Oral burning with dysphagia and weight loss

Fibromyalgia is a disorder characterized by an abnormal pain regulation. Widespread pain, fatigue, and sleep disturbance are the prevalent symptoms. When unusual symptoms are overbearingly predominant at clinical presentation, the diagnosis becomes challenging. We report on the case of a patient with fibromyalgia, who presented with dysphagia, odynophagia, and glossodynia as prevalent symptoms. Difficulty in swallowing gradually developed over a month prior hospitalization, and worsened progressively so that nourishment and fluid intake were impeded. Because anemia with mild iron deficiency was found, esophagogastroduodenoscopy was performed, but no lesions were seen in the upper digestive tract. Levels of zinc and vitamin B12 were normal. Intense pain at pelvis and the inferior limbs, which was at a first glance referred to as osteoarthrosis, associated with oral symptoms and feeling of being in the clouds allowed us to diagnose fibromyalgia. Amitriptyline was used, with relief of symptoms. Although oropharyngeal symptoms were occasionally reported in fibromyalgia, they are often overlooked. The present case, therefore, testifies the need to consider the diagnosis of fibromyalgia when the patient presents with such symptoms that cannot be readily explained on other grounds

Treatment of atherosclerotic renovascular hypertension: review of observational studies and a meta-analysis of randomized clinical trials.

open9Atherosclerotic renal artery stenosis can cause ischaemic nephropathy and arterial hypertension. We herein review the observational and randomized clinical trials (RCTs) comparing medical and endovascular treatment for control of hypertension and renal function preservation. Using the Population Intervention Comparison Outcome (PICO) strategy, we identified the relevant studies and performed a novel meta-analysis of all RCTs to determine the efficacy and safety of endovascular treatment when compared with medical therapy. The following outcomes were examined: baseline follow-up difference in mean systolic and diastolic blood pressure (BP), serum creatinine, number of drugs at follow-up, incident events (heart failure, stroke, and worsening renal function), mortality, cumulative relative risk of heart failure, stroke, and worsening renal function. Seven studies comprising a total of 2155 patients (1741 available at follow-up) were considered, including the recently reported CORAL Study. Compared with baseline, diastolic BP fell more at follow-up in patients in the endovascular than in the medical treatment arm (standard difference in means -0.21, 95% confidence interval (CI): -0.342 to -0.078, P = 0.002) despite a greater reduction in the mean number of antihypertensive drugs (standard difference in means -0.201, 95% CI: -0.302 to -0.1, P < 0.001). At variance, follow-up changes (from baseline) of systolic BP, serum creatinine, and incident cardiovascular event rates did not differ between treatment arms. Thus, patients with atherosclerotic renal artery stenosis receiving endovascular treatment required less anti-antihypertensive drugs at follow-up than those medically treated. Notwithstanding this, they evidenced a better control of diastolic BP.openopenCaielli P;Frigo AC;Pengo MF;Rossitto G;Maiolino G;Seccia TM;Calò LA;Miotto D;Rossi GPCaielli, P; Frigo, ANNA CHIARA; Pengo, Mf; Rossitto, G; Maiolino, G; Seccia, TERESA MARIA; Calò, La; Miotto, Diego; Rossi, Gianpaol

Endothelin-1 Drives Epithelial-Mesenchymal Transition In Hypertensive Nephroangiosclerosis

