14 research outputs found

    Population-based weight loss and gain do not explain trends in asthma mortality in Cuba: a prospective study from 1964 to 2014

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    Background The increase in prevalence of obesity is a possible risk factor for asthma in developed countries. As the people of Cuba experienced an acute population-based decrease in weight in the 1990s, we tested the hypothesis that national weight loss and subsequent weight gain was associated a reciprocal changes in asthma mortality. Methods Data were obtained on mortality rates from asthma and COPD in Cuba from 1964 to 2014, along with data on prevalence of obesity for this period. Joinpoint analysis was used to identify inflexion points in the data. Results Although the prevalence of obesity from 1990 to 1995 decreased from 14% to 7%, over the same time period the rate of asthma mortality increased from 4.5 deaths per 100,000 population to 5.4 deaths per 100,000 population. In 2010, the obesity prevalence subsequently increased to 15% in 2010, while the asthma mortality rate dropped to 2.3 deaths per 100,000 population. The optimal model for fit of asthma mortality over time gave an increasing linear association from 1964 to 1995 (95% confidence interval for inflexion point: 1993 to 1997), followed by a decrease in asthma mortality rates from 1995 to 1999 (95% confidence interval for inflexion point: 1997 to 2002). Conclusions These national data do not support the hypothesis that population-based changes in weight are associated with asthma mortality. Other possible explanations for the large decreases in asthma mortality rates include changes in pollution or better delivery of medical care over the same time period

    Astrocytes require insulin-like growth factor I to protect neurons against oxidative injury

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    Oxidative stress is a proposed mechanism in brain aging, making the study of its regulatory processes an important aspect of current neurobiological research. In this regard, the role of the aging regulator insulin-like growth factor I (IGF-I) in brain responses to oxidative stress remains elusive as both beneficial and detrimental actions have been ascribed to this growth factor. Because astrocytes protect neurons against oxidative injury, we explored whether IGF-I participates in astrocyte neuroprotection and found that blockade of the IGF-I receptor in astrocytes abrogated their rescuing effect on neurons. The protection mediated by IGF-I against oxidative stress (H 2O 2) in astrocytes is probably needed for these cells to provide adequate neuroprotection. Indeed, in astrocytes but not in neurons, IGF-I helps decrease the pro-oxidant protein thioredoxin-interacting protein 1 and normalizes the levels of reactive oxygen species. Furthermore, IGF-I cooperates with trophic signals produced by astrocytes in response to H 2O 2 such as stem cell factor (SCF) to protect neurons against oxidative insult. After stroke, a condition associated with brain aging where oxidative injury affects peri-infarcted regions, a simultaneous increase in SCF and IGF-I expression was found in the cortex, suggesting that a similar cooperative response takes place in vivo. Cell-specific modulation by IGF-I of brain responses to oxidative stress may contribute in clarifying the role of IGF-I in brain aging. © 2014 Genis L et al.This work was funded by grants of the Spanish Ministry of Science (SAF2010-17036) and Centro Investigacion Biomedica en red Enfermedades Neurodegenerativas (CIBERNED) to IT-A.Peer Reviewe

    The prevalence, clinical status and genotype of cystic fibrosis patients living in Cuba using national registry data

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    Background: We aimed to establish a national cystic fibrosis (CF) registry for Cuba, a developing country.Methods: Regional centres that deliver care for all CF patients provided information for a national database.Findings: The prevalence of CF in Cuba is 26.3 cases per 1,000,000 population. The median age at diagnosis is 2 years, and the median age of the total population was 15 years. Of those aged 16 years or older, the prevalence of Pseudomonas aeruginosa infection was 46%, the prevalence of Staphylococcus aureus infection was 36%, and 80% of individuals were receiving oral azithromycin. The commonest gene mutation was F508del which was observed in 50% of patients.Interpretation: These data demonstrate that it is possible to establish a national CF registry in a developing country such as Cuba. This provides baseline data to permit evaluation of health care delivery enable the spread of good clinical practice nationally

    Caracterización de las reacciones adversas por alimentos en un servicio hospitalario de alergia

