35 research outputs found

    Evaluating coasean bargaining experiments with meta-analysis

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    While the Coase Theorem has been a touchstone for understanding bargaining behavior, it has also been criticized for relying on unrealistic assumptions. In response, a line of experimental research analyzes bargaining behavior in laboratory settings. This paper uses meta-analysis to evaluate the Coasean bargaining literature by modeling the probability of an efficient bargain as a function of: (1) measures of transaction costs and related variables, and (2) measures of the social dimensions of a bargain. Results suggest that efficient solutions are more likely when explicit transaction costs do not exist, in the absence of a binding time limit, and when participants have perfect information on payoff schedules. Social dimension variables are found to have the potential to affect bargaining outcomes and are an important avenue for further research.Coase Theorem

    Differential effects of reduced cyclic stretch and perturbed shear stress within the arterial wall

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    Due to the pulsatile nature of blood flow, arteries are constantly exposed to dynamic mechanical forces; the pulsatility continuously stretches the vessel wall and the flow creates a frictional force on the interior surface. These stresses, referred to as cyclic circumferential stretch and shear stress, are known to determine arterial structure and morphology; modulation of which leads to the progression of vascular diseases such as hypertension and atherosclerosis. Yet the individual contributions of cyclic stretch and shear stress, with regards to vascular disease, have yet to be revealed. In this thesis I wish to identify the role of reduced cyclic stretch in the development of endothelial dysfunction and vascular remodeling, develop an experimental model for studying the autonomous effects of shear stress and cyclic stretch and how these two stimuli individually modulate markers of vascular disease in different regions of the vascular wall. I will begin by introducing the different structural and cellular components of the vascular wall and their individual functions. From here I will introduce how hemodynamic forces transmitted to the vascular wall due to the pulsatile nature of blood flow play an essential role maintaining arterial health and function. And as such, how deviations from a physiologic hemodynamic range can have catastrophic implications for the vasculature. Next I will introduce how certain hemodynamic conditions can stimulate cellular dysfunction and how this relates to initiation and progression of vascular disease. In the first paper, we set out to determine if reduction of cyclic stretch could be a factor which induces remodeling of the arterial wall. We found that reducing compliance caused a decrease in vascular smooth muscle function, as well as inducing switch in smooth muscle cell phenotype. Arteries exposed to a reduced cyclic stretch also exhibited increased matrix degradation and cellular proliferation than those allowed to stretch physiologically. These findings accent the importance of cyclic stretch in the maintenance of a differentiated and fully functional phenotype of vascular smooth muscle cells, as well as in the regulation of migratory properties, proliferation and matrix turnover in the vascular wall. In the second paper we investigated how reduction of cyclic stretch influences endothelial dysfunction and modulation of nitric oxide bioavailability. We observed that reduced compliance significantly decreases the activity of the enzyme responsible for producing nitric oxide (eNOS). Overall production of reactive oxygen species were also increased by reducing compliance, which we were able to attribute to stimulation of the superoxide generating NAD(P)H oxidase. We found that experimentally reduced compliance also caused a significant decrease in endothelial function, as assessed with bradykinin dependent vascular relaxation. The results from this study point out how reduced arterial compliance interrupts the eNOS activation pathway and increases vascular levels of oxidative stress, which together could explain the measured decreases on endothelial functionality. In the third article we used our experimental model to investigate how shear stress and cyclic stretch independently stimulate the vascular wall. We found that both oscillatory flow and reduced stretch are detrimental to endothelial function, whereas oscillatory flow alone, dominated total endogenous vascular wall superoxide anion production. Yet when superoxide anion production was analyzed in just the endothelial region we observed that it was modulated more significantly by reduced cyclic stretch than by oscillatory shear, emphasizing an important distinction between shear and stretch mediated effects to the vascular wall. Analysis of eNOS and nitro-tyrosine, the by-product of superoxide anion and nitric oxide, proved that they too are more significantly negatively modulated by oscillatory flow, than by reduced stretch. The findings from this study point out how shear and stretch stimulate regions of the vascular wall differently, affecting NO bioavailability and contributing to vascular disease. The goal of the fourth article is to further investigate how shear stress and cyclic stretch modulate markers of vascular remodelling in different regions of the arterial wall. We demonstrated that while total superoxide production, fibronectin expression and gelatinase activation are predominantly mediated by shear stress, their expression in the endothelial region is mediated by reduced cyclic stretch, which correlates well with results from total MMP-2 expression. By plotting intensity versus radius for these markers of vascular remodeling we are able to see that superoxide production and gelatinase activity follows trends indicating their expression is in part mediated by stress distributions through out the vascular wall, while fibronectin and p22-phox were much less or not at all. Most importantly these findings, when coupled with our results from tissue reactive studies, suggest that the arterial remodeling process triggered in the endothelial region due to reduced stretch causes the most significant changes in arterial smooth muscle function. Perturbed shear stress and reduced arterial compliance have both been implicated in the initiation and progression of vascular disease: this work provides a new perspective into how these stimuli are perceived through out the vascular wall. To conclude, this body of work has shown that cyclic stretching due to the pulsatile nature of blood flow is an essential stimulus regulating arterial remodeling and endothelial viability. We have performed experiments permitting the autonomous effects of cyclic stretch and shear stress to be studied. Yet more importantly, we have shown how cyclic stretch and shear stress stimulate the vascular wall in different regions and compared this data to arterial functionality studies. These results have indicated that although reduced cyclic stretch may not stimulate the total expression of certain markers of vascular disease as much as an OSC shear stress, it does so in specific regions of the vascular wall which can in fact have a more detrimental effect on arterial function. As reduced arterial cyclic stretching is associated with the aging process, this work gives insight into the progression of vascular disease over the course of a person's life time

