A comparison of lifelong and posttrauma nightmares in a civilian trauma sample: Nightmare characteristics, psychopathology, and treatment outcome.

Nightmares and sleep disturbances are thought to play a key role in the development of posttrauma problems. Research efforts have increased in an attempt to understand this association. The present study examined differences in nightmare characteristics, related psychopathology, treatment outcome, and trauma history among trauma-exposed individuals whose nightmares began before a traumatic event and those whose nightmares began after a traumatic event, while controlling for posttraumatic stress disorder status. Individuals whose nightmares began following a trauma experienced more depression and posttraumatic stress symptoms and poorer sleep quality, reported a higher number of traumatic events, and were more likely to report nightmares replicative of or similar to the trauma than those whose nightmares began before the trauma. No other between-groups differences were found for nightmare characteristics or response to treatment. This study is an important step in understanding the nature of nightmares and their relationship to traumatic events and consequences, but additional research is warranted. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Expression and activation of ephexin is altered after spinal cord injury

Failure of axon regeneration after traumatic spinal cord injury (SCI) is attributable in part to the presence of inhibitory molecular interactions. Recent evidence demonstrates that activation of Eph signaling pathways leads to modulation of growth cone dynamics and repulsion through the activation of ephexin, a novel guanine nucleotide exchange factor (GEF). However, little is known about the expression and modulation of Eph molecular targets in the injured spinal cord. In this study, we determined the expression profile of ephexin after a moderate spinal cord contusion at thoracic level (T10) in young adult rats. Western-blot studies showed increased protein expression in injured rats at 4 and 7 days postinjury (DPI) when compared with control animals. The protein levels returned to normal at 14 DPI and remained steady until 28 DPI. However, immunoprecipitation studies of the phosphorylated ephexin demonstrated that this protein is activated by day 2 until 14 DPI. Expression of ephexin was noticeable in neurons, axons, microglia/macrophages, and reactive astrocytes, and co-localized with EphA3, A4, and A7. These results demonstrate the presence of ephexin in the adult spinal cord and its activation after SCI. Therefore, we show, for the first time, the spatiotemporal pattern of ephexin expression and activation after contusive SCI. Collectively, our data support our previous findings on the putative nonpermissive roles of Eph receptors after SCI and the possible involvement of ephexin in the intracellular cascade of events.     

Rope trauma,sedation, disentanglement,and monitoring‐tag associated lesions in a terminally entangled North Atlantic right whale (Eubalaena glacialis)

A chronically entangled North Atlantic right whale, with consequent emaciation was sedated, disentangled to the extent possible, administered antibiotics, and satellite tag tracked for six subsequent days. It was found dead 11 d after the tag ceased transmission. Chronic constrictive deep rope lacerations and emaciation were found to be the proximate cause of death, which may have ultimately involved shark predation. A broadhead cutter and a spring‐loaded knife used for disentanglement were found to induce moderate wounds to the skin and blubber. The telemetry tag, with two barbed shafts partially penetrating the blubber was shed, leaving barbs embedded with localized histological reaction. One of four darts administered shed the barrel, but the needle was found postmortem in the whale with an 80º bend at the blubber‐muscle interface. This bend occurred due to epaxial muscle movement relative to the overlying blubber, with resultant necrosis and cavitation of underlying muscle. This suggests that rigid, implanted devices that span the cetacean blubber muscle interface, where the muscle moves relative to the blubber, could have secondary health impacts. Thus we encourage efforts to develop new tag telemetry systems that do not penetrate the subdermal sheath, but still remain attached for many months.     

