The Experts below are selected from a list of 15 Experts worldwide ranked by ideXlab platform
Chen Fuh Lam - One of the best experts on this subject based on the ideXlab platform.
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spinal cord injury enhances arterial expression and reactivity of α1 adrenergic receptors mechanistic investigation into autonomic dysreflexia
The Spine Journal, 2016Co-Authors: Jungshun Lee, Shih Yuan Fang, Jun Neng Roan, Iming Jou, Chen Fuh LamAbstract:Abstract Background Context Autonomic dysreflexia (AD) usually presents with a significant increase in blood pressure, and uncontrollable autonomic response to stimuli below the level of spinal cord injury (SCI). Purpose This study analyzed the vasomotor function and molecular changes in the peripheral arteries below the lesion of SCI to characterize the mechanism of autonomic dysreflexia. Study Design This was a randomized experimental study in rats. Methods Contusive SCI was induced using a force-Calibrated Weight-drop device at the T10 level in anesthetized rats. Two weeks after severe SCI, blood flow in the femoral arteries was measured, and the vasomotor function and expression of α1-adrenergic receptors were analyzed. Results Blood flow in the femoral artery was significantly reduced in rats with SCI (8.0±2 vs. 17.5±4 mL/min, SCI vs. control, respectively; p=.016). The contraction responses of femoral artery segments to cumulative addition of α1-adrenergic agonist phenylephrine were significantly enhanced in rats with SCI. Expression of α1-adrenergic receptor was upregulated in the medial layer of femoral artery vascular homogenates of these rats. Conclusion Our study provides evidence demonstrating that prolonged denervation below the lesion level following SCI results in a compensatory increased expression of α1-adrenergic receptors in the arterial smooth muscle layer, thereby enhancing the responsiveness to α1-adrenergic agonist and potentiating the development of AD.
Yi Ling Yang - One of the best experts on this subject based on the ideXlab platform.
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transient receptor potential vanilloid type 4 channels mediate na k cl co transporter induced brain edema after traumatic brain injury
Journal of Neurochemistry, 2017Co-Authors: Tai Chun Huang, Ya Hsin Tsai, Yi Ling YangAbstract:Abstract Na(+) -K(+) -2Cl(-) co-transporter (NKCC1) plays an important role in traumatic brain injury (TBI)-induced brain edema via the MAPK cascade. The transient receptor potential vanilloid type 4 (TRPV4) channel participates in neurogenic inflammation, pain transmission, and edema. In this study, we investigated the relationship between NKCC1 and TRPV4 and the related signaling pathways in TBI-induced brain edema and neuronal damage. TBI was induced by the Calibrated Weight-drop device. Adult male Wistar rats were randomly assigned into sham and experimental groups for time-course studies of TRPV4 expression after TBI. Hippocampal TRPV4, NKCC1, MAPK, and PI-3K cascades were analyzed by western blot, and brain edema was also evaluated among the different groups. Expression of hippocampal TRPV4 peaked at 8 h after TBI, and phosphorylation of the MAPK cascade and Akt was significantly elevated. Administration of either the TRPV4 antagonist, RN1734, or NKCC1 antagonist, bumetanide, significantly attenuated TBI-induced brain edema through decreasing the phosphorylation of MEK, ERK, and Akt proteins. Bumetanide injection inhibited TRPV4 expression, which suggests NKCC1 activation is critical to TRPV4 activation. Our results showed that hippocampal NKCC1 activation increased TRPV4 expression after TBI and then induced severe brain edema and neuronal damage through activation of the MAPK cascade and Akt-related signaling pathway.
Tai Chun Huang - One of the best experts on this subject based on the ideXlab platform.
