R. Yu

Publications11
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Citations78
Highly Influential Citations1
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Comparative mutagenicity testing of ceftiofur sodium. II. Cytogenetic damage induced in vitro by ceftiofur is reversible and is due to cell cycle delay.
Antiendotoxin Strategies for the Prevention and Treatment of Septic Shock
TLDR
It will require focused efforts by basic scientists, continued support by industry and enlightened study designs by clinical investigators to successfully develop antiendotoxin therapies for use in septic patients in the future.
Comparative mutagenicity testing of bropirimine, 3. Bropirimine does not induce cytogenetic damage in vivo in the rat but does produce micronuclei in the mouse.
Comparative mutagenicity testing of ceftiofur sodium: III. Ceftiofur sodium is not an in vivo clastogen.
Comparative mutagenicity testing of ceftiofur sodium: I. Positive results in in vitro cytogenetics.
End points for biomonitoring: assay sensitivity/selectivity.
TLDR
It is demonstrated in the monkey that hypoxanthine guanine phosphoribosyltransferase (hprt) mutations produced in vivo can be detected using technique originally worked out using human cells; cynomolgus monkeys were chosen to avoid many of the complications encountered in studying humans.
Lack of response to multiple genotoxic agents at the hprt locus in peripheral blood T‐lymphocytes of cynomolgus monkeys
TLDR
The results of the present study suggest a low sensitivity of the hprt mutation assay to certain classes of genotoxic agents in cynomolgus monkeys.
Micronuclei in mice treated with monocrotaline with and without phenobarbital pretreatment
TLDR
The goal of the experiments reported here was to confirm the reported clastogenesis induced by this agent in vivo and to evaluate the impact of modulation of metabolic activity by phenobarbital, a potent P‐450 inducer (both Phase I and Phase II enzymes).
Risk and benefit evaluation in development of pharmaceutical products.
TLDR
Several specific examples of risk assessments and some generic genotoxicity questions that are recurrent, including the question of the relevance of in vitro chromosomal aberration induction at high dose/sampling time, are raised.
Chromosomal breakage following treatment of CHO‐K1 Cells in Vitro With U‐68,553B is due to Induction of Undercondensation of Heterochromatin
TLDR
It is concluded that the positive results with CHO‐k1 cells treated with U‐68,553B are unlikely to be predictive of a genotoxic hazard and is a specific example of the importance of careful followup to an in vitro result in risk assessment.
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