bluuebunny/crossref_metadata_2025_split huggingface dataset:
A novel method for predicting chronic nickel bioavailability and toxicity toDaphnia magnain artificial and natural waters
Authors: Deleebeeck Nele M. E , De Schamphelaere Karel A. C , Janssen Colin R 
Published: April 2008

AbstractIn the present study, the individual effects of Ca, Mg, and pH on the chronic toxicity of Ni to Daphnia magna were examined in a series of 21-d reproduction tests in synthetic test solutions. Based on the linear increase of 21-d median effective concentrations expressed as Ni2+ activity (21-d EC50Ni2+) with increasing activities of Ca2+ and Mg2+, the effects of Ca and Mg were modeled according to single-site competition with log KCaBL = 3.53 and log KMgBL = 3.57 (BL = biotic ligand). Because the increase of 21-d EC50Ni2+ with increasing H+ activity was nonlinear, the effect of pH could not be described appropriately by singlesite competition between Ni2+ and H+. Instead, the effect of pH was modeled based on an empirical linear relationship between pH and 21-d EC50pNi2+* (equal to —log [21-d EC50Ni2+ corrected for the presence of Ca and Mg]) and was superimposed on the effects of Ca and Mg. For all test solutions used for model development, the developed model predicted the observed 21-d EC50 expressed as dissolved Ni concentration with an error of less than a factor of two. The importance of dissolved organic carbon in protecting D. magna against chronic Ni toxicity was demonstrated by conducting 21-d reproduction tests in a series of Ni-spiked natural waters. Because the model tended to systematically overestimate chronic Ni toxicity in these natural waters, it was further optimized to yield more accurate predictions in natural waters. Although some room still exists for improvement, the developed model is, to our knowledge, the first to present a useful tool for assessing the risk of Ni to aquatic invertebrates.
GRAVITY TECTONICS AND PLATE MOTIONS
Authors: Rangin Claude , Le Pichon Xavier , Martinez-Reyes Juventino , Aranda-Garcia Mario 
Published: April 2008

Abstract
This is an introduction to the series of papers presented in this volume that concerns the Cenozoic tectonics of the western margin of the Gulf of Mexico, from Texas in the north to the Veracruz area into the south. These combined offshore-onshore structural studies investigate the links between surperficial gravity slidings and deep crustal flow within the complex geodynamic framework of Mexico, located at the junction between the North America, Carribean and Pacific plates (including the earlier Farallon plate).
Cenozoic crustal deformation of the offshore Burgos basin region (NE Gulf of Mexico). A new interpretation of deep penetration multichannel seismic reflection lines
Authors: Le Roy Charlotte , Rangin Claude 
Published: April 2008

Abstract
Along northeastern Mexico close to the Texas-Mexico border, the Burgos basin and its extension offshore was developed and deformed from the Paleocene up to Present time. This is a key triple junction between the sub meridian dextral transtensive coastal plain of the Gulf of Mexico extending far to the south in Mexico, the NE Corsair fault zone offshore and the sinistral Rio Bravo fault zone, a reactivated segment of the Texas lineament.
Offshore NE Mexico, in the main study area covered by available seismic profiles, we have evidenced below the main well known gravitational décollement level (5 to 7 s twtt → 6 to 8 km) a Cenozoic deep-rooted deformation outlined by a N010° W trending deep-seated reverse fault zone and crustal folding down to the Moho (11 s twtt → ~ 20 km).
Based on extensive offshore 2D industrial multi-channel seismic reflection surveys, deep exploration wells and gravimetric data, we focus our study on the deep crustal fabric and its effects on the gravitational tectonics in the upper sedimentary layers: submeridian crustal transtensional normal faults and open folding of the identified Mesozoic basement were interpreted as Cenozoic buckling of the crust during a major phase of oblique crustal extension. This deformation has probably enhanced gravity sliding along N030° growth-faults related to salt withdrawal and halokinesis in the offshore Burgos basin. We have tentatively made a link between this crustal deformation episode and the Neogene tectonic inversion of the Laramide foredeep basin of the Sierra Madre Oriental. The latter is still affected by crustal strike slip faulting associated with basaltic volcanism observed into the gulf coastal plain.
This study favours a dominant crustal Cenozoic tectonic activity along the gulf margin without any clear evidence of Mesozoic tectonic reactivation. We propose that the large gravity collapse of the gulf margin was triggered by subsequent crustal deformation.
The southern Mexico block: main boundaries and new estimation for its Quaternary motion
Authors: Andreani Louis , Le Pichon Xavier , Rangin Claude , Martínez-Reyes Juventino 
Published: April 2008

