Collusions Between Patients and Clinicians in End-of-Life Care: Why Clarity Matters.

Collusion, an unconscious dynamic between patients and clinicians, may provoke strong emotions, unreflected behaviors, and a negative impact on care. Collusions, prevalent in the health care setting, are triggered by situations which signify an unresolved psychological issue relevant for both, patient and clinician. After an introductory definition of collusion, two archetypal situations of collusion-based on material from a regular supervision of a palliative care specialist by a liaison psychiatrist-and means of working through collusion are presented. The theoretical framework of collusion is then described and the conceptual shortcomings of the palliative care literature in this respect discussed, justifying the call for more clarity. Finally, cultural aspects and societal injunctions on the dying, contributing to the development of collusion in end-of-life care, are discussed

Theoretical and Numerical Analysis of an Optimal Execution Problem with Uncertain Market Impact

This paper is a continuation of Ishitani and Kato (2015), in which we derived a continuous-time value function corresponding to an optimal execution problem with uncertain market impact as the limit of a discrete-time value function. Here, we investigate some properties of the derived value function. In particular, we show that the function is continuous and has the semigroup property, which is strongly related to the Hamilton-Jacobi-Bellman quasi-variational inequality. Moreover, we show that noise in market impact causes risk-neutral assessment to underestimate the impact cost. We also study typical examples under a log-linear/quadratic market impact function with Gamma-distributed noise.Comment: 24 pages, 14 figures. Continuation of the paper arXiv:1301.648

Bowing of the band gap pressure coefficients in InGaN alloys

The hydrostatic pressure dependence of photoluminescence, dEPL/dp, of InxGa1−xN epilayers has been measured in the full composition range 0_x_1. Furthermore, ab initio calculations of the band gap pressure coefficient dEG/dp were performed. Both the experimental dEPL/dp values and calculated dEG/dp results show pronounced bowing and we find that the pressure coefficients have a nearly constant value of about 25 meV/GPa for epilayers with x_0.4 and a relatively steep dependence for x_0.4. On the basis of the agreement of the observed PL pressure coefficient with our calculations, we confirm that band-to-band recombination processes are responsible for PL emission and that no localized states are involved. Moreover, the good agreement between the experimentally determined dEPL/dp and the theoretical curve of dEG/dp indicates that the hydrostatic pressure dependence of PL measurements can be used to quantify changes of the band gap of the InGaN ternary alloy under pressure, demonstrating that the disorder-related Stokes shift in InGaN does not induce a significant difference between dEPL/dp and dEG/dp. This information is highly relevant for the correct analysis of pressure measurement

Are Student Loan Default Rates Linked to Institutional Capacity?

As more undergraduates have taken out loans to attend college, the number of borrowers who fail to repay their student loans has increased. While previous research has focused on students’ likelihood to default, this study employed institutional cohort default rates (CDRs) as an outcome variable. Using Integrated Postsecondary Education Data System, this study investigated the association between institutional effectiveness and CDRs. Coupled with multilevel modeling, the study also observed the effects of state-level factors, such as state appropriation and unemployment, on CDRs. The results showed that institutional characteristics—e.g., proportion of minority students, admission test scores, retention rates, and instructional expenses—are strongly associated with institutional CDRs. This suggests that institutional default rates are mainly a function of the students that institutions enroll, and future studies should include institutional as well as student factors to provide policy makers and researchers with a more comprehensive understanding of institutional CDRs

Technologies, Policies, and Measures for Mitigating Climate Change

This Technical Paper provides an overview and analysis of technologies and measures to limit and reduce greenhouse gas (GHG) emissions and to enhance GHG sinks under the United Nations Framework Convention on Climate Change (FCCC). The paper focuses on technologies and measures for the countries listed in Annex I of the FCCC, while noting information as appropriate for use by non- Annex I countries. Technologies and measures are examined over three time periods -- with a focus on the short term (present to 2010) and the medium term (2010-2020), but also including discussion of longer-term (e.g., 2050) possibilities and opportunities. For this analysis, the authors draw on materials used to prepare the IPCC Second Assessment Report (SAR) and previous IPCC assessments and reports. The Technical Paper includes discussions of technologies and measures that can be adopted in three energy end-use sectors (commercial/residential/institutional buildings, transportation, and industry), as well as in the energy supply sector and the agriculture, forestry, and waste management sectors. Broader measures affecting national economies are discussed in a final section on economic instruments. A range of potential measures are analyzed, including market-based programs; voluntary agreements; regulatory measures; research, development, and demonstration (RD&D); taxes on GHG emissions; and emissions permits/quotas. It should be noted that the choice of instruments could have economic impacts on other countries. The paper identifies and evaluates different options on the basis of three criteria. Because of the difficulty of estimating the economic and market potential (see Box 1) of different technologies and the effectiveness of different measures in achieving emission reduction objectives, and because of the danger of double-counting the results achieved by measures that tap the same technical potentials, the paper does not estimate total global emissions reductions. Nor does the paper recommend adoption of any particular approaches

