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39 results on '"Golomb, Mordechai"'

3. How Cox models react to a study-specific confounder in a patient-level pooled dataset: Random-effects better cope with an imbalanced covariate across trials unless baseline hazards differ

Author

McAndrew, Thomas, Redfors, Bjorn, Crowley, Aaron, Zhang, Yiran, Chen, Shmuel, Golomb, Mordechai, Alu, Maria, Francese, Dominic, Ben-Yehuda, Ori, Maehara, Akiko, Mintz, Gary, Stone, Gregg, and Jenkins, Paul

Subjects
Statistics - Applications
Abstract

Combining patient-level data from clinical trials can connect rare phenomena with clinical endpoints, but statistical techniques applied to a single trial may become problematical when trials are pooled. Estimating the hazard of a binary variable unevenly distributed across trials showcases a common pooled database issue. We studied how an unevenly distributed binary variable can compromise the integrity of fixed and random effects Cox proportional hazards models. We compared fixed effect and random effects Cox proportional hazards models on a set of simulated datasets inspired by a 17-trial pooled database of patients presenting with ST-segment elevation myocardial infarction (STEMI) and non-STEMI undergoing percutaneous coronary intervention. An unevenly distributed covariate can bias hazard ratio estimates, inflate standard errors, raise type I error, and reduce power. While uneveness causes problems for all Cox proportional hazards models, random effects suffer least. Compared to fixed effect models, random effects suffer lower bias and trade inflated type I errors for improved power. Contrasting hazard rates between trials prevent accurate estimates from both fixed and random effects models. When modeling a covariate unevenly distributed across pooled trials with similar baseline hazard rates, Cox proportional hazards models with a random trial effect more accurately estimate hazard ratios than fixed effects. Differing between-trial baseline hazard rates bias both random and fixed effect models. With an unevenly-distributed covariate and similar baseline hazard rates across trials, a random effects Cox proportional hazards model outperforms a fixed effect model, but cannot overcome contrasting baseline hazard rates., Comment: 9 Pages: Cox-Proportional Hazards, Frailty, Fixed-Effects, Random-Effects, Pooling Data

Published
2018

8. A Pregnant Woman With Severe Symptomatic Aortic Stenosis

Author

Yagel, Oren, primary, Alter, Roie, additional, Nissan, Batel, additional, Zwas, Donna R., additional, Rosenbloom, Joshua I., additional, Eyal, Ophir, additional, Golomb, Mordechai, additional, Planer, David, additional, and Elbaz-Greener, Gabby, additional

Published
2024
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12. Utility of the ACC/AHA Lesion Classification to Predict Outcomes After Contemporary DES Treatment: Individual Patient Data Pooled Analysis From 7 Randomized Trials

Author

Konigstein, Maayan, primary, Redfors, Björn, additional, Zhang, Zixuan, additional, Kotinkaduwa, Lak N., additional, Mintz, Gary S., additional, Smits, Pieter C., additional, Serruys, Patrick W., additional, von Birgelen, Clemens, additional, Madhavan, Mahesh V., additional, Golomb, Mordechai, additional, Ben‐Yehuda, Ori, additional, Mehran, Roxana, additional, Leon, Martin B., additional, and Stone, Gregg W., additional

Published
2022
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14. IGF2BP2 is Induced by Stress in the Heart and Mediates Dilated Cardiomyopathy

Author

Krumbein, Miriam, primary, Oberman, Froma, additional, Cinnamon, Yuval, additional, Golomb, Mordechai, additional, May, Dalit, additional, Vainer, Gilad, additional, Belzer, Vitali, additional, Meir, Karen, additional, Fridman, Irina, additional, Haybaeck, Johannes, additional, Poelzl, Gerhard, additional, Kehat, Izhak, additional, Beeri, Ronen, additional, Kessler, Sonja, additional, and Yisraeli, Joel K., additional

Published
2022
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20. Transgenic expression of human C-reactive protein suppresses endothelial nitric oxide synthase expression and bioactivity after vascular injury

Author

Grad, Etty, Golomb, Mordechai, Mor-Yosef, Irit, Koroukhov, Nikolay Lotan, Chaim, Edelman, Elazer R., and Danenberg, Haim D.

