bluuebunny/crossref_metadata_2025 huggingface dataset:
Electrochemical Impedance Spectroscopy Analysis of 2-Mercaptobenzimidazole (2MBI) as Corrosion Inhibitor in HCl 1M
Authors: Espinoza Araceli , Negrón Guillermo , Palomar-Pardavé Manuel , Romero-Romo Mario Alberto , Rodríguez- Torres Israel , Herrera-Hernández H.
Published: December 2009

This work presents the results concerning the effect of different concentrations of an organic heterocyclic compound that displays corrosion inhibiting properties, known as 2-mercaptobenzimidazole, 2MBI, in a system comprising samples of the steel type API 5L X52 exposed to HCl 1M. The impedance spectra revealed that there was a continuous increase of |Z| as a function of increasing inhibitor concentrations in the electrolyte. A 200 ppm 2MBI was tested also, however, the greatest corrosion inhibiting efficiency was attained 99%, IE, with much smaller concentrations of the compound. This is sufficient reason to consider it a good corrosion inhibitor in HCl, just as it was effective for H2SO4. Furthermore, the inhibition kinetics study undertaken indicated that the 2MBI added in a fairly large concentration of 200 ppm in 1M HCl maintains its effectivity up to 32 immersion days. Also, it was observed that the corrosion potential, Ecorr, became more negative as the 2MBI organic molecules concentration increased in the system, which suggests that this inhibitor may be acting on the cathodic and anodic sites, thus being considered a mixed type inhibitor, in agreement with the corrosion mixed potential theory.
Nano-architectured Pt-Mo Anode Electrocatalyst for High CO-tolerance in PEM Fuel Cells
Authors: Hu Jenny , Liu Zhufang , Eichhorn Bryan , Jackson Gregory S.
Published: December 2009

PEM fuel cell MEAs with Nafion electrolytes and common cathodes were tested with Pt0.8Mo0.2 alloy and MoOx@Pt core-shell anode electrocatalysts for anode CO tolerance and short-term stability to corroborate earlier thin-film RDE results. Polarization curves at 70 {degree sign}C for the Pt0.8Mo0.2 alloy in H2 with 25 to 1000 ppm CO showed a significant increase in CO tolerance in comparison to PtRu electrocatalysts. MoOx@Pt core-shell electrocatalysts, which showed extremely high activity for H2 in 1000 ppm CO during RDE studies, performed poorly in MEA testing, in comparison to the PtMo and PtRu alloys on a current per total catalyst loading basis. The discrepancy is attributed to residual stabilizer from the core-shell synthesis impacting catalyst-ionomer interfaces. Nonetheless, the MoOx@Pt electrochemical performance, with its reduced Pt content, is comparable or superior to the highly active Pt0.8Mo0.2 electrocatalyst for CO concentrations of 250 ppm or lower on a per gram of precious metal basis.
Investigation of the Oxygen Reduction Activity of non-Platinum Catalysts - a RDE Methodology
Authors: Wiberg Gustav , Mayhofer Karl , Arenz Matthias
Published: December 2009

The oxygen reduction reaction (ORR) is investigated on a non-platinum nanoparticulate electrocatalyst using a rotating disk electrode (RDE) setup. Rather than claiming the synthesis of a novel, improved catalyst, we focus on the general procedure for obtaining a meaningful electrochemical characterization of non-platinum systems and their comparison to state of the art platinum high surface area catalysts. The most important aspect in this respect is the determination of the electrochemically active surface area (ECA) or the number of electrochemical active sites (NECAS), respectively. Based on our results, the benefits of a general comparison of activities of different catalyst materials by turn over frequencies (TOF), i.e. normalization to the number of electrochemical active sites, is discussed. For this study unsupported silver nanoparticles in the size of about 100 nm (NP Ag) and a polycrystalline silver disk were chosen as a representative non-platinum catalyst system, due their significant activity for the ORR in alkaline electrolyte and their potential application in alkaline fuel cells.
Divergent roles of prokineticin receptors in the endothelial cells: angiogenesis and fenestration
Authors: Guilini Célia , Urayama Kyoji , Turkeri Gulen , Dedeoglu Deniz B. , Kurose Hitoshi , Messaddeq Nadia , Nebigil Canan G.
Published: December 2009

Prokineticins are secreted peptides that activate two G protein-coupled receptors: PKR1 and PKR2. Prokineticins induce angiogenesis and fenestration, but the cognate receptors involved in these functions are unknown. We hypothesized a role for prokineticin receptor signaling pathways and expression profiles in determining the selective effects of prokineticins on coronary endothelial cells (H5V). Activation of the PKR1/MAPK/Akt signaling pathway stimulates proliferation, migration, and angiogenesis in H5V cells, in which PKR1 predominates over PKR2. PKR1 was colocalized with Gα11 and was internalized following the stimulation of these cells with prokineticin-2. Knock down of PKR1 or Gα11 expression in H5V cells effectively inhibited prokineticin-2-induced vessel formation and MAPK/Akt activation, indicating a role for PKR1/Gα11 in this process. However, in conditions in which PKR2 predominated over PKR1, these cells displayed a fenestrated endothelial cell phenotype. H5V cells overexpressing PKR2 displayed large numbers of multivesicular bodies and caveolar clusters and a disruption of the distribution of zonula occluden-1 tight junction protein. Prokineticin-2 induced the colocalization of PKR2 with Gα12, and activated Gα12, which bound to zonula occluden-1 to trigger the degradation of this protein in these cells. Prokineticin-2 induced the formation of vessel-like structures by human aortic endothelial cells expressing only PKR1, and disorganized the tight junctions in human hepatic sinusoidal endothelial cells expressing only PKR2, confirming the divergent roles of these receptors. Our findings show the functional characteristics of coronary endothelial cells depend on the expression of PKR1 and PKR2 levels and the divergent signaling pathways used by these receptors.
What is the appropriate approach to prevention of thromboembolism in heart failure?
Authors: Schumaecker Matthew , Homma Shunichi , Freudenberger Ronald
Published: December 2009

