A5035223883- Neuroinflammation and Neurodegeneration Mechanisms
- Acute Ischemic Stroke Management
- Neonatal and fetal brain pathology
- Aortic aneurysm repair treatments
- Traumatic Brain Injury and Neurovascular Disturbances
- Peptidase Inhibition and Analysis
- Neurological Disease Mechanisms and Treatments
- Protease and Inhibitor Mechanisms
- Cerebrospinal fluid and hydrocephalus
- Intracerebral and Subarachnoid Hemorrhage Research
- Cellular transport and secretion
- Complement system in diseases
- S100 Proteins and Annexins
- Cardiac, Anesthesia and Surgical Outcomes
- Lipid Membrane Structure and Behavior
- Barrier Structure and Function Studies
- Stroke Rehabilitation and Recovery
- Nerve injury and regeneration
- Neuroscience and Neural Engineering
- Macrophage Migration Inhibitory Factor
- Alzheimer's disease research and treatments
- Neurological Disorders and Treatments
- Aortic Disease and Treatment Approaches
- Spinal Cord Injury Research
- Immune cells in cancer
Medical University of South Carolina
2019-2023
Clemson University
2016
Baylor College of Medicine
1983-1987
Cognitive deficits following traumatic brain injury (TBI) remain a major cause of disability and early-onset dementia, there is increasing evidence that chronic neuroinflammation occurring after TBI plays an important role in this process. However, little known about the molecular mechanisms responsible for triggering maintaining inflammation TBI. Here, we identify complement, specifically complement-mediated microglial phagocytosis synapses, as pathophysiological link between acute insult...
Abstract Traumatic brain injury (TBI) can result in progressive cognitive decline occurring for years after the initial insult, and which there is currently no pharmacological treatment. An ongoing chronic inflammatory response TBI thought to be an important factor driving this decline. Here, we investigate role of complement neuroinflammation up 6 months murine TBI. Male C57BL/6 mice were subjected open head using a controlled cortical impact device. At 2 post TBI, moved large cages with...
We previously reported that the cell fusion occurs during muscle development, when mononucleated myoblasts fuse to form multinucleated myotubes, requires endogenous metalloendoprotease activity at time of fusion. report here contain both soluble and membrane-associated metalloendoproteases, these proteases have different inhibitor specificities. Several inhibitors, shown block myoblast fusion, inhibit only not in myoblasts. Another inhibitor, phosphoramidon, which had no effect on inhibits...
Germinal matrix hemorrhage (GMH) is a devastating disease of infancy that results in intraventricular hemorrhage, post-hemorrhagic hydrocephalus (PHH), periventricular leukomalacia, and neurocognitive deficits. There are no curative treatments limited surgical options. We developed characterized mouse model GMH based on the injection collagenase into subventricular zone post-natal pups utilized to investigate role complement PHH development. The site-targeted inhibitor CR2Crry, which binds...
The angiotensin II type 1 receptor (AT1R) can be activated under conditions of mechanical stretch in some cellular systems. Whether this activity influences signaling within the abdominal aorta to promote aortic aneurysm (AAA) development remains unknown. We evaluated hypothesis that AT1R activation occur hypertension (HTN) and contribute AAA formation.BPH/2 mice, which demonstrate spontaneous neurogenic, low-renin HTN, normotensive BPN/3 mice underwent induction via calcium chloride model,...
Multiple neuroprotective agents have shown beneficial effects in rodent models of stroke, but they failed to translate the clinic. In this perspective, we consider that a likely explanation for failure, at least part, is there has been inadequate assessment functional outcomes preclinical stroke models, as well use young healthy animals are not representative clinical cohorts. Although impact older age and cigarette smoking comorbidities on documented clinically, these (and other)...
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Introduction: The gene expression profile of interleukin-6 (IL-6) signaling through the STAT3 transcription factor distinguishes it as a potential effector macrophage accumulation and abdominal aortic aneurysm (AAA) growth. This project aims to demonstrate that IL-6 is an integral component AAA development. Methods: C57Bl/6 knockout (IL-6KO) mice underwent induction by application peri-adventitial CaCl 2 (0.5M) +/- implantation osmotic mini-pump delivering (4.36υg/kg/day x 21 days). At...
Introduction: In addition to ligand-specific activation, the Angiotensin II Type 1 receptor (AT1R) has been shown activate under conditions of mechanical stretch. However, whether this activity contributes abdominal aortic aneurysm (AAA) development is unknown. Accordingly, study tested hypothesis that AAA attenuated by AT1R blockade (losartan) in mice with hypertension independent II. Methods: Commercially available, spontaneously hypertensive BPH/2J mice, which demonstrate neurogenic not...
OBJECTIVES/GOALS: Following stroke, complement-dependent neuroinflammation exacerbates secondary injury and worsens acute chronic outcomes. We have shown that an site-targeted complement inhibitor (B4Crry), targets specifically to the ischemic brain, inhibits activation leading improved Stroke comorbidities been promote a pro-inflammatory environment in brain systemically, exacerbate inflammatory responses after injury. investigated impact of age smoking on outcomes stroke assessed whether...
Following stroke, complement-dependent neuroinflammation exacerbates secondary injury and worsens acute chronic outcomes. We have shown that a complement inhibitor (B4Crry), targets specifically to the ischemic penumbra, inhibits activation leading improved outcomes following murine stroke. However, while multiple neuroprotective agents beneficial effects in rodent models of they failed translate clinic, likely explanation being there has been inadequate assessment functional stroke models,...
Abstract Introduction Germinal matrix hemorrhage (GMH) is a devastating disease of infancy that results in intraventricular hemorrhage, post-hemorrhagic hydrocephalus (PHH), periventricular leukomalacia and neurocognitive deficits. There are no curative treatments limited surgical options. We developed novel mouse model GMH investigated the role complement PHH development. Methods utilized neonatal involving injection collagenase into subventricular zone post-natal day four (P4) pups....