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A Karp

Publications and source records attributed to A Karp.

27 records · Page 2Linked to original sources

A prospective study of the effect of the appropriateness of foot-shoe fit and training shoe type on the incidence of overuse injuries among infantry recruits.

In a prospective study of the effect of the appropriateness of foot-shoe fit and training shoe type on the incidence of overuse injuries among infantry recruits, it was found that three shoe widths for each shoe length size were necessary to adequately accommodate the recruit population's foot anatomy. Recruits compensated for the lack of available shoe widths by choosing larger shoe sizes. However, this compensation did not result in an increase in the incidence of overuse injuries. Recruits who trained in basketball shoes had a lower incidence of overuse injuries of the feet than recruits who trained in infantry boots (p = 0.0001), but the overall incidence of overuse injuries was the same in both groups.

Cumulative Trauma Disorders↗

Cytosolic free calcium and NAD/NADH redox state in the cat cortex during in vivo activation of NMDA receptors.

Activation of the N-methyl-D-aspartate (NMDA) receptors and the concomitant Ca2+ entry have been implicated in neuronal injury in a variety of pathological states. The effects of extracellular Mg2+ concentrations and D,L-2-amino-5-phosphonovaleric acid (APV), a competitive NMDA receptor antagonist on the NMDA-induced responses were investigated in vivo. In vivo fluorometric measurements were made of changes in cytosolic free Ca2+ ([Ca2+]i) and NADH fluorescence directly from the cat cortex using indo-1, a fluorescent Ca2+ indicator. Changes in [Ca2+]i were assessed utilizing the ratio of indo-1 emission at two wavelengths (400 and 506 nm) during excitation with ultraviolet light (340 nm). Application of 100 microM NMDA to the cortex produced a significant increase in the [Ca2+]i signal ratio at physiological concentrations of Mg2+ (1.2 mM). This increase was enhanced in the absence of Mg2+ and was completely blocked either at 5 mM Mg2+ or in the presence of 50 microM APV. The NAD/NADH redox state was initially oxidized, which was also blocked by either high Mg2+ or APV. The application of NMDA elicited characteristic electroencephalogram (EEG) changes consisting of a marked reduction in amplitude and regular spikes (17-20 Hz). These EEG changes did not appear in the presence of APV. In addition to NMDA receptor antagonists, the level of extracellular Mg2+ is a potent physiological modulator of the NMDA response.

2-Amino-5-phosphonovalerate↗

Cytosolic free calcium, NAD/NADH redox state and hemodynamic changes in the cat cortex during severe hypoglycemia.

Using indo-1, a fluorescent Ca2+ indicator, in vivo fluorometric measurements were made of changes in cytosolic free Ca2+, NAD/NADH redox state, and hemodynamics directly from the cat cortex during and after severe insulin-induced hypoglycemia. Cytosolic free Ca2+ started to increase when the EEG became isoelectric, remained at a significantly high level (p less than 0.05) during the period of isoelectric EEG (IEEG), and recovered to the control level 6 min following an intravenous infusion of glucose. The NAD/NADH redox state oxidized significantly during IEEG and then recovered rapidly to the control level after the glucose infusion. Local cortical blood volume (LCBV) increased gradually during the progression of hypoglycemia, reaching the maximal level (146 +/- 7%) at the end of IEEG, and then started to recover. The mean transit time (MTT) through the cortical microcirculation was shortened during the IEEG (control: 3.84 +/- 0.41 s versus IEEG: 2.73 +/- 0.17 s, p less than 0.05), whereas it was prolonged during the 30-min recovery period (5.68 +/- 0.58 s, p less than 0.05). Local cortical blood flow calculated from the LCBV and MTT showed a twofold increase 5 min into IEEG (201 +/- 27% of control, p less than 0.05), recovered 15 min into the recovery period, and then decreased to 77% of control (p less than 0.05) by 30 min. The data support the hypothesis that hypoglycemic brain damage might be mediated by an elevation of cytosolic free calcium.

