bluuebunny/crossref_metadata_2025 huggingface dataset:
SUBGLACIAL PROCESSES
Authors: Clarke Garry K.C.
Published: January 2005

▪ Abstract  Processes operating beneath glaciers can have a greater influence on flow dynamics than those operating within them. The variety and complexity of these processes, which involve interactions among ice, water, and geological solids, resist efforts to establish simple truths and can lead to surprising outcomes. Thermal conditions at the ice-bed interface (melting or nonmelting) and the mechanical properties of the glacier substrate (soft or hard) determine which processes can be activated. The warm-soft case supports the greatest variety of processes and is the most important for fast-flow dynamics and for the mobilization of subglacial sediment. Process interactions can lead to oscillations and spatio-temporal switching behavior in glaciers and ice sheets as well as to the generation of subglacial landforms.
EVOLUTION OF THE CONTINENTAL LITHOSPHERE
Authors: Sleep Norman H.
Published: January 2005

▪Abstract   Stable cratons and stable continental platforms are salient features of the Earth. Mantle xenoliths provide detailed data on deep structure. Cratonal lithosphere is about 200 km thick. It formed in the Archean by processes analogous to modern tectonics and has been stable beneath the larger cratons since that time. Its high viscosity, high yield strength, and chemical buoyancy protected it from being entrained by underlying stagnant lid convection and by subduction. Chemically buoyant mantle does not underlie platforms. Platform lithosphere has gradually thickened with time as convection waned as the Earth's interior cooled. The thermal contraction associated with this thickening causes platforms to subside relative to cratons. At present, the thickness of platform lithosphere is comparable to that of cratonal lithosphere.
Robert T. Jones, One of a Kind
Authors: Vincenti Walter G.
Published: January 2005

His contemporaries saw R.T. Jones as one of the notably creative aerodynamicists of the twentieth century. This essay reviews his remarkable life and career, including his years as a farm-country boy, college dropout, and fledgling airplane designer in Missouri, his time as an elevator operator and self-directed student in Washington, D.C., and his long professional career as an aerodynamicist at the Langley and Ames Aeronautical Laboratories and Stanford University. The focus in his career is on his fundamental discovery of the benefits of sweepback for the wings of high-speed airplanes. This includes speculation about his highly intuitive thought processes in arriving at his creative ideas. I also give an account of his work on blood flow and the mechanical heart, his avocational accomplishments as a maker of telescopes and violins, and his philosophical interest in human affairs.
PRINCIPLES OF MICROFLUIDIC ACTUATION BY MODULATION OF SURFACE STRESSES
Authors: Darhuber Anton A. , Troian Sandra M.
Published: January 2005

▪ Abstract  Development and optimization of multifunctional devices for fluidic manipulation of films, drops, and bubbles require detailed understanding of interfacial phenomena and microhydrodynamic flows. Systems are distinguished by a large surface to volume ratio and flow at small Reynolds, capillary, and Bond numbers are strongly influenced by boundary effects and therefore amenable to control by a variety of surface treatments and surface forces. We review the principles underlying common techniques for actuation of droplets and films on homogeneous, chemically patterned, and topologically textured surfaces by modulation of normal or shear stresses.
MULTISCALE FLOW SIMULATIONS USING PARTICLES
Authors: Koumoutsakos Petros
Published: January 2005

▪ Abstract  Flow simulations are one of the archetypal multiscale problems. Simulations of turbulent and unsteady separated flows have to resolve a multitude of interacting scales, whereas molecular phenomena determine the structure of shocks and the validity of the no-slip boundary condition. Particle simulations of continuum and molecular phenomena can be formulated by following the motion of interacting particles that carry the physical properties of the flow. In this article we review Lagrangian, multiresolution, particle methods such as vortex methods and smooth particle hydrodynamics for the simulation of continuous flows and molecular dynamics for the simulation of flows at the atomistic scale. We review hybrid molecular-continuum simulations with an emphasis on the computational aspects of the problem. We identify the common computational characteristics of particle methods and discuss their properties that enable the formulation of a systematic framework for multiscale flow simulations.
GLOBAL INSTABILITIES IN SPATIALLY DEVELOPING FLOWS: Non-Normality and Nonlinearity
Authors: Chomaz Jean-Marc
Published: January 2005

▪ Abstract  The objective of this review is to critically assess the different approaches developed in recent years to understand the dynamics of open flows such as mixing layers, jets, wakes, separation bubbles, boundary layers, and so on. These complex flows develop in extended domains in which fluid particles are continuously advected downstream. They behave either as noise amplifiers or as oscillators, both of which exhibit strong nonlinearities ( Huerre & Monkewitz 1990 ). The local approach is inherently weakly nonparallel and it assumes that the basic flow varies on a long length scale compared to the wavelength of the instability waves. The dynamics of the flow is then considered as a superposition of linear or nonlinear instability waves that, at leading order, behave at each streamwise station as if the flow were homogeneous in the streamwise direction. In the fully global context, the basic flow and the instabilities do not have to be characterized by widely separated length scales, and the dynamics is then viewed as the result of the interactions between Global modes living in the entire physical domain with the streamwise direction as an eigendirection. This second approach is more and more resorted to as a result of increased computational capability. The earlier review of Huerre & Monkewitz (1990) emphasized how local linear theory can account for the noise amplifier behavior as well as for the onset of a Global mode. The present survey first adopts the opposite point of view by demonstrating how fully global theory accounts for the noise amplifier behavior of open flows. From such a perspective, there is strong emphasis on the very peculiar nonorthogonality of linear Global modes, which in turn allows a novel interpretation of recent numerical simulations and experimental observations. The nonorthogonality of linear Global modes also imposes severe constraints on the extension of linear global theory to the fully nonlinear régime. When the flow is weakly nonparallel, this limitation is so severe that the linear Global mode theory is of little help. It is then much more appropriate to develop a fully nonlinear formulation involving the presence of a front separating the base state region from the bifurcated state region.
THE DYNAMICAL SYSTEMS APPROACH TO LAGRANGIAN TRANSPORT IN OCEANIC FLOWS
Authors: Wiggins Stephen
Published: January 2005

