339 research outputs found

    Healthy babies through infant-centered feeding protocol: an intervention targeting early childhood obesity in vulnerable populations

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    <p>Abstract</p> <p>Background</p> <p>Poor feeding practices during infancy contribute to obesity risk. As infants transition from human milk and/or formula-based diets to solid foods, these practices interfere with infant feeding self-regulation and healthy growth patterns. Compared with other socioeconomic groups, lower-income mothers are more likely to experience difficulty feeding their infants. This may include misinterpreting feeding cues and using less-than-optimal feeding styles and practices, such as pressuring infants during mealtimes and prematurely introducing solid food and sweetened beverages. The Healthy Babies trial aims to determine the efficacy of a community-based randomized controlled trial of an in-home intervention with economically and educationally disadvantaged mother-infant dyads. The educational intervention is being conducted during the infant's first 6 months of life to promote healthy transition to solids during their first year and is based on the theory of planned behavior.</p> <p>Methods/Design</p> <p>We will describe our study protocol for a multisite randomized control trial being conducted in Colorado and Michigan with an anticipated sample of 372 economically and educationally disadvantaged African American, Hispanic, and Caucasian mothers with infants. Participants are being recruited by county community agency staff. Participants are randomly assigned to the intervention or the control group. The intervention consists of six in-home visits by a trained paraprofessional instructor followed by three reinforcement telephone contacts when the baby is 6, 8, and 10 months old. Main maternal outcomes include a) maternal responsiveness, b) feeding style, and c) feeding practices. Main infant outcome is infant growth pattern. All measures occur at baseline and when the infant is 6 and 12 months old.</p> <p>Discussion</p> <p>If this project is successful, the expected outcomes will address whether the home-based early nutrition education intervention is effective in helping mothers develop healthy infant feeding practices that contribute to improving infant health and development and reducing the risk of early-onset childhood obesity.</p> <p>Trial Registration</p> <p>Current Controlled Trials <a href="http://www.anzctr.org.au/ACTRN126100000415000.aspx">ACTRN126100000415000</a></p

    State of Type 1 Diabetes Management and Outcomes from the T1D Exchange in 2016–2018

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    Objective: To provide a snapshot of the profile of adults and youth with type 1 diabetes (T1D) in the United States and assessment of longitudinal changes in T1D management and clinical outcomes in the T1D Exchange registry. Research Design and Methods: Data on diabetes management and outcomes from 22,697 registry participants (age 1–93 years) were collected between 2016 and 2018 and compared with data collected in 2010–2012 for 25,529 registry participants. Results: Mean HbA1c in 2016–2018 increased from 65 mmol/mol at the age of 5 years to 78 mmol/mol between ages 15 and 18, with a decrease to 64 mmol/mol by age 28 and 58–63 mmol/mol beyond age 30. The American Diabetes Association (ADA) HbA1c goal of 10-fold in children <12 years old. HbA1c levels were lower in CGM users than nonusers. Severe hypoglycemia was most frequent in participants ≄50 years old and diabetic ketoacidosis was most common in adolescents and young adults. Racial differences were evident in use of pumps and CGM and HbA1c levels. Conclusions: Data from the T1D Exchange registry demonstrate that only a minority of adults and youth with T1D in the United States achieve ADA goals for HbA1c

    Regional and cellular gene expression changes in human Huntington's disease brain

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    Huntington's disease (HD) pathology is well understood at a histological level but a comprehensive molecular analysis of the effect of the disease in the human brain has not previously been available. To elucidate the molecular phenotype of HD on a genome-wide scale, we compared mRNA profiles from 44 human HD brains with those from 36 unaffected controls using microarray analysis. Four brain regions were analyzed: caudate nucleus, cerebellum, prefrontal association cortex [Brodmann's area 9 (BA9)] and motor cortex [Brodmann's area 4 (BA4)]. The greatest number and magnitude of differentially expressed mRNAs were detected in the caudate nucleus, followed by motor cortex, then cerebellum. Thus, the molecular phenotype of HD generally parallels established neuropathology. Surprisingly, no mRNA changes were detected in prefrontal association cortex, thereby revealing subtleties of pathology not previously disclosed by histological methods. To establish that the observed changes were not simply the result of cell loss, we examined mRNA levels in laser-capture microdissected neurons from Grade 1 HD caudate compared to control. These analyses confirmed changes in expression seen in tissue homogenates; we thus conclude that mRNA changes are not attributable to cell loss alone. These data from bona fide HD brains comprise an important reference for hypotheses related to HD and other neurodegenerative disease

    BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers

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    Background: The K3326X variant in BRCA2 (BRCA2*c.9976A&gt;T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed. Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations

    Connecting Earth Observation to High-Throughput Biodiversity Data

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    There is much interest in using Earth Observation (EO) technology to track biodiversity, ecosystem functions, and ecosystem services, understandable given the fast pace of biodiversity loss. However, because most biodiversity is invisible to EO, EO-based indicators could be misleading, which can reduce the effectiveness of nature conservation and even unintentionally decrease conservation effort. We describe an approach that combines automated recording devices, high-throughput DNA sequencing, and modern ecological modelling to extract much more of the information available in EO data. This approach is achievable now, 62 offering efficient and near-real time monitoring of management impacts on biodiversity and its functions and services
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