Journal of neurotrauma
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Journal of neurotrauma · Apr 2017
Leukemia Inhibitory Factor Contributed to Reactive Astrogliosis via activation of STAT3 signaling after Intracerebral Hemorrhage in Rats.
Reactive astrogliosis has occurred after intracerebral hemorrhage (ICH). Leukemia inhibitory factor (LIF) can act as a modulator for glial gene expression. Signal transducer and activator of transcription 3 (STAT3) is a critical regulator of reactive astrogliosis. ⋯ Moreover, LIF increased the number of PCNA+/GFAP+ nuclei and the expression of GFAP, LIFR, gp130, and p-STAT3. The number of PCNA+/ GFAP+ nuclei and GFAP protein levels were attenuated markedly after inhibition of p-STAT3. Together, these data suggest that LIF contributes to ICH-related reactive astrogliosis via activation of STAT3 signaling.
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Journal of neurotrauma · Apr 2017
Retracted PublicationSex And Age Differences In Epinephrine Mechanisms And Outcomes After Brain Injury.
Traumatic brain injury (TBI) is the leading cause of injury-related death in children, with boys and children <4 years of age having particularly poor outcomes. Cerebral autoregulation is often impaired after TBI, contributing to poor outcome. Cerebral perfusion pressure can be normalized by use of vasoactive agents. ⋯ Phosphorylated JNK MAPK was quantified by enzyme-linked immunosorbent assay (ELISA). Results show that EPI preserves autoregulation, prevents histopathology, and blocks phosphorylated JNK upregulation in newborn males and females and juvenile females but not juvenile males after TBI. These data indicate that EPI preserves cerebral autoregulation and limits histopathology after TBI through blockade of JNK in an age- and sex-dependent manner.
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Journal of neurotrauma · Apr 2017
Time-dependent effects of arginine-vasopressin V1 receptor inhibition on secondary brain damage after traumatic brain injury.
Arginine-vasopressin (AVP) V1 receptors are known to mediate brain edema formation after traumatic brain injury (TBI). So far, however, AVP V1 receptors were only inhibited by genetic deletion or prior to trauma. Therefore, the current study aimed to determine the therapeutic window of AVP V1 receptor antagonization after TBI. ⋯ Treatments initiated 6 h after TBI had no effect. The results of the current study demonstrate that inhibition of AVP V1 receptors improve outcome after experimental TBI when given within a clinically relevant time window. Therefore, AVP V1 receptors may represent a therapeutic target with clinical potential.
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Journal of neurotrauma · Apr 2017
Cognitive Deficits Post Traumatic Brain Injury and Their Association with Injury Severity and Gray Matter Volumes.
Traumatic brain injury (TBI) is known to have a substantial though highly variable impact on cognitive abilities. Due to the wide range of cognitive abilities among healthy individuals, an objective assessment of TBI-related cognitive loss requires an accurate measurement of pre-morbid cognitive performance. To address this problem, we recruited 50 adults who sustained a TBI and had performed a cognitive baseline assessment in adolescence as part of the aptitude tests mandated by the Israeli Defense Forces. ⋯ Mathematical reasoning was not affected by TBI. In the TBI patients, non-verbal abstract reasoning post-pre-injury change scores were negatively correlated with the volume of the insula. We conclude that access to pre-morbid neuropsychological data may have facilitated the discovery of the effects of mild TBI on abstract reasoning, as well as a significant correlation between TBI-related decline in this cognitive domain and the volume of the bilateral insula, both of which had not been appreciated in the past.