▪ Abstract  Chaotic advection and, more generally, ideas from dynamical systems, have been fruitfully applied to a diverse, and varied, collection of mixing and transport problems arising in engineering applications over the past 20 years. Indeed, the “dynamical systems approach” was developed, and tested, to the point where it can now be considered a standard tool for understanding mixing and transport issues in many disciplines. This success for engineering-type flows motivated an effort to apply this approach to transport and mixing problems in geophysical flows. However, there are fundamental difficulties arising in this endeavor that must be properly understood and overcome. Central to this approach is that the starting point for analysis is a velocity field (i.e., the “dynamical system”). In many engineering applications this can be obtained sufficiently accurately, either analytically or computationally, so that it describes particle trajectories for the actual flow. However, in geophysical flows (and we concentrate here almost exclusively on oceanographic flows), the wide range of dynamically significant time and length scales makes the justification of any velocity field, in the sense of reproducing particle trajectories for the actual flow, a much more difficult matter. Nevertheless, the case for this approach is compelling due to the advances in observational capabilities in oceanography (e.g., drifter deployments, remote sensing capabilities, satellite imagery, etc.), which reveal space-time structures that are highly suggestive of the structures one visualizes in the global, geometrical study of dynamical systems theory. This has been pursued in recent years through a combination of laboratory studies, kinematic models, and dynamically consistent models that have all been compared with observational data. During the course of these studies it has become apparent that a new type of dynamical system is necessary to consider in these studies (i.e., a finite time, aperiodically time-dependent velocity field defined as a data set), which requires the development of new analytical and computational tools, as well as the necessity to discard some of the standard ideas and results from dynamical systems theory. In this article we review a number of the key developments to date in this young, but rapidly developing, area at the interface between geophysical fluid dynamics and applied and computational mathematics. We also describe the wealth of new directions for research that this approach unlocks.
GEORGE GABRIEL STOKES ON WATER WAVE THEORY
Authors: Craik Alex D.D.
Published: January 2005

▪ Abstract  George Gabriel Stokes died just over 100 years ago, and it has been more than 150 years since he published his great 1847 paper on water waves. The work of Stokes' precursors, which informed his early publications of 1842–50, is described in the previous volume of the Annual Review of Fluid Mechanics ( Craik 2004 ). Here I examine Stokes' papers and letters concerning water waves.
Role of veins in regulation of pulmonary circulation
Authors: Gao Yuansheng , Raj J. Usha
Published: January 2005

Pulmonary veins have been seen primarily as conduit vessels; however, over the past two decades, a large amount of evidence has accumulated to indicate that pulmonary veins can exhibit substantial vasoactivity. In this review, the role of veins in regulation of the pulmonary circulation, particularly during the perinatal period and under certain pathophysiological conditions, is discussed. In the fetus, pulmonary veins contribute a significant fraction to total pulmonary vascular resistance. At birth, the veins as well as the arteries relax in response to endothelium-derived nitric oxide and dilator prostaglandins, thereby assisting in the fall in pulmonary vascular resistance. These effects are oxygen dependent and modulated by cGMP-dependent protein kinase. Under chronic hypoxic conditions, pulmonary veins undergo remodeling and demonstrate substantial constriction and hypertrophy. In a number of species, including the human, pulmonary veins are also the primary sites of action of certain vasoconstrictors such as endothelin and thromboxane. In various pathological conditions, there is an increased synthesis of these vasoactive agents that may lead to pulmonary venous constriction, increased microvascular pressures for fluid filtration, and formation of pulmonary edema. In conclusion, the significant role of veins in regulation of the pulmonary circulation needs to be appreciated to better prevent, diagnose, and treat lung disease.
Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation
Authors: Janic Branislava , Umstead Todd M. , Phelps David S. , Floros Joanna
Published: January 2005

Ozone (O3), a major component of air pollution and a strong oxidizing agent, can lead to lung injury associated with edema, inflammation, and epithelial cell damage. The effects of O3on pulmonary immune cells have been studied in various in vivo and in vitro systems. We have shown previously that O3exposure of surfactant protein (SP)-A decreases its ability to modulate proinflammatory cytokine production by cells of monocyte/macrophage lineage (THP-1 cells). In this report, we exposed THP-1 cells and/or native SP-A obtained from bronchoalveolar lavage of patients with alveolar proteinosis to O3and studied cytokine production and NF-κB signaling. The results showed 1) exposure of THP-1 cells to O3significantly decreased their ability to express TNF-α in response to SP-A; TNF-α production, under these conditions, was still significantly higher than basal (unstimulated) levels in filtered air-exposed THP-1 cells; 2) exposure of both THP-1 cells and SP-A to O3did not result in any significant differences in TNF-α expression compared with basal levels; 3) O3exposure of SP-A resulted in a decreased ability of SP-A to activate the NF-κB pathway, as assessed by the lack of significant increase and decrease of the nuclear p65 subunit of NF-κB and cytoplasmic IκBα, respectively; and 4) O3exposure of THP-1 cells resulted in a decrease in SP-A-mediated THP-1 cell responsiveness, which did not seem to be mediated via the classic NF-κB pathway. These findings indicate that O3exposure may mediate its effect on macrophage function both directly and indirectly (via SP-A oxidation) and by involving different mechanisms.
Nitric oxide decreases surfactant protein gene expression in primary cultures of type II pneumocytes
Authors: Lee Jae W. , Gonzalez Robert F. , Chapin Cheryl J. , Busch Justin , Fineman Jeffrey R. , Gutierrez Jorge A.
Published: January 2005