Many studies suggest a higher incidence of thromboembolic syndromes such as stroke, peripheral arterial thrombosis and pulmonary embolism in patients with heart failure (HF), particularly those with left ventricular systolic dysfunction. As a result, some clinicians have chosen to treat patients with HF with anticoagulants as primary prevention against thromboembolic events. However, this practice is not well-supported by scientific data. Retrospective analyses of large HF trials have yielded contradictory results and randomised trials designed to specifically address this question have been under-populated and under-powered. As a result, there is no general consensus among professional societies in either recommending or advising against anticoagulants in HF. We hope that ongoing clinical trials, WARCEF in particular, will yield results that will guide clinicians in deciding for or against routine use of anticoagulants in HF.
Loss of high-molecular-weight von Willebrand factor multimers mainly affects platelet aggregation in patients with aortic stenosis
Authors: Eslam Roza Badr , Schneller Alexandra , Kaider Alexandra , Koren Daniela , Eichelberger Beate , Rosenhek Raphael , Budde Ulrich , Lang Irene , Panzer Simon
Published: December 2009

Severe aortic stenosis is associated with a haemostatic abnormality that resembles acquired von Willebrand syndrome type 2. It is assumed that high shear conditions render large von Willebrand factor (VWF) multimers accessible to cleavage by ADAMTS-13. However, whether loss of these large multimers affects platelet function by impairing adhesion, aggregate formation, or both has not been evaluated in clinical studies. We prospectively enrolled 47 patients with severe aortic stenosis, and studied them prior to aortic valve surgery and at a median of six months after valve replacement. We investigated levels of large VWF multimers, platelet function under high shear conditions, and residual response to suboptimal concentrations of ADP to express P-selectin. As expected, there was a significant reduction of VWF large multimers before surgery that resolved thereafter in most patients (p<0.0001). The closure time of the ADP cartridge of the PFA-100 was also corrected in most patients after the operation (p<0.0001). We used the cone and plate(let) analyser Impact-R to differentiate between adhesion and aggregation. Both adhesion (p=0.03) and ADP-inducible platelet aggregation (p=0.002) improved considerably after valve replacement. Consequently, ADP-inducible expression of P-selectin was higher after valve replacement (p=0.001). We conclude that reduced levels of large VWF multimers associated with aortic stenosis lead to impairment of both adhesion and, especially, ADP-inducible platelet aggregation.
Impaired thrombin generation and fibrin clot formation in patients with dilutional coagulopathy during major surgery
Authors: Schols Saskia , Lancé Marcus , Feijge Marion , Damoiseaux Jan , Marcus Marco , Hamulyák Karly , Cate Hugo ten , van Pampus Elisabeth , Heemskerk Johan
Published: December 2009

Patients subjected to haemodilution during surgery are at increased risk of bleeding. We hypothesised that, in the acquired dilutional coagulopathy, insufficient haemostasis is due to either insufficient thrombin generation or insufficient fibrin clot formation. In tissue factor-activated plasmas from patients with coagulation deficiency, we measured time curves of thrombin generation and fibrin clot formation (thromboelastography). Investigated were in study A: 10 patients treated with vitamin K antagonist and five healthy subjects; in study B: 30 patients undergoing cardiopulmonary bypass (CPB) surgery and infused with on average 2,000 ml crystalloids and colloids (no major bleeding); in study C: 58 patients undergoing major general surgery, and transfused with >5,000 ml crystalloids, colloids and red cell concentrates, who experienced major bleeding and were post-transfused with fresh frozen plasma. The treatment with vitamin K antagonist led to a progressive reduction in thrombin generation but not fibrin clot formation. In CPB patients, plasma factor levels post-surgery were 53–60% of normal. This was accompanied by moderate reduction in both haemostatic processes. In plasmas from patients undergoing major surgery, factor levels were 38–41% of normal, and these levels increased after plasma transfusion. Taking preset thresholds for normal thrombin generation and fibrin clot formation, at least one of these processes was low in 88–93% of the patients with (persistent) bleeding, but only in 40–53% of the patients without bleeding. In conclusion, the ability of thrombin generation and fibrin clot formation is independently reduced in acquired dilutional coagulopathy, while minimal levels of both are required for adequate haemostasis.
Sulfated, low-molecular-weight lignins are potent inhibitors of plasmin, in addition to thrombin and factor Xa: Novel opportunity for controlling complex pathologies
Authors: Henry Brian , Aziz May Abdel , Zhou Qibing , Desai Umesh
Published: December 2009

