Dietary Interventions to Prevent Childhood Obesity: A Literature Review

Several dietary interventions have been conducted to prevent/reduce childhood obesity, but most of them are known to have failed in tackling the obesity epidemic. This study aimed to review the existing literature on dietary interventions for the prevention of childhood obesity and their effectiveness. A literature search was conducted using PubMed Central®. Only articles published between 2009 and 2021, written in English, conducted in humans, and including children and/or adolescents (<18 years old) were considered. The majority of studies were school-based interventions, with some addressing the whole community, and including some interventions in the food sector (e.g., taxation of high fat/sugar foods, front-of-pack labelling) and through mass media (e.g., restrictions on food advertising for children) that directly or indirectly could help to manage childhood obesity. Most of the programs/interventions conducted focus mainly on person-based educational approaches, such as nutrition/diet education sessions, allied to the promotion of physical activity and lifestyles to students, parents, and school staff, and less on environmental changes to offer healthier food choices. Only a few trials have focused on capacity building and macro-policy changes, such as the adaptation of the built environment of the school, serving smaller portion sizes, and increasing the availability and accessibility of healthy foods and water in schools, and restricting the access to vending machines, for example. Overall, most of the intervention studies showed no consistent effects on changing the body mass index of children; they have only reported small weight reductions, clinically irrelevant, or no effects at all. Little is known about the sustainability of interventions over time.The authors acknowledge FEDER from the Operational Programme Factors of Competitiveness—COMPETE and national funding from the Foundation for Science and Technology—FCT (Portuguese Ministry of Education and Science) under the projects “Appetite regulation and obesity in childhood: a comprehensive approach towards understanding genetic and behavioral influences” (POCI-01-0145-FEDER-030334; PTDC/SAUEPI/30334/2017) and “Appetite and adiposity—evidence for gene-environment interplay in children” (IF/01350/2015), and the Investigator Contract (IF/01350/2015—Andreia Oliveira)

Cardiac autonomic function, cardiovascular risk and physical activity in adolescents.

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this record.The aims of this study were to investigate in adolescents: 1) the relationships of physical activity (PA) and cardiorespiratory fitness (CRF) to traditional CVD risk factors, rest and recovery autonomic function; and 2) whether autonomic function strengthens the associations between PA, CRF and CVD risk. Fifty-four (22 girls) adolescents had traditional CVD risk factors, rest and recovery autonomic function evaluated. CRF was measured using a steep ramp cycle test and PA was assessed with accelerometers. Resting HRV (and RMSSD30) and heart rate recovery (T30, HHRτ) were used. Clustered traditional (CVDRtrad) and autonomic (CVDRauto) risk scores were created and added to form a composite clustered CVD risk score (CVDRcom). PA and CRF were significantly and negatively associated with traditional CVD risk factors. Moderate (MPA) and vigorous (VPA) were positively related to resting RMSSD, and negatively related to T30 and HHRτ (all P<0.05). RMSSD30 recovered faster in the high compared to low median split for VPA. Stronger associations for CVDRcom compared to CVDRtrad were observed for MPA (CVDRcom: r2=0.32, P=<0.001; CVDRtrad: r2=0.17, P=0.002), and VPA (CVDRcom: r2=0.18, P=0.001; CVDRtrad: r2=0.06, P=0.08). These findings strengthen the proposed additional beneficial effects of PA on autonomic function above traditional CVD risk factors.RSO is funded by Science Without Borders, CAPES, Brazil, under the process number:10423-13-3

Optical Coherence Tomography-Guided Full Plastic Jacket in Spontaneous Coronary Artery Dissection

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Reliability of autonomic and vascular components of baroreflex sensitivity in adolescents.