Inhaled nitric oxide (NO) is a selective pulmonary vasodilator effective in treating persistent pulmonary hypertension in newborns and in infants following congenital heart disease surgery. Recently, multiple in vivo and in vitro studies have shown a negative effect of NO on surfactant activity as well as surfactant protein gene expression. Although the relationship between NO and surfactant has been studied previously, the data has been hard to interpret due to the model systems used. The objective of the current study was to characterize the effect of NO on surfactant protein gene expression in primary rat type II pneumocytes cultured on a substratum that promoted the maintenance of type II cell phenotype. Exposure to a NO donor, S-nitroso-N-acetylpenicillamine (SNAP), decreased surfactant protein (SP)-A, (SP)-B, and (SP)-C mRNA levels in type II pneumocytes in a time- and dose-dependent manner. The effect was mediated in part by an increase in endothelin-1 secretion and a decrease in the intracellular messenger, phosphorylated ERK1/2 mitogen-activated protein kinases (MAPK). Exposing type II pneumocytes to endothelin-1 receptor antagonists PD-156707 or bosentan before exposure to SNAP partially prevented the decrease in surfactant protein gene expression. The results showed that NO mediated the decrease in surfactant protein gene expression at least in part through an increase in endothelin-1 secretion and a decrease in phosphorylated ERK1/2 MAPKs.
Developmental regulation of PV-1 in rat lung: association with the nuclear envelope and limited colocalization with Cav-1
Authors: Hnasko Robert , Ben-Jonathan Nira
Published: January 2005

Plasmalemma vesicle protein-1 (PV-1) is a caveolae-associated protein that is enriched in lung endothelial cells. The PV-1 protein is first detected in the lung at embryonic day 12, before that of caveolin-1 (Cav-1). There is a postnatal rise in PV-1 and Cav-1 mRNA levels, reaching a peak at the time of weaning and declining to their lowest levels in the adult lung. In contrast, the PV-1 protein progressively increases during postnatal development with its highest levels in the adult lung; the Cav-1 protein remains relatively constant throughout this period. Alveolar endothelial cells express both PV-1 and Cav-1 proteins, but PV-1, unlike Cav-1, is also detectable in some bronchial epithelial cells. Endothelial cells transfected with a rat PV-1 construct show a punctate membrane distribution of PV-1, perinuclear accumulation, and an association with the nuclear envelope. In these cells, PV-1 exhibits only partial perinuclear colocalization with Cav-1 and F-actin. In summary, PV-1 is developmentally regulated in the rat lung and shows a divergent intracellular localization, with a limited caveolae/Cav-1 colocalization in cultured endothelial cells.
Mechanism of eosinophil induced signaling in cholinergic IMR-32 cells
Authors: Curran David R. , Morgan Ross K. , Kingham Paul J. , Durcan Niamh , McLean W. Graham , Walsh Marie Therese , Costello Richard W.
Published: January 2005

Eosinophils interact with nerve cells, leading to changes in neurotransmitter release, altered nerve growth, and protection from cytokine-induced apoptosis. In part, these interactions occur as a result of activation of neural nuclear factor (NF)-κB, which is activated by adhesion of eosinophils to neural intercellular adhesion molecule-1 (ICAM-1). The mechanism and consequence of signaling after eosinophil adhesion to nerve cells were investigated. Eosinophil membranes, which contain eosinophil adhesion molecules but not other eosinophil products, were coincubated with IMR-32 cholinergic nerve cells. The studies showed that there were two mechanisms of activation of NF-κB, one of which was dependent on reactive oxygen species, since it was inhibited with diphenyleneiodonium. This occurred at least 30 min after coculture of eosinophils and nerves. An earlier phase of NF-κB activation occurred within 2 min of eosinophil adhesion and was mediated by tyrosine kinase-dependent phosphorylation of interleukin-1 receptor-associated kinase-1 (IRAK-1). Coimmunoprecipitation experiments showed that both extracellular signal-regulated kinase 1/2 and IRAK-1 were recruited to ICAM-1 rapidly after coculture with eosinophil membranes. This was accompanied by an induction of ICAM-1, which was mediated by an IRAK-1-dependent pathway. These data indicate that adhesion of eosinophils to IMR-32 nerves via ICAM-1 leads to important signaling events, mediated via IRAK-1, and these in turn lead to expression of adhesion molecules.
Prostanoid receptor expression by human airway smooth muscle cells and regulation of the secretion of granulocyte colony-stimulating factor
Authors: Clarke Deborah L. , Belvisi Maria G. , Smith Susan J. , Hardaker Elizabeth , Yacoub Magdi H. , Meja Koremu K. , Newton Robert , Slater Donna M. , Giembycz Mark A.
Published: January 2005