Recently we prepared sulfated, low-molecular-weight lignins (LMWLs) to mimic the biological activities of heparin and heparan sulfate. Chemo-enzymatically prepared sulfated LMWLs represent a library of diverse non-sugar, aromatic molecules with structures radically different from the heparins, and have been found to potently inhibit thrombin and factor Xa. To assess their effect on the fibrinolytic system, we studied the interaction of LMWLs with human plasmin. Enzyme inhibition studies indicate that the three sulfated LMWLs studied inhibit plasmin with IC50 values in the range of 0.24 and 1.3 μM, which are marginally affected in the presence of antithrombin. Similarly, plasmin degradation of polymeric fibrin is also inhibited by sulfated LMWLs. Michaelis-Menten kinetic studies indicate that maximal velocity of hydrolysis of chromogenic substrates decreases nearly 70% in the presence of LMWLs, while the effect on Michaelis constant is dependent on the nature of the substrate. Competitive binding studies indicate that the sulfated LMWLs compete with full-length heparin. Comparison with thrombin-heparin crystal structure identifies an anionic region on plasmin as a plausible sulfated LMWL binding site. Overall, the chemoenzymatic origin coupled with coagulation and fibrinolysis inhibition properties of sulfated LMWLs present novel opportunities for designing new pharmaceutical agents that regulate complex pathologies in which both systems are known to play important roles such as disseminated intravascular coagulation.
Economic evaluation of dabigatran etexilate for the prevention of venous thromboembolism in patients aged over 75 years or with moderate renal impairment undergoing total knee or hip replacement
Authors: Roskell Neil , Plumb Jonathan , Clemens Andreas , Noack Herbert , Robinson Paul , Dolan Gerry , Brenkel Ivan , Wolowacz Sorrel
Published: December 2009

Oral dabigatran etexilate is indicated for the prevention of venous thromboembolism (VTE) in patients undergoing total knee replacement or total hip replacement. We investigated the cost-effectiveness of the 150 mg once daily (od) dose recommended for patients aged over 75 or with moderate renal impairment, from a United Kingdom National Health Service perspective. Dabigatran etexilate was compared with subcutaneous enoxaparin 40 mg od, using a decision model. Risks for VTE and bleeding were derived from subgroup analyses of the phase III trials. Dabigatran etexilate was less costly than enoxaparin; cost savings varied from £62 to £274 (base-case analyses) and were primarily due to differences in administration costs. Results were robust across a range of sensitivity analyses. Dabigatran etexilate 150 mg od is cost saving compared with enoxaparin 40 mg od in patients aged over 75 years and in patients with moderate renal impairment, with comparable efficacy and safety.
Contribution of exosite occupancy by heparin to the regulation of coagulation proteases by antithrombin
Authors: Yang Likui , Manithody Chandrashekhara , Qureshi Shabir , Rezaie Alireza
Published: December 2009

Heparin promotes the antithrombin (AT) inactivation of factors IXa (fIXa) and Xa (fXa) through a conformational activation of the serpin and also by a template mechanism in the presence of physiological levels of Ca2+. Recently, it was reported that heparin induces conformational changes in the active-sites of fIXa and fXa, raising the possibility that heparin also modulates the reactivity of these proteases with AT by this mechanism. To test this possibility, we prepared an AT mutant in which four critical heparin-binding residues of the serpin (Arg-45, Arg-46, Lys-114, and Arg-129) were replaced with non-basic residues. This mutant lost its affinity for heparin, but retained its normal reactivity with coagulation proteases. Thus, the high-affinity AT-binding pentasaccharide fragment of heparin had no cofactor effect on the reactivity of the AT mutant with coagulation proteases. Full-length heparinconcentration dependence of the AT inhibition of fIXa and fXa revealed that in contrast to a greater than 4–5 orders of magnitude accelerating effect for heparin on the AT inhibition of fIXa and fXa, heparin exhibits a negligible cofactor effect (<2-fold) on the mutant AT inhibition of these proteases. The same results were obtained for the mutant AT inhibition of thrombin and factor VIIa, however, heparin accelerated the mutant AT inhibition of factor XIa ~10-fold. We conclude that, with the exception of factor XIa, heparin-mediated conformational modulation of the active-sites of coagulation proteases makes a minor contribution to the regulation of these proteases by AT.
Phosphorylation and Acetylation of Histone H3 and Autoregulation by Early Growth Response 1 Mediate Interleukin 1β Induction of Early Growth Response 1 Transcription
Authors: Wang Bo , Chen Jinbiao , Santiago Fernando S. , Janes Mary , Kavurma Mary M. , Chong Beng H. , Pimanda John E. , Khachigian Levon M.
Published: December 2009

Objective—

The transcription factor early growth response (EGR)-1 has been implicated as a key vascular phenotypic switch through its control of inducible transcription. EGR-1 autoregulation, and histone modification in the EGR-1 promoter, represent key mechanisms in EGR-1 control, but have not been explored.

