Glioma is the most common primary intracranial tumor. At present, the conventional treatment methods have limited effect and cannot significantly prolong the survival time of patients. Chemokine CCL2 is the most important member of the CC chemokine family, which can regulate glioma angiogenesis, immunosuppression, progression and invasion, and resistance to apoptosis. This article reviews the potential mechanism of CCL2 promoting the malignant progression of glioma, in order to provide new ideas and methods for the targeted therapy of glioma.

Objective:To explore the prognostic biomarkers of glioblastoma (GBM) in the tumor microenvironment (TME) and its function.Methods:A total of 169 GBM samples of 161 GBM patients were collected from the Cancer Genome Atlas (TCGA) database. ESTIMATE algorithm in R4.1.0 software was used to calculate the proportion of immune components and stromal components in TME, which were expressed as immune score and stromal score, respectively. According to the median value of the two scores, 169 GBM samples were divided into the high score group and the low score group, respectively, 84 each in each group (those whose scores were equal to the median were not involved in the grouping). The differentially expressed genes (DEG) [false discovery rate (FDR) < 0.05] between the high score group and the low score group of the two scores were obtained by using limma package, and the co-up-regulated and co-down-regulated DEG of the two scores were obtained by using Venn program. Based on the STRING database, the protein interaction (PPI) network of co-up-regulated and down-regulated DEG of immune score and stromal score was constructed, and the top 30 genes with connectivity were selected. Univariate Cox proportional hazard model analysis of overall survival (OS) of 161 GBM patients in the TCGA database was performed on co-up-regulated and down-regulated DEG between immune score and stromal score by using R4.1.0 software to obtain the DEG affecting OS. The intersection of the DEG obtained from PPI analysis and Cox analysis was taken as the prognostic core genes. According to the median expression value of prognostic core genes in GBM samples from the TCGA database, 161 patients were divided into prognostic core genes high expression group and low expression group (patients whose scores were equal to the median were not involved in the grouping), with 80 cases in each group. Kaplan-Meier survival analysis of OS was performed by using R4.1.0 software. GSEA 4.2.1 software was used to perform gene set enrichment analysis (GSEA) on all genes with transcriptome data of GBM patients in the two groups of the TCGA databases, and the main enriched functions of the two groups of genes were obtained. The CIBERSORT algorithm was used to test the accuracy of the proportion of tumor infiltrating immune cell (TIC) subsets in 169 GBM samples from the TCGA database, and 57 GBM samples were finally obtained. Immune cells with differential expression levels and immune cells related to the expression of prognostic core genes among the samples with different expression levels of prognostic core genes were analyzed; Venn program was used to obtain the intersection of immune cells with differential levels and related immune cells, and differentially expressed TIC related to expressions of prognostic core genes in GBM were obtained.Results:Based on the immune score and stromal score of GBM samples in the TCGA database, a total of 693 co-up-regulated and co-down-regulated DEG of both scores were screened out. After the intersection of 78 DEG related to OS obtained by univariate Cox regression analysis and 30 DEG obtained by PPI network results, CC motif chemokine receptor 2 (CCR2) was identified as the prognostic core gene ( HR = 1.294, 95% CI 1.060-1.579, P = 0.011). GBM patients with CCR2 high expression had worse OS compared with those with CCR2 low expression ( P = 0.009). GSEA analysis showed that genes in the CCR2 high expression group were mainly enriched in immune-related pathways, while genes in the CCR2 low expression group were mainly enriched in metabolism-related pathways. Among 57 screened GBM samples, there were differences in the levels of 3 immune cells between the CCR2 high expression group and the CCR2 low expression group ( P < 0.05). CCR2 expression was correlated with the levels of 9 immune cells (all P < 0.05). Venn program analysis showed that differentially expressed 3 TIC in GBM related to CCR2 gene expression were obtained; among them, M2 macrophages were positively correlated with CCR2 expression, while T follicular helper cell and activated NK cells were negatively correlated with CCR2 expression. Conclusions:CCR2 may be the core gene related to the prognosis in the TME of GBM. As reference, the level of CCR2 can help to predict the status of TME and prognosis in GBM patients, which is expected to provide a new direction for the treatment of GBM.

