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Blocked Pressure

The Experts below are selected from a list of 63 Experts worldwide ranked by ideXlab platform

Junichi Yoshikawa – 1st expert on this subject based on the ideXlab platform

  • Carvedilol inhibits Pressure-induced increase in oxidative stress in coronary smooth muscle cells.
    Hypertension Research, 2002
    Co-Authors: Kenichi Yasunari, Kensaku Maeda, Munehiro Nakamura, Junichi Yoshikawa

    Abstract:

    The cellular mechanisms by which hypertension enhances atherosclerosis are still not known in detail. Recently, evidence has been obtained that oxidative stress plays a role in the pathogenesis of Pressure-induced atherosclerosis. We examined the effects of Pressure on oxidative stress in cultured human coronary smooth muscle cells (SMCs). Application of increased Pressure (+100 mmHg) with He gas for 48 h increased oxidative stress of measured by flow cytometry by 71% and F2-isopretane by 77%. Increased Pressure also increased the activities of phospholipase D (PLD), and particulate protein kinase C (PKC). The PLD inhibitor suramin 100 μmol⁄l, 1-butanol 40 mmol⁄l, and the PKC inhibitors chelerythrine 1 μmol⁄l and calphostin C 100 nmol⁄l and completely Blocked the increase in oxidative stress induced by Pressure. Carvedilol 1 μmol⁄l but not propranolol 1 μmol⁄l Blocked Pressure-induced increases in oxidative stress in cultured SMCs. These findings suggest that Pressure increases oxidative stress and that carvedilol significantly inhibits Pressure-induced increase in oxidative stress in cultured human coronary smooth muscle cells. (Hypertens Res 2002; 25: 419-425)

  • Pressure Promotes Angiotensin II–Mediated Migration of Human Coronary Smooth Muscle Cells Through Increase in Oxidative Stress
    Hypertension, 2002
    Co-Authors: Kenichi Yasunari, Kensaku Maeda, Munehiro Nakamura, Junichi Yoshikawa

    Abstract:

    Angiotensin II–mediated oxidative stress may play a role in the pathogenesis of coronary atherosclerosis. We examined the effects of Pressure on the angiotensin II–mediated increase in oxidative stress and migration of cultured human coronary smooth muscle cells (SMCs). Increased Pressure (100 mm Hg) by helium gas for 48 hours increased angiotensin II–mediated oxidative stress as evaluated by flow cytometry and SMC migration (from 15.9±2.2 to 32.0±2.4 cells per 4 high-power fields, P P N -acetylcysteine (100 mmol/L) but not PD123319 (1 μmol/L) also Blocked Pressure-induced increases in angiotensin II–mediated oxidative stress and SMC migration ( P

Goran Pavić – 2nd expert on this subject based on the ideXlab platform

  • Experimental characterization of air-borne sound sources via surface coupling
    Applied Acoustics, 2018
    Co-Authors: Liangfen Du, Goran Pavić

    Abstract:

    Abstract The paper examines whether an advanced experimental method, the surface coupling method, could be used to intrinsically characterize a sound source. Such a characterization can be used in turn to predict sound radiation of the source into an arbitrary space. The surface coupling method considers the source as being made up of the physical source together with a part of the surrounding medium contained within an enveloping surface. The source is entirely characterized by two intrinsic descriptors measured across the interface surface – its Blocked Pressure and its surface impedance. In order to allow the use of a simple-shaped interface the identification of descriptors is done by the Patch Impedance approach. To demonstrate the principle of the surface coupling method a 1D experimental validation – prediction of sound radiated by a driver in a tube – is carried out first. The validation of the general 3D technique is then done by characterizing a 2-driver loudspeaker radiating into an irregular cavity. Both experiments confirm the feasibility of the sound prediction by experimental source characterization via surface coupling.

  • Air-borne sound source characterization by patch impedance coupling approach
    Journal of Sound and Vibration, 2010
    Co-Authors: Goran Pavić

    Abstract:

    An approach of independent sound source characterization is discussed. The source is defined by its Blocked sound Pressure and surface impedance via a suitable enveloping surface. Both the Blocked Pressure and the impedance are made discrete using the patch averaging concept. The approach is adapted to numerical as well as experimental implementation. The characterization of a source by patches allows for acoustical sub-structuring, which in turn enables the prediction of the sound field created by a source coupled to an arbitrary environment. Numerical simulations are presented which demonstrate the validity of the approach. (C) 2010 Elsevier Ltd. All rights reserved.

  • Modelling and characterization of airborne noise sources
    Journal of Sound and Vibration, 2003
    Co-Authors: Yu. I. Bobrovnitskii, Goran Pavić

    Abstract:

    Abstract A comprehensive model of an arbitrary airborne noise source is developed in this paper. It can be used for noise prediction in complex environment conditions. The model, described by a limited number of parameters—the source impedance and Blocked Pressure—is invariant with respect to the surrounding acoustical environment. Procedures for experimental identification of model parameters in an arbitrary enclosure are presented. These procedures require only conventional equipment and facilities, and thus can be applied widely. Two analytical examples confirm the validity of the approach.

Kenichi Yasunari – 3rd expert on this subject based on the ideXlab platform

  • Carvedilol inhibits Pressure-induced increase in oxidative stress in coronary smooth muscle cells.
    Hypertension Research, 2002
    Co-Authors: Kenichi Yasunari, Kensaku Maeda, Munehiro Nakamura, Junichi Yoshikawa

    Abstract:

    The cellular mechanisms by which hypertension enhances atherosclerosis are still not known in detail. Recently, evidence has been obtained that oxidative stress plays a role in the pathogenesis of Pressure-induced atherosclerosis. We examined the effects of Pressure on oxidative stress in cultured human coronary smooth muscle cells (SMCs). Application of increased Pressure (+100 mmHg) with He gas for 48 h increased oxidative stress of measured by flow cytometry by 71% and F2-isopretane by 77%. Increased Pressure also increased the activities of phospholipase D (PLD), and particulate protein kinase C (PKC). The PLD inhibitor suramin 100 μmol⁄l, 1-butanol 40 mmol⁄l, and the PKC inhibitors chelerythrine 1 μmol⁄l and calphostin C 100 nmol⁄l and completely Blocked the increase in oxidative stress induced by Pressure. Carvedilol 1 μmol⁄l but not propranolol 1 μmol⁄l Blocked Pressure-induced increases in oxidative stress in cultured SMCs. These findings suggest that Pressure increases oxidative stress and that carvedilol significantly inhibits Pressure-induced increase in oxidative stress in cultured human coronary smooth muscle cells. (Hypertens Res 2002; 25: 419-425)

  • Pressure Promotes Angiotensin II–Mediated Migration of Human Coronary Smooth Muscle Cells Through Increase in Oxidative Stress
    Hypertension, 2002
    Co-Authors: Kenichi Yasunari, Kensaku Maeda, Munehiro Nakamura, Junichi Yoshikawa

    Abstract:

    Angiotensin II–mediated oxidative stress may play a role in the pathogenesis of coronary atherosclerosis. We examined the effects of Pressure on the angiotensin II–mediated increase in oxidative stress and migration of cultured human coronary smooth muscle cells (SMCs). Increased Pressure (100 mm Hg) by helium gas for 48 hours increased angiotensin II–mediated oxidative stress as evaluated by flow cytometry and SMC migration (from 15.9±2.2 to 32.0±2.4 cells per 4 high-power fields, P P N -acetylcysteine (100 mmol/L) but not PD123319 (1 μmol/L) also Blocked Pressure-induced increases in angiotensin II–mediated oxidative stress and SMC migration ( P