The comet 17P/Holmes 2007 outburst: the early motion of the outburst material

Context. On October 24, 2007 the periodic comet 17P/Holmes underwent an astonishing outburst that increased its apparent total brightness from magnitude V\sim17 up to V\sim2.5 in roughly two days. We report on Wendelstein 0.8 m telescope (WST) photometric observations of the early evolution stages of the outburst. Aims. We studied the evolution of the structure morphology, its kinematic, and estimated the ejected dust mass. Methods. We analized 126 images in the BVRI photometric bands spread between 26/10/2007 and 20/11/2007. The bright comet core appeared well separated from that one of a quickly expanding dust cloud in all the data, and the bulk of the latter was contained in the field of view of our instrument. The ejected dust mass was derived on the base of differential photometry on background stars occulted by the moving cloud. Results. The two cores were moving apart from each other at a relative projected constant velocity of (9.87 +/- 0.07) arcsec/day (0.135 +/-0.001 km/sec). In the inner regions of the dust cloud we observed a linear increase in size at a mean constant velocity of (14.6+/-0.3) arcsec/day (0.200+/-0.004 km/sec). Evidence of a radial velocity gradient in the expanding cloud was also found. Our estimate for the expanding coma's mass was of the order of 10^{-2}-1 comet's mass implying a significant disintegration event. Conclusions. We interpreted our observations in the context of an explosive scenario which was more probably originated by some internal instability processes, rather than an impact with an asteroidal body. Due to the peculiar characteristics of this event, further observations and investigations are necessary in order to enlight the nature of the physical processes that determined it.Comment: 5 pages, 3 figures, A&A accepte

Meta-analysis of the impact of successful chronic total occlusion percutaneous coronary intervention on left ventricular systolic function and reverse remodeling

We sought to examine the impact of coronary chronic total occlusion (CTO) percutaneous coronary intervention (PCI) on left ventricular (LV) function.We performed a systematic review and meta-analysis of studies published between January 1980 and November 2017 on the impact of successful CTO PCI on LV function.A total of 34 observational studies including 2735 patients were included in the meta-analysis. Over a weighted mean follow-up of 7.9 months, successful CTO PCI was associated with an increase in LV ejection fraction by 3.8% (95%CI 3.0-4.7, P < 0.0001, I2 = 45%). In secondary analysis of 15 studies (1248 patients) that defined CTOs as occlusions of at least 3-month duration and reported follow-up of at least 3-months after the procedure, successful CTO PCI was associated with improvement in LV ejection fraction by 4.3% (95%CI [3.1, 5.6], P < 0.0001). In the 10 studies (502 patients) that reported LV end-systolic volume, successful CTO PCI was associated with a decrease in LV end-systolic volume by 4 mL, (95%CI -6.0 to -2.1, P < 0.0001, I2 = 0%). LV end-diastolic volume was reported in 9 studies with 403 patients and did not significantly change after successful CTO PCI (-2.3 mL, 95%CI -5.7 to 1.2 mL, P = 0.19, I2 = 0%).Successful CTO PCI is associated with a statistically significant improvement in LV ejection fraction and decrease in LV end-systolic volume, that may reflect a beneficial effect of CTO recanalization on LV remodeling. The clinical implications of these findings warrant further investigation

Nomograms including the UBC® Rapid test to detect primary bladder cancer based on a multicentre dataset

Objectives: To evaluate the clinical utility of the urinary bladder cancer antigen test UBC Rapid for the diagnosis of bladder cancer (BC) and to develop and validate nomograms to identify patients at high risk of primary BC. Patients and Methods: Data from 1787 patients from 13 participating centres, who were tested between 2012 and 2020, including 763 patients with BC, were analysed. Urine samples were analysed with the UBC Rapid test. The nomograms were developed using data from 320 patients and externally validated using data from 274 patients. The diagnostic accuracy of the UBC Rapid test was evaluated using receiver-operating characteristic curve analysis. Brier scores and calibration curves were chosen for the validation. Biopsy-proven BC was predicted using multivariate logistic regression. Results: The sensitivity, specificity, and area under the curve for the UBC Rapid test were 46.4%, 75.5% and 0.61 (95% confidence interval [CI] 0.58–0.64) for low-grade (LG) BC, and 70.5%, 75.5% and 0.73 (95% CI 0.70–0.76) for high-grade (HG) BC, respectively. Age, UBC Rapid test results, smoking status and haematuria were identified as independent predictors of primary BC. After external validation, nomograms based on these predictors resulted in areas under the curve of 0.79 (95% CI 0.72–0.87) and 0.95 (95% CI: 0.92–0.98) for predicting LG-BC and HG-BC, respectively, showing excellent calibration associated with a higher net benefit than the UBC Rapid test alone for low and medium risk levels in decision curve analysis. The R Shiny app allows the results to be explored interactively and can be accessed at www.blucab-index.net. Conclusion: The UBC Rapid test alone has limited clinical utility for predicting the presence of BC. However, its combined use with BC risk factors including age, smoking status and haematuria provides a fast, highly accurate and non-invasive tool for screening patients for primary LG-BC and especially primary HG-BC

