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    physical activity increased lower extremity muscle cross-sectional area in patients with myotonic dystrophy, preferentially in healthy-appearing muscle. © RSNA, 2020 Online supplemental material is available for this article.Background There is increasing research attention on the impact of overnight work on radiologist performance. Prior studies on overnight imaging interpretive errors have focused on radiology residents, not on the relative performance of board-eligible or board-certified radiologists at night compared with during the day. Purpose To analyze the rate of clinically important interpretation errors on CT examinations of the abdomen, pelvis, or both (“body CT studies”) committed by radiology fellows working off-hours based on day or night assignment. Materials and Methods Between July 2014 and June 2018, attending physicians at one tertiary care institution reviewed all body CT studies independently interpreted off-hours by radiologists in an academic fellowship within 10 hours of initial interpretation. Discrepancies affecting acute or follow-up clinical care were classified as errors. In this retrospective study, the error rate for studies interpreted during the day (between 700 am and 559 pm) was compared with tBruno in this issue.Background Cardiac involvement in liver cirrhosis in the absence of underlying cardiac disease is termed cirrhotic cardiomyopathy. The pathophysiology of this condition is still poorly understood. Purpose To investigate the extent of subclinical imaging changes in terms of fibrosis and inflammation and to explore the relationship between the severity of liver disease and the degree of myocardial involvement. selleckchem Materials and Methods In this prospective study from November 2018 to December 2019, participants with liver cirrhosis and healthy control participants underwent hepatic and cardiac MRI. The multiparametric scan protocol assessed hepatic (T1 and T2 relaxation times, extracellular volume [ECV], and MR elastography-based liver stiffness) and cardiac (T1 and T2 relaxation times, ECV, myocardial edema, late gadolinium enhancement [LGE], and myocardial strain) parameters. Student t tests, one-way analysis of variance, Pearson correlation, and multivariable binary regression analysis were used for statistical a less then .001), myocardial T1 relaxation times (r = 0.55; P less then .001), and ECV (r = 0.39; P = .01). Conclusion In participants with liver cirrhosis, systolic dysfunction and elevated parameters of myocardial edema and fibrosis were observed at MRI, which were more abnormal with greater severity of liver disease. © RSNA, 2020 Online supplemental material is available for this article. See also the editorial by de Roos and Lamb in this issue.Objective To develop a feasible protocol for testing maximum shoulder rotation strength in tetraplegic wheelchair athletes, and investigate concurrent validity of maximum isometric handheld dynamometer (HHD) towards maximum isokinetic dynamometer (ID) strength measurements; secondly, to study shoulder muscle activation during maximum shoulder rotation measurements, and the association between shoulder strength and shoulder pain. Design Descriptive methodological. Setting Danish Wheelchair Rugby (WCR) association for WCR tetraplegic athletes from local WCR-clubs. Participants Twelve adult tetraplegics. Interventions N/A. Outcome measures Wheelchair User’s Shoulder Pain Index (WUSPI) and Visual Analog Scale (VAS) measured shoulder pain, isometric HHD and ID (60°/s) measured maximum internal (IR) and external (ER) shoulder rotation strength. Surface Electromyography normalized to maximum EMG measured muscle activity (mm Infraspinatus and Latissimus Dorsi) during maximum shoulder rotation strength. Results Concurrent validity of isometric HHD towards ID showed Concordance Correlation Coefficients of left and right arms 0.90 and 0.86 (IR), and 0.89 and 0.91 (ER), with no difference in muscle activity between isometric HHD and ID, but larger co-activation during ER. There was no association between shoulder strength and pain, except for significantly weak negative associations between ID and pain during ER for left and right arms (P = 0.03; P = 0.04). Conclusion Standardized feasible protocol for tetraplegic wheelchair athletes for measuring maximum shoulder rotation strength was established. Isometric HHD is comparable with ID on normalized peak torques and muscle activity, but with larger co-activation. Strength was not clearly associated with shoulder pain.Hepatitis C virus (HCV) is a well-known pathogen to establish chronic infection leading to end-stage liver disease. The destruction of liver tissues takes its roots under chronic inflammation and proinflammatory signaling in liver microenvironment. The viral proteins interact with certain pattern recognition receptors, including Toll-like receptors, activating the innate immune system to clear the virus. HCV achieves immune evasion through other mechanisms and induce a continuous inflammatory microenvironment via Kupffer cells and Hepatic Stellate cells. This promotes disease progression. The current study aims to elucidate that the role of Toll-like receptor 4 (TLR4) induced innate immune response in chronic inflammation in patients chronically infected with HCV. For this purpose, changes in downstream signaling cascade of TLR4 during chronic HCV infection using peripheral blood mononuclear cells of chronic HCV patients were studied. We found significant increase in expression levels of proinflammatory and profibrotic genes induced by TLR4 Myeloid differentiation factor 88 (MyD88)-dependent pathway between treatment naive and healthy controls, while no significant difference between the expressions of genes involved in TLR4 signaling was found between treatment responders and healthy controls. Interestingly, both TLR4 MyD88-dependent and -independent pathways were found to be operational in nonresponders to interferon treatment. This further strengthens the involvement of innate immune signaling as a leading factor in HCV-mediated liver disease progression and the role of TLR4 MyD88-dependent and -independent pathway in ensuring the conditions for chronic inflammation.

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