Preterm babies have a higher risk of damage to their brain, lungs and liver. Also, babies born before 32 weeks of gestation have higher rates of death and disability. As such, it is vital to uncover ways to prevent preterm birth to give infants and children a better quality of life.
My research areas include preterm birth, pregnancy, genetics and genomics. One of the goals is discovering and improving our understanding of the molecular mechanisms associated with birth timing — one of the major unsolved questions in biology. We hope to develop methods to prevent preterm birth.
The most notable findings my colleagues and I uncovered in our lab to date were to identify the maternal genetic areas that lead to a higher risk of preterm birth in pregnant women. We have also looked at the endocrine stress response and the molecular systems responsible for birth in genetically altered mutant mice. We’ve researched the genetics and comparative genomics behind the birth timing molecular mechanisms.
I joined the team at Cincinnati Children’s Hospital Medical Center in 2012 as an adjunct faculty member. I have more than 30 years’ experience in the field of neonatology. In addition, I’m an elected member with the following notable associations:
Along with my academic research in preterm birth and pregnancy, I’m an adjunct professor at the University of Cincinnati College of Medicine and Cincinnati Children’s. I hold the positions of chief executive officer (CEO) and president of the Burroughs Wellcome Fund, which fosters diversity, equity and inclusion in science, education and society.
My research has been published in respected journals such as PLoS Biology, Nature, The New England Journal of Medicine, the Maternal and Child Health Journal and Genome Research.
BS: University of Michigan, Ann Arbor, MI, 1981.
PhD: University of Chicago, Chicago, IL, 1986.
MD: University of Chicago, Chicago, IL, 1988.
Prevention of Preterm Birth, Human Genetics
Anthropoid primate-specific retroviral element THE1B controls expression of CRH in placenta and alters gestation length. PLoS Biology. 2018; 16:e2006337.
Whole exome sequencing reveals HSPA1L as a genetic risk factor for spontaneous preterm birth. PLoS Genetics. 2018; 14:e1007394.
Inverted formin 2 regulates intracellular trafficking, placentation, and pregnancy outcome. eLife. 2018; 7:e31150.
Genetic Associations with Gestational Duration and Spontaneous Preterm Birth. The New England Journal of Medicine. 2017; 377:1156-1167.
Effect of Modifiable Risk Factors on Preterm Birth: A Population Based-Cohort. Maternal and Child Health Journal. 2017; 21:777-785.
Single-cell transcriptomics of the human placenta: inferring the cell communication network of the maternal-fetal interface. Genome research. 2017; 27:349-361.
Assessing the Causal Relationship of Maternal Height on Birth Size and Gestational Age at Birth: A Mendelian Randomization Analysis. PLoS Medicine. 2015; 12:e1001865.
An evolutionary genomic approach to identify genes involved in human birth timing. PLoS Genetics. 2011; 7:e1001365.
The Enigma of Spontaneous Preterm Birth REPLY. The New England Journal of Medicine. 2010; 362:2033-2034.
Corticotropin-releasing hormone deficiency reveals major fetal but not adult glucocorticoid need. Nature. 1995; 373:427-432.
Louis J. Muglia, MD, PhD, Ge Zhang, MD, PhD7/1/2019