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    Introducción: Las reacciones adversas por alimentos están aumentando en todo el mundo, y constituyen un problema de salud que afecta la calidad de vida de aquellos que las padecen. Objetivo: Caracterizar las reacciones adversas por alimentos en pacientes atendidos en el servicio de Alergia, para diseñar estrategias de intervención que permitan su prevención y un adecuado tratamiento. Métodos: Estudio descriptivo de corte transversal que incluyó 116 pacientes adultos atendidos en el servicio de Alergia del Hospital Universitario "General Calixto García", durante el periodo comprendido entre marzo 2017 y febrero 2019. A los pacientes se les realizó historia clínica e interrogó mediante cuestionario elaborado para el estudio, luego que dieran su consentimiento por escrito. Resultados: La rinitis alérgica fue el antecedente que prevaleció en los pacientes (47 %) y el asma en los familiares (41 %). Las manifestaciones cutáneas fueron las más frecuentes (79 %), seguidas de las digestivas (50 %). Los alimentos más implicados fueron los mariscos (42 %) y el pescado (40 %). La mayoría de las reacciones se presentaron en el propio hogar del paciente (86 %) y en menos de una hora (71 %). La combinación de antihistamínicos y esteroides (57 %) fue la más utilizada como medicamentos en dicho tratamiento. Conclusiones: Las reacciones por alimentos predominaron en el sexo femenino y se asociaron a enfermedad alérgica, en casi la mitad de los casos. Los mariscos y pescados fueron los principales alimentos causales. Se requiere investigar sobre los factores de riesgo y la prevalencia de reacciones adversas a los alimentos en la población cubana

    Epilepsy mortality trends in Cuba compared with England and Wales: 1987–2010

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    There are limited epilepsy mortality data from developing countries and Latin America in particular. We examined national epilepsy mortality data from Cuba and contrasted them with comparable data from England and Wales. National epilepsy mortality data for Cuba between the years 1987 and 2010 were obtained from the Medical Records and Health Statistics Bureau of the Cuban Public Health Ministry (www.sld.cu/sitios/dne/) with the corresponding mortality data from England and Wales obtained from the UK Office of National Statistics (ONS, www.ons.gov.uk). Indirect standardization with calculation of a standardized mortality ratio (SMR) was used to compare trends. The overall trend was of a slight decrease in mortality rates over the 23 years in Cuba, with higher mortality rates primarily occurring in young people. Annual age-adjusted rates were consistently lower in Cuba than those seen in England and Wales, with the SMR ranging from 0.35 (95% confidence interval (CI): 0.30 to 0.48) in 2007 to 1.00 (95% CI: 0.85 to 1.15) in 1994. Cuban epilepsy mortality rates are consistently lower than those of England and Wales. Reasons for this disparity in mortality rates are not immediately apparent but are likely to be multifactorial

    Prevalence and risk factors for wheeze, decreased forced expiratory volume in 1 s and bronchoconstriction in young children living in Havana, Cuba: a population-based cohort study

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    Objectives: Asthma has not been extensively studied in low-income and middle-income countries, where risk factors and access to treatment may differ from more affluent countries. We aimed to identify the prevalence of asthma and local risk factors in Havana, Cuba.Setting: Four municipalities in Havana, Cuba.Participants: A population-based cohort study design of young children living in Havana, Cuba. Children were recruited from primary care centres at age 12–15 months.Primary and secondary outcome measures: Data on wheeze in the past 12 months, asthma treatment and environmental exposures collected regularly until the age of 6 years, when forced expiratory volume in 1 s (FEV1) and reversibility to aerosolised salbutamol were also measured.Results: 1106 children provided data at the age of 6 years old. The prevalence of wheeze in the previous 12 months was 422 (38%), and 294 (33%) of the study population had bronchodilatation of 12% or more in FEV1 after administration of inhaled salbutamol. In the previous 12 months, 182 (16%) of the children had received inhaled corticosteroids, 416 (38%) salbutamol inhalers and 283 (26%) a course of systemic steroids.Wheeze in the first year and a family history of asthma were both positively associated with bronchodilatation to inhaled salbutamol (1.94%; 95% CI 0.81 to 3.08 and 1.85%; CI 0.14 to 3.57, respectively), while paracetamol use in the first year was associated with wheeze at 6 years (OR 1.64, 95% CI 1.14 to 2.35). There were large differences in FEV1, bronchodilatation and risk of wheeze across different geographical areas.Conclusions: Asthma is common in young children living in Havana, and the high prevalence of systemic steroids administrated is likely to reflect the underuse of regular inhaled corticosteroids. If replicated in other comparable low-income and middle-income countries, this represents an important global public health issue

