143 research outputs found

    Nativity and Country of Origin Variations in Life Expectancy With Functional Limitations Among Older Hispanics in the United States

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    This study examined racial/ethnic, nativity, and country of origin differences in life expectancy with and without functional limitations among older adults in the United States. We used data from the National Health Interview Survey (1999–2015) to estimate Sullivan-based life tables of life expectancies with functional limitations and without functional limitations by sex for U.S.-born Mexicans, foreign-born Mexicans, U.S.-born Puerto Ricans, island-born Puerto Ricans, foreign-born Cubans, and U.S.-born Whites. We find that Latinos exhibit heterogeneous life expectancies with functional limitations. Among females, U.S.-born Mexicans, foreign-born Mexicans, and foreign-born Cubans spend significantly fewer years without functional limitations, whereas island-born Puerto Ricans spend more years with functional limitations. For men, U.S.-born Puerto Ricans were the only Latino subgroup disadvantaged in the number of years lived with functional limitations. Conversely, foreign-born Cubans spend significantly fewer years without functional limitations. To address disparities in functional limitations, we must consider variation in health among Latino subgroups

    Puerta Interactiva para el acceso a una sala de clases

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    La tecnología moderna ha permitido actualmente que la sociedad como parte de una solución para sus actividades diarias, utilice equipos, aplicaciones y muchos otros dispositivos electrónicos que conjuntamente con la tecnología móvil permitan mejorar procesos y tareas, convirtiéndose en una herramienta de trabajo para la interacción hombre-máquina. En el presente trabajo se detalla el diseño y construcción de un prototipo de puerta interactiva controlada mediante módulo Arduino Uno y una aplicación de Android basada en el lenguaje de programación Eclipse permitiéndole a los docentes utilizarla como instrumento de trabajo durante sus horas laborables. Este tipo de puerta permitirá automatizar el ingreso al aula de clases, disminuyendo los inconvenientes que pueden presentarse ya sea por dejarla abierta o por no estar disponible la persona encargada de su apertura

    Smoking Dose Modifies the Association between C242T Polymorphism and Prevalence of Metabolic Syndrome in a Chinese Population

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    Background: The C242T polymorphism of the CYBA gene that encodes p22phox, a component of NADPH oxidase, has been found to modulate superoxide production. Oxidase is a major source of the superoxide anion that contributes to individual components of metabolic syndrome. We examined the relationship of the C242T polymorphism with the prevalence of metabolic syndrome in a Chinese population, taking account of consumed cigarette amounts. Methodology/Principal Findings: In 870 participants, we collected biomarkers related to metabolic syndrome and detailed history of smoking and genotyped the C242T polymorphisms. After adjustment for covariates, the CT/TT genotypes were associated with a lower risk of metabolic syndrome (P = 0.0008). The odds of having metabolic syndrome in the CT/TT participants were 0.439 (95%CI: 0.265, 0.726), while for CC participants the odds were 1.110 (95%CI: 0.904, 1.362). There was significant (P = 0.014) interaction between the C242T polymorphism and smoking status in relation to the prevalence of metabolic syndrome. For smokers who smoke no less than 25 pack-years, those with CT/TT genotypes had lower risk of metabolic syndrome as compared with CC polymorphism carriers (P = 0.015). In the multiple regression analysis, the CT/TT genotypes were significantly associated with lower serum concentration of triglycerides both in all subjects and smokers; furthermore, the CT/TT genotypes were also related to smaller waist circumference in smokers. Conclusions: Our study suggests that the C242T gene polymorphism is indeed related to the prevalence of metaboli

    Detection and Tertiary Treatment Technologies of Poly-and Perfluoroalkyl Substances in Wastewater Treatment Plants

