The Experts below are selected from a list of 237 Experts worldwide ranked by ideXlab platform

P C Johnson - One of the best experts on this subject based on the ideXlab platform.

  • Contribution of red blood Cell Aggregation to venous vascular resistance in skeletal muscle
    American Journal of Physiology-Heart and Circulatory Physiology, 1997
    Co-Authors: M Cabel, Herbert J. Meiselman, A S Popel, P C Johnson
    Abstract:

    The effects of red blood Cell Aggregation on venous vascular resistance and conductance were examined in the cat lateral gastrocnemius muscle. During perfusion with blood of normal hematocrit, veno...

  • Contribution of red blood Cell Aggregation to venous vascular resistance in skeletal muscle.
    The American journal of physiology, 1997
    Co-Authors: M Cabel, H J Meiselman, A S Popel, P C Johnson
    Abstract:

    The effects of red blood Cell Aggregation on venous vascular resistance and conductance were examined in the cat lateral gastrocnemius muscle. During perfusion with blood of normal hematocrit, venous conductance fell linearly by 41% when blood flow was reduced from 5 to 1 ml x min(-1) x 100 g tissue(-1) and increased linearly by 155% when flow was increased from 5 to 20 ml x min(-1) x 100 g tissue(-1). This effect was not seen when the muscle was perfused with an aCellular solution of 12% Dextran 40 in Ringer solution and was greatly reduced or absent with a nonaggregating suspension of red blood Cells in Ringer solution + Dextran 40. Also, the venous vascular conductance at a control flow of 5 ml x min(-1) x 100 g tissue(-1) during perfusion with the nonaggregating red blood Cell suspension was twice that with normal blood of the same hematocrit. The effect of flow on venous conductance was significantly reduced when red blood Cell Aggregation was increased by addition of Dextran 250 to the blood (200 mg/kg body wt) and was also reduced in animals with systemic hematocrit >50%. These findings suggest that red blood Cell Aggregation contributes importantly to venous vascular resistance in resting muscle.

Valérie Lobjois - One of the best experts on this subject based on the ideXlab platform.

  • Cell–Cell Adhesion and Cytoskeleton Tension Oppose Each Other in Regulating Tumor Cell Aggregation
    Cancer research, 2015
    Co-Authors: Laure Saias, Aurélie Gomes, Martine Cazales, Bernard Ducommun, Valérie Lobjois
    Abstract:

    Cell Aggregation is frequently impaired during the growth of primary tumors and the formation of metastatic lesions. Cell Aggregation depends on Cell–Cell adhesion; however, no rigorous approach exists to monitor and quantify it accurately in the absence of the confounding factors of Cell–substrate adhesion and the resulting Cell motility on the substrate. We report here a highly reproducible, automated, microscopy-based quantification of tumor-Cell spheroid formation in the absence of Cell–substrate adhesion and use it to characterize Cell Aggregation dynamics in the early steps of this process. This method is based on fluorescence and bright-field microscopy and on a custom MATLAB program to quantify automatically the Cells9 Aggregation kinetics. We demonstrate that the Cell–Cell adhesion protein E-cadherin and the desmosome proteins DSG2 and DSC2 are important for Aggregation. Furthermore, we show that inhibition or silencing of myosin IIa enhances Aggregation, suggesting that cytoskeleton tension inhibits tumor Cell Aggregation. This work opens new avenues to study the principles that govern multiCellular Aggregation, to characterize the Aggregation properties of various tumor Cell types, as well as to screen for drugs that inhibit or promote Aggregation. Cancer Res; 75(12); 2426–33. ©2015 AACR.

  • Cell Cell adhesion and cytoskeleton tension oppose each other in regulating tumor Cell Aggregation
    Cancer Research, 2015
    Co-Authors: Laure Saias, Aurélie Gomes, Martine Cazales, Bernard Ducommun, Valérie Lobjois
    Abstract:

    Cell Aggregation is frequently impaired during the growth of primary tumors and the formation of metastatic lesions. Cell Aggregation depends on Cell–Cell adhesion; however, no rigorous approach exists to monitor and quantify it accurately in the absence of the confounding factors of Cell–substrate adhesion and the resulting Cell motility on the substrate. We report here a highly reproducible, automated, microscopy-based quantification of tumor-Cell spheroid formation in the absence of Cell–substrate adhesion and use it to characterize Cell Aggregation dynamics in the early steps of this process. This method is based on fluorescence and bright-field microscopy and on a custom MATLAB program to quantify automatically the Cells9 Aggregation kinetics. We demonstrate that the Cell–Cell adhesion protein E-cadherin and the desmosome proteins DSG2 and DSC2 are important for Aggregation. Furthermore, we show that inhibition or silencing of myosin IIa enhances Aggregation, suggesting that cytoskeleton tension inhibits tumor Cell Aggregation. This work opens new avenues to study the principles that govern multiCellular Aggregation, to characterize the Aggregation properties of various tumor Cell types, as well as to screen for drugs that inhibit or promote Aggregation. Cancer Res; 75(12); 2426–33. ©2015 AACR.