The prostanoid receptors on human airway smooth muscle cells (HASMC) that augment the release by IL-1β of granulocyte colony-stimulating factor (G-CSF) have been characterized and the signaling pathway elucidated. PCR of HASM cDNA identified products corresponding to EP2, EP3, and EP4receptor subtypes. These findings were corroborated at the protein level by immunocytochemistry. IL-1β promoted the elaboration of G-CSF, which was augmented by PGE2. Cicaprost (IP receptor agonist) was approximately equiactive with PGE2, whereas PGD2, PGF2α, and U-46619 (TP receptor agonist) were over 10-fold less potent. Neither SQ 29,548 nor BW A868C (TP and DP1receptor antagonists, respectively) attenuated the enhancement of G-CSF release evoking any of the prostanoids studied. With respect to PGE2, the EP receptor agonists 16,16-dimethyl PGE2(nonselective), misoprostol (EP2/EP3selective), 17-phenyl-ω-trinor PGE2(EP1selective), ONO-AE1-259, and butaprost (both EP2selective) were full agonists at enhancing G-CSF release. AH 6809 (10 μM) and L-161,982 (2 μM), which can be used in HASMC as selective EP2and EP4receptor antagonists, respectively, failed to displace to the right the PGE2concentration-response curve that described the augmented G-CSF release. In contrast, AH 6809 and L-161,982 in combination competitively antagonized PGE2-induced G-CSF release. Augmentation of G-CSF release by PGE2was mimicked by 8-BrcAMP and abolished in cells infected with an adenovirus vector encoding an inhibitor protein of cAMP-dependent protein kinase (PKA). These data demonstrate that PGE2facilitates G-CSF secretion from HASMC through a PKA-dependent mechanism by acting through EP2and EP4prostanoid receptors and that effective antagonism is realized only when both subtypes are blocked concurrently.
Antioxidant properties of cystic fibrosis sputum
Authors: Dauletbaev Nurlan , Rickmann Jens , Viel Klaus , Diegel Holger , von Mallinckrodt Christian , Stein Jürgen , Wagner Thomas O. F. , Bargon Joachim
Published: January 2005

Oxidative stress is a likely contributor to the pathogenesis of cystic fibrosis (CF) lung disease. However, hydrogen peroxide (H2O2), a physiological oxidant, is not elevated in CF exhalates. H2O2may be neutralized by antioxidants in CF airway secretions. The H2O2-detoxifying capacity of CF airway secretions, obtained via sputum induction, was studied in an in vitro H2O2cytotoxicity model. 16HBE14o- cells were exposed to H2O2in culture medium containing either 0 or 10% fetal bovine serum (FBS) or 10% CF sputum supernatant (extracted without use of dithiothreitol). The efficiency of H2O2neutralization was estimated by measuring intracellular oxidant levels (dihydrorhodamine 123) after 2 h and cell viability (propidium iodide) after 24 h of H2O2exposure. Furthermore, the presence of reduced thiols (DTNB assay) and reduced glutathione (recycling assay) in CF sputum samples was evaluated. CF sputum extracts completely prevented intracellular oxidant accumulation seen in cells incubated with H2O2in both control media (i.e., 0 or 10% FBS). Furthermore, CF sputum abolished cell death in 16HBE14o- cells exposed to up to 1 mM H2O2. In contrast, there was 100% cytotoxicity in cells exposed to 600 μM H2O2in both control media. The H2O2-detoxifying potential of CF sputum was sustained after catalase and heme peroxidases were inactivated by sodium azide, which does not affect glutathione peroxidase. In addition, reduced protein thiols were found in abundance in CF sputum. In conclusion, CF sputum is capable to neutralize H2O2and abundant reduced thiols and/or glutathione peroxidase are fully sufficient to detoxify H2O2.
HMGB1 contributes to the development of acute lung injury after hemorrhage
Authors: Kim Jae Yeol , Park Jong Sung , Strassheim Derek , Douglas Ivor , Diaz del Valle Fernando , Asehnoune Karim , Mitra Sanchayita , Kwak Sang Hyun , Yamada Shingo , Maruyama Ikuro , Ishizaka Akitoshi , Abraham Edward
Published: January 2005

High mobility group box 1 (HMGB1) is a novel late mediator of inflammatory responses that contributes to endotoxin-induced acute lung injury and sepsis-associated lethality. Although acute lung injury is a frequent complication of severe blood loss, the contribution of HMGB1 to organ system dysfunction in this setting has not been investigated. In this study, HMGB1 was detected in pulmonary endothelial cells and macrophages under baseline conditions. After hemorrhage, in addition to positively staining endothelial cells and macrophages, neutrophils expressing HMGB1 were present in the lungs. HMGB1 expression in the lung was found to be increased within 4 h of hemorrhage and then remained elevated for more than 72 h after blood loss. Neutrophils appeared to contribute to the increase in posthemorrhage pulmonary HMGB1 expression since no change in lung HMGB1 levels was found after hemorrhage in mice made neutropenic with cyclophosphamide. Plasma concentrations of HMGB1 also increased after hemorrhage. Blockade of HMGB1 by administration of anti-HMGB1 antibodies prevented hemorrhage-induced increases in nuclear translocation of NF-κB in the lungs and pulmonary levels of proinflammatory cytokines, including keratinocyte-derived chemokine, IL-6, and IL-1β. Similarly, both the accumulation of neutrophils in the lung as well as enhanced lung permeability were reduced when anti-HMGB1 antibodies were injected after hemorrhage. These results demonstrate that hemorrhage results in increased HMGB1 expression in the lungs, primarily through neutrophil sources, and that HMGB1 participates in hemorrhage-induced acute lung injury.
Chronic endotoxin exposure does not cause sustained structural abnormalities in the fetal sheep lungs
Authors: Kallapur Suhas G. , Nitsos Ilias , Moss Timothy J. M. , Kramer Boris W. , Newnham John P. , Ikegami Machiko , Jobe Alan H.
Published: January 2005

