Search

Your search keyword '"Safford, Shawn D."' showing total 58 results
Start Over Author "Safford, Shawn D."
58 results on '"Safford, Shawn D."'

54. Thermal Preconditioning Before Rat Arterial Balloon Injury

Author

Neschis, David G., primary, Safford, Shawn D., additional, Raghunath, Puthiyaveettil N., additional, Langer, David J., additional, David, Mary L., additional, Hanna, Abigail K., additional, Tomaszewski, John E., additional, Kariko, Katalin, additional, Barnathan, Elliot S., additional, and Golden, Michael A., additional

Published
1998
Full Text
View/download PDF

56. HOW BODY SIZE AFFECTS MIDDLE-EAR STRUCTURE AND FUNCTION AND AUDITORY SENSITIVITY IN GEKKONOID LIZARDS.

Author

Werner, Yehudah L., Montgomery, Lynda G., Safford, Shawn D., Igic, Petar G., and Saunders, James C.

Subjects
GECKOS, AUDITORY perception, LIZARD anatomy, HEARING, ANATOMY
Abstract

Investigates whether changes in auditory function accompany increases in the body size of gekkonoid lizards. Study of middle-ear structure of adult and juvenile Eublepharis macularius and Oedura marmorata; Compound action potentials (CAPs) which were used as an indication of peripheral auditory function; Study of tympanic membrane velocity; Results, which indicated that significant changes occurred between the younger and older animals.

Published
1998
Full Text
View/download PDF

57. A Human Yeast Artificial Chromosome Containing the Multiple Endocrine Neoplasia Type 2B RetMutation Does Not Induce Medullary Thyroid Carcinoma but Does Support the Growth of Kidneys and Partially Rescues Enteric Nervous System Development in Ret-Deficient Mice

Author

Skinner, Michael A., Kalyanaraman, Somasundaram, Safford, Shawn D., Heuckeroth, Robert O., Tourtellotte, Warren, Goyeau, Dominique, Goodfellow, Paul, Milbrandt, Jeffrey D., and Freemerman, Alex

Abstract

We generated a line of transgenic mice using a yeast artificial chromosome containing the Retmutation responsible for the multiple endocrine neoplasia type 2B syndrome (MEN 2B). The resulting animals did not develop any of the expected neoplasms associated with MEN 2B. Transgenic animals were then bred with animals lacking murine Ret(RetM) to further evaluate the function of human mutated Ret(RetH2B) in the murine context. Whereas mice lacking RetMexhibit intestinal aganglionosis and the absence of kidneys with other genitourinary anomalies, expression of the RetH2Btransgene in RetM-deficient mice allowed significant renal development with a partial rescue of the enteric nervous system. These RetH2B-positive/RetM-deficient mice exhibit normal Retexpression and survive longer than RetM-deficient mice, but still die at 3 to 5 days of age with evidence of enterocolitis. We conclude that the normal expression of a human Retproto-oncogene with the MEN 2B mutation does not cause any features of MEN 2B in mice. Although the gene is normally expressed in the appropriate target tissues, there is incomplete phenotypic rescue in mice lacking murine Ret. These results suggest important interspecies differences between humans and mice in the function of the Retoncogene.

Published
2005
Full Text
View/download PDF

58. RET tyrosine kinase and medullary thyroid cells are unaffected by clinical doses of STI571.

Author

Skinner MA, Safford SD, and Freemerman AJ

Subjects
Benzamides, Carcinoma, Medullary enzymology, Carcinoma, Medullary pathology, Cell Death drug effects, Cell Division drug effects, Cell Line, Tumor, Humans, Imatinib Mesylate, Inhibitory Concentration 50, Phosphorylation drug effects, Proto-Oncogene Proteins metabolism, Proto-Oncogene Proteins c-ret, Receptor Protein-Tyrosine Kinases metabolism, Thyroid Neoplasms enzymology, Thyroid Neoplasms pathology, Antineoplastic Agents pharmacology, Carcinoma, Medullary drug therapy, Enzyme Inhibitors pharmacology, Piperazines pharmacology, Proto-Oncogene Proteins antagonists & inhibitors, Pyrimidines pharmacology, Receptor Protein-Tyrosine Kinases antagonists & inhibitors, Thyroid Neoplasms drug therapy
Abstract

Background: Activating mutations in the RET receptor tyrosine kinase are responsible for the development of medullary thyroid cancer (MTC) in persons with Multiple Endocrine Neoplasia type 2. We hypothesized that STI571 (Gleevec) would inhibit RET kinase and be a useful agent in the treatment of MTC., Materials and Methods: We determined the IC50 of STI571 for RET using an in vitro kinase assay and also examined the effects of STI571 on cellular proliferation and viability in TT cells, a human MTC cell line., Results: The average in vitro IC50 of STI571 for RET is 37 microM +/- 4 microM. Additionally, TT cells incubated with 10 microM STI571 for up to 8 days showed no apparent reduction in cell proliferation or viability. Higher concentrations of STI571, from 25 to 100 microM, induced necrosis of TT cells., Conclusion: The concentrations of STI571 required to significantly inhibit RET and to inhibit TT cell proliferation are not clinically achievable. We conclude that STI571 is not likely to be an effective treatment for MTC.

Published
2003

Catalog

Books, media, physical & digital resources
See catalog results