Like Mother, like Son: Physical Activity, Commuting, and Associated Demographic Factors

We would like to express our gratitude to the children, parents, and schools participating in the study.A mother’s healthy conduct may lead to the healthy conduct of their children. Thus, this study aimed to verify the role of demographic factors in the relationship between mothers’ physical activity (PA) and commuting to work with children and adolescent’s PA and commuting to school. This cross-sectional study comprised 1421 children and adolescents aged 6 to 17 years and 1421 mothers, from Brazil. PA, commuting, socioeconomic status (SES), skin color/ethnicity, and living area were evaluated by questionnaire. Logistic binary regression models were used. Results indicated that mothers’ PA and commuting were associated with children and adolescent’s PA and commuting to school in crude and adjusted models. Considering the role of the demographic factors, an association was only observed for girls in the relationship between mother’s PA with children’s PA. In adolescents, an association was observed in both high/low SES, boys/girls, and rural/urban areas. Regarding children and adolescent active commuting to school, there was an association with mothers commuting. All demographic factors were strongly associated, except for rural areas. Therefore, mothers’ PA as well as commuting to work are associated with children and adolescent’s PA and commuting to school. Sex, living area, and SES are the related demographic factors.CAPESPortuguese Foundation for Science and Technology SFRH/BSAB/142983/2018 UID/DTP/00617/20

From pregnancy to breastfeeding : adequate maternal body mass index is essential to prevent a high body mass index in your children

Objectives: To verify the associations between prenatal and perinatal factors with offspring body mass index (BMI) and the moderator role of maternal BMI in this relationship. Methods: Cross-sectional study developed with 1,562 children and adolescents aged between 6 and 17 years, as well as their mothers, from southern Brazil. The prenatal and perinatal factors, weight, and height for the calculation of maternal BMI were self-reported. For the calculation of BMI, weight and height of the child/adolescent were measured on an anthropometric scale with a coupled stadiometer. Linear regression models were used for the moderation analysis. All analyzes were adjusted for the mother’s and child’s age, sex, sexual maturation, skin color/race, and educational level. Results: cesarean as type of delivery (β=0.66; 95% CI=0.22 1.04; p=0.002) and pregnancy complications (β=0.60; 95% CI=0.15 1.04; p=0.002) were positively associated with offspring BMI. Schoolchildren who were breastfed for 4–6 months showed −0.56 kg/m2 of BMI (95% CI=−1.06– 0.06; p=0.02). Birth weight was also associated with BMI, with low weight being inversely (β=−0.59; 95% CI=−1.03– 0.15; p=0.008), while overweight was positively related (β=0.84; 95% CI=0.08 1.60; p=0.02). The moderation analysis indicated a positive interaction between the mother’s BMI and cesarean, pregnancy complications, and smoking with the offspring’s BMI. On the other hand, there was an inverse association between breastfeeding from 7 to 12 months and the offspring BMI, only in mothers with high BMI. Conclusions: Adequate maternal BMI is essential to prevent a high BMI in their children, especially when considering the influence of prenatal and perinatal risk factors

Influence of deformation and fluids on Ar retention in white mica: Dating the Dover Fault, Newfoundland Appalachians

White mica 40Ar/39Ar analyses may provide useful constraints on the timing of tectonic processes, but complex geological and thermal histories can perturb Ar systematics in a variety of ways. Ductile shear zones represent excellent case studies for exploring the link(s) between dynamic re-/neo-crystallization of white mica and coeval enhanced fluid flow, and their effect on 40Ar/39Ar dates. White mica 40Ar/39Ar dates were collected from compositionally similar granites that record different episodes of deformation with proximity to the Dover Fault, a terrane-bounding strike-slip shear zone in the Appalachian orogen, Newfoundland, Canada. 40Ar/39Ar data were collected in situ by laser ablation and by step heating single crystals. Results were compared to each other and against complementary U-Pb zircon and monazite, and K-Ar fault gouge analysis. Although step-heat 40Ar/39Ar is a widely applied method in orogenic settings, this dataset shows that relatively flat step-heat 40Ar/39Ar spectra are in contradiction with wide spreads in in-situ 40Ar/39Ar dates from the same samples, and that plateau dates in some cases yielded mixed dates of equivocal geological significance. This result indicates that the step-wise release of Ar from white mica likely homogenizes and obscures spatially-controlled Ar isotope reservoirs in white mica from sheared rocks. In contrast, in situ laser ablation 40Ar/39Ar analysis preserves the spatial resolution of 40Ar reservoirs that have been variably reset by deformation and fluid interaction. This study therefore suggests that laser ablation is the best method for dating the timing of deformation recorded by white mica. Final interpretation of results should be guided by microstructural analysis, estimation of deformation temperature, chemical characterization of white mica, and complementary chronometers. Overall the dataset shows that granitic protoliths were emplaced between 430-422 Ma (U-Pb zircon). High strain deformation along the Wing Pond Shear Zone occurred between ca. 422-405 Ma (U-Pb monazite and 40Ar/39Ar). Subsequent patchy Ar loss in white mica occurred locally during low T shear (40Ar/39Ar). K-Ar dating of authigenic illite in fault gouge from the broadly co-linear brittle Hermitage Bay Fault indicates that slip along the terrane boundary persisted until at least the Mississippian

