Molecular Diagnosis: And using Ubiquitous Transcription Factor and MAPK to Recover Thyroid Cells of Hyperthyroidism and Heart

This study sought to explore the Molecular Diagnosis (MD) mechanism and Targets of the Treatment effects on cardiovascular disease (CVD) by studying the regulatory effects of NF – κB and MAPK triggered in hyperthyroidism. Researchers have proposed a new MD paradigm to resolve this problem, which combines Nanoparticles-Medicine (NPs-M) with synthetic biology tools to provide biocomputing equipment redesign. The recombinant adenovirus of the TSHR-A subunit was injected into the anterior tibial muscle of BALB/C mice to create a model. The hyperthyroidism of those mice was taken to ensure a primary cell. Immunohistochemistry, techniques, and divisions into the groups and the medicated serum group were identified as thyroid cells, in terms of excess thyroid hormone affects CVD. These triggered pathways induce the content and expression of hyperthyroidism ICAM-1, cytokines IL-6, and CXCL10. In comparison with the model group, the medicated serum group had a significant callback effect, and the medicated serum had a significant callback effect on IL-6 levels. These results demonstrated that the regulatory effect on MAPK, NF – κB, and other cell triggered pathways in CVD and graves’ disease (GD) hyperthyroidism. We speculate that it can regulate the occurrence and development of targets of the treatment effects on Disease by inhibiting the activation of MAPK and NF – κB cell pathways and the expression of downstream cytokines. Furthermore, the possible direction of the MAPK and NF – NF – B pathway in soleus heart failure rats.