The role of hybrid ubiquitin chains in the MyD88 and other innate immune signalling pathways

The adaptor protein MyD88 is required for signal transmission by Toll-like Receptors (TLRs) and receptors of the interleukin 1 (IL-1) family of cytokines. MyD88 signalling triggers the formation of Lys63-linked and Met1-linked ubiquitin (K63-Ub, M1-Ub) chains within minutes. The K63-Ub chains, which are formed by the E3 ubiquitin ligases TRAF6, Pellino1 and Pellino2, activate TAK1, the master kinase that switches on mitogen-activated protein (MAP) kinase cascades and initiates activation of the canonical IκB kinase (IKK) complex. The M1-Ub chains, which are formed by the Linear Ubiquitin chain Assembly Complex (LUBAC), bind to the NEMO component of the IKK complex and are required for TAK1 to activate IKKs, but not MAP kinases. An essential E3 ligase-independent role of TRAF6 is to recruit LUBAC into the MyD88 signalling complex, where it recognises preformed K63-Ub chains attached to protein components of these complexes, such as IRAK1, producing ubiquitin chains containing both types of linkage, termed K63/M1-Ub hybrids. The formation of K63/M1-Ub hybrids, which is a feature of several innate immune signalling pathways, permits the co-recruitment of proteins that interact with either K63-Ub or M1-Ub chains. Two likely roles for K63/M1- Ub hybrids are to facilitate the TAK1-dependent activation of the IKK complex and to prevent the hyper-activation of these kinases by recruiting A20 and A20-binding inhibitor of NF-κB1 (ABIN1). These proteins restrict activation of the TAK1 and IKK complexes, probably by competing with them for binding to K63/M1-Ub hybrids. The formation of K63/M1-Ub hybrids may also regulate the rate at which the ubiquitin linkages in these chains are hydrolysed. The IKK-catalysed phosphorylation of some of its substrates permits their recognition by the E3 ligase SCFβ TRCP, leading to their Lys48-linked ubiquitylation and proteasomal degradation. Innate immune signalling is therefore controlled by the formation and destruction of three different types of ubiquitin linkage

Myofibroblast-Derived SFRP1 as Potential Inhibitor of Colorectal Carcinoma Field Effect

Epigenetic changes of stromal-epithelial interactions are of key importance in the regulation of colorectal carcinoma (CRC) cells and morphologically normal, but genetically and epigenetically altered epithelium in normal adjacent tumor (NAT) areas. Here we demonstrated retained protein expression of well-known Wnt inhibitor, secreted frizzled-related protein 1 (SFRP1) in stromal myofibroblasts and decreasing epithelial expression from NAT tissues towards the tumor. SFRP1 was unmethylated in laser microdissected myofibroblasts and partially hypermethylated in epithelial cells in these areas. In contrast, we found epigenetically silenced myofibroblast-derived SFRP1 in CRC stroma. Our results suggest that the myofibroblast-derived SFRP1 protein might be a paracrine inhibitor of epithelial proliferation in NAT areas and loss of this signal may support tumor proliferation in CRC

Inhibition of NOS- like activity in maize alters the expression of genes involved in H2O2 scavenging and glycine betaine biosynthesis

Nitric oxide synthase-like activity contributes to the production of nitric oxide in plants, which controls plant responses to stress. This study investigates if changes in ascorbate peroxidase enzymatic activity and glycine betaine content in response to inhibition of nitric oxide synthase-like activity are associated with transcriptional regulation by analyzing transcript levels of genes (betaine aldehyde dehydrogenase) involved in glycine betaine biosynthesis and those encoding antioxidant enzymes (ascorbate peroxidase and catalase) in leaves of maize seedlings treated with an inhibitor of nitric oxide synthase-like activity. In seedlings treated with a nitric oxide synthase inhibitor, transcript levels of betaine aldehyde dehydrogenase were decreased. In plants treated with the nitric oxide synthase inhibitor, the transcript levels of ascorbate peroxidase-encoding genes were down-regulated. We thus conclude that inhibition of nitric oxide synthase-like activity suppresses the expression of ascorbate peroxidase and betaine aldehyde dehydrogenase genes in maize leaves. Furthermore, catalase activity was suppressed in leaves of plants treated with nitric oxide synthase inhibitor; and this corresponded with the suppression of the expression of catalase genes. We further conclude that inhibition of nitric oxide synthase-like activity, which suppresses ascorbate peroxidase and catalase enzymatic activities, results in increased H2O2 content

Wnt signalling and cancer stem cells

[Abstract] Intracellular signalling mediated by secreted Wnt proteins is essential for the establishment of cell fates and proper tissue patterning during embryo development and for the regulation of tissue homeostasis and stem cell function in adult tissues. Aberrant activation of Wnt signalling pathways has been directly linked to the genesis of different tumours. Here, the components and molecular mechanisms implicated in the transduction of Wnt signal, along with important results supporting a central role for this signalling pathway in stem cell function regulation and carcinogenesis will be briefly reviewed.Ministerio de Ciencia e Innovación; SAF2008-0060