BACKGROUND: Tubulointerstitial fibrosis, the final outcome of most kidney diseases, involves activation of epithelial mesenchymal transition (EMT). Endothelin‐1 (ET‐1) activates EMT in cancer cells, but it is not known whether it drives EMT in the kidney. We therefore tested the hypothesis that tubulointerstitial fibrosis involves EMT driven by ET‐1. METHODS AND RESULTS: Transgenic TG[mRen2]27 (TGRen2) rats developing fulminant angiotensin II–dependent hypertension with prominent cardiovascular and renal damage were submitted to drug treatments targeted to ET‐1 and/or angiotensin II receptor or left untreated (controls). Expressional changes of E‐cadherin and α‐smooth muscle actin (αSMA) were examined as markers of renal EMT. In human kidney HK‐2 proximal tubular cells expressing the ET(B) receptor subtype, the effects of ET‐1 with or without ET‐1 antagonists were also investigated. The occurrence of renal fibrosis was associated with EMT in control TGRen2 rats, as evidenced by decreased E‐cadherin and increased αSMA expression. Irbesartan and the mixed ET‐1 receptor antagonist bosentan prevented these changes in a blood pressure–independent fashion (P < 0.001 for both versus controls). In HK‐2 cells ET‐1 blunted E‐cadherin expression, increased αSMA expression (both P < 0.01), collagen synthesis, and metalloproteinase activity (P < 0.005, all versus untreated cells). All changes were prevented by the selective ET(B) receptor antagonist BQ‐788. Evidence for involvement of the Rho‐kinase signaling pathway and dephosphorylation of Yes‐associated protein in EMT was also found. CONCLUSIONS: In angiotensin II–dependent hypertension, ET‐1 acting via ET(B) receptors and the Rho‐kinase and Yes‐associated protein induces EMT and thereby renal fibrosis

QPACE 2 and Domain Decomposition on the Intel Xeon Phi

We give an overview of QPACE 2, which is a custom-designed supercomputer based on Intel Xeon Phi processors, developed in a collaboration of Regensburg University and Eurotech. We give some general recommendations for how to write high-performance code for the Xeon Phi and then discuss our implementation of a domain-decomposition-based solver and present a number of benchmarks.Comment: plenary talk at Lattice 2014, to appear in the conference proceedings PoS(LATTICE2014), 15 pages, 9 figure

Using social robot NAO for emotional support to children at a paediatric emergency department: a randomised clinical trial

Background: Social robots have been used for improving anxiety in children in stressful clinical situations, as during painful procedures. No studies have been performed yet to assess their effect in children while waiting for emergency room consultations. Objective: To assess the impact of social robots in managing stress in children waiting for an emergency room procedure through the assessment of salivary cortisol levels. Methods: This was an open randomised clinical trial in children attending a paediatric emergency department. Children accessing the emergency room were randomised to one of three groups: 1) playing with a NAO social robot; 2) playing with a study nurse; 3) waiting with parents. All children were measured salivary cortisol levels through a swab. Salivary cortisol levels before and after the intervention were compared in the three groups. We calculated the effect size of our interventions through the Cohen's d-based effect size correlation (r). Results: A total of 109 children aged 3 to 10 years were enrolled in the study and 94 had complete data for the analyses. Salivary cortisol levels decreased significantly more in the group exposed to robot interaction than in the other two groups (r=0.75). Cortisol levels decreased more in girls (r=0.92) than boys (r=0.57). Conclusions: Social robots are efficacious in decreasing stress in children accessing the emergency room and may be considered as a tool for improving emotional perceptions of children and their families in such a critical setting. Clinicaltrial: Robot Therapy in Pediatric Emergency, NCT04627909, https://clinicaltrials.gov/ct2/show/study/NCT04627909

JANUS: an FPGA-based System for High Performance Scientific Computing

This paper describes JANUS, a modular massively parallel and reconfigurable FPGA-based computing system. Each JANUS module has a computational core and a host. The computational core is a 4x4 array of FPGA-based processing elements with nearest-neighbor data links. Processors are also directly connected to an I/O node attached to the JANUS host, a conventional PC. JANUS is tailored for, but not limited to, the requirements of a class of hard scientific applications characterized by regular code structure, unconventional data manipulation instructions and not too large data-base size. We discuss the architecture of this configurable machine, and focus on its use on Monte Carlo simulations of statistical mechanics. On this class of application JANUS achieves impressive performances: in some cases one JANUS processing element outperfoms high-end PCs by a factor ~ 1000. We also discuss the role of JANUS on other classes of scientific applications.Comment: 11 pages, 6 figures. Improved version, largely rewritten, submitted to Computing in Science & Engineerin

