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The pullets of Indian Rhode Island Red (RIR) breed of domestic fowl were reared under a step-down photoperiod of LD 18:6 (long photoperiod; LP) from day 1 to day 90 post-hatch, and then shifted to LD 12:12 (NLD), to assess its effect on growth kinetics of lymphoid and reproductive organs, and serum hormone profiles, the observations were made at 30,60 and 90 days and the results were compared with pullets reared under NLD alone. The weights of thyroid and ovary in LP chicks showed significant increment, whereas the weights of liver and lymphoid organs were identical to that of NLD chicks. The weights of adrenal and oviduct decreased significantly. In general, serum levels of T3, T4, corticosterone and progesterone tended to show a gradual decrement with age in NLD chicks, but the LP chicks showed a differential change marked by high T3 and T4 levels throughout and, increased corticosterone and decreased progesterone levels at 30 and 60 days. Long photoperiod seems to have an initial depressive, but later stimulatory effect on growth of thyroid, while it has an Inhibitory effect on adrenal. The histometric data of ovary suggest a stimulatory effect of light, indicated by increased number of follicles and decreased degree of follicular atresia. It is concluded from the present observations that exposure of chicks to LP has differential effects on growth kinetics and, a favourable influence on reproductive hormones suggesting inherent photosensitivity and, no setting in of photorefractoriness during this period.

Objective — to study the role and place of psychosomatic disorders and thyroid hormones in the pathogenesis of the comorbid course of gastroesophageal reflux disease and autoimmune thyroiditis, considering, on the one hand, the relationship between the psycho-vegetative state and the level of thyroid hormones, and, on the other, the effect of thyroid hormones on acid-forming processes.Materials and metods. For the study two groups of patients have been taken. The first group consisted of 30 patients suffering from isolated GERD, the second included 27 patients suffering from GERD in combination with hypothyroidism caused by AIT. All patients underwent a comprehensive examination according to the protocols for the diagnosis and treatment of GERD and AIT. The determination of the psychosomatic status and quality of life was carried out using Shihan, Eysenck, GERD-Q and GIQLI questionnaires. Patients were questioned upon admission to the hospital and 2 weeks after standard treatment.Results and discussion. It was established that patients with GERD with concomitant AIT compared with patients with isolated GERD showed a significantly increased level of anxiety, neuroticism and a lower level of quality of life. A clear correlation has been established between the indices of the motor-secretory function of the gastrointestinal tract, the level of thyroid hormones, the quality of life of patients and the peculiarity of psychosomatic disorders in the clinical course and prognosis of GERD. Conclusions. The findings suggest the role of psychosomatic disorders in the pathogenesis of disorders of thyroid hormone production and the motor-secretory function of the esophagus and stomach, which has a great influence on the formation of GERD in combination with AIT., Цель работы — изучить роль и место психосоматических расстройств и тиреоидных гормонов в патогенезе коморбидного течения гастроэзофагеальной рефлюксной болезни (ГЭРБ) и аутоиммунного тиреоидита (АИТ), учитывая, с одной стороны, взаимосвязь между психовегетативным состоянием и уровнем гормонов щитовидной железы, а с другой, влияние гормонов щитовидной железы на процессы кислотообразования.Материалы и методы. В исследовании приняли участие две группы больных. Первая состояла из 30 пациентов, страдающих изолированной ГЭРБ, вторая включала 27 пациентов, страдающих ГЭРБ в сочетании с гипотиреозом, вызванным АИТ. Всем больным было проведено комплексное обследование согласно протоколам диагностики и лечения ГЭРБ и АИТ. Определение психосоматического статуса и качества жизни проводили с помощью опросников Шихана, Айзенка, GERD-Q и GIQLI. Пациенты проходили анкетирование при поступлении в стационар и через 2 нед после стандартного лечения.Результаты и обсуждение. Установлено, что у больных ГЭРБ с сопутствующим АИТ по сравнению с больными с изолированной ГЭРБ отмечался достоверно повышенный уровень тревожности, нейротизма и более низкий уровень качества жизни. Обнаружена четкая корреляционная зависимость между показателями моторно-секреторной функции желудочно-кишечного тракта, клиническим течением, уровнем гормонов щитовидной железы, качеством жизни пациентов и особенностью психосоматических расстройств у больных ГЭРБ с сопутствующим АИТ.Выводы. Полученные данные свидетельствуют о роли психосоматических расстройств в патогенезе нарушений выработки гормонов щитовидной железы и моторно-секреторной функции пищевода и желудка, что влияет на формирование ГЭРБ в сочетании с АИТ., Мета роботи — вивчити роль і місце психосоматичних розладів і тиреоїдних гормонів у патогенезі коморбідного перебігу гастроезофагеальної рефлюксної хвороби (ГЕРХ) і автоімунного тиреоїдиту (АІТ), враховуючи, з одного боку, взаємозв’язок між психовегетативним станом і рівнем гормонів щитоподібної залози, а з іншого, вплив гормонів щитоподібної залози на процеси кислотоутворення.Матеріали та методи. У дослідженні взяли участь дві групи хворих. Перша складалася з 30 пацієнтів, які страждають на ізольовану ГЕРХ, друга включала 27 пацієнтів, що страждають на ГЕРХ в поєднанні з гіпотиреозом, викликаним АІТ. Всім хворим було проведено комплексне обстеження відповідно до протоколів діагностики та лікування ГЕРХ і АІТ. Визначення психосоматичного статусу і якості життя проводили за допомогою опитувальників Шихана, Айзенка, GERD-Q і GIQLI. Пацієнти проходили анкетування при надходженні до стаціонару і через 2 тиж після стандартного лікування.Результати та обговорення. Встановлено, що у хворих на ГЕРХ з супутнім АІТ в порівнянні з хворими на ізольовану ГЕРХ відзначався достовірно підвищений рівень тривожності, нейротизму і більш низький рівень якості життя. Виявлена чітка кореляційна залежність між показниками моторно-секреторної функції шлунково-кишкового тракту, клінічним перебігом, рівнем гормонів щитоподібної залози, якістю життя пацієнтів і особливістю психосоматичних розладів у хворих на ГЕРХ з супутнім АІТ. Висновки. Отримані дані свідчать про роль психосоматичних розладів в патогенезі порушень вироблення гормонів щитоподібної залози і моторно-секреторної функції стравоходу і шлунка, що впливає на формування ГЕРХ в поєднанні з АІТ.

