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S M Miller

Publications and source records attributed to S M Miller.

12 recordsLinked to original sources
PubMed1992

Comparison of recoveries from halothane vs isoflurane anesthesia in horses.

Recovery from isoflurane anesthesia was shorter, with no difference in quality, compared with halothane anesthesia in 2 groups of horses. In 1 group, 12 horses scheduled for elective arthroscopy were randomly assigned to receive halothane or isoflurane for maintenance of anesthesia during surgery. In the other group, 6 horses received anesthesia only, on 2 occasions, with halothane on 1 occasion, and isoflurane on the other. Difference in the quality of recovery was not seen between isoflurane and halothane anesthesia in either group. In the group that had surgery, recovery to sternal position was significantly shorter when isoflurane was used. In the group not treated surgically, recovery to sternal and standing positions was significantly shorter with isoflurane.

Acid-Base Equilibrium↗
PubMed1992

C-terminal cysteines of Tn501 mercuric ion reductase.

Mercuric ion reductase (MerA) catalyzes the reduction of Hg(II) to Hg(0) as the last step in the bacterial mercury detoxification pathway. A member of the flavin disulfide oxidoreductase family, MerA contains an FAD prosthetic group and redox-active disulfide in its active site. However, the presence of these two moieties is not sufficient for catalytic Hg(II) reduction, as other enzyme family members are potently inhibited by mercurials. We have previously identified a second pair of active site cysteines (Cys558 Cys559 in the Tn501 enzyme) unique to MerA, that are essential for high levels of mercuric ion reductase activity [Moore, M. J., & Walsh, C. T. (1989) Biochemistry 28, 1183; Miller, S. M., et al. (1989) Biochemistry 28, 1194]. In this paper, we have examined the individual roles of Cys558 and Cys559 by site-directed mutagenesis of each to alanine. Phenotypic analysis indicates that both merA mutations result in a total disruption of the Hg(II) detoxification pathway in vivo, while characterization of the purified mutant enzymes in vitro shows each to have differential effects on catalytic function. Compared to wild-type enzyme, the C558A mutant shows a 20-fold reduction in kcat and a 10-fold increase in Km, for an overall decrease in catalytic efficiency of 200-fold in kcat/Km. In contrast, mutation of Cys559 to alanine results in less than a 2-fold reduction in kcat and an increase in Km of only 4-5 fold for an overall decrease in catalytic efficiency of only ca. 10-fold in vitro. From these results, it appears that Cys558 plays a more important role in forming the reducible complex with Hg(II), while both Cys558 and Cys559 seem to be involved in efficient scavenging (i.e., tight binding) of Hg(II).

Alanine↗
PubMed1992

Policy options: early intervention services for substance-exposed infants.

Substance-exposed infants, or babies that have been victims of their mothers' drug use during pregnancy, have reached substantial proportions. Currently, no comprehensive public policy exists to deal with these infants as they enter a society unprepared to respond to an issue increasingly fraught with substantial adverse economic, social, and political ramifications. In order to address the needs of this emerging sub-population, California's governor and state legislature must develop and adopt a concerted interagency policy which outlines: a) uniform criteria for local health care workers, social service agencies, and educators; b) consistent guidelines governing the exchange of information among a range of agencies, including hospitals, schools, and other public and private agencies; and c) increased prevention and early intervention services for these babies and their families. Addressing the needs of these infants requires a bold, comprehensive, interdisciplinary approach from the creators of public policy.

California↗
PubMed1978

Cocaine toxicity.

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Anesthetics, Local↗
PubMed1975

Selenium in ruminant nutrition: a review.

The early interest in selenium related primarily to its toxicity, but since 1957 the element has been recognized as a dietary essential. The dietary requirement for selenium by most species is about .1 ppm. Deficiencies of selenium in cattle and sheep have been confirmed under natural grazing conditions in many countries of the world. Overt signs of inadequacy such as white muscle disease (nutritional muscular dystrophy) occur primarily in young calves or lambs born to selenium deficient dams. Infertility has increased in ewes grazing pastures low in selenium. In general, signs of deficiency have not occurred in older animals such as finishing beef cattle and lactating dairy cows. Subclinical deficiencies of selenium are not determined easily, however, and thus an inadequacy of the element may be limiting maximum animal performance under certain circumstances of drylot feeding. The current nutritional status of ruminant animals in many geographical areas and involving various feeding programs with this element has not been established. The recent widespread deficiency problems with nonruminants suggest that such an assessment should be made. Concentration of selenium in tissue, particularly in the liver, has been used in establishing selenium status of the animal. With lambs glutathione peroxidase activity in certain tissues may be a more accurate indicator of selenium adequacy than is selenium content of the tissue. Supplemental sodium selenite and sodium selenate by either oral administration or parenteral injection have prevented clinical signs of selenium deficiency and animal losses in both ruminant and nonruminant animals. Heavy pellets containing elemental selenium for placement in the rumen have proved effective. In general, organic forms of selenium are absorbed more readily by animals than are inorganic compounds. The dietary requirements for selenium and its metabolism are influenced by many nutrient interrelationships, including its interactions with sulfur, lipids, vitamin E, proteins, amino acids, and several microelements. The Food and Drug Administration gave approval in 1974 for the oral administration of supplemental selenium as either sodium selenite or sodium selenate to certain classes of swine and poultry. Similar approval in the United States for ruminants will require additional information, particularly with regard to the influence of dietary intake on concentrations of selenium in tissue and milk in beef and dairy animals.

Animal Feed↗