Jian Zheng, Zhen Liu, Weishan Li, Jiaxin Tang, Dongwei Zhang, and Xiaobo Tang
Inflammation and apoptosis are two key factors contributing to secondary brain injury after intracerebral hemorrhage (ICH). The objective of this study was to evaluate the effects of lithium posttreatment on behavior, brain atrophy, inflammation, and perihematomal cell death. Furthermore, the authors aimed to determine the role of the pro-apoptotic glycogen synthase kinase-3β (GSK-3β) after experimental ICH.
Male Sprague-Dawley rats (n = 108) were subjected to intracerebral infusion of semicoagulated autologous blood. Window of opportunity and dose optimization studies of lithium on ICH-induced injury were performed by measuring neurological deficits. Animals with ICH received vehicle administration or lithium posttreatment (60 mg/kg) for up to 21 days. Hemispheric atrophy was evaluated. Perihematomal cell death was quantified through terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling (TUNEL). The number of myeloperoxidase (MPO)-positive neutrophils and OX42-positive microglia in the perihematomal areas were calculated. Western blotting was used for the quantification of GSK-3β, heat shock protein 70 (HSP70), nuclear factor-κB p65 (NF-κB p65), and cy-clooxygenase-2 (COX-2).
Lithium, at a dose of 60 mg/kg initiated from 2 hours after injury, exhibited the best effects of improving neurological outcomes 3, 5, 7, 14, 21, and 28 days after ICH, reduced the hemispheric atrophy at 42 days after surgery, and reduced the number of TUNEL-positive cells, MPO-positive neutrophils, and OX42-positive microglia in the perihematomal areas. Furthermore, lithium posttreatment modulated GSK-3β, increased HSP70, and decreased NF-κB p65 and COX-2 expression in the ipsilateral hemisphere.
Lithium posttreatment at a dose of 60 mg/kg, initiated beginning 2 hours after injury, improves functional and morphological outcomes, and inhibits inflammation and perihematomal cell death in a rat model of semicoagulated autologous blood ICH through inactivation of GSK-3β.
Qi Wang, Chi Wang, Xiaobo Zhang, Fanqi Hu, Wenhao Hu, Teng Li, Yan Wang, and Xuesong Zhang
The aim of this study was to investigate whether bone mineral density (BMD) measured in Hounsfield units (HUs) is correlated with proximal junctional failure (PJF).
A retrospective study of 104 patients with adult degenerative lumbar disease was performed. All patients underwent posterior instrumented fusion of 4 or more segments and were followed up for at least 2 years. Patients were divided into two groups on the basis of whether they had mechanical complications of PJF. Age, sex ratio, BMI, follow-up time, upper instrumented vertebra (UIV), lower instrumented vertebra, and vertebral body osteotomy were recorded. The spinopelvic parameters were measured on early postoperative radiographs. The HU value of L1 trabecular attenuation was measured on axial and sagittal CT scans. Statistical analysis was performed to compare the difference of continuous and categorical variables. Receiver operating characteristic (ROC) curve analysis was used to obtain attenuation thresholds. A Kaplan-Meier curve and log-rank test were used to analyze the differences in PJF-free survival. Multivariate analysis via a Cox proportional hazards model was used to analyze the risk factors.
The HU value of L1 trabecular attenuation in the PJF group was lower than that in the control group (p < 0.001). The spinopelvic parameter L4–S1 lordosis was significantly different between the groups (p = 0.033). ROC curve analysis determined an optimal threshold of 89.25 HUs (sensitivity = 78.3%, specificity = 80.2%, area under the ROC curve = 0.799). PJF-free survival significantly decreased in patients with L1 attenuation ≤ 89.25 HUs (p < 0.001, log-rank test). When L1 trabecular attenuation was ≤ 89.25 HUs, PJF-free survival in patients with the UIV at L2 was the lowest, compared with patients with their UIV at the thoracolumbar junction or above (p = 0.028, log-rank test).
HUs could provide important information for surgeons to make a treatment plan to prevent PJF. L1 trabecular attenuation ≤ 89.25 HUs measured by spinal CT scanning could predict the incidence of PJF. Under this condition, the UIV at L2 significantly increases the incidence of PJF.