Endothelin-1 (ET-1) modulates epithelial-mesenchymal transition (EMT), which contributes to kidney tubulo-interstitial fibrosis in angiotensin II-dependent hypertension

The origin of myofibroblasts remains uncertain, but studies suggest that the epithelial cells may acquire a fibroblast-like phenotype via epithelial-mesenchymal transition (EMT). Objective of the study was to investigate whether EMT may contribute to the development of kidney fibrosis in a model of angiotensin II-dependent hypertension and to identify the role of ET-1 via ETA/ETB receptors. Transgenic rats TGRen2 (n=35) received for 4 weeks one of the following treatments a) irbesartan, b) bosentan, non selective ETA /ETB receptor antagonist, c) BMS-182874, selective ETA,antagonist, d) BMS+irbesartan, e) placebo. EMT was assessed by investigating coexpression of a marker of epithelial cell (E-cadherin) and one of myofibroblast (S100A4 or alfa-SMA) with double immunofluorescence. Specific immunoreactivity was measured using QWinStandard Leica ImageTMsoftware. A reduction in blood pressure was found only with irbesartan, whereas both bosentan and irbesartan significantly lowered tubulo-interstitial fibrosis. Coexpression of E-cadherin and S100A4, or E-cadherin and alfa-SMA, markedly decreased in the tubular cells of TGRen2 treated with irbesartan or bosentan. Alfa-SMA expression decreased after irbesartan, bosentan and BMS+irbesartan, but not after BMS. S100A4 expression was reduced after irbesartan, bosentan and BMS+irbesartan. E-cadherin increased only after irbesartan. Coexpression of the markers of myofibroblasts and kidney epithelial cells, by demonstrating the development of EMT during the onset of kidney hypertension-induced damage, suggests a crucial role of EMT in the pathogenesis of Ang II-mediated fibrosis. The reduction of myofibroblast markers not only after irbesartan, but also after blockade of ETA/ETB receptors, suggests an involvement of ET-1 in the development of Ang II-mediated EMT

Endothelin-1 (ET-1) modulates epithelial-mesenchymal transition (EMT), which contributes to kidney tubulo-interstitial fibrosis in angiotensin II-dependent hypertension

The origin of myofibroblasts remains uncertain, but studies suggest that the epithelial cells may acquire a fibroblast-like phenotype via epithelial-mesenchymal transition (EMT). Objective of the study was to investigate whether EMT may contribute to the development of kidney fibrosis in a model of angiotensin II-dependent hypertension and to identify the role of ET-1 via ETA/ETB receptors. Transgenic rats TGRen2 (n=35) received for 4 weeks one of the following treatments a) irbesartan, b) bosentan, non selective ETA /ETB receptor antagonist, c) BMS-182874, selective ETA,antagonist, d) BMS+irbesartan, e) placebo. EMT was assessed by investigating coexpression of a marker of epithelial cell (E-cadherin) and one of myofibroblast (S100A4 or alfa-SMA) with double immunofluorescence. Specific immunoreactivity was measured using QWinStandard Leica ImageTMsoftware. A reduction in blood pressure was found only with irbesartan, whereas both bosentan and irbesartan significantly lowered tubulo-interstitial fibrosis. Coexpression of E-cadherin and S100A4, or E-cadherin and alfa-SMA, markedly decreased in the tubular cells of TGRen2 treated with irbesartan or bosentan. Alfa-SMA expression decreased after irbesartan, bosentan and BMS+irbesartan, but not after BMS. S100A4 expression was reduced after irbesartan, bosentan and BMS+irbesartan. E-cadherin increased only after irbesartan. Coexpression of the markers of myofibroblasts and kidney epithelial cells, by demonstrating the development of EMT during the onset of kidney hypertension-induced damage, suggests a crucial role of EMT in the pathogenesis of Ang II-mediated fibrosis. The reduction of myofibroblast markers not only after irbesartan, but also after blockade of ETA/ETB receptors, suggests an involvement of ET-1 in the development of Ang II-mediated EMT