Fishes have developed many complex physiological mechanisms to combat osmotic challenges. In this study triiodothyronine (T3), thyroxine (T4) and cortisol in the plasma were quantified and the indices of metabolic and hydromineral regulations analyzed in the climbing perch Anabas testudineus after exposing the fish to a selected salinity (20 ppt) for varied intervals (1, 7, 14 and 21 days) to study the physiological basis of short- and long-term salinity acclimation. It was found that transfer of fish to 20 ppt salinity for a day after transient salinity changes, plasma T4 was elevated, and plasma T3 decreased whereas plasma cortisol remained unchanged. The levels of these hormones, however, returned to basal levels when these fish were kept for a prolonged acclimation of three weeks. Plasma glucose and lactate showed no change in response to salinity acclimation, whereas plasma urea showed an increase. Substantial increase in the gill Na+, K+-ATPase activity was found in these fish during salinity acclimation, which remained high even after three weeks. Salinity transfer for a day produced significant increase in the intestinal Na+, K+-ATPase activity, though it remained unaffected during the long-term acclimation. Kidney Na+, K+-ATPase activity decreased on day 1 salinity challenge, but remained unaltered after prolonged acclimation. Liver Na+, K+-ATPase activity increased upon transient salinity challenge but the levels were maintained during prolonged salinity challenge. Our results indicate that salinity acclimation in climbing perch demands thyroid hormone secretion and its action and not cortisol as part of co-ordinating the acclimation processes in the early phase of salinity acclimation. The results also point to the ability of climbing perch to tolerate osmotic challenge, and the fish becomes fully adaptive to brackish water salinity of 20 ppt after three weeks.

In this review, published data on the relationship occurring between melatonin - the main pineal hormone - and the thyroid gland, are briefly summarized. Numerous experimental data suggest an inhibitory influence of melatonin on thyroid growth and secretion. These effects have been presented in different experimental models in vivo and in vitro, the former including short-term and/or chronic melatonin administration to various animal species, in pinealectomized animals, also following light restriction which is known to increase the activity of the pineal. On the other hand, stimulatory effects of thyroid hormones on the pineal growth and function have been demonstrated. Oxidative stress is involved in physiological and pathological processes in the thyroid gland. Recent results of experimental studies suggest that melatonin can protect against oxidative damage in the thyroid. A confirmation of the mutual relationship between the pineal gland and the thyroid is - in clinical studies, in humans - rather difficult, as both human beings and animal species used in experimental studies, live far away from their natural/original habitats. It makes almost impossible to compare the results of studies on the pineal-thyroid interrelationship, obtained in particular experiments in different animal species.

