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Objectives Undiagnosed osteoporosis may lead to severe complications after spinal surgery. This study aimed to construct and validate a radiomic signature based on CT scans to screen for lumbar spine osteoporosis. Methods Using a stratified random sample method, 386 vertebral bodies were randomly divided into a training set (n = 270) and a test set (n = 116). A total of 1040 radiomics features were automatically retracted from lumbar spine CT scans using the 3D slicer pyradiomics module, and a radiomic signature was created. The sensitivity, specificity, accuracy, and area under the receiver operating characteristic curve (AUC) of the Hounsfield and radiomics signature models were calculated. The AUCs of the two models were compared using the DeLong test. Their clinical usefulness was assessed using a decision curve analysis. Results Twelve features were chosen to establish the radiomic signature. The AUCs of the radiomics signature and Hounsfield models were 0.96 and 0.88 in the training set and 0.92 and 0.84 in the test set, respectively. According to the DeLong test, the AUCs of the two models were significantly different (p < 0.05). The radiomics signature model indicated a higher overall net benefit than the Hounsfield model, as determined by decision curve analysis. Conclusions The CT-based radiomic signature can differentiate patients with/without osteoporosis prior to lumbar spinal surgery. Without additional medical cost and radiation exposure, the radiomics method may provide valuable information facilitating surgical decision-making. Key Points • The goal of the study was to evaluate the efficacy of a radiomics signature model based on routine preoperative lumbar spine CT scans in screening osteoporosis. • The radiomics signature model demonstrated excellent prediction performance in both the training and test sets. • This radiomics method may provide valuable information and facilitate surgical decision-making without additional medical costs and radiation exposure.

ObjectBaicalein has been shown to offer neuroprotection in the ischemic brain, but its effect in subarachnoid hemorrhage (SAH) is unknown. The authors used a double-hemorrhage model to study the role of early baicalein treatment in SAH.MethodsSubarachnoid hemorrhage was induced in male Wistar rats through a repeat injection of autologous blood at a 48-hour interval. Rats subjected or not subjected to SAH received a 30-mg/kg baicalein injection 3 hours after SAH and daily for 6 consecutive days, and results were compared with those obtained in vehicle-treated control rats. Mortality of the rats was recorded. Neurological outcome was assessed daily. Cerebrospinal fluid dialysates were collected and examined for glutamate concentrations. Cerebral vasospasm (CVS), brain water content, neuron variability, expression of glutamate transporter–1 (GLT-1), immunoreactivity of astrocyte, and level of malondialdehyde, activities of superoxide dismutase (SOD), and catalase in brain tissues content were determined on post-SAH Day 7.ResultsMortality rate, neuronal degeneration, brain water content, and CVS were decreased and neurological function improved in the baicalein-treated rats. Baicalein increased astrocyte activity and preserved GLT-1, which attenuated the glutamate surge after SAH. Baicalein also provided antioxidative stress by preserving activities of SOD and catalase and decreased malondialdehydelevel after SAH. The glutamate, body weight, neurological scores, and glial fibrillary acidic protein activity were significantly correlated. The CVS was correlated with neuronal degeneration, and GLT-1 was correlated with oxidative stress.ConclusionsEarly baicalein treatment attenuated CVS and limited neurological injury following SAH. These data may indicate clinical utility for baicalein as an adjunct therapy to reduce brain injury and improve patient outcomes.

Allograft inflammatory factor-1 (AIF-1) plays an important role in various inflammatory conditions. Our previous study demonstrated that AIF-1 was over-expressed in the liver of BALB/c mice infected with Schistosoma japonicum and played significant role in the pathogenesis of schistosomiasis. The aim of this study was to focus on the effect of AIF-1 treatment on liver fibrosis and necrosis of BALB/c mice infected with S. japonicum. Seventy-two BALB/c mice were infected with cercariae of S. japonicum and then divided into three groups: AIF-1-treated group, saline-treated group, and control group. The vital signs, liver function, egg load, and hepatic pathological changes of the mice were assessed, and the levels of AIF-1 and TNF-α in the liver and spleen were measured at 5, 8, and 14 weeks postinfection. The treatment of AIF-1 on the mice infected with S. japonicum suppressed the expression of TNF-α and increased the effectiveness of AIF-1 in the liver and spleen at 14 weeks postinfection. Histopathological analysis and Masson trichrome staining for the liver tissues showed that the liver fibrosis and necrosis were alleviated previously compared with other infected mice at 14 weeks postinfection. The treatment of AIF-1 on the mice infected with S. japonicum can alleviate hepatic fibrosis and necrosis which indicate that AIF-1 use may prevent and cure the liver fibrosis.