Methods and Results—

We demonstrate that EGR-1 regulates its own transcription and that this involves histone H3 phosphorylation and acetylation. EGR-1 transactivates its promoter in smooth muscle cells exposed to interleukin (IL) 1β through a novel
cis
-acting element (−211/−203). PD98059, which inhibits mitogen-activated protein kinase kinase/extracellular regulated kinase (MEK/ERK) attenuates IL-1β–inducible phosphorylation of extracellular signal–regulated kinase 1/2 and mitogen and stress–activated protein kinases 1/2; and reduces levels of phosphorylated and acetylated histone H3. Histone deacetylase inhibition enhances EGR-1 transcription in response to cytokine. Conversely, suppression of histone modification with mitogen and stress–activated protein kinase 1/2 short interfering RNA, or the histone H3 acetyltransferase inhibitor Garcinol, inhibits IL-1β–inducible EGR-1 transcription. EGR-1 interacts with the acetyltransferase p300. Acetylated H3 and phosphorylated H3 are enriched at the promoter of EGR-1; and EGR-1 is enriched at the promoters of tissue factor and plasminogen activator inhibitor 1 in response to IL-1β, and attenuated by PD98059, Garcinol, and mitogen and stress–activated protein kinase 1/2 short interfering RNA.

Conclusion—

IL-1β induction of EGR-1 transcription involves histone H3 phosphorylation, acetylation, and autoregulation by EGR-1.
Local Atherosclerotic Plaques Are a Source of Prognostic Biomarkers for Adverse Cardiovascular Events
Authors: de Kleijn Dominique P.V. , Moll Frans L. , Hellings Willem E. , Ozsarlak-Sozer Gonen , de Bruin Peter , Doevendans Pieter A. , Vink Aryan , Catanzariti Louise M. , Schoneveld Arjan H. , Algra Ale , Daemen Mat J. , Biessen E.A. , de Jager W. , Zhang Huoming , de Vries Jean-Paul , Falk Erling , Lim Sai K. , van der Spek Peter J. , Sze Siu Kwan , Pasterkamp Gerard
Published: December 2009

Objective—

Atherosclerotic cardiovascular disease is a major burden to health care. Because atherosclerosis is considered a systemic disease, we hypothesized that one single atherosclerotic plaque contains ample molecular information that predicts future cardiovascular events in all vascular territories.

Methods and Results—

AtheroExpress is a biobank collecting atherosclerotic lesions during surgery, with a 3-year follow-up. The composite primary outcome encompasses all cardiovascular events and interventions, eg, cardiovascular death, myocardial infarction, stroke, and endovascular interventions. A proteomics search identified osteopontin as a potential plaque biomarker. Patients undergoing carotid surgery (n=574) served as the cohort in which plaque osteopontin levels were examined in relation to their outcome during follow-up and was validated in a cohort of patients undergoing femoral endarterectomy (n=151). Comparing the highest quartile of carotid plaque osteopontin levels with quartile 1 showed a hazard ratio for the primary outcome of 3.8 (95% confidence interval, 2.6–5.9). The outcome did not change after adjustment for plaque characteristics and traditional risk factors (hazard ratio, 3.5; 95% confidence interval, 2.0–5.9). The femoral validation cohort showed a hazard ratio of 3.8 (95% confidence interval 2.0 to 7.4) comparing osteopontin levels in quartile 4 with quartile 1.

Conclusion—

Plaque osteopontin levels in single lesions are predictive for cardiovascular events in other vascular territories. Local atherosclerotic plaques are a source of prognostic biomarkers with a high predictive value for secondary manifestations of atherosclerotic disease.
Cardiac-Specific Overexpression of Catalase Identifies Hydrogen Peroxide-Dependent and -Independent Phases of Myocardial Remodeling and Prevents the Progression to Overt Heart Failure in Gαq-Overexpressing Transgenic Mice
Authors: Qin Fuzhong , Lennon-Edwards Shannon , Lancel Steve , Biolo Andreia , Siwik Deborah A. , Pimentel David R. , Dorn Gerald W. , Kang Y. James , Colucci Wilson S.
Published: December 2009

Background—

Although it seems that reactive oxygen species contribute to chronic myocardial remodeling, questions remain about (1) the specific types of reactive oxygen species involved, (2) the role of reactive oxygen species in mediating specific cellular events, and (3) the cause-and-effect relationship between myocardial reactive oxygen species and the progression to heart failure. Transgenic mice with myocyte-specific overexpression of Gαq develop a dilated cardiomyopathy that progresses to heart failure. We used this model to examine the role of H
2
O
2
in mediating myocardial remodeling and the progression to failure.

Methods and Results—

In Gαq myocardium, markers of oxidative stress were increased at 4 weeks and increased further at 20 weeks. Gαq mice were crossbred with transgenic mice having myocyte-specific overexpression of catalase. At 4 weeks of age, left ventricular end-diastolic dimension was increased and left ventricular fractional shortening decreased in Gαq mice and deteriorated further through 20 weeks. In Gαq mice, myocardial catalase overexpression had no effect on left ventricular end-diastolic dimension or fractional shortening at 4 weeks but prevented the subsequent deterioration in both. In Gαq mice, myocyte hypertrophy; myocyte apoptosis; interstitial fibrosis; and the progression to overt heart failure, as reflected by lung congestion and exercise intolerance, were prevented by catalase overexpression.

