Changes in screen time from 4 to 7 years of age, dietary patterns and obesity: Findings from the Generation XXI birth cohort

Background and aims Increased screen exposure is associated with unhealthy eating behaviours and obesity. Screen time (ST) changes from pre-school to school age, and associations with dietary patterns (DP) and obesity remain unknown. We, therefore, analysed ST changes from 4 to 7 years of age, associated factors, and the relation with DP and obesity. Methods and results We included 4531 children evaluated at 4 and 7 years, as part of the Generation XXI birth cohort (Porto, Portugal). ST was assessed for weekdays and weekend, and average daily time was estimated. Associations between covariates and ST changes, and between ST changes and 3 DP previously identified (Energy-dense foods, Snacking, and Healthier) were estimated by odds ratios (OR) and 95% confidence interval (95%CI), using adjusted multinomial regression models. From 4 to 7 years, 31.5% of the children decreased their ST, 21.8% increased, 16.5% maintained low (≤60 min), and 30.2% maintained high (61–120 min or >120 min) ST. After adjustment, lower maternal education (OR = 2.33, 95%CI:1.82–2.99) and lower family income (OR = 1.72, 95%CI:1.35–2.21) were associated with higher odds of increasing ST, while being a girl was associated with 35% decreased odds of increasing ST. Children that increased and those that maintained high ST showed greater odds of presenting a Snacking DP at 7 years (OR = 2.34, 95%CI:1.64–3.35) and (OR = 2.65, 95%CI:1.89–3.72), respectively. No statistically significant differences were found regarding changes in ST and the child's BMI. Conclusion Children increasing screen exposure during this period were more frequently from lower socioeconomic strata and presented unhealthier DP.The authors gratefully acknowledge the families enrolled in Generation XXI for their kindness, all members of the research team for their enthusiasm and perseverance, and the participating hospitals and their staff for their help and support. This study was supported by national funding through Programa Operacional de Saúde – Saúde XXI, Quadro Comunitário de Apoio III and Administração Regional de Saúde Norte (Regional Department of Ministry of Health) and by FCT (Foundation for Science and Technology, I.P.), under the Epidemiology Research Unit (EPIUnit), from the Institute of Public Health of the University of Porto (UIDB/04750/2020), and by the Stimulus of Scientific Employment – Individual Support (CEECIND/01271/2018) and the FCT Investigator contract IF/01060/2015

Divergent trophic responses to biogeographic and environmental gradients

Following environmental changes, communities disassemble and reassemble in seemingly unpredictable ways. Whether species respond to such changes individualistically or collectively (e.g. as functional groups) is still unclear. To address this question, we used an extensive new dataset for the lake communities in the Azores' archipelago to test whether: 1) individual species respond concordantly within trophic groups; 2) trophic groups respond concordantly to biogeographic and environmental gradients. Spatial concordance in individual species distributions within trophic groups was always greater than expected by chance. In contrast, trophic groups varied non-concordantly along biogeographic and environmental gradients revealing idiosyncratic responses to them. Whether communities respond individualistically to environmental gradients thus depends on the functional resolution of the data. Our study challenges the view that modelling environmental change effects on biodiversity always requires an individualist approach. Instead, it finds support for the longstanding idea that communities might be modelled as a cohort if the functional resolution is appropriate

"Freshwater killer whales": beaching behavior of an alien fish to hunt land birds

The behavioral strategies developed by predators to capture and kill their prey are fascinating, notably for predators that forage for prey at, or beyond, the boundaries of their ecosystem. We report here the occurrence of a beaching behavior used by an alien and large-bodied freshwater predatory fish (Silurus glanis) to capture birds on land (i.e. pigeons, Columbia livia). Among a total of 45 beaching behaviors observed and filmed, 28% were successful in bird capture. Stable isotope analyses (δ¹³C and δ¹⁵N) of predators and their putative prey revealed a highly variable dietary contribution of land birds among individuals. Since this extreme behavior has not been reported in the native range of the species, our results suggest that some individuals in introduced predator populations may adapt their behavior to forage on novel prey in new environments, leading to behavioral and trophic specialization to actively cross the water-land interface

Interaction of paraoxonase-192 polymorphism with low HDL-cholesterol in coronary artery disease risk.