    Effects of Reduced Cyclic Stretch on Vascular Smooth Muscle Cell Function of Pig Carotids Perfused Ex Vivo

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    Background With advancing age arteries stiffen, reducing arterial compliance and leading to the development of systolic hypertension and to a substantial increase in pulse pressure. An augmented pulse pressure can be a predictor of the development of hypertension, which has been linked to several cardiovascular diseases including atherosclerosis, and to pathologies such as diabetes and renal dysfunction. In this study, we tested the hypothesis that reduced wall compliance induces pulse-pressure-mediated changes in arterial wall metabolism and remodeling. Methods Porcine carotid arteries were perfused for 24 h using an ex vivo arterial support system. Control arteries were exposed to a pulse shear stress (6 ± 3 dynes/cm2) combined with a pulse pressure of 80 ± 10 mm Hg, yielding a physiological cyclic stretch of 4-5%. A reduced compliance group was also studied, in which arteries were wrapped with an external band, thereby decreasing cyclic stretch to levels <1%. Results The experimentally reduced compliance caused a decreased contraction capacity induced by norepinephrine(NE), and this was associated with lower levels of α-smooth muscle cell-actin (α-SMC-actin) and desmin protein expressions. Arteries that were exposed to a reduced cyclic stretch exhibited a higher level of matrix metalloproteinase-2 (MMP-2) expression activity as well as an increase in Ki67 expression, thereby suggesting that matrix degradation and cellular proliferation had been initiated. Furthermore, the expression of plasminogen activator inhibitor-1 (PAI-1) in stiffened arteries was lower than in the control arteries. Conclusions These findings underline the importance of cyclic stretch in the maintenance of a differentiated and fully functional phenotype of vascular SMCs, as well as in the regulation of migratory properties, proliferation, and matrix turnove

    Differential Effects of Reduced Cyclic Stretch and Perturbed Shear Stress Within the Arterial Wall and on Smooth Muscle Function

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    Background Cyclic circumferential stretch and shear stress act in concert and yet are capable of independently mediating arterial smooth muscle function, modulating the production of superoxide and stimulating arterial remodeling. Methods Porcine carotid arteries were perfused ex vivo for 72 h. Groups combining normal (5%) and reduced (1%) stretch with high shear (6 ± 3 dyn/cm2) and oscillatory shear (0.3 ± 3 dyn/cm2) stress were created, while maintaining a pulse pressure of 80 ± 10 mm Hg. Results Total superoxide production, fibronectin expression, and gelatinase activation were mediated by shear stress, but expression in the endothelial region was mediated by reduced cyclic stretch. By plotting intensity vs. radius, we saw that superoxide and gelatinase activity were in part mediated by stress distributions throughout the vascular wall, whereas fibronectin and p22-phox were much less or not at all. These findings, when coupled with our results from tissue reactive studies, suggest that the arterial remodeling process triggered in the endothelial region due to reduced stretch causes the most significant changes in arterial smooth muscle function. Conclusions We have found that the remodeling process triggered by reduced compliance in the endothelial region of large conduit arteries has a more profound detrimental effect to smooth muscle function than that brought on by perturbed shear stress. This work provides new insight by suggesting that although mechanical stimuli such as cyclic stretch and shear stress are known to augment similar markers of vascular remodeling, the location of their expression throughout the vascular wall differs greatly and this can have dramatic effects on vascular function. American Journal of Hypertension 2009; 22:1250-1257 © 2009 American Journal of Hypertension, Lt

    Building Social Capital in Forest Communities: Analysis of New Mexico\u27s Collaborative Forest Restorative Program

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    In part because of its emphasis on building social capital, the Collaborative Forest Restoration Program (CFRP) in New Mexico represents a unique experiment in public lands management. This study uses logit probability modeling to investigate what factors determined CFRP funding, which totaled $26 million between 2001 and 2006. Results reveal program preferences for projects that encourage collaboration and improve forest health, especially in poor counties. Negative determinants of funding include measures of small-diameter material utilization and whether a project takes place across multiple land jurisdictions. There is no evidence of bias toward funding any particular applicant type or land jurisdiction

    Differential effects of reduced cyclic stretch and perturbed shear stress within the arterial wall and on smooth muscle function

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    Cyclic circumferential stretch and shear stress act in concert and yet are capable of independently mediating arterial smooth muscle function, modulating the production of superoxide and stimulating arterial remodeling

    Effects of reduced cyclic stretch on vascular smooth muscle cell function of pig carotids perfused ex vivo

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    With advancing age arteries stiffen, reducing arterial compliance and leading to the development of systolic hypertension and to a substantial increase in pulse pressure. An augmented pulse pressure can be a predictor of the development of hypertension, which has been linked to several cardiovascular diseases including atherosclerosis, and to pathologies such as diabetes and renal dysfunction. In this study, we tested the hypothesis that reduced wall compliance induces pulse-pressure-mediated changes in arterial wall metabolism and remodeling

    Real-time Full Field Laser Doppler Imaging

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    We present a full field laser Doppler imaging instrument that enables real-time in vivo assessment of blood flow in dermal tissue and skin. The instrument monitors the blood perfusion in an area of about 50cm2 with 480 x 480 pixels per frame at a rate of 12-14 frames per second. Smaller frames can be monitored at much higher frame rates. We recorded the microcirculation in healthy skin before, during and after arterial occlusion. In initial clinical case studies, we imaged the microcirculation in burned skin and monitored the recovery of blood flow in a skin flap during reconstructive surgery indicating the high potential of LDI for clinical applications
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