Hospital Acquired Pneumonia (HAP) is one of the most common complications and late causes of death in TBI patients. Targeted prevention and treatment of HAP are of great significance for improving the prognosis of TBI patients. In the previous clinical observation, we found that folic acid treatment for TBI patients has a good effect on preventing and treating HAP. We conducted this retrospective cohort study to demonstrate what we observed by selecting 293 TBI patients from two medical centers and analyzing their hospitalization data. The result showed that the incidence of HAP was significantly lower in TBI patients who received folic acid treatment (44.1% vs. 63.0%, p = 0.012). Multivariate logistic regression analysis showed that folic acid treatment was an independent protective factor for the occurrence of HAP in TBI patients (OR = 0.418, p = 0.031), especially in high-risk groups of HAP, such as the old (OR: 1.356 vs. 2.889), ICU (OR: 1.775 vs. 5.996) and severe TBI (OR: 0.975 vs. 5.424) patients. At the same time, cohort studies of HAP patients showed that folic acid also had a good effect on delaying the progression of HAP, such as reducing the chance of tracheotomy (26.1% vs. 50.8%, p = 0.041), and reduced the length of hospital stay (15 d vs. 19 d, p = 0.029) and ICU stay (5 d vs. 8 d, p = 0.046). Therefore, we believe that folic acid treatment in TBI patients has the potential for preventing and treating HAP, and it is worthy of further clinical research.

Glioma is the most common primary brain tumors and has a high recurrence and mortality rate after surgery. Most gliomas are of astrocytic origin. We recently demonstrated that Celsr2 is essential for injury-induced responses and functions of astrocytes, while its role in the development and treatment of gliomas remains unexplored. In this study, an increase of CELSR2 expression was identified in patient glioma samples and glioma cell lines, and higher levels of CELSR2 correlate with poorer patient survival as indicated by TCGA data. In cultured glioma cells, CELSR2 knockdown reduced proliferation and caused cell cycle arrest, which was further supported by proteomic analysis. CELSR2 knockdown inhibited Wnt/β-catenin signaling, and the effect could be reversed by activating β-catenin using GSK-3β inhibitor in glioma cells. WNT3A efficiently enhanced the proliferation of glioma cells and activated the downstream signaling, which were significantly compromised by CELSR2 knockdown. We developed magnetic nanoparticles loaded with CELSR2 -siRNA, which suppressed tumor growth in glioma-inoculated nude mice. In conclusion, CELSR2 positively regulates glioma development through WNT3A/β-catenin signaling and inhibiting CESLR2 is a novel therapeutic strategy for gliomas.