bluuebunny/crossref_metadata_2025 huggingface dataset:
PRECISE VORONOI CELL EXTRACTION OF FREE-FORM PLANAR PIECEWISE C1-CONTINUOUS CLOSED RATIONAL CURVES
Authors: HANNIEL I. , RAMANATHAN M. , ELBER G. , KIM M. -S.
Published: November 2007

We present an algorithm for generating Voronoi cells for a set of planar piecewise C1-continuous closed rational curves, which is precise up to machine precision. The algorithm starts with the symbolically generated bisectors for pairs of C1-continuous curve segments (C(t),Ci(r)). The bisectors are represented implicitly in the tr-parameter space. Then, they are properly trimmed after being split into monotone pieces. The trimming procedure uses the orientation of the original curves as well as their curvature fields, resulting in a set of trimmed-bisector segments represented as implicit curves in a parameter space.

A lower-envelope algorithm is then used in the parameter space of the curve whose Voronoi cell is sought. The lower envelope represents the exact boundary of the Voronoi cell. The algorithm also supports piecewise C1-continuous curves and generates the Voronoi cell of such input curves using additional point/curve bisector segments.
Electrochemical Formation of A Novel Conducting Poylmer Membrane on CPE from Aqueous Solution Containing Pb(II) Acetate
Authors: Avila-Jiménez Miguel , Ramírez-Silva María Teresa , Rosquete Pina Giselle , Palomar-Pardavé Manuel , Romero-Romo Mario
Published: November 2007

A membrane was synthesized to prepare a selective electrode to Pb(II) based on a complex Pb (II)-acetate: the effects of experimental conditions on the synthesis were analyzed, like that of the potential range used and of the lead and acetates concentration in solution were investigated during the formation process of the surface film. The lead concentration had a direct effect on the current's response. The process of electrochemical formation of the film was found to be directly dependent on the lead-acetates species predominating in solution.
Autonomic effects on QT-RR interval dynamics after exercise
Authors: Sundaram Sri , Carnethon Mercedes , Polito Karla , Kadish Alan H. , Goldberger Jeffrey J.
Published: November 2007

This study was designed to assess autonomic effects on the QT interval during recovery from exercise. Exercise is associated with an acute increased risk of sudden cardiac death. Evidence of impaired parasympathetic activity, such as low heart rate variability and heart rate recovery, and an increased QT interval are also associated with increased mortality. However, there is no clear pathophysiological link among these findings. Bicycle exercise testing was performed serially in 33 healthy volunteers (19 men; ages, 54 ± 7 yr) under four conditions: 1) baseline, 2) β-adrenergic blockade-intravenous propranolol (0.2 mg/kg) administered during exercise, 3) parasympathetic blockade-intravenous atropine (0.04 mg/kg) administered during exercise, and 4) double blockade with propranolol and atropine. ECGs were obtained every minute in recovery for 10 min and then at the 15th and 20th min, from which the QT and RR intervals were measured. Linear regression analyses were used to assess the individual QT-RR relationships for each subject for each condition. Relative to baseline, the QT-RR relationship with parasympathetic blockade was shifted to the left and had a steeper slope. In contrast, the QT-RR relationship with β-adrenergic blockade was shifted to the right and had a less steep slope. The baseline and double-blockade QT-RR relationships were in the middle and essentially superimposable. There was a negative relationship between QT-RR slope and heart rate or RR interval recoveries, but it was significant only for the 1- and 2-min RR interval recoveries with low R2 values of 0.124 and 0.114. The main parasympathetic effect in the postexercise recovery period is to counteract the sympathetically mediated QT prolongation. These data support the concept that parasympathetic tone may provide a natural antiarrhythmic effect during this time.
Cardiovascular response to acute hypoxemia induced by prolonged breath holding in air
Authors: Pingitore Alessandro , Gemignani Angelo , Menicucci Danilo , Di Bella Gianluca , De Marchi Daniele , Passera Mirko , Bedini Remo , Ghelarducci Brunello , L'Abbate Antonio
Published: November 2007

Prolonged breath hold (BH) represents a valid model for studying the cardiac adaptation to acute hypoxemia in humans. Cardiac magnetic resonance (CMR) allows a three-dimensional, high-resolution, noninvasive, and nonionizing anatomical and functional evaluation of the heart. The aim of the study was to assess the adaptation of the cardiovascular system to prolonged BH in air. Ten male volunteer diving athletes (age 30 ± 6 yr) were studied during maximal BH duration with CMR. Four epochs were studied: I, rest; II and III, intermediate BH; and IV, peak BH. Oxygen saturation (So2), heart rate (HR), blood pressure (BP), systemic vascular resistance (VR), end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), cardiac output (CO), ejection fraction (EF), maximal elastance index (EL), systolic wall thickening (SWT), and end-systolic wall stress (ESWS) of the left ventricle (LV) were measured in all four BH epochs. Average BH duration was 3.7 ± 0.3 min. So2 was reduced ( I: 97 ± 0.2%, range 96–98%, vs. IV: 84 ± 2.0%, range 76–92%; P < 0.00001). BP, EDV, ESV, SV, CO, and ESWS linearly increased from epochs I to IV, whereas EF, EL, and SWT showed an opposite behavior, decreasing from resting to epoch IV (all trends are P < 0.01). During prolonged BH in air, a marked enlargement of the LV chamber occurs in healthy diving athletes. This response to acute hypoxemia allows SV,CO, and arterial pressure to be maintained despite the severe reduction in LV contractile function.
Effects of myocardial constraint on the passive mechanical behaviors of the coronary vessel wall
Authors: Liu Yi , Zhang Wei , Kassab Ghassan S.
Published: November 2007

