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Your search keyword '"Koenig, Steven C."' showing total 150 results
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150 results on '"Koenig, Steven C."'

20. Development of Inspired Therapeutics Pediatric VAD: Benchtop Evaluation of Impeller Performance and Torques for MagLev Motor Design

Author

Tompkins, Landon H., primary, Prina, Steven R., additional, Gellman, Barry N., additional, Morello, Gino F., additional, Roussel, Thomas, additional, Kopechek, Jonathan A., additional, Williams, Stuart J., additional, Petit, Priscilla C., additional, Slaughter, Mark S., additional, Koenig, Steven C., additional, and Dasse, Kurt A., additional

Published
2021
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26. A Novel Closed-Loop Electrical Brain Stimulation Device Featuring Wireless Low-Energy Ultrasound Power and Communication

Author

Neimat, Joseph S., Bina, Robert W., Koenig, Steven C., Demirors, Emrecan, Guida, Raffaele, Burke, Ryan, Melodia, Tommaso, and Jimenez, Jorge

Abstract

This study aimed to indicate the feasibility of a prototype electrical neuromodulation system using a closed-loop energy-efficient ultrasound-based mechanism for communication, data transmission, and recharging.

Published
2024
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30. Erratum to: Mechanistic insight of platelet apoptosis leading to non-surgical bleeding among heart failure patients supported by continuous-flow left ventricular assist devices

Author

Mondal, Nandan K., primary, Li, Tieluo, additional, Chen, Zengsheng, additional, Chen, Hegang H., additional, Sorensen, Erik N., additional, Pham, Si M., additional, Sobieski, Michael A., additional, Koenig, Steven C., additional, Slaughter, Mark S., additional, Griffith, Bartley P., additional, and Wu, Zhongjun J., additional

Published
2017
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31. Continuous-Flow Left Ventricular Assist Device Support Improves Myocardial Supply:Demand in Chronic Heart Failure

Author

Soucy, Kevin G., primary, Bartoli, Carlo R., additional, Phillips, Dustin, additional, Giridharan, Guruprasad A., additional, Sobieski, Michael A., additional, Wead, William B., additional, Dowling, Robert D., additional, Wu, Zhongjun J., additional, Prabhu, Sumanth D., additional, Slaughter, Mark S., additional, and Koenig, Steven C., additional

Published
2017
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32. Systemic inflammatory response syndrome in end stage heart failure patients following continuous-flow left ventricular assist devices implantation: differences in plasma redox status and leukocyte activation

Author

Mondal, Nandan K, Sorensen, Erik N, Pham, Si M., Koenig, Steven C, Griffith, Bartley P, Slaughter, Mark S, and W, Zhongjun J

Subjects
Adult, Heart Failure, Male, Middle Aged, Article, Systemic Inflammatory Response Syndrome, Lipoproteins, LDL, Oxidative Stress, Malondialdehyde, Leukocytes, Humans, Female, Heart-Assist Devices, Oxidation-Reduction, Aged
Abstract

The role of oxidative stress and leukocyte activation has not been elucidated in developing systemic inflammatory response syndrome (SIRS) in heart failure (HF) patients after continuous-flow left ventricular assist device (CF-LVAD) implantation. The objective of this study was to investigate the change of plasma redox status and leukocyte activation in CF-LVAD implanted HF patients with or without systemic inflammatory response syndrome (SIRS). We recruited 31 CF-LVAD implanted HF patients (16 SIRS and 15 Non-SIRS) and 11 healthy volunteers as the control. Pre and post implant blood samples were collected from the HF patients. Plasma levels of oxidized low density lipoprotein (oxLDL), malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD) in erythrocyte, myeloperoxidase (MPO) and polymorphonuclear elastase (PMN-elastase) were measured. The HF patients had preexisting condition of oxidative stress than healthy controls as evident from the higher oxLDL and MDA levels as well as depleted SOD and TAC. Leukocyte activation in terms of higher plasma MPO and PMN-elastase were also prominent in HF patients than control. Persistent oxidative stress and reduced antioxidant status were found more belligerent in HF patients with SIRS after the implantation of CF-LVAD when compared to Non-SIRS patients. Similar to oxidative stress, the activation of blood leukocyte were significantly highlighted in SIRS patients after implantation compared to Non-SIRS. We identified that the plasma redox status and leukocyte activation became more prominent in CF-LVAD implanted HF patients who developed SIRS. Our findings suggest that plasma biomarkers of oxidative stress and leukocyte activation may be associated with the development of SIRS after CF-LVAD implant surgery.

