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Biomedical subjects

A Salinger

Publications and source records attributed to A Salinger.

4 recordsLinked to original sources
PubMed2000

Optimal N-ethyl-N-nitrosourea (ENU) doses for inbred mouse strains.

ENU is a powerful germline mutagen in the mouse, providing the opportunity to analyze the functions of large numbers of genes in the mammalian genome. In many mutagenesis experiments, it would be beneficial to exploit the advantages of inbred mouse strains. To perform an effective ENU mutagenesis screen using inbred mice, a dosage regimen is required to determine the optimal dose of ENU for that inbred strain, a time-consuming preliminary process. We have carried out dosage regimens for mutagenizing doses of ENU in ten inbred strains of mouse: 129X1/SvJ, 129S6/SvEv, A/J, BALB/cJ, BTBR/N, C3He/J, C3HeB/FeJ, C57BL/6J, C57BR/cdJ, and CBA/CaJ, and determined an optimal dose for each strain, defined by length of sterile period and number of males to survive treatment. Three strains: A/J, BALB/cJ and C57BL/6J, are able to tolerate high doses, up to 300 mg/kg body weight, and are highly recommended for mutagenesis studies.

Alkylating Agents↗
PubMed1997

The role of the EST genes in yeast telomere replication.

We have recently completed a large mutant screen designed to identify new mutants of Saccharomyces cerevisiae with a telomerase-like defect. From this screen; 22 mutants were identified that mapped to three genes, called EST1, EST2 and EST3, as well as a novel EST-like mutation in a fourth gene, previously identified as CDC13. Mutations in each of these genes give rise to phenotypes that are indistinguishable from those observed when TLC1, encoding the yeast telomerase RNA, is deleted. In addition, genetic analysis indicates that all four genes function in the same pathway for telomere replication as defined by TLC1, the one known component of telomerase. This indicates that these genes encode factors that are essential in vivo for telomerase function. Genetic and biochemical analyses have shown that EST1 and CDC13 encode single-stranded telomeric DNA-binding proteins, suggesting that these two proteins may function to mediate access of telomerase to the end of the telomere.

DNA Replication↗
PubMed1995

Effects of lysine clonixinate and ketorolac tromethamine on prostanoid release from various rat organs incubated ex vivo.

The release of prostanoids from rat brain, gastric mucosa, lungs and kidneys incubated ex vivo has been investigated for up to 5 h after oral administration of 10 mg/kg lysine clonixinate or 1 mg/kg ketorolac tromethamine. Additionally, 60 min after drug administration, a time point of near-maximal inhibition of prostanoid release, the effects of 2.5, 10 and 30 mg/kg lysine clonixinate and of 0.0225, 0.15 and 1 mg/kg ketorolac tromethamine were compared. In all organs investigated both drugs inhibited fatty acid cyclooxygenase (COX) in a dose-dependent manner, but ketorolac tromethamine was more potent and had a longer-lasting effect than lysine clonixinate. While the ID50 values for lysine clonixinate were in the same order of magnitude for all 4 organs investigated, ketorolac tromethamine exhibited some organ selectivity with a particularly high activity in the kidneys. This effect might be related to the renal toxicity of ketorolac tromethamine. On the other hand, the difference in potency was smallest in brain suggesting that inhibition of central prostanoid biosynthesis could contribute to the rapid and effective inhibition of pain by both drugs. IC50 values for inhibition of purified COX-1 and COX-2 in vitro were slightly lower for lysine clonixinate (2.4 and 24.6 micrograms/ml, respectively) than for ketorolac tromethamine (3.7 and 25.6 micrograms/ml, respectively).

6-Ketoprostaglandin F1 alpha↗