VITAMIN A AND THE THYROID

High serum levels of thyroxine and triiodothyronine were observed in vitamin A-deficient rats. Thyrotropin (TSH) content of pituitary and Thyrotropin Releasing Hormone (TRH) content of hypothalamus were also raised. It is postulated that in vitamin A deficiency the negative feedback regulation of the brain by thyroid hormone is disturbed.     

Responsiveness of glycosyltransferases to thyrotropin in a serum-free culture of porcine thyroid cells

Administration of thyrotropin to porcine thyroid follicles, obtained in a serum-free chemically defined medium, provoked marked increases in the activities of several glycosyltransferases involved in protein N-glycosylation. The coincidence of these effects with a previously demonstrated enhancement of thyroglobulin production renders a relationship between these events likely. The most important stimulation was for peptide oligosaccharyltransferase (3-fold). Among the enzymes involved in the synthesis of the lipid oligosaccharide donor, Dol-P glycosyl- and mannosyltransferases were increased 1.5-fold, and Dol-P N-acetylglucosaminylphosphotransferase only 1.15-fold. As regards terminal glycosyltransferases, asialofetuin sialyltransferase was increased 2-fold and ovomucoid galactosyltransferase only 1.2-fold. There was a continuous release of the latter two enzymes into the culture medium.     

Autoimmune thyroiditis in 18q deletion syndrome

Deletion of a segment of the long arm of chromosome 18 causes characteristic physical features and mental retardation. Autoimmune disorders have been described with this syndrome in a limited number of reports. We describe 2 cases of autoimmune hypothyroidism in children with 18q deletion syndrome.     

Generation of a transgenic animal model of hyperthyroid Graves' disease

Graves' disease (GD) is an organ-specific autoimmune disease characterized by hyperthyroidism. Agonistic anti-thyrotropin receptor antibodies (thyroid-stimulating antibodies, TSAb), which mimic the thyrotropin (TSH) action, are thought to cause GD. The precise immunological mechanism of TSAb production, however, remains elusive. Previous immunization approaches using TSH receptor led to transient hyperthyroidism, but did not seem sufficient for comprehensive understanding of the development of autoimmune responses. To create GD-related autoimmunity in mice, we here generated TSAb-transgenic mice in which a patient-derived TSAb is expressed in B cells. Expression of the human TSAb in mice resulted in various manifestations of hyperthyroidism including increased free thyroxine levels with concomitantly decreased TSH levels, increased thyroid uptake of technetium pertechnetate, hyperthermia and thyroid hyperplasia. We found a correlation between the serum levels of human TSAb immunoglobulin and free thyroxine. In addition, conventional B cells expressing the TSAb were partially deleted in the periphery while B1 cells expressing the TSAb persisted and accumulated in the peritoneal cavity, a finding consistent with previous demonstrations that the maintenance of B1 cells plays an important role in the development of autoimmune diseases. Thus, our transgenic mouse may provide a novel and useful animal model for elucidating the pathogenesis and pathophysiology of GD.     

Cloning of cDNAs encoding the three pituitary glycoprotein hormone beta subunit precursor molecules in the Japanese toad,Bufo japonicus

Complementary DNAs encoding precursor molecules of the beta subunits of three pituitary glycoprotein hormones (LH, FSH, and TSH) of the Japanese toad (Bufo japonicus) were isolated and sequenced. Unexpectedly large numbers of single nucleotide substitutions were found in all three beta subunit cDNAs. The eight isolated LH beta precursor cDNA clones were classified into six forms of nucleotide sequence, with four nucleotide substitutions each in the apoprotein coding region and in the 3' untranslated region (UTR). In the deduced amino acid sequence, the LH beta subunit showed two forms with a single amino acid substitution. The seven isolated FSH beta subunit cDNAs were classified into two forms, which differed from each other at 11 positions in the 3' UTR. The six isolated TSH beta subunit clones were classified into four forms with 2 and 5 nucleotide substitutions in the signal peptide and apoprotein coding regions, respectively. However, all the substitutions in the apoprotein coding region were silent. The substitution in the signal peptide coding region could produce three forms of signal peptide. Amino acid sequence comparison revealed that the toad LH beta subunit is more similar to the fish GTH II beta subunit than to mammalian and avian LH beta subunits. We found that the toad LH beta subunit molecule is a partial chimera of LH and FSH; amino acid residues located in 36th to 42nd and 96th to 99th are identical or similar to those of not LH- but FSH-beta subunit in mammalian, whereas it is more similar to LH- than FSH-beta subunit in total. We also found that the toad FSH beta subunit is more similar to the fish GTH II beta subunit than to the fish GTH I beta subunit and that the toad TSH beta subunit is more similar to tetrapod TSH beta subunits than to fish TSH beta subunits.     

