A5080174490- S100 Proteins and Annexins
- Acute Ischemic Stroke Management
- Protease and Inhibitor Mechanisms
- RNA Interference and Gene Delivery
- Mesenchymal stem cell research
- Neurological Disease Mechanisms and Treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Apelin-related biomedical research
- Nanoparticle-Based Drug Delivery
- Traumatic Brain Injury and Neurovascular Disturbances
- Advanced biosensing and bioanalysis techniques
- Advanced MRI Techniques and Applications
- Calcium signaling and nucleotide metabolism
- Integrated Circuits and Semiconductor Failure Analysis
- PARP inhibition in cancer therapy
- Erythropoietin and Anemia Treatment
- RNA regulation and disease
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- 3D Printing in Biomedical Research
- Pluripotent Stem Cells Research
- Genetic Associations and Epidemiology
- Amyotrophic Lateral Sclerosis Research
- IL-33, ST2, and ILC Pathways
- Extracellular vesicles in disease
- Angiogenesis and VEGF in Cancer
University of California, San Francisco
2022
University of Tennessee Health Science Center
2020-2021
Hanyang University
2008-2016
Hanyang University Guri Hospital
2016
University of South Florida
2014-2015
Treatment with tissue plasminogen activator (tPA) beyond the therapeutic time window (>4.5 hours post stroke) may produce hemorrhagic transformation (HT). Strategies that could extend narrow of tPA will benefit a significant number stroke patients. Male Sprague—Dawley rats underwent middle cerebral artery occlusion (MCAo) and given vehicle, (10 mg/kg), or granulocyte colony-stimulating factor (G-CSF, 300 μg/kg), at 6 after MCAo. Twenty-four treatment, G-CSF+tPA-treated displayed 25%...
Aim: The abnormal proliferation of vascular smooth muscle cells (VSMCs) in arterial walls is an important pathogenic factor disorders such as atherosclerosis and restenosis after angioplasty. During atherogenesis or response to vessel injury, VSMC induced by a number peptide growth factors released from platelets VSMCs. Cilostazol phosphodiesterase (PDE) 3 inhibitor that increases intracellular cAMP levels decreases Ca2+ levels, inhibiting platelet aggregation inducing vasodilatation. also...
Understanding Alzheimer's disease (AD) in terms of its various pathophysiological pathways is essential to unravel the complex nature process and identify potential therapeutic targets. The renin-angiotensin system (RAS) has been implicated several brain diseases, including traumatic injury, ischemic stroke, AD.This study was designed evaluate protein expression levels RAS components postmortem cortical hippocampal samples obtained from AD versus non-AD individuals.We analyzed cortex...
Bone marrow-derived mesenchymal stromal cells (MSCs) have been used successfully as a source of stem for treating neurodegenerative diseases. However, reasons that are not clear, autologous MSC transplants yielded successful results in human trials. To test one possible reason, we compared the migratory ability MSCs from amyotrophic lateral sclerosis (ALS) patients with those healthy controls. We found derived ALS (ALS-MSCs) had reduced to migrate, which may explain why transplantation is...
Cerebral infarction causes permanent neuronal loss inducing severe morbidity and mortality. Because hypertension is the main risk factor for cerebral most patients with take antihypertensive drugs daily, neuroprotective effects mechanisms of anti-hypertensive need to be investigated. Cilnidipine, a long-acting, new generation 1,4-dihydropyridine inhibitor both L- N-type calcium channels, was reported reduce oxidative stress. In this study, we investigated whether cilnidipine has therapeutic...
Abstract Poly(ADP‐ribose) polymerase (PARP)‐1 plays an important role in the pathogenic mechanism of ischemic stroke. A number studies have been undertaken to develop PARP‐1 inhibitors for clinical use. We report on newly developed inhibitors, among which 12a showed good activity (IC 50 =7.8 nM enzyme‐based assay and=0.73 µM a cell‐based assay) and pharmacokinetic profiles. Treatment middle cerebral artery (MCA) occluded rats with 3 mg/kg reduced infarct volume suggesting that, may be...
Abstract The authors have requested that this preprint be removed from Research Square.
Cerebral infarction causes permanent neuronal loss inducing severe morbidity and mortality. Because hypertension is the main risk factor for cerebral most patients with take daily antihypertensive drugs, neuroprotective effects mechanisms of anti-hypertensive drugs need to be investigated. Cilnidipine, a long-acting, second-generation 1,4-dihydropyridine inhibitor both L- N-type calcium channels, was reported reduce oxidative stress. In this study, we investigated whether cilnidipine has...
Background and Purpose: Thrombolytic therapy has remained utterly challenging in hyperglycemic patients for poor prognosis increased hemorrhagic conversions. We have recently shown that tissue plasminogen activator (tPA)-induced cerebrovascular damage is associated with thioredoxin interacting protein (TXNIP) upregulation, which an established role the detrimental effects of hyperglycemia. In present work, we investigated whether verapamil, as TXNIP inhibitor may provide protection against...
Background and Hypothesis: Acute hyperglycemia (AHG) worsens stroke outcome increases the risk of intracerebral hemorrhage after tissue plasminogen activator (tPA) treatment, independent preexisting diabetes. We have previously reported that genetic deletion thioredoxin interacting protein exerts neuroprotection experimental stroke. Here we tested hypothesis pharmacological inhibition TXNIP, with verapamil protects against tPA-induced brain damage under AHG in a mouse model focal cerebral...