30 research outputs found

    Assessment of the scientific evidence of the potential use of açaí (Euterpe oleracea, Mart.) in clinical outcomes: analysis with focus on antioxidant and anti-inflammatory action

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    The a√ßa√≠ berry (Euterpe oleracea, Mart.), fruit native to the Amazon region and explored mainly in the region of Par√°, gained importance in recent years due to potential health benefits, associated with its phytochemical composition and antioxidant capacity, related to its high content of flavonoids. Among these, anthocyanins are responsible for the anti-inflammatory and antioxidant capacity of this fruit. Experimental studies show that due to its composition, the acai berry has antioxidant activity related to its ability to reduce the reactive oxygen species (ROS) and its potential to inhibit cyclooxygenase 2 (COX-2). Another benefit studied is the analysis of their effectiveness in the anti-inflammatory process, being observed inhibition of araqued√īnico acid-derived mediators, suggesting that the fruit can act in the chronic inflammatory process. Also it was possible to observe that the fruit may have anti-inflammatory effects in healthy patients. Thus, the supplementation of diets with use of acai berry could attenuate inflammation process and oxidative stress, today with more consistent evidence derived primarily from in vitro studies. However, there is still need for further studies to prove the action of this fruit in the mechanisms involved in these processes, isolation of specific compounds and determining their optimal dosage

    Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

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    In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

    Cancer Incidence, Mortality, Years of Life Lost, Years Lived With Disability, and Disability-Adjusted Life Years for 29 Cancer Groups From 2010 to 2019: A Systematic Analysis for the Global Burden of Disease Study 2019.