The large epicardial coronary arteries and veins span the surface of the heart and gradually penetrate into the myocardium. It has recently been shown that remodeling of the epicardial veins in response to pressure overload strongly depends on the degree of myocardial support. The nontethered regions of the vessel wall show significant intimal hyperplasia compared with the tethered regions. Our hypothesis is that such circumferentially nonuniform structural adaptation in the vessel wall is due to nonuniform wall stress and strain. Transmural stress and strain are significantly influenced by the support of the surrounding myocardial tissue, which significantly limits distension of the vessel. In this finite-element study, we modeled the nonuniform support by embedding the left anterior descending artery into the myocardium to different depths and analyzed deformation and strain in the vessel wall. Circumferential wall strain was much higher in the untethered than tethered region at physiological pressure. On the basis of the hypothesis that elevated wall strain is the stimulus for remodeling, the simulation results suggest that large epicardial coronary vessels have a greater tendency to become thicker in the absence of myocardial constraint. This study provides a mechanical basis for understanding the local growth and remodeling of vessels subjected to various degrees of surrounding tissue.
Postconditioning fails to improve no reflow or alter infarct size in an open-chest rabbit model of myocardial ischemia-reperfusion
Authors: Hale Sharon L. , Mehra Ankur , Leeka Justin , Kloner Robert A.
Published: November 2007

Postconditioning (PoC) with brief intermittent ischemia after myocardial reperfusion has been shown to lessen some elements of postischemic injury including arrhythmias and, in some studies, the size of myocardial infarction. We hypothesized that PoC could improve reflow to the risk zone after reperfusion. Anesthetized, open-chest rabbits were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion. In protocol 1, rabbits were randomly assigned to the control group ( n = 10, no further intervention after reperfusion) or to the PoC group, which consisted of four cycles of 30-s reocclusions with 30 s of reperfusion in between starting at 30 s after the initial reperfusion (4 × 30/30, n = 10). In protocol 2, rabbits were assigned to the control group ( n = 7) or the PoC group, which received PoC consisting of four cycles of 60-s intervals of ischemia and reperfusion starting at 30 s after the initial reperfusion (4 × 60/60, n = 7). No reflow was determined by injecting thioflavine S (a fluorescent marker of capillary perfusion), risk zone by blue dye, and infarct size by triphenyltetrazolium chloride. In protocol 1, there were no statistical differences in hemodynamics, ischemic risk zone, or infarct size (35 ± 6% of the risk zone in the PoC group vs. 29 ± 4% in the control group, P = 0.38) between the groups. Similarly, in protocol 2, PoC failed to reduce infarct size compared with the control group (45 ± 4% of the risk zone in the PoC group vs. 42 ± 6% in the control group, P = 0.75). There was a strong correlation in both protocols between the size of the necrotic zone and the portion of the necrotic zone that contained an area of no reflow. However, PoC did not affect this relationship. PoC did not reduce infarct size in this model, nor did it reduce the extent of the anatomic zone of no reflow, suggesting that this intervention may not impact postreperfusion microvascular damage due to ischemia.
Impaired serotonergic regulation of heart rate may underlie reduced baroreflex sensitivity in an animal model of depression
Authors: Hildreth Cara M. , Padley James R. , Pilowsky Paul M. , Goodchild Ann K.
Published: November 2007

Serotonin (5-HT) is crucial to normal reflex vagal modulation of heart rate (HR). Reduced baroreflex sensitivity [spontaneous baroreflex sensitivity (sBRS)] and HR variability (HRV) reflect impaired neural, particularly vagal, control of HR and are independently associated with depression. In conscious, telemetered Flinders-Sensitive Line (FSL) rats, a well-validated animal model of depression, we tested the hypothesis that cardiovascular regulatory abnormalities are present and associated with deficient serotonergic control of reflex cardiovagal function. In FSL rats and control Flinders-Resistant (FRL) and Sprague-Dawley (SD) rat strains, diurnal measurements of HR, arterial pressure (AP), activity, sBRS, and HRV were made. All strains had normal and similar diurnal variations in HR, AP, and activity. In FRL rats, HR was elevated, contributing to the reduced HRV and sBRS in this strain. In FSL rats, sBRS and high-frequency power HRV were reduced during the night, indicating reduced reflex cardiovagal activity. The ratio of low- to high-frequency bands of HRV was increased in FSL rats, suggesting a relative predominance of cardiac sympathetic and/or reflex activity compared with FRL and SD rats. These data show that conscious FSL rats have cardiovascular regulatory abnormalities similar to depressed humans. Acute changes in HR, AP, temperature, and sBRS in response to 8-hydroxy-2-(di- n-propylamino)tetralin, a 5-HT1A, 5-HT1B, and 5-HT7 receptor agonist, were also determined. In FSL rats, despite inducing an exaggerated hypothermic effect, 8-hydroxy-2-(di- n-propylamino)tetralin did not decrease HR and AP or improve sBRS, suggesting impaired serotonergic neural control of cardiovagal activity. These data suggest that impaired serotonergic control of cardiac reflex function could be one mechanism linking reduced sBRS to increased cardiac risk in depression.
Hydroxyurea attenuates activated neutrophil-mediated sickle erythrocyte membrane phosphatidylserine exposure and adhesion to pulmonary vascular endothelium
Authors: Haynes Johnson , Obiako Boniface , Hester Raymond B. , Baliga B. Surendra , Stevens Troy
Published: November 2007