Emery-Dreifuss muscular dystrophy Type 1 is associated with a high risk of malignant ventricular arrhythmias and end-stage heart failure

\ua9 2023 The Author(s). Published by Oxford University Press on behalf of the European Society of Cardiology.Background and Aims: Emery-Dreifuss muscular dystrophy (EDMD) is caused by variants in EMD (EDMD1) and LMNA (EDMD2). Cardiac conduction defects and atrial arrhythmia are common to both, but LMNA variants also cause end-stage heart failure (ESHF) and malignant ventricular arrhythmia (MVA). This study aimed to better characterize the cardiac complications of EMD variants. Methods: Consecutively referred EMD variant-carriers were retrospectively recruited from 12 international cardiomyopathy units. MVA and ESHF incidences in male and female variant-carriers were determined. Male EMD variant-carriers with a cardiac phenotype at baseline (EMDCARDIAC) were compared with consecutively recruited male LMNA variant-carriers with a cardiac phenotype at baseline (LMNACARDIAC). Results: Longitudinal follow-up data were available for 38 male and 21 female EMD variant-carriers [mean (SD) ages 33.4 (13.3) and 43.3 (16.8) years, respectively]. Nine (23.7%) males developed MVA and five (13.2%) developed ESHF during a median (inter-quartile range) follow-up of 65.0 (24.3-109.5) months. No female EMD variant-carrier had MVA or ESHF, but nine (42.8%) developed a cardiac phenotype at a median (inter-quartile range) age of 58.6 (53.2-60.4) years. Incidence rates for MVA were similar for EMDCARDIAC and LMNACARDIAC (4.8 and 6.6 per 100 person-years, respectively; log-rank P =. 49). Incidence rates for ESHF were 2.4 and 5.9 per 100 person-years for EMDCARDIAC and LMNACARDIAC, respectively (log-rank P =. 09). Conclusions: Male EMD variant-carriers have a risk of progressive heart failure and ventricular arrhythmias similar to that of male LMNA variant-carriers. Early implantable cardioverter defibrillator implantation and heart failure drug therapy should be considered in male EMD variant-carriers with cardiac disease

Emery-Dreifuss muscular dystrophy Type 1 is associated with a high risk of malignant ventricular arrhythmias and end-stage heart failure

BACKGROUND AND AIMS: Emery-Dreifuss muscular dystrophy (EDMD) is caused by variants in EMD (EDMD1) and LMNA (EDMD2). Cardiac conduction defects and atrial arrhythmia are common to both, but LMNA variants also cause end-stage heart failure (ESHF) and malignant ventricular arrhythmia (MVA). This study aimed to better characterise the cardiac complications of EMD variants. METHODS: Consecutively referred EMD variant-carriers were retrospectively recruited from 12 international cardiomyopathy units. MVA and ESHF incidence in male and female variant-carriers was determined. Male EMD variant-carriers with a cardiac phenotype at baseline (EMDCARDIAC) were compared to consecutively recruited male LMNA variant-carriers with a cardiac phenotype at baseline (LMNACARDIAC). RESULTS: Longitudinal follow-up data were available for 38 male and 21 female EMD variant-carriers (mean [SD] ages 33.4 [13.3] and 43.3 [16.8] years, respectively). Nine (23.6%) males developed MVA and five (13.2%) developed ESHF during a median [IQR] follow-up of 65.0 [24.3, 109.5] months. No female EMD variant-carrier had MVA or ESHF, but nine (42.8%) developed a cardiac phenotype at a median [IQR] age of 58.6 [53.2, 60.4] years. Incidence rates for MVA were similar for EMDCARDIAC and LMNACARDIAC (4.8 and 6.6 per 100 person-years, respectively; log-rank p = 0.49). Incidence rates for ESHF were 2.4 and 5.9 per 100 person-years for EMDCARDIAC and LMNACARDIAC, respectively (log-rank p = 0.09). CONCLUSIONS: Male EMD variant-carriers have a risk of progressive heart failure and ventricular arrhythmias similar to that of male LMNA variant-carriers. Early implantable cardioverter defibrillator implantation and heart failure drug therapy should be considered in male EMD variant-carriers with cardiac disease

Emery-Dreifuss Muscular Dystrophy 1 is associated with high risk of malignant ventricular arrhythmias and end-stage heart failure.