A doença coronária (DC) é a principal causa de mortalidade nos países desenvolvidos. O aumento da peroxidação lipídica está associado com a progressão acelerada da arteriosclerose. A Paraoxonase (PON1) é uma enzima antioxidante, que protege contra a peroxidação lipídica e a DC. A actividade da PON1 está sob controlo genético e a sua base molecular consiste num polimorfismo do gene da PON1 que apresenta duas isoformas comuns: a forma nativa, Q (192 Gln) com elevada capacidade de protecção das LDL da peroxidação lipídica in vitro, e a isoforma mutada R (192 Arg) com baixa capacidade de protecção. Objectivo: O objectivo deste trabalho foi investigar a interacção entre o alelo R do gene da PON 1 e os níveis plasmáticos baixos de colesterol HDL, no risco do aparecimento da DC. Métodos: Participaram no estudo 818 indivíduos, 298 doentes coronários com idade média 55.0±10.3 anos, 78.9% do sexo masculino, e 520 controlos, com uma idade média de 53.3±11, 7 anos, 72, 5% do sexo masculino, tendo casos e controlos sido emparelhados por idade e sexo. Foi considerado um valor <de 40 mg/dl (0,90 mmol/L), nos homens e <de 50 mg/dl (1,11 mmol/L), nas mulheres como um nível baixo de Colesterol HDL. As comparações genotípicas, entre casos e controlos, foram efectuadas pelo teste do Chi-quadrado. A significância estatística foi aceite para valores de p <0,05. Para determinar o risco relativo de DC, em relação ao genótipo RR e aos níveis baixos de colesterol HDL, foi usada uma análise univariada e foram utilizadas as tabelas epidemiológicas 4x2 e medidas de sinergismo (modelo aditivo - SI e multiplicativo - SIM) para determinar a interacção entre o genótipo RR e os níveis baixos de colesterol HDL. Foi finalmente calculado o excesso de risco relativo (RERI) e proporção atribuída à interacção (AP). Resultados: A PON 1 192 RR está associada à DC [OR=1,61; p=0,043] para toda a população. A associação de níveis baixos de HDL com o genótipo 192 RR mostrou um aumento do risco de DC (OR=17,38; p <0,0001) comparada aos níveis normais de HDL associados ao mesmo genótipo (OR=1,39; p=0,348) e aos níveis baixos de HDL sem o genótipo RR (OR=7,79; p <0,0001). Índices de Sinergismo: SI= 2,3; SIM = 1.6; RERI=9,2; AP=0,53. Conclusão: Estes dados sugerem a existência de um efeito sinérgico entre o genótipo 192 RR da PON1 e os valores baixos de colesterol HDL, na emergência de DC, pois este genótipo aumentou o risco de DC, em especial, na população com níveis plasmáticos baixos de colesterol HDL. A proporção de DC que pode ser atribuída a esta interacção (AP) foi de 0,53 significando que 53% da DC que surgiu nestes indivíduos, foi explicada por esta interacção.INTRODUCTION: Coronary artery disease (CAD) is the main cause of mortality in developed countries. Increased lipid peroxidation is associated with accelerated progression of atherosclerosis. Paraoxonase (PON1) is an antioxidant enzyme bound to high-density lipoprotein (HDL), which protects against lipid peroxidation and coronary artery disease. PON1 activity is under genetic control and its molecular basis is a polymorphism in the PON1 gene that shows two common isoforms: the wild Q form (192 Gln) with high ability to protect LDL from lipid peroxidation in vitro, and the mutated R (Arg) form with lower ability. AIM: To explore the interaction of the R allele of the paraoxonase gene and low HDL-cholesterol concentrations in CAD risk. METHODS: The study population consisted of 818 individuals, 298 coronary patients, aged 55.0 +/- 10.3 years, 78.9% male, and 520 age and gender matched healthy controls, aged 53.3 +/- 11.7 years, 72.5% male. Low HDL-cholesterol was defined as < 0.90 mmol/l in men and < 1.11 mmol/l in women. Comparisons of genotypes between cases and controls were performed by a chi-square test. Statistical significance was accepted at p < 0.05. Odds ratios and 95% confidence intervals for the RR genotypes and HDL-deficient subjects were computed using univariate analysis (2 x 2 tables). To determine the interaction between the RR paraoxonase genotype and HDL-deficient subjects, we used 4 x 2 epidemiologic tables and synergy measures: the additive model (Rothman's synergy index, SI) and multiplicative model (Khoury's synergy index, SIM). The relative excess risk due to interaction (RERI) and the attributable proportion (AP) due to interaction (Rothman) were calculated. RESULTS: The PON1 RR192 polymorphism was associated with coronary heart disease (OR = 1.61; p = 0.043) in the whole population. HDL-deficient subjects with the RR192 genotype showed increased risk for CAD (OR = 17.38; p < 0.0001) compared to those with normal HDL and RR192 (OR = 1.39; p = 0.348) and HDL-deficient subjects not carrying the RR genotype (OR = 7.79; p < 0.0001). Synergy measures were SI = 2.3, SIM = 1.6; RERI = 9.2. CONCLUSION: These data suggest the existence of a synergistic effect of the PON1 RR192 genotype (with lower antioxidant ability) and HDL-deficient subjects in risk for development of CAD. The AP due to this interaction was 0.53, meaning that 53% of CAD was explained by this interaction.info:eu-repo/semantics/publishedVersio

