Serum thyroid-stimulating hormone receptor antibody levels and thyroid dysfunction after hysterosalpingography: a case-control study.

OBJECTIVE: Hysterosalpingography (HSG) performed with an iodine contrast media can cause thyroid dysfunction, including thyrotoxicosis and hypothyroidism. We investigated the association between the serum levels of thyroid-stimulating hormone receptor antibody (TRAb), an indicator of Graves' disease, and abnormal thyroid function after performing HSG. METHODS: The screening of TRAb was conducted in 362 patients who first visited the Tawara IVF Clinic between April and September 2018. The association between TRAb levels and the effects of HSG examinations on thyroid function were evaluated. RESULTS: Of the 362 patients, 2 (0.55%) had high levels (>2.0 IU/L) of TRAb, whereas 18 (5.0%) had intermediate TRAb levels, ranging from 0.3 to 1.9 IU/L. Of the 98 women (including 7 of the 18 women with TRAb level 0.3-1.9 IU/L, and 91 of the 342 women with TRAb level <0.3 IU/L) who had undergone HSG, two women developed overt thyrotoxicosis after HSG, and the frequency was significantly higher (p = .0044) in the group with intermediate levels of TRAb (28.6%, 2 of 7) than that in the group with low TRAb levels (<0.3 IU/L; 0.0%, 0 of 91). CONCLUSIONS: These findings indicate that increased serum levels of TRAb are significantly associated with the development of thyrotoxicosis after HSG.

Nickel ion inhibits nuclear factor-kappa B activity in human oral squamous cell carcinoma.

BACKGROUND: The spontaneous IL-8 secretion observed in OSCC is partially dependent on the disregulated activity of transcription factor NF-κB. Nickel compounds are well established human carcinogens, however, little is known about the influence of nickel on the spontaneous secretion of IL-8 in oral squamous cell carcinoma (OSCC) cells. The aim of the present study was to investigate whether Ni(2+) ions can influence on IL-8 secretion by OSCC. METHODS AND RESULTS: The IL-8 secretion was measured by ELISA. The expression of IL-8 mRNA was examined by real-time PCR. The NF-κB activity was measured by luciferase assay. The phosphorylation status and nuclear localization of NF-κB subunits were examined by Western blotting or Transfactor kit and immunofluorescence staining, respectively. The interaction of NF-κB p50 subunit and Ni(2+) ions was examined by Ni(2+)-column pull down assay. The site-directed mutagenesis was used to generate a series of p50 mutants. Scratch motility assay was used to monitor the cell mobility. Our results demonstrated that, on the contrary to our expectations, Ni(2+) ions inhibited the spontaneous secretion of IL-8. As IL-8 reduction was observed in a transcriptional level, we performed the luciferase assay and the data indicated that Ni(2+) ions reduced the NF-κB activity. Measurement of p50 subunit in the nucleus and the immunofluorescence staining revealed that the inhibitory effect of Ni(2+) ions was attributed to the prevention of p50 subunit accumulation to the nucleus. By Ni(2+)-column pull down assay, Ni(2+) ions were shown to interact directly with His cluster in the N-terminus of p50 subunit. The inhibitory effect of Ni(2+) ions was reverted in the transfectant expressing the His cluster-deleted p50 mutant. Moreover, Ni(2+) ions inhibited the OSCC mobility in a dose dependent fashion. CONCLUSIONS: Taken together, inhibition of NF-κB activity by Ni(2+) ion might be a novel therapeutic strategy for the treatment of oral cancer.

Reduced production of polymeric immunoglobulin receptor in murine dextran sodium sulfate-induced colitis.

Polymeric immunoglobulin receptor (pIgR) plays an intrinsic role in protecting the intestinal tract from invading pathogens. In the present study, we observed a decrease in pIgR in colon lysate from mice with dextran sodium sulfate (DSS) colitis. A decrease in pIgR was detected in both mRNA and protein levels. Histologic examinations revealed marked destruction of intestinal epithelial cells (IECs), and only a small number of regenerating IECs expressed pIgR. These results suggest that the decrease in pIgR was due to the destruction of IECs. Because activation of toll-like receptor 3 slows the progression of DSS colitis, we injected polyriboinosinic: polyribocytidylic acid (poly I:C) intraperitoneally and observed the correlation between pIgR level and severity of DSS colitis. Poly I:C markedly decreased progression of DSS colitis, and pIgR levels significantly recovered. Furthermore, we found that expressions of IFN-γ and TNF-α were higher in DSS colitis. These results indicate that the decrease in pIgR was not compensated for by increased expression of these cytokines. In sum, our findings show that pIgR levels vary according to the severity of DSS colitis and that these changes might be useful as a biomarker of the severity of inflammatory bowel disease.