AbstractNumerous studies, mainly based on structural and paleomagnetic data, consider southern Mexico as a crustal block (southern Mexico block, SMB) uncoupled from the North American plate with a southeast motion with respect to North America, accommodated by extension through the central Trans-Mexican volcanic belt (TMVB). On the other hand, the accommodation of this motion on the southeastward boundary, especially at the Cocos–Caribbean–North American triple junction, is still debated.The boundary between the SMB and the North American plate is constituted by three connected zones of deformation: (1) left-lateral transtension across the central TMVB, (2) left-lateral strike-slip faulting along the eastern TMVB and Veracruz area and (3) reverse and left-lateral strike-slip faulting in the Chiapas area. We show that these three active deformation zones accommodate a counterclockwise rotation of the SMB with respect to the North American plate. We specially discuss the Quaternary motion of the SMB with respect to the surrounding plates near the Cocos–Caribbean–North American triple junction. The model we propose predicts a Quaternary counterclockwise rotation of 0.45°/Ma with a pole located at 24.2°N and 91.8°W.Finally we discuss the geodynamic implications of this counterclockwise rotation. The southern Mexico block motion is generally assumed to be the result of slip partitioning at the trench. However the obliquity of the subduction is too small to explain slip partitioning. The motion could be facilitated by the high thermal gradient and gravitational collapse that affects central Mexico and/or by partial coupling with the eastward motion of the Caribbean plate.
The Mean Filtration Pressure of Leukocyte Suspensions and Its Relation to the Passage of Leukocytes through Nuclepore Filters and Capillary Networks
Authors: EPPIHIMER M. J. , LIPOWSKY H. H. 
Published: April 2008

ABSTRACTObjective: To quantitatively evaluate the deformability of bulk suspensions of leukocytes (WBCs), account for the variance of individual cell mechanical properties, and deduce the potential for WBC entrapment within the capillary network in response to alterations in cell properties.Methods: The transient washout of WBCs initially trapped under low perfusion pressure in 5‐μm pores of Nuclepore filters was analyzed for a 0.2‐ml bolus of WBCs (derived from hamsters) with equal numbers of filter pores and cells, to characterize the statistical distribution of pressures, pyield, required to dislodge the cells. Contributions of the variance in WBC diameter, pore diameter, and cremaster muscle capillary diameter to pyield were estimated with a WBC cortical shell model and an analysis of the probability function of the ratio of WBC to pore diameter, Λ.Results: For normal WBCs, pyield exhibited a log‐normal distribution with mean ((pyield)) of 0.59 cmH2O. Incubation of cells in cytochalasin‐B reduced (pyield) almost 50%, whereas phorbol myristate acetate increased (pyield) twofold. Incubation in N‐formyl‐methiolnyl‐leucyl‐phenylalanine had no significant effect on (pyield), as polymorphonuclear cells became permanently trapped in the filter. The fluorescent dyes acridine orange, acridine red, and tetramethylrhodamine isothiocyanate increased (pyield) as much as 10‐fold, whereas steady‐flow filtration methods showed no alteration. Analysis of the distribution of Λ revealed that due to their smaller pore diameters, in vitro filtration methods may overestimate in vivo values of (pyield) by almost twofold.Conclusions: The transient filtration of WBC suspensions appears to be much more sensitive to subtle alterations in WBC deformability than steady‐flow methods and may provide greater insight into the determinants of capillary perfusion. Estimates of (pyield) are comparable to those obtained with micropipettes and permit analysis of substantially greater numbers of cells within a sample. Fluorescence labeling techniques should be used with caution, as they may dramatically alter cell properties to an extent undetectable by direct in vivo observations.
An Adenosine Agonist Increases Blood Flow and Density of Capillary Branches in the Optic Tectum of Xenopus laevis Tadpoles
Authors: Jen Shyian Charcha , Rovainen Carl M. 
Published: April 2008