    Repositioning of the global epicentre of non-optimal cholesterol

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    High blood cholesterol is typically considered a feature of wealthy western countries(1,2). However, dietary and behavioural determinants of blood cholesterol are changing rapidly throughout the world(3) and countries are using lipid-lowering medications at varying rates. These changes can have distinct effects on the levels of high-density lipoprotein (HDL) cholesterol and non-HDL cholesterol, which have different effects on human health(4,5). However, the trends of HDL and non-HDL cholesterol levels over time have not been previously reported in a global analysis. Here we pooled 1,127 population-based studies that measured blood lipids in 102.6 million individuals aged 18 years and older to estimate trends from 1980 to 2018 in mean total, non-HDL and HDL cholesterol levels for 200 countries. Globally, there was little change in total or non-HDL cholesterol from 1980 to 2018. This was a net effect of increases in low- and middle-income countries, especially in east and southeast Asia, and decreases in high-income western countries, especially those in northwestern Europe, and in central and eastern Europe. As a result, countries with the highest level of non-HDL cholesterol-which is a marker of cardiovascular riskchanged from those in western Europe such as Belgium, Finland, Greenland, Iceland, Norway, Sweden, Switzerland and Malta in 1980 to those in Asia and the Pacific, such as Tokelau, Malaysia, The Philippines and Thailand. In 2017, high non-HDL cholesterol was responsible for an estimated 3.9 million (95% credible interval 3.7 million-4.2 million) worldwide deaths, half of which occurred in east, southeast and south Asia. The global repositioning of lipid-related risk, with non-optimal cholesterol shifting from a distinct feature of high-income countries in northwestern Europe, north America and Australasia to one that affects countries in east and southeast Asia and Oceania should motivate the use of population-based policies and personal interventions to improve nutrition and enhance access to treatment throughout the world.Peer reviewe

    Frataxin deficiency unveils cell-context dependent actions of insulin-like growth factor I on neurons

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    Abstract Background Friedreich’s ataxia (FRDA) is a neurodegenerative disease caused by deficiency of the mitochondrial iron chaperone frataxin (Fxn). FRDA has no cure, but disease-modifying strategies to increase frataxin are under study. Because insulin-like growth factor I (IGF-I) has therapeutic effects in various types of cerebellar ataxia and exerts protective actions on mitochondrial function, we explored the potential Fxn-stimulating activity of this growth factor on brain cells. Results IGF-I normalized frataxin levels in frataxin-deficient neurons and astrocytes through its canonical Akt/mTOR signaling pathway. IGF-I also stimulated frataxin in normal astrocytes but not in normal neurons, whereas IGF-I stimulated the Akt/mTOR pathway in both types of cells. This cell context-dependent action of IGF-I on neurons suggested that the intrinsic regulation of Fxn in neurons is different than in astrocytes. Indeed, neurons express much higher levels of frataxin and are much more sensitive to Fxn deficiency than astrocytes; i.e.: only neurons die in the absence of frataxin. In addition, the half-life of frataxin is shorter in neurons than in astrocytes, while after blockade of the proteasome only neurons responded to IGF-I with an increase in frataxin levels. We also explore a potential therapeutic utility of IGF-I in FRDA-like transgenic mice (YG8R mice) and found that treatment with IGF-I normalized motor coordination in these moderately ataxic mice. Conclusion Exposure to IGF-I unveiled a cell-specific regulation of frataxin in neurons as compared to astrocytes. Collectively, these results indicate that IGF-I exerts cell-context neuroprotection in frataxin deficiency that maybe therapeutically effective.This work was funded by Spanish Ministry of Science (SAF2007-60051 and SAF2010-17036) and by CIBERNEDPeer Reviewe

    Calcineurin in Reactive Astrocytes Plays a Key Role in the Interplay between Proinflammatory and Anti-Inflammatory Signals

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    12 pages, 7 figures, 1 table,Supplemental Data . - PMID: 17699657 [PubMed - indexed for MEDLINE] Free ArticleMaladaptive inflammation is a major suspect in progressive neurodegeneration, but the underlying mechanisms are difficult to envisage in part because reactive glial cells at lesion sites secrete both proinflammatory and anti-inflammatory mediators. We now report that astrocytes modulate neuronal resilience to inflammatory insults through the phosphatase calcineurin. In quiescent astrocytes, inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha) recruits calcineurin to stimulate a canonical inflammatory pathway involving the transcription factors nuclear factor kappaB (NFkappaB) and nuclear factor of activated T-cells (NFAT). However, in reactive astrocytes, local anti-inflammatory mediators such as insulin-like growth factor I also recruit calcineurin but, in this case, to inhibit NFkappaB/NFAT. Proof of concept experiments in vitro showed that expression of constitutively active calcineurin in astrocytes abrogated the inflammatory response after TNF-alpha or endotoxins and markedly enhanced neuronal survival. Furthermore, regulated expression of constitutively active calcineurin in astrocytes markedly reduced inflammatory injury in transgenic mice, in a calcineurin-dependent manner. These results suggest that calcineurin forms part of a molecular pathway whereby reactive astrocytes determine the outcome of the neuroinflammatory process by directing it toward either its resolution or its progressionThis work was supported by Ministerio de Educacion y Ciencia Grants SAF2001-1722 and 2004-0446 and by NeuropharmaPeer reviewe
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