Tumor-associated macrophage (TAM) is a group of heterogeneous cells and a major component of inflammatory cells in the tumor microenvironment. Parts of these cells in gliomas are derived from central nervous system microglia and circulating monocytes, and have been implicated in angiogenesis, immunosuppression, tumor progression and invasion of gliomas. This article reviews the potential mechanisms of TAM promoting glioma development through various pathways to provide new possibilities for targeted therapy of gliomas.

Objective To investigate the effect of hyperuricemia (HUA) on nuclear factor-κB (NF-κB) in myocardial tissue,Mn superoxide dismutases (Mn-SOD) activity in mitochondria,cardiac function of rats with HUA.Methods Sixty SD male rats,including 30 young rats and 30 aged rats,were randomly divided into four groups:the young control group,the young HUA group,the aged control group and the aged HUA group.Fifteen rats were in each group.The HUA rat models were set up by lavage method with yeast extract and ethambutol.Left ventricular systolic pressure (LVSP),left ventricular end-diastolic pressure (LVEDP) and left ventricular pressure at the end of the rising and falling maximum velocity (+dp/dtmax) were determined by intubation in the left ventricle with cardiac catheter.Mn-SOD activity in the mitochondria of rat myocardial tissue was detected by chemical colorimetry.The expressions of NF-κB in rats myocardial tissue were measured by immunohistochemistry (IHC) and reverse transcription polymerase chain reaction (RT-PCR).Differences between groups were analyzed with One way analysis of variance,Student-Newman-Keuls q test was used to compare the mean of multiple samples.Results Hyperuricemia had no significant effect on the cardiac function of HUA groups (P＞0.05).But the gene and protein expression of NF-κB in myocardial tissue and Mn-SOD activity of mitochondria were impacted by HUA.Both the gene and protein expression of NF-κB and the activity of Mn-SOD in HUA groups were increased (F=85.428 4,120.683 0 and 398.228 3,P＜0.01).Furthermore,the increase of gene and protein expression of NF-κB and the Mn-SOD activity in rats myocardial tissue of young HUA group were higher than those in aged HUA group (q=6.818 6,10.693 6 and 18.877 9,P＜0.05).Conclusion Hyperuricemia may cause inflammation and increase oxygen free radicals in myocardial tissue on one hand,and it may reduce inflammation and protect the myocardial tissue by increasing the activity of Mn-SOD in myocardial mitochondria of HUA rats,and removing the oxygen free radicals on the other hand.The response to uric acid in young HUA group is stronger than that in the aged HUA group.

Objective To investigate the expression level of nuclear factor-kappa(NF-κB),substance P(SP)and aquaporin 4(AQP4)gene and the change of discharge frequency of pain sensitive neurons (PSN)in the ventral posteriolateral thalamic nucleus(VPL)of acute gout(AG)rats.The neuro-genic inflammation of AG was explored.Methods Forty-eight rats were randomly divided into two groups:the control group and the AG group. According to the time interval after injection of monosodiumurate(MSU)into the the unilateral ankle joint,the AG group was subdivided into seven groups,ie.0.5 hours group,2 hours group,6 hours group,12 hours group,24 hours group,48 hours group and 72 hours group.There were 6 rats in each group.After recording of the discharge frequency of PSN in rats VPL nucleus,the expression level of NF-κB,SP and AQP4 gene in the rats joint synovium were evaluated at mRNA level by PCR in above mentioned time.Results In the 0.5 hours group,the discharge frequency of PSN in the rats VPL nueleus and the expression level of SP gene in the rats joint synovium had increased immediately after the injection of MSU(P＜0.05).In the 6 hours group,they reached the peak level(P＜0.05),and in the 12 hours group,they began to decrease gradually(P＜0.05).In the 0.5 hours group,the expression level of NF-κB and AQP4 gene increased after the injection of MSU(P＜0.05).However,their peak level presented at the 12 hours(P＜0.05),and they decreaged after 24 hours(P＜0.05).The statistical analysis of correlation had shown that there were positive correlation among the expression level of NF-κB,substance P.AQP4 gene and the change of discharge frequency of PSN in the rats VPL nucleus.Conclusion The discharge frequency of PSN in the rats VPL and the expression level of SP gene in the rats ioint synovium can be used to evaluate the Severity of pain in the AG rats.The expression level of NF-κB and SP gene can reflect the severity of neurogenic intlammation.We can know the severity of edema of the joint synovium by detecting the expression level of AQP4 gene.Pain and neurogenic inflammation play an important role in the pathogenesis of AG.Combingelectrophysiology and biochemical technique can shade light on the pathogenesis of AG from different aspects.In the meantime,it may provide a new method for developing new drugs and new approaches for clinical treatment.