Alcohol decreases the nocturnal peak of TSH in healthy volunteers

Rationale Studies of ethanol's effects on TSH carried out during the daytime, when its secretion is at its nadir, do not reflect the true action of alcohol on TSH secretion since TSH peak occurs at night.Objective The present study investigated the effects of alcohol on the serum concentrations of TSH in healthy volunteers during a 26-h session.Methods The trial included a 26-h session during which alcohol was administered at a rate similar to that found in heavy drinkers, i.e. 256 g per day and a 26-h placebo session. Volunteers functioned as their own controls, and we controlled for masking effects in both sessions.Results The usual TSH circadian rhythm flattened during the alcohol session, and the usual peak in the middle of the night completely disappeared.Conclusion Alcohol dramatically decreased nocturnal TSH secretion in healthy volunteers.     

Differential effects of microsomal enzyme inducers on in vitro thyroxine (T(4)) and triiodothyronine (T(3)) glucuronidation.

Microsomal enzyme inducers that increase UDP-glucuronosyltransferase (UDP-GT) activity are suspected to affect the thyroid gland by increasing the glucuronidation of T(4), which reduces serum thyroxine (T(4)). In response to reduced serum T(4), serum thyroid-stimulating hormone (TSH) increases. However, not all microsomal enzyme inducers that reduce serum T(4) produce an increase in serum TSH. We have shown that serum TSH is increased the most in rats treated with the microsomal enzyme inducers phenobarbital (PB) or pregnenolone-16alpha-carbonitrile (PCN), whereas TSH is affected less in rats treated with 3-methylcholanthrene (3MC) and Aroclor 1254 (PCB). It is unclear why serum TSH is differentially affected by various microsomal enzyme inducers. We propose that the glucuronidation of T(3) might be the reason serum TSH is increased by some microsomal enzyme inducers but not by others. Male Sprague-Dawley rats were fed either a basal diet or a diet containing PB (at 300, 600, 1200, or 2400 ppm), PCN (at 200, 400, 800, or 1600 ppm), 3MC (at 50, 100, 200, or 400 ppm), or PCB (at 25, 50, 100, or 200 ppm) for 7 days; and T(4) and T(3) UDP-GT activities were then determined. T(4) UDP-GT activity was increased in rats treated with PB (120%), PCN (250 to 400%), 3MC (400 to 600%), or PCB (300 to 430%). In contrast, T(3) UDP-GT activity was increased in rats treated with PB (90%) or PCN (120 to 200%), whereas 3MC and PCB treatments did not have an appreciable effect. In conclusion, differential effects on T(3) glucuronosyltransferase activity were found in rats treated with microsomal enzyme inducers.     

HCG分泌与类甲亢关系的临床研究

目的　探讨妊娠早期HCG分泌与甲状腺功能的关系。方法　将 12 0例妊娠 6～ 12周孕妇分为单胎初产、单胎经产、双胎、妊娠剧吐四组 ,抽空腹肘静脉血 2ml采用酶联免疫吸附测定法观察T3 ,T4,TSH与HCG的关系及各组间HCG的定量关系。结果　单胎初产组 :T3 2 6 10 7± 1.2 8nmol L ,T416 0 .71± 4 8.16nmol L ,TSH 5 .14± 1.4 2nmol L ,HCG 4 997.5 0± 14 4 8.4 0nmol L ,单胎经产组 :T3 2 .4 8± 0 .6 1nmol L ,T416 0 .6 1± 5 0 .2 1nmol L ,TSH 5 .35± 1.4 0nmol L ,HCG 5 2 6 7.18± 10 84 .5 5nmol L ,双胎组 :T3 2 .10± 0 .6 6nmol L ,T416 8.11± 4 7.4 7nmol L ,TSH 4 .93± 1.4 2nmol L ,HCG 5 74 1.6 7± 1189.0 5nmol L ,妊娠剧吐组 :T3 2 .5 8± 1.5 3nmol L ,T4176 .2 5± 6 7.5 0nmol L ,TSH 4 .9179±0 .93nmol L ,HCG 6 0 35 .2 9± 12 6 4.85nmol L。结论　妊娠剧吐与双胎组中HCG与TSH呈相关性 ,双胎组HCG与T4有相关性 ,双胎与妊娠剧吐组HCG有差异。提示HCG对垂体 甲状腺轴有一定的调节作用。     

45岁以下出血性脑卒中患者血清水平动态变化对预后评估及影响因素分析

目的 探讨45岁以下出血性脑卒中患者人群血清FT3、FT4、TSH水平动态变化的流行病学特征,并对这些指标进行预后评估及影响因素分析.方法 选取2017年1月至2020年1月间,纳入成都市第六人民医院出血性脑卒中患者227例.收集并分析基线和随访12个月内预后(死亡,再出血,未见不良预后)相关信息;随访期间同时于治疗时...