Deep Convolutional Neural Networks for Breast Cancer Histology Image Analysis

Breast cancer is one of the main causes of cancer death worldwide. Early diagnostics significantly increases the chances of correct treatment and survival, but this process is tedious and often leads to a disagreement between pathologists. Computer-aided diagnosis systems showed potential for improving the diagnostic accuracy. In this work, we develop the computational approach based on deep convolution neural networks for breast cancer histology image classification. Hematoxylin and eosin stained breast histology microscopy image dataset is provided as a part of the ICIAR 2018 Grand Challenge on Breast Cancer Histology Images. Our approach utilizes several deep neural network architectures and gradient boosted trees classifier. For 4-class classification task, we report 87.2% accuracy. For 2-class classification task to detect carcinomas we report 93.8% accuracy, AUC 97.3%, and sensitivity/specificity 96.5/88.0% at the high-sensitivity operating point. To our knowledge, this approach outperforms other common methods in automated histopathological image classification. The source code for our approach is made publicly available at https://github.com/alexander-rakhlin/ICIAR2018Comment: 8 pages, 4 figure

Independent association of the variant rs1333049 at the 9p21 locus and coronary heart disease.

Introdução: Estudos recentes de associação genómica em larga escala (GWAS) identificaram vários polimorfismos de um único nucleótido (SNP), localizados no locus 9p21, associados com doença arterial coronária (DAC). De entre eles o SNP rs1333049 demonstrou uma associação consistente com a DAC tendo sido reproduzida, com sucesso, em várias populações. Objectivo: Investigar se a nova variante rs1333049, no cromossoma 9p21, é um factor de risco independente para DAC, na população Portuguesa. Material e métodos: Estudo caso-controlo, que incluiu 1406 indivíduos, 723 doentes coronários internados consecutivamente (idade média de 53,7±8,9 anos 79,9% do sexo masculino) e 683 controlos sem doença coronária (idade média de 53,3±10,5 anos, 73,9 % do sexo masculino) seleccionados para não serem significativamente diferentes quanto ao sexo e idade. Estudou-se o SNP rs1333049, em todos os indivíduos, com recurso à técnica convencionada de PCR combinada com a técnica TaqMan (Applied Biosystems). Determinou-se a distribuição alélica e genotípica (C/G), odds ratio e respectivo intervalo de confiança para risco de DAC. Foi construído um modelo de regressão logística forward wald ajustado para a idade, sexo, factores de risco convencionais, marcadores bioquímicos e genótipos em estudo, afim de avaliar quais as variáveis associadas de forma significativa e independente com DAC. Resultados: 60% dos doentes coronários e 53% dos controlos apresentaram o alelo C (OR=1,33; p=0,0002), 35,7% dos doentes e 29,3% dos controlos tinham o genótipo homozigoto CC (OR=1,34;p=0,010). O heterozigoto CG estava presente em 48,1% dos doentes e 47% nos controlos, não atingindo significância estatística, para risco vascular (OR=1,05;p=0,670). Após análise multivariada de regressão logística o genótipo CC do cromossoma 9p21 ficou na equação com um OR=1,7, p=0,018 e o genótipo heterozigoto CG com um OR=1,5, p=0,048. Conclusão: Com o presente trabalho replicou-se, numa população portuguesa, o risco coronário ligado à nova variante rs1333049 do cromossoma 9p21. A robustez deste genótipo, tanto em homo como em heterozigotia, tem sido consistente e relevante na estratificação de risco para a DAC, mesmo em contextos populacionais muito diversos. Nestas circunstâncias, a utilização do genótipo CC ou CG poderá vir a revelar-se útil para a previsão do risco de DAC na nossa população.INTRODUCTION: Recent genome-wide association studies have identified single-nucleotide polymorphisms (SNPs) at the 9p21 locus as risk factors for coronary artery disease (CAD). Among them, the SNP rs1333049 has demonstrated a consistent association with CAD, which has been successfully replicated in several populations. AIM: To investigate whether the SNP rs1333049 located on the 9p21 chromosome is an independent risk factor for CAD in a Portuguese population. METHODS: We performed a case-control study which included 1406 individuals, 723 consecutive coronary patients (mean age 53.71 +/- 8.9 years, 79.9% male and 683 controls without coronary disease (mean age 53.3 +/- 10.5 years, 73.9% male). Cases and controls were selected so as not to be significantly different in terms of gender and age. We studied the SNP rs1333049 at the 9p21 locus in all individuals, using standard PCR combined with the TaqMan technique (Applied Biosystems). The allelic and genotype distribution (C/G), odds ratios and corresponding confidence intervals for CAD risk were determined. A forward Wald logistic regression analysis model was constructed, adjusted for age, gender, conventional risk factors, biochemical markers and the genotypes under study, in order to determine which variables were linked significantly and independently with CAD. RESULTS: The C allele was found in 60% of the CAD patients and 53% of the controls, with OR = 1.33; p = 0.0002. The CC genotype appeared in 35.7% of CAD patients, with OR = 1.34, p = 0.010. The heterozygous CG genotype was present in 48.1% of the CAD patients and 47% of the controls, and did not present vascular risk (OR = 1.05, p = 0.670). After logistic regression analysis, the CC genotype remained in the equation with OR = 1.7; p = 0.018 and CG with OR = 1.5, p = 0.048. CONCLUSION: In the present study we replicated the coronary risk linked to the recently discovered variant rs1333049 on the 9p21 chromosome in a Portuguese population. Although the mechanism underlying the risk is still unknown, the robustness of this risk allele in risk stratification for CAD has been consistent, even in very different populations. The presence of the CC or CG genotype may thus prove to be useful for predicting the risk of developing CAD in the Portuguese population.info:eu-repo/semantics/publishedVersio