BACKGROUND AND AIMS Emery-Dreifuss muscular dystrophy (EDMD) is caused by variants in EMD (EDMD1) and LMNA (EDMD2). Cardiac conduction defects and atrial arrhythmia are common to both, but LMNA variants also cause end-stage heart failure (ESHF) and malignant ventricular arrhythmia (MVA). This study aimed to better characterise the cardiac complications of EMD variants. METHODS Consecutively referred EMD variant-carriers were retrospectively recruited from 12 international cardiomyopathy units. MVA and ESHF incidence in male and female variant-carriers was determined. Male EMD variant-carriers with a cardiac phenotype at baseline (EMDCARDIAC) were compared to consecutively recruited male LMNA variant-carriers with a cardiac phenotype at baseline (LMNACARDIAC). RESULTS Longitudinal follow-up data were available for 38 male and 21 female EMD variant-carriers (mean [SD] ages 33.4 [13.3] and 43.3 [16.8] years, respectively). Nine (23.6%) males developed MVA and five (13.2%) developed ESHF during a median [IQR] follow-up of 65.0 [24.3, 109.5] months. No female EMD variant-carrier had MVA or ESHF, but nine (42.8%) developed a cardiac phenotype at a median [IQR] age of 58.6 [53.2, 60.4] years. Incidence rates for MVA were similar for EMDCARDIAC and LMNACARDIAC (4.8 and 6.6 per 100 person-years, respectively; log-rank p = 0.49). Incidence rates for ESHF were 2.4 and 5.9 per 100 person-years for EMDCARDIAC and LMNACARDIAC, respectively (log-rank p = 0.09). CONCLUSIONS Male EMD variant-carriers have a risk of progressive heart failure and ventricular arrhythmias similar to that of male LMNA variant-carriers. Early implantable cardioverter defibrillator implantation and heart failure drug therapy should be considered in male EMD variant-carriers with cardiac disease.The work reported in this publication was funded by: a British Heart Foundation Clinical Research Training Fellowship to D.E.C. (FS/CRTF/ 20/24022); a British Heart Foundation Clinical Research Training fellowship to A.P. (FS/18/82/34024); The Ministry of Health, Italy, project RC-2022-2773270 to E.B.; the National Institutes of Health (NIH) (R01HL69071, R01HL116906, R01HL147064, NIH/NCATS UL1 TR002535, and UL1 TR001082) to L.M.; and support from the Rose Foundation for K.M.S

Non-erythropoietic erythropoietin derivatives protect from light-induced and genetic photoreceptor degeneration

Given the high genetic heterogeneity of inherited retinal degenerations (IRDs), a wide applicable treatment would be desirable to halt/slow progressive photoreceptor (PR) cell loss in a mutation-independent manner. In addition to its erythropoietic activity, erythropoietin (EPO) presents neurotrophic characteristics. We have previously shown that adeno-associated viral (AAV) vector-mediated systemic EPO delivery protects from PR degeneration. However, this is associated with an undesired hematocrit increase that could contribute to PR protection. Non-erythropoietic EPO derivatives (EPO-D) are available which allow us to dissect erythropoiesis's role in PR preservation and may be more versatile and safe than EPO as anti-apoptotic agents. We delivered in animal models of light-induced or genetic retinal degeneration either intramuscularly or subretinally AAV vectors encoding EPO or one of the three selected EPO-D: the mutant S100E, the helix A- and B-derived EPO-mimetic peptides. We observed that (i) systemic expression of S100E induces a significantly lower hematocrit increase than EPO and provides similar protection from PR degeneration, and (ii) intraocular expression of EPO-D protects PR from degeneration in the absence of significant hematocrit increase. On the basis of this, we conclude that erythropoiesis is not required for EPO-mediated PR protection. However, the lower efficacy observed when EPO or S100E is expressed intraocularly rather than systemically suggests that hormone systemic effects contribute to PR protection. Unlike S100E, EPO-mimetic peptides preserve PR only when given locally, suggesting that different EPO-D have a different potency or mode of action. In conclusion, our data show that subretinal delivery of AAV vectors encoding EPO-D protects from light-induced and genetic PR degeneration

Anxiety and Depression in Adults with Autism Spectrum Disorder: A Systematic Review and Meta-analysis

Adults with autism spectrum disorder (ASD) are thought to be at disproportionate risk of developing mental health comorbidities, with anxiety and depression being considered most prominent amongst these. Yet, no systematic review has been carried out to date to examine rates of both anxiety and depression focusing specifically on adults with ASD. This systematic review and meta-analysis examined the rates of anxiety and depression in adults with ASD and the impact of factors such as assessment methods and presence of comorbid intellectual disability (ID) diagnosis on estimated prevalence rates. Electronic database searches for studies published between January 2000 and September 2017 identified a total of 35 studies, including 30 studies measuring anxiety (n = 26 070; mean age = 30.9, s.d. = 6.2 years) and 29 studies measuring depression (n = 26 117; mean age = 31.1, s.d. = 6.8 years). The pooled estimation of current and lifetime prevalence for adults with ASD were 27% and 42% for any anxiety disorder, and 23% and 37% for depressive disorder. Further analyses revealed that the use of questionnaire measures and the presence of ID may significantly influence estimates of prevalence. The current literature suffers from a high degree of heterogeneity in study method and an overreliance on clinical samples. These results highlight the importance of community-based studies and the identification and inclusion of well-characterized samples to reduce heterogeneity and bias in estimates of prevalence for comorbidity in adults with ASD and other populations with complex psychiatric presentations