Construction management contracts: law and practice

The context of construction management (CM) reveals that this method of procurement is as much a management philosophy as a contract structure. It is important to consider legal and contractual issues in this context. The interplay between management and law is complex and often misunderstood. Before considering specific issues, the use of contractual remedies in business agreements is discussed. In addition, the extent to which standardising a form of contract detracts or contributes to the success of projects is also considered. The dearth of judicial decisions, and the lack of a standard form, render it difficult to be specific about legal issues. Therefore, the main discussion of legal issues is centred around a recently completed research project which involved eliciting the views of a cross-section of experienced construction management clients, consultants and trade contractors. These interviews are used as the basis for highlighting some of the most important legal points to consider when setting up CM projects. The interviews revealed that the advantage of CM is the proximity of the client to the trade contractors and the disadvantage is that it depends on a high degree of professionalism and experience; qualities which are unfortunately difficult to find in the UK construction industry

High resolution infrared absorption spectra, crystal field, and relaxation processes in CsCdBr_3:Pr^3+

High resolution low-temperature absorption spectra of 0.2% Pr^3+ doped CsCdBr_3 were measured in the spectral region 2000--7000 cm-1. Positions and widths of the crystal field levels within the 3H5, 3H4, 3F2, and 3F3 multiplets of the Pr^3+ main center have been determined. Hyperfine structure of several spectral lines has been found. Crystal field calculations were carried out in the framework of the semiphenomenological exchange charge model (ECM). Parameters of the ECM were determined by fitting to the measured total splittings of the 3H4 and 3H6 multiplets and to the observed in this work hyperfine splittings of the crystal field levels. One- and two-phonon relaxation rates were calculated using the phonon Green's functions of the perfect (CsCdBr_3) and locally perturbed (impurity dimer centers in CsCdBr_3:Pr^3+) crystal lattice. Comparison with the measured linewidths confirmed an essential redistribution of the phonon density of states in CsCdBr_3 crystals doped with rare-earth ions.Comment: 16 pages, 5 tables, 3 figure

Coronary CT Angiography and 5-Year Risk of Myocardial Infarction.

BACKGROUND: Although coronary computed tomographic angiography (CTA) improves diagnostic certainty in the assessment of patients with stable chest pain, its effect on 5-year clinical outcomes is unknown. METHODS: In an open-label, multicenter, parallel-group trial, we randomly assigned 4146 patients with stable chest pain who had been referred to a cardiology clinic for evaluation to standard care plus CTA (2073 patients) or to standard care alone (2073 patients). Investigations, treatments, and clinical outcomes were assessed over 3 to 7 years of follow-up. The primary end point was death from coronary heart disease or nonfatal myocardial infarction at 5 years. RESULTS: The median duration of follow-up was 4.8 years, which yielded 20,254 patient-years of follow-up. The 5-year rate of the primary end point was lower in the CTA group than in the standard-care group (2.3% [48 patients] vs. 3.9% [81 patients]; hazard ratio, 0.59; 95% confidence interval [CI], 0.41 to 0.84; P=0.004). Although the rates of invasive coronary angiography and coronary revascularization were higher in the CTA group than in the standard-care group in the first few months of follow-up, overall rates were similar at 5 years: invasive coronary angiography was performed in 491 patients in the CTA group and in 502 patients in the standard-care group (hazard ratio, 1.00; 95% CI, 0.88 to 1.13), and coronary revascularization was performed in 279 patients in the CTA group and in 267 in the standard-care group (hazard ratio, 1.07; 95% CI, 0.91 to 1.27). However, more preventive therapies were initiated in patients in the CTA group (odds ratio, 1.40; 95% CI, 1.19 to 1.65), as were more antianginal therapies (odds ratio, 1.27; 95% CI, 1.05 to 1.54). There were no significant between-group differences in the rates of cardiovascular or noncardiovascular deaths or deaths from any cause. CONCLUSIONS: In this trial, the use of CTA in addition to standard care in patients with stable chest pain resulted in a significantly lower rate of death from coronary heart disease or nonfatal myocardial infarction at 5 years than standard care alone, without resulting in a significantly higher rate of coronary angiography or coronary revascularization. (Funded by the Scottish Government Chief Scientist Office and others; SCOT-HEART ClinicalTrials.gov number, NCT01149590 .)

