高压氧治疗重型颅脑损伤的临床疗效观察

目的:观察高压氧辅助治疗重型颅脑损伤的临床疗效。方法:68例重型颅脑损伤患者随机分为观察组和对照组各34例,所有患者均根据病情选择手术或保守治疗,观察组在患者病情稳定后加用高压氧辅助治疗,治疗结束后比较两组患者的临床疗效。结果:观察组治疗有效率为91.2%,显著高于对照组的76.5%(P<0.05);治疗后1周和2周观察组的GCS评分均显著高于对照组(P<0.05),治疗后6个月观察组的GOS评分显著高于对照组(P<0.05);治疗后两组患者脑动脉血流速度均较治疗前有明显的改善(P<0.05),且观察的的改善情况优于对照组。结论:选择高压氧辅助治疗重型颅脑损伤的临床疗效好,可改善患者的临床情况和预后,值得临床应用。     

Hyperbaric Oxygen Therapy Can Improve Post Concussion Syndrome Years after Mild Traumatic Brain Injury - Randomized Prospective Trial

Background

Traumatic brain injury (TBI) is the leading cause of death and disability in the US. Approximately 70-90% of the TBI cases are classified as mild, and up to 25% of them will not recover and suffer chronic neurocognitive impairments. The main pathology in these cases involves diffuse brain injuries, which are hard to detect by anatomical imaging yet noticeable in metabolic imaging. The current study tested the effectiveness of Hyperbaric Oxygen Therapy (HBOT) in improving brain function and quality of life in mTBI patients suffering chronic neurocognitive impairments.

Methods and Findings

The trial population included 56 mTBI patients 1–5 years after injury with prolonged post-concussion syndrome (PCS). The HBOT effect was evaluated by means of prospective, randomized, crossover controlled trial: the patients were randomly assigned to treated or crossover groups. Patients in the treated group were evaluated at baseline and following 40 HBOT sessions; patients in the crossover group were evaluated three times: at baseline, following a 2-month control period of no treatment, and following subsequent 2-months of 40 HBOT sessions. The HBOT protocol included 40 treatment sessions (5 days/week), 60 minutes each, with 100% oxygen at 1.5 ATA. “Mindstreams” was used for cognitive evaluations, quality of life (QOL) was evaluated by the EQ-5D, and changes in brain activity were assessed by SPECT imaging. Significant improvements were demonstrated in cognitive function and QOL in both groups following HBOT but no significant improvement was observed following the control period. SPECT imaging revealed elevated brain activity in good agreement with the cognitive improvements.

Conclusions

HBOT can induce neuroplasticity leading to repair of chronically impaired brain functions and improved quality of life in mTBI patients with prolonged PCS at late chronic stage.

Trial Registration

ClinicalTrials.gov {"type":"clinical-trial","attrs":{"text":"NCT00715052","term_id":"NCT00715052"}}NCT00715052     

Effect of Early Normobaric Hyperoxia on Blast-Induced Traumatic Brain Injury in Rats

Neurochemical Research - Blast-induced traumatic brain injury (bTBI) is a leading cause of disability and mortality in soldiers during the conflicts in Iraq and Afghanistan. Although substantial...     

Propofol Administration Modulates AQP-4 Expression and Brain Edema After Traumatic Brain Injury

The increased intracranial pressure caused by brain edema following traumatic brain injury (TBI) always leads to poor patient prognosis. Aquaporin-4 (AQP-4) plays an important role in edema formation and resolution, which may provide a novel therapeutic target for edema treatment. In this present study, we found that propofol treatment, within a short time, after TBI significantly reduced brain edema in a controlled cortical injury rat model and suppressed in vivo expression of AQP-4. The ameliorating effect of propofol was associated with attenuated expression of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). In addition, the regulatory effect of propofol on AQP-4 expression was investigated in cultured astrocytes. Results showed that propofol could block the stimulatory effect of IL-1β and TNF-α on AQP-4 expression in cultured astrocytes. We also found that both NFκB and p38/MAPK pathways were involved in IL-1β and TNF-α-induced AQP-4 expression and that propofol functions as a dual inhibitor of NFκB and p38/MAPK pathways. In conclusion, treatment with propofol, within a short time, after TBI attenuates cerebral edema and reduces the expression of AQP-4. Propofol modulates acute AQP-4 expression by attenuating IL-1β and TNF-α expression and inhibiting IL-1β and TNF-α induced AQP-4 expression.     