Animals↗

In vivo measurement of cytosolic free calcium during cerebral ischemia and reperfusion.

An increase in cytosolic free calcium concentration ([Ca2+]i) may trigger irreversible cell injury following cerebral ischemia. We have measured changes in [Ca2+]i in cat cortex in vivo during ischemia produced by 1 hour of middle cerebral artery occlusion and during 30 minutes of reperfusion. Indo-1, a fluorescent Ca2+ indicator, was loaded into the exposed cortex by superfusion, and changes in the [Ca2+]i signal (400/506 nm ratio) were measured microfluorometrically during ultraviolet excitation (340 nm). The nicotinamide adenine dinucleotide/reduced nicotinamide adenine dinucleotide (NAD/NADH) redox state and hemodynamic changes were measured simultaneously. The animals showing severe deterioration in their electroencephalograms (EEG) showed a progressive increase in the [Ca2+]i signal during ischemia (baseline: 1.46 +/- 0.05; 60 minutes after occlusion: 2.99 +/- 0.37; n = 7). At 30 minutes following reperfusion, the animals showing little recovery in their EEG exhibited a further increase in [Ca2+]i (4.71 +/- 0.87, n = 3), whereas animals showing significant recovery in their EEG also showed recovery of [Ca2+]i (1.55 +/- 0.09, n = 4). By contrast, the moderate or mild stroke animals with less deterioration in their EEGs showed no increase in [Ca2+]i during either ischemia or reperfusion. These data suggest that the increase in [Ca2+]i might be closely related not only to deterioration of brain function during ischemia but also to poor recovery during the reperfusion period.

Animals↗

Calcium channel blockers in systemic hypertension.

Alterations in transmembrane flux of calcium ions may be playing a role in the pathophysiology of systemic hypertension. Calcium channel blockers have been shown to be effective antihypertensive drugs with excellent safety profiles. They are efficacious in the long term treatment of systemic hypertension in all population subgroups, and have special applicability for treating patients with hypertensive urgencies and individuals with concomitant diseases such as angina pectoris and arrhythmias.

Animals↗

In vivo fluorometric measurement of changes in cytosolic free calcium from the cat cortex during anoxia.

A new approach to assess the mean changes in intracellular free calcium [Ca2+]i directly from the cortex in situ is described along with the [Ca2+]i changes during nitrogen anoxia. Following incision of the dura and part of the pia-arachnoid membrane, quin2 acetoxymethyl ester, 100 microM in artificial CSF, was superfused for 60 min onto the cat cortex. A small cortical area was irradiated with ultraviolet rays (350/30 nm) and the changes in the fluorescence and reflectance were recorded microfluorometrically at 506 and 366 nm, respectively. The net change in the quin2-Ca2+ fluorescence was calculated after correction for the hemodynamic artifact and subtraction of the basal NADH change. The quin2-Ca2+ fluorescence began to increase significantly (48.0 +/- 13.4 units; p less than 0.05) 20 s prior to the isoelectric electrocorticogram (ECoG) and remained elevated during nitrogen anoxia. It decreased steeply 7.3 +/- 1.7 s prior to the recovery of the ECoG activity after the animal was reoxygenated. Thus, the changes in the intracellular free calcium preceded those of the ECoG during a reversible anoxic insult, suggesting that the increase in the [Ca2+]i might be related to the electrical failure during anoxia.

Aminoquinolines↗

Retinitis pigmentosa and progressive hearing loss.

Much material has been written about the deaf-blind patient diagnosed as having Usher's syndrome, a pathologic condition involving hearing impairment and retinitis pigmentosa. Contrary to the accepted pattern of prelingual deafness in such cases, however, there are a number of patients who report a progressive, postlingual hearing loss associated with retinitis pigmentosa. These patients may suffer from a variation of classical Usher's syndrome. An attempt is made to verify this statement through presentation of case histories and audiologic findings. In addition, diagnostic and rehabilitative techniques employed in assisting patients with these dual impairments are offered.

Audiometry, Pure-Tone↗