Aims: To describe a type 1 diabetes melllitus (T1DM) transition care model by assessing clinic attendance, glycemic management, and diabetes-related hospitalizations.
Methods: This is a descriptive longitudinal single-center study of patients with T1DM aged 18 to 25 referred to our transition clinic from 2012 to 2021 (N=179).
Results: Our data analysis demonstrates an average clinic attendance rate of 79% and mean time between last pediatric and first adult visit of 6.
Background/objective: Although retinoid-associated central hypothyroidism has been reported on several occasions, there are very few studies on retinoid-associated central adrenal insufficiency. Here, we present the case of a patient with alitretinoin-induced central hypothyroidism and adrenal insufficiency.
Case Report: An 86-year-old man with a diagnosis of cutaneous T-cell lymphoma, treated with oral alitretinoin 30 mg po daily, topical steroids, and ultraviolet light therapy presented to the emergency department with generalized weakness, decreased energy, orthostasis, and unexplained falls.
Objective: Prader-Willi syndrome (PWS) is associated with multiple endocrinopathies, including hypogonadism. The mechanism underlying hypogonadism in PWS is thought to be secondary to hypothalamic dysfunction, primary gonadal defect, or a combination of both. Here, we present a case of hyperestrogenism in PWS due to concomitant polycystic ovary syndrome (PCOS) and therapeutic considerations regarding hormone replacement therapy (HRT).
View Article and Find Full Text PDFJ Thorac Cardiovasc Surg
January 2021
Objectives: Aortic valve stenosis (AVS) is the most common cause of surgical valve replacement worldwide. The vasoactive peptide urotensin II (UII) is upregulated in atherosclerosis and several other cardiovascular diseases; however, its role in the pathogenesis of AVS remains to be determined. Here, we investigated the expression of UII, urotensin-related peptide (URP), and the urotensin receptor (UT) and the role this system plays in AVS.
View Article and Find Full Text PDFSeveral previous studies outlined the importance of the histone H2A deubiquitinase MYSM1 in the regulation of stem cell quiescence and haematopoiesis. In this study we investigated the role of MYSM1 in T-cell development. Using mouse models that allow conditional Mysm1 ablation at late stages of thymic development, we found that MYSM1 is intricately involved in the maintenance, activation and survival of CD8 T cells.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
March 2017
Objective: The mechanisms underlying the pathogenesis of aortic valve calcification remain unclear. With accumulating evidence demonstrating that valve calcification recapitulates bone development, the crucial roles of noncanonical Wnt ligands WNT5a, WNT5b, and WNT11 in osteogenesis make them critical targets in the study of aortic valve calcification.
Approach And Results: Using immunohistochemistry, real-time qPCR, Western blotting, and tissue culture, we examined the tissue distribution of WNT5a, WNT5b, and WNT11 in noncalcified and calcified aortic valves and their effects on human aortic valve interstitial cells (HAVICs).
Background And Aims: The aims of the present study were to determine the expression of urotensin II (UII), urotensin-II related peptide (URP), and their receptor (UT) in stable and unstable carotid atherosclerosis, and determine the effects of UII on human aortic smooth muscle cell (SMCs) calcification.
Methods And Results: We examined UII, URP, and UT protein expression in 88 carotid endarterectomy specimens using immunohistochemistry. Expression of UII, URP, and UT was more evident in unstable compared to stable plaques (P < 0.
Urotensin II (UII) is a vasoactive peptide with various roles in cardiovascular physiology and pathophysiology. There is an accumulating evidence implicating UII in atherosclerosis and coronary artery disease, making it an important target in acute coronary syndrome (ACS). In this study, we sought to determine the plasma levels of UII in ACS patients within 48 h of clinical presentation and after a 12-week recovery period.
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