Conclusion—

In Gαq mice, myocyte-specific overexpression of catalase had no effect on the initial phenotype of left ventricular dilation and contractile dysfunction but prevented the subsequent progressive remodeling phase leading to heart failure. Catalase prevented the cellular hallmarks of adverse remodeling (myocyte hypertrophy, myocyte apoptosis, and interstitial fibrosis) and the progression to overt heart failure. Thus, H
2
O
2
, associated oxidant pathways, or both play a critical role in adverse myocardial remodeling and the progression to failure.
Oxygen-Wasting Effect of Inotropy
Authors: Müller Stig , How Ole-Jakob , Jakobsen Øyvind , Hermansen Stig Eggen , Røsner Assami , Stenberg Thor Allan , Myrmel Truls
Published: December 2009

Background—We addressed the hypothesis that the inotropic drugs dobutamine and levosimendan both induce surplus oxygen consumption (oxygen wasting) relative to their contractile effect in equipotent therapeutic doses, with levosimendan being energetically more efficient.

Methods and Results—Postischemically reduced left ventricular function (stunning) was created by repetitive left coronary occlusions in 22 pigs. This contractile dysfunction was reversed by infusion of either levosimendan (24 μg/kg loading and 0.04 μg · kg−1· min−1infusion) or an equipotent dose of dobutamine (1.25 μg · kg−1· min−1). Contractility and cardiac output were normalized by both drug regimens. The energy cost of drug-induced contractility enhancement was assessed by myocardial oxygen consumption related to the mechanical indexes tension-time index, pressure-volume area, and total mechanical energy. ANCOVA did not reveal any increased oxygen cost of contractility for either drug in these doses. However, both dobutamine and levosimendan at supratherapeutic levels (10 μg · kg−1· min−1and 48 μg/kg loading with 0.2 μg · kg−1· min−1infusion, respectively) induced a highly significant increase in oxygen consumption related to mechanical work, compatible with the established oxygen-wasting effect of inotropy (P<0.001 for all mechanical indexes with dobutamine;P=0.007 for levosimendan as assessed by pressure-volume area).

Conclusion—Therapeutic levels of neither dobutamine nor levosimendan showed inotropic oxygen wasting in this in vivo pig model. Thus, relevant hemodynamic responses can be achieved with an adrenergic inotrope without surplus oxygen consumption.
Brain-Derived Neurotrophic Factor Stimulates Production of Prostacyclin in Cerebral Arteries
Authors: Santhanam Anantha Vijay R. , Smith Leslie A. , Katusic Zvonimir S.
Published: December 2009

Background and Purpose—

The role of brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B, in control of cerebral circulation is poorly understood. The present study was designed to investigate the cerebral vascular effects of BDNF in vivo.

Methods—

Replication incompetent adenovirus encoding either rat BDNF (AdBDNF) or green fluorescent protein was injected intracisternally into rabbits. Forty-eight hours later, animals were euthanized. Plasma and cerebrospinal fluid levels of BDNF were measured by enzyme-linked immunosorbent assay, vasomotor function of isolated basilar arteries was studied in organ chambers, protein expression in the basilar arteries was studied by Western blotting, prostanoid levels were measured by enzyme-linked immunosorbent assay, and cyclic adenosine 3′,5′-monophosphate levels were measured by radioimmunoassay.

Results—

The levels of BDNF in the cerebrospinal fluid were significantly elevated in AdBDNF-treated rabbits as compared with adenovirus encoding green fluorescent protein-treated rabbits (37±5 ng/mL versus 0.006±0.003 ng/mL, respectively;
P
<0.05; n=14). Western blotting studies revealed that in basilar arteries, AdBDNF increased protein expression of prostacyclin synthase, whereas expression of endothelial nitric oxide synthase and phosphorylated (Ser 1177) endothelial nitric oxide synthase remained unchanged. During incubation with arachidonic acid (1 μmol/L), PGI
2
production and levels of cyclic adenosine 3′,5′-monophosphate were significantly elevated only in AdBDNF-treated rabbit basilar arteries (
P
<0.05, n=6). Relaxations to acetylcholine (10
−9
to 10
−5
mol/L) and arachidonic acid (10
−9
to 10
−5
mol/L) were significantly potentiated in basilar arteries from rabbits injected with AdBDNF. Potentiation of relaxations to acetylcholine in AdBDNF-treated basilar arteries was inhibited by the nonselective cyclooxygenase inhibitor, indomethacin (10
−5
mol/L,
P
<0.05, n=6) and constitutive phospholipase A
2
inhibitor, AACOCF3 (2×10
−5
mol/L,
P
<0.05, n=5).

Conclusion—

Our results demonstrate that in cerebral arteries, BDNF-induced activation of tropomyosin receptor kinase B receptor signaling in vivo promotes prostacyclin biosynthesis. These findings provide novel mechanistic insight into the vascular protective effect of BDNF in cerebral circulation.
The Potential for Actigraphy to Be Used as an Indicator of Sitting Discomfort
Authors: Telfer Scott , Spence William D. , Solomonidis Stephan E.
Published: December 2009

