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Biomedical subjects

P R Adams

Publications and source records attributed to P R Adams.

At least 19 recordsLinked to original sources
PubMed2000

Optimal sample preparation conditions for the determination of uranium in biological samples by kinetic phosphorescence analysis (KPA).

Kinetic phosphorescence analysis (KPA) is a proven technique for rapid, precise, and accurate determination of uranium in aqueous solutions. Uranium analysis of biological samples require dry-ashing in a muffle furnace between 400 and 600 degrees C followed by wet-ashing with concentrated nitric acid and hydrogen peroxide to digest the organic component in the sample that interferes with uranium determination by KPA. The optimal dry-ashing temperature was determined to be 450 degrees C. At dry-ashing temperatures greater than 450 degrees C, uranium loss was attributed to vaporization. High temperatures also caused increased background values that were attributed to uranium leaching from the glass vials. Dry-ashing temperatures less than 450 degrees C result in the samples needing additional wet-ashing steps. The recovery of uranium in urine samples was 99.2+/-4.02% between spiked concentrations of 1.98-1980 ng (0.198-198 microg l(-1)) uranium, whereas the recovery in whole blood was 89.9+/-7.33% between the same spiked concentrations. The limit of quantification in which uranium in urine and blood could be accurately measured above the background was determined to be 0.05 and 0.6 microg l(-1), respectively.

Humans↗
PubMed1997

Traumatic aortic transections: eight-year experience with the "clamp-sew" technique.

BACKGROUND: Because traumatic aortic transection is associated with high mortality rates, great debate exists about the appropriate operative technique for treatment of patients who have acute traumatic aortic transection. METHODS: To determine the safety and efficacy of the "clamp-sew" method, we retrospectively reviewed our 8-year experience treating 75 patients who had aortic injuries secondary to blunt trauma. Seventy-one of these patients were treated surgically. The clamp-sew method was used in all of these operations. RESULTS: Aortic cross-clamp time averaged 24 minutes (range, 14 to 36 minutes), with 4/71 having times in excess of 30 minutes. One patient (clamp time, 28 minutes) became paraplegic. Significant associated injuries were seen in 51/75 patients (48/71 patients with operation), including intrathoracic (35 patients), orthopedic (28 patients), intraabdominal (24 patients), and central nervous system (17 patients) damage. No patient died within 24 hours of operation. Overall 30-day mortality was 12% (9/75), with 7/9 having two or more aforementioned associated injuries. Of these 7, 5 had central nervous system injuries. Two of 9 died within 30 days without two or more associated injuries: 1 Jehovah's Witness of low hemoglobin, and 1 patient of sepsis. CONCLUSIONS: Although any of several maneuvers may be appropriate in managing traumatic aortic injuries, the simple "clamp-sew" technique is a safe and effective method for the treatment of traumatic aortic transections.

Adolescent↗
PubMed1997

Visualization of calcium influx through channels that shape the burst and tonic firing modes of thalamic relay cells.

Thalamic neurons have two firing modes: "tonic" and "burst." During burst mode, both low-threshold (LT) and high-threshold (HT) calcium channels are activated, while in tonic mode, only the HT-type of calcium channel is activated. The calcium signals associated with each firing mode were investigated in rat thalamic slices using whole cell patch clamping and confocal calcium imaging. Action potentials were induced by direct current injection into thalamic relay cells loaded with a fluorescent calcium indicator. In both tonic and burst firing modes, large calcium signals were recorded throughout the soma and proximal dendrites. To map the distribution of the channels mediating these calcium fluxes, LT and HT currents were independently activated using specific voltage-clamp protocols. We focused on the proximal region of the cell (up to 50 microm from the soma) because it appeared to be well clamped. For a voltage pulse of a given size, the largest calcium signals were observed in the proximal dendrites with smaller signals occurring in the soma and nucleus. This was true for both LT and HT signals. Rapid imaging, using one-dimensional linescans, was used to more precisely localize the calcium influx. For both LT and HT channels, calcium influx occurred simultaneously throughout all imaged regions including the soma and proximal dendrites. The presence of sizable calcium signals in the dendrites, soma, and nucleus during both firing modes, and the presence of LT calcium channels in the proximal dendrite where sensory afferents synapse, have implications for both the electrical functioning of relay cells and the transmission of sensory information to cortex.

