Psychiatric disorders in myasthenia gravis

OBJECTIVE: To investigate the prevalence of psychiatric disorders in patients with myasthenia gravis (MG). METHOD: Forty-one patients with MG answered to a structured psychiatric interview (MINI-Plus). RESULTS: Eleven (26.1%) patients were diagnosed with a depressive disorder and 19 (46.3%) were diagnosed with an anxiety disorder. Patients with dysthymia were older (p=0.029) and had longer disease duration (p=0.006). Patients with social phobia also had longer disease duration (p=0.039). CONCLUSION: Psychiatric disorders in MG are common, especially depressive and anxiety disorders

Biomechanical factors in atherosclerosis: mechanisms and clinical implications

Blood vessels are exposed to multiple mechanical forces that are exerted on the vessel wall (radial, circumferential and Longitudinal forces) or on the endothelial surface (shear stress). The stresses and strains experienced by arteries influence the initiation of atherosclerotic Lesions, which develop at regions of arteries that are exposed to complex blood flow. In addition, plaque progression and eventually plaque rupture is influenced by a complex interaction between biological and mechanical factors mechanical forces regulate the cellular and molecular composition of plaques and, conversely, the composition of plaques determines their ability to withstand mechanical load. A deeper understanding of these interactions is essential for designing new therapeutic strategies to prevent lesion development and promote plaque stabilization. Moreover, integrating clinical imaging techniques with finite element modelling techniques allows for detailed examination of local morphological and biomechanical characteristics of atherosclerotic lesions that may be of help in prediction of future events. In this ESC Position Paper on biomechanical factors in atherosclerosis, we summarize the current 'state of the art' on the interface between mechanical forces and atherosclerotic plaque biology and identify potential clinical applications and key questions for future research

Divergent Modulation of Proteostasis in Prostate Cancer

Ballar, Petek/0000-0002-6189-1818WOS: 000530838600006PubMed: 32274755Proteostasis regulates key cellular processes such as cell proliferation, differentiation, transcription, and apoptosis. the mechanisms by which proteostasis is regulated are crucial and the deterioration of cellular proteostasis has been significantly associated with tumorigenesis since it specifically targets key oncoproteins and tumor suppressors. Prostate cancer (PCa) is the second most common cause of cancer death in men worldwide. Androgens mediate one of the most central signaling pathways in all stages of PCa via the androgen receptor (AR). in addition to their regulation by hormones, PCa cells are also known to be highly secretory and are particularly prone to ER stress as proper ER function is essential. Alterations in various complex signaling pathways and cellular processes including cell cycle control, transcription, DNA repair, apoptosis, cell adhesion, epithelial-mesenchymal transition (EMT), and angiogenesis are critical factors influencing PCa development through key molecular changes mainly by posttranslational modifications in PCa-related proteins, including AR, NKX3.1, PTEN, p53, cyclin D1, and p27. Several ubiquitin ligases like MDM2, Siah2, RNF6, CHIP, and substrate-binding adaptor SPOP; deubiquitinases such as USP7, USP10, USP26, and USP12 are just some of the modifiers involved in the regulation of these key proteins via ubiquitin-proteasome system (UPS). Some ubiquitin-like modifiers, especially SUMOs, have been also closely associated with PCa. on the other hand, the proteotoxicity resulting from misfolded proteins and failure of ER adaptive capacity induce unfolded protein response (UPR) that is an indispensable signaling mechanism for PCa development. Lastly, ER-associated degradation (ERAD) also plays a crucial role in prostate tumorigenesis. in this section, the relationship between prostate cancer and proteostasis will be discussed in terms of UPS, UPR, SUMOylation, ERAD, and autophagy.Scientific and Technological Research Council of Turkey (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [SBAG-108S056/114S062]; Ege University internal funds; BAGEP Award of the Science Academy; Pfizer-TurkeyPfizer; COST Action (PROTEOSTASIS)European Cooperation in Science and Technology (COST) [BM1307]; COST (European Cooperation in Science and Technology)European Cooperation in Science and Technology (COST)Work by PBK is supported by the Scientific and Technological Research Council of Turkey (TUBITAK, SBAG-108S056/114S062), Ege University internal funds, BAGEP Award of the Science Academy with funding supplied by Pfizer-Turkey, COST Action (PROTEOSTASIS BM1307), and by COST (European Cooperation in Science and Technology)