Candidalysin is required for neutrophil recruitment and virulence during systemic Candida albicans infection

Background Candidalysin is a cytolytic peptide toxin secreted by Candida albicans hyphae and has significantly advanced our understanding of fungal pathogenesis. Candidalysin is critical for mucosal C albicans infections and is known to activate epithelial cells to induce downstream innate immune responses that are associated with protection or immunopathology during oral or vaginal infections. Furthermore, candidalysin activates the NLRP3 inflammasome and causes cytolysis in mononuclear phagocytes. However, the role of candidalysin in driving systemic infections is unknown. Methods In this study, using candidalysin-producing and candidalysin-deficient C albicans strains, we show that candidalysin activates mitogen-activated protein kinase (MAPK) signaling and chemokine secretion in endothelial cells in vitro. Results Candidalysin induces immune activation and neutrophil recruitment in vivo, and it promotes mortality in zebrafish and murine models of systemic fungal infection. Conclusions The data demonstrate a key role for candidalysin in neutrophil recruitment and fungal virulence during disseminated systemic C albicans infections

Dust Lifting Through Surface Albedo Changes at Jezero Crater, Mars

We identify temporal variations in surface albedo at Jezero crater using first-of-their-kind high-cadence in-situ measurements of reflected shortwave radiation during the first 350 sols of the Mars 2020 mission. Simultaneous Mars Environmental Dynamics Analyzer (MEDA) measurements of pressure, radiative fluxes, winds, and sky brightness indicate that these albedo changes are caused by dust devils under typical conditions and by a dust storm at Ls ∼ 155°. The 17% decrease in albedo caused by the dust storm is one order of magnitude larger than the most apparent changes caused during quiescent periods by dust devils. Spectral reflectance measurements from Mastcam-Z images before and after the storm indicate that the decrease in albedo is mainly caused by dust removal. The occurrence of albedo changes is affected by the intensity and proximity of the convective vortex, and the availability and mobility of small particles at the surface. The probability of observing an albedo change increases with the magnitude of the pressure drop (ΔP): changes were detected in 3.5%, 43%, and 100% of the dust devils with ΔP 2.5 Pa and ΔP > 4.5 Pa, respectively. Albedo changes were associated with peak wind speeds above 15 m·s−1. We discuss dust removal estimates, the observed surface temperature changes coincident with albedo changes, and implications for solar-powered missions. These results show synergies between multiple instruments (MEDA, Mastcam-Z, Navcam, and the Supercam microphone) that improve our understanding of aeolian processes on Mars.This research has been funded by the Comunidad de Madrid Project S2018/NMT-4291 (TEC2SPACE-CM), by the Spanish State Research Agency (AEI) Project MDM-2017-0737 Unidad de Excelencia “María de Maeztu”- Centro de Astrobiología (CSIC/INTA), by the Spanish Ministry of Science and Innovation (MCIN)/State Agency of Research (10.13039/501100011033) project RTI2018-098728-B-C31, and by the project PID2021-126719OB-C41, funded by MCIN/AEI/10.13039/501100011033/FEDER, UE. RH, ASL and AM were supported by Grant PID2019-109467GB-I00 funded by MCIN/AEI/10.13039/501100011033/. Part of the research was carried out at the Jet Propulsion Laboratory, California Institute of Technology, under a contract with the National Aeronautics and Space Administration (80NM0018D0004). We want to thank J. Bell for processing Mastcam-Z projections showing the entire TIRS FOV and to S. Navarro and the entire team for generating the processed wind sensor data

A critical role for muscle ring finger-1 in acute lung injury-associated skeletal muscle wasting

Rationale: Acute lung injury (ALI) is a debilitating condition associated with severe skeletal muscle weakness thatpersists in humans long after lung injury has resolved. The molecular mechanisms underlying this condition are unknown. Objectives: To identify the muscle-specific molecular mechanisms responsible for muscle wasting in a mouse model of ALI. Methods:Changes in skeletal muscle weight, fiber size, in vivo contractile performance, and expression of mRNAs and proteins encoding muscle atrophy-associated genes for muscle ring finger-1 (MuRF1) and atrogin1 were measured. Genetic inactivation of MuRF1 or electroporation-mediated transduction of miRNA-based short hairpin RNAs targeting either MuRF1 or atrogin1 were used to identify their role in ALI-associated skeletal muscle wasting. Measurements and Main Results: Mice with ALI developed profound muscle atrophy and preferential loss of muscle contractile proteins associatedwith reducedmuscle function in vivo. Although mRNA expression of the muscle-specific ubiquitin ligases, MuRF1 and atrogin1, was increased in ALI mice, only MuRF1 protein levels were up-regulated. Consistent with these changes, suppression of MuRF1 by genetic or biochemical approaches prevented muscle fiber atrophy, whereas suppression of atrogin1 expression was without effect. Despite resolution of lung injury and down-regulation of MuRF1 and atrogin1, force generation in ALI mice remained suppressed. Conclusions: These data show that MuRF1 is responsible for mediating muscle atrophy that occurs during the period of active lung injury inALI mice and that, as in humans, skeletal muscle dysfunction persists despite resolution of lung injury