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    PFAS are a very diverse group of anthropogenic chemicals used in various consumer and industrial products. The properties that characterize are their low degradability as well as their resistance to water, oil and heat. This results in their high persistence in the environment and bioaccumulation in different organisms, causing many adverse effects on the environment as well as in human health. Some of their effects remain unknown to this day. As there are thousands of registered PFAS, it is difficult to apply traditional technologies for an efficient removal and detection for all. This has made it difficult for wastewater treatment plants to remove or degrade PFAS before discharging the effluents into the environment. Also, monitoring these contaminants depends mostly on chromatography-based methods, which require expensive equipment and consumables, making it difficult to detect PFAS in the environment. The detection of PFAS in the environment, and the development of technologies to be implemented in tertiary treatment of wastewater treatment plants are topics of high concern. This study focuses on analyzing and discussing the mechanisms of occurrence, migration, transformation, and fate of PFAS in the environment, as well the main adverse effects in the environment and human health. The following work reviews the recent advances in the development of PFAS detection technologies (biosensors, electrochemical sensors, microfluidic devices), and removal/degradation methods (electrochemical degradation, enzymatic transformation, advanced oxidation, photocatalytic degradation). Understanding the risks to public health and identifying the routes of production, transportation, exposure to PFAS is extremely important to implement regulations for the detection and removal of PFAS in wastewater and the environment.This work is part of the project entitled “Contaminantes emergentes y prioritarios en las aguas reutilizadas en agricultura: riesgos y efectos en suelos, producción agrícola y entorno ambiental” funded by CSIC-Tecnológico de Monterrey under i-Link + program (LINKB20030).Peer reviewe

    Familial hypercholesterolaemia in children and adolescents from 48 countries: a cross-sectional study

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    Background Approximately 450 000 children are born with familial hypercholesterolaemia worldwide every year, yet only 2·1% of adults with familial hypercholesterolaemia were diagnosed before age 18 years via current diagnostic approaches, which are derived from observations in adults. We aimed to characterise children and adolescents with heterozygous familial hypercholesterolaemia (HeFH) and understand current approaches to the identification and management of familial hypercholesterolaemia to inform future public health strategies. Methods For this cross-sectional study, we assessed children and adolescents younger than 18 years with a clinical or genetic diagnosis of HeFH at the time of entry into the Familial Hypercholesterolaemia Studies Collaboration (FHSC) registry between Oct 1, 2015, and Jan 31, 2021. Data in the registry were collected from 55 regional or national registries in 48 countries. Diagnoses relying on self-reported history of familial hypercholesterolaemia and suspected secondary hypercholesterolaemia were excluded from the registry; people with untreated LDL cholesterol (LDL-C) of at least 13·0 mmol/L were excluded from this study. Data were assessed overall and by WHO region, World Bank country income status, age, diagnostic criteria, and index-case status. The main outcome of this study was to assess current identification and management of children and adolescents with familial hypercholesterolaemia. Findings Of 63 093 individuals in the FHSC registry, 11 848 (18·8%) were children or adolescents younger than 18 years with HeFH and were included in this study; 5756 (50·2%) of 11 476 included individuals were female and 5720 (49·8%) were male. Sex data were missing for 372 (3·1%) of 11 848 individuals. Median age at registry entry was 9·6 years (IQR 5·8–13·2). 10 099 (89·9%) of 11 235 included individuals had a final genetically confirmed diagnosis of familial hypercholesterolaemia and 1136 (10·1%) had a clinical diagnosis. Genetically confirmed diagnosis data or clinical diagnosis data were missing for 613 (5·2%) of 11 848 individuals. Genetic diagnosis was more common in children and adolescents from high-income countries (9427 [92·4%] of 10 202) than in children and adolescents from non-high-income countries (199 [48·0%] of 415). 3414 (31·6%) of 10 804 children or adolescents were index cases. Familial-hypercholesterolaemia-related physical signs, cardiovascular risk factors, and cardiovascular disease were uncommon, but were more common in non-high-income countries. 7557 (72·4%) of 10 428 included children or adolescents were not taking lipid-lowering medication (LLM) and had a median LDL-C of 5·00 mmol/L (IQR 4·05–6·08). Compared with genetic diagnosis, the use of unadapted clinical criteria intended for use in adults and reliant on more extreme phenotypes could result in 50–75% of children and adolescents with familial hypercholesterolaemia not being identified. Interpretation Clinical characteristics observed in adults with familial hypercholesterolaemia are uncommon in children and adolescents with familial hypercholesterolaemia, hence detection in this age group relies on measurement of LDL-C and genetic confirmation. Where genetic testing is unavailable, increased availability and use of LDL-C measurements in the first few years of life could help reduce the current gap between prevalence and detection, enabling increased use of combination LLM to reach recommended LDL-C targets early in life. Funding Pfizer, Amgen, Merck Sharp & Dohme, Sanofi–Aventis, Daiichi Sankyo, and Regeneron