Activated neutrophils increase erythrocyte phosphatidylserine (PS) exposure. PS-exposed sickle red blood cells (SSRBCs) are more adhesive to vascular endothelium than non-PS-exposed cells. An increase in SSRBC fetal hemoglobin (HbF) concentration has been associated with improved rheology and decreased numbers of vasoocclusive episodes. This study examined the effects of HbF, PS-exposed SSRBCs, and chronic hydroxyurea (HU) treatment on activated neutrophil-mediated SSRBC retention/adherence in isolated-perfused rat lungs. Lungs were perfused with erythrocyte suspensions from 1) individuals homozygous for hemoglobin S with 0–7% HbF (SS), 2) with ≥8% HbF (SS + F), and 3) individuals homozygous for hemoglobin S treated with HU therapy for ≥1 yr (SS + HU). Retention of SSRBCs from the SS + HU group was significantly less than that seen in both the SS and SS + F groups. No difference was observed between the SS and SS + F groups. The percentage of HbF and F-cells did not differ between the SS + F and SS + HU groups. At baseline, the proportion of PS-exposed SSRBCs was not different between the SS and SS + HU groups. However, SSRBC treatment with activated neutrophil supernatant caused a twofold increase in PS-exposed SSRBCs in the SS control and no change in the SS + HU group. We conclude that 1) HU attenuates SSRBC retention/adherence in the pulmonary circulation seen in response neutrophil activation, 2) HU stabilizes SSRBC membrane PS, and 3) HU attenuation SSRBC retention/adherence in the pulmonary circulation occurs through a mechanism(s) independent of HbF.
Angiotensin II type 1 receptor blockade corrects cutaneous nitric oxide deficit in postural tachycardia syndrome
Authors: Stewart Julian M. , Taneja Indu , Glover June , Medow Marvin S.
Published: November 2007

Low-flow postural tachycardia syndrome (POTS) is associated with increased plasma angiotensin II (ANG II) and reduced neuronal nitric oxide (NO), which decreases NO-dependent vasodilation. We tested whether the ANG II type 1 receptor (AT1R) antagonist losartan would improve NO-dependent vasodilation in POTS patients. Furthermore, if the action of ANG II is dependent on NO, then the NO synthase inhibitor nitro-l-arginine (NLA) would reverse this improvement. We used local heating of the skin of the left calf to 42°C and laser-Doppler flowmetry to assess NO-dependent conductance [percent maximum cutaneous vascular conductance (%CVCmax)] in 12 low-flow POTS patients aged 22.5 ± 0.8 yr and in 15 control subjects aged 22.0 ± 1.3 yr. After measuring the baseline local heating response at three separate sites, we perfused individual intradermal microdialysis catheters at those sites with 2 μg/l losartan, 10 mM NLA, or losartan + NLA. The predrug heat response was reduced in POTS, particularly the plateau phase reflecting NO-dependent vasodilation (50 ± 5 vs. 91 ± 7 %CVCmax; P < 0.001 vs. control). Losartan increased baseline flow in both POTS and control subjects (from 6 ± 1 to 21 ± 3 vs. from 10 ± 1 to 21 ± 2 %CVCmax; P < 0.05 compared with predrug). The baseline increase was blunted by NLA. Losartan increased the POTS heat response to equal the control subject response (79 ± 7 vs. 88 ± 6 %CVCmax; P = 0.48). NLA decreased both POTS and control subject heat responses to similar conductances (38 ± 4 vs. 38 ± 3 %CVCmax; P < 0.05 compared with predrug). The addition of NLA to losartan reduced POTS and control subject conductances compared with losartan alone (48 ± 3 vs. 53 ± 2 %CVCmax). The data suggest that the reduction in cutaneous NO-dependent vasodilation in low-flow POTS is corrected by AT1R blockade.
Phosphodiesterase 4 inhibitor GPD-1116 markedly attenuates the development of cigarette smoke-induced emphysema in senescence-accelerated mice P1 strain
Authors: Mori Hiroaki , Nose Takashi , Ishitani Kouki , Kasagi Satoshi , Souma Sanae , Akiyoshi Taeko , Kodama Yuzo , Mori Takanori , Kondo Miwa , Sasaki Shinichi , Iwase Akihiko , Takahashi Kazuhisa , Fukuchi Yoshinosuke , Seyama Kuniaki
Published: November 2007