Subjects
C-reactive protein -- Research, Blood circulation disorders -- Research, Ion channels -- Research, Vascular endothelium -- Research, Cellular control mechanisms -- Research, Cardiovascular research, Biological sciences
Abstract

C-reactive protein (CRP) is a risk marker and a potential modulator of vascular disease. Whether CRP modulates nitric oxide (NO) synthase (NOS) activity and NO metabolism remains unclear. We studied the effect of CRP on NO metabolism in transgenic mice that express human CRP (CRPtg). CRPtg and wild-type mice were subjected to controlled femoral artery wire injury. CRP serum levels at baseline and 6 and 24 h after injury were 12.4 [+ or -] 9, 18.6 [+ or -] 6.9, and 58.4 [+ or -] 13 mg/l, respectively, in CRPtg mice but were undetectable at all time points in wild-type mice. Endothelial NOS protein and mRNA expression were significantly suppressed in the injured arteries of CRPtg mice (n = 5, P < 0.05). A similar reduction in eNOS expression was observed in the distant lung and heart. NO release after injury was significantly lower in CRPtg mice, as measured by nitrate and nitrite breakdown products, with a concomitant suppression of cGMP NO signaling after injury. Endothelial NOS and NO expression after vascular injury are locally and systemically suppressed in mice that express human CRP. These in vivo observations support the hypothesis that CRP modulates NO metabolism and may have implications regarding the mechanisms by which CRP modulates vascular disease. vascular disease; inflammatory response doi:10.1152/ajpheart.01418.2006

Published
2007

22. Reply

Author

Golomb, Mordechai, primary and Stone, Gregg W., additional

Published
2020
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27. Supplements - Augmentation of Ouabain-Induced Increase in Heart Muscle Contractility by Akt Inhibitor MK-2206

Author

Buzaglo, Nahum, Golomb, Mordechai, Rosen, Haim, Beeri, Ronen, Ami, Hagit Cohen-Ben, Fattal Langane, Pierre, Sandrine, and Lichtstein, David

Subjects
110203 Respiratory Diseases, FOS: Clinical medicine, education, Cardiology, 110323 Surgery, 110306 Endocrinology, humanities, 111599 Pharmacology and Pharmaceutical Sciences not elsewhere classified
Abstract

Supplements for Augmentation of Ouabain-Induced Increase in Heart Muscle Contractility by Akt Inhibitor MK-2206 by Nahum Buzaglo, Mordechai Golomb, Haim Rosen, Ronen Beeri, Hagit Cohen-Ben Ami, Fattal Langane, Sandrine Pierre, and David Lichtstein in The Journal of Clinical Pharmacology

Published
2018
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28. How Cox models react to a study-specific confounder in a patient-level pooled dataset: random effects better cope with an imbalanced covariate across trials unless baseline hazards differ

Author

McAndrew, Thomas, primary, Redfors, Bjorn, additional, Crowley, Aaron, additional, Zhang, Yiran, additional, Chen, Shmuel, additional, Golomb, Mordechai, additional, Alu, Maria C., additional, Francese, Dominic P., additional, Ben-Yehuda, Ori, additional, Maehara, Akiko, additional, Mintz, Gary S., additional, Stone, Gregg W., additional, and Jenkins, Paul L., additional

Published
2019
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29. TCT-795 Prognostic Impact of Race in Patients Undergoing PCI: Analysis of 22,638 Patients from 10 Randomized Coronary Stent Trials

Author

Golomb, Mordechai, primary, Redfors, Bjorn, additional, Crowley, Aaron, additional, Ben-Yehuda, Ori, additional, Smits, Pieter, additional, Serruys, Patrick, additional, von Birgelen, Clemens, additional, Madhavan, Mahesh, additional, Mehran, Roxana, additional, Leon, Martin, additional, and Stone, Gregg, additional

Published
2018
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30. TCT-499 Prognostic Implications of Pre-procedural TIMI Flow in Patients with STEMI Undergoing PCI with Drug-Eluting Stent Implantation

Author

Golomb, Mordechai, primary, Wolny, Rafal, additional, Liu, Yangbo, additional, Smits, Pieter, additional, von Birgelen, Clemens, additional, Redfors, Bjorn, additional, Madhavan, Mahesh, additional, Ben-Yehuda, Ori, additional, Mehran, Roxana, additional, Leon, Martin, additional, and Stone, Gregg, additional

Published
2018
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31. TCT-500 Prognostic Implications of Reduced Pre-procedural TIMI Flow in Patients with Non–ST-Segment Elevation Acute Coronary Syndromes Undergoing PCI

Author

Golomb, Mordechai, primary, Wolny, Rafal, additional, Liu, Yangbo, additional, Serruys, Patrick, additional, von Birgelen, Clemens, additional, Smits, Pieter, additional, Redfors, Bjorn, additional, Madhavan, Mahesh, additional, Ben-Yehuda, Ori, additional, Mehran, Roxana, additional, Leon, Martin, additional, and Stone, Gregg, additional

Published
2018
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34. Augmentation of Ouabain-Induced Increase in Heart Muscle Contractility by Akt Inhibitor MK-2206.