    Why Are Outcomes Different for Registry Patients Enrolled Prospectively and Retrospectively? Insights from the Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF).

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    Background: Retrospective and prospective observational studies are designed to reflect real-world evidence on clinical practice, but can yield conflicting results. The GARFIELD-AF Registry includes both methods of enrolment and allows analysis of differences in patient characteristics and outcomes that may result. Methods and Results: Patients with atrial fibrillation (AF) and ≥1 risk factor for stroke at diagnosis of AF were recruited either retrospectively (n = 5069) or prospectively (n = 5501) from 19 countries and then followed prospectively. The retrospectively enrolled cohort comprised patients with established AF (for a least 6, and up to 24 months before enrolment), who were identified retrospectively (and baseline and partial follow-up data were collected from the emedical records) and then followed prospectively between 0-18 months (such that the total time of follow-up was 24 months; data collection Dec-2009 and Oct-2010). In the prospectively enrolled cohort, patients with newly diagnosed AF (≤6 weeks after diagnosis) were recruited between Mar-2010 and Oct-2011 and were followed for 24 months after enrolment. Differences between the cohorts were observed in clinical characteristics, including type of AF, stroke prevention strategies, and event rates. More patients in the retrospectively identified cohort received vitamin K antagonists (62.1% vs. 53.2%) and fewer received non-vitamin K oral anticoagulants (1.8% vs . 4.2%). All-cause mortality rates per 100 person-years during the prospective follow-up (starting the first study visit up to 1 year) were significantly lower in the retrospective than prospectively identified cohort (3.04 [95% CI 2.51 to 3.67] vs . 4.05 [95% CI 3.53 to 4.63]; p = 0.016). Conclusions: Interpretations of data from registries that aim to evaluate the characteristics and outcomes of patients with AF must take account of differences in registry design and the impact of recall bias and survivorship bias that is incurred with retrospective enrolment. Clinical Trial Registration: - URL: http://www.clinicaltrials.gov . Unique identifier for GARFIELD-AF (NCT01090362)

    Phenotypical, Clinical, and Molecular Aspects of Adults and Children With Homozygous Familial Hypercholesterolemia in Iberoamerica