Objective: A novel technique that uses actigraphy, the study of activity involving the use of body-mounted accelerometers, to detect the discomfort-related movements of a sitting individual has been proposed as a potential indicator of sitting discomfort, and the purpose of this study was to test its validity. Background: Objective measurement of sitting discomfort has always been challenging for researchers. Electromyographic measurements, pressure mapping, and a wide range of other techniques have all been investigated with limited success. Method: The activity monitor’s ability to detect and measure seated movement was assessed, and 12 participants were tested on four different chairs (100-min sessions for each). Results: The activity monitor was able to detect participants’ sitting movements (Pearson coefficients > 0.9). The chairs were shown to have significantly different subjective discomfort ratings, all of which increased over time. The movements detected by the activity monitor also increased significantly with time, and the amount measured was greater in the chairs rated as most uncomfortable. Regression analysis indicated that the actigraphy data were able to account for 29.6% of the variation in perceived discomfort ratings. Conclusion: Actigraphy can reliably detect sitting movements and may be of use in measuring sitting discomfort. Application: Potential applications of this technique exist for seating research in the automotive industry, health care, and office and leisure chairs.
Text Messaging During Simulated Driving
Authors: Drews Frank A. , Yazdani Hina , Godfrey Celeste N. , Cooper Joel M. , Strayer David L.
Published: December 2009

Objective: This research aims to identify the impact of text messaging on simulated driving performance. Background: In the past decade, a number of on-road, epidemiological, and simulator-based studies reported the negative impact of talking on a cell phone on driving behavior. However, the impact of text messaging on simulated driving performance is still not fully understood. Method: Forty participants engaged in both a single task (driving) and a dual task (driving and text messaging) in a high-fidelity driving simulator. Results: Analysis of driving performance revealed that participants in the dual-task condition responded more slowly to the onset of braking lights and showed impairments in forward and lateral control compared with a driving-only condition. Moreover, text-messaging drivers were involved in more crashes than drivers not engaged in text messaging. Conclusion: Text messaging while driving has a negative impact on simulated driving performance. This negative impact appears to exceed the impact of conversing on a cell phone while driving. Application: The results increase our understanding of driver distraction and have potential implications for public safety and device development.
“Presidents of Color,” Globalization, and Social Inequality
Authors: Germain Felix
Published: December 2009

In this era of globalization, social inequality based on racial attributes is increasingly perceived as anachronistic. Moreover, citizens of racially diverse countries have gained a new consciousness, which occasionally translates into electing a president from a racially underrepresented group. However, although members of these racially underrepresented groups have obtained presidential appointments, racism and social inequality persist. This article sheds light on the trans-national discourses of reverse discrimination that result from the election of “presidents of color.” It suggests that while these discourses take different shapes and forms, they aim to minimize the continuities of racialized relations, thereby painting utopian pictures of modern societies. The article also reveals the extent to which these leaders can reduce the social inequalities and racism plaguing their countries. By examining the legacy of Nelson Mandela in South Africa and the presidency of Bolivia’s Evo Morales, this article argues that to accomplish these intertwined goals, Barack Obama and other presidents from racially underrepresented groups must enact local policies that contradict the logics of globalization, which is based on the free movement of labor and capital.
“Yes We Can” or “Yes We Did”?
Authors: Ford Pearl K. , Johnson Tekla A. , Maxwell Angie
Published: December 2009

The election of Barack Obama as the first African American president speaks to the progress made in fulfilling the promise of one nation for all people. Obama’s success reflects retrospective changes, such as the advent of viral technology, the mobilization of Black voters, and the shift toward tolerance in White racial attitudes, all of which allowed a strategic Obama campaign to make landmark gains. But are these changes permanent? Moreover, will these retrospective changes benefit future African American candidates seeking political office? On the other hand, following an extremely unpopular Bush administration, the Obama victory could reflect the prospective changes that many voters believed would follow, including the restoration of American credibility abroad, economic recovery, and the move toward a postracial state. Have Obama’s first 100 days fulfilled these prospective visions? And if so, will Obama’s actions in these areas prove advantageous to minority candidates who follow in his historic footsteps?
Southern Strategy 2.0
Authors: Edge Thomas
Published: December 2009

In the rush of excitement over Barack Obama’s nomination and ascension to the presidency of the United States, many media figures were loathe to analyze the impact of race on both the rhetoric of the election and the actual results. From across the political spectrum, pundits argued that race did not play a major role on Election Day, without offering any context to such comments. Likewise, conservatives in particular have used that idea to assert that racism is no longer a hindrance to advancement in American society. This article seeks to examine the role of race in the election, both in political attacks on Barack Obama and in an analysis of the voting patterns, with a particular emphasis on how conservatives have tried to shape the contours of these discussions. Their purpose, it is argued, is to launch Southern Strategy 2.0, which seeks to use Obama’s victory to attack some of the results of the civil rights movement that helped make his rise possible. At the same time, it still plays on some of the overt racism of the first Southern Strategy, using Obama’s racial identity and politics to challenge whether he is “American” enough to lead the nation. Thus, conservatives use Obama’s image as a sign that racism is dead, while simultaneously attacking him with the same race-based tactics that have played such an important role in the recent history of the Republican Party.
Turning Out the Center
Authors: Howard Philip S. S.
Published: December 2009

