and Afghanistan have brought heightened awareness of military related PTSD, as well as the intimate relationship problems that accompany the disorder and can influence the course of veterans' trauma recovery. In this paper, we review recent research that documents the association between PTSD and intimate relationship problems in the most recent cohort of returning veterans and also synthesize research on prior eras of veterans and their intimate relationships in order to inform future research and treatment efforts with recently returned veterans and their families. We highlight the need for more theoretically-driven research that can account for the likely reciprocally causal association between PTSD and intimate relationship problems to advance understanding and inform prevention and treatment efforts for veterans and their families. Future research directions are offered to advance this field of study.     

Mild traumatic brain injury and posttraumatic stress disorder in returning veterans: Perspectives from cognitive neuroscience

A significant proportion of military personnel deployed in support of Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) has been exposed to war-zone events potentially associated with traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD). There has been significant controversy regarding healthcare policy for those service members and military veterans who returned from OEF/OIF deployments with both mild TBI and PTSD. There is currently little empirical evidence available to address these controversies. This review uses a cognitive neuroscience framework to address the potential impact of mild TBI on the development, course, and clinical management of PTSD. The field would benefit from research efforts that take into consideration the potential differential impact of mild TBI with versus without persistent cognitive deficits, longitudinal work examining the trajectory of PTSD symptoms when index trauma events involve TBI, randomized clinical trials designed to examine the impact of mild TBI on response to existing PTSD treatment interventions, and development and examination of potential treatment augmentation strategies.     

Glial reactions in a rodent cauda equina injury and repair model

In the adult rat, an avulsion injury of lumbosacral ventral roots results in a progressive and pronounced loss of the axotomized motoneurons. A subsequent acute implantation of an avulsed ventral root into the spinal cord has neuroprotective effects. However, it has not been known whether a surgical implantation of an avulsed ventral root into the spinal cord for neural repair purposes affects intramedullary glial and microglial reactions. Here, adult female Sprague-Dawley rats underwent a unilateral L5-S2 ventral root avulsion injury with or without acute implantation of the L6 ventral root into the spinal cord. At 4 weeks postoperatively, immunohistochemistry using primary antibodies to GFAP (astrocytes), Ox-42 (microglia), and ED-1 (macrophages) was performed at the L6 spinal cord segment, and quantified using densitometry. Our results show that a lumbosacral ventral root avulsion injury induces an activation of astrocytes, microglia, and macrophages in the ventral horn. Interestingly, an acute implantation of an avulsed root into the white matter does not significantly affect the activation of glial cells or macrophages in the ventral horn. We speculate that neuroprotective and axonal growth promoting benefits of the combined glial and microglial/ macrophage responses may outweigh their potential negative effects, as previous studies have shown that implantation of avulsed roots is a successful strategy in promoting reinnervation of peripheral targets.     

组织损伤修复中的生物力学问题

生物力学对损伤组织修复的影响及调控研究方兴未艾。组织修复与再生医学的发展为生物力学的研究提供了新平台,而生物力学则成为推动组织修复与再生医学发展的重要因素。对《医用生物力学》2016年第5期发表的"生物力学与组织修复"专栏论文进行简要的分析、述评,同时对该领域的研究进行回顾和展望。     

Autophagy in renal tubular injury and repair

Autophagy is a fundamental cellular process that maintains normal function and structure of the cell. It can be induced during stress and serves as an adaptive response for cell survival. Normal kidneys have high metabolic demands yet are relatively hypoxic, especially in the medulla and papilla. Injury or ageing aggravates metabolic perturbation and activates autophagy in many types of renal cells. In the kidney, tubular epithelial cells consume the most energy due to active transport mechanisms and therefore are the most susceptible to injuries from hypoxic or low‐energy states. This brief review will summarize current understandings of the biological function and molecular regulation of epithelial autophagy during tubular injury and repair.     

Putting the pieces together: preliminary efficacy of a web-based family intervention for children with traumatic brain injury

OBJECTIVE: To report preliminary efficacy data from a Web-based family problem-solving intervention to improve parent and child adaptation. METHOD: Eight parents and six children with moderate to severe traumatic brain injury (TBI) who were injured more than 15 months earlier (M = 16 months) participated in the intervention. Families were given computers, Web cameras, and high-speed Internet access. Weekly videoconferences with the therapist were conducted after they completed self-guided Web exercises on problem-solving, communication, and antecedent behavior management strategies. RESULTS: Paired t tests comparing pre- and post-intervention scores revealed significant improvements in injury-related burden, parental psychiatric symptoms, depression, and parenting stress. There were also significant reductions in antisocial behaviors in the injured child, but not in self-reported depressive symptoms. CONCLUSIONS: These findings suggest that a computer-based intervention may successfully be used to improve both parent and child outcomes following TBI in children.     