Objective To investigate the role of microRNA?96?5p in the proliferation and invasion of gastric cancer cells and its molecular mechanism. Methods From June 2015 to January 2017, 53 resected specimens were collected. The transcriptional levels of microRNA?96?5p and forkhead box Q1 (FoxQ1) in gastric cancer tissues and the matched para?cancerous tissues were quantified by quantitative real?time PCR (qRT?PCR). The expression of FoxQ1 protein was also detected by immunohistochemistry (IHC). The relationship between microRNA?96?5p expression and the clinicopathological features of gastric cancer and its correlation with FoxQ1 expression were analyzed. The expressions of miRNA?96?5p in gastric cancer tissue and adjacent normal tissue were detected by qRT?PCR. miRNA?96?5p mimics was transfected to BGC?823 gastric cancer cells. The effects of miRNA?96?5p on cell proliferation and invasion were detected by cell counting kit?8 (CCK?8) assay and Transwell assay, respectively. The protein expressions of FoxQ1, E?cadherin and vimentin were determined by western blot. The relationship between FoxQ1 and miRNA?96?5p expressed in BGC?823 cells was detected by dual?luciferase reporter assay. Results The median expression of miRNA?96?5p in gastric cancer tissue was 1.05, significantly lower than 3.23 of para?cancerous tissues (P＜0.05).The positive rate of FoxQ1 expression in gastric cancer tissue was 71.7%, significantly higher than 28.3% of para?cancerous tissues ( P＜0.05). The expression of FoxQ1 was negatively corelated with the level of miRNA?96?5p (r＝－0.613, P＝0.006). The expression of miRNA?96?5p in gastric cancer cell BGC?823 was significantly decreased compared with normal gastric epithelial cell (0.96±0.08 vs 2.84± 0.15, P＜0.05). The results of CCK?8 assay and Transwell assay showed that overexpression of miRNA?96?5p significantly reduced the proliferation and invasion abilities of gastric cancer cells ( P＜ 0.05 ). Overexpression of miRNA?96?5p decreased the protein level of FoxQ1. Moreover, it upregulated the expression of E?cadherin and downregulated the expression of vimentin. The result of dual?luciferase?3′?UTR reporter assay confirmed that miRNA?96?5p binds to the 3′UTR of FoxQ1. Conclusion miRNA?96?5p may suppress the proliferation, migration and epithelial?mesenchymal transition (EMT) of gastric cancer cell by down?regulation of FoxQ1.

Objective To investigate the role of microRNA?96?5p in the proliferation and invasion of gastric cancer cells and its molecular mechanism. Methods From June 2015 to January 2017, 53 resected specimens were collected. The transcriptional levels of microRNA?96?5p and forkhead box Q1 (FoxQ1) in gastric cancer tissues and the matched para?cancerous tissues were quantified by quantitative real?time PCR (qRT?PCR). The expression of FoxQ1 protein was also detected by immunohistochemistry (IHC). The relationship between microRNA?96?5p expression and the clinicopathological features of gastric cancer and its correlation with FoxQ1 expression were analyzed. The expressions of miRNA?96?5p in gastric cancer tissue and adjacent normal tissue were detected by qRT?PCR. miRNA?96?5p mimics was transfected to BGC?823 gastric cancer cells. The effects of miRNA?96?5p on cell proliferation and invasion were detected by cell counting kit?8 (CCK?8) assay and Transwell assay, respectively. The protein expressions of FoxQ1, E?cadherin and vimentin were determined by western blot. The relationship between FoxQ1 and miRNA?96?5p expressed in BGC?823 cells was detected by dual?luciferase reporter assay. Results The median expression of miRNA?96?5p in gastric cancer tissue was 1.05, significantly lower than 3.23 of para?cancerous tissues (P＜0.05).The positive rate of FoxQ1 expression in gastric cancer tissue was 71.7%, significantly higher than 28.3% of para?cancerous tissues ( P＜0.05). The expression of FoxQ1 was negatively corelated with the level of miRNA?96?5p (r＝－0.613, P＝0.006). The expression of miRNA?96?5p in gastric cancer cell BGC?823 was significantly decreased compared with normal gastric epithelial cell (0.96±0.08 vs 2.84± 0.15, P＜0.05). The results of CCK?8 assay and Transwell assay showed that overexpression of miRNA?96?5p significantly reduced the proliferation and invasion abilities of gastric cancer cells ( P＜ 0.05 ). Overexpression of miRNA?96?5p decreased the protein level of FoxQ1. Moreover, it upregulated the expression of E?cadherin and downregulated the expression of vimentin. The result of dual?luciferase?3′?UTR reporter assay confirmed that miRNA?96?5p binds to the 3′UTR of FoxQ1. Conclusion miRNA?96?5p may suppress the proliferation, migration and epithelial?mesenchymal transition (EMT) of gastric cancer cell by down?regulation of FoxQ1.

