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Errata
Duh EJ. Sema 3A resists retinal revascularization. Blood. 2011;117(22):5785-5786.
On page 5785 in the 2 June 2011 issue, there is an error in the Inside Blood title. There should be no spaces in the abbreviation for
Semaphorin 3A (Sema3A). The title reads, “Sema 3A resists retinal revascularization.” The title should have read, “Sema3A resists retinal
revascularization.”
© 2014 by The American Society of Hematology
Hole PS, Darley RL, Tonks A. Do reactive oxygen species play a role in myeloid
leukemias? Blood. 2011;117(22):5816-5826.
On page 5817 in the 2 June 2011 issue, there is an error in Figure 1: the Fenton chemistry cycle is drawn with the arrows in the opposing
direction to the true nature of the cycle. The corrected Figure 1 is shown.
Figure 1. Physiologic ROS homeostasis networks.
Univalent reduction of oxygen results in the formation of
superoxide (O2•2), which can occur as a result of NADPH
oxidase (NOX) activity, and also as a by-product of
oxidative phosphorylation, primarily at complex I in the
mitochondrial electron transport chain (ETC). Superoxide
may act as a reductant or an oxidant and is a key molecule
in several subsequent physiologic reactions. Most of the
superoxide generated in vivo is converted into hydrogen
peroxide (H2O2) primarily by the actions of superoxide
dismutases, which exist in cytosolic (SOD1), mitochondrial
(SOD2), and extracellular (SOD3) isoforms. H2O2 levels
are tightly regulated by several mechanisms, including
the actions of catalase, the glutathione peroxidase (GPX)
system, and peroxiredoxins (Prx). H2O2 may be further
processed by the actions of myeloperoxidase (MPO) during
an immune response to form hypochlorous acid (HOCl),
which may in turn react with superoxide to form hydroxyl
radicals. Hydroxyl radicals may also be formed from H2O2
by Fenton chemistry, which may occur in the presence of
free metal cations such as Fe21 or Cu1. Where superoxide
production and production of nitric oxide (NO • ) are
colocalized, reactive nitrogen species (RNS) may be
formed, with the proximal species being peroxynitrite.
Various RNS may then form via further chemical reactions
with other ROS or RNS. This network of ROS and RNS
production can be disrupted or biased in the presence of
various compounds such as diphenyleneiodonium (DPI),
which inhibits flavoproteins including the NOX oxidase
family, ion chelators that can terminate Fenton chemistry
cycles, and L -arginine analogs such as L-monomethyl
arginine (L-NMMA), which inhibits nitric oxide synthase.
Green represents molecular oxygen, blue are ROS derived
from O2, and red represents nitric oxide and other RNS.
© 2014 by The American Society of Hematology
Hsu LL. Hydroxyurea makes inflammation “just right”? Blood. 2012;119(8):1796-1798.
On page 1797 in the 23 February 2012 issue, there is an error in the text. The first sentence of the seventh paragraph of the article reads, “Their
final experiment used clinical SCD blood samples obtained during the Pediatric Hydroxyurea Phase III Clinical (BABY HUG) randomized
trial.7” The sentence should have read, “Their final experiment used clinical SCD blood samples obtained during the pediatric Hydroxyurea
Study of Long-Term Effects (HUSTLE, NCT00305175).7”
Furthermore, on page 1798, the citation at the end of the corrected sentence is incorrect in “References.” Reference 7 reads, “Wang WC,
Ware RE, Miller ST, et al. Hydroxycarbamide in very young children with sickle-cell anaemia: a multicentre, randomised, controlled
trial (BABY HUG). Lancet. 2011;377(9778):1663-1672.” Reference 7 should have read, “Flanagan JM, Steward S, Howard TA, et al.
Hydroxycarbamide alters erythroid gene expression in children with sickle cell anaemia. Br J Haematol. 2012;157(2):240-248.”
© 2014 by The American Society of Hematology
798
BLOOD, 30 JANUARY 2014 x VOLUME 123, NUMBER 5
From www.bloodjournal.org by guest on June 17, 2017. For personal use only.
2014 123: 798
doi:10.1182/blood-2013-12-545137
Duh EJ. Sema 3A resists retinal revascularization. Blood.
2011;117(22):5785-5786.
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