JNK3 involvement in nerve cell apoptosis and neurofunctional recovery after traumatic brain injury

Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in celt apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1,3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.

Role of Xuesaitong in Amelioration of Neural Function and Alteration of Bax Expression in Rats with Brain Trauma

Traumatic brain injury (TBI) is one of the most common diseases in clinical neurosurgery characterized with high incidence rate, mortality and many complications. Objectives: The purpose of this study is to explore the roles of Xuesaitong in the therapeutic effect of brain trauma and alteration of expression in Bax, a kind of promoting apoptosis factor. Methods: The rat traumatic brain injury models were established by using modified free falling body impact method. Thereafter, Xuesaitong was employed to be administered to TBI rats, and NSS Score Rating Scale was used to evaluate the effect of Xuesaitong. Moreover, real-time PCR was used to detect the Bax expression changes before and after the Xuesaitong administration. Results: Xuesaitong could accelerate the neurofunctional recovery of TBI rats, accompanied by NSS Scores significant decrease. Simultaneously, it also could inhibit the expression of Bax factor. Conclusions: Xusaitong could markedly ameliorate TBI restoration, in which it promotes the neurofunctional recovery, and at the same time it inhibits the expression of Bax.

1 Case Clinical Report of Cranium Aggressive Fibromatosis and Literature Review

Objective: The purpose of this study is to explore the clinical characteristics and therapeutic methods of aggressive fibromatosis (AF) in skull. Methods: The clinical data and operative therapy of one case of aggressive fibromatosis in skull in our department were examined and reviewed. The associated literatures were reviewed and discussed. Results: It was indicated that the main manifestation of AF in skull was headache and skull tumor. There was prominent osteolytic destruction found in X-ray plain film for skull AF. And CT scanning showed that skull sclerotin was disorganized and inhomogeneous, with widen diploe. The skull fibromatosis constituted by fibroblasts and myofibroblas, which were mainly spindle-shaped without heteromorphism. Immunohistochemistry showed positive expression of β-catenin and Vim in these cells. The enlarged incision was adopted for the strategy of operation in this patient of skull AF. After follow-up, there was no recurrence of AF discovered. Conclusions: Skull AF is very rare in neurosurgical clinic. The clinical manifestation and iconography of AF were lack of specificity. Therefore, skull AF is hard to diagnose preoperatively. The effective diagnose is mainly dependant on histopathologic examination. As for treatment, operation is the most optimal method so far, which has a good therapeutic effect.