The functional role of thyroid hormone (TH) in the cortex and hippocampus of mouse during neuronal development was investigated in this study. TH insufficiency showed a decrease in the expression of parvalbumin (PV) in the cortex and hippocampus of pups at postnatal day (PD) 14, while treatment with thyroxine from PD 0 to PD 14 ameliorated the PV loss. On the other hand, treatment with antithyroid agents in adulthood did not result in a decrease in the expression of PV in these areas. These results indicate the existence of a critical period of TH action during the early postnatal period. A decrease in MeCP2-positive neuronal nuclei was also observed in the cortical layers II–IV of the cerebral cortex. The brains were then stained with CUX1, a marker for cortical layers II–IV. In comparison with normal mice, CUX1 signals were decreased in the somatosensory cortex of the hypothyroid mice, and the total thickness of cortical layers II–IV of the mice was lower than that of normal mice. These results suggest that TH insufficiency during the perinatal period strongly and broadly affects neuronal development.
Renal cell carcinoma, which has clear cells in 70% of cases, has a high frequency of hematogenous distant metastases to lung, bone, liver, and other areas. Metastatic cancer accounts for 1 to 3% of malignant tumors in the stomatognathic region, and the metastasis of renal cell carcinoma to the oral mucosal tissue, though extremely rare, does occur. In addition, clear cells have been observed in some salivary gland cancers in the oral cavity. Therefore, the differential diagnosis of metastatic renal cell carcinoma and salivary gland cancer is important. This review discusses the differential diagnosis between metastatic renal cell carcinoma and malignant tumors of the salivary gland.
The [1,3]-nitrogen rearrangement reactions of O-aryl ketoximes were promoted by N-heterocyclic carbene (NHC)-copper catalysts and BF3·OEt2 as an additive, affording ortho-aminophenol derivatives in good yields. The reaction of substrates with...
Thyroid hormones play an important role in brain development, and thyroid hormone insufficiency during the perinatal period results in severe developmental delays. Perinatal thyroid hormone deficiency is clinically known as congenital hypothyroidism, which is caused by dysgenesis of the thyroid gland or low iodine intake. If the disorder is not diagnosed or not treated early, the neuronal architecture is perturbed by thyroid hormone insufficiency, and neuropathological findings, such as abnormal synapse formation, defects in neuronal migration, and impairment of myelination, are observed in the brains of such patients. Furthermore, the expression of psychiatric disorder-related molecules, especially parvalbumin, is significantly decreased by thyroid hormone insufficiency during the perinatal period. Animal experiments using hypothyroidism models display decreased parvalbumin expression and abnormal brain architecture, and these experimental results show reproducibility and stability. These basic studies reinforce the results of epidemiological studies, suggesting the relevance of thyroid dysfunction in psychiatric disorders. In this review, we discuss the disruption of brain function associated with congenital hypothyroidism from the perspective of basic and clinical research.
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