The incidence of thyroid cancer has significantly increased in the past decade or so.The tumor tissues,stromal cells and immune cells that exist in thyroid cancer itself constitute the dynamic and changing tumor microenvironment of thyroid cancer.The tumor microenvironment plays a decisive role in the occurrence,development and treatment of thyroid cancer,among which B lymphocytes have received increasing attention.This review systematically summarizes the latest research progress of B lymphocytes in the tumor microenvironment of thyroid cancer,to better explore the characteristics of the tumor microenvironment of thyroid cancer.

The incidence of thyroid cancer has significantly increased in the past decade or so.The tumor tissues,stromal cells and immune cells that exist in thyroid cancer itself constitute the dynamic and changing tumor microenvironment of thyroid cancer.The tumor microenvironment plays a decisive role in the occurrence,development and treatment of thyroid cancer,among which B lymphocytes have received increasing attention.This review systematically summarizes the latest research progress of B lymphocytes in the tumor microenvironment of thyroid cancer,to better explore the characteristics of the tumor microenvironment of thyroid cancer.

Objective:To investigate the correlation between different serum uric acid (SUA) levels and impaired fasting glucose (IFG) in adults.Methods:From March 2019 to February 2020, 5006 adults in Wuxi area of Taihu Sanatorium in Jiangsu Province were selected as subjects. Quintile method was divided into the following five groups: Q1: SUA<270 μmol/L, Q2: 270 μmol/L SUA 318 μmol/L or less, Q3: 319 μmol/L ≤SUA≤360 μmol/L, Q4: 361 μmol/L SUA 410 μmol/L or less, and Q5: SUA>410 μmol/L. Correlation was analyzed by logistic analysis, with IFG as the outcome index, five SUA groups as the observation index, and gender, age, body mass index (BMI), blood lipid, and blood pressure as confounding factors. Three logistic regression analysis models were constructed to explore the relationship between different SUA level groups and IFG risk, as well as the influence of BMI on the risk correlation between SUA and IFG.Results:The BMI, DBP, FPG, TC, TG, and LDL-C all increased with the increase in SUA level; however, HDL-C gradually decreased with the increase in SUA level (P<0.01). The SUA levels among the five groups were positively correlated with fasting blood glucose level in the IFG group ( r=0.589, P<0.001). After adjusting for age, sex, and BMI, SUA level was strongly associated with fasting glucose in the IFG group ( r=0.534, P<0.001). After further adjustment for blood lipid and blood pressure, the correlation persisted ( r=0.523, P<0.001). With Q1 as the control group, the calculated OR values of IFG risk were 1.199, 2.660, 2.784 and 3.629, respectively. After further adjustment for various confounding factors, the calculated OR values of each group were 1.130, 2.389, 2.350 and 2.895, respectively. The IFG risk in the group with SUA level in the corresponding Q2 and Q5 groups was 1.13 times and 2.90 times higher, respectively, than that in the normal group, indicating that with the increase in SUA level, the IFG risk in the population increased. With the increase in BMI and SUA levels after BMI stratification, the mean fasting glucose level increased ( P<0.001). Conclusion:The SUA level and IFG risk are closely related. Increased SUA level increases IFG risk, and SUA and IFG are associated with weight gain, which should be paid attention to.

UbcH5c belongs to the ubiquitin-conjugating enzyme family and plays an important role in catalyzing ubiquitination during TNF---triggered NF-B activation. Therefore, UbcH5c is a potent therapeutic target for the treatment of inflammatory and autoimmune diseases induced by aberrant activation of NF-B. In this study, we established a stable expression system for recombinant UbcH5c and solved the crystal structure of UbcH5c belonging to space group P222with one molecule in the asymmetric unit. This study provides the basis for further study of UbcH5c including the design of UbcH5c inhibitors.