Equity in healthcare: status, barriers, and challenges

Global health provides a challenge for primary care and general practice which will become increasingly important in the future as the prevalence of multimorbidity increases. There is increasing likelihood of survival from acute illnesses and increase an in the elderly population. This literature review focuses on the health inequities, the role of family medicine and the factors that are essential in overcoming these inequalities. Health disparities refer to gaps in the quality of health and delivery of health care across racial, ethnic, gender and socioeconomic groups. The health disparities vary among different countries and the factors that lead to these disparities differ across the world. Family medicine plays a crucial role in bridging this gap and is an essential backbone of the society in developing nations as well as the wealthier nations in providing equity in health care to all people. There are many factors leading to inequity in health care. Family medicine should be recognized as a specialty across the world, as family medicine with its person centered care can bring about a global change in health care. This issue has to be taken up more seriously by the institutions like the WHO, UN and also individual governments along with the political parties to create uniformity in health care. In the current setting of the global economic and financial crisis, a truly global solution is needed. The WHO has come up with various strategies to solve the issue of financial crises and ensuring equity in health globally. This will ensure equal health care to all people especially the underprivileged in developing countries who do not have access to better healthcare due to lack of resources. This factor is a major contributor to the premature death of individuals at all stages of life from new born to the elderly and includes infant mortality and mortality due to chronic diseases. This is important in creating uniformity in health care across the world but has to be considered at a global level to have an impact

First mirror test in JET for ITER : Complete overview after three ILW campaigns

The First Mirror Test for ITER has been carried out in JET with mirrors exposed during: (i) the third ILW campaign (ILW-3, 2015-2016, 23.33 h plasma) and (ii) all three campaigns, i.e. ILW-1 to ILW-3: 2011-2016, 63,52 h in total. All mirrors from main chamber wall show no significant changes of the total reflectivity from the initial value and the diffuse reflectivity does not exceed 3% in the spectral range above 500 nm. The modified layer on surface has very small amount of impurities such as D, Be, C, N, O and Ni. All mirrors from the divertor (inner, outer, base under the bulk W tile) lost reflectivity by 20-80% due to the beryllium-rich deposition also containing D, C, N, O, Ni and W. In the inner divertor N reaches 5 x 10(17) cm(-2), W is up to 4.3 x 10(17) cm(-2), while the content of Ni is the greatest in the outer divertor: 3.8 x 10(17) cm(-2). Oxygen-18 used as the tracer in experiments at the end of ILW-3 has been detected at the level of 1.1 x 10(16) cm(-2). The thickness of deposited layer is in the range of 90 nm to 900 nm. The layer growth rate in the base (2.7 pm s(-1)) and inner divertor is proportional to the exposure time when a single campaign and all three are compared. In a few cases, on mirrors located at the cassette mouth, flaking of deposits and erosion occurred.Peer reviewe

Serial selection for invasiveness increases expression of miR-143/miR-145 in glioblastoma cell lines

<p>Abstract</p> <p>Background</p> <p>Glioblastoma multiforme (GBM) is the most common primary central nervous system malignancy and its unique invasiveness renders it difficult to treat. This invasive phenotype, like other cellular processes, may be controlled in part by microRNAs - a class of small non-coding RNAs that act by altering the expression of targeted messenger RNAs. In this report, we demonstrate a straightforward method for creating invasive subpopulations of glioblastoma cells (IM3 cells). To understand the correlation between the expression of miRNAs and the invasion, we fully profiled 1263 miRNAs on six different cell lines and two miRNAs, miR-143 and miR-145, were selected for validation of their biological properties contributing to invasion. Further, we investigated an ensemble effect of both miR-143 and miR-145 in promoting invasion.</p> <p>Methods</p> <p>By repeated serial invasion through Matrigel^®-coated membranes, we isolated highly invasive subpopulations of glioma cell lines. Phenotypic characterization of these cells included <it>in vitro </it>assays for proliferation, attachment, and invasion. Micro-RNA expression was compared using miRCURY arrays (Exiqon). In situ hybridization allowed visualization of the regional expression of miR-143 and miR-145 in tumor samples, and antisense probes were used investigate <it>in vitro </it>phenotypic changes seen with knockdown in their expression.</p> <p>Results</p> <p>The phenotype we created in these selected cells proved stable over multiple passages, and their microRNA expression profiles were measurably different. We found that two specific microRNAs expressed from the same genetic locus, miR-143 and miR-145, were over-expressed in our invasive subpopulations. Further, we also found that combinatorial treatment of these cells with both antisense-miRNAs (antimiR-143 and -145) will abrogated their invasion without decreasing cell attachment or proliferation.</p> <p>Conclusions</p> <p>To best of our knowledge, these data demonstrate for the first time that miR-143 and miR-145 regulate the invasion of glioblastoma and that miR-143 and -145 could be potential therapeutic target for anti-invasion therapies of glioblastoma patients.</p

