291 research outputs found
Recommended from our members
Does the built-environment industry attract risk-taking individuals?
This exploratory research examines whether or not those attracted to professional-level occupations in the built-environment industry are innately physical risk-takers and hence potentially, thereby, more likely to countenance or contribute to physically risky workplace climates. Using individual-level data, the occupational attractiveness of the built-environment industry subsectors of construction management and architecture are each found positively and significantly to be predicted by physical risk-taking propensity, but not by a comparator risk-taking propensity, gambling. Conversely, the occupational attractiveness of a comparator profession in financial services is found to be significantly predicted by gambling risk-taking propensity, but not by physical risk-taking propensity. Although exploratory, our finding that two key professions in the built-environment industry are each discretely found to be attractive to physical risk-takers suggests not only that constituent occupations within the industry, but that the industry as a whole might perhaps engender a self-reinforcing suboptimal workplace safety climate. Accordingly, constituent subsectors of the industry may need both separately and collectively to consider the phenomenon of physical risk-taking propensity amongst the professionals it attracts in order effectively to set and manage the site work-place safety climate that such professionals are ultimately responsible for creating and delivering in a sector fraught with physical risks for site workers
Recommended from our members
Building bridges: the bilingual language work of migrant construction workers
N-terminal pro-BNP predicts mortality better than procalcitonin in abdominal severe sepsis and septic shock
Markers of focal and diffuse nonischemic myocardial fibrosis are associated with adverse cardiac remodeling and prognosis in patients with hypertension: the REMODEL study
Background: The prognostic significance of focal and diffuse myocardial fibrosis in patients with cardiovascular risk factors is unclear. Methods: REMODEL (Response of the Myocardium to Hypertrophic Conditions in the Adult Population) is an observational cohort of asymptomatic patients with essential hypertension. All participants underwent cardiovascular magnetic resonance to assess for myocardial fibrosis: nonischemic late gadolinium enhancement (LGE), native myocardial T1, postcontrast myocardial T1, extracellular volume fraction including/excluding LGE regions, interstitial volume (extracellular volume×myocardial volume), and interstitial/myocyte ratio. Primary outcome was a composite of first occurrence acute coronary syndrome, heart failure hospitalization, strokes, and cardiovascular mortality. Patients were recruited from February 2016 and followed until June 2021. Results: Of the 786 patients with hypertension (58±11 years; 39% women; systolic blood pressure, 130±14 mm Hg), 145 (18%) had nonischemic LGE. Patients with nonischemic LGE were more likely to be men, have diabetes, be current smokers, and have higher blood pressure (P<0.05 for all). Compared with those without LGE, patients with nonischemic LGE had greater left ventricular mass (66±22 versus 49±9 g/m2; P<0.001), worse multidirectional strain (P<0.001 for all measures), and elevated circulating markers of myocardial wall stress and myocardial injury, adjusted for potential confounders. Twenty-four patients had primary outcome over 39 (30–50) months of follow-up. Of all the cardiovascular magnetic resonance markers of myocardial fibrosis assessed, only nonischemic LGE (hazard ratio, 6.69 [95% CI, 2.54–17.60]; P<0.001) and indexed interstitial volume (hazard ratio, 1.11 [95% CI, 1.04–1.19]; P=0.002) demonstrated independent association with primary outcome. Conclusions: In patients with hypertension, myocardial fibrosis on cardiovascular magnetic resonance is associated with adverse cardiac remodeling and outcomes
Vertical accuracy comparison of multi-source Digital Elevation Model (DEM) with Airborne Light Detection and Ranging (LiDAR)
Digital Elevation Model (DEM) is a digital representation of ground surface topography or terrain. There are many freely available DEM data with a spatial resolution of 30 m to 90 m. Nevertheless, their vertical accuracy may vary, depending on the vegetation cover and terrain characteristics. This study examined the vertical accuracy of open-access global DEMs (ALOS PALSAR, ASTER GDEM3, SRTM, TanDEM-X) and fused DEM (EarthEnvDEM90, MERIT DEM). Their performances were assessed using a Digital Terrain Model (DTM) generated using airborne LiDAR data that had an outstanding absolute vertical accuracy (mean error (ME) = 0.24 m; root mean square error (RMSEz) = 1.20 m). Height differences between the global DEMs and the LiDAR DTM were calculated and examined their performances by forested vs. non-forested, slope, and elevation classes. The results showed the MERIT DEM was superior to other DEMs in most of the testing methods. It outperformed other DEMs with an RMSEz value of 3.02 m in the forested areas, followed by ALOS PALSAR (9.29 m), EarthEnv-DEM90 (9.40 m), SRTM (9.80 m), TanDEM-X (10.41 m), and ASTER GDEM3 (12.57 m). The MERIT DEM also had the best accuracy in the higher elevation areas. Overall, the ASTER GDEM3 had the worst accuracies, with relatively large over-estimations compared to other DEMs. Despite its low spatial resolution, the MERIT DEM was the best for representing terrain elevation for applications over a large area
Difference in pulmonary permeability between indirect and direct acute respiratory distress syndrome assessed by the transpulmonary thermodilution technique: a prospective, observational, multi-institutional study
Quantum Physics and Human Language
Human languages employ constructions that tacitly assume specific properties
of the limited range of phenomena they evolved to describe. These assumed
properties are true features of that limited context, but may not be general or
precise properties of all the physical situations allowed by fundamental
physics. In brief, human languages contain `excess baggage' that must be
qualified, discarded, or otherwise reformed to give a clear account in the
context of fundamental physics of even the everyday phenomena that the
languages evolved to describe. The surest route to clarity is to express the
constructions of human languages in the language of fundamental physical
theory, not the other way around. These ideas are illustrated by an analysis of
the verb `to happen' and the word `reality' in special relativity and the
modern quantum mechanics of closed systems.Comment: Contribution to the festschrift for G.C. Ghirardi on his 70th
Birthday, minor correction
Soluble Triggering Receptor Expressed on Myeloid cells-1 in bronchoalveolar lavage fluid is not predictive for ventilator-associated pneumonia
Gelsolin dysfunction causes photoreceptor loss in induced pluripotent cell and animal retinitis pigmentosa models
Mutations in the Retinitis Pigmentosa GTPase Regulator (RPGR) cause X-linked RP (XLRP), an untreatable, inherited retinal dystrophy that leads to premature blindness. RPGR localises to the photoreceptor connecting cilium where its function remains unknown. Here we show, using murine and human induced pluripotent stem cell models, that RPGR interacts with and activates the actin-severing protein gelsolin, and that gelsolin regulates actin disassembly in the connecting cilium, thus facilitating rhodopsin transport to photoreceptor outer segments. Disease-causing RPGR mutations perturb this RPGR-gelsolin interaction, compromising gelsolin activation. Both RPGR and Gelsolin knockout mice show abnormalities of actin polymerisation and mislocalisation of rhodopsin in photoreceptors. These findings reveal a clinically-significant role for RPGR in the activation of gelsolin, without which abnormalities in actin polymerisation in the photoreceptor connecting cilia cause rhodopsin mislocalisation and eventual retinal degeneration in XLRP.Mutations in the Retinitis Pigmentosa GTPase Regulator (RPGR) cause retinal dystrophy, but how this arises at a molecular level is unclear. Here, the authors show in induced pluripotent stem cells and mouse knockouts that RPGR mediates actin dynamics in photoreceptors via the actin-severing protein, gelsolin
The pseudokinase SgK223 promotes invasion of pancreatic ductal epithelial cells through JAK1/Stat3 signaling
- …