不同时间高压氧治疗对颅脑损伤患者认知功能障碍的影响

目的:探讨不同时间高压氧治疗对颅脑损伤患者认知功能障碍的影响。方法:选择了2006年5月-2015年5月在我院接受高压氧治疗的500例颅脑损伤手术或非手术患者,根据患者开始采取高压氧治疗时间的不同分为A(入院后7d内)、B(7-30 d)、C(30 d后)三组,通过相应的治疗比较三组患者认知功能评分、FIM评分及治疗效果。结果:高压氧治疗后,三组患者较治疗前都有了不同程度上的改善,但A组在定向能力、专注能力、理解能力、复述能力、结构组织能力、记忆能力、计算能力以及自我照顾、转移、行走、交流、社会认知较B组、C组改善显著(P0.05),而B组与C组间认知功能各项评分、FIM评分比较差异无统计学意义(P0.05);A组患者治疗后总有效率为90.63%,显著优于B组73.89%的总有效率及C组70.00%的总有效率(P0.05),而B组与C组比较差异无统计学意义(P0.05)。结论:颅脑伤患者尽早的接受高压氧治疗其认知功能改善越明显,治疗效果越好。     

目标导向液体治疗联合右美托咪定对创伤性颅脑损伤患者血流动力学、脑氧代谢及炎症因子的影响

目的:探讨目标导向液体(GDFT)治疗联合右美托咪定对创伤性颅脑损伤(TBI)患者血流动力学、脑氧代谢及炎症因子的影响。方法:选取2016年3月~2019年3月期间我院收治的TBI患者142例,根据随机数字表法分为对照组1(n=47,GDFT治疗)、对照组2(n=47,常规液体联合右美托咪定)和研究组(n=48,GDFT联合右美托咪定),比较三组患者围术期指标、血流动力学、脑氧代谢及炎症因子变化情况,记录三组围术期间不良反应状况。结果:三组患者术后12、24 h心率(HR)、呼吸频率(RR)及动脉-颈内静脉血氧含量差(AVDO2)均较术前降低,且研究组低于对照组1、对照组2(P<0.05);三组患者术后12、24 h血氧饱和度(Sjv O2)较术前升高,且研究组高于对照组1、对照组2(P<0.05);三组患者术后12、24 h白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)呈逐渐下降趋势(P<0.05);研究组术后12、24 h的IL-6、TNF-α低于对照组1、对照组2(P<0.05)。对照组2、对照组1、研究组术中总液体量、胶体量、晶体量依次减少(P<0.05),住院天数依次缩短(P<0.05)。三组不良反应发生率对比未见显著差异(P>0.05)。结论:TBI患者手术麻醉过程中给予GDFT联合右美托咪定方案,促进机体HR、RR趋于平稳的同时还可改善脑氧代谢及炎性因子水平,且不增加不良反应发生率。     

Attenuation of Acute Phase Injury in Rat Intracranial Hemorrhage by Cerebrolysin that Inhibits Brain Edema and Inflammatory Response

The outcome of intracerebral hemorrhage (ICH) is mainly determined by the volume of the hemorrhage core and the secondary brain damage to penumbral tissues due to brain swelling, microcirculation disturbance and inflammation. The present study aims to investigate the protective effects of cerebrolysin on brain edema and inhibition of the inflammation response surrounding the hematoma core in the acute stage after ICH. The ICH model was induced by administration of type VII bacterial collagenase into the stratum of adult rats, which were then randomly divided into three groups: ICH + saline; ICH + Cerebrolysin (5 ml/kg) and sham. Cerebrolysin or saline was administered intraperitoneally 1 h post surgery. Neurological scores, extent of brain edema content and Evans blue dye extravasation were recorded. The levels of pro-inflammatory factors (IL-1β, TNF-α and IL-6) were assayed by Real-time PCR and Elisa kits. Aquaporin-4 (AQP4) and tight junction proteins (TJPs; claudin-5, occludin and zonula occluden-1) expression were measured at multiple time points. The morphological and intercellular changes were characterized by Electron microscopy. It is found that cerebrolysin (5 ml/kg) improved the neurological behavior and reduced the ipsilateral brain water content and Evans blue dye extravasation. After cerebrolysin treated, the levels of pro-inflammatory factors and AQP4 in the peri-hematomal areas were markedly reduced and were accompanied with higher expression of TJPs. Electron microscopy showed the astrocytic swelling and concentrated chromatin in the ICH group and confirmed the cell junction changes. Thus, early cerebrolysin treatment ameliorates secondary injury after ICH and promotes behavioral performance during the acute phase by reducing brain edema, inflammatory response, and blood–brain barrier permeability.     