The application of biological technology and the deepening of tumor research have effectively improved the level of tumor diagnosis, treatment and clinical outcome prediction. However, the specific mechanisms of tumorigenesis and development are still unclear, and tumor drug resistance has also become an urgent problem that needs to be solved to improve the clinical outcome of patients. Considerable studies have shown that the extrachromosomal DNA (ecDNA) can promote tumorigenesis, development and drug resistance. EcDNA is a looser, rounded form of DNA with unique genetic properties that carry specific genes and regulatory elements. This paper will discuss the biological characteristics, tumor-promoting mechanisms and drug resistance-facilitating of ecDNA.

Vascular nutrition transmission is an irreplaceable factor in the process of tumor formation. Blocking or reducing the energy transmission pathway of tumor can effectively resist the development of tumor. There is a close relationship between JAK-STAT signaling pathway and angiogenesis, especially research on the relationship between this pathway and vascular endothelial growth factor (VEGF) signal has produced many results in recent years. This review summarizes the induction of angiogenesis, drug development, and the discovery of antiangiogenic targets in the JAK pathway, providing some ideas for the treatment of glioma.

Glioma is one of the most common and invasive malignant tumors in the central nervous system. The Wnt-β-catenin signaling pathway is a classical Wnt pathway, which is involved in the occurrence and development of glioma and other tumors. Long non-coding RNA (LncRNA) is a functional RNA molecule without protein coding function, which plays a regulatory role in the occurrence and development of various tumors. Recent studies have shown that LncRNA and Wnt-β-catenin signaling pathways are jointly involved in glioma growth, invasion, migration and other processes, but the complex mechanism has not been thoroughly elaborated. In this paper, the influence of Wnt-β-catenin signaling pathway and its related LncRNA on glioma was reviewed, and the pathogenesis of glioma was deeply understood, so as to find a better way for the diagnosis and treatment of glioma.

