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Biomedical subjects

R T Blaszak

Publications and source records attributed to R T Blaszak.

2 recordsLinked to original sources

The use of short-acting nifedipine in pediatric patients with hypertension.

OBJECTIVE: To evaluate the use of short-acting nifedipine for treatment of severe hypertension in children. STUDY DESIGN: A retrospective chart review of 520 nifedipine doses given for severe hypertension in 117 pediatric patients was completed. Nifedipine dose, systolic and diastolic blood pressures before and within 2 hours of the dose, and side effects were recorded. Pre- and post-dose mean arterial pressure (MAP) and percent reductions in MAP and systolic and diastolic blood pressure were calculated. Age, dose, primary diagnosis, and use of other antihypertensive agents were examined with respect to blood pressure reduction. RESULTS: Of the doses received, 35% were associated with > or =25% reduction in MAP, a degree of MAP reduction previously associated with hypertension treatment complications. MAP percent reduction was correlated with nifedipine dose adjusted for weight (r = 0.24, P<.001). Mean nifedipine doses per kilogram were larger in patients who had > or =25% MAP reduction compared with those who had <25% MAP reduction (0.26 +/- 0.12 mg/kg vs. 0.21 +/- 0.11 mg/kg, F = 29.01, P <.001). Adolescents received lower nifedipine doses per kilogram and had lower percent reduction in blood pressure compared with younger children. No clinically significant side effects were noted after administration of nifedipine. CONCLUSION: Precipitous reductions in blood pressure are ameliorated by decreasing the initial nifedipine dose to < or =0.25 mg/kg in pediatric patients. Short-acting nifedipine use in pediatric patients with hypertension in a hospital setting is safe.

Adolescent↗

DNA structural transitions within the PKD1 gene.

Autosomal dominant polycystic kidney disease (ADPKD) affects over 500 000 Americans. Eighty-five percent of these patients have mutations in the PKD1 gene. The focal nature of cyst formation has recently been attributed to innate instability in the PKD1 gene. Intron 21 of this gene contains the largest polypurine. polypyrimidine tract (2.5 kb) identified to date in the human genome. Polypurine.polypyrimidine mirror repeats form intramolecular triplexes, which may predispose the gene to mutagenesis. A recombinant plasmid containing the entire PKD1 intron 21 was analyzed by two-dimensional gel electrophoresis and it exhibited sharp structural transitions under conditions of negative supercoiling and acidic pH. The superhelical density at which the transition occurred was linearly related to pH, consistent with formation of protonated DNA structures. P1 nuclease mapping studies of a plasmid containing the entire intron 21 identified four single-stranded regions where structural transitions occurred at low superhelical densities. Two-dimensional gel electrophoresis and chemical modification studies of the plasmid containing a 46 bp mirror repeat from one of the four regions demonstrated the formation of an H-y3 triplex structure. In summary, these experiments demonstrate that a 2500 bp polypurine.polypyrimidine tract within the PKD1 gene is capable of forming multiple non-B-DNA structures.

Base Sequence↗