Thyroid : official journal of the American Thyroid Association
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Comparative Study
Differential regulation of the myosin heavy chain genes alpha and beta in rat atria and ventricles: role of antisense RNA.
The myosin heavy chain (MHC) genes are regulated by triiodothyronine (T3) in a reciprocal and chamber-specific manner. To further our understanding of the potential mechanisms involved, we determined the T3 responsiveness of the MHC genes, alpha and beta, and the beta-MHC antisense (AS) gene in the rat ventricles and atria. ⋯ In the hypothyroid rat heart ventricle, beta-MHC AS RNA expression increases in response to T3 similar to that of alpha-MHC. Simultaneous measures of beta-MHC sense RNA are decreased, suggesting a possible mechanism for AS to regulate sense expression. In atria, while alpha-MHC is not influenced by thyroid state, beta-MHC sense and AS RNA were simultaneously and inversely altered in response to T3. This confirms a close positive relationship between T3 and beta-MHC AS RNA in both the atria and ventricles, while demonstrating for the first time that alpha- and beta-MHC expression is not coupled in the atria.
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Surgeons may assume intuitively that preservation of a palsied recurrent laryngeal nerve (RLN) in patients with preoperative vocal cord paralysis is not meaningful. Here we present our experience in four cases with preoperative vocal cord paralysis, and show that preservation of a palsied RLN may be important in maintaining patients' voice. ⋯ Even on a palsied RLN, a positive electrophysiological response may still be yielded by intraoperative neuromonitoring. This means that there may retain residual innervations in laryngeal muscles. To prevent atrophy of a paralyzed vocal cord, further injury to a palsied RLN should be avoided. Even the palsied nerve should be saved whenever possible.
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Controlled Clinical Trial
Serial changes in liver function tests in patients with thyrotoxicosis induced by Graves' disease and painless thyroiditis.
When the liver function tests are aggravated after starting antithyroid drugs (ATDs) in Graves' hyperthyroidism, discontinuation of ATDs is generally considered. However, a question arises whether such aggravation constitutes an adverse effect of the drugs or not. ⋯ Similar serial changes in liver function tests in both Graves' disease and painless thyroiditis strongly suggest that increases of AST and ALT after starting ATD therapy may not be due to ATD side effects but may be induced by changes in thyroid function.