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Biomedical subjects

J A Warren

Publications and source records attributed to J A Warren.

At least 19 recordsLinked to original sources
PubMed2004

Phase field modeling of electrochemistry. I. Equilibrium.

A diffuse interface (phase field) model for an electrochemical system is developed. We describe the minimal set of components needed to model an electrochemical interface and present a variational derivation of the governing equations. With a simple set of assumptions: mass and volume constraints, Poisson's equation, ideal solution thermodynamics in the bulk, and a simple description of the competing energies in the interface, the model captures the charge separation associated with the equilibrium double layer at the electrochemical interface. The decay of the electrostatic potential in the electrolyte agrees with the classical Gouy-Chapman and Debye-Hückel theories. We calculate the surface free energy, surface charge, and differential capacitance as functions of potential and find qualitative agreement between the model and existing theories and experiments. In particular, the differential capacitance curves exhibit complex shapes with multiple extrema, as exhibited in many electrochemical systems.

Journal Article↗
PubMed2004

Phase field modeling of electrochemistry. II. Kinetics.

The kinetic behavior of a phase field model of electrochemistry is explored for advancing (electrodeposition) and receding (electrodissolution) conditions in one dimension. We previously described the equilibrium behavior of this model [J. E. Guyer, W. J. Boettinger, J. A. Warren, and G. B. McFadden, Phys. Rev. E 69, 021603 (2004)]. We examine the relationship between the parameters of the phase field method and the more typical parameters of electrochemistry. We demonstrate ohmic conduction in the electrode and ionic conduction in the electrolyte. We find that, despite making simple, linear dynamic postulates, we obtain the nonlinear relationship between current and overpotential predicted by the classical "Butler-Volmer" equation and observed in electrochemical experiments. The charge distribution in the interfacial double layer changes with the passage of current and, at sufficiently high currents, we find that the diffusion limited deposition of a more noble cation leads to alloy deposition with less noble species.

Journal Article↗
PubMed2001

Sharp interface limit of a phase-field model of crystal grains.

We analyze a two-dimensional phase field model designed to describe the dynamics of crystalline grains. The phenomenological free energy is a functional of two order parameters. The first one reflects the orientational order, while the second reflects the predominantally local orientation of the crystal. We consider the gradient flow of this free energy. Solutions can be interpreted as ensembles of grains (in which the orientation is constant in space) separated by grain boundaries. We study the dynamics of the boundaries as well as the rotation of the grains. In the limit of an infinitely sharp interface, the normal velocity of the boundary is proportional to both its curvature and its energy. We obtain explicit formulas for the interfacial energy and mobility, and study their behavior in the limit of a small misorientation. We calculate the rate of rotation of a grain in the sharp interface limit, and find that it depends sensitively on the choice of the model.

Journal Article↗
PubMed1999

A preview of implantable cardioverter defibrillator systems in the next millennium: an integrative cardiac rhythm management approach.

The implantable cardioverter defibrillator (ICD), a primary therapeutic option for preventing sudden cardiac death, has rapidly evolved since being introduced clinically in 1980. Technologic advances in several key areas have enabled ICDs to provide more sophisticated rhythm management. Recent emphasis has been placed on dual-chamber ICDs possessing adaptive-rate pacing capabilities. Adoption of dual-chamber ICD systems has been rapid. The capabilities of future ICD systems will be governed by an integrative strategy that brings together sets of features specifically targeted at multifaceted rhythm disorders. The addition of atrial therapy will require more sophisticated rhythm discrimination algorithms. ICD technology will improve on several fronts including leads, integrated circuits, batteries, and capacitors. Additionally, state-of-the-art pacemaker technology will continue to be incorporated into ICDs. As these new ICD systems become increasingly sophisticated from an engineering viewpoint, tremendous emphasis will be placed on decreasing the complexity of programming, device interrogation, and patient monitoring during routine patient follow-up. Vast improvements in ICD programming systems may ultimately permit the 1-minute follow-up.

Death, Sudden, Cardiac↗
PubMed1999

Future of bradyarrhythmia therapy systems: automaticity.

Since the first fixed-rate ventricular pacemaker was introduced in the late 1950s, pacing systems have evolved rapidly. Current developments focus on making devices more sophisticated and less complex--a challenging combination. Automaticity features such as beat-by-beat capture verification, sensitivity threshold adaptation, and algorithms to govern dynamically the maximum sensor rate have either recently been introduced or are likely to be introduced in the near future. Technologic advances are likely to allow meaningful improvements in current drain, battery performance, memory capacity, signal processing, telemetry, and programmer interface. Bradyarrhythmia therapy devices of the future promise to go beyond the pacemaker. Ultimately, pacing systems will become part of integrated cardiac rhythm management systems.

Bradycardia↗
PubMed1994

Maternal influences on growth and development of full-sibling foals.