Objective:To investigate the status and influencing factors of skin cleaning outside wound (hereinafter referred to as skin) in adult trauma patients.Methods:A multicenter cross-sectional investigation was conducted. From September 1 to 30, 2020, a total of 952 adult trauma patients who met the inclusion criteria were admitted to wound care clinics or trauma surgery wards of 13 military or local Grade Ⅲ Level A hospitals, including the General Hospital of the Eastern Theater Command of People's Liberation Army and the Army Medical Center, etc. A self-designed questionnaire on cleaning status of skin in trauma patients was released through the "questionnaire star" website to investigate basic information such as gender, age, education level, living status, and self-care ability, trauma information such as cause of injury, wound duration, trauma site, trauma depth, wound pain, wound peculiar smell, and wound cleaning solution, and skin cleaning status after injury such as whether to clean or not, cleaning method, cleaning frequency, cleaning duration in each time, or reasons for not cleaning. The patients who cleaned skin regularly after injury were included in cleaning group, and the other patients were included in no cleaning group. The basic information, trauma information, and skin cleaning status after injury of patients in 2 groups were investigated. Data were statistically analyzed with chi-square test, and binary multivariate logistic regression analysis was performed on indicators with statistically significant differences between the two groups to screen the independent influencing factors of skin cleaning in trauma patients.Results:A total of 952 questionnaires were received, and the recovery rate was 100%. Three invalid questionnaires were eliminated, and 949 valid questionnaires were obtained, with an effective rate of 99.68%. In 949 patients, there were 461 (48.6%) males and 488 (51.4%) females, aged 18-100 (50±18) years. Most patients were less than 60 years old, lived with their families, and could take care of themselves completely. Nearly half of the patients were with junior high school or below education level. The main causes of injury were sharp cutting injury and falling injury, the wound duration was 2-365 days, most of the injured parts were limbs and trunk, the wound depth was mostly full-thickness injury, and most patients had wound-related pain and no peculiar smell and used 5 g/L iodophor to clean the wound. Totally 684 (72.1%) patients cleaned their skin after injury, mainly by scrubbing with warm water, the cleaning frequency was mainly once or twice a week, and the cleaning time was mainly 10 or 15 min for each time. Totally 265 (27.9%) patients didn't clean their skin after injury, and the main causes for not cleaning were following the doctor's advice, followed by worrying about wound infection and loss of self-care ability. There were significantly statistical differences in constituent ratios of education level, self-care ability, cause of injury, wound pain, and wound peculiar smell of patients in 2 groups ( χ2=12.365, 24.519, 22.820, 9.572, 92.342, P<0.01). Education level, self-care ability, cause of injury, wound pain, and wound peculiar smell were potential influencing factors of skin cleaning in patients. Binary multivariate logistic regression analysis showed that self-care ability, wound pain, and wound peculiar smell were independent influencing factors of skin cleaning in patients (odds ratio=1.51, 0.52, 3.72, 95% confidence interval=1.08-2.12, 0.42-0.89, 2.66-5.22, P<0.05 or P<0.01). Conclusions:Self-care ability, wound pain, and wound peculiar smell are independent influencing factors of skin cleaning in adult trauma patients.

Objective:To investigate the effect of inhibitory activity of high mobility group protein B1 (HMGB1), signal transduction and activator of transcription 3 (STAT3) on myocardial ischemia-reperfusion injury in rats.Methods:In vivo and in vitro models of MIRI were established. SD rats were randomly divided into a sham group, a model group, a glycyrrhizic acid group, and a NSC74859 group, with 6 rats in each group. Rats in the sham group were not ligation, and rats in the sham group and model group were not given medication. The rats in the glycyrrhizic acid group and the NSC74859 group were injected with HMGB1 antagonist glycyrrhizic acid or STAT3 inhibitor NSC74859 5 mg/kg in the tail vein at 12 h 30 min before ischemia/reperfusion and 30 min after ischemia, respectively. Left ventricular shortening fraction (FS) and left ventricular ejection fraction (EF) were evaluated by echocardiography, and apoptosis of cardiomyocytes was evaluated by hematoxylin-eosin (HE) and TUNEL staining. The expression levels of HMGB1, STAT3, and phosphorylated STAT3 (p-STAT3) were detected by real-time fluorescence quantitative PCR and Western Blot. The viability of H9C2 cells was determined by the MTS assay, intracellular ATP content was determined, and the mitochondrial membrane potential of H9C2 cells was measured by flow cytometry to evaluate the survival of cardiomyocytes. The action mode of HMGB1/STAT3 was studied by the immunoprecipitation method. The expression and migration of HMGB1/STAT3 in the nucleus and cytoplasm were detected by immunostaining. Results:After inhibiting the expression of HMGB1 or STAT3, EF and FS were increased, and immune infiltration and apoptosis of cardiomyocytes were decreased. Inhibition of HMGB1 expression could decrease the expression of STAT3, but inhibition of STAT3 expression didn’t affect the expression of HMGB1. Hypoxia could lead to increased expression of HMGB1 and p-STAT3, and decreased expression of STAT3. After 8 hours of hypoxia, the expression level of STAT3 suddenly increased. After reoxygenation, the expression of HMGB1 and STAT3 decreased, and the expression of p-STAT3 increased, but p-STAT3 (Ser 727) didn’t participate in this process. After ischemia-reperfusion injury, HMGB1 and STAT3 binded firmly in cardiomyocytes, but inhibition of STAT3 or HMGB1 weakened this binding. Inhibition of HMGB1 or STAT3 expression could reduce myocardial ischemia-reperfusion injury. The expression of HMGB1 in reoxygenated cardiomyocytes increased after hypoxia, and HMGB1 migrated from the nucleus to the cytoplasm.Conclusions:Inhibiting the activity of the HMGB1/STAT3 axis effectively reduces MIRI in rats.

