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MR Angiography String: Essentials regarding Non-Contrast-enhanced MR Angiography.
To extract the items most suitable for a short version of the 15-item Geriatric Depression Scale (GDS-15) in a sample of adults aged ≥ 85 years using item response theory (IRT).

This population-based cross-sectional study included 651 individuals aged ≥ 85 years from the Umeå 85+/GErontological Regional DAtabase (GERDA) study. Participants were either community dwelling (approximately 70%) or resided in institutional care (approximately 30%) in northern Sweden and western Finland in 2000-2002 and 2005-2007. The psychometric properties of GDS-15 items were investigated using an IRT-based approach to find items most closely corresponding to the GDS-15 cut off value of ≥5 points. Receiver operating characteristic curves were used to compare the performance of the proposed short version with that of previously proposed short GDS versions.

GDS-15 items 3, 8, 12, and 13 best differentiated respondents' levels of depressive symptoms corresponding to the GDS-15 cut off value of ≥5, regardless of age or sex, and thus comprise the proposed short version of the scale (GDS-4 GERDA). For the identification of individuals with depression (total GDS-15 score ≥ 5), the GDS-4 GERDA with a cut-off score of ≥2 had 92.9% sensitivity and 85.0% specificity.

The GDS-4 GERDA could be used as an optimized short version of the GDS-15 to screen for depression among adults aged ≥ 85 years.
The GDS-4 GERDA could be used as an optimized short version of the GDS-15 to screen for depression among adults aged ≥ 85 years.Recurrent epithelial erosion and refractory corneal ulcer are the clinical features of diabetic keratopathy (DK), which eventually lead to corneal scar and visual disturbance. In this study, we sought to determine the abnormalities of cell junction in diabetic corneal epithelial cells and the effect of high glucose on the β-catenin/E-cadherin complex. Corneal histology showed that corneal epithelial cells of high glucose mice were loosely arranged, and the immunohistochemistry showed that the expression of E-cadherin decreased, the levels of β-catenin increased in nuclear. High glucose-induced degradation and endocytosis of E-cadherin of corneal epithelial cells reduce the formation of β-catenin/E-cadherin complex and promote the nuclear translocation of β-catenin. Moreover, high glucose also activated the transcription and expression of matrix metallopeptidase and snail, which interfered with the adhesion of corneal epithelial cells to the basement membrane. These findings reveal that DK is associated with the dissociation of cell junctions. The maintenance of the stability of the β-catenin/E-cadherin complex may be a potential therapeutic target of refractory corneal ulcers in patients with diabetes.Under pathological conditions and excessive stress, mitochondria may experience a severe and irreversible loss of function. Both strenuous exhaustive exercise and neurodegenerative disorders appear to share defects in mitochondrial function that may fiercely disrupt the integrity and homeostasis of the organelle, leading to perennial pathological substrates. Here, we overview similarities of mitochondrial dysfunction in two conditions and discuss possible areas of interdisciplinary collaboration and research translation between sports medicine and neurology.An optimally functional brain requires both excitatory and inhibitory inputs that are regulated and balanced. A perturbation in the excitatory/inhibitory balance-as is the case in some neurological disorders/diseases (e.g. traumatic brain injury Alzheimer's disease, stroke, epilepsy and substance abuse) and disorders of development (e.g. schizophrenia, Rhett syndrome and autism spectrum disorder)-leads to dysfunctional signaling, which can result in impaired cognitive and motor function, if not frank neuronal injury. At the cellular level, transmission of glutamate and GABA, the principle excitatory and inhibitory neurotransmitters in the central nervous system control excitatory/inhibitory balance. Herein, we review the synthesis, release, and signaling of GABA and glutamate followed by a focused discussion on the importance of their transport systems to the maintenance of excitatory/inhibitory balance.The myometrium is the smooth muscle layer of the uterus that generates the contractions that drive processes such as menstruation and childbirth. Aberrant contractions of the myometrium can result in preterm birth, insufficient progression of labor, or other difficulties that can lead to maternal or fetal complications or even death. To investigate the underlying mechanisms of these conditions, the most common model systems have conventionally been animal models and human tissue strips, which have limitations mostly related to relevance and scalability, respectively. AZD1656 Myometrial smooth muscle cells have also been isolated from patient biopsies and cultured in vitro as a more controlled experimental system. However, in vitro approaches have focused primarily on measuring the effects of biochemical stimuli and neglected biomechanical stimuli, despite the extensive evidence indicating that remodeling of tissue rigidity or excessive strain is associated with uterine disorders. In this review, we first describe the existing approaches for modeling human myometrium with animal models and human tissue strips and compare their advantages and disadvantages. Next, we introduce existing in vitro techniques and assays for assessing contractility and summarize their applications in elucidating the role of biochemical or biomechanical stimuli on human myometrium. Finally, we conclude by proposing the translation of "organ on chip" approaches to myometrial smooth muscle cells as new paradigms for establishing their fundamental mechanobiology and to serve as next-generation platforms for drug development.Cancer-associated sarcopenia is a complex metabolic syndrome marked by muscle mass wasting. Muscle wasting is a serious complication that is a primary contributor to cancer-related mortality. The underlying molecular mechanisms of cancer-associated sarcopenia have not been completely described to date. In general, evidence shows that the main pathophysiological alterations in sarcopenia are associated with the degradation of cellular components, an exceptional inflammatory secretome and mitochondrial dysfunction. Importantly, we highlight the prospect that several miRNAs carried by tumor-derived exosomes that have shown the ability to promote inflammatory secretion, activate catabolism, and even participate in the regulation of cellular degradation pathways can be delivered to and exert effects on muscle cells. In this review, we aim to describe the current knowledge about the functions of exosomal miRNAs in the induction of cancer-associated muscle wasting and propose potential treatment strategies.
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