Phosphodiesterase 4 (PDE4) is an intracellular enzyme specifically degrading cAMP, a second messenger exerting inhibitory effects on many inflammatory cells. To investigate whether GPD-1116 (a PDE4 inhibitor) prevents murine lungs from developing cigarette smoke-induced emphysema, the senescence-accelerated mouse (SAM) P1 strain was exposed to either fresh air or cigarette smoke for 8 wk with or without oral administration of GPD-1116. We confirmed the development of smoke-induced emphysema in SAMP1 [air vs. smoke (means ± SE); the mean linear intercepts (MLI), 52.9 ± 0.8 vs. 68.4 ± 4.2 μm, P < 0.05, and destructive index (DI), 4.5% ± 1.3% vs. 16.0% ± 0.4%, P < 0.01]. Emphysema was markedly attenuated by GPD-1116 (MLI = 57.0 ± 1.4 μm, P < 0.05; DI = 8.2% ± 0.6%, P < 0.01) compared with smoke-exposed SAMP1 without GPD-1116. Smoke-induced apoptosis of lung cells were also reduced by administration of GPD-1116. Matrix metalloproteinase (MMP)-12 activity in bronchoalveolar lavage fluid (BALF) was increased by smoke exposure (air vs. smoke, 4.1 ± 1.1 vs. 40.5 ± 16.2 area/μg protein; P < 0.05), but GPD-1116 significantly decreased MMP-12 activity in smoke-exposed mice (5.3 ± 2.1 area/μg protein). However, VEGF content in lung tissues and BALF decreased after smoke exposure, and the decrease was not markedly restored by oral administration of GPD-1116. Our study suggests that GPD-1116 attenuates smoke-induced emphysema by inhibiting the increase of smoke-induced MMP-12 activity and protecting lung cells from apoptosis, but is not likely to alleviate cigarette smoke-induced decrease of VEGF in SAMP1 lungs.
Neutrophil caveolin-1 expression contributes to mechanism of lung inflammation and injury
Authors: Hu Guochang , Ye Richard D. , Dinauer Mary C. , Malik Asrar B. , Minshall Richard D.
Published: November 2007

Caveolin-1 present in immune cells may be involved in regulation of the inflammatory response. Here, using caveolin-1-null ( Cav-1−/−) mice, we addressed the role of caveolin-1 in polymorphonuclear neutrophils (PMNs) in regulating PMN activation-mediated lung injury. In lungs of wild-type ( Cav-1+/+) mice perfused at constant flow with Krebs-Henseleit solution, addition of Cav-1+/+PMNs (4 × 106cells) into the perfusate followed by their activation with formyl-Met-Leu-Phe (fMLP, 1.0 μM) plus platelet-activating factor (1.0 nM) increased pulmonary microvessel filtration coefficient by 150% and wet-to-dry lung weight ratio by 50% as well as PMN accumulation in lungs. These responses were markedly reduced in lungs perfused with Cav-1−/−PMNs followed by addition of the same activating agents. fMLP-stimulated adhesion of Cav-1−/−PMNs to pulmonary microvascular endothelial cells and migration of Cav-1−/−PMNs across endothelial monolayers were also impaired compared with Cav-1+/+PMNs. Cav-1−/−PMNs showed 50–80% reduction in PMA- or fMLP-stimulated superoxide production compared with Cav-1+/+PMNs. In addition, Cav-1−/−PMNs had decreased migratory activity (50%) and adhesion to fibrinogen (40%) in response to fMLP. Rac1 and Rac2 were activated in Cav-1+/+PMNs after stimulation of fMLP but not in Cav-1−/−PMNs. Exogenous expression of caveolin-1 in COS-phox cells augmented the fMLP-induced Rac1 activation and superoxide production, indicating a direct role of caveolin-1 in the mechanism of superoxide production. Thus caveolin-1 expression in PMNs plays a key role in mediating PMN activation, adhesion, and transendothelial migration and in PMN activation-induced lung inflammation and vascular injury.
Protective effect of purinergic agonist ATPγS against acute lung injury
Authors: Kolosova Irina A. , Mirzapoiazova Tamara , Moreno-Vinasco Liliana , Sammani Saad , Garcia Joe G. N. , Verin Alexander D.
Published: November 2007

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are major causes of acute respiratory failure associated with high morbidity and mortality. Although ALI/ARDS pathogenesis is only partly understood, pulmonary endothelium plays a major role by regulating lung fluid balance and pulmonary edema formation. Consequently, endothelium-targeted therapies may have beneficial effects in ALI/ARDS. Recently, attention has been given to the therapeutic potential of purinergic agonists and antagonists for the treatment of cardiovascular and pulmonary diseases. Extracellular purines (adenosine, ADP, and ATP) and pyrimidines (UDP and UTP) are important signaling molecules that mediate diverse biological effects via cell-surface P2Y receptors. We previously described ATP-induced endothelial cell (EC) barrier enhancement via a complex cell signaling and hypothesized endothelial purinoreceptors activation to exert anti-inflammatory barrier-protective effects. To test this hypothesis, we used a murine model of ALI induced by intratracheal administration of endotoxin/lipopolysaccharide (LPS) and cultured pulmonary EC. The nonhydrolyzed ATP analog ATPγS (50–100 μM final blood concentration) attenuated inflammatory response with decreased accumulation of cells (48%, P < 0.01) and proteins (57%, P < 0.01) in bronchoalveolar lavage and reduced neutrophil infiltration and extravasation of Evans blue albumin dye into lung tissue. In cell culture model, ATPγS inhibited junctional permeability induced by LPS. These findings suggest that purinergic receptor stimulation exerts a protective role against ALI by preserving integrity of endothelial cell-cell junctions.
Murine models of pulmonary fibrosis
Authors: Moore Bethany B. , Hogaboam Cory M.
Published: November 2007

Human pulmonary fibrosis is characterized by alveolar epithelial cell injury, areas of type II cell hyperplasia, accumulation of fibroblasts and myofibroblasts, and the deposition of extracellular matrix proteins. The result is a progressive loss of normal lung architecture and impairment in gas exchange. Pertinent features of the human disease include temporal heterogeneity of the fibrotic lesions, progressive nature of the disease, development of fibrotic foci, and in some patients, a rapid worsening of symptoms known as an acute exacerbation. No current animal model recapitulates all of these cardinal manifestations of the human disease. However, investigations using murine models have led to the identification of many pathological cells and mediators that are believed to be important in human disease as well. In this review, we will summarize the characteristics, advantages, and disadvantages of many of the currently utilized murine models of pulmonary fibrosis.
Inhibition of human airway smooth muscle cell proliferation by β2-adrenergic receptors and cAMP is PKA independent: evidence for EPAC involvement
Authors: Kassel Karen M. , Wyatt Todd A. , Panettieri Reynold A. , Toews Myron L.
Published: November 2007