Objective: To investigate the role of microRNA-96-5p in the proliferation and invasion of gastric cancer cells and its molecular mechanism. Methods: From June 2015 to January 2017, 53 resected specimens were collected. The transcriptional levels of microRNA-96-5p and forkhead box Q1 (FoxQ1) in gastric cancer tissues and the matched para-cancerous tissues were quantified by quantitative real-time PCR (qRT-PCR). The expression of FoxQ1 protein was also detected by immunohistochemistry (IHC). The relationship between microRNA-96-5p expression and the clinicopathological features of gastric cancer and its correlation with FoxQ1 expression were analyzed. The expressions of miRNA-96-5p in gastric cancer tissue and adjacent normal tissue were detected by qRT-PCR. miRNA-96-5p mimics was transfected to BGC-823 gastric cancer cells. The effects of miRNA-96-5p on cell proliferation and invasion were detected by cell counting kit-8 (CCK-8) assay and Transwell assay, respectively. The protein expressions of FoxQ1, E-cadherin and vimentin were determined by western blot. The relationship between FoxQ1 and miRNA-96-5p expressed in BGC-823 cells was detected by dual-luciferase reporter assay. Results: The median expression of miRNA-96-5p in gastric cancer tissue was 1.05, significantly lower than 3.23 of para-cancerous tissues (P<0.05). The positive rate of FoxQ1 expression in gastric cancer tissue was 71.7%, significantly higher than 28.3% of para-cancerous tissues (P<0.05). The expression of FoxQ1 was negatively corelated with the level of miRNA-96-5p (r=-0.613, P=0.006). The expression of miRNA-96-5p in gastric cancer cell BGC-823 was significantly decreased compared with normal gastric epithelial cell (0.96±0.08 vs 2.84±0.15, P<0.05). The results of CCK-8 assay and Transwell assay showed that overexpression of miRNA-96-5p significantly reduced the proliferation and invasion abilities of gastric cancer cells (P<0.05). Overexpression of miRNA-96-5p decreased the protein level of FoxQ1. Moreover, it upregulated the expression of E-cadherin and downregulated the expression of vimentin. The result of dual-luciferase-3′-UTR reporter assay confirmed that miRNA-96-5p binds to the 3′UTR of FoxQ1. Conclusion miRNA-96-5p may suppress the proliferation, migration and epithelial-mesenchymal transition (EMT) of gastric cancer cell by down-regulation of FoxQ1.

Traumatic supraorbital fissure syndrome (TSOFS) is a symptom complex caused by nerve entrapment in the supraorbital fissure after skull base trauma. If the compressed cranial nerve in the supraorbital fissure is not decompressed surgically, ptosis, diplopia and eye movement disorder may exist for a long time and seriously affect the patients′ quality of life. Since its overall incidence is not high, it is not familiarized with the majority of neurosurgeons and some TSOFS may be complicated with skull base vascular injury. If the supraorbital fissure surgery is performed without treatment of vascular injury, it may cause massive hemorrhage, and disability and even life-threatening in severe cases. At present, there is no consensus or guideline on the diagnosis and treatment of TSOFS that can be referred to both domestically and internationally. To improve the understanding of TSOFS among clinical physicians and establish standardized diagnosis and treatment plans, the Skull Base Trauma Group of the Neurorepair Professional Committee of the Chinese Medical Doctor Association, Neurotrauma Group of the Neurosurgery Branch of the Chinese Medical Association, Neurotrauma Group of the Traumatology Branch of the Chinese Medical Association, and Editorial Committee of Chinese Journal of Trauma organized relevant experts to formulate Chinese expert consensus on the diagnosis and treatment of traumatic supraorbital fissure syndrome ( version 2024) based on evidence of evidence-based medicine and clinical experience of diagnosis and treatment. This consensus puts forward 12 recommendations on the diagnosis, classification, treatment, efficacy evaluation and follow-up of TSOFS, aiming to provide references for neurosurgeons from hospitals of all levels to standardize the diagnosis and treatment of TSOFS.