Six pairs of full-sibling Quarter Horse foals were produced by non-surgical embryo transfer and immediate rebreeding of donor mares. Each pair of donor/recipient mares consisted of one multiparous (donor) and one nulliparous (recipient) mare of similar body type and size. Milk yield was determined within 2 d of 8, 15, 22, 29 d (early lactation); 45, 60 d (midlactation); and 90, 120 d (late lactation) postpartum by the weigh-suckle-weigh method. On the following day, milk samples were collected, and foals were weighed and measured for wither height, heart girth, metacarpal length, metatarsal length, carpus height, tarsus height, and hip height. Mean gestation length was longer (P < .05) in nulliparous mares than multiparous mares (343 vs 333 d). Daily milk production was greater (P < .05) during early lactation (12.1 vs 10.8 kg) and tended to be greater (P = .08) during midlactation (11.7 vs 10.4) in multiparous mares but was similar between groups in late lactation. Milk composition was similar between groups throughout lactation. Foals produced by multiparous mares weighed more (P < .03) throughout early lactation (70.4 vs 63.1 kg), but no differences in weights occurred between foals from multiparous and nulliparous mares through mid- and late lactation. Average daily weight gain (ADG) was similar between foal groups through early and midlactation. During late lactation, ADG tended to be greater (P = .07) in foals from nulliparous mares (1.05 vs .92 kg/d). These data suggest that nulliparous and multiparous mares of the same breed and similar body type and size produce foals with no differences in size and weight by 4 mo of age.

Age Factors↗
PubMed1992

Elevated muscle vitamin E does not attenuate eccentric exercise-induced muscle injury.

The purpose of this study was to evaluate the effect of elevated muscle vitamin E content on skeletal muscle damage from eccentric exercise. Sixty Sprague-Dawley rats were put on a normal (40 IU vitamin E/kg food) or supplemented (10,000 IU vitamin E/kg food) diet for 5 wk. Injury in soleus muscle was determined using several criteria: reductions in maximal tetanic force and number of intact fibers per square millimeter and elevations in muscle glucose 6-phosphate dehydrogenase activity and plasma creatine kinase activity, either immediately (0 h) or 2 days (48 h) after a downhill walking protocol. Sedentary animals were also tested but did not exercise. Muscle vitamin E levels were significantly elevated (approximately 3- to 4-fold), and susceptibility of the muscles to oxidant stress was decreased, after supplementation. However, vitamin E supplementation did not attenuate injury by any of the criteria employed. Maximal tetanic force decreased approximately 20% at 0 and 48 h after exercise in both groups. The number of intact fibers per square millimeter decreased approximately 30-35% in both groups at 0 and 48 h. Glucose 6-phosphate dehydrogenase activity increased approximately 50-100% in both groups at 48 h, and plasma creatine kinase activity was elevated approximately 2- to 2.5-fold at 0 h in both groups. These findings do not support a major role for free radical damage to muscle membranes in the initiation of injury from eccentric exercise, although they do not disprove free radical involvement in the etiology.

Animals↗
PubMed1991

Mechanisms of exercise-induced muscle fibre injury.

Exercise for which a skeletal muscle is not adequately conditioned results in focal sites of injury distributed within and among the fibres. Exercise with eccentric contractions is particularly damaging. The injury process can be hypothesised to occur in several stages. First, an initial phase serves to inaugurate the sequence. Hypotheses for the initial event can be categorised as either physical or metabolic in nature. We argue that the initial event is physical, that stresses imposed on sarcolemma by sarcomere length inhomogeneities occurring during eccentric contractions cause disruption of the normal permeability barrier provided by the cell membrane and basal lamina. This structural disturbance allows Ca++ to enter the fibre down its electrochemical gradient, precipitating the Ca++ overload phase. If the breaks in the sarcolemma are relatively minor, the entering Ca++ may be adequately handled by ATPase pumps that sequester and extrude Ca++ from the cytoplasm ('reversible' injury). However, if the Ca++ influx overwhelms the Ca++ pumps and free cytosolic Ca++ concentration rises, the injury becomes 'irreversible'. Elevations in intracellular Ca++ levels activate a number of Ca(++)-dependent proteolytic and phospholipolytic pathways that are indigenous to the muscle fibres, which respectively degrade structural and contractile proteins and membrane phospholipids; for instance, it has been demonstrated that elevation of intracellular Ca++ levels with Ca++ ionophores results in loss of creatine kinase activity from the fibres through activation of phospholipase A2 and subsequent production of leukotrienes. This autogenetic phase occurs prior to arrival of phagocytic cells, and continues during the inflammatory period when macrophages and other phagocytic cells are active at the damage site. The phagocytic phase is in evidence by 2 to 6 hours after the injury, and proceeds for several days. The regenerative phase then restores the muscle fibre to its normal condition. Repair of the muscle fibres appears to be complete; the fibres adapt during this process so that future bouts of exercise of similar type, intensity, and duration cause less injury to the muscle.

Body Temperature↗
PubMed1991

Red blood cell pulmonary capillary transit time during exercise in athletes.