Identification of Injury Specific Proteins in a Cell Culture Model of Traumatic Brain Injury

The complicated secondary molecular and cellular mechanisms following traumatic brain injury (TBI) are still not fully understood. In the present study, we have used mass spectrometry to identify injury specific proteins in an in vitro model of TBI. A standardized injury was induced by scalpel cuts through a mixed cell culture of astrocytes, oligodendrocytes and neurons. Twenty-four hours after the injury, cell culture medium and whole-cell fractions were collected for analysis. We found 53 medium proteins and 46 cell fraction proteins that were specifically expressed after injury and the known function of these proteins was elucidated by an extensive literature survey. By using time-lapse microscopy and immunostainings we could link a large proportion of the proteins to specific cellular processes that occur in response to trauma; including cell death, proliferation, lamellipodia formation, axonal regeneration, actin remodeling, migration and inflammation. A high percentage of the proteins uniquely expressed in the medium after injury were actin-related proteins, which normally are situated intracellularly. We show that two of these, ezrin and moesin, are expressed by astrocytes both in the cell culture model and in mouse brain subjected to experimental TBI. Interestingly, we found many inflammation-related proteins, despite the fact that cells were present in the culture. This study contributes with important knowledge about the cellular responses after trauma and identifies several potential cell-specific biomarkers.     

Repetitive Long-Term Hyperbaric Oxygen Treatment (HBOT) Administered after Experimental Traumatic Brain Injury in Rats Induces Significant Remyelination and a Recovery of Sensorimotor Function

Cells in the central nervous system rely almost exclusively on aerobic metabolism. Oxygen deprivation, such as injury-associated ischemia, results in detrimental apoptotic and necrotic cell loss. There is evidence that repetitive hyperbaric oxygen therapy (HBOT) improves outcomes in traumatic brain-injured patients. However, there are no experimental studies investigating the mechanism of repetitive long-term HBOT treatment-associated protective effects. We have therefore analysed the effect of long-term repetitive HBOT treatment on brain trauma-associated cerebral modulations using the lateral fluid percussion model for rats. Trauma-associated neurological impairment regressed significantly in the group of HBO-treated animals within three weeks post trauma. Evaluation of somatosensory-evoked potentials indicated a possible remyelination of neurons in the injured hemisphere following HBOT. This presumption was confirmed by a pronounced increase in myelin basic protein isoforms, PLP expression as well as an increase in myelin following three weeks of repetitive HBO treatment. Our results indicate that protective long-term HBOT effects following brain injury is mediated by a pronounced remyelination in the ipsilateral injured cortex as substantiated by the associated recovery of sensorimotor function.     

丙泊酚镇静对颅脑损伤患者脑氧供需平衡的影响

目的:探讨丙泊酚实施不同程度镇静对颅脑损伤患者脑氧供需平衡的影响。方法:选择急性闭合性颅脑损伤需行机械通气患者46例,随机分为轻度镇静组(A组),设定目标脑电双频谱指数(BIS)值75%;中度镇静组(B组),设定目标BIS值65%。主要观察达设定目标BIS值时丙泊酚靶控输注(TCI)浓度、Ramsay镇静评分、脑氧供需平衡指标颈内静脉血氧饱和度(SjvO_2)和脑氧摄取率(CERO_2)以及心率(HR)、平均动脉压(MAP)。结果:两组设定镇静目标需丙泊酚TCI浓度有明显差异(P0.05),但Ramsay评分比较差异无统计学意义;中度镇静组SjvO_2较基础值增加约12%(P0.05),CERO_2较基础值下降约15%(P0.05);而轻度镇静组对SjvO_2和CERO_2基础值没有影响。两组HR均较基础值减慢(P0.05),但对MAP均没有影响。结论:颅脑损伤患者维持目标镇静BIS值65%,调控丙泊酚靶浓度1.5-1.6μg/mL,更有利于改善脑氧供需平衡。     