Mechanisms by which β-adrenergic receptor (βAR) agonists inhibit proliferation of human airway smooth muscle (HASM) cells were investigated because of their potential relevance to smooth muscle hyperplasia in asthma. We hypothesized that βAR agonists would inhibit mitogenesis in HASM cells via the β2AR, an increase in cAMP, and PKA activation. HASM cells were treated for 24 h with various agents and then analyzed for [3H]thymidine incorporation as a measure of cell proliferation. EGF stimulated proliferation by ∼10-fold. The nonselective βAR agonist isoproterenol and the β2AR-selective agonists albuterol and salmeterol inhibited EGF-stimulated proliferation by more than 50%, with half-maximal effects at 4.8 nM, 110 nM, and 6.7 nM, respectively. A β2AR-selective antagonist inhibited the isoproterenol effect with 100-fold greater potency than a β1AR-selective antagonist, confirming β2AR involvement in the inhibition of proliferation. The cAMP-elevating agents PGE2and forskolin decreased EGF-induced proliferation, suggesting cAMP as the mediator. β2AR agonists and forskolin also inhibited proliferation stimulated by lysophosphatidic acid (LPA) as well as the synergistic proliferation stimulated by LPA+EGF. Importantly, PKA-selective cAMP analogs did not inhibit proliferation at concentrations that maximally activated PKA (10–100 μM), whereas a cAMP analog selective for the exchange protein directly activated by cAMP (EPAC), 8-(4-chlorophenylthio)-2′-O-methyl-cAMP, maximally inhibited proliferation at a concentration that did not activate PKA (10 μM). These data show that β2AR agonists and other cAMP-elevating agents decrease proliferation in HASM cells via a PKA-independent mechanism, and they provide pharmacological evidence for involvement of EPAC or an EPAC-like cAMP effector protein instead.
Airway smooth muscle relaxation is impaired in mice lacking the p47phoxsubunit of NAD(P)H oxidase
Authors: Chitano Pasquale , Wang Lu , Mason Stanley N. , Auten Richard L. , Potts Erin N. , Foster William M. , Sturrock Anne , Kennedy Thomas P. , Hoidal John R. , Murphy Thomas M.
Published: November 2007

NAD(P)H oxidase is one of the critical enzymes mediating cellular production of reactive oxygen species and has a central role in airway smooth muscle (ASM) cell proliferation. Since reactive oxygen species also affect ASM contractile response, we hypothesized a regulatory role of NAD(P)H oxidase in ASM contractility. We therefore studied ASM function in wild-type mice (C57BL/6J) and mice deficient in a component (p47phox) of NAD(P)H oxidase. In histological sections of the trachea, we found that the area occupied by ASM was 17% more in p47phox−/−than in wild-type mice. After correcting for the difference in ASM content, we found that force generation did not vary between the two genotypes. Similarly, their ASM shortening velocity, maximal power, and sensitivity to acetylcholine, as well as airway responsiveness to methacholine in vivo, were not significantly different. The main finding of this study was a significantly reduced ASM relaxation in p47phox−/−compared with wild-type mice both during the stimulus and after the end of stimulation. The tension relaxation attained at the 20th second of electric field stimulation was, respectively, 17.6 ± 2.4 and 9.2 ± 2.3% in null and wild-type mice ( P <0.01 by t-test). Similar significant differences were found in the rate of tension relaxation and the time required to reduce tension by one-half. Our data suggest that NAD(P)H oxidase may have a role in the structural arrangement and mechanical properties of the airway tissue. Most importantly, we report the first evidence that the p47phoxsubunit of NAD(P)H oxidase plays a role in ASM relaxation.
Impaired VEGF and nitric oxide signaling after nitrofen exposure in rat fetal lung explants
Authors: Muehlethaler Vincent , Kunig Anette M. , Seedorf Gregory , Balasubramaniam Vivek , Abman Steven H.
Published: November 2007

We hypothesized that abnormal fetal lung growth in experimental congenital diaphragmatic hernia after maternal nitrofen exposure alters lung structure due to impaired VEGF signaling, which can be reversed with VEGF or nitric oxide (NO) treatment. Timed-pregnant Sprague-Dawley rats were treated with nitrofen on embryonic day 9 (E9), and fetal lungs were harvested for explant culture on E15. Explants were maintained in 3% O2for 3 days and were treated with NO gas or recombinant human VEGF protein for 3 days. To determine the effects of VEGF inhibition on lung structure, normal fetal lung explants were treated with SU-5416, a VEGF receptor inhibitor, with or without exogenous NO or VEGF. We found that nitrofen treatment impaired lung structure, as evidenced by decreased branching at day 0, but lung structure was not different from controls after 3 days in culture. Nitrofen reduced lung VEGF but not endothelial NO synthase protein level. Treatment with NO enhanced lung growth in control and nitrofen-exposed lungs; however, the response to NO in the nitrofen-treated lungs was reduced when compared with controls. VEGF treatment did not cause a further increase in lung complexity after nitrofen exposure. SU-5416 treatment altered lung structure, which improved with NO but not VEGF treatment. Both nitrofen and SU-5416 treatment increased apoptosis in the mesenchyme of fetal lung explants. We conclude that nitrofen exposure increased apoptosis, decreased lung growth and reduced VEGF expression, and that exogenous NO but not VEGF treatment enhances lung growth. Disruption of lung architecture after VEGF receptor blockade was similar to nitrofen-induced changes but was more responsive to NO.
Latent Class Analysis of Differential Item Functioning on the Peabody Picture Vocabulary Test–III
Authors: Lee Webb Mi-young , Cohen Allan S. , Schwanenflugel Paula J.
Published: November 2007