护理干预对大鼠脊髓损伤后运动功能修复的脊髓形态学研究

目的研究护理干预对大鼠脊髓损伤后脊髓运动功能修复的脊髓形态学变化。方法将60只SD成年大鼠随机分为3组,分别为正常对照组、实验对照组、实验组,每组20只,每组分4个时相点,即脊髓损伤后1 d、7 d、30 d、60 d(n=5)。实验对照组和实验组均采用切割加挤压脊髓L4平面横断制备脊髓损伤大鼠模型。正常对照组为正常大鼠未经处理,实验对照组大鼠脊髓损伤后给予排尿、排便等常规护理,实验组除常规护理之外,还给予关节活动度训练和肌肉按摩训练,每日2次,每次10 min。采用常规HE染色、免疫组织化学染色法观察护理干预对脊髓损伤后大鼠脊髓的形态学变化。结果 HE染色结果以及GFAP和NF-200免疫组织化学染色结果显示,实验组和实验对照组未见明显区别,但与正常对照组比较差异非常明显。结论护理干预对损伤区脊髓组织形态学研究未见明显改变。     

流感病毒致小鼠急性肺损伤模型建立及利巴韦林干预作用研究

目的 建立A/FM/1/47/(H1N1)流感病毒感染诱导的小鼠急性肺损伤模型,并使用利巴韦林对其进行治疗,观察其保护机制.方法 将30只13-15g的昆明(KM)小鼠随机分为三组(正常组、模型组和利巴韦林组),每组10只,模型组与利巴韦林组采用H1N1流感病毒经鼻腔接种,利巴韦林组小鼠配以药物治疗,定时称量各组小鼠的体质量、观察记录小鼠存活状态,连续观察15d;另取36只13-15g的KM小鼠,如上随机分为三组,每组12只,模型组与利巴韦林组采用H1N1流感病毒经鼻腔接种,利巴韦林组小鼠配以药物治疗,感染后第6d测量肺系数、肺湿/干重比、观察肺病理组织学变化、动脉血气分析、血清细胞因子含量和肺部病毒载量.结果 实验结果显示,流感病毒滴鼻感染可诱发小鼠病毒性肺损伤.利巴韦林可延长感染小鼠生存时间,降低肺水肿,改善低氧血症,抑制炎性细胞的分泌,抑制病毒在体内的复制.结论 本研究利用流感病毒感染小鼠的病毒性肺损伤,分析了利巴韦林对流感病毒诱发的病毒性肺损伤的保护作用.该模型对进一步开发抑制流感病毒性肺损伤的新药有重要意义.     

The zebrafish swimbladder: A simple model for lung elastin injury and repair

In this communication we offer data to suggest that the zebrafish swimbladder may provide a simple model of elastin injury and repair which is amenable to genetic analysis and pertinent to lung physiology. In situ hybridization of zebrafish embryos illustrated that elastin gene expression is evident in the developing gut tract prior to swimbladder morphogenesis. Northern blot analysis demonstrated that the major zebrafish elastin mRNA is 2.0 kb which is significantly smaller than its higher vertebrate counterpart. Amino acid analysis of alkali-resistant protein from the anterior chamber of the adult zebrafish swimbladder showed a composition similar to higher vertebrate elastins including significant amounts of desmosine crosslinks. Electron microscopic investigations of the swimbladder wall indicate a simple structure with an inner layer of elastin fibers. Elastase delivery to the swimbladder in vitro resulted in significant fragmentation of elastin in the anterior chamber providing an environment for studying elastin repair within the tissue.     

