Lynwood H. Smith

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The evolutionary origins of the protistan phylum, Myxozoa, have long been questioned. Although these obligate parasites are like protozoans in many features, several aspects of their ontogeny and morphology have implied a closer relationship to metazoan lineages. Phylogenetic analyses of 18S ribosomal RNA sequences from myxozoans and other eukaryotes, with(More)
Despite the frequency and morbidity of nephrolithiasis in autosomal dominant polycystic kidney disease (ADPKD), this association has not been subject to a detailed study. One hundred fifty-one of 751 ADPKD patients seen at the Mayo Clinic between 1976 and 1986 had nephrolithiasis. Seventy-four had passed calculi or had stones surgically removed. Stone(More)
A method is described for quantitatively determining the inhibitory activity of pure components, isolates, or mixtures of components (such as urine) on the growth of calcium oxalate crystals. Results with known calcium phosphate crystal growth inhibitors--magnesium, citrate, and pyrophosphate--suggest that these components contribute little to the ability(More)
BACKGROUND The prognosis for patients with primary hyperoxaluria has been ominous, with the expectation of renal failure, poor results with transplantation, and early death. METHODS We studied the long-term effects of orthophosphate and pyridoxine therapy in 25 patients with primary hyperoxaluria who were treated for an average of 10 years (range, 0.3 to(More)
BACKGROUND The primary hyperoxalurias are autosomal recessive disorders resulting from deficiency of hepatic alanine:glyoxylate aminotransferase (PHI) or D-glycerate dehydrogenase/glyoxylate reductase (PHII). Marked hyperoxaluria results in urolithiasis, renal failure, and systemic oxalosis. A direct comparison of PHI and PHII has not previously been(More)
Primary hyperoxaluria type II (PH-II) or L-glyceric aciduria was first reported by Williams and Smith in 1968 (N Engl J Med 278:233-239, 1968). Deficiencies of D-glycerate dehydrogenase and glyoxylate reductase activity in patients with this disorder leads to increases in urinary oxalate and glycerate excretion. Clinically, PH-II presents in a similar(More)
The 5′-triphosphates of adenosine, guanosine, uridine, and cytidine inhibited the crystallization of calcium phosphate from stable supersaturated solutions that had been seeded with crystals of hydroxyapatite. Concentrations of the nucleoside triphosphates in the micromolar range were sufficient to have a significant effect on the crystal growth process.(More)