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transient receptor potential vanilloid type 4 channels mediate na k cl co transporter induced brain edema after traumatic brain injury
Journal of Neurochemistry, 2017Co-Authors: Tai Chun Huang, Ya Hsin Tsai, Yi Ling YangAbstract:Abstract Na(+) -K(+) -2Cl(-) co-transporter (NKCC1) plays an important role in traumatic brain injury (TBI)-induced brain edema via the MAPK cascade. The transient receptor potential vanilloid type 4 (TRPV4) channel participates in neurogenic inflammation, pain transmission, and edema. In this study, we investigated the relationship between NKCC1 and TRPV4 and the related signaling pathways in TBI-induced brain edema and neuronal damage. TBI was induced by the Calibrated Weight-drop device. Adult male Wistar rats were randomly assigned into sham and experimental groups for time-course studies of TRPV4 expression after TBI. Hippocampal TRPV4, NKCC1, MAPK, and PI-3K cascades were analyzed by western blot, and brain edema was also evaluated among the different groups. Expression of hippocampal TRPV4 peaked at 8 h after TBI, and phosphorylation of the MAPK cascade and Akt was significantly elevated. Administration of either the TRPV4 antagonist, RN1734, or NKCC1 antagonist, bumetanide, significantly attenuated TBI-induced brain edema through decreasing the phosphorylation of MEK, ERK, and Akt proteins. Bumetanide injection inhibited TRPV4 expression, which suggests NKCC1 activation is critical to TRPV4 activation. Our results showed that hippocampal NKCC1 activation increased TRPV4 expression after TBI and then induced severe brain edema and neuronal damage through activation of the MAPK cascade and Akt-related signaling pathway.
Gunar Schirner - One of the best experts on this subject based on the ideXlab platform.
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rapid high level performance estimation for dse using Calibrated Weight tables
International Embedded Systems Symposium, 2015Co-Authors: Kasra Moazzemi, Smit Patel, Shen Feng, Gunar SchirnerAbstract:Automated Design Space Exploration (DSE) is a critical part of system-level design. It relies on performance estimation to evaluate design alternatives. However, since a plethora of design alternatives need to be compared, the run-time of performance estimation itself may pose a bottleneck. In DSE, fastest performance estimation is of essence while some accuracy may be sacrificed. Fast estimation can be realised through capturing application demand, as well as Processing Element (PE) supply (later on called Weight table) in a matrix each. Then, performance estimation (retargeting) is reduced to a matrix multiplication. However, defining the Weight table from a data sheet is impractical due to the multitude of (micro-) architecture aspects.
Ya Hsin Tsai - One of the best experts on this subject based on the ideXlab platform.
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transient receptor potential vanilloid type 4 channels mediate na k cl co transporter induced brain edema after traumatic brain injury
Journal of Neurochemistry, 2017Co-Authors: Tai Chun Huang, Ya Hsin Tsai, Yi Ling YangAbstract:Abstract Na(+) -K(+) -2Cl(-) co-transporter (NKCC1) plays an important role in traumatic brain injury (TBI)-induced brain edema via the MAPK cascade. The transient receptor potential vanilloid type 4 (TRPV4) channel participates in neurogenic inflammation, pain transmission, and edema. In this study, we investigated the relationship between NKCC1 and TRPV4 and the related signaling pathways in TBI-induced brain edema and neuronal damage. TBI was induced by the Calibrated Weight-drop device. Adult male Wistar rats were randomly assigned into sham and experimental groups for time-course studies of TRPV4 expression after TBI. Hippocampal TRPV4, NKCC1, MAPK, and PI-3K cascades were analyzed by western blot, and brain edema was also evaluated among the different groups. Expression of hippocampal TRPV4 peaked at 8 h after TBI, and phosphorylation of the MAPK cascade and Akt was significantly elevated. Administration of either the TRPV4 antagonist, RN1734, or NKCC1 antagonist, bumetanide, significantly attenuated TBI-induced brain edema through decreasing the phosphorylation of MEK, ERK, and Akt proteins. Bumetanide injection inhibited TRPV4 expression, which suggests NKCC1 activation is critical to TRPV4 activation. Our results showed that hippocampal NKCC1 activation increased TRPV4 expression after TBI and then induced severe brain edema and neuronal damage through activation of the MAPK cascade and Akt-related signaling pathway.
