Patients with thyrotoxicosis had a normal circadian rhythm of ACTH and F,but the level of serum F was lower than controls due to excessive degradation.The responsiveness of ACTH to dexamet-hasone suppression or insulin hypoglycemic stimulation was normal.Whereas the circadian secretion of ACTH and F was also normal in patients with primary hypothyroidism,and the concentration of F was inreased with normal ACTH level.There were stunted responses of ACTH to suppressing and stimulating tests,which were thought to be due to the fact that the corticotropes were impaired by hypertrophy or hyperplasia of thyrotropes in primary hypothyroidism.

Objective To observe the effect of diabetes on the activation of kinin-system and the role of the system in development of diabetic nephropathy. Methods The TKA activation was measured and the function of kinin-system was changed by the antagonist of bradykinin B2 receptor-HOE 140 and kallikrein. Results The activation of TKA decreased sharply at 18 week in diabetic acts and was much lower than the levels of TKA at & week or in control rats (P

Objective To understand the trajectory and classification of adult body mass index(BMI)in Jiangsu Province.Methods Based on China Health and Nutrition Survey,this study used the linear mixed model tree to explore the trajectory and classification of BMI of people aged 18-65 in Jiangsu Province.Results The linear mixed model tree had 13 nodes and the depth was 6.The classification nodes were baseline BMI,average calorie intake and baseline age.Conclusion The linear mixed model tree can identify the trajectory of BMI and expand the research method of longitudinal data.

Metabolic reprogramming is a hallmark of cancer, including lung cancer. However, the exact underlying mechanism and therapeutic potential are largely unknown. Here we report that protein arginine methyltransferase 6 (PRMT6) is highly expressed in lung cancer and is required for cell metabolism, tumorigenicity, and cisplatin response of lung cancer. PRMT6 regulated the oxidative pentose phosphate pathway (PPP) flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phospho-gluconate dehydrogenase (6PGD) and α-enolase (ENO1). Furthermore, PRMT6 methylated R324 of 6PGD to enhancing its activity; while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate (2-PG) binding to ENO1, respectively. Lastly, targeting PRMT6 blocked the oxidative PPP flux, glycolysis pathway, and tumor growth, as well as enhanced the anti-tumor effects of cisplatin in lung cancer. Together, this study demonstrates that PRMT6 acts as a post-translational modification (PTM) regulator of glucose metabolism, which leads to the pathogenesis of lung cancer. It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.