Traumatic Brain Injury
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2021 ◽  
Vol 150 ◽  
pp. 105173
Lauren D. Moss ◽  
Derek Sode ◽  
Rekha Patel ◽  
Ashley Lui ◽  
Charles Hudson ◽  

2021 ◽  
Vol 11 (12) ◽  
pp. 2321-2328
Zihuan Zeng ◽  
Hao Zhang ◽  
Jianwu Wu ◽  
Liangfeng Wei ◽  
Weiqiang Chen ◽  

To investigate the effect of mouse nerve growth factor (mNGF) on axonal injury after traumatic brain injury (TBI) combined with seawater drowning (SWD) in rats and the possible mechanism, we assigned 78 SD rats by random into sham group (Group A, n = 14), TBI+SWD group (Group B, n = 32), and mNGF group (Group C, n = 32). The compound injury model of rats was established by Marmarou method (450 g×1.5 m) and intratracheal pumping seawater (3 ml/kg). Rats in Group C were subject to intraperitoneal injection of mNGF (3 ug/kg) immediately after injury, and Group A as well as Group B were intraperitoneally injected the same amount of normal saline. Modified neurological severity scores(mNSS) was performed on rats at 12 h, 24 h, 72 h as well as 168 h, respectively after injury. HE staining showed that 24 h after injury, the swelling of nerve cells in Group C was relatively milder and the tissue edema was similar to that in Group B. At 72 h and 168 h after injury, the matrix looseness, cell swelling, and nuclear condensation in Group C were improved in comparison with Group B. (2) Compared with group B, mNSS of group C decreased signally at 72 h and 68 h after injury (P <0.05). (3) IHC staining showed that the protein expressions of β-APP, NF-L, and AQP4 were decreased in Group C in comparison with Group B at 12 h, 24 h, 72 h and 168 h after injury. (4) Brain water content in Group C was similar to that in Group B (P >0.05). (5) At 12 h after injury, the expression of TNF-α in Group C was signally lower than that in Group B (P < 0.05). Our reseache showed that mNGF might play a neuroprotective role by reducing cerebral edema and inflammatory response after TBI+SWD injury in rats, thereby restoring part of the injured axons in TBI+SWD rats.

2021 ◽  
Vol 11 (4) ◽  
pp. 396-403
Abraham Tsedalu Amare ◽  
Tadesse Dagget Tesfaye ◽  
Awole Seid Ali ◽  
Tamiru Alene Woelile ◽  
Tekalign Amera Birlie ◽  

2021 ◽  
Vol 154 ◽  
pp. 105805
J. Fortin ◽  
S. Grondin ◽  
S. Blanchet

2021 ◽  
Vol 9 (1) ◽  
Miguel A. Gama Sosa ◽  
Rita De Gasperi ◽  
Dylan Pryor ◽  
Georgina S. Perez Garcia ◽  
Gissel M. Perez ◽  

AbstractCerebral vascular injury as a consequence of blast-induced traumatic brain injury is primarily the result of blast wave-induced mechanical disruptions within the neurovascular unit. In rodent models of blast-induced traumatic brain injury, chronic vascular degenerative processes are associated with the development of an age-dependent post-traumatic stress disorder-like phenotype. To investigate the evolution of blast-induced chronic vascular degenerative changes, Long-Evans rats were blast-exposed (3 × 74.5 kPa) and their brains analyzed at different times post-exposure by X-ray microcomputed tomography, immunohistochemistry and electron microscopy. On microcomputed tomography scans, regional cerebral vascular attenuation or occlusion was observed as early as 48 h post-blast, and cerebral vascular disorganization was visible at 6 weeks and more accentuated at 13 months post-blast. Progression of the late-onset pathology was characterized by detachment of the endothelial and smooth muscle cellular elements from the neuropil due to degeneration and loss of arteriolar perivascular astrocytes. Development of this pathology was associated with vascular remodeling and neuroinflammation as increased levels of matrix metalloproteinases (MMP-2 and MMP-9), collagen type IV loss, and microglial activation were observed in the affected vasculature. Blast-induced chronic alterations within the neurovascular unit should affect cerebral blood circulation, glymphatic flow and intramural periarterial drainage, all of which may contribute to development of the blast-induced behavioral phenotype. Our results also identify astrocytic degeneration as a potential target for the development of therapies to treat blast-induced brain injury.