常压氧与高压氧对成年大鼠脑缺血再灌注损伤后 微血管新生影响的比较

目的:研究常压氧与高压氧对成年大鼠脑缺血再灌注损伤后微血管新生影响的差异。方法:将成年SD雄性大鼠随机分为三组:假手术组(SS组)、常压氧治疗组(NBO组)、高压氧治疗组(HBO组),每组又随机分为3、7、10天三个亚组。采用线栓法对NBO组和HBO组大鼠进行大脑中动脉栓塞(MCAO),缺血1.5小时后拔出栓子再灌注,NBO组进行常压氧治疗,HBO组进行高压氧治疗。大鼠分别在3、7、10天麻醉处死,取脑组织切片,血管内皮生长因子(VEGF)、VEGF受体-1(FLT-1)和CD34免疫组化染色,光镜观察取图和统计分析。结果:NBO各组与SS各组相比,VEGF、FLT-1和CD34阳性细胞数目均明显增多(P<0.05);HBO各组与NBO各组比较,7天、10天组VEGF、FLT-1和CD34阳性细胞数目均显著增多(P<0.05)。结论:HBO治疗较NBO治疗对成年大鼠微血管的新生更有促进作用。     

Reactive Oxygen Species-Activated Nanoprodrug of Ibuprofen for Targeting Traumatic Brain Injury in Mice

Traumatic brain injury (TBI) is an enormous public health problem, with 1.7 million new cases of TBI recorded annually by the Centers for Disease Control. However, TBI has proven to be an extremely challenging condition to treat. Here, we apply a nanoprodrug strategy in a mouse model of TBI. The novel nanoprodrug contains a derivative of the nonsteroidal anti-inflammatory drug (NSAID) ibuprofen in an emulsion with the antioxidant α-tocopherol. The ibuprofen derivative, Ibu₂TEG, contains a tetra ethylene glycol (TEG) spacer consisting of biodegradable ester bonds. The biodegradable ester bonds ensure that the prodrug molecules break down hydrolytically or enzymatically. The drug is labeled with the fluorescent reporter Cy5.5 using nonbiodegradable bonds to 1-octadecanethiol, allowing us to reliably track its accumulation in the brain after TBI. We delivered a moderate injury using a highly reproducible mouse model of closed-skull controlled cortical impact to the parietal region of the cortex, followed by an injection of the nanoprodrug at a dose of 0.2 mg per mouse. The blood brain barrier is known to exhibit increased permeability at the site of injury. We tested for accumulation of the fluorescent drug particles at the site of injury using confocal and bioluminescence imaging of whole brains and brain slices 36 hours after administration. We demonstrated that the drug does accumulate preferentially in the region of injured tissue, likely due to an enhanced permeability and retention (EPR) phenomenon. The use of a nanoprodrug approach to deliver therapeutics in TBI represents a promising potential therapeutic modality.     

Stretch-Induced Deformation as a Model to Study Dopaminergic Dysfunction in Traumatic Brain Injury

Neurochemical Research - Traumatic brain injury (TBI) is defined as damage to the brain that consequently disrupts normal function. Neuronal death, a hallmark of TBI, has been related to the...     

Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice

Traumatic brain injury (TBI) research has attained renewed momentum due to the increasing awareness of head injuries, which result in morbidity and mortality. Based on the nature of primary injury following TBI, complex and heterogeneous secondary consequences result, which are followed by regenerative processes ^1,2. Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement ^3,4. The resulting hematomas and lacerations cause a vascular response ^3,5, and the morphological and functional damage of the white matter leads to diffuse axonal injury ^6-8. Additional secondary changes commonly seen in the brain are edema and increased intracranial pressure ⁹. Following TBI there are microscopic alterations in biochemical and physiological pathways involving the release of excitotoxic neurotransmitters, immune mediators and oxygen radicals ^10-12, which ultimately result in long-term neurological disabilities ^13,14. Thus choosing appropriate animal models of TBI that present similar cellular and molecular events in human and rodent TBI is critical for studying the mechanisms underlying injury and repair.Various experimental models of TBI have been developed to reproduce aspects of TBI observed in humans, among them three specific models are widely adapted for rodents: fluid percussion, cortical impact and weight drop/impact acceleration ¹. The fluid percussion device produces an injury through a craniectomy by applying a brief fluid pressure pulse on to the intact dura. The pulse is created by a pendulum striking the piston of a reservoir of fluid. The percussion produces brief displacement and deformation of neural tissue ^1,15. Conversely, cortical impact injury delivers mechanical energy to the intact dura via a rigid impactor under pneumatic pressure ^16,17. The weight drop/impact model is characterized by the fall of a rod with a specific mass on the closed skull ¹⁸. Among the TBI models, LFP is the most established and commonly used model to evaluate mixed focal and diffuse brain injury ¹⁹. It is reproducible and is standardized to allow for the manipulation of injury parameters. LFP recapitulates injuries observed in humans, thus rendering it clinically relevant, and allows for exploration of novel therapeutics for clinical translation ²⁰.We describe the detailed protocol to perform LFP procedure in mice. The injury inflicted is mild to moderate, with brain regions such as cortex, hippocampus and corpus callosum being most vulnerable. Hippocampal and motor learning tasks are explored following LFP.     

