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hypothyroidism/proline
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Lack of effect of the TRH related dipeptide histidyl-proline diketopiperazine on TSH and PRL secretion in normal subjects, in patients with microprolactinomas and in primary hypothyroidism.
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We have studied the effects of the TRH related dipeptide histidyl-proline diketopiperazine [cyclo (His-Pro)] on basal and stimulated TSH and PRL secretion in normal volunteers, in patients with microprolactinomas and in patients with primary hypothyroidism. Cyclo (His-Pro), 400 micrograms
[Influence of experimental hypothyroidism on C-14-labeled proline incorporation in dental and bone tissues].
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Histidyl-proline diketopiperazine cyclo (His-Pro): measurement by radioimmunoassay in human blood in normal subjects and in patients with hyper- and hypothyroidism.
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A new PAX8 mutation causing congenital hypothyroidism in three generations of a family is associated with abnormalities in the urogenital tract.
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BACKGROUND
Although thyroid dysgenesis is the most common cause of congenital hypothyroidism (CH), its molecular basis remains largely elusive. Indeed, in only a minority of cases with thyroid dysgenesis (2%-3%) was it possible to identify an underlying genetic defect. The objective of this study
A novel mutation (Q40P) in PAX8 associated with congenital hypothyroidism and thyroid hypoplasia: evidence for phenotypic variability in mother and child.
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Congenital hypothyroidism associated with thyroid hypoplasia can be caused by several genetic defects, including mutations in the TSHbeta-subunit, the TSH receptor, the G(s)alpha-subunit, and the transcription factor PAX8. Four girls with sporadic congenital hypothyroidism and hypoplastic thyroid
A Novel Thyrotropin-Releasing Hormone Receptor Missense Mutation (P81R) in Central Congenital Hypothyroidism.
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BACKGROUND
Isolated central congenital hypothyroidism (CCH) is rare and evades diagnosis on TSH-based congenital hypothyroidism (CH) screening programs in the United Kingdom. Accordingly, genetic ascertainment facilitates diagnosis and treatment of familial cases. Recognized causes include TSH β
The influence of hyperthyroidism and hypothyroidism on the wound healing of experimental myocardial infarction in the rat.
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In hyperthyroid and hypothyroid rats myocardial infarction was produced by coronary artery ligature. At different times following the ligature the animals were given 3H-thymidine or 3H-proline. The following parameters were determined: the number of DNA- and tropocollagen-synthesizing
Identification of a structural requirement for thyroid Na+/I- symporter (NIS) function from analysis of a mutation that causes human congenital hypothyroidism.
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Patients with congenital lack of I transport do not accumulate I in their thyroids, often resulting in severe hypothyroidism. A single amino acid substitution in the thyroid Na+/I- symporter (NIS), proline replacing threonine at position 354 (T354P), was recently identified as the cause of this
Low prevalence of thyrotropin receptor mutations in a large series of subjects with sporadic and familial nonautoimmune subclinical hypothyroidism.
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Subclinical hypothyroidism of chronic autoimmune thyroiditis must be distinguished from the rare condition of thyroid resistance to TSH in which variable degrees of congenital insensitivity of the thyroid to a biologically active TSH molecule are present. We studied 42 subjects with slight to
Detection in human serum by radioimmunoassay of histidyl-proline diketopiperazine, a metabolite of thyrotropin-releasing hormone.
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Cyclo(His-Pro) is believed to be a metabolite of TRH. A specific antiserum directed against cyclo(His-Pro) was used to detect immunoreactive material in human serum. Gel filtration column chromatography was used to establish that cyclo(His-Pro)-like immunoreactivity was found not only in free form
Thyroid resistance to TSH complicated by autoimmune thyroiditis.
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In this report we describe a 47-yr-old woman who was referred to our department for elevated serum TSH associated with normal free thyroid hormone levels, suggesting subclinical hypothyroidism. When first seen she was clinically euthyroid, and her thyroid gland was normal in size both at palpation
16p13.11 microdeletion uncovers loss-of-function of a MYH11 missense variant in a patient with megacystis-microcolon-intestinal-hypoperistalsis syndrome.
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Megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS), a rare condition that affects smooth muscle cells, is caused by biallelic null alleles in MYH11. We report on a girl with MMIHS in addition to growth hormone deficiency, central hypothyroidism and a tonically dilated pupil with
The epidermal response to change in thyroid status.
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Epidermal dimensions, replication, and anabolic activity have been studied before and after treatment in 10 patients with thyrotoxicosis and 7 patients with hypothyroidism. Following treatment of thyrotoxicosis there was a significant decrease in epidermal thickness, and also in cell replication as
Thyrotropin-releasing hormone-degrading enzyme in human serum is classified as type II of pyroglutamyl aminopeptidase: influence of thyroid status.
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The characteristics of thyrotropin-releasing hormone (TRH)-degrading enzyme in human serum were studied. Serum was incubated in 0.1 M phosphate buffer containing [proline-3H]TRH at 37 degrees C. A thin layer chromatography analysis of TRH degradation did not show any radioactive peak located in an
Thyrotropin-releasing hormone and insulin release: in vitro studies with islets of normal and dysthyroid mice.
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Pancreatic islets contain large-quantities of thyrotropin-releasing hormone (TRH) and of its metabolite Histidyl-Proline diketopiperazine (Cyclo His-Pro). The effects of these two putative neurotransmitters on the pancreatic B-cell function have been evaluated in vitro, with islets of normal or
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