Titlebook: Syndromes of Hormone Resistance on the Hypothalamic-Pituitary-Thyroid Axis; Paolo Beck-Peccoz Textbook 2004 Kluwer Academic Publishers 200

渐变

Molecular Basis of Thyroid Hormone Action,sm of virtually all tissues (1–3). TH exerts its major effects at the genomic level, although it also may have activities at nongenomic sites such as the plasma membrane, cytoplasm, and mitochondrion. A general schema for TH effects on gene transcription is shown in Fig. 1.

ABASH

Ischemic-Stroke

,Learning from Nature’s Experiments on the Thyroid Hormone Receptor; X-Ray Structures of RTH Mutant oid hormone receptor-β (hTR β) genes. It is an uncommon disorder, but thyroid hormone receptor-β (hTR β) genes. It is an uncommon disorder, but nonetheless one that requires diagnosis by the physician to avoid mismanagement of the patient. Study of the syndrome has resulted in substantial insights i

faultfinder

Molecular Pathogenesis of Resistance to Thyroid Hormone,nd in turn, T4 and T3 regulate TRH and TSH production as part of a negative feedback loop. The feedback effects of thyroid hormones on TSH production are mediated by inhibition of hypothalamic TRH and pituitary TSHα and β subunit gene expression. Target genes which are induced by thyroid hormone inc

AMPLE

Syndromes of Resistance to Thyroid Hormone: Clinical Aspects,ponsiveness of target tissues to the action of thyroid hormones. Despite of the specific biochemical presentation, characterized by elevated thyroid hormone levels in the presence of detectable concentration of TSH, the resulting clinical phenotype is extremely variable. Early recognition of RTH is

高调

Resistance to Thyroid Hormone in the Absence of Mutations in the Thyroid Hormone Receptor Genes,nt thyroid hormone receptors (TR) ß molecules that interfere with the function of the normal TRß, thus resulting in a dominant mode of inheritance. RTH caused by . gene deletion, on the other hand, is inherited as a recessive trait. In as many as 15% of families, RTH manifests in the absence of a .

反话

MIRTH

Overstate

,Multi-Factorial Regulation of , Action of TRβ Mutants. Lessons Learned from RTH Mice with a Targeteβ (TRβ) gene locus ushered in an exciting opportunity to study the molecular basis of RTH (1). Indeed, shortly thereafter, a Pro453His mutation was identified in the TRβ gene of one kindred (2) and a Gly345rg mutation in another (3), establishing that mutations of the TRβ gene cause RTH. To date, ab

mendacity

The Effect of Vitamin A, Retinoids and Retinoid Receptors on the Hypothalamic-Pituitary-Thyroid Axih hyperthyroidism, were successfully treated with high dose of vitamin A (1) . When treated with vitamin A, these hyperthyroid patients had decreased symptoms of hyperthyroidism as well as decreased metabolic rate. Shadu and Brody studied this effect in euthyroid rats which were fed 30,000 IU of vit