Necrostatin-1 Suppresses Autophagy and Apoptosis in Mice Traumatic Brain Injury Model

Traumatic brain injury (TBI) results in neuronal apoptosis, autophagic cell death and necroptosis. Necroptosis is a newly discovered caspases-independent programmed necrosis pathway which can be triggered by activation of death receptor. Previous works identified that necrostatin-1 (NEC-1), a specific necroptosis inhibitor, could reduce tissue damage and functional impairment through inhibiting of necroptosis process following TBI. However, the role of NEC-1 on apoptosis and autophagy after TBI is still not very clear. In this study, the amount of TBI-induced neural cell deaths were counted by PI labeling method as previously described. The expression of autophagic pathway associated proteins (Beclin-1, LC3-II, and P62) and apoptotic pathway associated proteins (Bcl-2 and caspase-3) were also respectively assessed by immunoblotting. The data showed that mice pretreated with NEC-1 reduced the amount of PI-positive cells from 12 to 48?h after TBI. Immunoblotting results showed that NEC-1 suppressed TBI-induced Beclin-1 and LC3-II activation which maintained p62 at high level. NEC-1 pretreatment also reversed TBI-induced Bcl-2 expression and caspase-3 activation, as well as the ratio of Beclin-1/Bcl-2. Both 3-MA and NEC-1 suppressed TBI-induced caspase-3 activation and LC3-II formation, Z-VAD only inhibited caspase-3 activation but increased LC3-II expression at 24?h post-TBI. All these results revealed that multiple cell death pathways participated in the development of TBI, and NEC-1 inhibited apoptosis and autophagy simultaneously. These coactions may further explain how can NEC-1 reduce TBI-induced tissue damage and functional deficits and reflect the interrelationship among necrosis, apoptosis and autophagy.     

家兔自发性蛛网膜下腔出血早期脑损伤模型的初步研究

目的：建立一种可重复的、有典型神经损伤症状的自发性蛛网膜下腔出血（sAH）动物模型,为研究蛛网膜下腔出血后早期脑损伤（EBI）的机制提供可靠的动物模型。方法：选用新西兰大耳白兔60只,随机分为实验组、对照组、空白组。采用枕大池穿刺一次注入自体动脉血法建立SAH模型。在4h、8h、12h、24h、48h、72h时间点,观察比较行为学与脑组织形态学的变化。结果：（1）实验组枕大池和蛛网膜下腔内发现大量的血凝块和血液。（2）实验组光镜下可观察到蛛网膜下腔大量红细胞,神经元细胞水肿,电镜下可见胶质细胞空泡样改变,神经元细胞线粒体肿胀,髓鞘内存在空泡和板层分离现象。（3）实验组造模后均出现明显的神经系统损伤,对照组4h出现典型神经系统损伤表现,12h后恢复正常,空白组未见神经系统损伤表现。结论：枕大池一次注血法是一种简便、可重复的症状性自发性蛛网膜下腔出血早期脑损伤模型,适宜于研究早期脑损伤的致病机制。     

Formulation,Optimization, Characterization,and Pharmacokinetics of Progesterone Intravenous Lipid Emulsion for Traumatic Brain Injury Therapy