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    The Global Burden of Diseases, Injuries, and Risk Factors Study 2019 (GBD 2019) provided systematic estimates of incidence, morbidity, and mortality to inform local and international efforts toward reducing cancer burden. To estimate cancer burden and trends globally for 204 countries and territories and by Sociodemographic Index (SDI) quintiles from 2010 to 2019. The GBD 2019 estimation methods were used to describe cancer incidence, mortality, years lived with disability, years of life lost, and disability-adjusted life years (DALYs) in 2019 and over the past decade. Estimates are also provided by quintiles of the SDI, a composite measure of educational attainment, income per capita, and total fertility rate for those younger than 25 years. Estimates include 95% uncertainty intervals (UIs). In 2019, there were an estimated 23.6 million (95% UI, 22.2-24.9 million) new cancer cases (17.2 million when excluding nonmelanoma skin cancer) and 10.0 million (95% UI, 9.36-10.6 million) cancer deaths globally, with an estimated 250 million (235-264 million) DALYs due to cancer. Since 2010, these represented a 26.3% (95% UI, 20.3%-32.3%) increase in new cases, a 20.9% (95% UI, 14.2%-27.6%) increase in deaths, and a 16.0% (95% UI, 9.3%-22.8%) increase in DALYs. Among 22 groups of diseases and injuries in the GBD 2019 study, cancer was second only to cardiovascular diseases for the number of deaths, years of life lost, and DALYs globally in 2019. Cancer burden differed across SDI quintiles. The proportion of years lived with disability that contributed to DALYs increased with SDI, ranging from 1.4% (1.1%-1.8%) in the low SDI quintile to 5.7% (4.2%-7.1%) in the high SDI quintile. While the high SDI quintile had the highest number of new cases in 2019, the middle SDI quintile had the highest number of cancer deaths and DALYs. From 2010 to 2019, the largest percentage increase in the numbers of cases and deaths occurred in the low and low-middle SDI quintiles. The results of this systematic analysis suggest that the global burden of cancer is substantial and growing, with burden differing by SDI. These results provide comprehensive and comparable estimates that can potentially inform efforts toward equitable cancer control around the world.Funding/Support: The Institute for Health Metrics and Evaluation received funding from the Bill & Melinda Gates Foundation and the American Lebanese Syrian Associated Charities. Dr Aljunid acknowledges the Department of Health Policy and Management of Kuwait University and the International Centre for Casemix and Clinical Coding, National University of Malaysia for the approval and support to participate in this research project. Dr Bhaskar acknowledges institutional support from the NSW Ministry of Health and NSW Health Pathology. Dr B√§rnighausen was supported by the Alexander von Humboldt Foundation through the Alexander von Humboldt Professor award, which is funded by the German Federal Ministry of Education and Research. Dr Braithwaite acknowledges funding from the National Institutes of Health/ National Cancer Institute. Dr Conde acknowledges financial support from the European Research Council ERC Starting Grant agreement No 848325. Dr Costa acknowledges her grant (SFRH/BHD/110001/2015), received by Portuguese national funds through Funda√ß√£o para a Ci√™ncia e Tecnologia, IP under the Norma Transit√≥ria grant DL57/2016/CP1334/CT0006. Dr Ghith acknowledges support from a grant from Novo Nordisk Foundation (NNF16OC0021856). Dr Glasbey is supported by a National Institute of Health Research Doctoral Research Fellowship. Dr Vivek Kumar Gupta acknowledges funding support from National Health and Medical Research Council Australia. Dr Haque thanks Jazan University, Saudi Arabia for providing access to the Saudi Digital Library for this research study. Drs Herteliu, Pana, and Ausloos are partially supported by a grant of the Romanian National Authority for Scientific Research and Innovation, CNDS-UEFISCDI, project number PN-III-P4-ID-PCCF-2016-0084. Dr Hugo received support from the Higher Education Improvement Coordination of the Brazilian Ministry of Education for a sabbatical period at the Institute for Health Metrics and Evaluation, between September 2019 and August 2020. Dr Sheikh Mohammed Shariful Islam acknowledges funding by a National Heart Foundation of Australia Fellowship and National Health and Medical Research Council Emerging Leadership Fellowship. Dr Jakovljevic acknowledges support through grant OI 175014 of the Ministry of Education Science and Technological Development of the Republic of Serbia. Dr Katikireddi acknowledges funding from a NHS Research Scotland Senior Clinical Fellowship (SCAF/15/02), the Medical Research Council (MC_UU_00022/2), and the Scottish Government Chief Scientist Office (SPHSU17). Dr Md Nuruzzaman Khan acknowledges the support of Jatiya Kabi Kazi Nazrul Islam University, Bangladesh. Dr Yun Jin Kim was supported by the Research Management Centre, Xiamen University Malaysia (XMUMRF/2020-C6/ITCM/0004). Dr Koulmane Laxminarayana acknowledges institutional support from Manipal Academy of Higher Education. Dr Landires is a member of the Sistema Nacional de Investigaci√≥n, which is supported by Panama‚Äôs Secretar√≠a Nacional de Ciencia, Tecnolog√≠a e Innovaci√≥n. Dr Loureiro was supported by national funds through Funda√ß√£o para a Ci√™ncia e Tecnologia under the Scientific Employment Stimulus‚ÄďInstitutional Call (CEECINST/00049/2018). Dr Molokhia is supported by the National Institute for Health Research Biomedical Research Center at Guy‚Äôs and St Thomas‚Äô National Health Service Foundation Trust and King‚Äôs College London. Dr Moosavi appreciates NIGEB's support. Dr Pati acknowledges support from the SIAN Institute, Association for Biodiversity Conservation & Research. Dr Rakovac acknowledges a grant from the government of the Russian Federation in the context of World Health Organization Noncommunicable Diseases Office. Dr Samy was supported by a fellowship from the Egyptian Fulbright Mission Program. Dr Sheikh acknowledges support from Health Data Research UK. Drs Adithi Shetty and Unnikrishnan acknowledge support given by Kasturba Medical College, Mangalore, Manipal Academy of Higher Education. Dr Pavanchand H. Shetty acknowledges Manipal Academy of Higher Education for their research support. Dr Diego Augusto Santos Silva was financed in part by the Coordena√ß√£o de Aperfei√ßoamento de Pessoal de N√≠vel Superior - Brasil Finance Code 001 and is supported in part by CNPq (302028/2018-8). Dr Zhu acknowledges the Cancer Prevention and Research Institute of Texas grant RP210042

    Influência da suplementação de açaí (Euterpe oleracea Mart.) na ração sobre a remodelação cardíaca em ratos submetidos a infarto agudo do miocárdio

