Background The WHO's Vision 2020 global initiative against blindness, launched in 2000, prioritises children. Progress has been hampered by the global paucity of epidemiological data about childhood visual disability. The British Childhood Visual Impairment and Blindness Study 2 (BCVIS2) was undertaken to address this evidence gap. Methods UK-wide prospective population-based observational study of all those aged under 18 years newly diagnosed with visual impairment or blindness between Oct 1, 2015 and Nov 1 2016. Eligible children were notified simultaneously but independently by their managing ophthalmologists and paediatricians via the two national active surveillance schemes, the British Ophthalmic and Paediatric Surveillance Units. Standardised detailed data were collected at diagnosis and one year later. Incidence estimates and relative rates by key sociodemographic factors were calculated. Descriptive analyses were undertaken of underlying ophthalmic disorders and nonophthalmic comorbidities. FindingsOf 784 cases, 72% had additional non-ophthalmic impairments/disorders and 4% died within the year. Annual incidence was highest in the first year of life, 5•2 per 10,000 (95% CI 4•7-5•7) with cumulative incidence by 18 years of 10•0 per 10,000 (95% CI 9•4 to 10•8). Rates were higher for those from any ethnic minority group, the lowest quintile of socio-economic status, born preterm or with low birthweight. Only 44% had a single ophthalmic condition: disorders of the brain/visual pathways affected 48% overall. Prenatal or perinatal aetiological factors accounted for 84% of all conditions. InterpretationBCVIS2 provides a contemporary snapshot of the heterogeneity, multi-morbidity and vulnerability associated with childhood visual disability in a high income country, and the arising complex needs. These findings will facilitate developing and delivering healthcare and planning interventional research. They highlight the importance of including childhood visual disability as a sentinel event and metric in global child health initiatives.
Placental fatty acid oxidation (FAO) is impaired and lipid storage is increased in pregnancy states associated with chronic oxidative stress. The effect of acute oxidative stress, as seen in pregnancies complicated with asthma, on placental lipid metabolism is unknown. We hypothesized that induction of acute oxidative stress would decrease FAO and increase esterification. We assessed [3H]-palmitate oxidation and esterification in term placental explants from lean women after exposure to hydrogen peroxide (H2O2) for 4 hours. Fatty acid oxidation decreased 16% and 24% in placental explants exposed to 200 ( P = .02) and 400 µM H2O2 ( P = .01), respectively. Esterification was not altered with H2O2 exposure. Neither messenger RNA nor protein expression of key genes involved in FAO (eg, peroxisome proliferator-activated receptor α, carnitine palmitoyl transferase 1b) were altered. Adenosine triphosphate (ATP) levels decreased with induction of oxidative stress, without increasing cytotoxicity. Acute oxidative stress decreased FAO and ATP production in the term placenta without altering fatty acid esterification. As decreases in placental FAO and ATP production are associated with impaired fetal growth, pregnancies exposed to acute oxidative stress may be at risk for fetal growth restriction.
This study examined iron status and nutrient intake in highly active (n = 28; 20 +/- 2 yr, >/=12 hr purposeful physical activity per week [PPA/wk]) and sedentary (n = 28; 24 +/- 3 yr, =2 hr PPA/wk) women. Participants completed a 7-day weighed-food record (energy, protein, fiber, alcohol, and micronutrients), 7-day pedometer/activity log, and fasting blood draw (hemoglobin, hematocrit, red blood cell indices, C-reactive protein, serum iron, percent transferrin saturation, total iron-binding capacity, ferritin, transferrin receptor [sTfR], and sTfR index). Independent-sample t tests and the Mann-Whitney nonparametric test compared mean values between groups. Lower serum ferritin (p = .01) and mean cell hemoglobin (p < .01) concentrations were found in active than in sedentary women. Higher mean sTfR (p = .01) and sTfR index (p < .01) values were found in the active women. No significant differences were found between groups for the other blood markers. Serum ferritin concentrations (storage iron) indicated iron depletion (Stage I) in 21% of active and 18% of sedentary participants. Nonetheless, 50% of active and 18% of sedentary participants were iron depleted as evidenced by the sTfR index (ratio of functional-to-storage iron). Elevated sTfR concentrations (functional iron) were observed in 25% of active and 3% of sedentary participants. Although the active women reported greater iron (p < .01) but similar heme iron intakes, they had higher mean sTfR, higher sTfR index, and lower serum ferritin concentrations than the sedentary women. Assessment of iron status may require measures not commonly used in routine assessments.
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