Buerger's Disease (Thromboangiitis Obliterans): a Diagnostic Challenge

Buerger's disease or Thromboangiitis obliterans is a segmental inflammatory disease that affects the vessels and nerves of the extremities. It usually affects men below 45 years old and correlates with tobacco, as a predisposing factor. The authors present the case of a 34-year-old male, with ulcers in the fingertips with progressive worsening: acrocyanosis, slow healing, necrosis and finally loss of substance. Dorsalis pedis and posterior tibial pulses were not palpable. Personal history of heavy smoking was (20 pack-years). The angiography revealed proximal occlusion of the left posterior tibial and interosseal arteries, with distal circulation by the anterior tibial artery. He was submitted to disarticulation of the second left toe and therapy with pentoxifyline and iloprost infusion, calcium antagonist, antiplatelet drugs, statin and low molecular weight heparin (later replaced by oral anticoagulation). Improvement was seen of active vascular lesions and pain symptoms.info:eu-repo/semantics/publishedVersio

Exposure of humans to the zoonotic nematode Dirofilaria immitis in Northern Portugal

Dirofilariosis caused by Dirofilaria immitis (heartworm) is a zoonosis, considered an endemic disease of dogs and cats in several countries of Western Europe, including Portugal. This study assesses the levels of D. immitis exposure in humans from Northern Portugal, to which end, 668 inhabitants of several districts belonging to two different climate areas (Csa: Bragança, Vila Real and Csb: Aveiro, Braga, Porto, Viseu) were tested for anti-D. immitis and anti-Wolbachia surface proteins (WSP) antibodies. The overall prevalence of seropositivity to both anti-D. immitis and WSP antibodies was 6.1%, which demonstrated the risk of infection with D. immitis in humans living in Northern Portugal. This study, carried out in a Western European country, contributes to the characterisation of the risk of infection with D. immitis among human population in this region of the continent. From a One Health point of view, the results of the current work also support the close relationship between dogs and people as a risk factor for human infectio

Human paraoxonase gene polymorphisms and coronary artery disease risk.

