Birth Defects Research Part B: Developmental and Reproductive Toxicology, 2013
Pfaff T, Rhodes J, Bergmann M, Weinbauer GF
- HESI - Health and Environmental Sciences Institute
This study was designed to determine the effects of Compound A on spermatogenesis including assessment of inhibin B levels and on fertility in the male rat over a 15 to 19 weeks treatment and a 19 weeks treatment-free period in control and 30, 60, and 180 mg/kg dose groups (n = 22/group).
Birth Defects Research Part B: Developmental and Reproductive Toxicology, 2013
Sonee M, Bogdan N, Hall L, Bryant S, Vinken P
- HESI - Health and Environmental Sciences Institute
This study was conducted as part of an ILSI-HESI International Life Sciences Institute-Health & Environmental Sciences Institute consortium effort to assess the utility of circulating Inhibin B as an early biomarker of Sertoli cell-specific testicular toxicity in rats.
Birth Defects Research Part B: Developmental and Reproductive Toxicology, 2013
Stewart J, Bickerton S, Betts CJ, Kirk S
- HESI - Health and Environmental Sciences Institute
Inhibin B was measured in plasma samples obtained from 34 healthy male subjects selected on criteria typical for a phase I clinical trial across a wide age range (19–70 years).
Birth Defects Research Part B: Developmental and Reproductive Toxicology, 2013
Ziejewski MK, Vidal JD, Stanislaus D, Apostoli A, Chowdhury P, ...
- HESI - Health and Environmental Sciences Institute
In a repeat oral dose toxicity study, all of 16 male rats given 100 mg/kg/day GSK1322888 sustained testicular injury after 4 weeks of treatment; the findings were not reversible after 12 weeks off-dose.
Birth Defects Research Part B: Developmental and Reproductive Toxicology, 2013
Chapin RE, Kim JH
- HESI - Health and Environmental Sciences Institute
Birth Defects Research Part B: Developmental and Reproductive Toxicology. 2013;98(1):1-3.
Toxicologic Pathology, 2013
Reagan WJ, York M, Berridge B, Schultze E, Walker D, Pettit S
- HESI - Health and Environmental Sciences Institute
Cardiac troponin (cTn) has been utilized to assess acute myocardial injury, but the cTn response in active/ongoing chronic injury is not well documented.
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