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  • Munkholm Johansen posted an update 1 day, 23 hours ago

    To assess whether volumetric vertebral bone mineral density (BMD) measured with opportunistic quantitative computed tomography (QCT) (i.e., CT acquired for other reasons) can predict osteoporotic fracture occurrence in a prospective clinical cohort and how this performs in comparison to dual-energy X-ray absorptiometry (DXA) measurements.

    In the database of our fracture liaison service, 58 patients (73 ± 11 years, 72% women) were identified that had at least one prevalent low-energy fracture and had undergone CT of the spine. BMD was determined by converting HU using scanner-specific conversion equations. Baseline DXA was available for 31 patients. During a 3-year follow-up, new fractures were diagnosed either by (i) recent in-house imaging or (ii) clinical follow-up with validated external reports. Associations were assessed using logistic regression models, and cut-off values were determined with ROC/Youden analyses.

    Within 3 years, 20 of 58 patients presented new low-energy fractures (34%). Mean QCT easurements attained through QCT predicted fractures during a 3-year follow-up. Fostamatinib This suggests that opportunistic measurements are useful to reduce the diagnostic gap and evaluate the fracture risk in osteoporotic patients.Inhibition of neuropeptide Y1 receptor stimulates osteogenesis in vitro and in vivo. However, the underlying mechanisms involved in these effects remain poorly understood. Here we identify the effects of Y1 receptor deficiency on osteogenic differentiation in human bone marrow stromal cells (BMSCs) by using genetic and pharmacological regulation, and to explore the pathways mediating these effects. In BMSCs, inhibition of Y1 receptor stimulates osteogenesis and upregulates the expression levels of the master transcriptional factor RUNX2. Mechanistically, Y1 receptor deficiency increases the levels of intracellular cAMP, which via protein kinase A (PKA) mediated pathways results in activation of phospho-CREB (p-CREB). We find RUNX2 activation induced by Y1 receptor deficiency is reversed by H-89, a PKA inhibitor. These results indicate Y1 receptor deficiency activates PKA-mediated phosphorylation of CREB, leading to activation of RUNX2 and enhances osteogenic differentiation in BMSCs. In conclusion, these data indicate that Y1 receptor deficiency promotes osteogenic differentiation by RUNX2 stimulation through cAMP/PKA/CREB pathway.The brain is responsible for maintaining whole-body energy homeostasis by changing energy input and availability. The hypothalamus and dorsal vagal complex (DVC) are the primary sites of metabolic control, able to sense both hormones and nutrients and adapt metabolism accordingly. The mitochondria respond to the level of nutrient availability by fusion or fission to maintain energy homeostasis; however, these processes can be disrupted by metabolic diseases including obesity and type II diabetes (T2D). Mitochondrial dynamics are crucial in the development and maintenance of obesity and T2D, playing a role in the control of glucose homeostasis and whole-body metabolism across neurons and glia in the hypothalamus and DVC.

    Bisphosphonates (BPs) are first-line therapy for osteoporosis. Adherence is usually low in chronic, asymptomatic diseases, but gastrointestinal (GI) side-effects can also contribute to low adherence in BP therapy and may necessitate a review by a gastroenterologist with or without gastroscopy.

    Our meta-analysis aims to determine the risk of severe GI adverse events due to oral BP therapy in osteoporotic patients.

    A systematic search was conducted in three databases up to September 2020 for randomized controlled trials (RCTs) detailing GI adverse events in adults with osteoporosis on BP compared to placebo.Risk ratios (RRs) with 95% confidence intervals (CI) were calculated for non-severe and severe adverse events indicating endoscopic procedure with the random-effects model. Statistical heterogeneity was assessed using chi

    and I

    statistics.

    Forty-two RCTs with 39,047 patients with 9,999 non-severe and 1,503 severe GI adverse events were included. The incidence of non-severe and severe adverse evenh caution.

    Our results show that bisphosphonates do not increase the risk of severe GI adverse events. However, the marked variability of the screening for side effects in the included studies, and the fact that in most of the studies GI diseases were exclusion criteria limits the strenght of evidence of our results. The conclusions drawn from the meta-analysis are therefore restricted to selected populations, and the results must be interpreted with caution.Covid19 is a worldwide pandemic challenge that started in Wuhan, China and spread to almost all countries on the planet within a few months. The causative virus was found to be highly contagious and, until now, considerably difficult to contain. A look at the epidemiological distribution of the disease over the planet has raised a number of questions whose answers could help us understand the behavior of the virus and consequently leads us to possible means of limitation of its spread or even flattening of the curve of morbidity and mortality. After the third decade of life, there is a progressive decline of growth hormone (GH) secretion by approximately 15% for every decade of adult life. The data from highly affected countries suggest a more aggressive course in the elderly, a double-time affection of males more than females, and the vulnerability of some risk groups of patients. Our observation is that GH deficiency is a common factor in all vulnerable patient groups. We think that there is a need for studying the role of growth hormone in the unique epidemiological pattern of Covid-19 so that it might help in the early detection and management of the high-risk groups as appropriate.Purpose The purpose of this study is to explore the differences in transcriptome expression profiles between healthy subjects and type 2 diabetes mellitus patients with thirst and fatigue (D-T2DM) and, in addition, to investigate the possible role of noncoding ribonucleic acids (RNAs) in the pathogenesis of D-T2DM. Methods We constructed the expression profiles of RNAs by RNA sequencing in the peripheral blood of D-T2DM patients and healthy subjects and analyzed differentially expressed RNAs. Results Compared with healthy subjects, a total of 469 mRNAs, 776 long non-coding RNAs (lncRNAs), and 21 circular RNAs (circRNAs) were differentially expressed in D-T2DM patients. Furthermore, several genes associated with insulin resistance, inflammation, and mitochondrial dysfunction were identified within the differentially expressed mRNAs. Differentially expressed lncRNAs were primarily involved in biological processes associated with immune responses. In addition, differentially expressed circRNAs may target miRNAs associated with glucose metabolism and mitochondrial function.

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