Jill J. F. Belch - One of the best experts on this subject based on the ideXlab platform.

  • A study of whole blood platelet and white Cell Aggregation using a laser flow aggregometer.
    Platelets, 2003
    Co-Authors: J. Sun, Eric Abel, A. Bancroft, Margaret Mclaren, Jill J. F. Belch
    Abstract:

    Both platelet Aggregation and white blood Cell Aggregation are involved in pathological processes such as thrombosis, atherosclerosis and chronic inflammation. People in older age groups are likely to suffer from cardiovascular diseases and may have increased white Cell and platelet Aggregation which could contribute to this increased risk. This study aimed to compare white Cell and platelet Aggregation between different age and gender groups. Whole blood white Cell Aggregation and platelet Aggregation were carried out on healthy volunteers using cytometric techniques. It was found that both white Cell and platelet Aggregation in the elderly group (white Cell Aggregation median value, 0.08; range, 0.02-0.14; platelet Aggregation median value, 0.32; range, 0.1-0.39) were significantly higher ( P = 0.017 for white Cell Aggregation, P = 0.007 for platelet Aggregation) than in the younger group (white Cell Aggregation median value, 0.05; range, 0.01-0.14; platelet Aggregation median value, 0.18; range, 0.07-0...

  • Cigarette smoking increases white blood Cell Aggregation in whole blood.
    Journal of the Royal Society of Medicine, 1993
    Co-Authors: A. B. Bridges, Alexander Hill, Jill J. F. Belch
    Abstract:

    We studied the effect of chronic cigarette smoking on white blood Cell Aggregation, increased Aggregation predisposes to microvascular occlusion and damage. Current smokers had significantly increased white blood Cell Aggregation when compared with non smokers. The presence of chronically activated white blood Cells in current smokers may be relevant in the pathogenesis of ischaemic vascular disease.

Herbert J. Meiselman - One of the best experts on this subject based on the ideXlab platform.

M Cabel - One of the best experts on this subject based on the ideXlab platform.

  • Contribution of red blood Cell Aggregation to venous vascular resistance in skeletal muscle
    American Journal of Physiology-Heart and Circulatory Physiology, 1997
    Co-Authors: M Cabel, Herbert J. Meiselman, A S Popel, P C Johnson
    Abstract:

    The effects of red blood Cell Aggregation on venous vascular resistance and conductance were examined in the cat lateral gastrocnemius muscle. During perfusion with blood of normal hematocrit, veno...

  • Contribution of red blood Cell Aggregation to venous vascular resistance in skeletal muscle.
    The American journal of physiology, 1997
    Co-Authors: M Cabel, H J Meiselman, A S Popel, P C Johnson
    Abstract:

    The effects of red blood Cell Aggregation on venous vascular resistance and conductance were examined in the cat lateral gastrocnemius muscle. During perfusion with blood of normal hematocrit, venous conductance fell linearly by 41% when blood flow was reduced from 5 to 1 ml x min(-1) x 100 g tissue(-1) and increased linearly by 155% when flow was increased from 5 to 20 ml x min(-1) x 100 g tissue(-1). This effect was not seen when the muscle was perfused with an aCellular solution of 12% Dextran 40 in Ringer solution and was greatly reduced or absent with a nonaggregating suspension of red blood Cells in Ringer solution + Dextran 40. Also, the venous vascular conductance at a control flow of 5 ml x min(-1) x 100 g tissue(-1) during perfusion with the nonaggregating red blood Cell suspension was twice that with normal blood of the same hematocrit. The effect of flow on venous conductance was significantly reduced when red blood Cell Aggregation was increased by addition of Dextran 250 to the blood (200 mg/kg body wt) and was also reduced in animals with systemic hematocrit >50%. These findings suggest that red blood Cell Aggregation contributes importantly to venous vascular resistance in resting muscle.