Objective To study the value of upbuilding heartcare network in metabolic syndrome.Methods Body mass index,waist and breech circumference,waist hip ratio,blood pressure,fasting plasma glucose,lipid profile, plasma insulin,and urine albumin were determined.Various risk factors were assessed and intervention measures were made.Results Various risk factors in metabolic syndrome were decreased after treatment intervention for 3,6 months,1 and 2 years.Conclusion Taking integrated intervention measures with heartcarc network was significant for hygiene.

Members of the inhibitors of differentiation (Id) family of helix-loop-helix (HLH) proteins are known to play important roles in the proliferation and differentiation of many cell types. Thyroid-stimulating hormone (TSH) regulates proliferation and differentiation by activating TSH receptor (TSHR) in thyrocytes. In this study, we found that Id2, one of the Id family proteins, is a major target for regulation by TSH in FRTL-5 thyroid cells. TSH rapidly increases the Id2 mRNA level in FRTL-5 thyroid cells but the Id2 protein showed biphasic regulatory patterns, being transiently reduced and subsequently induced by TSH treatment. Transient reduction of Id2 protein was noted within 2 hr of TSH treatment and was mediated by proteasomal degradation. Moreover, reduced Id2 expression correlated with the activity of the phosphatidylinositol 3 kinase pathway, which is activated by TSH. Although TSH increases the activity of the Id2 promoter, TSH-induced activation of this promoter was independent of c-Myc. Id2 did not alter TTF-1- and Pax-8-mediated effects on the regulation of the Tg promoter. Thus, in summary, we found that TSH regulates Id2 expression, but that Id2 does not alter the expression of thyroid-specific genes, such as Tg, in FRTL-5 thyroid cells.
1-Phosphatidylinositol 3-Kinase/metabolism ; Animals ; Cattle ; Cell Differentiation ; Cell Proliferation ; *Gene Expression Regulation ; Inhibitor of Differentiation Protein 2/metabolism ; Insulin/metabolism ; Paired Box Transcription Factors/metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-myc/metabolism ; Rats ; Thyroglobulin/metabolism ; Thyroid Gland/*cytology ; Thyrotropin/*metabolism