The goal of the research is to determine the mechanism by which thyroid hormone (T3) affects bone, and the cause of the osteoporosis that can result when T3 concentrations are excessive. Our previous publications had shown that T3 increases the production of the bone growth factor insulin-like growth factor-I (IGF-I) in osteoblastic cells and promotes the production of the osteoclastogenic cytokine interleukin-6. The experiments carried out during the first grant year evaluated models that could be used to study the roles of these local factors in the anabolic and resorptive effects of T3 on bone and the molecular mechanisms by which T3 stimulated their production. The early findings using antibodies to the IGF-I and IL-6 receptors and antisense oligonucleotides to the IGF-I receptor support a role for these factors in the thyroid hormone effects. Studies at the level of gene expression show T3 augmentation of IL-6 production in human and rodent osteosarcoma cells, a lack of effect of T3 on IL-i receptor expression, and T3 potentiation of parathyroid hormone-induced IL-6 mRNA production.

Understanding the molecular basis of breast carcinoma is central to designing rational and effective therapy for this prevalent disease.

The marked and protracted hypermetabolic and catabolic response in major burn and other severe traumatic injury has been appreciated for most of this century. This response includes elevated body temperature, high cardiac output, and decreased peripheral resistance, and resolves in survivors as the wounds heal over weeks to months. During this time before wound closure, a condition resembling thyrotoxicosis is thus present. Because of this and the long-standing speculation that stress is the etiology of hyperthyroidism, Oliver Cope et al recognized the importance of determining whether the post-burn hypermetabolic condition is a function of transient hyperthyroidism. They found that thyroidal radioactive iodine uptake (RAIU) and serum protein bound iodine measurements were normal in burn patients and concluded that hyperthyroidism was not present and was not the mediator of the hypermetabolism. Later, others found a widely varying thyroidal RAIU in burn patients. However, in their patients with the most severe burns, a low RAIU clearly predominated during the 3 months after injury and ultimately resolved in survivors. RAIU measurements could have been influenced by a number of variables such as changing fluid and circulatory status, and thyroidal and renal iodide delivery, or iodine exposure or deprivation before or during the hospital course.

Evidence suggests that thyroid hormone acts by binding to nuclear receptors which regulate expression of a discrete number of proteins, including cardiac ventricular myosin isoenzymes. Administration of thyroid hormone is known to stimulate synthesis of ventricular α-myosin heavy chain and inhibit production of a (beta)-myosin heavy chain. The first part of this study examines the effects of naturally occurring and synthetic thyroid analogs, catecholamines and high carbohydrate diets on ventricular myosin isoenzyme expression in thyroidectomized and hypophysectomized rats. Also, the effects on myosin isoenzyme expression of adrenalectomy and hydrocortisone replacement have been studied in euthyroid animals. Myocardial CO₂ production and hepatic α-glycerol phosphate dehydrogenase activity were measured to monitor the effects of these interventions on tissue respiration. The results indicate that thyroid hormone analogs do not selectively stimulate myosin isoenzyme expression as compared with their effects on energy production. No significant separation between the actions of these analogs on metabolic parameters and myosin isoenzyme patterns was found. However, high carbohydrate feeding in thyroidectomized and hypophysectomized rats increased the content of the α-myosin heavy chain. β-Adrenergic stimulation with isoproterenol and blockade with propranalol did not affect myosin isoenzyme expression. Adrenalectomy in euthyroid rats decreased the α-myosin heavy chain with a corresponding increase in the β-myosin heavy chain. This could be reversed by treatment with hydrocortisone. The results suggest that the mechanism for regulation of cardiac myosin isoenzymes may involve a primary signal related to dietary carbohydrate, which is modulated by thyroid hormone, and possibly glucocorticoids. The method for purification of the T₃-receptor-DNA complex is described. This complex is thought to mediate the action of T₃ on gene expression. The results indicate that a relativel