ABSTRACT Objective: To test the hypothesis that adenosine can increase capillary densities in developing brain tissue. Methods: Transparent tadpoles of albino Xenopus laevis were exposed to adenosine agonists, mainly 5′‐N‐ethylcarboxamidoadenosine (NECA), and to antagonists, mainly 8‐phenyltheophylline (8PT) in aquarium water. After 2 weeks in drugs, networks of blood vessels on the dorsal surface of the optic tectum were scanned in vivo by videomicroscopy. Densities of surface capillaries and venules, of deep branches, and of deep perfused capillaries were calculated. Results: NECA initially dilated brain blood vessels and chronically increased blood flow by a simple subjective index. 8PT diminished diameters and prevented the subjective flow increase. Chronic 3 μM NECA significantly increased densities of total deep branches from pial vessels into the tectum. Conclusions: In an in vivo amphibian assay, NECA dilated brain capillaries and venules and increased their flow and density. Adenosine was present chemically and increased during metabolic stress. These results are consistent with adenosine as a metabolic signal for growth of blood vessels during brain development. In addition, it appeared that short‐term dilation and flow increase in tectal capillaries in acute NECA was followed over a period of weeks in chronic NECA by vascular remodeling and return of diameters to normal.
Fluid Flow Modulates Vascular Endothelial Cytosolic Calcium Responses to Adenine Nucleotides
Authors: Shen Jian , Luscinskas Francis W. , Gimbrone Michael A , Dewey C. Forbes 
Published: April 2008

ABSTRACT Objective: To determine whether fluid flow influences the action of soluble vasoactive agonists on vascular endothelium. Methods: Confluent monolayers of bovine aortic endothelial cells (BAEC) were cultured on glass coverslips, prelabeled with the Ca2+‐sensitive dye fura‐2, and placed in a parallel‐plate flow chamber designed to generate defined laminar fluid flow. Cytosolic free Ca2+ concentration ([Ca2+];) in individual BAEC was monitored during perfusion with medium containing adenine nucleotide under defined flow conditions. Results: Continuous perfusion with ATP (0.3–3.0 μM) or ADP (0.1–1.0 μM) evoked repetitive oscillations in [Ca2+]; in individual BAEC. The frequency of the [Ca2+]; oscillations was dependent on both nucleotide concentration and levels of applied shear stress; at constant bulk concentration of nucleotide, the frequency increased with shear stress. Stopping flow in the continuous presence of agonists immediately extinguished the oscillatory response. Elimination of extracellular Ca2+ did not inhibit the [Ca2+]; oscillations. In the presence of nonhydrolyzable nucleotide analog, ATPγS or ADPβS, application of flow resulted in similar shear‐dependent [Ca2+]; oscillations, suggesting that flow modulation of the [Ca2+]; response was not simply due to depletion of ATP or ADP in the vicinity of BAEC monolayers as a result of hydrolysis of nucleotides by ectonucleotidases. Conclusions: These findings suggest that local hemodynamic conditions may modulate the action of vasoactive agents on the vascular endothelium in vivo.
Acidic Fibroblast Factor Induction of Cyclooxygenase II in Rabbit Cardiac Muscle Microvessel Endothelial Cells: Mediation by Protein Kinase C
Authors: Moatter Tariq , Gerritsen Mary E. 
Published: April 2008

ABSTRACT Objective: To determine if the novel cyclooxygenase, COX II, was induced by acidic fibroblast growth factor (aFGF) in rabbit cardiac muscle microvessel (RCME) endothelial cells and to determine the role of protein kinase C (PKC) activation in the mediation of the aFGF induction of COX activity. Methods: Cultured RCME cells were treated with aFGF (200 ng/ml). Induction of COX II activity was assessed by determination of COX activity (PGE2 production), by immunoprecipitation of metabolically labeled COX II, and by Northern analyses. The role of PKC was assessed using phorbol myristate acetate and PKC inhibitors and by determination of PKC activity in cytosol and membrane fractions of RCME cells treated with aFGF and phorbol myristate acetate. Results: aFGF selectively induced COX II protein and mRNA. Protein kinase C activation was implicated in the transduction of the effects of aFGF for the following reasons: (1) phorbol myristate acetate (PMA), a direct activator of protein kinase C, was a potent inducer of COX II mRNA, COX activity and synthesis of COX II protein. (2) H‐7, an inhibitor of PKC, but not the inactive control, HA‐1004, blocked aFGF induction of COX II mRNA, COX II protein synthesis, and COX activity. Two additional inhibitors of PKC, calphostin C and staurosporine, also inhibited aFGF induction of COX activity. (3) Downregulation of PKC by overnight incubation with 1 μM PMA blocked subsequent induction of COX II protein synthesis by aFGF. (4) aFGF treatment of RCME cells resulted in the translocation of PKC activity from the cytosol to the membrane fraction. However, aFGF, at concentrations that elicited COX II, neither induced Ca2+ mobilization from intracellular stores nor increased the accumulation of inositol phosphates. Conclusion: aFGF induces COX II in RCME and this response in mediated, at least in part, by protein kinase C activation. However, aFGF mediated activation of PKC activation must stimulate this kinase through a pathway of signal transduction distinct from inositol phospholipid accumulation or elevation of intracellular Ca2+.
Desensitization of 5HT2 Receptors by Protein Kinase C Activation in Distal Pulmonary Vascular Smooth Muscle Cells in Culture
Authors: Weng Weili , Reynolds Ian J. , Jani Jitesh P. , Blaskovich Michelle , Sebti Said M. , Davies Paul , Pitt Bruce R. 
Published: April 2008

