The ethics of inherent trust in care robots for the elderly

The way elderly care is delivered is changing. Attempts are being made to accommodate the increasing number of elderly, and the decline in the number of people available to care for them, with care robots. This change introduces ethical issues into robotics and healthcare. The two-part study (heuristic evaluation and survey) reported here examines a phenomenon which is a result of that change. The phenomenon rises out of a contradiction. All but 2 (who were undecided) of the 12 elderly survey respondents, out of the total of 102 respondents, wanted to be able to change how the presented care robot made decisions and 7 of those 12 elderly wanted to be able to examine its decision making process so as to ensure the care provided is personalized. However, at the same time, 34% of the elderly participants said they were willing to trust the care robot inherently, compared to only 16% of the participants who were under fifty. Additionally, 66% of the elderly respondents said they were very likely or likely to accept and use such a care robot in their everyday lives. The contradiction of inherent trust and simultaneous wariness about control gives rise to the phenomenon: elderly in need want control over their care to ensure it is personalized, but many may desperately take any help they can get. The possible causes, and ethical implications, of this phenomenon are the focus of this paper

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Obesity, metabolic syndrome, diabetes and smoking

It is becoming increasingly clear that arterial stiffness may be determined not only by age(ing) and blood pressure, but also by exposure to other cardiovascular risk factors. This chapter reviews the evidence provided by studies adopting an aetiological model of analyses of determinants of arterial stiffness, mainly derived, if available, from prospective designs. Specifically, the following risk factors are examined: the critical axis (central) obesity – metabolic syndrome – (type 2) diabetes, and also smoking. There is convincing evidence, reinforced by recent aetiological prospective studies, that these risk factors, all of which may be preventable, increase arterial stiffness. This may explain, at least in part, the increased cardiovascular disease risk observed in these conditions. However, the molecular basis of greater arterial stiffness associated with these risk factors remains to be fully elucidated. In addition, the prognostic significance of arterial stiffness indices in individuals with these risk factors, and the extent to which intervention on these risk factors improves cardiovascular outcome through beneficial impact on arterial stiffness, is still unclear. Given the high and/or increasing prevalence of these risk factors, these issues constitute an important research agenda

T1 Values in Hydride and New Molecular Hydrogen Phosphite Complexes of Comparable Structure

The molecular hydrogen complexes {MH(η2-H 2)[PhP(OEt)2]4} BPh4 (M = Fe, Ru, Os) and dihydride species {CoH2[PhP(OEt)2] 4}BPh4 have been prepared and T1 measurements for H- and η2-H2 resonances give T 1 <100 ms for all complexes at 80 MHz