Sociopolitical consequences of COVID-19 in the Americas, Europe, and Asia: A multilevel, multicountry investigation of risk perceptions and support for antidemocratic practices

Although different social crises may eventually favor undemocratic and authoritarian forms of governance, at some point, such antidemocratic practices require the support of a significant part of the population to be implemented. The present research investigates how and whether the COVID-19 pandemic might have favoured greater support for antidemocratic governmental practices, on the premise of regaining control and security. Using data from 17 countries (N = 4364) and national-level indicators (i.e., real number of contagions and deaths, and sociopolitical indicators), we test how the risk of contagion and death from COVID-19, along with personal orientations (i.e., social dominance orientation [SDO], right-wing authoritarianism [RWA], and perceived anomie) motivate authoritarian and antidemocratic practices. Results from multilevel models indicate that risk perception and perceptions of political instability predict a wish for stronger leadership, agreement with martial law, and support for a controlling government especially when SDO and RWA are high, while more egalitarian and less conservative people agree less with these authoritarian measures in spite of the levels of risk perception. We discuss the implications for these findings for future research on similar but also dissimilar external events (natural disasters, war, or terror incidents) and the consequences for societies with higher authoritarian tendencies.Fil: Pizarro, José J.. Universidad Católica del Norte; Chile. Universidad del País Vasco; EspañaFil: Cakal, Huseyin. Keele University; Reino UnidoFil: Méndez, Lander. Universidad del País Vasco; EspañaFil: Zumeta, Larraitz N.. Universidad del País Vasco; EspañaFil: Gracia-Leiva, Marcela. Universidad del País Vasco; EspañaFil: Basabe, Nekane. Universidad del País Vasco; EspañaFil: Navarro-Carrillo, Ginés. Universidad de Jaén; EspañaFil: Cazan, Ana Maria. Transilvania University of Brasov; RumaniaFil: Keshavarzi, Saeed. Independent Researcher; IránFil: López López, Wilson. Pontificia Universidad Javeriana; ColombiaFil: Yahiiaiev, Illia. Taras Shevchenko National University of Kyiv; UcraniaFil: Alzugaray Ponce, Carolina. Universidad Santo Tomas; ChileFil: Villagrán, Loreto. Universidad de Concepción; ChileFil: Moyano Díaz, Emilio. Universidad de Talca; ChileFil: Petrović, Nebojša. University of Belgrade; SerbiaFil: Mathias, Anderson. Universidad Autonoma de Coahuila; MéxicoFil: Techio, Elza M.. Universidade Federal da Bahia; BrasilFil: Wlodarczyk, Anna. Universidad Católica del Norte; ChileFil: Alfaro-Beracoechea, Laura. Universidad de Guadalajara; MéxicoFil: Ibarra, Manuel L.. Universidad Nacional Autónoma de México; MéxicoFil: Michael, Andreas. University of Cyprus; ChipreFil: Mhaskar, Sumeet. O.p. Jindal Global University; IndiaFil: Martínez Zelaya, Gonzalo. Universidad Viña del Mar; ChileFil: Bilbao, Marian. Universidad Alberto Hurtado; ChileFil: Delfino, Gisela Isabel. Universidad Pontificia Comillas; España. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Carvalho, Catarina L.. Universidad de Porto; PortugalFil: Pinto, Isabel R.. Universidad de Porto; PortugalFil: Mohsin, Falak Zehra. Karachi School Of Business And Leadership; PakistánFil: Espinosa, Agustín. Pontificia Universidad Católica de Perú; PerúFil: Cueto, Rosa María. Pontificia Universidad Católica de Perú; PerúFil: Cavalli, Stefano. Scuola Universitaria Professionale Della Svizzera Italiana; ItaliaFil: da Costa, Silvia. Universidad de Zaragoza; EspañaFil: Amutio, Alberto. Universidad Andrés Bello; Chile. Universidad del País Vasco; EspañaFil: Alonso Arbiol, Itziar. Universidad del País Vasco; EspañaFil: Páez, Darío. Universidad Andrés Bello; Chil

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.

Estimating global injuries morbidity and mortality : methods and data used in the Global Burden of Disease 2017 study

Background: While there is a long history of measuring death and disability from injuries, modern research methods must account for the wide spectrum of disability that can occur in an injury, and must provide estimates with sufficient demographic, geographical and temporal detail to be useful for policy makers. The Global Burden of Disease (GBD) 2017 study used methods to provide highly detailed estimates of global injury burden that meet these criteria. Methods: In this study, we report and discuss the methods used in GBD 2017 for injury morbidity and mortality burden estimation. In summary, these methods included estimating cause-specific mortality for every cause of injury, and then estimating incidence for every cause of injury. Non-fatal disability for each cause is then calculated based on the probabilities of suffering from different types of bodily injury experienced. Results: GBD 2017 produced morbidity and mortality estimates for 38 causes of injury. Estimates were produced in terms of incidence, prevalence, years lived with disability, cause-specific mortality, years of life lost and disability-adjusted life-years for a 28-year period for 22 age groups, 195 countries and both sexes. Conclusions: GBD 2017 demonstrated a complex and sophisticated series of analytical steps using the largest known database of morbidity and mortality data on injuries. GBD 2017 results should be used to help inform injury prevention policy making and resource allocation. We also identify important avenues for improving injury burden estimation in the future

Contributions of mean and shape of blood pressure distribution to worldwide trends and variations in raised blood pressure: A pooled analysis of 1018 population-based measurement studies with 88.6 million participants

© The Author(s) 2018. Background: Change in the prevalence of raised blood pressure could be due to both shifts in the entire distribution of blood pressure (representing the combined effects of public health interventions and secular trends) and changes in its high-blood-pressure tail (representing successful clinical interventions to control blood pressure in the hypertensive population). Our aim was to quantify the contributions of these two phenomena to the worldwide trends in the prevalence of raised blood pressure. Methods: We pooled 1018 population-based studies with blood pressure measurements on 88.6 million participants from 1985 to 2016. We first calculated mean systolic blood pressure (SBP), mean diastolic blood pressure (DBP) and prevalence of raised blood pressure by sex and 10-year age group from 20-29 years to 70-79 years in each study, taking into account complex survey design and survey sample weights, where relevant. We used a linear mixed effect model to quantify the association between (probittransformed) prevalence of raised blood pressure and age-group- and sex-specific mean blood pressure. We calculated the contributions of change in mean SBP and DBP, and of change in the prevalence-mean association, to the change in prevalence of raised blood pressure. Results: In 2005-16, at the same level of population mean SBP and DBP, men and women in South Asia and in Central Asia, the Middle East and North Africa would have the highest prevalence of raised blood pressure, and men and women in the highincome Asia Pacific and high-income Western regions would have the lowest. In most region-sex-age groups where the prevalence of raised blood pressure declined, one half or more of the decline was due to the decline in mean blood pressure. Where prevalence of raised blood pressure has increased, the change was entirely driven by increasing mean blood pressure, offset partly by the change in the prevalence-mean association. Conclusions: Change in mean blood pressure is the main driver of the worldwide change in the prevalence of raised blood pressure, but change in the high-blood-pressure tail of the distribution has also contributed to the change in prevalence, especially in older age groups