Objective To detect the changes of cellular immune level in patients with different grades of glioma in perioperative period, and to investigate its relationship with the postoperative intracranial infection. Methods A total of 53 patients with glioma newly diagnosed by pathology who underwent the surgical treatment in the First Hospital of Shanxi Medical University from September 2017 to September 2018 were collected. According to the World Health Organization (WHO) classification criteria, the patients were divided into the low-grade group (grade Ⅰ-Ⅱ, 21 cases) and the high-grade group (grade Ⅲ-Ⅳ, 32 cases). The peripheral blood at the time of 1 day before the operation, 1 day and 7 days after the operation was drawn to detect the T lymphocyte subsets, and then the differences of cell immunity indexes from different grade gliomas were analyzed. The relationship between immune level and postoperative intracranial infection was analyzed. SPSS 22.0 statistical software was used to analyze the data. Results The levels of CD3+, CD4+, CD8+, CD4+CD25+Foxp3+and CD4+/CD8+in the high-grade group at the time of 1 day before the operation were (54.09±4.25)％, (31.93±3.08)％, (34.23±2.48)％, (9.66±1.47)％, 0.93±0.06, respectively; the levels at the time of 1 day after the operation were (48.84±3.69)％, (27.49±2.41)％, (34.99±2.96)％, (11.09±1.70)％, 0.84± 0.05, respectively; the levels at the time of 7 days after the operation were (59.45 ±3.47)％, (33.59 ±2.66)％, (31.99±1.97)％, (7.45±1.48)％, 1.05±0.07, respectively. The levels of CD3+, CD4+, CD8+, CD4+CD25+Foxp3+and CD4+/CD8+in the low-grade group at the time of 1 day before the operation were (62.37±6.57)％, (34.88± 4.43)％, (30.16 ±3.75)％, (6.30 ±1.29)％, 1.16 ±0.11, respectively; the levels at the time of 1 day after the operation were (55.44 ±7.25)％, (29.05 ±4.04)％, (31.66 ±3.13)％, (7.95 ±1.67)％, 0.92 ±0.11, respectively; the levels at the time of 7 days after the operation were (67.73 ±7.18)％, (35.55 ±4.95)％, (28.10 ±3.12)％, (5.50 ± 1.25)％, 1.27±0.12, respectively. The levels of CD3+, CD4+, CD4+/CD8+before and after the operation in the high-grade group were lower than those in the low-grade group (all P< 0.05), while the levels of CD8+and CD4+CD25+Foxp3+were higher than those in the low-grade group (all P<0.05). Compared with the levels at the time of 1 day before the operation, the levels of CD3+, CD4+, CD4+/CD8+at the time of 1 day after the operation of both groups were decreased, while the levels of CD8+and CD4+CD25+Foxp3+were increased (all P< 0.05). The levels of CD3+, CD4+and CD4+/CD8+ at the time of 7 days after the operation in the both groups were increased, while the levels of CD8+ and CD4+ CD25+ Foxp3+ were decreased (all P< 0.05). Among 53 patients, 8 cases had postoperative intracranial infection, and the infection rate was 15.09％. Age, duration of surgery, pathological stage, and intraoperative blood transfusion were the independent affecting factors of postoperative intracranial infection of cerebral glioma (OR= 1.513, P= 0.024; OR= 1.722, P<0.01; OR= 1.365, P= 0.001; OR= 1.262, P< 0.01). Conclusions The peripheral blood cellular immune level of glioma patients is related with the malignancy of glioma. The inhibition degree of the cellular immunity could be relieved after the resection of glioma. The detection of T lymphocyte subsets could be considered as an evaluating index for the malignancy and prognosis in patients with glioma. The clinical detection of cellular immune can play a positive role in predicting and preventing the postoperative intracranial infection in patients with glioma.

Glioma is a common primary malignant brain neoplasms which is characterized with easy recurrence and poor prognosis. The overall survival of glioma patients is not satisfying. Tumor treating fields (TTFields) is an emerging low-toxicity treatment for solid neoplasms, and its technical basis is to form an anti-tumor electric field in a specific area. TTFields can inhibit the proliferation of tumor cells through inhibiting cell mitosis, replicating stress, inducing autophagy and apoptosis, and inhibiting DNA damage and repair, and induce the cell death without affecting normal cells in the resting phase. At present, TTFields has been approved for various types of gliomas and is gradually becoming an effective treatment protocol for glioma following surgery, radiotherapy and chemoradiotherapy. Many preclinical and clinical studies have confirmed that TTFields inhibits glioma cells and significantly increases the overall survival rates of patients.This paper reviews the progress of related researches.

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.

Heat shock protein 47 (HSP47) is mainly involved in regulating collagen folding, secretion and maturation in the tumor microenvironment (TME) and is widely amplified in human cancers. HSP47 has been shown to be overexpressed in a variety of extracranial tumors. In glioma, the expression of HSP47 correlates with the grading of glioma and is involved in proliferation, invasion, angiogenesis, and immune regulation of glioma, regulates the TME of glioma, and promotes the survival of glioma stem cells, which may be related to the heterogeneity of glioma. This article reviews the progress of HSP47 in the development and progression of glioma, and discusses the significances of HSP47 in the proliferation, invasion, targeted therapy and immunotherapy of glioma.