Chronic early gestational chorioamnionitis is associated with development of bronchopulmonary dysplasia in preterm infants. A single intra-amniotic exposure to endotoxin decreased alveolarization and reduced expression of endothelial proteins in 125-day gestational age preterm lambs. We hypothesized that prolonged exposure to intra-amniotic endotoxin would cause progressive lung inflammation and inhibit alveolar and pulmonary vascular development. Endotoxin (1 mg/day) or saline was administered via an intra-amniotic osmotic pump from 80 to 108 days of gestational age (continuous pump) or by four weekly 10-mg intra-amniotic endotoxin injections starting at 100 days of gestational age (multiple dose). Lung morphometry, lung inflammation, vascular effects, and lung maturation were measured at delivery. The continuous pump lambs delivered at 100 days (∼70% of total endotoxin exposure) had lung inflammation, fewer saccules, and decreased endothelial proteins endothelial nitric oxide synthase and VEGF receptor 2 expression compared with controls. The continuous pump (delivered at 138 days) and multiple dose lambs (delivered at 130 and 145 days) had mild persistent lung inflammation and no significant differences in lung morphometry or expression of endothelial proteins compared with controls. Surfactant saturated phosphatidylcholine pool sizes were increased in all endotoxin-exposed groups, but lung function was not changed relative to controls. Contrary to our hypothesis, a prolonged fetal exposure to intra-amniotic endotoxin caused mild persistent inflammation but did not lead to progressive structural abnormalities in lungs of near-term gestation lambs.
Leptin gene expression and systemic levels in healthy men: effect of exercise, carbohydrate, interleukin-6, and epinephrine
Authors: Keller Pernille , Keller Charlotte , Steensberg Adam , Robinson Lindsay E. , Pedersen Bente K.
Published: January 2005

Leptin, an adipose tissue-derived cytokine, is correlated with adipose mass as obese persons have increased levels of leptin that decrease with weight loss. Previous studies demonstrate that high-energy-expenditure exercise decreases circulating leptin levels, whereas low-energy-expenditure exercise has no effect. We aimed to test the hypothesis that acute exercise reduced leptin mRNA levels in human adipose tissue and that this effect would be ameliorated by carbohydrate supplementation. Because exercise markedly increases circulating IL-6 and epinephrine, we investigated whether the changes in leptin seen with acute exercise could be mediated by IL-6 or epinephrine infusion. Abdominal subcutaneous adipose tissue mRNA and plasma levels of leptin were measured in healthy men in response to 3-h ergometer exercise with or without carbohydrate (CHO) ingestion ( n = 8) and in response to infusion with recombinant human (rh)IL-6 ( n = 11) or epinephrine ( n = 8) or saline. Plasma leptin declined in response to exercise ( P < 0.05) compared with rest, whereas mRNA expression in adipose tissue was unaffected. The exercise-induced decrease in plasma leptin was attenuated by CHO ingestion ( P < 0.001). A 3-h epinephrine infusion decreased plasma leptin ( P < 0.001) to the same level seen with 3 h of exercise, whereas leptin levels were unaffected by rhIL-6 infusion. In conclusion, both acute exercise and epinephrine infusion decreased plasma leptin to a similar extent, whereas there was no effect with rhIL-6 infusion. Acute exercise solely affected leptin plasma levels, as mRNA levels were unchanged. The exercise-induced decrease in circulating leptin was counteracted by CHO ingestion, suggesting a posttranscriptional regulatory mechanism of leptin involving substrate availability.
Adaptation of pulmonary O2 uptake kinetics and muscle deoxygenation at the onset of heavy-intensity exercise in young and older adults
Authors: DeLorey Darren S. , Kowalchuk John M. , Paterson Donald H.
Published: January 2005

The purpose was to examine the adaptation of pulmonary O2 uptake (V̇o2p) and deoxygenation of the vastus lateralis muscle at the onset of heavy-intensity, constant-load cycling exercise in young (Y; 24 ± 4 yr; mean ± SD; n = 5) and older (O; 68 ± 3 yr; n = 6) adults. Subjects performed repeated transitions on 4 separate days from 20 W to a work rate corresponding to heavy-intensity exercise. V̇o2p was measured breath by breath. The concentration changes in oxyhemoglobin, deoxyhemoglobin (HHb), and total hemoglobin/myoglobin were determined by near-infrared spectroscopy (Hamamatsu NIRO-300). V̇o2p data were filtered, interpolated to 1 s, and averaged to 5-s bins. HHb-near-infrared spectroscopy data were filtered and averaged to 5-s bins. A monoexponential model was used to fit V̇o2p [phase 2, time constant (τ) of V̇o2p] and HHb [following the time delay (TD) from exercise onset to the start of an increase in HHb] data. The τV̇o2p was slower ( P < 0.001) in O (49 ± 8 s) than Y (29 ± 4 s). The HHb TD was similar in O (8 ± 3 s) and Y (7 ± 1 s); however, the τ HHb following TD was faster ( P < 0.05) in O (8 ± 2 s) than Y (14 ± 2 s). The slower V̇o2p kinetics and faster muscle deoxygenation in O compared with Y during heavy-intensity exercise imply that the kinetics of muscle perfusion are slowed relatively more than those of V̇o2p in O. This suggests that the slowed V̇o2p kinetics in O may be a consequence of a slower adaptation of local muscle blood flow relative to that in Y.
Artifactual contractions triggered by field stimulation of cardiomyocytes
Authors: Bøkenes Janny , Sjaastad Ivar , Sejersted Ole M.
Published: January 2005

