Mitochondrial Cyclophilin D as a Potential Therapeutic Target for Ischemia-Induced Facial Palsy in Rats.

Many studies have demonstrated that ischemia could induce facial nerve (FN) injury. However, there is a lack of a suitable animal model for FN injury study and thus little knowledge is available about the precise mechanism for FN injury. The aims of this study were to establish a reliable FN injury model induced by blocking the petrosal artery and to investigate whether dysfunctional interaction between cyclophilin D (CypD) and mitochondrial permeability transition pore (MPTP) can mediate cell dysfunction in ischemic FN injury. The outcomes of ischemia-induced FN injury rat model were evaluated by behavioral assessment, histological observation, electrophysiology, and electron microscopy. Then the levels of CypD and protein that forms the MPTP were evaluated under the conditions with or without the treatment of Cyclosporin A (CsA), which has been found to disrupt MPTP through the binding of CypD. The blocking of petrosal artery caused significant facial palsy signs in the ischemia group but not in the sham group. Furthermore, ischemia can induce the dysfunction of facial nucleus neurons and destruction of the myelin sheath and increase the protein levels of CypD and MPTP protein compared with sham group. Interestingly, treatment with CsA significantly improved neurological function and reversed the ischemia-induced increase of CypD and MPTP proteins in ischemia group. These results demonstrated that blocking of petrosal artery in rats can induce FN injury and the mechanism may be related to the disruption of MPTP by CypD.

A predictive model for the risk of sepsis within 30 days of admission in patients with traumatic brain injury in the intensive care unit: a retrospective analysis based on MIMIC-IV database.

PURPOSE: Traumatic brain injury (TBI) patients admitted to the intensive care unit (ICU) are at a high risk of infection and sepsis. However, there are few studies on predicting secondary sepsis in TBI patients in the ICU. This study aimed to build a prediction model for the risk of secondary sepsis in TBI patients in the ICU, and provide effective information for clinical diagnosis and treatment. METHODS: Using the MIMIC IV database version 2.0 (Medical Information Mart for Intensive Care IV), we searched data on TBI patients admitted to ICU and considered them as a study cohort. The extracted data included patient demographic information, laboratory indicators, complications, and other clinical data. The study cohort was divided into a training cohort and a validation cohort. In the training cohort, variables were screened by LASSO (Least absolute shrinkage and selection operator) regression and stepwise Logistic regression to assess the predictive ability of each feature on the incidence of patients. The screened variables were included in the final Logistic regression model. Finally, the decision curve, calibration curve, and receiver operating character (ROC) were used to test the performance of the model. RESULTS: Finally, a total of 1167 patients were included in the study, and these patients were randomly divided into the training (N = 817) and validation (N = 350) cohorts at a ratio of 7:3. In the training cohort, seven features were identified as key predictors of secondary sepsis in TBI patients in the ICU, including acute kidney injury (AKI), anemia, invasive ventilation, GCS (Glasgow Coma Scale) score, lactic acid, and blood calcium level, which were included in the final model. The areas under the ROC curve in the training cohort and the validation cohort were 0.756 and 0.711, respectively. The calibration curve and ROC curve show that the model has favorable predictive accuracy, while the decision curve shows that the model has favorable clinical benefits with good and robust predictive efficiency. CONCLUSION: We have developed a nomogram model for predicting secondary sepsis in TBI patients admitted to the ICU, which can provide useful predictive information for clinical decision-making.

The Value of CD64 in the Early Diagnosis for Intracranial Infection After Craniocerebral Surgery.

PURPOSE: To investigate the value of CD64 in the early diagnosis of intracranial infection after craniocerebral surgery. METHODS: A total of 93 patients who met the inclusion and exclusion criteria after neurosurgery in Lianyungang First People's Hospital and Lianyungang Second People's Hospital were admitted and divided into experimental group with intracranial infection (n = 32) and uninfected control group (n = 61) according to the results of cerebrospinal fluid culture. We performed relevant statistical analysis, drew the receiver operating characteristic curve and calculated area under the curve (AUC). RESULTS: The sensitivity and specificity of the CD64, c-reactive protein (CRP), and white blood cell (WBC) counts were 84.38% and 86.89%, 78.13% and 75.41%, and 75.00% and 67.21%, respectively; the AUCs were 0.912, 0.858, and 0.851, respectively. Accuracy was the highest when the 3 diagnosis were combined, reaching 93.75%; the AUC could reach 0.948. CONCLUSIONS: Serum CD64, CRP, and WBC count in the diagnosis of intracranial infection after craniocerebral surgery were significant. CD64 was more valuable than the others. The diagnostic efficiency could be improved when CD64, CRP, and WBC count were combined.

Coactosin-Like Protein (COTL1) Promotes Glioblastoma (GBM) Growth in vitro and in vivo.

OBJECTIVE: To assess the expression levels of COTL1 in human GBM tissues and evaluate the potential involvement of COTL1 in cancer progression. METHODS: Bioinformation analysis was performed to evaluate COTL1 mRNA levels in GBM tissues and normal tissues, according to the TCGA database, and explore the effects on prognosis. Immunohistochemical (IHC) assays were performed to evaluate COTL1 expression in human GBM tissues and the clinical pathological analysis was performed. Colony formation and MTT assays were performed to evaluate the effects of COTL1 on GBM cell proliferation. Immunoblot assays were performed to detect the expression level of COTL1, Ki67, and PCNA. A xenograft model was developed in mice to assess the effects of COTL1 on tumor growth in vivo. RESULTS: We found COTL1 had an obvious high expression in human GBM tissues. The expression of COTL1 was related to recurrence (P=0.006**) and prognosis of patients with GBM. Our data further demonstrated COTL1 promoted cell proliferation in vitro and contributed to tumor growth of GBM cells in mice. CONCLUSION: We therefore identified a novel and promising therapeutic target for the treatment of GBM.