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Biomedical subjects

H S Martin

Publications and source records attributed to H S Martin.

3 recordsLinked to original sources
PubMed2000

Cost-effectiveness of childhood immunization reminder/recall systems in urban private practices.

OBJECTIVE: To assess cost and cost-effectiveness of immunization reminder/recall systems in the private sector. METHODS: A manual postcard system (mail) was compared with a computer-based telephone system (autodialer) and control. Costs included time costs and the cost of equipment and supplies. The cost per child and the incremental cost of the intervention relative to control were computed. Cost-effectiveness ratios were computed for return visits and for immunizations delivered. RESULTS: The average cost per child was $2.28 for the mail group and $1.47 for the autodialer group. The incremental visit cost relative to the control was higher for the mail group ($9.52) than for the autodialer group ($3.48). The autodialer was more cost-effective in delivering immunizations: $4. 06 per extra immunization (autodialer) versus $12.82 (mail). CONCLUSIONS: Excluding start-up costs, the autodialer system was most cost-effective. Including autodialer equipment costs, the autodialer system is more cost-effective only for larger practices.

Cost-Benefit Analysis↗
PubMed1999

Effects of glucose and PaO2 modulation on cortical intracellular acidosis, NADH redox state, and infarction in the ischemic penumbra.

BACKGROUND AND PURPOSE: During focal cerebral ischemia, the ischemic penumbra or border-zone regions of moderate cortical blood flow reductions have a heterogeneous development of intracellular cortical acidosis. This experiment tested the hypotheses that (1) this acidosis is secondary to glucose utilization and (2) this intracellular acidosis leads to recruitment of potentially salvageable tissue into infarction. METHODS: Brain pHi, regional cortical blood flow, and NADH redox state were measured by in vivo fluorescent imaging, and infarct volume was assessed by triphenyltetrazolium chloride histology. Thirty fasted rabbits divided into 6 groups of 5 each were subjected to 4 hours of permanent focal ischemia in the presence of hypoglycemia ( approximately 2.8 mmol/L), moderate hyperglycemia ( approximately 11 mmol/L), and severe hyperglycemia (>28 mmol/L) under either normoxia or moderate hypoxia (PaO2 approximately 50 mm Hg). RESULTS: Preischemic hyperglycemia led to a more pronounced intracellular acidosis and retardation of NADH regeneration than in the hypoglycemia groups under both normoxia and moderate hypoxia in the ischemic penumbra. For example, 4 hours after ischemia, brain pHi in the severe hyperglycemia/normoxia group measured 6.46, compared with 6.84 in the hypoglycemia/normoxia group (P<0.01), and NADH fluorescence measured 173% compared with 114%. Infarct volume in the severe hyperglycemia/normoxia group measured 35.1+/-6.9% of total hemispheric volume, compared with 13.5+/-4.2% in the hypoglycemia/normoxia group (P<0.01). CONCLUSIONS: Hyperglycemia significantly worsened both cortical intracellular brain acidosis and mitochondrial function in the ischemic penumbra. This supports the hypothesis that the evolution of acidosis in the ischemic penumbra is related to glucose utilization. Furthermore, the observation that hypoglycemia significantly decreased infarct size supports the postulate that cortical acidosis leads to recruitment of ischemic penumbra into infarction.

Acidosis↗