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    A remodela√ß√£o card√≠aca tem papel importante na disfun√ß√£o ventricular p√≥sinfarto. Alguns mecanismos como estresse oxidativo, metabolismo energ√©tico e processo inflamat√≥rio modulam este processo. Neste contexto, h√° interesse em utilizar alimentos naturais, com propriedades antioxidantes e anti-inflamat√≥rias, destacando-se o a√ßa√≠ (Euterpe oleracea Mart). Objetivo: Avaliar a influ√™ncia da suplementa√ß√£o de a√ßa√≠ na ra√ß√£o sobre a remodela√ß√£o card√≠aca ap√≥s o infarto do mioc√°rdio (IM) em ratos. M√©todos: Ratos Wistar machos, com peso entre 200-250g, foram submetidos ao infarto experimental ou √† cirurgia simulada (Sham) e alocados em seis grupos ap√≥s estudo ecocardiogr√°fico, para verificar o tamanho do infarto: 1) grupo Sham alimentado com ra√ß√£o padr√£o (SA0, n=14); 2) grupo Sham alimentado com ra√ß√£o padr√£o suplementada com 2% de polpa de a√ßa√≠ pasteurizado (SA2, n=13); 3) grupo Sham alimentado com ra√ß√£o padr√£o suplementada com 5% de polpa de a√ßa√≠ pasteurizado (SA5, n=14); 4) grupo infartado alimentado com ra√ß√£o padr√£o (IA0, n=12); 5) grupo infartado, alimentado com ra√ß√£o padr√£o suplementada com 2% de polpa de a√ßa√≠ pasteurizado (IA2, n=12); 6) grupo infartado, alimentado com ra√ß√£o padr√£o suplementada com 5% de polpa de a√ßa√≠ pasteurizado (IA5, n=12). Os animais foram suplementados por tr√™s meses e foi observada a mortalidade. Ap√≥s esse per√≠odo, os animais foram submetidos √† segunda avalia√ß√£o ecocardiogr√°fica e posteriormente √† eutan√°sia e coleta de material biol√≥gico para realiza√ß√£o das demais avalia√ß√Ķes. Os dados foram apresentados como m√©dia ¬Ī erro padr√£o. As compara√ß√Ķes foram feitas por teste ANOVA de duas vias, com n√≠vel de signific√Ęncia adotado de 5%. Resultados: infarto induziu altera√ß√Ķes card√≠acas morfol√≥gicas e funcionais (sist√≥licas e diast√≥licas), com hipertrofia do ventr√≠culo, maior concentra√ß√£o de hidroper√≥xido de lip√≠deo e malondialde√≠do, maior atividade de super√≥xido dismutase, menor atividade da glutationa peroxidase e menor express√£o de fator nuclear eritr√≥ide 2, menor atividade do complexo piruvato desidrogenase, de citrato sintase, do Complexo I e II da cadeia respirat√≥ria, da ATP sintase e de beta-hodroxiacil Coenzima A desidrogenase, maior atividade do lactato desidrogenase, maior concentra√ß√£o de interleucina-10, menor concentra√ß√£o de interferon gama, maior concentra√ß√£o de inibidor tecidual de metaloproteinase e maior express√£o de col√°geno I. Os animais infartados que receberam suplementa√ß√£o de polpa de a√ßa√≠ apresentaram menor concentra√ß√£o do malondialde√≠do e menor atividade de super√≥xido dismutase, maior atividade do complexo piruvato desidrogenase, de citrato sintase, do Complexo I da cadeia respirat√≥ria, de betahidroxiacil Coenzima A desidrogenase, menor atividade de ATP sintase, do lactato desidrogenase, menor concentra√ß√£o de interleucina-10 e de inibidor tecidual de metaloproteinase. Conclus√£o: A suplementa√ß√£o de polpa de a√ßa√≠ nos animais infartados atenuou o estresse oxidativo, melhorou o metabolismo energ√©tico e modulou o processo inflamat√≥rio no cora√ß√£o. A influ√™ncia da suplementa√ß√£o de a√ßa√≠ foi dose dependente.Cardiac remodeling plays a key role in post-infarction ventricular dysfunction. Some mechanism, such as oxidative stress, energy metabolism and inflammation can modulate this process. In this context, there is great interest in natural foods, with antioxidant and anti-inflammatory properties, as a√ßa√≠ (Euterpe oleracea Mart). Objective: To analyze the influence of a√ßa√≠ supplementation in chow on cardiac remodeling after myocardial infarction (MI) in rats. Methods: Male Wistar rats with 200-250 g, were submitted to the experimental infarction or simulated surgery and divided into six groups: 1) Sham group fed standard chow and not subjected to the IM (SA0, n=14); 2) Sham group fed standard chow supplemented with 2% a√ßa√≠ pulp pasteurized and not subjected to IM (SA2, n=13); 3) Sham group fed standard chow supplemented with 5% a√ßa√≠ pulp pasteurized and not subjected to IM (SA5, n=14); 4) group submitted to MI and fed standard chow (IA0, n=12); 5) group submitted to MI and fed standard chow supplemented with 2% a√ßa√≠ pulp pasteurized (IA2, n=12); 6) group submitted to MI and fed standard chow supplemented with 5% a√ßa√≠ pulp pasteurized (IA5, n=12). The animals were supplemented for three months and observed mortality. After this period, the animals underwent echocardiography and subsequently euthanized and collecting biological material for other evaluations. The values were expressed as mean ¬Ī standard error. The comparisons were made by two-way ANOVA test with significance level of 5%. Results: Infarction induced heart morphological and functional changes (systolic and diastolic), ventricular hypertrophy, higher concentration of lipid hydroperoxide and malondialdehyde, higher activity of superoxide dismutase, decrease glutathione peroxidase activity and lower expression of Nrf-2, decrease pyruvate dehydrogenase complex, citrate synthase, complex I and II, ATP synthase and ő≤-hydroxyacyl CoA dehydrogenase activity, higher activity of lactate dehydrogenase, higher concentration of interleukin-10 and lower concentration of interferon gamma, higher concentration of tissue inhibitor of metalloproteinase and higher expression of collagen I. The infarcted animals that received a√ßa√≠ pulp supplementation decrease malondialdehyde concentration and decrease superoxide dismutase activity, higher activity of pyruvate dehydrogenase complex, citrate synthase, complex I, ő≤-hydroxyacyl CoA dehydrogenase, decrease ATP synthase and lactate dehydrogenase activity, decrease interleukin-10 and tissue inhibitor of metalloproteinase concentration. Conclusion: The supplementation with a√ßa√≠ pulp attenuated cardiac remodeling after infarction by acting on oxidative stress, energy metabolism, inflammation and tissue inhibitor of metalloproteinase in heart. The findings of this study also suggest that supplementation with a√ßa√≠ pulp appears to be dose dependent response.Coordena√ß√£o de Aperfei√ßoamento de Pessoal de N√≠vel Superior (CAPES

