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  • Book
    Thomas W. Hale.
    Summary: "Written by a world-renowned expert in perinatal pharmacology, this essential reference contains current, complete, and evidence-based information on the transmission of maternal drugs into human milk. Because so many women ingest medications while breastfeeding, one of the most common questions encountered in pediatrics is: Which drugs are safe and which are hazardous for the infant? This 2019 edition has been extensively revised, and now includes 39 completely new and 331 updated medications, and state-of-the-art coverage of multiple diseases, vaccines, and syndromes. It addresses the use of radiopharmaceuticals, chemotherapeutic agents, and vaccines in breastfeeding mothers, and covers adult concerns, methods of reducing risk to infants, and infant monitoring."--Publisher's description.
    Digital Access R2Library 2019
    Limited to 1 simultaneous user
  • Article
    Jain K, Logothetopoulos J.
    Biochem J. 1978 Mar 15;170(3):461-7.
    Inosine, guanosine and adenosine strongly stimulated proinsulin biosynthesis and insulin secretion in isolated mouse pancreatic islets. None of the purine ribonucleosides stimulated insulin secretion in rat islets, although as reported [jain & Logothetopoulos (1977) Endocrinilogy 100, 923-927] inosine and guanosine, but no adenosine, were potent stimulants of proinsulin biosynthesis in this species. The purine bases had no effect in either species. D-Ribose, which enhanced proinsulin biosynthesis at 0.3 and 0.6 mM but not at 5mM in rat pancreatic islets [jain & Logothetopoulos (1977) Endocrinology 100, 923-927], produced no secretory signals in rat islets and was without any effect on proinsulin biosynthesis and insulin secretion in mouse islets. The rates of oxidation of 14C-labelled purine ribonucleosides and D-ribose in islets of the two species correlated well with their effectiveness as inducers of insulin secretion and proinsulin biosynthesis. Specific inhibitors of purine ribonucleoside phosphorylase, adenosine deaminiase and of purine ribonucleoside transport suppressed the stimulatory effects of nucleosides in pancreatic islets without altering the effect of D-glucose. The same inhibitors also markedly diminished the oxidation rats of the labelled purine ribonucleosides. The experiments clearly indicate that porinsulin biosynthesis and insulin secretion are modulated through metabolic signals and not through interactions of intact substrate molecules with cell receptors.
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