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The approaches to correct thyroid deficiency include replacement therapy with thyroid hormones (THs), but such therapy causes a number of side effects. A possible alternative is thyroid-stimulating hormone (TSH) receptor activators, including allosteric agonists. The aim of this work was to study the effect of ethyl-2-(4-(4-(5-amino-6-(-butylcarbamoyl)-2-(methylthio)thieno[2,3-d]pyrimidin-4-yl)phenyl)--1,2,3-triazol-1-yl) acetate (TPY3m), a TSH receptor allosteric agonist developed by us, on basal and thyroliberin (TRH)-stimulated TH levels and the hypothalamic-pituitary-thyroid (HPT) axis in male rats with high-fat diet/low-dose streptozotocin-induced type 2 diabetes mellitus (T2DM).

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Since the early discovery of QRFP43, intensive research has been primarily focused on its role in the modulation of food intake. As is widely recognised, the regulation of the body's energy status is a highly complex process involving numerous systems, hormones and neurotransmitters. Among the most important regulators of energy status, alongside the satiety and hunger centre located in the hypothalamus, is the HPT axis, which directly and indirectly affects the regulation of metabolism in all cells of the body.

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Background: In prolactinoma diagnosis, current guidelines recommend prolactin (PRL) assessment, considering values exceeding 200 ng/mL highly suggestive of prolactinoma. However, subtler hyperprolactinemia is more common, and to rule out potential prolactinomas, pituitary resonance magnetic imaging (MRI) studies are necessary. These present limitations in terms of availability, costs, and delays in diagnosis.

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Objective: To compare the effect of varying durations of noise exposure on the histomorphological and endocrine profile of the thyroid gland in male and female adult rats.

Study Design: An experimental study. Place and Duration of the Study: Department of Anatomy, Army Medical College, Rawalpindi / NUMS, from January to December 2020.

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Aim: To analyze the relationship between the occurrence of atrial fibrillation (AF) and thyroid dysfunction caused by low concentrations of free triiodothyronine (FT3), free triiodothyronine and free thyroxine (FT3 and FT4), and high concentrations of free thyroxine (FT4) with normal values of thyroid-stimulating hormone (TSH) in experiments on outbred rats.

Material And Methods: The pathogenesis of AF with low concentrations of FT3, FT3 and FT4, and a high concentration of FT4 was studied in an experiment on 146 outbred rats. In the experiment, hypothyroidism, euthyroidism, and thyrotoxicosis were modeled by changing the concentrations of thyroid hormones, and the effect of these conditions on ECG and the incidence of AF was evaluated.

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