Circulating CD62E+ Microparticles and Cardiovascular Outcomes

BACKGROUND: Activated endothelial cells release plasma membrane submicron vesicles expressing CD62E (E-selectin) into blood, known as endothelial microparticles (EMPs). We studied whether the levels of endothelial microparticles expressing CD62E(+), CD31(+)/Annexin-V(+), or CD31(+)/CD42(-) predict cardiovascular outcomes in patients with stroke history. METHODS/PRINCIPAL FINDINGS: Patients with stroke history at least 3 months prior to enrolment were recruited. Peripheral blood EMP levels were measured by flow cytometry. Major cardiovascular events and death were monitored for 36 months. Three hundred patients were enrolled, of which 298 completed the study according to protocol. Major cardiovascular events occurred in 29 patients (9.7%). Nine patients died, five from cardiovascular causes. Cumulative event-free survival rates were lower in patients with high levels of CD62E(+) microparticles. Multivariate Cox regression analysis adjusted for cardiovascular risk factors, medications and stroke etiologic groups showed an association between a high CD62E(+) microparticle level and a risk of major cardiovascular events and hospitalization. Levels of other kinds of EMPs expressing CD31(+)/Annexin-V(+) or CD31(+)/CD42(-) markers were not predictive of cardiovascular outcomes. CONCLUSION: A high level of CD62E(+) microparticles is associated with cardiovascular events in patients with stroke history, suggesting that the systemic endothelial activation increases the risk for cardiovascular morbidities

Protective paraspeckle hyper-assembly downstream of TDP-43 loss of function in amyotrophic lateral sclerosis

Background Paraspeckles are subnuclear bodies assembled on a long non-coding RNA (lncRNA) NEAT1. Their enhanced formation in spinal neurons of sporadic amyotrophic lateral sclerosis (ALS) patients has been reported but underlying mechanisms are unknown. The majority of ALS cases are characterized by TDP-43 proteinopathy. In current study we aimed to establish whether and how TDP-43 pathology may augment paraspeckle assembly. Methods Paraspeckle formation in human samples was analysed by RNA-FISH and laser capture microdissection followed by qRT-PCR. Mechanistic studies were performed in stable cell lines, mouse primary neurons and human embryonic stem cell-derived neurons. Loss and gain of function for TDP-43 and other microRNA pathway factors were modelled by siRNA-mediated knockdown and protein overexpression. Results We show that de novo paraspeckle assembly in spinal neurons and glial cells is a hallmark of both sporadic and familial ALS with TDP-43 pathology. Mechanistically, loss of TDP-43 but not its cytoplasmic accumulation or aggregation augments paraspeckle assembly in cultured cells. TDP-43 is a component of the microRNA machinery, and recently, paraspeckles have been shown to regulate pri-miRNA processing. Consistently, downregulation of core protein components of the miRNA pathway also promotes paraspeckle assembly. In addition, depletion of these proteins or TDP-43 results in accumulation of endogenous dsRNA and activation of type I interferon response which also stimulates paraspeckle formation. We demonstrate that human or mouse neurons in vitro lack paraspeckles, but a synthetic dsRNA is able to trigger their de novo formation. Finally, paraspeckles are protective in cells with compromised microRNA/dsRNA metabolism, and their assembly can be promoted by a small-molecule microRNA enhancer. Conclusions Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA

Can houseplants improve indoor air quality by removing CO2 and increasing relative humidity?

High indoor CO2 concentrations and low relative humidity (RH) create an array of well-documented human health issues. Therefore, assessing houseplants’ potential as a low-cost approach to CO2 removal and increasing RH is important. We investigated how environmental factors such as ’dry’ ( 0.30 m3 m-3) growing substrates, and indoor light levels (‘low’ 10 µmol m-2 s-1, ‘high’ 50 µmol m-2 s-1 and ‘very high’ 300 µmol m-2 s-1), influence the plants’ net CO2 assimilation (‘A’) and water-vapour loss. Seven common houseplant taxa – representing a variety of leaf types, metabolisms and sizes – were studied for their ability to assimilate CO2 across a range of indoor light levels. Additionally, to assess the plants’ potential contribution to RH increase, the plants’ evapo-transpiration (ET) was measured. At typical ‘low’ indoor light levels ‘A’ rates were generally low (< 3.9 mg hr-1). Differences between ‘dry’ and ’wet’ plants at typical indoor light levels were negligible in terms of room-level impact. Light compensation points (i.e. light levels at which plants have positive ‘A’) were in the typical indoor light range (1-50 µmol m-2 s-1) only for two studied Spathiphyllum wallisii cultivars and Hedera helix; these plants would thus provide the best CO2 removal indoors. Additionally, increasing indoor light levels to 300 µmol m-2 s-1 would, in most species, significantly increase their potential to assimilate CO2. Species which assimilated the most CO2 also contributed most to increasing RH