Prevention of adverse health effects from environmental exposure is the major focus of the research in the Allard laboratory. Faced with the tens of thousands of untested chemicals released in the environment, we are developing technologies that can rapidly and reliably determine whether these chemicals are safe. We concentrate our efforts on aspects of health that are particularly difficult to examine with current toxicity testing methods such as reproduction, aging and heritable health effects spanning several generations.
The Allard laboratory is part of the department of Environmental Health Sciences at the UCLA Fielding School of Public Health and the UCLA Institute for Society and Genetics. We are also affiliated with the Jonsson Comprehensive Cancer Center, the Institute of the Environment and Sustainability and the Molecular Toxicology Interdepartmental Graduate Program. This gives us a unique angle to examine environmental effects on health from both a molecular and a societal standpoint.
Dr. Patrick Allard, Assistant Professor, leads the laboratory and trained as a Reproductive Biologist, Developmental Biologist and Geneticist at McGill University and Harvard Medical School. The laboratory works closely with the National Institute of Environmental Health Sciences and the Environmental Protection Agency and receives funding from these agencies, the Center for Alternatives to Animal Testing and others.
For more information, please contact: firstname.lastname@example.org or visit: http://www.theallardlabatucla.org/
Toxicity screening, Reproduction, Genetics, Policy applications
Ferreira D, Chen Y, Allard P. “Use of the alternative model system C. elegans in developmental and Reproductive Toxicology”. In Developmental & Reproductive Toxicology (ed. Dr Ali Faqi). Springer, 2014. Chapter.
Allard P. Biomarkers of Bisphenol A Toxicity. In Biomarkers in Toxicology (ed. Dr Ramesh Gupta). Elsevier Inc., 2013. Chapter.
Allard P, Kleinstreuer N, Knudsen T, Colaiacovo MP. A screening platform for the rapid assessment of chemical disruption of germline function. Environmental Health Perspectives. 2013 Jun;121(6):717-24.
Allard P, Colaiacovo MP. Mechanistic insights into the action of Bisphenol A on the germline using C. elegans. Cell Cycle. 2011 Jan 15;10(2):183-4. Review.
Allard P, Colaiacovo MP. Bisphenol A impairs the double-strand break repair machinery in the germline and causes chromosome abnormalities. Proc Natl Acad Sci U S A. 2010 Nov 23; 107(47): 20405-10.*Featured in JAMA. 2011;305(1):28.
Allard P, Colaiacovo MP. Bisphenol A: metabolism, mechanisms and toxicity. In Reproductive and Developmental Toxicology (ed. Ramesh C. Gupta). Elsevier Inc., 2011. Chapter.
Yang Q*, Allard P*, Huang M, Zheng W, Clarke HJ. Proteasomal activity is required to initiate and to sustain translational activation of messenger RNA encoding the Stem-Loop-Binding Protein during meiotic maturation in mice. Biology of Reproduction. 2010 Jan;82(1):123-31.
Allard P, Tabin CJ. Achieving bilateral symmetry during vertebrate limb development. Seminars in Cell & Developmental Biology. 2009 Jun;20(4):479-84. Review.
Nissim S, Allard P, Bandyopadhyay A, Harfe BD, Tabin CJ. Characterization of a novel ectodermal signaling center regulating Tbx2 and Shh in the vertebrate limb. Developmental Biology. 2007 Apr 1;304(1):9-21.
Villaescusa JC, Allard P, Carminati E, Kontogiannea M, Talarico D, Blasi F, Farookhi R, Verrotti AC. Clast4, the murine homologue of human 4E-T, is expressed and post-translationally regulated during follicular development. Gene. 2006 Feb 15; 367:101-9.
Allard P, Young Q, Marzluff WF, Clarke HJ. Stem-Loop Binding Protein accumulation during meiotic maturation is required for normal histone synthesis and embryonic chromatin assembly. Developmental Biology. 2005 Oct 1;286(1):195-206.
Allard P*, Champigny MJ*, Skoggard S*, Erkmann JA, Whitfield ML, Marzluff WF, Clarke HJ. Stem-loop binding protein accumulates during oocyte maturation and is not cell-cycle-regulated in the early mouse embryo. Journal of Cell Science. 2002 Dec 1; 4577-86. * Contributed equally to the work.
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