Thalidomide embryopathy : an enigmatic challenge

Thanks go to Dr. Chris Mahony, Prof. Martin Collinson, Shaunna-Leigh Beedie and Alexandra Diamond for critical comments on the paper. Thanks also go to Prof. Lynda Erskine, Dr. W. D. Figg, Dr. Lavinia Schuler-Faccini, Dr. Robert L. Smith, Prof. Nigel Brown, Prof. Ruth Ross, Prof. Cheryll Tickle and Prof. Lewis Wolpert for fantastic discussions on thalidomide. This work is dedicated to C. G. V. and C. W. M. V.Peer reviewedPublisher PD

Arterial dysgenesis and limb defects : Clinical and experimental examples

Acknowledgements This article is dedicated to Dr David S. Packard Jr. With thanks to Dr John DeSesso, Dr Lewis B. Holmes, Dr Mark Levinsohn, Dr David S. Packard Jr, Prof Lewis Wolpert for discussions on vascular disruption, particularly arterial dysgenesis and limb defects. We apologise to the many authors whose work we were unable to cite due to space limitations. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.Peer reviewedPostprin

Quantitative assessment of intrinsic noise for visually guided behaviour in zebrafish

Supported by Royal Society of London (University Research Fellowship), Medical Research Council (New Investigator Research Grant) and CNRS.Peer reviewedPostprin

The teratogenic effects of thalidomide on limbs

Acknowledgements Thanks to members of the Thalidomide Society for helpful discussions on thalidomide-induced limb damage. Funding The author disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: Research in the lab has previously been sponsored by Wellcome Trust, Royal Society and University of Aberdeen.Peer reviewedPostprin

Smad7 Misexpression during Embryonic Angiogenesis Causes Vascular Dilation and Malformations Independently of Vascular Smooth Muscle Cell Function

AbstractNumerous in vitro and in vivo studies implicate transforming growth factor-β (TGFβ) superfamily signaling in vascular development and maintenance. Mice and humans with mutations in TGFβ superfamily signaling pathway genes exhibit a range of vascular defects that include dilated, fragile and hemorrhagic vessels, defective angiogenic remodeling, severe vascular malformations including arterio-venous malformations, and disrupted vascular smooth muscle cell recruitment and maintenance. Despite a wealth of data, the functions of TGFβ superfamily signals during angiogenesis are poorly defined, since early embryonic lethality and difficulty distinguishing between primary and secondary defects frequently confound phenotypic interpretation. To perturb TGFβ superfamily signaling during angiogenesis, we have misexpressed Smad7, an intracellular antagonist of TGFβ superfamily signaling, in the developing chick limb and head. We find that the great vessels are strikingly dilated and frequently develop intra and intervascular shunts. Neither noggin nor dominant negative BMP receptor misexpression causes similar vascular phenotypes. However, simultaneous misexpression of constitutively active BMP receptors with Smad7 suppresses the Smad7-induced phenotype, suggesting that a BMP-like intracellular pathway is the target of Smad7 action. Despite the gross morphological defects, further analyses find no evidence of hemorrhage and vessel structure is normal. Furthermore, enlarged vessels and vascular malformations form in either the presence or absence of vascular smooth muscle, and vascular smooth muscle cell recruitment is unperturbed. Our data define the TGFβ superfamily pathway as an integral regulator of vessel caliber that is also essential for appropriate vessel connectivity. They demonstrate that dilation need not result in vessel rupture or hemorrhage, and dissociate vessel maintenance from the presence of a vascular smooth muscle cell coat. Furthermore they uncouple vascular smooth muscle cell recruitment and differentiation from TGFβ superfamily signaling

Thalidomide: History, withdrawal, renaissance and safety concerns

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Thalidomide and birth defects

Apologies to the many papers we were unable to cite, due to space constraints. We thank Lynda Erskine, Shaunna Beedie and Chris Mahony for helpful discussions. Lucas Rosa Fraga is funded by a PhD scholarship from the Science without Borders program - CNPq Brazil - INAGEMP/ Grant CNPq 573993/2008-4. Alex J. Diamond is funded by a BBSRC DTP PhD Scholarship.Peer reviewedPostprin

Vascular anomalies of the upper limb

Acknowledgements: The authors would like to thank Selina Ackermann for her great help with the editing of this article. Funding: The authors received no financial support for the research, authorship, and/or publication of this article.Peer reviewedPostprin

The chick limb: embryology, genetics and teratology

MD is supported by the BBSRC through a BBSRC Institute Strategic Grant, MT is a Wellcome Trust Senior Fellow and NV’s studies on thalidomide were supported by The Wellcome Trust. We all thank lab members past and present for their help and support. We apologize to those whose work we have not referenced due to lack of space.Peer reviewedPublisher PD

Considerations for future quantitative structure-activity relationship (QSAR) modelling for heavy metals : A case study of mercury

Acknowledgements The authors would like to acknowledge the in-kind contribution of the National Decommissioning Centre of the use of the mercury analyser, and the support of the Net Zero Technology Centre. Funding This work was supported by the University of Aberdeen [grant no. RG13793-67], the UK Energy Research Centre [grant no. UKERC-4 EP/S029575/1], DEFRA [grant no. ETPP-33/C10], and the National Decommissioning Centre through the University of Aberdeen [grant no. RG15508-11].Peer reviewedPublisher PD