Chronic kidney disease and valvular heart disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference

Chronic kidney disease (CKD) is a major risk factor for valvular heart disease (VHD). Mitral annular and aortic valve calcifications are highly prevalent in CKD patients and commonly lead to valvular stenosis and regurgitation, as well as complications including conduction system abnormalities and endocarditis. VHD, especially mitral regurgitation and aortic stenosis, is associated with significantly reduced survival among CKD patients. Knowledge related to VHD in the general population is not always applicable to CKD patients because the pathophysiology may be different, and CKD patients have a high prevalence of comorbid conditions and elevated risk for periprocedural complications and mortality. This Kidney Disease: Improving Global Outcomes (KDIGO) review of CKD and VHD seeks to improve understanding of the epidemiology, pathophysiology, diagnosis, and treatment of VHD in CKD by summarizing knowledge gaps, areas of controversy, and priorities for research

Molecular imaging of inflammation and intraplaque vasa vasorum: A step forward to identification of vulnerable plaques?

Current developments in cardiovascular biology and imaging enable the noninvasive molecular evaluation of atherosclerotic vascular disease. Intraplaque neovascularization sprouting from the adventitial vasa vasorum has been identified as an independent predictor of intraplaque hemorrhage and plaque rupture. These intraplaque vasa vasorum result from angiogenesis, most likely under influence of hypoxic and inflammatory stimuli. Several molecular imaging techniques are currently available. Most experience has been obtained with molecular imaging using positron emission tomography and single photon emission computed tomography. Recently, the development of targeted contrast agents has allowed molecular imaging with magnetic resonance imaging, ultrasound and computed tomography. The present review discusses the use of these molecular imaging techniques to identify inflammation and intraplaque vasa vasorum to identify vulnerable atherosclerotic plaques at risk of rupture and thrombosis. The available literature on molecular imaging techniques and molecular targets associated with inflammation and angiogenesis is discussed, and the clinical applications of molecular cardiovascular imaging and the use of molecular techniques for local drug delivery are addressed

Optical novae: the major class of supersoft X-ray sources in M 31

We searched for X-ray counterparts of optical novae detected in M 31 and M 33. We combined an optical nova catalogue from the WeCAPP survey with optical novae reported in the literature and correlated them with the most recent X-ray catalogues from ROSAT, XMM-Newton and Chandra, and - in addition - searched for nova correlations in archival data. We report 21 X-ray counterparts for novae in M 31 - mostly identified as supersoft sources (SSS) by their hardness ratios - and two in M 33. Our sample more than triples the number of known optical novae with supersoft X-ray phase. Most of the counterparts are covered in several observations allowing us to constrain their X-ray light curves. Selected brighter sources were classified by their XMM-Newton EPIC spectra. We use the well determined start time of the SSS state in two novae to estimate the hydrogen mass ejected in the outburst to ~10^{-5}M_sun and ~10^{-6}M_sun, respectively. The supersoft X-ray phase of at least 15% of the novae starts within a year. At least one of the novae shows a SSS state lasting 6.1 years after the optical outburst. Six of the SSSs turned on between 3 and 9 years after the optical discovery of the outburst and may be interpreted as recurrent novae. If confirmed, the detection of a delayed SSS phase turn-on may be used as a new method to classify novae as recurrent. At the moment, the new method yields a ratio of recurrent novae to classical novae of 0.3 which is in agreement (within the errors) with previous works.Comment: 16 pages, 7 figures, A&A revised version, 1 nova in M33 added, restructured discussion, summary and conclusion

Chronic kidney disease and valvular heart disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies conference

Chronic kidney disease (CKD) is a major risk factor for valvular heart disease (VHD). Mitral annular and aortic valve calcifications are highly prevalent in CKD patients and commonly lead to valvular stenosis and regurgitation, as well as complications including conduction system abnormalities and endocarditis. VHD, especially mitral regurgitation and aortic stenosis, is associated with significantly reduced survival among CKD patients. Knowledge related to VHD in the general population is not always applicable to CKD patients because the pathophysiology may be different, and CKD patients have a high prevalence of comorbid conditions and elevated risk for periprocedural complications and mortality. This Kidney Disease: Improving Global Outcomes (KDIGO) review of CKD and VHD seeks to improve understanding of the epidemiology, pathophysiology, diagnosis, and treatment of VHD in CKD by summarizing knowledge gaps, areas of controversy, and priorities for research