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MingMing Ning

Researcher at Harvard University

Publications -  100
Citations -  3199

MingMing Ning is an academic researcher from Harvard University. The author has contributed to research in topics: Stroke & Medicine. The author has an hindex of 25, co-authored 90 publications receiving 2699 citations. Previous affiliations of MingMing Ning include Capital Medical University.

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Hemorrhage Burden Predicts Recurrent Intracerebral Hemorrhage After Lobar Hemorrhage

TL;DR: Hemorrhages identified by MRI predict clinically important events in survivors of lobar ICH, and detection of microhemorrhage may be useful for assessing risk in ICH patients and as a surrogate marker for clinical studies.
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Mechanisms of hemorrhagic transformation after tissue plasminogen activator reperfusion therapy for ischemic stroke.

TL;DR: By augmenting matrix metalloproteinase (MMP) dysregulation after stroke, tPA may degrade extracellular matrix integrity and increase risks of neurovascular cell death, blood–brain barrier leakage, edema, and hemorrhage.
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Comparison of clinical characteristics and functional outcomes of ischemic stroke in different vascular territories.

TL;DR: The initial functional status at admission, rather than the stroke subgroup, better predicts discharge functional outcomes postrehabilitation, and patients with stroke made significant functional gains and should be offered rehabilitation regardless of stroke vascular territory.
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Oxidative Stress and Matrix Metalloproteinase-9 in Acute Ischemic Stroke: The Biomarker Evaluation for Antioxidant Therapies in Stroke (BEAT-Stroke) Study

TL;DR: In early human stroke, evidence of increased oxidative stress and a relationship with MMP-9 expression is found, supporting findings from experimental studies.
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Association between tPA therapy and raised early matrix metalloproteinase-9 in acute stroke.

TL;DR: Tissue plasminogen activator independently predicted plasma matrix metalloproteinase-9 (MMP9) in the first 8 hours after human ischemic stroke as MMP9 may be an important mediator of hemorrhagic transformation, alternative thrombolytic agents or therapeutic M MP9 inhibition may increase the safety profile of acute stroke thromBOlysis.