Given President Obama’s current ambiguous stand on racial matters, many African Americans are asking legitimate questions about the implications of his presidency for African Americans and for antiracist struggle. They speculate about whether he has “sold out” or whether he is strategizing for a future moment when he will act decisively in the interest of African Americans in fulfilling his duty to serve all Americans. This article contends that Obama’s ambiguity and the need to pose the above questions flow from the contradictions involved with an African American occupying the presidential office in a country that has yet to eradicate anti-Black racism. The fundamental question, then, is one about the limits around African agency within dominant institutions. Through a discussion of African agency and African conceptions of community, this article contributes to a conversation about how African Americans might maximize African agency where it is found within dominant institutions.
Barack Obama and the Politics of Race
Authors: Teasley Martell , Ikard David
Published: December 2009

Many scholars across racial lines argue that the historic election of Barack Obama as the first African American president of the United States marks the dawning of a “postracial era” in our country. Despite this claim and unprecedented enthusiasm that abounds within African American circles about the direction of race relations in this country, there seems to be a glaring ideological disconnect between the desire and reality of a race-free society. Focusing attention on this disconnect and the symbolic capital of “hope” that Obama’s presidency constitutes for the Black community, this article exposes the potential pitfalls of wholesale investment in postracial thinking, particularly for the most economically vulnerable African American populations. Chief among the questions that the authors ask is how African Americans can productively address the continuing challenges of race-centric oppression under an Obama administration that is itself an embodiment of this postrace thinking.
Coping Styles and Strategies: A Comparison of Adolescent Students With and Without Learning Disabilities
Authors: Firth Nola , Greaves Daryl , Frydenberg Erica
Published: December 2009

In this study, the authors compared the results of a coping measure completed by 98 seventh through ninth grade students who were assessed as having learning disabilities with published means from the general Australian student population. The Adolescent Coping Scale was the measure used. The results suggested higher use by students aged 12 to 13 years who had learning disabilities of an overall nonproductive coping style and in particular of the nonproductive strategies of ignoring the problem and not coping. Although there was no difference in overall productive or nonproductive coping style for 14- to 15-year-olds, the students in this age group who had learning disabilities reported higher use of the strategies of not coping and ignoring the problem. These findings are discussed in relation to a need for interventions that give students who have learning disabilities strategies that address the risk of a passive coping style.
Transnational Alliances
Authors: Churchill Lindsey
Published: December 2009

An examination of U.S. feminists’ attempts at solidarity and interactions with Latin American movements and activists between 1970 and 1989 focuses on two radical feminist organizations—the Atlanta Lesbian Feminist Alliance (ALFA) and the Women’s International Resource Exchange (WIRE)—in order to illuminate the complicated nature of solidarity between First World and Third World feminism. Although solidarity with Latin America was central to many leftwing organizations during the 1970s and 1980s, the experience of radical feminist groups demonstrates how alliances of gender and sexuality altered these relationships of solidarity. Indeed, when socialist Cuba marginalized homosexuals, some radical feminists questioned which political identity to privilege—that of socialist or that of lesbian feminist.
CAFTA Opposition
Authors: Finley-Brook Mary , Hoyt Katherine
Published: December 2009

Overlapping transnational networks attempted to reconcile divergent perspectives— some favoring rejection, others reform—and leverage change in the U.S. government’s framing of the Central American Free Trade Agreement (CAFTA). The experience of the Stop CAFTA Coalition shows that protest movements cannot be fully understood from the perspective of a single period in time. Core coalition members began organizing decades prior to CAFTA’s proposal, generally on a topic other than free trade, and their solidarity-based decision-making model was fundamental to their decision to reject rather than attempt to reform CAFTA—since this was the position of their Central American partner organizations. A split between reforming CAFTA and more radically transforming free trade with the United States emerged as a fault line in CAFTA opposition, but solidarity groups maintained their anti-free-trade position even as they cooperated within networks representing distinct interests.
Solidarity with Sandino
Authors: Grossman Richard
Published: December 2009

The intervention of the U.S. Marines in Nicaragua in 1926 inspired opposition of two kinds, one against any U.S. intervention and the other specifically aligned with the Nicaraguan guerrillas under Augusto Sandino. These groups succeeded in having limits placed on the war but, by abandoning Sandino at a critical moment, set the stage for the creation of a new pro-U.S. Nicaraguan military that was able to seize power and control Nicaragua without the need for U.S. troops. The Somoza dictatorship was an unintended Nicaragua without the need for U.S. troops. The Somoza dictatorship was an unintended consequence of the organized opposition to U.S. intervention.
The Sanctuary Movement and Central American Activism in Los Angeles
Authors: Stoltz Chinchilla Norma , Hamilton Nora , Loucky James
Published: December 2009

The Sanctuary movement of the 1980s combined religious faith and social activism to provide refuge for Central Americans fleeing violence and persecution and to raise awareness of the responsibility associated with U.S. policy in the region. Features of the Los Angeles area, such as its large Latino population, provided support and a sense of community; in this sense the city itself was a sanctuary. The presence of many Central Americans who brought their experience and skills in organizing in their home countries to the development of solidarity and refugee organizations in Los Angeles were also an important resource for the Sanctuary movement. The development of the Sanctuary movement was characterized by the interaction of spiritual ethics and religious practice with activism in raising consciousness and providing legitimacy. The strength of the movement lay particularly in the profound experiences and narratives of refugees, shared through personal connections that spanned cultures and countries.
Strategies for Union Renewal in the Context of Public Sector Outsourcing
Authors: Cunningham Ian , James Philip
Published: December 2009

