Access Rate to the Emergency Department for Venous Thromboembolism in Relationship with Coarse and Fine Particulate Matter Air Pollution

Particulate matter (PM) air pollution has been associated with cardiovascular and respiratory disease. Recent studies have proposed also a link with venous thromboembolism (VTE) risk. This study was aimed to evaluate the possible influence of air pollution-related changes on the daily flux of patients referring to the Emergency Department (ED) for VTE, dissecting the different effects of coarse and fine PM. From July 1st, 2007, to June 30th, 2009, data about ED accesses for VTE and about daily concentrations of PM air pollution in Verona district (Italy) were collected. Coarse PM (PM10-2.5) was calculated by subtracting the finest PM2.5 from the whole PM10. During the index period a total of 302 accesses for VTE were observed (135 males and 167 females; mean age 68.3±16.7 years). In multiple regression models adjusted for other atmospheric parameters PM10-2.5, but not PM2.5, concentrations were positively correlated with VTE (beta-coefficient = 0.237; P = 0.020). During the days with high levels of PM10-2.5 (≥75th percentile) there was an increased risk of ED accesses for VTE (OR 1.69 with 95%CI 1.13–2.53). By analysing days of exposure using distributed lag non-linear models, the increase of VTE risk was limited to PM10-2.5 peaks in the short-term period. Consistently with these results, in another cohort of subjects without active thrombosis (n = 102) an inverse correlation between PM10-2.5 and prothrombin time was found (R = −0.247; P = 0.012). Our results suggest that short-time exposure to high concentrations of PM10-2.5 may favour an increased rate of ED accesses for VTE through the induction of a prothrombotic state

Cytoskeletal control of B cell responses to antigens.

The actin cytoskeleton is essential for cell mechanics and has increasingly been implicated in the regulation of cell signalling. In B cells, the actin cytoskeleton is extensively coupled to B cell receptor (BCR) signalling pathways, and defects of the actin cytoskeleton can either promote or suppress B cell activation. Recent insights from studies using single-cell imaging and biophysical techniques suggest that actin orchestrates BCR signalling at the plasma membrane through effects on protein diffusion and that it regulates antigen discrimination through the biomechanics of immune synapses. These mechanical functions also have a role in the adaptation of B cell subsets to specialized tasks during antibody responses

Early influences on cardiovascular and renal development

The hypothesis that a developmental component plays a role in subsequent disease initially arose from epidemiological studies relating birth size to both risk factors for cardiovascular disease and actual cardiovascular disease prevalence in later life. The findings that small size at birth is associated with an increased risk of cardiovascular disease have led to concerns about the effect size and the causality of the associations. However, recent studies have overcome most methodological flaws and suggested small effect sizes for these associations for the individual, but an potential important effect size on a population level. Various mechanisms underlying these associations have been hypothesized, including fetal undernutrition, genetic susceptibility and postnatal accelerated growth. The specific adverse exposures in fetal and early postnatal life leading to cardiovascular disease in adult life are not yet fully understood. Current studies suggest that both environmental and genetic factors in various periods of life may underlie the complex associations of fetal growth retardation and low birth weight with cardiovascular disease in later life. To estimate the population effect size and to identify the underlying mechanisms, well-designed epidemiological studies are needed. This review is focused on specific adverse fetal exposures, cardiovascular adaptations and perspectives for new studies. Copyrigh

Multifrequency studies of the peculiar quasar 4C+21.35 during the 2010 flaring activity

The discovery of rapidly variable Very High Energy ( VHE; E &gt; 100 GeV). - ray emission from 4C + 21.35 ( PKS 1222+ 216) by MAGIC on 2010 June 17, triggered by the high activity detected by the Fermi Large Area Telescope ( LAT) in high energy ( HE; E &gt; 100 MeV). - rays, poses intriguing questions on the location of the. - ray emitting region in this flat spectrum radio quasar. We present multifrequency data of 4C + 21.35 collected from centimeter to VHE during 2010 to investigate the properties of this source and discuss a possible emission model. The first hint of detection at VHE was observed by MAGIC on 2010 May 3, soon after a gamma- ray flare detected by Fermi-LAT that peaked on April 29. The same emission mechanism may therefore be responsible for both the HE and VHE emission during the 2010 flaring episodes. Two optical peaks were detected on 2010 April 20 and June 30, close in time but not simultaneous with the two gamma- ray peaks, while no clear connection was observed between the X-ray and gamma- ray emission. An increasing flux density was observed in radio and mm bands from the beginning of 2009, in accordance with the increasing gamma- ray activity observed by Fermi-LAT, and peaking on 2011 January 27 in the mm regime ( 230 GHz). We model the spectral energy distributions ( SEDs) of 4C + 21.35 for the two periods of the VHE detection and a quiescent state, using a one-zone model with the emission coming from a very compact region outside the broad line region. The three SEDs can be fit with a combination of synchrotron self-Compton and external Compton emission of seed photons from a dust torus, changing only the electron distribution parameters between the epochs. The fit of the optical/UV part of the spectrum for 2010 April 29 seems to favor an inner disk radius of &lt; six gravitational radii, as one would expect from a prograde-rotating Kerr black hole.</p

The Rotterdam Study: 2012 objectives and design update

The Rotterdam Study is a prospective cohort study ongoing since 1990 in the city of Rotterdam in The Netherlands. The study targets cardiovascular, endocrine, hepatic, neurological, ophthalmic, psychiatric, dermatological, oncological, and respiratory diseases. As of 2008, 14,926 subjects aged 45 years or over comprise the Rotterdam Study cohort. The findings of the Rotterdam Study have been presented in over a 1,000 research articles and reports (see www.erasmus-epidemiology.nl/rotterdamstudy). This article gives the rationale of the study and its design. It also presents a summary of the major findings and an update of the objectives and methods

Higher temperatures increase suicide rates in the United States and Mexico

Linkages between climate and mental health are often theorized but remain poorly quantified. In particular, it is unknown whether the rate of suicide, a leading cause of death globally, is systematically affected by climatic conditions. Using comprehensive data from multiple decades for both the United States and Mexico, we find that suicide rates rise 0.7% in US counties and 2.1% in Mexican municipalities for a 1 °C increase in monthly average temperature. This effect is similar in hotter versus cooler regions and has not diminished over time, indicating limited historical adaptation. Analysis of depressive language in >600 million social media updates further suggests that mental well-being deteriorates during warmer periods. We project that unmitigated climate change (RCP8.5) could result in a combined 9–40 thousand additional suicides (95% confidence interval) across the United States and Mexico by 2050, representing a change in suicide rates comparable to the estimated impact of economic recessions, suicide prevention programmes or gun restriction laws