The Central Laboratory for Human Embryology is a national resource for the collection, study, description and distribution of human embryonic and fetal tissue. During the past 30 years, our ability to reliably obtain, stage, identify and distribute conceptal tissues nationwide has resulted in approximately 600 publications from several hundred laboratories. Additionally, intramural research has yielded several hundred more published manuscripts including some that serve as standards for human prenatal growth and development. Although specimens are routinely shipped to widely dispersed sites, this laboratory has served as a nucleus for the many research programs that employ human prenatal tissues at the University of Washington. The success of this program is facilitated by the continued cooperation of obstetricians and pathologists in the Seattle area. We encourage this cooperation by carefully examining and reporting our findings to referring physicians. In addition to performing this service to the community, our extensive experience in embryonic and fetal pathology enables us to fulfill a surveillance function by monitoring abortuses for changes in malformation incidences. This laboratory also serves as a repository for teratogen information, answering calls from health professionals, nationwide. The importance of embryonic tissue has increased significantly with the power of molecular biology. In response to the requirements of these methods, we now collect and process specimens in ways that will maximize their usefulness. This includes new protocols for fixation and embedding that are compatible with immunocytochemistry and in situ hybridization. The Central Laboratory for Human Embryology represents a unique, dynamic resource for the collection and distribution of prenatal human tissue to laboratories throughout the United States, as well as a nucleus for research on human embryos and fetuses.
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| Sivananthan, S N; Lee, A W; Goodyer, C G et al. (2010) Familial amyloid precursor protein mutants cause caspase-6-dependent but amyloid *-peptide-independent neuronal degeneration in primary human neuron cultures. Cell Death Dis 1:e100 |
| Jodoin, Julie; Misiewicz, Micheal; Makhijani, Priya et al. (2009) Loss of anti-Bax function in Gerstmann-Straussler-Scheinker syndrome-associated prion protein mutants. PLoS One 4:e6647 |
| Sneitz, Nina; Court, Michael H; Zhang, Xiuling et al. (2009) Human UDP-glucuronosyltransferase UGT2A2: cDNA construction, expression, and functional characterization in comparison with UGT2A1 and UGT2A3. Pharmacogenet Genomics 19:923-34 |