    Association of high-fat diet with neuroinflammation, anxiety-like defensive behavioral responses, and altered thermoregulatory responses in male rats.

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    Overweight and obesity are a worldwide pandemic affecting billions of people. These conditions have been associated with a chronic low-grade inflammatory state that is recognized as a risk factor for a range of somatic diseases as well as neurodevelopmental disorders, anxiety disorders, trauma- and stressor-related disorders, and affective disorders. We previously reported that the ingestion of a high-fat diet (HFD; 45% fat kcal/g) for nine weeks was capable of inducing obesity in rats in association with increased reactivity to stress and increased anxiety-related defensive behavior. In this study, we conducted a nine-week diet protocol to induce obesity in rats, followed by investigation of anxiety-related defensive behavioral responses using the elevated T-maze (ETM), numbers of FOS-immunoreactive cells after exposure of rats to the avoidance or escape task of the ETM, and neuroinflammatory cytokine expression in hypothalamic and amygdaloid nuclei. In addition, we investigated stress-induced cutaneous thermoregulatory responses during exposure to an open-field (OF). Here we demonstrated that nine weeks of HFD intake induced obesity, in association with increased abdominal fat pad weight, increased anxiety-related defensive behavioral responses, and increased proinflammatory cytokines in hypothalamic and amygdaloid nuclei. In addition, HFD exposure altered avoidance- or escape task-induced FOSimmunoreactivity within brain structures involved in control of neuroendocrine, autonomic, and behavioral responses to aversive stimuli, including the basolateral amygdala (BLA) and dorsomedial (DMH), paraventricular (PVN) and ventromedial (VMH) hypothalamic nuclei. Furthermore, rats exposed to HFD, relative to control dietfed rats, responded with increased tail skin temperature at baseline and throughout exposure to an open-field apparatus. These data are consistent with the hypothesis that HFD induces neuroinflammation, alters excitability of brain nuclei controlling neuroendocrine, autonomic, and behavioral responses to stressful stimuli, and enhances stress reactivity and anxiety-like defensive behavioral responses
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