ABSTRACTObjective: Although acute and chronic roles of microvascular smooth muscle cells as effectors of pulmonary vascular resistance and remodeling are well appreciated, relatively little is known regarding the direct effects of neurohumoral agents on these cells. We recently reported that microvascular smooth muscle cells isolated from distal rat lung (RPC) express mRNA and binding sites for 5HT2 receptors. The objective of the current study was to determine if protein kinase C (PKC) affected 5HT‐induced changes in intracellular calcium and phosphoinositide metabolism in RPC.Methods: 5HT‐induced changes in intracellular calcium ([Ca2+]i) in single RPC were determined microspectrofluorometrically using the calcium‐sensitive dye, Fura‐2.Results: Phorbol 12‐myristate 13‐acetate (PMA: 100 nM) caused a rapid desensitization of 5HT‐induced increases in [Ca2+]i. Staurosporine, a putative PKC inhibitor, abolished the PMA‐induced desensitization. Downregulation of PKC with prolonged (24 hr) PMA exposure also abolished subsequent PMA‐induced desensitization of 5HT response. Neither short‐ nor long‐term exposure of RPC to PMA affected binding of [125I]LSD. Activation of PKC by PMA was associated, however, with complete inhibition of 5HT‐induced increases in intracellular inositol monophosphate.Conclusions: These data are consistent with PKC causing desensitization of 5HT2 receptors by affecting elements of signal transduction and uncoupling receptor‐G protein complex from phospholipase C in RPC.
Cellular Aspects of Transvascular Exchange: A 40‐Year Perspective
Authors: Renkin Eugene M. 
Published: April 2008

ABSTRACTStudy of the microcirculation began with microscopic anatomy in the 17th century, but it was not until the mid‐19th century that the concept of microcirculatory exchange was developed, in association with the great expansion in knowledge of physical chemistry and cell biology. In the first half of the 20th century, the roles of diffusion and osmosis (ultrafiltration) were put on a quantitative foundation and the physiological basis for regulation of the microcirculation was established. During the past 40 years, our understanding of transvascular exchange has been deepened and widened through two major developments: 1) the application of electron microscopy to the study of microvascular structure and 2) the use of sophisticated physical and mathematical models of passive transport processes to analyze and interpret experimental data. In the past few years, the focus of microvascular research has been returning to cell biology and the role of endothelial cells in controlling transvascular exchange. The 21st century holds promise of many exciting new developments.
Ischemia/Reperfusion‐Induced Granulocyte Influx is a Multistep Process Mediated by Mast Cells
Authors: Kanwar Samina , Kubes Paul 
Published: April 2008

ABSTRACTObjective: The influx of polymorphonuclear leukocytes (PMNs) that occurs at the onset of reperfusion of postischemic tissue is a multistep mechanism that includes initial rolling of PMNs, a progressive reduction in PMN rolling velocity, and ultimately PMN adhesion and emigration. In this study we assessed whether mast cells play a role in reperfusion‐induced PMN recruitment with emphasis on PMN rolling, adhesion, and emigration.Methods: Cat small intestinal venules were visualized using intravital microscopy during control, 60 min of ischemia (intestinal blood flow 20% of control), and 60 min of reperfusion in untreated and cromolyn‐ (mast cell stabilizer) pretreated animals.Results: Between 1 and 5 min of reperfusion, there was a very dramatic rise in PMN rolling which persisted for the next 60 min. In cromolyn‐pretreated animals, the flux of rolling PMNs increased in the very early (5 min) reperfusion period, but by 10 min the number of rolling leukocytes was significantly reduced, an event that persisted for the next 60 min. PMNs rolled at a velocity of 40% of control values for the first 10 min of reperfusion without a change in hemodynamic values but returned toward control values by 60 min of reperfusion. An identical velocity profile was observed for the cromolyn‐treated animals. In untreated animals, PMN adhesion and emigration was significantly increased throughout the reperfusion period, whereas the cromolyn‐pretreated animals had reduced adhesion (60 min of reperfusion) and a reduced rate of emigration throughout the reperfusion period.Conclusions: Interstitial mast cells contribute significantly to the multistep recruitment (rolling, adhesion, and emigration) of PMNs from blood to postischemic tissues and raise the possibility that antiallergy agents such as cromolyn may be a useful form of therapy in the postischemic intestine.
The Influence of Flow and Hematocrit on the Laser Doppler Flux Signal from the Surface of the Perfused Pig Liver
Authors: WHEATLEY ANTHONY M. , HICKMAN ROSEMARY 
Published: April 2008