Published
2015

33. High shear induces platelet dysfunction leading to enhanced thrombotic propensity and diminished hemostatic capacity.

Author

Chen, Zengsheng, Griffith, Bartley P., Wu, Zhongjun J., Mondal, Nandan K., Zheng, Shirong, Slaughter, Mark S., and Koenig, Steven C.

Subjects
BLOOD platelet aggregation, SHEARING force
Abstract

Thrombosis and bleeding are devastating adverse events in patients supported with blood-contacting medical devices (BCMDs). In this study, we delineated that high non-physiological shear stress (NPSS) caused platelet dysfunction that may contribute to both thrombosis and bleeding. Human blood was subjected to NPSS with short exposure time. Levels of platelet surface GPIbα and GPVI receptors as well as activation level of GPIIb/IIIa in NPSS-sheared blood were examined with flow cytometry. Adhesion of sheared platelets on fibrinogen, von Willibrand factor (VWF), and collagen was quantified with fluorescent microscopy. Ristocetin- and collagen-induced platelet aggregation was characterized by aggregometry. NPSS activated platelets in a shear and exposure time-dependent manner. The number of activated platelets increased with increasing levels of NPSS and exposure time, which corresponded well with increased adhesion of sheared platelets on fibrinogen. Concurrently, NPSS caused shedding of GPIbα and GPVI in a manner dependent on shear and exposure time. The loss of intact GPIbα and GPVI increased with increasing levels of NPSS and exposure time. The number of platelets adhered on VWF and collagen decreased with increasing levels of NPSS and exposure time, respectively. The decrease in the number of platelets adhered on VWF and collagen corresponded well with the loss in GPIbα and GPVI on platelet surface. Both ristocetin- and collagen-induced platelet aggregation in sheared blood decreased with increasing levels of NPSS and exposure time. The study clearly demonstrated that high NPSS causes simultaneous platelet activation and receptor shedding, resulting in a paradoxical effect on platelet function via two distinct mechanisms. The results from the study suggested that the NPSS could induce the concurrent propensity for both thrombosis and bleeding in patients. [ABSTRACT FROM AUTHOR]

Published
2019
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37. Flow features and device‐induced blood trauma in CF‐VADs under a pulsatile blood flow condition: A CFD comparative study.

Author

Chen, Zengsheng, Jena, Sofen K., Giridharan, Guruprasad A., Koenig, Steven C., Slaughter, Mark S., Griffith, Bartley P., and Wu, Zhongjun J.

Subjects
BLOOD flow, FLUID dynamics, SHEARING force, HEART assist devices, HEMOLYSIS & hemolysins
Abstract

Abstract: In this study, the flow features and device‐associated blood trauma in 4 clinical ventricular assist devices (VADs; 2 implantable axial VADs, 1 implantable centrifugal VAD, and 1 extracorporeal VAD) were computationally analyzed under clinically relevant pulsatile flow conditions. The 4 VADs were operated at fixed pump speed at a mean rate of 4.5 L/min. Mean pressure difference, wall shear stress, volume distribution of scalar shear stress (SSS), and shear‐induced hemolysis index (HI) were derived from the flow field of each VAD and were compared. The computationally predicted mean pressure difference across the 3 implantable VADs was ~70 mmHg, and the extracorporeal VAD was ~345 mmHg, which matched well with their reported pressure‐flow curves. The axial VADs had higher mean wall shear stress and SSS compared with the centrifugal VADs. However, the residence time of the centrifugal VADs was much longer compared with the axial VADs because of the large volume of the centrifugal VADs. The highest SSS was observed in one axial VAD, and the longest exposure time was observed in 1 centrifugal VAD. These 2 VADs generated the highest HI. The shear‐induced HI varied as a function of flow rate within each cardiac cycle. At fixed pump speed, the HI was greatest at low flow rate due to longer exposure time to shear stress compared with at high flow rate. Subsequently, we hypothesize that to reduce the risk of blood trauma during VAD support, shear stress magnitude and exposure time need to be minimized. [ABSTRACT FROM AUTHOR]