液体负平衡对腹部外伤患者血流动力学指标变化与炎症因子浓度的影响及其相关因素分析

目的:探讨液体负平衡对腹部外伤患者血流动力学指标变化与炎症因子浓度的影响并分析其相关因素。方法:选取2015年10月-2018年9月期间在我院接受治疗的腹部外伤患者120例,以随机数字表法分为对照组(n=60)和研究组(n=60)。对照组患者采用常规的抗感染的治疗方法,研究组患者在对照组患者的基础上保持该组患者的液体负平衡,比较两组患者炎症因子水平、血流动力学指标、体内氧合情况及呼吸机机械通气状况,多因素Logistic回归分析研究组患者的生存率的影响因素。结果:两组患者治疗后白介素-6(IL-6)、动脉血氧分压差[P(A-a)O2]均降低,且研究组低于对照组(P0.05),动脉血氧分压(PaO2)升高,且研究组高于对照组(P0.05)。两组患者脱机时平台压(Pplat)、呼气末正压(PEEP)、吸氧浓度(Fi O2)均降低,且研究组低于对照组(P0.05)。两组患者治疗后血管外肺水(EVLWI)降低,且研究组低于对照组(P0.05),心输出量(CO)、心指数(CI)与治疗前比较无差异(P0.05)。单因素分析结果显示,研究组患者生存率与患者的年龄、腹部创伤严重度评分(ISS)、手术前体温和碱剩余(BE)绝对值、ICU入室体温有关(P0.05),而与手术时间无关(P0.05)。Logistic回归分析结果显示,年龄、ISS、手术前BE绝对值、ICU入室体温均是研究组患者生存率的影响因素。结论:液体负平衡对腹部外伤患者的心肺功能具有一定的改善作用,可降低患者体内炎症因子的水平。年龄、ISS、ICU入室体温以及手术前BE绝对值均会影响腹部外伤患者的生存率。     

End-to-end military pain management

The last three years have seen significant changes in the Defence Medical Services approach to trauma pain management. This article seeks to outline these changes that have occurred at every level of the casualty's journey along the chain of evacuation, from the point of injury to rehabilitation and either continued employment in the Services or to medical discharge. Particular attention is paid to the evidence for the interventions used for both acute pain and chronic pain management. Also highlighted are possible differences in pain management techniques between civilian and military casualties.     

New therapeutic strategy of hinokitiol in haemorrhagic shock‐induced liver injury

Haemorrhagic shock and resuscitation (HS/R) may cause global ischaemia‐reperfusion injury, which can result in systemic inflammation, multiorgan failure (particularly liver failure) and high mortality. Hinokitiol, a bioactive tropolone‐related compound, exhibits antiplatelet and anti‐inflammatory activities. Targeting inflammatory responses is a potential strategy for ameliorating hepatic injury during HS/R. Whether hinokitiol prevents hepatic injury during HS/R remains unclear. In the present study, we determined the role of hinokitiol following HS/R. The in vivo assays revealed that hinokitiol markedly attenuated HS/R‐induced hepatic injury. Hinokitiol could inhibited NF‐κB activation and IL‐6 and TNF‐α upregulation in liver tissues. Moreover, hinokitiol reduced caspase‐3 activation, upregulated Bax and downregulated Bcl‐2. These findings suggest that hinokitiol can ameliorate liver injury following HS/R, partly through suppression of inflammation and apoptosis. Furthermore, the in vitro data revealed that hinokitiol significantly reversed hypoxia/reoxygenation (H/R)‐induced cell death and apoptosis in the primary hepatocytes. Hinokitiol prevented H/R‐induced caspase‐3 activation, PPAR cleavage, Bax overexpression and Bcl‐2 downregulation. Moreover, hinokitiol attenuated H/R‐stimulated NF‐κB activation and reduced the levels of IL‐6 and TNF‐α mRNAs, suggesting that hinokitiol can protect hepatocytes from H/R injury. Collectively, our data suggest that hinokitiol attenuates liver injury following HS/R, partly through the inhibition of NF‐κB activation.     

Estimating the risk of PTSD in recent trauma survivors: results of the International Consortium to Predict PTSD (ICPP)

A timely determination of the risk of post‐traumatic stress disorder (PTSD) is a prerequisite for efficient service delivery and prevention. We provide a risk estimate tool allowing a calculation of individuals’ PTSD likelihood from early predictors. Members of the International Consortium to Predict PTSD (ICPP) shared individual participants’ item‐level data from ten longitudinal studies of civilian trauma survivors admitted to acute care centers in six countries. Eligible participants (N=2,473) completed an initial clinical assessment within 60 days of trauma exposure, and at least one follow‐up assessment 4‐15 months later. The Clinician‐Administered PTSD Scale for DSM‐IV (CAPS) evaluated PTSD symptom severity and diagnostic status at each assessment. Participants’ education, prior lifetime trauma exposure, marital status and socio‐economic status were assessed and harmonized across studies. The study's main outcome was the likelihood of a follow‐up PTSD given early predictors. The prevalence of follow‐up PTSD was 11.8% (9.2% for male participants and 16.4% for females). A logistic model using early PTSD symptom severity (initial CAPS total score) as a predictor produced remarkably accurate estimates of follow‐up PTSD (predicted vs. raw probabilities: r=0.976). Adding respondents’ female gender, lower education, and exposure to prior interpersonal trauma to the model yielded higher PTSD likelihood estimates, with similar model accuracy (predicted vs. raw probabilities: r=0.941). The current model could be adjusted for other traumatic circumstances and accommodate risk factors not captured by the ICPP (e.g., biological, social). In line with their use in general medicine, risk estimate models can inform clinical choices in psychiatry. It is hoped that quantifying individuals’ PTSD risk will be a first step towards systematic prevention of the disorder.     