ABSTRACTObjective: We tested the hypothesis that the measurement volume of the laser Doppler flowmeter (LDF) is too small to provide reliable quantitative estimates of total liver blood flow of large mammals, such as the pig.Methods: In a perfused pig liver, the influence of changing (i) hepatic arterial (HA) and portal venous flows individually (n = 9), (ii) HA flow at fixed portal venous flow (50%, 70%, and 100% expected total liver blood flow), and (iii) hematocrit (0–30%) at fixed total liver blood flow on LDF flux was tested (n = 8).Results: Linearity of LDF with hepatic arterial flow and portal venous flow was confirmed; however, the slope of the regression lines was higher for hepatic artery [1.92 ± 0.60 (SD)] than portal vein perfused livers (0.66 ± 0.34; P < 0.001). With portal venous flow at 50% and 70% total liver blood flow, changing hepatic arterial flow produced linear LDF versus flow responses, but at 100% total liver blood flow, linearity was achieved in only 6/9 livers. The coefficient of variation for the slopes of regression lines was always > 30%. At constant total liver blood flow (100 ml/min per 100 g), LDF response decreased linearly by a factor of about 2 on changing the hematocrit from 30% to 5% and markedly fell as the hematocrit was further decreased to zero.Conclusions: These results suggest that (i) the LDF flux signal from the liver surface provides a poor measure of hepatic microcirculatory blood flow during changes in total liver blood flow as the LDF responds with about three times greater sensitivity to changes in hepatic arterial than in portal venous flow, and (ii) when hematocrit is falling, LDF may underestimate hepatic perfusion to a significant extent. In addition, due to high measurement variability, the LDF flux signal cannot be quantified in absolute perfusion units.
Nitric Oxide Mediates C5a‐Induced Vasodilation in the Small Intestine
Authors: LUO HONG Y. , WEAD WILLIAM B. , YANG SAI , WILSON MARK A. , Harris Patrick D. 
Published: April 2008

ABSTRACTObjective: This study was designed to investigate the microvascular responses of the small intestine to complement C5a and to define the role of nitric oxide in the C5a‐induced response.Methods: Male Sprague–Dawley rats were anesthetized with pentobarbital, and a loop of small intestine was exteriorized and suffused with Krebs solution. The diameters of large and small arterioles of the small intestinal wall were measured with in vivo videomicroscopy following the application of experimental mediators. Four 1‐hr C5a dose‐response trials were performed (10−14 M, 10−12 M, 10−10 M, and 10−8 M). Then, we completed acetylcholine dose‐response curves with and without Nω‐nitro‐L‐arginine (N‐Arg) to document the adequacy of nitric oxide synthase inhibition. The microvascular response to the topical application of C5a (10−12 M) was recorded in the presence of 2 × 10−4 M N‐Arg. Additionally, experiments of C5a‐induced response with N‐Arg were repeated in the presence of L‐arginine (L‐Arg; the precursor of nitric oxide synthesis) or with systemic administration of superoxide dismutase (SOD).Results: (1) C5a induces a dose‐dependent vasodilation in the small intestine, and the maximal vasodilation occurs in A3 arterioles at C5a concentration of 10−12 M; (2) N‐Arg inhibits the Ach‐induced vasodilation in the rat small intestine; and (3) L‐Arg or SOD partially reverses the inhibitory effect of N‐Arg.Conclusions: Nitric oxide mediates the C5a‐induced vasodilation in small intestinal microvessels. Superoxide is, at least partially, responsible for the vasoconstrictor response to C5a in the presence of N‐Arg.