Published
2018
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40. Hemodynamic Changes and Retrograde Flow in LVAD Failure

Author

Giridharan, Guruprasad A., primary, Koenig, Steven C., additional, Soucy, Kevin G., additional, Choi, Young, additional, Pirbodaghi, Tohid, additional, Bartoli, Carlo R., additional, Monreal, Gretel, additional, Sobieski, Michael A., additional, Schumer, Erin, additional, Cheng, Allen, additional, and Slaughter, Mark S., additional

Published
2015
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42. Feasibility Study of Particulate Extracellular Matrix (P-ECM) and Left Ventricular Assist Device (HVAD) Therapy in Chronic Ischemic Heart Failure Bovine Model

Author

Soucy, Kevin G., primary, Smith, Erin F., additional, Monreal, Gretel, additional, Rokosh, Gregg, additional, Keller, Brad B., additional, Yuan, Fangping, additional, Matheny, Robert G., additional, Fallon, Anna M., additional, Lewis, Beecher C., additional, Sherwood, Leslie C., additional, Sobieski, Michael A., additional, Giridharan, Guruprasad A., additional, Koenig, Steven C., additional, and Slaughter, Mark S., additional

Published
2015
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49. Paradoxical Effect of Nonphysiological Shear Stress on Platelets and von Willebrand Factor.

Author

Chen, Zengsheng, Mondal, Nandan K., Ding, Jun, Koenig, Steven C., Slaughter, Mark S., and Wu, Zhongjun J.

Subjects
SHEARING force, BLOOD platelets, GLYCOPROTEIN receptors, HYPERCOAGULATION disorders, VON Willebrand factor
Abstract

Blood can become hypercoagulable by shear-induced platelet activation and generation of microparticles. It has been reported that nonphysiological shear stress (NPSS) could induce shedding of platelet receptor glycoprotein (GP) Iba, which may result in an opposite effect to hemostasis. The aim of this study was to investigate the influence of the NPSS on platelets and von Willebrand factor (vWF). Human blood was exposed to two levels of NPSS (25 Pa, 125 Pa) with an exposure time of 0.5 s, generated by using a novel blood-shearing device. Platelet activation (P-selectin expression, GPIIb/IIIa activation and generation of microparticles) and shedding of three platelet receptors (GPIbα, GPVI, GPIIb/IIIa) in sheared blood were quantified using flow cytometry. Aggregation capacity of sheared blood induced by ristocetin and collagen was evaluated using an aggregometer. Shear-induced vWF damage was characterized with Western blotting. Consistent with the published data, the NPSS caused significantly more platelets to become activated with increasing NPSS level. Meanwhile, the NPSS induced the shedding of platelet receptors. The loss of the platelet receptors increased with increasing NPSS level. The aggregation capacity of sheared blood induced by ristocetin and collagen decreased. There was a loss of high molecular weight multimers (HMWMs) of vWF in sheared blood. These results suggest that the NPSS induced a paradoxical effect. More activated platelets increase the risk of thrombosis, while the reduction in platelet receptors and the loss of HMWM-vWF increased the propensity of bleeding. The finding might provide a new perspective to understand thrombosis and acquired bleeding disorder in patients supported with blood contacting medical devices. [ABSTRACT FROM AUTHOR]

Published
2016
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