178 research outputs found

    Multimorbidity: What do we know? What should we do?

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    Multimorbidity, which is defined as the co-occurrence of two or more chronic conditions, has moved onto the priority agenda for many health policymakers and healthcare providers. Patients with multimorbidity are high utilizers of healthcare resources and are some of the most costly and difficult-to-treat patients in Europe. Preventing and improving the way multimorbidity is managed is now a key priority for many countries, and work is at last underway to develop more sustainable models of care. Unfortunately, this effort is being hampered by a lack of basic knowledge about the aetiology, epidemiology, and risk factors for multimorbidity, and the efficacy and cost-effectiveness of different interventions. The European Commission recognizes the need for reform in this area and has committed to raising awareness of multimorbidity, encouraging innovation, optimizing the use of existing resources, and coordinating the efforts of different stakeholders across the European Union. Many countries have now incorporated multimorbidity into their own healthcare strategies and are working to strengthen their prevention efforts and develop more integrated models of care. Although there is some evidence that integrated care for people with multimorbidity can create efficiency gains and improve health outcomes, the evidence is limited, and may only be applicable to high-income countries with relatively strong and well-resourced health systems. In low- to middle-income countries, which are facing the double burden of infectious and chronic diseases, integration of care will require capacity building, better quality services, and a stronger evidence base. Journal of Comorbidity 2016;6(1):4–1

    What's in a name? A call to reframe non-communicable diseases.

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    The global health community does not spend much time on branding, which perhaps explains why existing classifications for the three largest groups of diseases are both outdated and counterproductive. The first Global Burden of Disease study1 described infectious diseases, non-communicable diseases (NCDs), and injuries. This grouping reflected a predominantly infectious disease burden in low-income and middle-income countries, which has since tilted towards NCDs. A name that is a longwinded non-definition, and that only tells us what this group of diseases is not, is not befitting of a group of diseases that now constitute the world's largest killer

    In Posidonia oceanica cadmium induces changes in DNA methylation and chromatin patterning

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    In mammals, cadmium is widely considered as a non-genotoxic carcinogen acting through a methylation-dependent epigenetic mechanism. Here, the effects of Cd treatment on the DNA methylation patten are examined together with its effect on chromatin reconfiguration in Posidonia oceanica. DNA methylation level and pattern were analysed in actively growing organs, under short- (6 h) and long- (2 d or 4 d) term and low (10 μM) and high (50 μM) doses of Cd, through a Methylation-Sensitive Amplification Polymorphism technique and an immunocytological approach, respectively. The expression of one member of the CHROMOMETHYLASE (CMT) family, a DNA methyltransferase, was also assessed by qRT-PCR. Nuclear chromatin ultrastructure was investigated by transmission electron microscopy. Cd treatment induced a DNA hypermethylation, as well as an up-regulation of CMT, indicating that de novo methylation did indeed occur. Moreover, a high dose of Cd led to a progressive heterochromatinization of interphase nuclei and apoptotic figures were also observed after long-term treatment. The data demonstrate that Cd perturbs the DNA methylation status through the involvement of a specific methyltransferase. Such changes are linked to nuclear chromatin reconfiguration likely to establish a new balance of expressed/repressed chromatin. Overall, the data show an epigenetic basis to the mechanism underlying Cd toxicity in plants

    Comparing the effects of excess copper in the leaves of Brassica juncea (L. Czern) and Brassica napus (L.) seedlings: Growth inhibition, oxidative stress and photosynthetic damage

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    Hydroponic experiments were conducted to compare the effects of excess copper (Cu) on growth and photosynthesis in young Indian mustard (Brassica juncea) and oilseed rape (Brassica napus). We compared the effects of excess Cu on the two Brassica species at different physiological levels from antioxidant levels to photosynthetic activity. Nine-day-old plants were treated with Cu (10, 25 and 50 μM CuSO4) for 7 and 14 days. Both species took up Cu from the external solution to a similar degree but showed slight root-to-shoot translocation. Furthermore, after seven days of treatment, excess Cu significantly decreased other microelement content, such as iron (Fe) and manganese (Mn), especially in the shoots of B. napus. As a consequence, the leaves of young Brassica napus plants showed decreased concentrations of photosynthetic pigments and more intense growth inhibition; however, accumulation of highly reactive oxygen species (hROS) were not detected. After 14 days of Cu exposure the reduction of Fe and Mn contents and shoot growth proved to be comparable in the two species. Moreover, a significant Cu-induced hROS accumulation was observed in both Brassica species. The diminution in pigment contents and photosynthetic efficiency were more pronounced in B. napus during prolonged Cu exposure. Based on all the parameters, B. juncea appears to be more resistant to excess Cu than B. napus, rendering it a species with higher potential for phytoremediation
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