THE Newborn survival: a multi-country analysis of a decade of change

1. Joy E Lawn, 
2. Mary V Kinney, 
3. Robert E Black, 
4. Catherine Pitt, 
5. Simon Cousens,
6. Kate Kerber, 
7. Erica Corbett, 
8. Allisyn C Moran, 
9. Claudia S Morrissey and
10. Mikkel Z Oestergaard

Health Policy & Planning volume 27 supplement 3: A decade of change for newborn survival, policy and programmes (2000–2010), July 2012 pp. iii6–iii28

doi:10.1093/heapol/czs053

This article contained errors on p. 8, para 1 and in Table 3. The health density figures should refer to the number of midwives, nurses and physicians per 100 000, not per 10 000. The sentence on p. 8 should read:

The density of midwives and nurses is over 30-fold higher in Category 1 (664 per 100 000 population) compared with Category 4 (57 per 100 000 population) and Category 5 (30 per 100 000), and the density of doctors is 50 times higher.

A corrected version of Table 3 appears on the following page.

The authors apologise for these errors.

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Table 3

Countries (193) organized according to five levels of neonatal mortality, showing the variation in context, health system capacity and funding around the year 2010

Medicine: Carcinogenesis

Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including viral, chemical and physical carcinogenesis, metabolism of carcinogens, and the formation, detection, identification and quantification of environmental carcinogens).

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Carcinogenesis: Targeting of magnolin on ERKs inhibits Ras/ERKs/RSK2-signaling-mediated neoplastic cell transformation

Abstract

Mitogen-activated protein kinases play a key role in cell proliferation, cell cycle progression and cell transformation, and activated Ras/extracellular signal-regulated kinases (ERKs)/ribosomal S6 kinase 2 (RSK2) signaling pathways have been widely identified in many solid tumors. In this study, we found that magnolin, a compound found in the Magnolia species, directly targeted and inhibited ERK1 and ERK2 kinase activities with IC₅₀values of 87 and 16.5 nM by competing with adenosine triphosphate in an active pocket. Further, we demonstrated that magnolin inhibited epidermal growth factor (EGF)-induced p90RSKs phosphorylation at Thr359/Ser363, but not ERKs phosphorylation at Thr202/Tyr204, and this resulted in inhibition of cell proliferation by suppression of the G₁/S cell cycle transition. Additionally, p38 kinases, Jun N-terminal kinases and Akts were not involved in the magnolin-mediated inhibitory signaling. Magnolin targeting of ERK1 and 2 activities suppressed the phosphorylation of RSK2 and downstream target proteins including ATF1 and c-Jun and AP-1, a dimer of Jun/Fos, and the transactivation activities of ATF1 and AP-1. Notably, ERKs inhibition by magnolin suppressed EGF-induced anchorage-independent cell transformation and colony growth of Ras^G12V-harboring A549 human lung cancer cells and NIH3T3 cells stably expressing Ras^G12V in soft agar. Taken together, these results demonstrated that magnolin might be a naturally occurring chemoprevention and therapeutic agent capable of inhibiting cell proliferation and transformation by targeting ERK1 and ERK2.

Summary: Targeting of magnolin, a natural compound found in theMagnolia species, on ERKs active pocket inhibits EGF-induced cell proliferation and transformation. Thus, magnolin might be a naturally occurring chemoprevention and therapeutic agent by targeting ERK1 and ERK2.

Abbreviations:

ATP

adenosine triphosphate

DMEM

Dulbecco’s modified Eagle’s medium

DMSO

dimethyl sulfoxide

EGF

epidermal growth factor

ERK

extracellular signal-regulated kinase

FACS

fluorescence-activated cell sorting

FBS

fetal bovine serum

JNK

c-Jun N-terminal kinase

MAPK

mitogen-activated protein kinases

MEM

modified Eagle’s medium

MTS

3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium

PDB

Protein Data Bank

RSK2

ribosomal S6 kinase 2

SDS

sodium dodecyl sulfate.