Microvascular injury and repair in acute human bacterial pyelonephritis

Summary Acute inflammatory cell-capillary endothelial cell interactions, related to injury and repair, were investigated light and electron microscopically in acute human bacterial pyelonephritis. In inflammatory infiltrate-adjacent microvessels, the small capillaries were completely occluded by leukocyte plugs and the large capillaries were densely filled with acute inflammatory cells adhering to the endothelium. Severe damage to small and large capillaries was observed around endothelium adherent, degranulated neutrophil granulocytes containing phagocytosed bacteria. There were spaces in the endothelium, degradation of the vascular basement membrane, of the perivascular interstitial matrix and of collagen fibrils, with fibrin deposition and vessel wall fragmentation. In the small capillaries relatively distant from the interstitial infiltrates, emigration of leukocytes was frequently seen. Around the escaping cells the endothelial lining displayed occasional discontinuities, allowing leakage of vascular fluid into the interstitial space. Some small capillaries not related to the infiltrate were occluded by fibrin thrombi with apparent damage to the endothelial cells and disruption of the capillary wall. Various reparative changes were noticed in association with this change including capillary neovascularization. The findings confirm the existence of polymorphonuclear leukocyte-mediated injury of capillaries during the development of inflammatory responses in acute pyelonephritis.Some parts of this paper were presented at the XVIth Congress of the IAP, Vienna, Austria, August 31–September 5, 1986A Fellow of the Deutscher Akademischer Austauschdienst, Bonn, FRG     

A murine model of acute lung injury identifies growth factors to promote tissue repair and their biomarkers

Type II alveolar epithelial cells (AEC2s) play a crucial role in the regeneration of type I AECs after acute lung injury. The mechanisms underlying the regeneration of AEC2s are not fully understood. To address this issue, here, we investigated a murine model of acute lung injury using mice expressing human Diphtheria Toxin Receptor (DTR) under the control of Lysozyme M promoter (LysM‐DTR). DT injection induced the depletion of AEC2s, alveolar macrophages, and bone marrow (BM)‐derived myeloid cells in LysM‐DTR mice, and the mice died within 6 days after DT injection. Apoptotic AEC2s and bronchiolar epithelial cells appeared at 24 hr, whereas Ki67‐positive proliferating cells appeared in the alveoli and bronchioles in the lung of LysM‐DTR mice at 72–96 hr after DT injection. Transfer of wild‐type BM cells into LysM‐DTR mice accelerated the regeneration of AEC2s along with the up‐regulation of several growth factors. Moreover, several metabolites were significantly decreased in the sera of LysM‐DTR mice compared with WT mice after DT injection, suggesting that these metabolites might be biomarkers to predict AEC2s injury. Together, LysM‐DTR mice might be useful to identify growth factors to promote lung repair and the metabolites to predict the severity of lung injury.     

Diffuse axonal injury in head injury: definition, diagnosis and grading

Diffuse axonal injury is one of the most important types of brain damage that can occur as a result of non-missile head injury, and it may be very difficult to diagnose post mortem unless the pathologist knows precisely what he is looking for. Increasing experience with fatal non-missile head injury in man has allowed the identification of three grades of diffuse axonal injury. In grade 1 there is histological evidence of axonal injury in the white matter of the cerebral hemispheres, the corpus callosum, the brain stem and, less commonly, the cerebellum; in grade 2 there is also a focal lesion in the corpus callosum; and in grade 3 there is in addition a focal lesion in the dorsolateral quadrant or quadrants of the rostral brain stem. The focal lesions can often only be identified microscopically. Diffuse axonal injury was identified in 122 of a series of 434 fatal non-missile head injuries--10 grade 1, 29 grade 2 and 83 grade 3. In 24 of these cases the diagnosis could not have been made without microscopical examination, while in a further 31 microscopical examination was required to establish its severity.     

辐射致雄性小鼠不育症模型的建立及生精细胞损伤的初步分析

目的：构建辐射致雄性小鼠不育症模型,并对模型小鼠的生精细胞损伤进行初步分析。方法：不育症模型构建：65只雄性C57BL/6小鼠随机分为7组,正常对照组(A组)及6组60Co γ照射组,后者包括B组(12 Gy)、C组(6+6 Gy)、D组(10 Gy)、E组(6+4 Gy)、F组(8 Gy)、G组(4+4 Gy)。观察分析小鼠死亡情况(24w)及30、50、70 d受孕率。生精细胞损伤分析：72只雄鼠随机分为4组：正常对照组、6+4 Gy组、4+4 Gy组、6 Gy组。30、50、70 d观察睾丸组织切片(HE染色)并评估其生精功能( Johnsen评分);对PLZF阳性标记的精原干细胞(免疫组化法)计数。结果：A、E、F、G组生存时间较长,B、C组生存时间较短。30、50、70 d,D、E组受孕率均为0%。各照射组Johnsen评分均低于对照组(P<0.05);6+4 Gy组的PLZF阳性细胞计数呈逐渐上升趋势,但均明显低于对照组(P<0.05)。结论：6+4 Gy的60Co-γ射线照射7周龄的C57BL/6雄性小鼠,可以构建不育症模型。模型小鼠的PLZF标记的精原干细胞计数虽然低于对照组,但并非完全消失,提示不育症的原因并非精原干细胞的完全消亡。