Introdução: As doenças complexas como a doença das artérias coronárias (DAC), a hipertensão e a diabetes, são usualmente causadas pela susceptibilidade individual a múltiplos genes, factores ambientais e pela interacção entre eles. As enzimas da paraoxonase humana (PON), particularmente a PON1, têm sido implicadas na patogenia da aterosclerose e da DAC. Dois polimorfismos comuns na região codificante do gene, com substituição Glutamina (Q) /Arginina (R) na posição 192 e Leucina /Metionina na posição 55 influenciam a actividade da PON1. Vários estudos têm investigado a associação entre os polimorfismos da PON1 e a DAC, com resultados contraditórios. Objectivo: 1- Avaliar a associação dos polimorfismos da PON1 com o risco de DAC. 2-Estudar a interacção destes polimorfismos com outros situados em genes candidatos diferentes, na susceptibilidade para o aparecimento da DAC. Material e Métodos: Estudámos em 298 doentes coronários e 298 controlos saudáveis, através de um estudo caso/controlo, o risco de DAC associado aos polimorfismos da PON1, 192Q/R e 55L/M. Numa segunda fase avaliámos o risco das interacções polimórficas PON1 192 RR + MTHFR 1298 AA; PON1 192 R/R + ECA DD; PON1 192 R/R + ECA 8 GG. Finalmente construímos um modelo de regressão logística (no qual entraram todas as variáveis genéticas, ambientais e bioquímicas, que tinham mostrado significância estatística na análise univariada), para determinar quais as que se relacionavam de forma significativa e independente com DAC. Resultados: Verificámos que o genótipo PON1 55 MM tinha uma distribuição superior na população doente mas não atingia significância estatística como factor de risco para DAC. O PON1 199 RR apresentou um risco relativo 80% superior relativamente à população que o não possuía (p=0,04). A interacção da PON1 192 RR e da MTHFR 1298 AA, polimorfismos sedeados em genes diferentes, apresentou um risco relativo de DAC de 2,76 (OR=2,76;IC=1,20- 6,47; P=0,009), bastante superior ao risco de cada polimorfismo isolado, assim como a associação da PON1 RR + ECA DD (com polimorfismos também sedeados em genes diferentes), que apresentou um risco 337% superior relativamente aos que não possuíam esta associação (OR=4,37;IC=1,47- 13,87; P=0,002). Da mesma forma a associação entre a PON1 RR e ECA 8 GG, revelou um risco ainda mais elevado (OR=6;23; IC=1,67- 27,37; P<0,001). Após modelo de Regressão Logística as variáveis que ficaram na equação representando factores de risco significativos e independentes para DAC, foram os hábitos tabágicos, doença familiar, diabetes, fibrinogénio, Lp (a) e a associação PON1 192 RR + ECA 8 GG. Esta última associação apresentou, na regressão logística, um OR=14,113; p=0,018 Conclusões: O genótipo PON1 192 RR apresentou, se avaliado isoladamente, um risco relativo de DAC 80% superior relativamente à população que não possuía este genótipo. A associação deste polimorfismo com outros polimorfismos sedeados em genes diferentes, codificando para diferentes enzimas e pertencendo a sistemas fisiopatológicos distintos (MTHFR1298 AA, ECA DD e ECA 8 GG), aumentou