Although cell shortening in patch-clamped cells (current-clamp mode) is triggered by an ordinary action potential, the trigger mechanism in field-stimulated cells is not so obvious. The contraction characteristics of the two methods differ, and we, therefore, examined the triggering sequence in field-stimulated cells. Isolated rat cardiomyocytes were plated on laminin-coated coverslips that were mounted on an inverted light microscope and superfused with HEPES-Tyrode buffer (pH 7.4; 37°C). The cells were stimulated to contract either by a 0.5-ms current injection (CC cells) through high-resistance electrodes or a 5-ms biphasic field-stimulation pulse (FS cells), and drugs were added to block sarcolemmal proteins involved in excitation-contraction coupling. Time to peak contraction (TTP) was significantly longer in FS cells and was not affected by the polarity or the length of the stimulus pulse. Tetrodotoxin (TTX; 20 μM) blocked cell shortening in CC cells but not in FS cells. Ni2+ (5 mM) blocked cell shortening in FS cells, whereas KB-R7943 (KB; 5 μM) had no effect either on cell shortening or TTP. In FS cells, nifedipine (Nif; 100 μM) and Cd2+ (300 μM) reduced fractional shortening by 34 and 63%, respectively, but only Cd2+ affected TTP (reduced by 48%). A combination of Nif and KB reduced cell shortening by 50%, whereas a combination of Cd2+ and KB almost abolished cell shortening. We conclude that field stimulation per se prolongs TTP and that cell shortening in FS cells is not dependent on Na+ current but is triggered by a combination of L-type Ca2+ current and reverse mode Na+/Ca2+ exchange.
Effects of elastase on the mechanical and failure properties of engineered elastin-rich matrices
Authors: Black Lauren D. , Brewer Kelly K. , Morris Shirley M. , Schreiber Barbara M. , Toselli Paul , Nugent Matthew A. , Suki Bela , Stone Phillip J.
Published: January 2005

Pulmonary emphysema and vessel wall aneurysms are diseases characterized by elastolytic damage to elastin fibers that leads to mechanical failure. To model this, neonatal rat aortic smooth muscle cells were cultured, accumulating an extracellular matrix rich in elastin, and mechanical measurements were made before and during enzymatic digestion of elastin. Specifically, the cells in the cultures were killed with sodium azide, the cultures were lifted from the flask, cut into small strips, and fixed to a computer-controlled lever arm and a force transducer. The strips were subjected to a broadband displacement signal to study the dynamic mechanical properties of the samples. Also, quasi-static stress-strain curves were measured. The dynamic data were fit to a linear viscoelastic model to estimate the tissues' loss (G) and storage (H) modulus coefficients, which were evaluated before and during 30 min of elastase treatment, at which point a failure test was performed. G and H decreased significantly to 30% of their baseline values after 30 min. The failure stress of control samples was ∼15 times higher than that of the digested samples. Understanding the structure-function relationship of elastin networks and the effects of elastolytic injury on their mechanical properties can lead to the elucidation of the mechanism of elastin fiber failure and evaluation of possible treatments to enhance repair in diseases involving elastolytic injury.
Short-term high- vs. low-velocity isokinetic lengthening training results in greater hypertrophy of the elbow flexors in young men
Authors: Shepstone Tim N. , Tang Jason E. , Dallaire Stephane , Schuenke Mark D. , Staron Robert S. , Phillips Stuart M.
Published: January 2005

We performed two studies to determine the effect of a resistive training program comprised of fast vs. slow isokinetic lengthening contractions on muscle fiber hypertrophy. In study I, we investigated the effect of fast (3.66 rad/s; Fast) or slow (0.35 rad/s; Slow) isokinetic high-resistance muscle lengthening contractions on muscle fiber and whole muscle cross-sectional area (CSA) of the elbow flexors was investigated in young men. Twelve subjects (23.8 ± 2.4 yr; means ± SD) performed maximal resistive lengthening isokinetic exercise with both arms for 8 wk (3 days/wk), during which they trained one arm at a Fast velocity while the contralateral arm performed an equivalent number of contractions at a Slow velocity. Before (Pre) and after (Post) the training, percutaneous muscle biopsies were taken from the midbelly of the biceps brachii and analyzed for fiber type and CSA. Type I muscle fiber size increased Pre to Post ( P < 0.05) in both Fast and Slow arms. Type IIa and IIx muscle fiber CSA increased in both arms, but the increases were greater in the Fast- vs. the Slow-trained arm ( P < 0.05). Elbow flexor CSA increased in Fast and Slow arms, with the increase in the Fast arm showing a trend toward being greater ( P = 0.06). Maximum torque-generating capacity also increased to a greater degree ( P < 0.05) in the Fast arm, regardless of testing velocity. In study II, we attempted to provide some explanation of the greater hypertrophy observed in study I by examining an indicator of protein remodeling (Z-line streaming), which we hypothesized would be greater in the Fast condition. Nine men (21.7 ± 2.4 yr) performed an acute bout ( n = 30, 3 sets × 10 repetitions/set) of maximal lengthening contractions at Fast and Slow velocities used in the training study. Biopsies revealed that Fast lengthening contractions resulted in more (185 ± 1 7%; P < 0.01) Z-band streaming per millimeter squared muscle vs. the Slow arm. In conclusion, training using Fast (3.66 rad/s) lengthening contractions leads to greater hypertrophy and strength gains than Slow (0.35 rad/s) lengthening contractions. The greater hypertrophy seen in the Fast-trained arm ( study I) may be related to a greater amount of protein remodeling (Z-band streaming; study II).
Episodic hypoxia induces long-term facilitation of neural drive to tongue protrudor and retractor muscles
Authors: Fuller D. D.
Published: January 2005

