B
Benjamin Hassid
Researcher at Columbia University
Publications - 16
Citations - 873
Benjamin Hassid is an academic researcher from Columbia University. The author has contributed to research in topics: Ischemia & Complement system. The author has an hindex of 13, co-authored 16 publications receiving 794 citations. Previous affiliations of Benjamin Hassid include University of California, San Francisco & Stanford University.
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Journal ArticleDOI
Oxidative stress and neuronal death/survival signaling in cerebral ischemia
Atsushi Saito,Carolina M. Maier,Purnima Narasimhan,Tatsuro Nishi,Yun Seon Song,Fengshan Yu,Jing Liu,Yong-Sun Lee,Chikako Nito,Hiroshi Kamada,Robert L. Dodd,Lily B. Hsieh,Benjamin Hassid,Esther Kim,Maricela González,Pak H. Chan +15 more
TL;DR: Genetic manipulation of intrinsic antioxidants and factors in the signaling pathways has provided substantial understanding of the mechanisms involved in cell death/survival signaling pathways and the role of oxygen radicals in ischemic cerebral injury.
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Complement Component C3 Mediates Inflammatory Injury Following Focal Cerebral Ischemia
J. Mocco,William J. Mack,Andrew F. Ducruet,Sergei A. Sosunov,Michael E. Sughrue,Benjamin Hassid,M. Nathan Nair,Ilya Laufer,Ricardo J. Komotar,M. Claire,H. Holland,David J. Pinsky,E. Sander Connolly +12 more
TL;DR: C3 activation is established as the key constituent in complement-related inflammatory tissue injury following stroke and a C3a anaphylatoxin-mediated mechanism is suggested.
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Celiac disease in normal-weight and overweight children: clinical features and growth outcomes following a gluten-free diet.
Norelle R. Reilly,Kathleen Aguilar,Benjamin Hassid,Jianfeng Cheng,Amy R. DeFelice,Philip Kazlow,Govind Bhagat,Peter H.R. Green +7 more
TL;DR: In this paper, the authors describe the presentation of celiac disease among children with a normal and an elevated body mass index (BMI) for age, and study their BMI changes following a gluten-free diet (GFD).
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C3a Receptor Modulation of Granulocyte Infiltration after Murine Focal Cerebral Ischemia is Reperfusion Dependent
Andrew F. Ducruet,Benjamin Hassid,William J. Mack,Sergei A. Sosunov,Marc L. Otten,David J Fusco,Zachary L. Hickman,Grace H. Kim,Ricardo J. Komotar,J. Mocco,E. Sander Connolly +10 more
TL;DR: The data suggest that blocking the binding of C3a to C3AR modulates tissue injury in reperfused stroke by inhibiting the recruitment of neutrophils to the ischemic zone, and establishes antagonism of the C 3a anaphylatoxin as a promising strategy for ameliorating injury after ischemia/reperfusion.
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C3a receptor antagonist attenuates brain injury after intracerebral hemorrhage.
Michal A. Rynkowski,Grace H. Kim,Matthew C. Garrett,Brad E. Zacharia,Marc L. Otten,Sergei A. Sosunov,Ricardo J. Komotar,Benjamin Hassid,Andrew F. Ducruet,John D. Lambris,E. Sander Connolly +10 more
TL;DR: Results of this study suggest that the C3a receptor may be a promising target for therapeutic intervention in hemorrhagic stroke.