Action Potentials↗
PubMed1994

Extracellular amylase activities of Rhizomucor pusillus and Humicola lanuginosa at initial stages of growth.

Among thermophilic fungi, Rhizomucor Pusillus and Humicola lanuginosa have been reported to be among the most prolific producers of amylase, an apparently heat stable enzyme vital to the incorporation of carbon from macromolecular sources such as starch. Yet the highest levels of extracellular amylase in starch-yeast cultures of these fungi were measured after most of the growth had occurred; pre-growth levels appeared to be very small. Since these low levels are the significant ones for growth, a procedure was devised to measure them: 1.162 x 10(-2) units (mg maltose/ml/min) were measured after two days of growth of R. pusillus and 6.230 x 10(-3) units measured after four days of the slower-growing H. lanuginosa. Re-assays of these after dialysis to remove most of the reducing sugars gave 1.689 x 10(-2) units and 1.234 x 10(-2) units, respectively, with all correlation coefficients 0.96 or better.

Amylases↗
PubMed1994

Regulation of M current by intracellular calcium in bullfrog sympathetic ganglion neurons.

Regulation of M current (lM) by intracellular free calcium was studied in dissociated bullfrog sympathetic ganglion B cells using whole-cell recording, intracellular perfusion, and confocal calcium imaging. BAPTA (20 mM) and appropriate amounts of calcium were added to pipette solutions to clamp calcium at different levels. A high concentration of BAPTA itself mildly inhibited lM. Intracellular perfusion effectively controlled cellular free calcium; this was confirmed by confocal imaging with the calcium indicator fluo-3. In a calcium-free environment (no calcium added to either side of the cell membrane), average lM was 166 pA. Raising intracellular free calcium to 60 nM or higher reversibly enhanced lM by more than 100%. The maximum M conductance doubled upon raising calcium from 0 to 120 nM, and was accompanied by a -11 mV shift of the half-activation voltage. The kinetics of the closing and reopening relaxations of lM were also altered by raising calcium. Enhancement of lM by calcium required ATP in the pipette. TEA (5 mM) and d-tubocurarine (d-TC; 100 microM) did not alter the calcium effect, indicating that it was the M current being modulated and not other K+ currents. High calcium (450 nM) reduced lM. The up- and downregulation of lM paralleled the increases and decreases of fluorescence intensity observed via calcium imaging. Changing extracellular calcium had no significant effect on lM or cellular fluorescence. The role of calcium in muscarinic and peptidergic modulation of lM was also explored. Muscarine (1 or 10 microM) inhibited lM less at zero calcium than at higher calcium. Nearly complete suppression occurred with 120 nM calcium in the presence of 20 mM BAPTA. lM overrecovered upon washout of muscarine at 120 nM calcium, while little overrecovery of lM developed at zero calcium. Similar effects were observed at zero and 120 nM calcium when using the peptide LHRH to inhibit lM. We conclude that the absolute level of free calcium determines the size of lM, and that a minimum sustained level of calcium is required both for optimal suppression of lM by muscarine and for overrecovery. While our data suggest that resting calcium levels play a permissive role in muscarinic suppression, an additional role for agonist-induced calcium increases cannot be ruled out.

Animals↗
PubMed1992

Multiple kinetic states underlying macroscopic M-currents in bullfrog sympathetic neurons.