Hypoxic episodes can evoke a prolonged augmentation of inspiratory motor output called long-term facilitation (LTF). Hypoglossal (XII) LTF has been assumed to represent increased tongue protrudor muscle activation and pharyngeal airway dilation. However, recent studies indicate that tongue protrudor and retractor muscles are coactivated during inspiration, a behavior that promotes upper airway patency by reducing airway compliance. These experiments tested the hypothesis that XII LTF is manifest as increased inspiratory drive to both tongue protrudor and retractor muscles. Neurograms were recorded in the medial XII nerve branch (XIIMED; contains tongue protrudor motor axons), the lateral XII nerve branch (XIILAT; contains tongue retractor motor axons), and the phrenic nerve in anesthetized, vagotomized, paralyzed, ventilated male rats. Strict isocapnia was maintained for 60 min after five 3-min hypoxic episodes (arterial Po2 = 35 ± 2 Torr) or sham treatment. Peak inspiratory burst amplitude showed a persistent increase in XIIMED, XIILAT, and phrenic nerves during the hour after episodic hypoxia ( P < 0.05 vs. sham). This effect was present regardless of the quantification method (e.g., % baseline vs. percent maximum); however, comparisons of the relative magnitude of LTF between neurograms (e.g., XIIMED vs. XIILAT) varied with the normalization procedure. There was no persistent effect of episodic hypoxia on inspiratory burst frequency ( P > 0.05 vs. sham). These data demonstrate that episodic hypoxia induces LTF of inspiratory drive to both tongue protrudor and retractor muscles and underscore the potential contribution of tongue muscle coactivation to regulation of upper airway patency.
Ultrasound: a reproducible method to measure conduit vein compliance
Authors: de Groot Patricia C. E. , Bleeker Michiel W. P. , Hopman Maria T. E.
Published: January 2005

Classical venous occlusion plethysmography (VOP) of the leg, often used to assess venous compliance, measures properties of the whole calf, including volume changes at the arterial side and the interstitial fluid accumulation that occurs as a result of the enhanced capillary pressure during venous occlusion. We present an ultrasound technique to measure the compliance of one major conduit vein in the leg. Ultrasound measurements of the popliteal vein were compared with classical VOP measurements, which were performed simultaneously in one subject. Six healthy individuals were measured on three occasions to assess short- and long-term reproducibility of the measurements. Six motor complete spinal cord-injured (SCI) individuals were included to compare venous compliance in subjects with known pathological changes of the venous system with controls. The ultrasound and VOP measurements of venous compliance correlated significantly ( r2= 0.39, P = 0.001). Ultrasound provides reproducible measurements with short- and long-term coefficients of variation ranging from 10 to 15% for popliteal vein compliance and from 2 to 9% for absolute diameters at the different venous pressure steps. In addition, by using ultrasound, we were able to detect an 80% reduction in the compliance of the popliteal vein in SCI individuals compared with controls ( P < 0.01). In conclusion, ultrasound is a suitable and reproducible method to measure conduit vein compliance and provides the possibility to specifically assess compliance of one vein instead of the whole calf.
Mechanical deformation of neutrophils into narrow channels induces pseudopod projection and changes in biomechanical properties
Authors: Yap Belinda , Kamm Roger D.
Published: January 2005

Neutrophils traversing the pulmonary microcirculation are subjected to mechanical stimulation during their deformation into narrow capillaries. To better understand the time-dependant changes caused by this mechanical stimulus, neutrophils were caused to flow into a microchannel, which allowed simultaneous visualization of cell morphology and passive rheological measurement by tracking the Brownian motion of endogenous granules. Above a threshold stimulus, mechanical deformation resulted in neutrophil activation with pseudopod projection. The activation time was inversely correlated to the rate of mechanical deformation experienced by the neutrophils. A reduction in shear moduli was observed within seconds after the onset of the mechanical stimulus, suggesting a sudden disruption of the neutrophil cytoskeleton when subjected to mechanical deformation. However, the magnitude of the reduction in moduli was independent of the degree of deformation. Recovery to nearly the initial values of viscoelastic moduli occurred within 1 min. These observations confirm that mechanical deformation of neutrophils, similar to conditions encountered in the pulmonary capillaries, is not a passive event; rather, it is capable of activating the neutrophils and enhancing their migratory tendencies.
Empirical Bayes methods for disease mapping
Authors: Leyland Alastair H , Davies Carolyn A
Published: January 2005

