Efficacy of atorvastatin administration after surgery in patients with chronic subdural hematoma.

To explore the clinical efficacy of atorvastatin administration after surgery in patients with chronic subdural hematoma. We conducted a retrospective study to analyze the clinical data of patients with chronic subdural hematoma. Patients receiving atorvastatin treatment after surgery were divided into the study group while others were divided into the control group. As the primary outcome, we compared the hematoma recurrence rate. The secondary outcomes were the remaining volume of hematoma and the activities of daily living (Barthel index) score at 3 months after discharge. A total of 53 patients were included in the study: 30 patients in the study group (n = 30) and 23 patients in the control group (n = 23). The baseline clinical data were similar in the 2 groups (P > .05). Four patients had recurrence of hematoma in the study group, while 5 patients had recurrence of hematoma in the control group [4/30 (13.3%) versus 5/23 (21.7%), P = .661] at 3 months after discharge. The mean remaining volume of hematoma was 12.10 ±â€…8.80 mL in the study group and 17.30 ±â€…9.50 mL in the control group at 3 months after discharge, respectively. The remaining volume of hematoma in the study group was less than that in the control group (P = .045).The activities of daily living score in the study group were higher than those in the control group (97.83 ±â€…4.48 vs 94.78 ±â€…5.73, P = .034) at 3 months after discharge. Atorvastatin administration after surgery barely reduce the recurrence rate of chronic subdural hematoma, however, reduced the remaining volume of hematoma and improved neurological function.

Claudin 4 enhances the malignancy of glioma cells via NNAT/Wnt signaling.

Gliomas are the most common malignancies of the central nervous system and are associated with high mortality rates. However, the pathogenesis of gliomas is unclear. In this study, we show that elevated claudin-4 (CLDN4) levels in glioma tissues are associated with poor clinical outcomes. We found that upregulating the expression of CLND4 enhanced the proliferative and migratory capacities of glioma cells. Mechanistically, CLND4 upregulated Neuronatin (NNAT) by activating Wnt3A signaling, and aided in the progression of the glioma. Most importantly, our in vivo data demonstrated that CLND4 overexpression caused rapid tumor growth in mice injected with LN229 cells and reduced the survival of these mice. Our findings reveal that CLND4 modulates malignancy in glioma cells; targeting CLDN4 may open up new avenues for glioma treatment.