M-current is a time- and voltage-dependent potassium current which is suppressible by muscarinic receptor activation. We have used curve fitting and noise analysis to determine if macroscopic M-currents deviate from a previously predicted simple two-state kinetic scheme. The M-current was best described by three kinetically distinct components: 'fast' (tau 0), 'intermediate' (tau 1) and 'slow' (tau 2) time constants. The 'fast' (tau 0) and 'intermediate' (tau 1) components were identified from the spectra of M-current noise at potentials positive to the cells' resting membrane potential. The 'intermediate' (tau 1) and 'slow' (tau 2) components were seen by curve fitting M-current deactivation currents. The 'intermediate' (tau 1) time constant was voltage dependent (decreasing e-fold in 23 mV), but voltage dependence of the 'fast' (tau 0) and 'slow' (tau 2) components was not obvious. All kinetic components were sensitive to muscarine, with the 'intermediate' (tau 1) and 'slow' (tau 2) being equally so. These data suggest that all components may derive from the same channel population, and that the M-channel may have at least four kinetic states.

Animals↗
PubMed1992

Release of intracellular calcium and modulation of membrane currents by caffeine in bull-frog sympathetic neurones.

1. Calcium release and sequestration were studied in whole-cell voltage-clamped bull-frog sympathetic neurones by image analysis of Fura-2 signals. 2. Application of caffeine (10 mM) to cells voltage clamped at -38 mV caused a rapid increase in intracellular calcium concentration ([Ca2+]i) to a mean value of 352 +/- 33 nM, which activated an outward current. In the continued presence of caffeine the rise in [Ca2+]i slowly declined to a sustained plateau of 196 +/- 20 nM (112 nM above control levels), while the outward current rapidly decayed. Peak calcium release was highest at the edge of the cell. 3. The caffeine-evoked intracellular calcium increase was reduced by two inhibitors of calcium-induced calcium release, ryanodine and procaine. The residual non-suppressible increase in [Ca2+]i may indicate that caffeine can release calcium from two pharmacologically distinct intracellular stores. 4. Inhibition of the caffeine-evoked release of calcium by ryanodine was both concentration and 'use dependent' so that the full inhibitory effect was only observed when caffeine was applied for the second time in the presence of ryanodine. In contrast, the action of procaine did not show any 'use dependence' and unlike ryanodine was fully reversible. 5. The outward current was sensitive to blockers of the large conductance calcium-activated potassium current, Ic. Analysis of variance from this current indicated that it arose at least partly from summation of spontaneous miniature outward currents. 6. The magnitude and duration of calcium release by caffeine was dependent on the resting level of intracellular calcium and the caffeine exposure time. This, together with the pharmacology of the release, suggests that caffeine increases intracellular calcium by sensitizing calcium-induced calcium release. 7. The evoked [Ca2+]i increase was enhanced in amplitude by intracellular application of Ruthenium Red. This effect was mimicked by extracellular application of the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (FCCP) but not by internal application of FCCP or other inhibitors of mitochondrial Ca2+ uptake. This suggests that the evoked increase in [Ca2+]i is predominantly buffered by a Ruthenium Red-sensitive sequestration process which is not mitochondrial.

Animals↗
PubMed1991

Modulation of M-current by intracellular Ca2+.

IM is a voltage- and time-dependent K+ current that is suppressed by muscarinic receptor activation. IM augmentation following agonist washout was blocked by heavily buffering [Ca2+]i using BAPTA. Although IM is not primarily Ca2+ dependent, small increases in [Ca2+]i by photolysis of the "caged" Ca2+ chelator nitr-5 or by evoking action potentials augmented, while larger increases inhibited, IM. Raising [Ca2+]i for prolonged periods, by nitr-5 photolysis, reduced its sensitivity to agonist, leaving a poorly reversible response. These results suggest that IM can be regulated by physiologically relevant changes in [Ca2+]i, placing IM in a unique position to modulate cell excitability.

Animals↗
PubMed1991

Arrest and reversal of atherosclerosis with parenteral nutrition.