Author

Buzaglo, Nahum, Golomb, Mordechai, Rosen, Haim, Beeri, Ronen, Ami, Hagit Cohen-Ben, Langane, Fattal, Pierre, Sandrine, and Lichtstein, David

Subjects
CARDIAC contraction, OUABAIN, CONGESTIVE heart failure treatment, ANIMAL experimentation, BIOLOGICAL models, CARDIAC glycosides, CARDIOTONIC agents, CELL culture, CELLS, CELLULAR signal transduction, COMBINATION drug therapy, DRUG synergism, LEFT heart ventricle, HEART physiology, HETEROCYCLIC compounds, MYOCARDIAL infarction, RATS, TRANSFERASES, PROTEIN kinase inhibitors, PHARMACODYNAMICS
Abstract

Cardiac steroids (CSs), such as ouabain and digoxin, increase the force of contraction of heart muscle and are used for the treatment of congestive heart failure (CHF). However, their small therapeutic window limits their use. It is well established that Na+, K+-ATPase inhibition mediates CS-induced increase in heart contractility. Recently, the involvement of intracellular signal transduction was implicated in this effect. The aim of the present study was to test the hypothesis that combined treatment with ouabain and Akt inhibitor (MK-2206) augments ouabain-induced inotropy in mammalian models. We demonstrate that the combined treatment led to an ouabain-induced increase in contractility at concentrations at which ouabain alone was ineffective. This was shown in 3 experimental systems: neonatal primary rat cardiomyocytes, a Langendorff preparation, and an in vivo myocardial infarction induced by left anterior descending coronary artery (LAD) ligation. Furthermore, cell viability experiments revealed that this treatment protected primary cardiomyocytes from MK-2206 toxicity and in vivo reduced the size of scar tissue 10 days post-LAD ligation. We propose that Akt activity imposes a constant inhibitory force on muscle contraction, which is attenuated by low concentrations of MK-2206, resulting in potentiation of the ouabain effect. This demonstration of the increase in the CS effect advocates the development of the combined treatment in CHF. [ABSTRACT FROM AUTHOR]

Published
2019
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35. Heparanase Regulates Thrombosis in Vascular Injury and Stent-Induced Flow Disturbance

Author

Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Harvard University--MIT Division of Health Sciences and Technology, Gibson, William J., Kolachalama, Vijaya Bhasker, Indolfi, Laura, Edelman, Elazer R., Baker, Aaron B., Golomb, Mordechai, Spruell, Christopher, Zcharia, Eyal, Vlodavsky, Israel, Gibson, William J., Ph. D. Massachusetts Institute of Technology, Massachusetts Institute of Technology. Institute for Medical Engineering & Science, Harvard University--MIT Division of Health Sciences and Technology, Gibson, William J., Kolachalama, Vijaya Bhasker, Indolfi, Laura, Edelman, Elazer R., Baker, Aaron B., Golomb, Mordechai, Spruell, Christopher, Zcharia, Eyal, Vlodavsky, Israel, and Gibson, William J., Ph. D. Massachusetts Institute of Technology

Abstract

Objectives The purpose of this study was to examine the role of heparanase in controlling thrombosis following vascular injury or endovascular stenting. Background The use of endovascular stents are a common clinical intervention for the treatment of arteries occluded due to vascular disease. Both heparin and heparan sulfate are known to be potent inhibitors of thrombosis. Heparanase is the major enzyme that degrades heparan sulfate in mammalian cells. This study examined the role of heparanase in controlling thrombosis following vascular injury and stent-induced flow disturbance. Methods This study used mice overexpressing human heparanase and examined the time to thrombosis using a laser-induced arterial thrombosis model in combination with vascular injury. An ex vivo system was used to examine the formation of thrombus to stent-induced flow disturbance. Results In the absence of vascular injury, wild type and heparanase overexpressing (HPA Tg) mice had similar times to thrombosis in a laser-induced arterial thrombosis model. However, in the presence of vascular injury, the time to thrombosis was dramatically reduced in HPA Tg mice. An ex vivo system was used to flow blood from wild type and HPA Tg mice over stents and stented arterial segments from both animal types. These studies demonstrate markedly increased thromboses on stents with blood isolated from HPA Tg mice in comparison to blood from wild type animals. We found that blood from HPA Tg animals had markedly increased thrombosis when applied to stented arterial segments from either wild type or HPA Tg mice. Conclusions Taken together, this study's results indicate that heparanase is a powerful mediator of thrombosis in the context of vascular injury and stent-induced flow disturbance.

Published
2014

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