sempre o risco de eclosão da DAC. Após correcção para os outros factores de risco clássicos e bioquímicos, a associação PON1 192 RR + ECA 8 GG, continuou a ser um factor de risco significativo e independente para CAD.BACKGROUND: Complex diseases such as coronary artery disease (CAD), hypertension and diabetes are usually caused by individual susceptibility to multiple genes, environmental factors, and the interaction between them. The paraoxonase 1 (PON1) enzyme has been implicated in the pathogenesis of atherosclerosis and CAD. Two common polymorphisms in the coding region of the PON1 gene, which lead to a glutamine (Q)/arginine (R) substitution at position 192 and a leucine (L)/methionine (M) substitution at position 55, influence PON1 activity. Studies have investigated the association between these polymorphisms and CAD, but with conflicting results. AIMS: 1) To evaluate the association between PON1 polymorphisms and CAD risk; and 2) to study the interaction between PON1 polymorphisms and others in different candidate genes. METHODS: We evaluated the risk of CAD associated with PON1 Q192R and L55M polymorphisms in 298 CAD patients and 298 healthy individuals. We then evaluated the risk associated with the interaction of the PON1 polymorphisms with ACE DD, ACE 8 GG and MTHFR 1298AA. Finally, using a logistic regression model, we evaluated which variables (genetic, biochemical and environmental) were linked significantly and independently with CAD. RESULTS: We found that the PON1 55MM genotype was more common in the CAD population, but this did not reach statistical significance as a risk factor for CAD, while PON1 192RR presented an 80% higher relative risk compared to the population without this polymorphism. The interaction between PON1 192RR and MTHFR 1298AA, sited in different genes, increased the risk for CAD, compared with the polymorphisms in isolation (OR=2.76; 95% CI=1.20-6.47; p=0.009), as did the association of PON1 192RR with ACE DD, which presented a 337% higher risk compared to the population without this polymorphic association (OR=4.37; 95% CI=1.47-13.87; p=0.002). Similarly, the association between PON1 192RR and ACE 8 GG was linked to an even higher risk (OR=6.23; 95% CI=1.67-27.37; p<0.001). After logistic regression, smoking, family history, fibrinogen, diabetes, Lp(a) and the association of PON1 192RR + ACE 8 GG remained in the regression model and proved to be significant and independent risk factors for CAD. In the regression model the latter association had OR=14.113; p=0.018. CONCLUSION: When analyzed separately, the PON1 192RR genotype presented a relative risk for CAD 80% higher than in the population without this genotype. Its association with other genetic polymorphisms sited in different genes, coding for different enzymes and belonging to different physiological systems, always increased the risk for CAD. After correction for other conventional and biochemical risk factors, the PON1 192RR + ACE 8 GG association remained a significant and independent risk factor for CAD.info:eu-repo/semantics/publishedVersio