In a large subset of patients with atherosclerotic cardiovascular disease, all medical and surgical treatment alternatives have been exhausted or have proved to be ineffective. Intravenous infusion of specially formulated amino acid solutions, developed in the animal laboratory, has been efficacious in arresting and reversing atherosclerosis in humans for the first time. It is anticipated that the principles derived from these precise parenteral studies will eventually permit development of oral and enteral dietary formulations effective for the systemic control and management of atherosclerosis.

Animals↗
PubMed1990

Subcellular calcium transients visualized by confocal microscopy in a voltage-clamped vertebrate neuron.

Confocal laser-scanned microscopy and long-wavelength calcium (Ca2+) indicators were combined to monitor both sustained and rapidly dissipating Ca2+ gradients in voltage-clamped sympathetic neurons isolated from the bullfrog. After a brief activation of voltage-dependent Ca2+ channels, Ca2+ spreads inwardly, and reaches the center of these spherical cells in about 300 milliseconds. Although the Ca2+ redistribution in the bulk of the cytosol could be accounted for with a radial diffusion model, local nonlinearities, suggesting either nonuniform Ca2+ entry or spatial buffering, could be seen. After electrical stimulation, Ca2+ signals in the nucleus were consistently larger and decayed more slowly than those in the cytosol. A similar behavior was observed when release of intracellular Ca2+ was induced by caffeine, suggesting that in both cases large responses originate from Ca2+ release sites near or within the nucleus. These results are consistent with an amplification mechanism involving Ca2(+)-induced Ca2+ release, which could be relevant to activity-dependent, Ca2(+)-regulated nuclear events.

Animals↗
PubMed1990

N-methyl-D-aspartate receptors contribute to excitatory postsynaptic potentials of cat lateral geniculate neurons recorded in thalamic slices.

Neurons of the cat's dorsal lateral geniculate nucleus were recorded intracellularly to study the contribution of N-methyl-D-aspartate (NMDA) receptors to excitatory postsynaptic potentials (EPSPs) and low-threshold calcium spikes. EPSPs were evoked by stimulation of retinogeniculate axons in the optic tract and/or corticogeniculate axons in the optic radiations; EPSPs from both sources were similar. These EPSPs had one or two components, and the second component had several characteristics of NMDA receptor-mediated events. For example, EPSP amplitude decreased when neurons were hyperpolarized and increased when stimulus frequency was increased; these EPSPs could also be blocked reversibly by application of the selective NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV). We also studied the influence of NMDA receptors on low-threshold calcium spikes, which are large, voltage- and calcium-dependent depolarizations that are often accompanied by high-frequency action potential discharge. APV blocked synaptically activated low-threshold calcium spikes, but APV had no effect on low-threshold calcium spikes that were elicited by current injection. Therefore, APV does not appear to have a direct effect on the T-type calcium channel that is involved in generation of low-threshold calcium spikes. The voltage and frequency dependence of the NMDA receptor-mediated component of the EPSPs, as well as its ability to trigger low-threshold calcium spikes, provide for complex signal processing in the lateral geniculate nucleus.

2-Amino-5-phosphonovalerate↗
PubMed1989

Bradykinin inhibits a potassium M-like current in rat pheochromocytoma PC12 cells.

We studied the action of bradykinin (BK) on ionic currents in fused pheochromocytoma PC12 cells under voltage-clamp in whole-cell mode, and on intracellular calcium using fura-2 BK induced the development of an outward current associated with an increase in intracellular calcium, followed by inhibition of an M-like current. The outward current was blocked by (+)-tubocurarine, and prevented when the calcium BAPTA or high concentrations of inositol 1,4,5-triphosphate were introduced into the cell, whereas the M-like current and its inhibition by BK remained unaffected. The protein kinase activator phorbol 12,13 dibutyrate partially reduced the M-current. M-current density did not substantially change after prolonged treatment with nerve growth factor.

Animals↗