The purpose of this study was to test the hypothesis that the exercise-induced hypoxemia observed in endurance athletes is due to a reduction in the mean red blood cell pulmonary capillary transit time consequent to a plateau in pulmonary capillary blood volume (Vc) as exercise intensity progresses from moderate to heavy levels. Measurements of Vc, mean transit time, arterial O2 tension (PaO2), and end tidal-arterial O2 tension difference (AaDO2) were made in 16 subjects (mean maximal oxygen uptake (VO2max) = 4.90 l.min-1) at rest and during five cycle exercise bouts designed to elicit 55, 65, 75, 85, and 95% VO2max. Mean PaO2 fell from 101 mm Hg at rest to 85 mm Hg during heavy exercise. Mean AaDO2 increased linearly from one stage to the next and at the highest work rate equaled 22.3 mm Hg. Mean Vc failed to plateau with increasing exercise intensity and increased on average by 16 ml from one stage to the next. Mean transit time, on average, dropped from 1.05 s at rest to 0.46 s at the lowest work rate. Mean transit time did not decrease further with increasing exercise intensity (range, 0.42-0.46 s). We conclude that, under the conditions of this study, the AaDO2 increases and PaO2 decreases observed in endurance athletes during exercise of increasing intensity is not caused by a plateau in Vc and a consequent reduction in mean transit time.

Adult↗
PubMed1990

Shark myelin basic protein: amino acid sequence, secondary structure, and self-association.

Myelin basic protein (MBP) from the Whaler shark (Carcharhinus obscurus) has been purified from acid extracts of a chloroform/methanol pellet from whole brains. The amino acid sequence of the majority of the protein has been determined and compared with the sequences of other MBPs. The shark protein has only 44% homology with the bovine protein, but, in common with other MBPs, it has basic residues distributed throughout the sequence and no extensive segments that are predicted to have an ordered secondary structure in solution. Shark MBP lacks the triproline sequence previously postulated to form a hairpin bend in the molecule. The region containing the putative consensus sequence for encephalitogenicity in the guinea pig contains several substitutions, thus accounting for the lack of activity of the shark protein. Studies of the secondary structure and self-association have shown that shark MBP possesses solution properties similar to those of the bovine protein, despite the extensive differences in primary structure.

Amino Acid Sequence↗
PubMed1990

Hemodynamic responses during exercise at and above VO2max in swine.

Mean arterial pressure (Pa), heart rate, cardiac output (Q), and Q distribution (with radiolabeled microspheres) were measured in miniature swine as they ran at high levels on a motor-driven treadmill. Each animal ran on two occasions: once during exercise at maximal O2 uptake (VO2max) and once at an intensity estimated to require approximately 115% VO2max. The purpose was to assess these cardiovascular variables to determine whether the calculated resistance to blood flow during supramaximal exercise was different from that during maximal exercise. A total of 114 tissues/organs were dissected for blood flow analysis. Pa and Q were unaltered between the two exercise conditions. Blood flow to all but one of the 62 skeletal muscles sampled was unchanged between conditions as were the blood flows to the visceral organs and brain. The results demonstrate that vascular resistance was constant in all these tissues between maximal and supramaximal exercise intensities. Elevated blood flows were measured in 7 of the 11 coronary sites sampled. Calculated resistance to blood flow indicated that a decrease in resistance occurred in most of the samples having elevated blood flow. Because heart rate was elevated during the supramaximal exercise, the increase in blood flow was probably in response to the greater myocardial work and concomitant elevation in O2 demand. In summary, it was shown that Pa, Q, and Q distribution in most tissues remained unchanged during exercise at intensities above VO2max. Thus a precise matching occurs between the increasingly powerful vasoconstrictor drive initiated by the sympathetic nervous system and the elevated local vasodilatory drive responding to the greater O2 demand during the supramaximal exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Monoclonal antibodies reactive with the breast carcinoma-associated mucin core protein repeat sequence peptide also recognise the ovarian carcinoma-associated sebaceous gland antigen.

The monoclonal antibody (Mab) OM-1, which defines the ovarian carcinoma-associated sebaceous gland antigen (SGA), and Mab F36/22, which defines the ductal carcinoma antigen (DCA), were tested for reactivity against a synthetic peptide representing the repeat twenty amino acid sequence of the human polymorphic epithelial mucin core protein plus four amino acids of the adjacent sequence (p1-24). OM-1 bound strongly to the peptide by direct dot blot assay and ELISA and the minimum epitope for OM-1 was shown to be APDTRP(A) by inhibition assay. F36/22 reacted weakly with the peptide under the same conditions and its affinity for peptide in solution was relatively very low. Mab OC125, which defines the ovarian cancer-associated antigen CA125, did not react with the p1-24 peptide. Five other anti-mucin Mabs (HMFG1, HMFG2, BC1, BC2, BC3), previously shown to bind to the p1-24 peptide, reacted strongly with SGA by direct binding and in a sandwich assay with OM-1 as the capture Mab. F36/22 was weakly positive under the same conditions suggesting that both peptide and SGA do not express the optimal epitope for F36/22 binding. These results indicate that SGA and possibly DCA have the repeat sequence core protein of the breast carcinoma-associated human polymorphic epithelial mucin.

Amino Acid Sequence↗