Traumatic brain injury (TBI) is a major cause of mortality and disability throughout the world. Progesterone (PROG) plays an important role in neurologic treatment. The aim of this study was to develop a progesterone formulation with good physical and chemical stability. Progesterone intravenous lipid emulsion (PILE) was prepared based on one-factor-at-a-time experiments and orthogonal design. The optimal PILE was evaluated for mean particle size, particle size distribution, zeta potential, morphology, pH, osmolarity, entrapment efficiency, storage stability, and pharmacokinetics in ICR mice compared with the commercial progesterone products. The droplets of PILE had the smallest possible diameters of 218.0?±?1.8 nm and adequate zeta potential of ?41.1?±?0.9 mV. The volume percentage of droplets exceeding 5 μm (PFAT₅) of PILE was 0.003?±?0.0015% and much less than the specified standard. The TEM imaging proved that emulsion droplets had a smooth spherical appearance. Chemically and physically stable PILE was obtained with excellent entrapment efficiency that was up to 95.23%, with suitable pH at 7.15?±?0.01 and osmolarity at 301.3?±?1.2 mOsmol/l. Storage stability tests indicated that the emulsion was stable long term under ambient temperature conditions. Animal studies demonstrated that the emulsion was more effective with the higher progesterone concentration in the brain compared with commercial products. Therefore, the optimized PILE would offer great promise as a means of progesterone delivery for TBI therapy.     

Identification of Serum MicroRNA Signatures for Diagnosis of Mild Traumatic Brain Injury in a Closed Head Injury Model

Wars in Iraq and Afghanistan have highlighted the problems of diagnosis and treatment of mild traumatic brain injury (mTBI). MTBI is a heterogeneous injury that may lead to the development of neurological and behavioral disorders. In the absence of specific diagnostic markers, mTBI is often unnoticed or misdiagnosed. In this study, mice were induced with increasing levels of mTBI and microRNA (miRNA) changes in the serum were determined. MTBI was induced by varying weight and fall height of the impactor rod resulting in four different severity grades of the mTBI. Injuries were characterized as mild by assessing with the neurobehavioral severity scale-revised (NSS-R) at day 1 post injury. Open field locomotion and acoustic startle response showed behavioral and sensory motor deficits in 3 of the 4 injury groups at day 1 post injury. All of the animals recovered after day 1 with no significant neurobehavioral alteration by day 30 post injury. Serum microRNA (miRNA) profiles clearly differentiated injured from uninjured animals. Overall, the number of miRNAs that were significantly modulated in injured animals over the sham controls increased with the severity of the injury. Thirteen miRNAs were found to identify mTBI regardless of its severity within the mild spectrum of injury. Bioinformatics analyses revealed that the more severe brain injuries were associated with a greater number of miRNAs involved in brain related functions. The evaluation of serum miRNA may help to identify the severity of brain injury and the risk of developing adverse effects after TBI.     

Voluntary Alcohol Intake following Blast Exposure in a Rat Model of Mild Traumatic Brain Injury

Alcoholism is a frequent comorbidity following mild traumatic brain injury (mTBI), even in patients without a previous history of alcohol dependence. Despite this correlational relationship, the extent to which the neurological effects of mTBI contribute to the development of alcoholism is unknown. In this study, we used a rodent blast exposure model to investigate the relationship between mTBI and voluntary alcohol drinking in alcohol naïve rats. We have previously demonstrated in Sprague Dawley rats that blast exposure leads to microstructural abnormalities in the medial prefrontal cortex (mPFC) and other brain regions that progress from four to thirty days. The mPFC is a brain region implicated in alcoholism and drug addiction, although the impact of mTBI on drug reward and addiction using controlled models remains largely unexplored. Alcohol naïve Sprague Dawley rats were subjected to a blast model of mTBI (or sham conditions) and then tested in several common measures of voluntary alcohol intake. In a seven-week intermittent two-bottle choice alcohol drinking test, sham and blast exposed rats had comparable levels of alcohol intake. In a short access test session at the conclusion of the two-bottle test, blast rats fell into a bimodal distribution, and among high intake rats, blast treated animals had significantly elevated intake compared to shams. We found no effect of blast when rats were tested for an alcohol deprivation effect or compulsive drinking in a quinine adulteration test. Throughout the experiment, alcohol drinking was modest in both groups, consistent with other studies using Sprague Dawley rats. In conclusion, blast exposure had a minimal impact on overall alcohol intake in Sprague Dawley rats, although intake was increased in a subpopulation of blast animals in a short access session following intermittent access exposure.     

Mapping Spatiotemporal Microproteomics Landscape in Experimental Model of Traumatic Brain Injury Unveils a link to Parkinson's Disease,

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Highlights

• •Spatiotemporal microproteomics analysis of TBI.
• •Injury site microproteomics reveal distinct phases in 10-day frame post TBI.
• •Uninjured proteomic profile is restored in TBI at 10 days post injury.
• •Substantia nigra protein post 3 days suggest link to Parkinson's disease.