Minocycline attenuates neuronal apoptosis and improves motor function after traumatic brain injury in rats.

Minocycline is a type of tetracycline antibiotic with broad-spectrum antibacterial activity that has been demonstrated to protect the brain against a series of central nervous system diseases. However, the precise mechanisms of these neuroprotective actions remain unknown. In the present study, we found that minocycline treatment significantly reduced HT22 cell apoptosis in a mechanical cell injury model. In addition, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining confirmed the neuroprotective effects of minocycline in vivo through the inhibition of apoptosis in a rat model of controlled cortical impact (CCI) brain injury. The western blotting analysis revealed that minocycline treatment significantly downregulated the pro-apoptotic proteins BAX and cleaved caspase-3 and upregulated the anti-apoptotic protein BCL-2. Furthermore, the beam-walking test showed that the administration of minocycline ameliorated traumatic brain injury (TBI)-induced deficits in motor function. Taken together, these findings suggested that minocycline attenuated neuronal apoptosis and improved motor function following TBI.

Take it seriously or not: postoperative pneumocephalus in CSDH patients?

Background: Pneumocephalus is a common finding after burr-hole drainage of chronic subdural hematoma (CSDH). Its effects have not been specifically studied.Methods: A retrospective analysis was performed in 140 patients with CSDH with single burr-hole drainage. The pre- and postoperative volumes of intracranial hematoma and the postoperative volume of pneumocephalus were calculated and analyzed with their relationships with Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS) scores.Results: The preoperative hematoma volume and the patient ages are positively correlated with the 1-day postoperative pneumocephalus volume (p < 0.001, p < 0.01). There is no correlation between postoperative pneumocephalus volume and GCS/GOS scores (p > 0.05) and there is no difference of GCS/GOS scores or CSDH recurrence rate between patients with and without pneumocephalus (p > 0.05). The age and the volume of 1-day postoperative pneumocephalus are positively correlated with the absorbing rate of pneumocephalus (p < 0.01, p < 0.001).Conclusions: The pneumocephalus at a certain range has no effect on the prognosis of patients with CSDH and requires no specific intervention due to its self-absorbing capacity in the normal progress after surgery.HighlightsNo correlation between postoperative pneumocephalus volume and GCS/GOS scores.No difference of GCS/GOS or recurrence between patients with pneumocephalus or not.Pneumocephalus at certain range has no effect on the prognosis of patients.

Serum caspase-cleaved cytokeratin-18 levels and outcomes after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: Cell apoptosis is involved in acute brain injury after aneurysmal subarachnoid hemorrhage (aSAH). The protein cytokeratin-18 (CK-18) is cleaved by the action of caspases during apoptosis, and the resulting fragments are released into the blood as caspase-cleaved CK (CCCK)-18. Our study examined the relationship between circulating CCCK-18 levels and long-term clinical outcomes among aSAH patients. METHODS: We recruited 128 aSAH patients and 128 controls (matched on age and sex). Serum was collected at admission to the emergency department. Unfavorable outcome was defined as the Glasgow Outcome Score scores of 1-3. After a 6-month follow-up period, outcomes were assessed using a logistic regression analyses. The prognostic predictive values were evaluated according to receiver operating curves analysis. RESULTS: aSAH patients had higher plasma CCCK-18 levels compared to controls (235.1 ± 86.8 U/L vs. 25.6 ± 23.4 U/L, P<0.001). CCCK-18 was independently associated with World Federation of Neurological Surgeons (WFNS) scores (t=4.460, P<0.001) and modified Fisher scores (t=3.781, P<0.001). Furthermore, CCCK-18 levels were markedly higher among patients with an unfavorable outcome and among non-survivors. CCCK-18 was yet identified as an independent prognostic predictor for mortality (odds ratio, 5.769; 95% confidence interval, 1.196-27.832; P=0.029) and unfavorable outcome (odds ratio, 4.909; 95% confidence interval, 1.521-15.838; P=0.008), as well as had similar predictive values for them compared with WFNS scores and modified Fisher scores. CONCLUSIONS: High circulating CCCK-18 levels were associated with injury severity and a poor clinical outcome after aSAH and CCCK-18 had the potential to be a good prognostic biomarker for aSAH.