This study investigated the improvement and safety of intrathecal meropenem and vancomycin in the treatment of postoperative intracranial infection in patients with severe traumatic brain injury (STBI). A retrospective analysis was performed on 86 patients with intracranial infections after cranial trauma operation in Tai'an Traditional Chinese Medicine Hospital and Affiliated Hospital of Taishan Medical University from May 2004 to June 2017. The patients were divided into the control group (43 patients) and the experimental group (43 patients) according to the treatment. Patients in the control group were intravenously infused with vancomycin hydrochloride (1.0 g, Q12H) and meropenem (2.0 g, Q8H). After lumbar cistern drainage was performed for the release of cerebrospinal fluid (CSF), patients in the experimental group were slowly given vancomycin 20 mg. After the tube was flushed with 2 ml of 0.9% sodium chloride injection, the patients were slowly given meropenem 20 mg, bid. The clinical efficacy, cure time and treatment cost of patients in the two groups were observed. The adverse reactions and sequelae after 6 months of treatment were recorded. The response rate (RR) of patients in the experimental group was significantly higher than that in the control group (P<0.05). The cure time of patients in the experimental group was significantly lower than that in the control group (P<0.05). The treatment cost of patients in the experimental group was significantly lower than that in the control group (P<0.05). The incidence of adverse reactions of patients, incidence of sequelae of patients in the experimental group was significantly lower than that in the control group (P<0.05). Intrathecal meropenem and vancomycin is more effective than intravenous administration in the treatment of intracranial infection after craniotomy. It can significantly shorten the treatment time and reduce the treatment cost, with better safety.

BackgroundNon-small cell lung cancer (NSCLC) is the most common histological type of lung cancer, and brain metastasis (BM) is the most lethal complication of NSCLC. The predictive biomarkers and risk factors of asynchronous BM are still unknown.Materials and methodsA total of 203 patients with NSCLC were enrolled into our cohort and followed up. The clinicopathological factors such as tumor size, T stage, lymphatic invasion, metastasis and asynchronous BM were investigated. CCKAR expression in NSCLC and resected BM was assessed by IHC, and CCKAR mRNAs in NSCLC and para-tumor tissues were estimated by qRT-PCR. The correlations between CCKAR expression, BM and other clinicopathological factors were assessed by chi-square test, and prognostic significance of CCKAR was estimated by univariate and multivariate analyses.ResultsCCKAR was highly expressed in NSCLC tissues compared with para-tumor tissues. CCKAR expression in NSCLC was significantly associated with asynchronous BM. The BM percentages for NSCLC patients with low and high CCKAR were surprisingly 5.2% and 66.6%, respectively. CCKAR expression and BM were unfavorable factors predicting unfavorable outcome of NSCLC. Moreover, CCKAR expression in NSCLC was an independent risk factor of asynchronous BM.ConclusionsCCKAR is a prognostic biomarker of NSCLC. CCKAR expression in NSCLC is positively associated with asynchronous BM, and is a risk factor of asynchronous BM from NSCLC.

Background Glioma is the most prevalent brain tumors with extremely poor prognosis, but the prognostic biomarkers of high-grade (grade III and IV) gliomas (HGG) are still insufficient. Methods In our study, we investigated the expression of GPBAR1 in HGG by qRT-PCR and immunohistochemistry (IHC), and evaluated the clinical significance of GPBAR1 with univariate and multivariate analyses. By retrieving the data from TCGA, we screened the genes significantly associated with GPBAR1, and identified the correlation between GPBAR1 and MAFB. By experiments in vitro, we showed the pivotal role of MAFB in GPBAR1-induced proliferation of HGG. Results GPBAR1 expression in HGGs was significantly higher than that in normal brain tissues. GPBAR1 was an independent prognostic biomarker of HGG. GPBAR1 promoted the proliferation of HGG by inducing MAFB expression. MAFB was also a prognostic biomarker of HGG, and patients with co-expression of MAFB and GPBAR1 had worse prognosis. Conclusions GPBAR1 promoted the proliferation of HGG by inducing MAFB expression. Both GPBAR1 and MAFB were prognostic biomarkers of HGG, and patients with co-expression of MAFB and GPBAR1 had worse prognosis than those with only GPBAR1 or MAFB expression.