Post‐traumatic stress disorder: a state‐of‐the‐art review of evidence and challenges

Post‐traumatic stress disorder (PTSD) is arguably the most common psychiatric disorder to arise after exposure to a traumatic event. Since its formal introduction in the DSM‐III in 1980, knowledge has grown significantly regarding its causes, maintaining mechanisms and treatments. Despite this increased understanding, however, the actual definition of the disorder remains controversial. The DSM‐5 and ICD‐11 define the disorder differently, reflecting disagreements in the field about whether the construct of PTSD should encompass a broad array of psychological manifestations that arise after trauma or should be focused more specifically on trauma memory phenomena. This controversy over clarifying the phenotype of PTSD has limited the capacity to identify biomarkers and specific mechanisms of traumatic stress. This review provides an up‐to‐date outline of the current definitions of PTSD, its known prevalence and risk factors, the main models to explain the disorder, and evidence‐supported treatments. A major conclusion is that, although trauma‐focused cognitive behavior therapy is the best‐validated treatment for PTSD, it has stagnated over recent decades, and only two‐thirds of PTSD patients respond adequately to this intervention. Moreover, most people with PTSD do not access evidence‐based treatment, and this situation is much worse in low‐ and middle‐income countries. Identifying processes that can overcome these major barriers to better management of people with PTSD remains an outstanding challenge.     

Quantitative analysis of brain microstructure following mild blunt and blast trauma

We induced mild blunt and blast injuries in rats using a custom-built device and utilized in-house diffusion tensor imaging (DTI) software to reconstruct 3-D fiber tracts in brains before and after injury (1, 4, and 7 days). DTI measures such as fiber count, fiber length, and fractional anisotropy (FA) were selected to characterize axonal integrity. In-house image analysis software also showed changes in parameters including the area fraction (AF) and nearest neighbor distance (NND), which corresponded to variations in the microstructure of Hematoxylin and Eosin (H&E) brain sections. Both blunt and blast injuries produced lower fiber counts, but neither injury case significantly changed the fiber length. Compared to controls, blunt injury produced a lower FA, which may correspond to an early onset of diffuse axonal injury (DAI). However, blast injury generated a higher FA compared to controls. This increase in FA has been linked previously to various phenomena including edema, neuroplasticity, and even recovery. Subsequent image analysis revealed that both blunt and blast injuries produced a significantly higher AF and significantly lower NND, which correlated to voids formed by the reduced fluid retention within injured axons. In conclusion, DTI can detect subtle pathophysiological changes in axonal fiber structure after mild blunt and blast trauma. Our injury model and DTI method provide a practical basis for studying mild traumatic brain injury (mTBI) in a controllable manner and for tracking injury progression. Knowledge gained from our approach could lead to enhanced mTBI diagnoses, biofidelic constitutive brain models, and specialized pharmaceutical treatments.     

Trophy heads from Nawinpukio, Perú: physical and chemical analysis of Huarpa-era modified human remains

Rescue excavations at the site of Nawinpukio in Perú's Ayacucho Valley exposed a cache of fragmented skulls dating to the Huarpa-era, about AD 400-700. Physical analysis of these remains revealed that they belonged to individuals of both sexes and a range of ages (MNI = 8), and that four crania had been modified through drilling, cutting, and scraping. The occipital and parietal bones of one cranium had been modified to form a shallow basin. Carbon stable isotope analysis of these remains revealed that five individuals had isotopic signatures consistent with maize consumption and one individual exhibited a carbon isotope value indicative of a C(3) plant based diet. Such a nonmaize diet distinguishes this individual from all other prehistoric humans analyzed from the Ayacucho Valley and is consistent with an origin a different ecozone of the valley. On the basis of their physical properties it is argued that these remains represent trophies obtained during raiding. Drawing on the formal properties of the specimens as well as ethnographic and archaeological analogies, it is suggested that the cranial basin served as a vessel for liquid.