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context. To analyze the dynamic changes of serum thyrotrophin receptor antibody (TRAb) and thyroid peroxidase antibody (TPOAb) in Graves' disease (GD) patients before and after radioactive iodine (RAI) treatment and to investigate if TRAb and TPOAb play a role in the occurrence of early hypothyroidism after 131 I therapy for Graves' hyperthyroidism. subjects and methods. A total of 240 patients newly diagnosed with GD were selected to study. A clinical and laboratory assessment was performed before and at 3, 6, and 12 months after 131 I therapy. Chemiluminescent immunoassays were used to detect serum free triiodothyronine (FT3), free thyroxine (FT4), sensitive thyroid-stimulating hormone (TSH) and TPOAb concentration. Radio-receptor assay was used to measure serum TRAb concentration. According to the early onset of hypothyroidism in a year after RAI therapy, patients were divided into early hypothyroidism group (group A) and non-early hypothyroidism group (group B). Results. In both groups, serum TRAb and TPOAb increased at 3 months, reached the highest level at 6 months and returned to the baseline at 12 months after RAI therapy. TRAb showed a significant difference between the two groups at 6 months (P<0.01). Serum TPOAb in group A was higher than that in group B before and at 3, 6, 12 months after RAI therapy (P<0.05). conclusions. Serum TRAb and TPOAb are closely related to the occurrence of the early hypothyroidism, and play an important role in judging prognosis after 131 I treatment in Graves' disease.

Hyperlipidemia adversely affects bone metabolism, often resulting in compromised osseointegration and implant loss. In addition, genetic networks associated with osseointegration have been proposed. Serologically defined colon cancer antigen 3 (Sdccag3) is a novel endosomal protein that functions in actin cytoskeleton remodeling, protein trafficking and secretion, cytokinesis, and apoptosis, but its roles in the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and in implant osseointegration under hyperlipidemic conditions have not been uncovered. Here, we performed microarray and RNA sequencing analysis to determine the differential expression of the Sdccag3 gene and related noncoding RNAs (ncRNAs) and to assess the long noncoding RNA (lncRNA) MSTRG.97162.4-miR-193a-3p-Sdccag3 coexpression network in bone tissues within the region 0.5 mm around implants in hyperlipidemic rats. In this experiment, we found that Sdccag3 and the previously uncharacterized lncRNA-MSTRG.97162.4 were downregulated during hyperlipidemia, while miR-193a-3p was upregulated. Sdccag3 overexpression increased new trabecular formation, the bone volume/total volume (BV/TV) (1.24-fold), and bone-implant combination ratio (BIC%) (1.26-fold). An RNA pulldown experiment revealed that Sdccag3 protein targeted lncRNA-MSTRG.97162.4 nucleotides 361 to 389. In addition, lncRNA-MSTRG.97162.4 overexpression significantly enhanced Sdccag3 (2.78-fold) expression and increased BV/TV (1.45-fold) and BIC% (1.07-fold) at the bone-implant interface. Taken together, these findings indicate that Sdccag3 overexpression enhances implant osseointegration under hyperlipidemic conditions by binding to lncRNA-MSTRG.97162.4. Furthermore, miR-193a-3p overexpression inhibited lncRNA-MSTRG.97162.4 (0.63-fold) and Sdccag3 (0.88-fold) expression and induced poor implant osseointegration (BV/TV, 0.86-fold; BIC%, 0.82-fold), while miR-193a-3p downregulation produced the opposite results (lncRNA-MSTRG.97162.4, 10.69-fold; Sdccag3, 6.96-fold; BV/TV, 1.20-fold; BIC%, 1.26-fold). Therefore, our findings show that Sdccag3 promotes implant osseointegration, and its related lncRNA-MSTRG.97162.4 and miR-193a-3p play an important role in osseointegration during hyperlipidemia, which might be a promising therapeutic target for improving dental implantation success rates.