This is the author accepted manuscript. The final version is available from Wiley via the DOI in this record.Improvements in the autonomic and vascular systems are implicated in cardiovascular disease risk reduction. Baroreflex sensitivity (BRS) is composed of vascular and autonomic components. This study aimed to investigate between- and within-day reliability of BRS and its autonomic and vascular determinants in adolescents. Thirteen male adolescents (14·1 ± 0·5 y) participated in this study. For between-day reliability, participants completed four experimental visits separated by a minimum of 48-h. For within-day reliability, participants repeated BRS assessments three times in the morning with one hour between the measures. BRS was evaluated using the cross-spectral gain (LFgain) between blood pressure and heart rate interval. BRS was further divided into: 1) vascular component using arterial compliance (AC); and 2) autonomic component measured as LFgain divided by AC (LFgain/AC). LFgain, AC and LFgain/AC presented between-day coefficient of variation (CV) of 20%, 17%, and 20%, respectively. Similarly, variables associated with blood pressure control, such as cardiac output, mean arterial pressure, heart rate and total peripheral resistance, presented CVs ranging from 6% to 15%. Within-day reliability was poorer compared to between-day for LFgain (25%), AC (25%), and LFgain/AC (31%), as well as all hemodynamic variables (CVs from 11% to 22%, except heart rate with presented CV of 6%). This study indicates suitable between- and within-reliability of BRS and its autonomic and vascular determinants, as well as hemodynamic variables associated with BRS, in adolescents.This research was partially funded by Science Without Borders, CAPES, Brazil, under the process number:10423‐13‐3

Three-dimensional culture of single embryonic stem-derived neural/stem progenitor cells in fibrin hydrogels: neuronal network formation and matrix remodelling

In an attempt to improve the efficacy of neural stem/progenitor cell (NSPC) based therapies, fibrin hydrogels are being explored to provide a favourable microenvironment for cell survival and differentiation following transplantation. In the present work, the ability of fibrin to support the survival, proliferation, and neuronal differentiation of NSPCs derived from embryonic stem (ES) cells under monolayer culture was explored. Single mouse ES-NSPCs were cultured within fibrin (fibrinogen concentration: 6 mg/ml) under neuronal differentiation conditions up to 14 days. The ES-NSPCs retained high cell viability and proliferated within small-sized spheroids. Neuronal differentiation was confirmed by an increase in the levels of ßIII-tubulin and NF200 over time. At day 14, cell-matrix constructs mainly comprised NSPCs and neurons (46.5% ßIII-tubulin + cells). Gamma-aminobutyric acid (GABA)ergic and dopaminergic/noradrenergic neurons were also observed, along with a network of synaptic proteins. The ES-NSPCs expressed matriptase and secreted MMP-2/9, with MMP-2 activity increasing along time. Fibronectin, laminin and collagen type IV deposition was also detected. Fibrin gels prepared with higher fibrinogen concentrations (8/10 mg/ml) were less permissive to neurite extension and neuronal differentiation, possibly owing to their smaller pore area and higher rigidity. Overall, it is shown that ES-NSPCs within fibrin are able to establish neuronal networks and to remodel fibrin through MMP secretion and extracellular matrix (ECM) deposition. This three-dimensional (3D) culture system was also shown to support cell viability, neuronal differentiation and ECM deposition of human ES-NSPCs. The settled 3D platform is expected to constitute a valuable tool to develop fibrin-based hydrogels for ES-NSPC delivery into the injured central nervous system.The authors would like to acknowledge Prof. Domingos Henrique (Instituto de Medicina Molecular, Lisbon) for providing the ES 46C cell line. This work was supported by FEDER funds through the Programa Operacional Factores de Competitividade – COMPETE (FCOMP‐01–0124‐FEDER‐021125) and by National funds FCT – Fundação para a Ciência e a Tecnologia (PTDC/SAU‐BMA/118869/2010). A.R.B. and M.J. Oliveira are supported by FCT (SFRH/BD/86200/2012; Investigator FCT)

Regional White Matter Atrophy Correlates with Spike Activity in Encephalopathy Related to Status Epilepticus During Slow Sleep (ESES) After Early Thalamic Lesions