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    Fil: Alves, Ana Catarina. Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisboa; Portugal.Fil: Alonso, Rodrigo. Center for Advanced Metabolic Medicine and Nutrition, Santiago; Chile.Fil: Diaz-Diaz, José Luís. Hospital Universitario A Coruña. Department of Internal Medicine; España.Fil: Medeiros, Ana Margarida. Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisboa; Portugal.Fil: Jannes, Cinthia E. University of São Paulo. Medical School. Hospital São Paulo. Heart Institute (InCor); Brasil.Fil: Merchan, Alonso. Fundación Clinica SHAIO, Cardiología, Bogotá; Colombia.Fil: Vasques-Cardenas, Norma A. Universidad Autónoma de Guadalajara. Facultad de Medicina Zapopan; México.Fil: Cuevas, Ada. Center for Advanced Metabolic Medicine and Nutrition, Santiago; Chile.Fil: Chacra, Ana Paula. University of São Paulo. Medical School. Hospital São Paulo. Heart Institute (InCor); Brasil.Fil: Krieger, Jose E. University of São Paulo. Medical School. Hospital São Paulo. Heart Institute (InCor); Brasil.Fil: Arroyo, Raquel. Fundación Hipercolesterolemia Familiar, Madrid; España.Fil: Arrieta, Francisco. Hospital Ramón y Cajal. Departamento de Endocrinología, Madrid; España.Fil: Schreier, Laura. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica, Laboratorio de Lípidos y Aterosclerosis; Argentina.Fil: Corral, Pablo. Universidad FASTA. Facultad de Medicina. Cátedra Farmacología e Investigación, Mar del Plata; Argentina.Fil: Bañares, Virginia. ANLIS Dr.C.G.Malbrán. Centro Nacional de Genética Médica. Departamento de Genética Experimental; Argentina.Fil: Araujo, Maria B. Hospital Garrahan. Servicio de Nutrición; Argentina.Fil: Bustos, Paula. Universidad de Concepción. Facultad de Farmacia; Chile.Fil: Asenjo, Sylvia. Universidad de Concepción. Facultad de Medicina; Chile.Fil: Stoll, Mario. Programa GENYCO, Laboratorio de Genética Molecular. Comisión Honoraria de Salud Cardiovascular, Montevideo; Uruguay.Fil: Dell'Oca, Nicolás. Programa GENYCO, Laboratorio de Genética Molecular. Comisión Honoraria de Salud Cardiovascular, Montevideo; Uruguay.Fil: Reyes, Maria. Fundación Cardiovascular de Colombia. Cardiología; Bogotá.Fil: Ressia, Andrés. Fundación Cardiovascular de Colombia. Cardiología; Bogotá.Fil: Campo, Rafael. Instituto Mexicano del Seguro Social. Centro de Investigación Biomédica del Occidente, Guadalajara; México.Fil: Magaña-Torres, Maria T. Instituto Nacional de Ciencias Médicas y Nutrición. Unidad de Investigación de Enfermedades Metabólicas; México.Fil: Metha, Roopa. Instituto Nacional de Ciencias Médicas y Nutrición. Unidad de Investigación de Enfermedades Metabólicas; México.Fil: Aguilar-Salinas, Carlos A. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán. Departamento de Endocrinología y Metabolismo. Secretaría de la Defensa Nacional. Unidad de Especialidades Médicas. Servicio de Endocrinología; México.Fil: Ceballos-Macias, José J. Pontificia Universidad Javerina. Facultad de Medicina. Departamento de Medicina Interna, Bogotá; Colombia.Fil: Ruiz Morales, Álvaro J. Pontificia Universidad Javerina. Facultad de Medicina. Departamento de Medicina Interna, Bogotá; Colombia.Fil: Mata, Pedro. Fundación Hipercolesterolemia Familiar, Madrid; España.Fil: Bourbon, Mafalda. Instituto Nacional de Saúde Doutor Ricardo Jorge, Lisboa; Portugal.Fil: Santos, Raul D. University of São Paulo. Medical School. Hospital São Paulo. Heart Institute (InCor); Brasil.OBJECTIVE: Characterize homozygous familial hypercholesterolemia (HoFH) individuals from Iberoamerica. APPROACH AND RESULTS: In a cross-sectional retrospective evaluation 134 individuals with a HoFH phenotype, 71 adults (age 39.3±15.8 years, 38.0% males), and 63 children (age 8.8±4.0 years, 50.8% males) were studied. Genetic characterization was available in 129 (96%). The majority (91%) were true homozygotes (true HoFH, n=79, 43.0% children, 46.8% males) or compound heterozygotes (compound heterozygous familial hypercholesterolemia, n=39, 51.3% children, 46.2% males) with putative pathogenic variants in the LDLR. True HoFH due to LDLR variants had higher total (P=0.015) and LDL (low-density lipoprotein)-cholesterol (P=0.008) compared with compound heterozygous familial hypercholesterolemia. Children with true HoFH (n=34) tended to be diagnosed earlier (P=0.051) and had a greater frequency of xanthomas (P=0.016) than those with compound heterozygous familial hypercholesterolemia (n=20). Previous major cardiovascular events were present in 25 (48%) of 52 children (missing information in 2 cases), and in 43 (67%) of 64 adults with LDLR variants. Children who are true HoFH had higher frequency of major cardiovascular events (P=0.02), coronary heart (P=0.013), and aortic/supra-aortic valve diseases (P=0.022) than compound heterozygous familial hypercholesterolemia. In adults, no differences were observed in major cardiovascular events according to type of LDLR variant. From 118 subjects with LDLR variants, 76 (64%) had 2 likely pathogenic or pathogenic variants. In 89 subjects with 2 LDLR variants, those with at least one null allele were younger (P=0.003) and had a greater frequency of major cardiovascular events (P=0.038) occurring at an earlier age (P=0.001). CONCLUSIONS: There was a high frequency of cardiovascular disease even in children. Phenotype and cardiovascular complications were heterogeneous and associated with the type of molecular defect