The hypothalamic-pituitary-thyroid axis operates to maintain the circulating concentration of thyroid hormones. Thyrotropin releasing hormone (TRH) is the major hypothalamic messenger controlling the pituitary-thyroid unit. However, the pituitary-thyroid unit responses to various modalities of TRH exposure are not well characterized. Also, interactions between the thyroid axis and other mammalian organ systems, specifically other hormone axes, to maintain the organism's homeostatic state are not well characterized. This work was designed to clarify the response of the pituitary-thyroid unit to TRH and to assess the effects of physiological levels of the rat's primary adrenal cortical hormone, corticosterone, on the thyroid axis. Adult rats were given equal amounts of TRH by intravenous (I.V.) bolus injection or constant intraperitoneal (I.P.) infusion. Both methods resulted in significant increases in plasma thyroid stimulating hormone (TSH), although the time course and peak plasma value varied with the TRH dosage and administration method. Despite the differences in plasma TSH elicited, the thyroid gland responses were similar. Thus, the pituitary is sensitive to the rate and dose of TRH administration. Also, the thyroid is sensitive to plasma levels of TSH but reaches maximum stimulation at submaximal circulating TSH levels. Adrenalectomized female rats, with I.P. and I.V. catheters, were infused with corticosterone (B) to achieve plasma levels within the rat's physiological range. Plasma samples were drawn before and after submaximal TRH (250 ng/100 g Body Weight) administration for assay of TSH and B concentrations. B in the lower half of its physiological range significantly inhibited the increase in plasma TSH observed 10 and 30 minutes after TRH administration. Also, direct stereotaxic infusion of B (50 ng) followed by TRH (1 ng) into the anterior pituitary inhibited the observed increase in plasma TSH. These studies indicate that homeostatic thyroid axis ho

The C57 BL/KsJ db/db mouse is obese, hyperglycemic, hyperinsulinemic and serves as a model for noninsulin dependent diabetes mellitus (NIDDM). This study reports a dysfunction in the pituitary-thyroid axis and apparent peripheral resistence to thyroid hormones due to a reduction in T3 receptor binding. Diabetic mice have subnormal serum T4 concentrations and supranormal T3 concentrations which are most pronounced between 8 and 10 weeks of age. Thyroid glands of diabetic animals appear hypoactive histologically. Serum TSH concentrations approximate those found in normal mice. In vitro studies show that thryroid glands from diabetic animals are responsive to TSH. Pituitary glands from the same animals hypersecrete TSH and are responsive to TRH. Ultrastructural analysis of pituitary thyrotropes from diabetic mice indicate that these cells are hypersecretory and may be under chronic stimulation by TRH. Diet restriction maintains diabetic mice at a normal total body weight but these animals still possess abnormally large fat deposits. The thyroid hormone profile of these mice appears normal as does the histological appearance of the thyroid gland. Similarly, the blockade of peripheral deiodination by daily injection of iopanoic acid returns the thyroid hormone profile to normal.

Myosin heavy chain (MHC) isoforms in vertebrate striated muscles are encoded by a highly conserved multigene family. Seven sarcomeric MHCs are known to be expressed in cardiac and skeletal muscles of the rat. These isoforms show distinct patterns of tissue-specific expression which are hormonally and developmentally regulated. Thyroid hormone has been shown to regulate the expression of the ventricular isoforms by causing an accumulation of alpha-MHC and a repression of beta-MHC. Alterations in thyroid status have also been reported to affect MHC isoforms in skeletal muscles. The first part of this study describes the development of a dot-blot assay with which to measure the levels of the sarcomeric MHC mRNAs. This assay was utilized in part two of this dissertation to analyze the effects of thyroid hormone administration on the expression of MHC and actin mRNAs in ventricular muscle, as well as in representative fast and slow skeletal muscles of the hypothyroid rat. The results indicate that expression of all of the MHC genes is regulated by thyroid hormone in a highly complex, tissue specific manner. Also, thyroid hormone caused transient increases in the expression of cardiac actin mRNA in the ventricle, but no actin isoform transitions were observed in any muscle type. The third portion of this dissertation describes the development of a cultured cell system that has been used to analyze changes in MHC and alpha-actin gene expression in response to thyroid hormone in vitro. Cultured primary fetal cardiomyocytes were found to express only the cardiac MHC and actin isoforms. In addition, the alpha- and beta-MHC isoforms were found to be regulated by thyroid hormone in a similar manner to that observed in the intact rat ventricle. In the final portion of this study, the promoter region of the thyroid hormone inducible gene, alpha-MHC, was isolated and ligated to the bacterial chloramphenicol acetyltransferase gene. Chimeric genes were utilized in transfection studi