Encephalopathy related to Status Epilepticus during slow Sleep (ESES) is an age-related, epileptic syndrome, which associates cognitive/behavioral disturbances with a peculiar pattern of spike activity. One promising line of research is the study of ESES in cases of early thalamic lesions. We studied 7 ESES patients with unilateral thalamic lesions using magnetic resonance imaging to assess regional white matter (WM) and thalamic nuclei volume differences, and long-term electroencephalogram recordings to localize the epileptogenic cortex. N170 event-related potentials were used to demonstrate the dysfunctional character of the WM abnormalities. Diffusion-weighted images in a subset of 4 patients were used to parcellate the thalamus and evaluate volume asymmetries, based on cortical connectivity. Large WM regional atrophy in the hemisphere with the thalamic lesion was associated with both cortical dysfunction and epileptic activity. A correlation was demonstrated between lesions in the pulvinar and the mediodorsal thalamic nuclei and WM atrophy of the corresponding cortical projection areas. We propose that these abnormalities are due to the widespread structural disconnection produced by the thalamic lesions associated to a yet unknown age-dependent factor. Further exploration of WM regional atrophy association with the spike activity in other etiologies could lend support to the cortical disconnection role in ESES genesis.info:eu-repo/semantics/publishedVersio

Effects of exercise intensity on vascular and autonomic components of the baroreflex following glucose ingestion in adolescents.

This is the final version. Available from the publisher via the DOI in this record.PURPOSE: To investigate the effects of an oral glucose tolerance test (OGTT) on baroreflex sensitivity (BRS) in a sample of healthy adolescents, and how acute exercise bouts of different intensities alter the effects of the OGTT on BRS. METHODS: Thirteen male adolescents (14.0 ± 0.5 years) completed three conditions on separate days in a counterbalanced order: (1) high-intensity interval exercise (HIIE); (2) moderate-intensity interval exercise (MIIE); and (3) resting control (CON). At ~ 90 min following the conditions, participants performed an OGTT. Supine heart rate and blood pressure were monitored continuously at baseline, 60 min following the conditions, and 60 min following the OGTT. A cross-spectral method (LFgain) was used to determine BRS gain. Arterial compliance (AC) was assessed as the BRS vascular component. LFgain divided by AC (LFgain/AC) was used as the autonomic component. RESULTS: Although non-significant, LFgain moderately decreased post-OGTT when no exercise was performed (pre-OGTT = 24.4 ± 8.2 ms mmHg- 1; post-OGTT = 19.9 ± 5.6 ms mmHg- 1; ES = 0.64, P > 0.05). This was attributed to the decrease in LFgain/AC (pre-OGTT = 1.19 ± 0.5 ms µm- 1; post-OGTT = 0.92 ± 0.24 ms µm- 1; ES = 0.69, P > 0.05). Compared to CON (Δ = - 4.4 ± 8.7 ms mmHg- 1), there were no differences for the pre-post-OGTT delta changes in LF/gain for HIIE (Δ = - 3.5 ± 8.2 ms mmHg- 1) and MIIE (Δ = 1.3 ± 9.9 ms mmHg- 1) had no effects on BRS following the OGTT (all ES < 0.5). Similarly, compared to CON (Δ = - 0.23 ± 0.40 ms µm- 1) there were no differences for the pre-post-OGTT delta changes in LF/gain for HIIE (Δ = - 0.22 ± 0.49 ms µm- 1) and MIIE (Δ = 0.13 ± 0.36 ms µm- 1). CONCLUSION: A moderate non-significant decrease in BRS was observed in adolescents following a glucose challenge with no apparent effects of exercise.Science Without Border

Atypical Phenotype in Two Patients with LAMA2 Mutations

Congenital muscular dystrophy type 1A is caused by mutations in the LAMA2 gene, which encodes the a2-chain of laminin. We report two patients with partial laminin-a2 deficiency and atypical phenotypes, one with almost exclusive central nervous system involvement (cognitive impairment and refractory epilepsy) and the second with marked cardiac dysfunction, rigid spine syndrome and limb-girdle weakness. Patients underwent clinical, histopathological, imaging and genetic studies. Both cases have two heterozygous LAMA2 variants sharing a potentially pathogenic missense mutation c.2461A>C (p.Thr821Pro) located in exon 18. Brain MRI was instrumental for the diagnosis, since muscular examination and motor achievements were normal in the first patient and there was a severe cardiac involvement in the second. The clinical phenotype of the patients is markedly different which could in part be explained by the different combination of mutations types (two missense versus a missense and a truncating mutation)