This study investigated the use of latent class analysis for the detection of differences in item functioning on the Peabody Picture Vocabulary Test—Third Edition (PPVT-III). A two-class solution for a latent class model appeared to be defined in part by ability because Class 1 was lower in ability than Class 2 on both the PPVT-III and the Expressive Vocabulary Test (EVT). This difference was much larger on the PPVT-III for the low-ability class. No difference was found for the high-ability latent class, suggesting that the difference was a result of something in the PPVT-III that was not present in the EVT. The difference on the PPVT-III for low-ability children appeared to be a result of the structure of the items on the test, which seems to encourage the overriding use of the novel name—nameless category strategy for the selection of an answer—a strategy not available on the EVT.
Polytomous Differential Item Functioning and Violations of Ordering of the Expected Latent Trait by the Raw Score
Authors: DeMars Christine E.
Published: November 2007

The graded response (GR) and generalized partial credit (GPC) models do not imply that examinees ordered by raw observed score will necessarily be ordered on the expected value of the latent trait (OEL). Factors were manipulated to assess whether increased violations of OEL also produced increased Type I error rates in differential item functioning (DIF) procedures conditioned on the raw score. Shorter tests and greater variance in item slope parameters increased OEL violations for the GR data but not for the GPC data. These same factors, combined with group mean differences between the reference and focal groups, increased the Type I error rate for the observed raw score DIF methods for both the GR and GPC data. A procedure conditioned on the classical test theory latent score estimate instead of the observed score helped reduce the Type I error in some of the conditions but not for the shortest tests.
Baker Revisited 2007
Authors: Rowe Roger
Published: November 2007

A landmark case in Canadian administrative law, Baker set new standards for the review of administrative discretion and the content of the duty of procedural fairness. Baker's stipulations regarding procedural fairness, the duty to give reasons, and the requirement for decision makers to be alive to the best interests of children gave many Canadians a sense of hope that all immigrants seeking legal status— including those with Canadian-born children—would at least receive a fair consideration of their cases before being removed from Canada. Unfortunately, Baker created expectations that have not been fulfilled. The Supreme Court of Canada's failure to address the racism permeating Baker is symptomatic of the larger problem of Canadian society's ongoing failure to come to terms with the reality of systemic anti-Black discrimination. Black people cannot rely on the courts alone to put an end to systemic discrimination. The solution to this challenge may ultimately be political.
Ghosts in the Canadian Multicultural Machine
Authors: Brown Yvonne
Published: November 2007

The author, who is an African Canadian, was a beneficiary of the 1967 Immigration and Manpower Act. She embraced the Canadian Multicultural Policy and subsequent Multiculturalism Act and its programs as means to validate the identities and cultures of Black people. She tells a tale of her disillusionment and how multiculturalism has concealed the brutal histories of enslavement, colonization, and empire. She uses the metaphor of ghosts to describe her project of directed self-study to understand the subjugation of knowledge about the colonized Other. She offers implications for educational institutions.
“I'm Glad That Someone Is Telling the Nursing Story”
Authors: Flynn Karen
Published: November 2007

The paucity of historical materials on Black Canadian women does not necessarily mean the sources are unavailable. To recuperate and reconstruct Black Canadian women's subjugated knowledge requires drawing from fragments of materials available within and outside the archives. Using oral history as the primary methodology, as well as archival and nursing sources, coupled with secondary research, this essay exploits these sources to piece together the story of a group of women about whom very little is known. This research not only contributes to the history of nursing in Canada but also challenges the national narrative that touts the benign treatment of Black people in Canada.
The Possibilities of Home
Authors: Littlewood McKibbin Molly
Published: November 2007

This discussion of Dionne Brand's novel What We All Long For focuses on the degree to which the second-generation characters are able to feel at home in Toronto. The article treats the city as the location where immigration, Blackness, racism, and other social factors meet and analyzes how each character negotiates space in his or her efforts to claim a home.
So Seldom for Us, So Often Against Us
Authors: Thornhill Esmeralda M. A.
Published: November 2007

One unprobed strand of Canada-U.S. racial history demanding examination and explanation is law's obfuscated role of collusion with race—a role that more often than not has aided and abetted racism and racial discrimination. Knowledge of this historical complicity and duplicity between law and race constitutes a precondition for understanding the material reality of the racism that daily blights and scars the lifescapes of Blacks in Canada today. Diasporic literacy demands that we start opening up the Canadian record so as to better comprehend how law as an institution has so often behaved with impunity and continues to operate as if there were nothing about Black people worth honoring! Though in matters of racism and racial discrimination we in Canada have experienced the law too often as a sword of oppression and so seldom as a shield of protection, law nevertheless remains too precious a tool for Black people to abandon.
Child Abuse and Chronic Pain in a Community Survey of Women
Authors: Walsh Christine A. , Jamieson Ellen , MacMillan Harriet , Boyle Michael
Published: November 2007