In the face of significant declines in union membership and organizing, a variety of strategies for union renewal have been identified. Views differ, however, concerning how far these strategies should be seen as mutually supportive. This article explores this issue drawing on research findings that shed light on the challenges that unions face in recruiting and organizing voluntary sector workers employed in the provision of outsourced public social care services in the UK. It concludes that unions, at least in certain contexts, can potentially utilize a combination of the strategies identified, but that the effective adoption of such an approach requires them to successfully address a number of difficult s trategic challenges.
Anger and Retribution After Collective Overuse: The Role of Blaming and Environmental Uncertainty in Social Dilemmas
Authors: de Kwaadsteniet Erik W. , van Dijk Eric , Wit Arjaan , De Cremer David
Published: December 2009

This article investigates how group members respond to one another when collective overuse occurs. The authors argue that interpersonal reactions after overuse in a common-resource dilemma are largely determined by the environmental characteristics of the social dilemma. More specifically, under environmental certainty they expect people to show more anger to group members than under uncertainty (Study 1). Additionally, they expect stronger retributive reactions to high harvesters than to moderate harvesters, and they expect this difference to be larger under certainty than under uncertainty (Study 2 and 3). Moreover, they predict that these effects are mediated by blaming. The results of three experiments corroborate these predictions.
Coping With Memory Effect and Serial Correlation When Estimating Reliability in a Longitudinal Framework
Authors: Laenen Annouschka , Alonso Ariel , Molenberghs Geert , Vangeneugden Tony , Mallinckrodt Craig H.
Published: December 2009

Longitudinal studies are permeating clinical trials in psychiatry. Therefore, it is of utmost importance to study the psychometric properties of rating scales, frequently used in these trials, within a longitudinal framework. However, intrasubject serial correlation and memory effects are problematic issues often encountered in longitudinal data. In the present work the authors study, via simulation, the impact of uncontrolled sources of serial correlation on newly proposed measures, designed to evaluate reliability in a longitudinal scenario. This study also addresses the relationship between serial correlation and memory effect. The simulations illustrate that ignoring serial correlation can have a severe impact on the estimates of reliability and on inferences related to it. Importantly, the authors show that the underlying modeling framework used in this new approach allows correcting for this type of correlation and avoiding bias. Moreover, it can adjust for the presence of a memory effect. Nevertheless, to achieve that, a careful model building is required.
Roles for Inflammation and Regulatory T Cells in Colon Cancer
Authors: Erdman Susan E. , Poutahidis Theofilos
Published: December 2009

Risk for developing cancer rises substantially as a result of poorly regulated inflammatory responses to pathogenic bacterial infections. Anti-inflammatory CD4+ regulatory cells (TREG) function to restore immune homeostasis during chronic inflammatory disorders. It seems logical that TREG cells would function to reduce risk of inflammation-associated cancer in the bowel by down-regulating inflammation. It is widely believed, however, that T REG function in cancer mainly to suppress protective anticancer inflammatory responses. Thus roles for inflammation, TREG cells, and gut bacteria in cancer are paradoxical and are the subject of controversy. Our accumulated data build upon the ‘‘hygiene hypothesis’’ model in which gastrointestinal (GI) infections lead to changes in TREG that reduce inflammation-associated diseases. Ability of TREG to inhibit or suppress cancer depends upon gut bacteria and IL-10, which serve to maintain immune balance and a protective anti-inflammatory TREG phenotype. However, under poorly regulated pro-inflammatory conditions, TREG fail to inhibit and may instead contribute to a T helper (Th)-17-driven procarcinogenic process, a cancer state that is reversible by down-regulation of inflammation and interleukin (IL)-6. Consequently, hygienic individuals with a weakened IL-10— and TREG—mediated inhibitory loop are highly susceptible to the carcinogenic consequences of elevated inflammation and show more frequent inflammation-associated cancers. Taken together, these data help explain the paradox of inflammation and TREG in cancer and indicate that targeted stimulation of TREG may promote health and significantly reduce risk of cancer.
Precancer: Sequentially Acquired or Predetermined?
Authors: Cardiff Robert D. , Borowsky Alexander D.
Published: December 2009

Recognition of focal morphological intraepithelial lesions associated with the eventual development of invasive cancer has long been the sine qua non of precancer. Empirically, precancers are associated with a morphological continuum from atypia to dysplasia and invasive neoplasia. Such lesions are used as early indicators of cancers and have dramatically reduced mortality from cancers of the colon, uterine cervix, and breast. Progression has been modeled as a linear, stepwise process. Some molecular evidence supports a linear model. However, clinical studies now suggest that preexisting cofactors such as human papilloma virus (HPV) in cervical cancer determines the cell fate. Other clinical studies such as bladder, prostate, and breast suggest that many intraepithelial lesions do not progress to malignancy. The more recent experimental analyses reveal that the key molecular and genetic events even predate the emergence of visible lesions. Thus, a new nonlinear, parallel model is proposed. The parallel model suggests an origin in a putative progenitor cell that expands and invades. The clinical outcome is thus predetermined. If correct, this model suggests that ‘‘progression’’ to malignancy is epigenetic. Further, future assessment of biological potential will involve identification and genetic analysis of the progenitor cell populations.