Pancreatic atrophy caused by dietary selenium deficiency induces hypoinsulinemic hyperglycemia via global down-regulation of selenoprotein encoding genes in broilers - Fig 4

<p><b>Effects of dietary Se deficiency on relative mRNA levels of the selenoprotein encoding genes in liver (A), muscle (B) and pancreas (C) of chickens compared with those fed the control diet at fifth week</b>. Data are presented as means ± SE (<i>n</i> = 6). Asterisks indicate different from control: *<i>P</i> < 0.05, **<i>P</i> < 0.01.</p

Effects of dietary Se deficiency on body weight of broiler for 5 week.

<p>Data are presented as means ± SE (<i>n</i> = 11–60). **<i>P</i> < 0.01.</p

Pancreatic atrophy caused by dietary selenium deficiency induces hypoinsulinemic hyperglycemia via global down-regulation of selenoprotein encoding genes in broilers - Fig 4

<p><b>Effects of dietary Se deficiency on relative mRNA levels of the selenoprotein encoding genes in liver (A), muscle (B) and pancreas (C) of chickens compared with those fed the control diet at fifth week</b>. Data are presented as means ± SE (<i>n</i> = 6). Asterisks indicate different from control: *<i>P</i> < 0.05, **<i>P</i> < 0.01.</p

Comparison of the pancreas of broiler fed on Se deficient and control diet at fifth week.

<p>Gross morphometry (A), and histopathological view: control group (B) and Se-deficient group (C).</p

Effects of dietary Se deficiency on antioxidant attributes measurements in plasma, liver, muscle and pancreas at fifth week.

<p>Effects of dietary Se deficiency on antioxidant attributes measurements in plasma, liver, muscle and pancreas at fifth week.</p

Week-wise incidence of Se deficient symptoms and mortality in broilers fed on Se deficient diet over five weeks.

<p>Week-wise incidence of Se deficient symptoms and mortality in broilers fed on Se deficient diet over five weeks.</p

Effects of dietary Se deficiency on liver Se deposition, plasma biochemical attributes and inflammatory cytokine at fifth week.

<p>Effects of dietary Se deficiency on liver Se deposition, plasma biochemical attributes and inflammatory cytokine at fifth week.</p

Incidence of Se deficiency symptoms and cumulative mortality in broilers fed Se deficient diets over five week period.

<p>Figures on incidence of Se deficiency symptoms and cumulative/total mortality in birds are expressed in percentage.</p

Cohort Profile: The Chongqing Longitudinal Twin Study (LoTiS)

We aim to define the relative contribution of genetic factors and the environment to early onset morbidity of infancy and to identify specific ‘biomarkers’ and critical time points from pregnancy onwards for emergence of differences in illness in infancy-associated phenotypes, by establishing a longitudinal twin pregnancy birth cohort. The Chongqing Longitudinal Twin Study (LoTiS) cohort was established in January 2016 at Chongqing, China, with the aim of enrolling 300 women, aged 20–40 years, pregnant with twins, and their offspring. The women were followed up in early, middle and late pregnancy and at delivery, and their offspring were followed up at birth, 6 weeks and 3, 6, 12, 18, 24, 30 and 36months of age. Currently, there were 439 participants recruited and 333 completed the visits during pregnancy. Maternal social demography, laboratory examinations, perinatal outcomes, neonatal outcomes, infantile growth data and assessment were collected. The study collaborated with Murdoch Children’s Research Institute, Royal Children's Hospital, Australia and the University of Birmingham, UK. Data were assessed at the website: [https://www.medscinet.com/Lotis/empty.aspx].</p