This paper reviews empirical Bayes methods for disease mapping. A distinction is made between spatial models (which take into account the geographical distribution of disease) and nonspatial models. Several estimators are presented, and methods of estimation are described. Empirical Bayes methods are compared with full Bayes methods, and we argue that both have their place.
Towards joint disease mapping
Authors: Held Leonhard , Natário Isabel , Fenton Sarah Elaine , Rue Håvard , Becker Nikolaus
Published: January 2005

This article discusses and extends statistical models to jointly analyse the spatial variation of rates of several diseases with common risk factors. We start with a review of methods for separate analyses of diseases, then move to ecological regression approaches, where the rates from one of the diseases enter as surrogate covariates for exposure. Finally, we propose a general framework for jointly modelling the variation of two or more diseases, some of which share latent spatial fields, but with possibly different risk gradients. In our application, we consider mortality data on oral, oesophagus, larynx and lung cancers for males in Germany, which all share smoking as a common risk factor. Furthermore, the first three cancers are also known to be related to excessive alcohol consumption. An empirical comparison of the different models based on a formal model criterion as well as on the posterior precision of the relative risk estimates strongly suggests that the joint modelling approach is a useful and valuable extension over individual analyses.
Pitfalls in Teaching Judgment Heuristics
Authors: Shepperd James A. , Koch Erika J.
Published: January 2005

Demonstrations of judgment heuristics typically focus on how heuristics can lead to poor judgments. However, exclusive focus on the negative consequences of heuristics can prove problematic. We illustrate the problem with the representativeness heuristic and present a study (N = 45) that examined how examples influence understanding of the representativeness heuristic. Students received a definition of the heuristic, a definition plus examples of the heuristic leading to poor judgment, or a definition plus examples of the heuristic leading to both good and poor judgments. The results suggest that providing examples of heuristics leading only to poor judgments undermined comprehension.
Integrating Online Instruction in a College Classroom to Improve Cost Effectiveness
Authors: Buzhardt Jay , Semb George
Published: January 2005

We compared online study guides to pen-and-paper study guides in terms of academic performance, the amount of time instructors spent grading study guides, and student preferences. Students in 3 sections of a child psychology course used online study guides (n = 46), and students in 3 other sections used pen-and-paper study guides (n = 64). Instructors spent 14.3 hr during the semester grading the pen-and-paper study guides and no time grading the online study guides. Students who used the online study guides reported higher satisfaction than the students who used pen-and-paper study guides. Our results suggest that integrating online study guides saved labor costs and increased student satisfaction while maintaining student performance.
Sniffing Out Efficacy: Sniffy Lite, a Virtual Animal Lab
Authors: Venneman Sandy S. , Knowles Laura Ruth
Published: January 2005

We investigated the benefits of using a virtual laboratory, Sniffy Lite CD—ROM (Alloway, Wilson, Graham, & Krames, 2000), as a supplemental teaching tool to present schedules of reinforcement in operant conditioning. Our results suggest that using the virtual laboratory significantly enhanced understanding. Students who used the virtual laboratory earned a mean score of 76% on the measure of comprehension, whereas control group participants who studied an equivalent period of time as the virtual laboratory assignments earned 63%, as did those who received no intervention. Increased student comprehension supports the efficacy of this low-cost learning tool.
Integration of Computer Technology into an Introductory-Level Neuroscience Laboratory
Authors: Evert Denise L. , Goodwin Gregory , Stavnezer Amy Jo
Published: January 2005

We describe 3 computer-based neuroscience laboratories. In the first 2 labs, we used commercially available interactive software to enhance the study of functional and comparative neuroanatomy and neurophysiology. In the remaining lab, we used customized software and hardware in 2 psychophysiological experiments. With the use of the computer-based technology, we have successfully met our pedagogical objectives while minimizing operating costs and maintaining flexibility of the lab space. Student response to the lab experience was overwhelmingly positive.
Lessons in Teaching Hope: An Interview with C. R. Snyder
Authors: Ritschel Lorie
Published: January 2005

Lorie Ritschel received her undergraduate degrees in French and psychology from the University of Georgia in 1999. In 2002, she received her MA in clinical psychology from the University of Kansas, where she currently is pursuing a doctoral degree. Lorie is the clinic systems coordinator and a therapist at the University of Kansas Psychological Clinic. She also has taught undergraduate courses in abnormal psychology. Lorie's research examines the roles of mindfulness and hope in psychotherapy.

C. R. (Rick) Snyder received his PhD in clinical psychology from Vanderbilt University in 1971. His entire career has been at the Department of Psychology, University of Kansas, Lawrence, where he was promoted to full professor in 1980. Director of the Kansas Clinical Program from 1974 to 2001, he became the Wright Distinguished Professor of Clinical Psychology in 2002. Editor of the Journal of Social and Clinical Psychology from 1987 to 2001, he presently edits the Oxford University Press Book Series in Human Motivation. With longstanding interests in human strengths, his research has been at the interface of clinical, social, personality, and health psychology. His theories, in chronological order, have entailed how people react to personal feedback, the need for uniqueness, the ubiquitous drive to excuse transgressions, and, most recently, the hope motive. Recognized with fellow status in various psychological societies, Snyder also has received awards for his teaching and research.
Advice on Advising: Improving a Comprehensive University's Program
Authors: Johnson Emily J. , Morgan Betsy L.
Published: January 2005

This article reports on a systematic revision of our psychology department's advising system. Assessment results indicate a change from 38% to 70% of our seniors endorsing advising as “good” or “high quality” from 1993 to 2003. We present the individual components of our advising plan and recommendations for improving advising.