    New insights into the genetic etiology of Alzheimer's disease and related dementias

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    Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

    Improved risk stratification of patients with atrial fibrillation: an integrated GARFIELD-AF tool for the prediction of mortality, stroke and bleed in patients with and without anticoagulation.

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    OBJECTIVES: To provide an accurate, web-based tool for stratifying patients with atrial fibrillation to facilitate decisions on the potential benefits/risks of anticoagulation, based on mortality, stroke and bleeding risks. DESIGN: The new tool was developed, using stepwise regression, for all and then applied to lower risk patients. C-statistics were compared with CHA2DS2-VASc using 30-fold cross-validation to control for overfitting. External validation was undertaken in an independent dataset, Outcome Registry for Better Informed Treatment of Atrial Fibrillation (ORBIT-AF). PARTICIPANTS: Data from 39 898 patients enrolled in the prospective GARFIELD-AF registry provided the basis for deriving and validating an integrated risk tool to predict stroke risk, mortality and bleeding risk. RESULTS: The discriminatory value of the GARFIELD-AF risk model was superior to CHA2DS2-VASc for patients with or without anticoagulation. C-statistics (95% CI) for all-cause mortality, ischaemic stroke/systemic embolism and haemorrhagic stroke/major bleeding (treated patients) were: 0.77 (0.76 to 0.78), 0.69 (0.67 to 0.71) and 0.66 (0.62 to 0.69), respectively, for the GARFIELD-AF risk models, and 0.66 (0.64-0.67), 0.64 (0.61-0.66) and 0.64 (0.61-0.68), respectively, for CHA2DS2-VASc (or HAS-BLED for bleeding). In very low to low risk patients (CHA2DS2-VASc 0 or 1 (men) and 1 or 2 (women)), the CHA2DS2-VASc and HAS-BLED (for bleeding) scores offered weak discriminatory value for mortality, stroke/systemic embolism and major bleeding. C-statistics for the GARFIELD-AF risk tool were 0.69 (0.64 to 0.75), 0.65 (0.56 to 0.73) and 0.60 (0.47 to 0.73) for each end point, respectively, versus 0.50 (0.45 to 0.55), 0.59 (0.50 to 0.67) and 0.55 (0.53 to 0.56) for CHA2DS2-VASc (or HAS-BLED for bleeding). Upon validation in the ORBIT-AF population, C-statistics showed that the GARFIELD-AF risk tool was effective for predicting 1-year all-cause mortality using the full and simplified model for all-cause mortality: C-statistics 0.75 (0.73 to 0.77) and 0.75 (0.73 to 0.77), respectively, and for predicting for any stroke or systemic embolism over 1 year, C-statistics 0.68 (0.62 to 0.74). CONCLUSIONS: Performance of the GARFIELD-AF risk tool was superior to CHA2DS2-VASc in predicting stroke and mortality and superior to HAS-BLED for bleeding, overall and in lower risk patients. The GARFIELD-AF tool has the potential for incorporation in routine electronic systems, and for the first time, permits simultaneous evaluation of ischaemic stroke, mortality and bleeding risks. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier for GARFIELD-AF (NCT01090362) and for ORBIT-AF (NCT01165710)
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