This study examined the relationship between a self-reported history of child physical and sexual abuse and chronic pain among women ( N = 3381) in a provincewide community sample. Chronic pain was significantly associated with physical abuse, education, and age of the respondents and was unrelated to child sexual abuse alone or in combination with physical abuse, mental disorder (anxiety, depression, or substance abuse), or low income. Number of health problems and mental health disorders did not mediate the relationship between physical abuse and chronic pain. Despite considerable evidence from the clinical literature linking exposure to child maltreatment and chronic pain in adulthood, this may well be the first population-based study to investigate this relationship for child physical and sexual abuse independently. The significant association between childhood history of physical abuse and pain in adulthood calls for a greater awareness of the potential for chronic pain problems associated with this type of maltreatment. Further research is needed to understand the mechanism for this complex relationship.
Compliance and Learning in an Intervention Program for Partner-Violent Men
Authors: Contrino Kathleen M. , Dermen Kurt H. , Nochajski Thomas H. , Wieczorek William F. , Navratil Peter K.
Published: November 2007

Although research has yielded mixed findings regarding the effectiveness of intervention programs for partner-violent men, it appears that greater participant compliance with such programs is associated with better outcomes. However, no research to date has jointly examined compliance with intervention programs and the extent to which partner-violent men learn specific information presented during the programs. The current study makes use of existing data to evaluate general and specific elements of partner-violent men's compliance with (i.e., active, appropriate participation in) an intervention program and recall of key points from the program. Results from a subsample of 22 men indicate that at program termination, those rated as having been “process conscious” during intervention group sessions, having self-disclosed during sessions, having evidenced awareness and use of techniques to avoid violence, and having used respectful language show greater recall of material taught in the program. This finding points to the potential benefit of taking steps to increase men's active participation in programs and of studying active engagement as a mediator of program effects on men's violence toward partners.
A Comparison of Men Who Committed Different Types of Sexual Assault in a Community Sample
Authors: Abbey Antonia , Parkhill Michele R. , Clinton-Sherrod A. Monique , Zawacki Tina
Published: November 2007

This study extends past research by examining predictors of different types of sexual assault perpetration in a community sample. Computer-assisted self-interviews were conducted with a representative sample of 163 men in one large urban community. As hypothesized, many variables that are significant predictors of sexual assault perpetration in college student samples were also significant predictors in this sample, including empathy, adult attachment, attitudes about casual sex, sexual dominance, alcohol consumption in sexual situations, and peer approval of forced sex. For most measures, the strongest differences were between nonassaulters and men who committed acts that met standard legal definitions of rape. Men who committed forced sexual contact and verbal coercion tended to have scores that fell in between those of the other two groups. The implications of these findings are discussed for community-based sexual assault prevention programs.
The Role of Cognitive Coping in Female Victims of Stalking
Authors: Kraaij Vivian , Arensman Ella , Garnefski Nadia , Kremers Ismay
Published: November 2007

The aim of the study is to examine the role of cognitive coping in a sample of 47 female victims of stalking. Stalking victims who blamed themselves more for the stalking report significantly higher symptoms of depression, anxiety, and posttraumatic stress disorder (PTSD). Respondents who ruminated more about the stalking experience, or respondents who explicitly emphasized the terror of the stalking to a higher extent, also report significantly higher symptom levels. Finally, respondents who thought more about what steps to take and how to handle the stalking report significantly higher symptom levels of depression, anxiety, and PTSD. This conclusion holds also after controlling for the severity of stalking. If the findings of the present study can be confirmed, this could possibly contribute to the help provided to victims of stalking.
Representative Sampling of Maritally Violent and Nonviolent Couples
Authors: Farris Coreen , Holtzworth-Munroe Amy
Published: November 2007

Despite the methodological advantages of representative sampling, few researchers in the field of marital violence have employed random samples for laboratory assessments of couples. The current study tests the feasibility and sampling success of three recruitment methods: (a) random digit dialing, (b) directory-assisted recruitment, and (c) a hybrid method. The number of successful telephone contacts with couples does not differ across the three methods; most successful calls contact nonviolent couples. The sample recruited through all three methods does not appear to match the demographics of the calling area, and all methods require a high monetary and human resource investment.
Who Is Most at Risk for Intimate Partner Violence?
Authors: Romans Sarah , Forte Tonia , Cohen Marsha M. , Du Mont Janice , Hyman Ilene
Published: November 2007

Whole population studies on intimate partner violence (IPV) have given contradictory information about prevalence and risk factors, especially concerning gender. The authors examined the 1999 Canadian General Social Survey data for gender patterns of physical, sexual, emotional, or financial IPV from a current or ex-partner. More women (8.6%) than men (7.0%, p = .001) reported partner physical abuse in general, physical IPV causing physical injury ( p < .0001), sexual abuse (1.7% vs. 0.2%, p < .0001), and financial abuse (4.1% vs. 1.6%, p < .0001). There were no gender differences for partner emotional abuse. Significant risk factors after multivariate modeling for physical/sexual IPV were younger age, being divorced/separated or single, having children in the household, and poor self-rated physical health. These findings from a large, randomly generated data set further refine our understanding of the risk profile for IPV in the developed world.
Motivations Underlying Power Dynamics in Hierarchically Structured Groups
Authors: van Dijke Marius , Poppe Matthijs
Published: November 2007

