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Non-Western immigrant children have lower 25-hydroxyvitamin D than children from Western families – CORRIGENDUM
- Jessica A Omand, Pauline B Darling, Patricia C Parkin, Catherine S Birken, Marina Khovratovich, Kevin E Thorpe, Sarah Carsley, Julie DeGroot, Jonathon L Maguire
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- Journal:
- Public Health Nutrition / Volume 17 / Issue 7 / July 2014
- Published online by Cambridge University Press:
- 28 June 2013, p. 1668
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Non-Western immigrant children have lower 25-hydroxyvitamin D than children from Western families
- Jessica A Omand, Pauline B Darling, Patricia C Parkin, Catherine S Birken, Marina Khovratovich, Kevin E Thorpe, Sarah Carsley, Julie DeGroot, Jonathon L Maguire, on behalf of the TARGet Kids! Collaboration
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- Journal:
- Public Health Nutrition / Volume 17 / Issue 7 / July 2014
- Published online by Cambridge University Press:
- 24 May 2013, pp. 1547-1554
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Objective
To determine if children aged 1–6 years from non-Western immigrant families have lower serum 25-hydroxyvitamin D (25(OH)D) levels than children from Western-born families and examine which factors influence this relationship.
DesignCross-sectional study.
SettingToronto, Canada.
SubjectsHealthy children (n 1540) recruited through the TARGet Kids! practice-based research network. Serum 25(OH)D concentrations of non-Western immigrants were compared with those of children from Western-born families. Children from non-Western immigrant families were defined as those born, or their parents were born, outside a Western country. Univariate and multiple linear regression analyses were used to identify factors which might influence this relationship.
ResultsMedian age was 36 months, 51 % were male, 86 % had ‘light’ skin pigmentation, 55 % took vitamin D supplements, mean cow's milk intake was 1·8 cups/d and 27 % were non-Western immigrants. Median serum 25(OH)D concentration was 83 nmol/l, with 5 % having 25(OH)D < 50 nmol/l. Univariable analysis revealed that non-Western immigrant children had serum 25(OH)D lower by 4 (95 % CI 1·3, 8·0) nmol/l (P = 0·006) and increased odds of 25(OH)D < 50 nmol/l (OR = 1·9; 95 % CI 1·3, 2·9). After adjustment for known vitamin D determinants the observed difference attenuated to 0·04 (95 % CI −4·8, 4·8) nmol/l (P = 0·99), with higher cow's milk intake (P < 0·0001), vitamin D supplementation (P < 0·0001), summer season (P = 0·008) and increased age (P = 0·04) being statistically significant covariates. Vitamin D supplementation was the strongest explanatory factor of the observed difference.
ConclusionsThere is an association between non-Western immigration and lower 25(OH)D in early childhood. This difference appears related to known vitamin D determinants, primarily vitamin D supplementation, representing opportunities for intervention.
Contributors
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- By Rose Teteki Abbey, K. C. Abraham, David Tuesday Adamo, LeRoy H. Aden, Efrain Agosto, Victor Aguilan, Gillian T. W. Ahlgren, Charanjit Kaur AjitSingh, Dorothy B E A Akoto, Giuseppe Alberigo, Daniel E. Albrecht, Ruth Albrecht, Daniel O. Aleshire, Urs Altermatt, Anand Amaladass, Michael Amaladoss, James N. Amanze, Lesley G. Anderson, Thomas C. Anderson, Victor Anderson, Hope S. Antone, María Pilar Aquino, Paula Arai, Victorio Araya Guillén, S. Wesley Ariarajah, Ellen T. Armour, Brett Gregory Armstrong, Atsuhiro Asano, Naim Stifan Ateek, Mahmoud Ayoub, John Alembillah Azumah, Mercedes L. García Bachmann, Irena Backus, J. Wayne Baker, Mieke Bal, Lewis V. Baldwin, William Barbieri, António Barbosa da Silva, David Basinger, Bolaji Olukemi Bateye, Oswald Bayer, Daniel H. Bays, Rosalie Beck, Nancy Elizabeth Bedford, Guy-Thomas Bedouelle, Chorbishop Seely Beggiani, Wolfgang Behringer, Christopher M. Bellitto, Byard Bennett, Harold V. Bennett, Teresa Berger, Miguel A. 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- Edited by Daniel Patte, Vanderbilt University, Tennessee
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- The Cambridge Dictionary of Christianity
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- 05 August 2012
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- 20 September 2010, pp xi-xliv
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64 - Platelet–Endothelial Interactions
- from PART II - ENDOTHELIAL CELL AS INPUT-OUTPUT DEVICE
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- By Patricia B. Maguire, Conway Institute, University College Dublin, Ireland, Orina Belton, Conway Institute, University College Dublin, Ireland, Niaobh O'Donoghue, Conway Institute, University College Dublin, Ireland, Sandra Austin, Conway Institute, University College Dublin, Ireland, Judith Coppinger, Conway Institute, University College Dublin, Ireland
- Edited by William C. Aird, Harvard University, Massachusetts
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- Endothelial Biomedicine
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- 04 May 2010
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- 03 September 2007, pp 587-601
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Summary
Platelets are anucleate, discoid cell fragments measuring 1.5 to 3.0 μM in diameter. They are derived from bone-marrow megakaryocytes that are normally maintained in a nonadhesive state, whereby they circulate freely in blood. Anucleate platelets are unique to mammals, with nonmammalian vertebrates (such as zebrafish) possessing nucleated thrombocytes. In 1865, a German anatomist Max Schultze (1825–1874) first described platelets as “spherules” much smaller than red blood cells. A few years later, in 1882, Giulio Bizzozero (1846–1901) found that platelets played a role in coagulation because they could clump and form a blood clot at the site of vessel wall injury. It was not until 1961, however, that the platelet aggregating effect of adenosine diphosphate was discovered (1) and, in the following year, that a machine for measuring aggregation (an aggregometer) was developed (2). The most important breakthroughs surrounded the discovery of proaggregatory platelet thromboxane A2 (TXA2) and antiaggregatory endothelial cell (EC) prostacyclin (PGI2), both discovered in the 1970s, along with the finding that aspirin inhibited prostaglandin synthesis and platelet activation. Indeed, finding inhibitors to platelets was exciting because it established the therapeutic possibility of preventing arterial thrombosis and ultimately vessel occlusion (the precipitating event in most myocardial infarctions and many strokes) by means of antiplatelet therapy.
The activation of platelets to arrest bleeding at sites of vascular damage results in platelet adhesion to the vessel wall, where they convert from passive, small discs into larger, flattened structures with extended pseudopods that act as a surface for the propagation of the clotting cascade. Activated platelets secrete and synthesize further platelet agonists, inflammatory mediators, and vasoactive substances.
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