The price you pay for the drug not taken.
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Biomedical subjects
Publications and source records attributed to R McCarthy.
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Intraosseous infusion is a well accepted means of obtaining emergency intravascular access in children. Despite the low incidence of serious complications from intraosseous infusions, the potential exists for growth plate injury and subsequent growth disturbance following intraosseous infusion. We conducted a prospective, blinded observational study of 10 subjects to evaluate tibial length discrepancy radiographically one year or more following intraosseous infusion. We found no significant difference in mean tibial length between the legs that had intraosseous infusions and the opposite legs, which served as controls. We conclude that intraosseous infusion does not appear to produce subsequent leg length discrepancy one year after infusion.
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While the term coined to characterize 24-hour advice lines has been copyrighted and castigated, demand management itself has grown into a major force in health care.
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Electroconvulsive therapy (ECT) is associated with dramatic increases in arterial blood pressure and heart rate (HR) that may precipitate new left ventricular regional wall motion abnormalities (RWMAs) suggestive of myocardial ischemia. The purpose of this study was to investigate the effect of pretreatment with esmolol on the incidence of RWMAs after ECT. Thirteen patients served as their own controls and, in a random fashion, received a standard succinylcholine/methohexital anesthetic for one of two ECT sessions, and an identical anesthetic with esmolol 1 mg/kg for their other ECT session. Systolic (SBP), diastolic (DBP), mean arterial pressures (MAP) and HR were recorded after drug administration and before ECT and at 1-, 2-, 4-, 5-, 10-, and 15-min intervals after ECT. Echocardiograms were obtained at baseline, after drug administration, 1 min after ECT, and at recovery 15 min later. All patients had significant increases in SBP, DBP, and MAP at 1, 2 and 4 min after ECT versus baseline, whereas HR was significantly faster at all times in the control sessions. HR was significantly slower after anesthetic induction until 2 min after ECT in the esmolol versus the control group (P < 0.05). New RWMAs were seen in only 1 of 26 (4%) ECT sessions, despite the presence of baseline RWMAs in 31% of the patients. We conclude that contrary to previously reported data, new RWMAs after ECT are uncommon. Consequently, this study was unable to demonstrate any beneficial effect of pretreatment with esmolol on the incidence of ECT-induced RWMAs.
We studied excitatory postsynaptic potentials (EPSPs) arising in single spinal motoneurons (composite EPSPs) induced by Ia afferent and magnetic cortical stimulation in 28 normal subjects ranging in age from 24 to 84 years and 28 patients with amyotrophic lateral sclerosis (ALS) aged 34 to 82 years. The subjects voluntarily recruited single motor units of the first dorsal interosseous muscle. Using peristimulus time histograms, we determined changes in the firing probability of the first dorsal interosseous motor units and measured the magnitude of the EPSP. An early period of increased firing probability (primary peak) occurred at approximately 30 msec after la afferent and 25 msec after cortical stimulation, reflecting underlying EPSPs arising in spinal motoneurons induced by either projection. The latency of the primary peaks for both Ia afferent and cortical stimulation was mildly prolonged in ALS, suggesting a loss of the fastest-conducting spinal motoneurons. Patients with ALS had la afferent-driven EPSPs whose amplitude and rise time were equivalent to those of normal subjects. However, the ratio of cortical to la afferent-driven composite EPSPs in ALS was significantly lower than that for normal subjects. Fourteen of 28 ALS motor units had cortically driven EPSPs that were small or large only because of a prolonged rise time. The findings suggest that in ALS, corticomotoneuronal attrition or dispersion of the descending volley occurs in the presence of normally functioning spinal motoneurons to which they project.
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We investigated the sequence of expression of osteoblast gene markers during bone formation in vivo by in situ hybridization. Cylindrical lesions were induced in the femora of sheep with titanium analytic bone implants that allow removal of serial core samples to study bone formation. At 2 weeks (2W), granulation tissue made up of spindle-shaped cells had partially replaced the blood clot. Islands of osseous tissue, first noted in the periphery of the ingrowing tissue at 3W, became the predominant tissue by 6W. The surfaces of newly forming bone at 3W were apposed by cuboidal cells, which in some areas were several layers thick. By 6W, most of the cells lining bone trabeculae had assumed a flattened morphology. The temporal and spatial distribution of osteoblast gene markers was examined by in situ hybridization with nonradioactive digoxigenin probes for alpha 1(I) procollagen, alkaline phosphatase (ALP), osteopontin (OP), and bone Gla protein (BGP). The spindle-shaped cells in the granulation tissue expressed mRNA for alpha 1(I) procollagen, ALP, and OP but not BGP, suggesting that they may be osteoblast precursor cells. alpha 1(I) procollagen mRNA was strongly expressed by all cells on the surface of bone, with a peak intensity at 3W and then reducing sharply by 6W. Initially, only pockets of cuboidal cells on bone surfaces expressed ALP mRNA, with a peak intensity at 5W. Similarly, only a proportion of cuboidal cells expressed OP mRNA early in bone formation, but the number of cells expressing OP mRNA increased with time. Clumps of cuboidal cells expressed BGP mRNA only when bone was present, and the degree of expression increased with the amount of bone formed. This model allows the study of temporal and spatial sequence of gene expression in cells participating in osteogenesis. The temporal sequence is similar to that shown in vitro in other models of mineralization. The geographic localization of cells expressing mRNA for alpha 1(I) procollagen, ALP, OP, and BGP implies subspecialization of osteoblasts in bone formation.