The authors studied tendencies to change power differences with others in hierarchically structured groups. Specifically, they contrasted predictions from two theories based on a power motive approach that have recently inspired power dynamics research. Social comparison theory predicts that people want to be somewhat more powerful than comparison others. A competing prediction from power distance theory is that people are more inclined to further increase their power, the more power they have already. In an experiment, 79 students participated in a decision-making task in a hierarchical group. They advised their subordinates and received advice from their superiors. Subsequently, they indicated their preferred changes in power differences. Social comparison theory was mostly supported: Participants mainly wanted slight power superiority over comparison others. The discussion focuses on implications for various theories in the field, such as expectation states theory, and on understanding behavior aimed at improving or securing power positions in hierarchical groups.
Neuroprotection by Cell Permeable TAT-mGluR1 Peptide in Ischemia: Synergy between Carrier and Cargo Sequences
Authors: Wei Xu  , Miou Zhou  , Baudry Michel
Published: November 2007

Overactivation of glutamate receptors is a critical mechanism for neuronal death in ischemic stroke. Previously, we reported that overactivation of N-methyl-D-aspartate (NMDA)—type glutamate receptor induced calpain-mediated truncation of metabotropic glutamate receptor mGluR1α, resulting in suppression of its neuroprotective signaling pathway. A fusion peptide containing the transactivating regulatory protein (TAT) protein transduction domain (PTD) and the mGluR1α sequence spanning the calpain cleavage site effectively blocked mGluR1α truncation and protected neurons against NMDA-induced neuronal toxicity. We recently evaluated the role of this mechanism in ischemia-induced cell death. We found that mGluR1α was truncated in both in vitro and in vivo models of stroke and that this truncation was accompanied by the typical calpain-mediated proteolysis of spectrin. The TAT-mGluR1 fusion peptide produced robust neuroprotective effect in the in vitro model of stroke. In addition, we found that the TAT protein transduction domain peptide itself altered the function of membrane channels through some unknown mechanisms and showed some mild neuroprotective effects. Together, these experiments indicated a synergistic relationship between the TAT carrier sequence and the mGluR1α peptide cargo sequence, and this synergy might account for the neuroprotective properties of the TAT-mGluR1 peptide. NEUROSCIENTIST 14(5):409—414, 2008. DOI: 10.1177/1073858407309762
P2Y receptor signaling regulates phenotype and IFN-α secretion of human plasmacytoid dendritic cells
Authors: Shin Amanda , Toy Tracey , Rothenfusser Simon , Robson Neil , Vorac Julia , Dauer Marc , Stuplich Moritz , Endres Stefan , Cebon Jonathan , Maraskovsky Eugene , Schnurr Max
Published: November 2007

Plasmacytoid dendritic cells (PDCs) play powerful regulatory roles in innate and adaptive immune responses and are a major source of type I interferon (IFN) following viral infection. During inflammation and mechanical stress, cells release nucleotides into the extracellular space where they act as signaling molecules via G protein–coupled P2Y receptors. We have previously reported on the regulation of myeloid dendritic cell (DC) function by nucleotides. Here, we report that human PDCs express several subtypes of P2Y receptors and mobilize intracellular calcium in response to nucleotide exposure. As a functional consequence, PDCs acquire a mature phenotype that is further enhanced in the context of CD40 ligation. Strikingly, nucleotides strongly inhibit IFN-α secretion induced by influenza virus or CpG-A. This effect is most pronounced for the uridine nucleotides UDP and UTP and the sugar nucleotide UDP-glucose, ligands of P2Y6, P2Y4, and P2Y14, respectively. Nucleotide-induced inhibition of IFN-α production is blocked by suramin, a P2Y receptor antagonist. Pharmacological data point toward a role of protein kinase C in the negative regulation of type I IFN. Manipulating PDC function with P2Y receptor agonists may offer novel therapeutic strategies for autoimmune diseases or cancer.
Dendritic cells loaded with apoptotic antibody-coated tumor cells provide protective immunity against B-cell lymphoma in vivo
Authors: Franki Suzanne N. , Steward Kristopher K. , Betting David J. , Kafi Kamran , Yamada Reiko E. , Timmerman John M.
Published: November 2007

The in vitro priming of tumor-specific T cells by dendritic cells (DCs) phagocytosing killed tumor cells can be augmented in the presence of antitumor monoclonal antibody (mAb). We investigated whether DCs phagocytosing killed lymphoma cells coated with tumor-specific antibody could elicit antitumor immunity in vivo. Irradiated murine 38C13 lymphoma cells were cocultured with bone marrow–derived DCs in the presence or absence of tumor-specific mAb. Mice vaccinated with DCs cocultured with mAb-coated tumor cells were protected from tumor challenge (60% long-term survival), whereas DCs loaded with tumor cells alone were much less effective. The opsonized whole tumor cell–DC vaccine elicited significantly better tumor protection than a traditional lymphoma idiotype (Id) protein vaccine, and in combination with chemotherapy could eradicate preexisting tumor. Moreover, the DC vaccine protected animals from both wild-type and Id-negative variant tumor cells, indicating that Id is not a major target of the induced tumor immunity. Protection was critically dependent upon CD8+ T cells, with lesser contribution by CD4+ T cells. Importantly, opsonized whole tumor cell–DC vaccination did not result in tissue-specific autoimmunity. Since opsonized whole tumor cell–DC and Id vaccines appear to target distinct tumor antigens, optimal antilymphoma immunity might be achieved by combining these approaches.