2021 ◽  
Vol 70 (41) ◽  
pp. 1447-1452
Jill Daugherty ◽  
Hong Zhou ◽  
Kelly Sarmiento ◽  
Dana Waltzman

2021 ◽  
Halle Quang ◽  
Skye McDonald ◽  
Phuong Huynh-Le ◽  
Tuong-Vu Nguyen ◽  
Ngoc-Anh Le ◽  

2021 ◽  
pp. 1-8
Bryon P. Jackson ◽  
Jason L. Sperry ◽  
Mark H. Yazer

<b><i>Background:</i></b> Early initiation of blood products transfusion after injury has been associated with improved patient outcomes following traumatic injury. The ability to transfuse patients’ plasma in the prehospital setting provides a prime opportunity to begin resuscitation with blood products earlier and with a more balanced plasma:RBC ratio than what has traditionally been done. Published studies on the use of prehospital plasma show a complex relationship between its use and improved survival. <b><i>Summary:</i></b> Examination of the literature shows that there may be a mortality benefit from the use of prehospital plasma, but that it may be limited to certain subgroups of trauma patients. The likelihood of realizing these survival benefits appears to be predicted by several factors including the type of injury, length of transport time, presence of traumatic brain injury, and total number of blood products transfused, whether the patient required only a few products or a massive transfusion. When taken as a whole the evidence appears to show that prehospital plasma may have a mortality benefit that is most clearly demonstrated in patients with blunt injuries, moderate transfusion requirements, traumatic brain injury, and/or transport time greater than 20 min, as well as those who demonstrate a certain cytokine expression profile. <b><i>Key Messages:</i></b> The evidence suggests that a targeted use of prehospital plasma will most likely maximize the benefits from the use of this limited resource. It is also possible that prehospital plasma may best be provided through whole blood as survival benefits were greatest in patients who received both prehospital plasma and RBCs.

2021 ◽  
Vol 23 (5) ◽  
Andrew Chen ◽  
Nidhi Sharoha

2021 ◽  
Tobias J. Krämer ◽  
Per Hübener ◽  
Bruno Pöttker ◽  
Christina Gölz ◽  
Axel Neulen ◽  

Abstract Traumatic brain injury (TBI) involves primary mechanical damage and delayed secondary damage caused by vascular dysfunction and neuroinflammation. Intracellular components released into the parenchyma and systemic circulation, termed danger-associated molecular patterns (DAMPs), are major drivers of vascular dysfunction and neuroinflammation. These DAMPs include cell-free RNAs (cfRNAs), which damage the blood–brain barrier (BBB), thereby promoting edema, procoagulatory processes, and infiltration of inflammatory cells. We tested the hypothesis that intraperitoneal injection of Ribonuclease-1 (RNase1, two doses of 20, 60, or 180 µg/kg) at 30 min and 12h after controlled-cortical-impact (CCI) can reduce secondary lesion expansion compared to vehicle treatment 24h and 120h post-CCI. The lowest total dose (40 µg/kg) was most effective at reducing lesion volume (−31% RNase 40µg/kg vs. vehicle), brain water accumulation (−5.5%), and loss of BBB integrity (−21.6%) at 24h post-CCI. RNase1 also reduced perilesional leukocyte recruitment (−53.3%) and microglial activation (−18.3%) at 120h post-CCI, but there was no difference in lesion volume at this time and no functional benefit. Treatment with RNase1 in the early phase following TBI stabilizes the BBB and impedes leukocyte immigration, thereby suppressing neuroinflammation. RNase1-treatment may be a novel approach to delay brain injury to extend the window for treatment opportunities after TBI.

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