Frank C. Barone

ORCID: 0000-0001-8509-3936
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurological Disease Mechanisms and Treatments
  • Neuroscience and Neuropharmacology Research
  • Acute Ischemic Stroke Management
  • S100 Proteins and Annexins
  • Immune Response and Inflammation
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Neurological Disorders and Treatments
  • Sleep and Wakefulness Research
  • Regulation of Appetite and Obesity
  • Cell Adhesion Molecules Research
  • Nitric Oxide and Endothelin Effects
  • Cerebrovascular and Carotid Artery Diseases
  • Biochemical Analysis and Sensing Techniques
  • Neuroscience of respiration and sleep
  • Cardiac Ischemia and Reperfusion
  • Neuropeptides and Animal Physiology
  • Gastroesophageal reflux and treatments
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Gastrointestinal motility and disorders
  • Dysphagia Assessment and Management
  • Melanoma and MAPK Pathways
  • Biochemical effects in animals
  • Advanced MRI Techniques and Applications
  • Neurotransmitter Receptor Influence on Behavior

SUNY Downstate Health Sciences University
2016-2025

State University of New York
2009-2025

Northwestern University
2019

Hôpital Saint-Michel
2014

Interfaith Medical Center
2012

GlaxoSmithKline (United States)
2001-2010

High Throughput Biology (United States)
2001-2008

GlaxoSmithKline (United Kingdom)
2001-2007

University of Pittsburgh
2003

New Frontier
1993-2002

Background and Purpose Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine that rapidly upregulates in the brain after injury. The present study was designed to explore pathophysiological significance of TNF-α ischemic by systematically evaluating effects lateral cerebroventricular administration exogenous agents block on focal stroke examining potential direct toxic cultured neurons better understand how might mediate Methods (2.5 or 25 pmol) administered intracerebroventricularly...

10.1161/01.str.28.6.1233 article EN Stroke 1997-06-01

Tumor necrosis factor-alpha (TNF-alpha) is a cytokine with diverse proinflammatory actions, including endothelial leukocyte adhesion molecule expression. Since leukocytes infiltrate into ischemic brain lesions, the present study was conducted to examine whether TNF-alpha messenger RNA (mRNA) and peptide are expressed in after experimental focal stroke before accumulation.TNF-alpha mRNA protein expression were monitored nonischemic cerebral cortex of rats ischemia produced by permanent middle...

10.1161/01.str.25.7.1481 article EN Stroke 1994-07-01

Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that degrade the extracellular matrix and implicated in numerous pathological conditions including atherosclerosis, inflammation, tumor growth metastasis. In brain, endothelial cell wall, strengthened by tight junctions, defines blood-brain barrier (BBB). The molecules constitute basement membrane underlying vasculature play critical role maintaining integrity BBB. After focal stroke, there is breakdown BBB with an...

10.1161/01.str.29.5.1020 article EN Stroke 1998-05-01

Background and Purpose —A short duration of ischemia (ie, ischemic preconditioning [PC]) can provide significant brain protection to subsequent events tolerance [IT]). The present series studies was conducted characterize the temporal pattern a PC paradigm, systematically evaluate importance protein synthesis in PC-induced IT, explore candidate gene expression changes associated with IT. Methods —Temporary middle cerebral artery occlusion (MCAO) (10 minutes) used for PC. Various periods...

10.1161/01.str.29.9.1937 article EN Stroke 1998-09-01

Cerebral infarction initiates a cascade of molecular events, leading to proteolytic cell death. Matrix-degrading metalloproteinases (MMPs) are neutral proteases involved in extracellular matrix damage. Type IV collagenase is an MMP that increases cerebral capillary permeability after intracerebral injection and may be important along with plasminogen activators (PA) secondary brain edema stroke. Therefore, we measured MMPs PAs spontaneously hypertensive (SHR) or Wistar-Kyoto (WKY) rats...

10.1097/00004647-199605000-00002 article EN Journal of Cerebral Blood Flow & Metabolism 1996-05-01

Two different techniques were utilized to identify the infiltration of polymorphonuclear leukocytes (PMN) into cerebral tissue following focal ischemia: histologic analysis and a modified myeloperoxidase (MPO) activity assay. Twenty-four hours after producing permanent cortical ischemia by occluding severing middle artery male spontaneously hypertensive rats, contralateral hemiparalysis sensory-motor deficits observed due infarction frontal parietal cortex. In hematoxylin-and-eosin-stained...

10.1002/jnr.490290309 article EN Journal of Neuroscience Research 1991-07-01

Interleukin-1 beta is a proinflammatory cytokine produced by blood-borne and resident brain inflammatory cells. The present study was conducted to determine if interleukin-1 mRNA in the of rats subjected permanent focal ischemia. Rat cDNA, synthesized from stimulated rat peritoneal macrophage RNA reverse transcription polymerase chain reaction cloned plasmid Bluescript KS+, used evaluate expression cerebral cortex spontaneously hypertensive normotensive middle artery occlusion. quantified...

10.1161/01.str.24.11.1746 article EN Stroke 1993-11-01

The consequences of cerebral ischemia were studied in three different strains (BDF, CFW, and BALB/C) mice. exhibited significant differences susceptibility to 24-h focal ischemia. Following middle artery occlusion (MCAO), infarct volumes (mm3) 5 +/- 3 BDF, 15 23 BALB/C mice (p < 0.05). MCAO plus ipsilateral common carotid (CCAO) resulted 9 38 10 72 12 In addition, CCAO produced death by 24 h 42% CFW 67% mice, but not any BDF alone multifocal hemispheric infarctions 36% the other two strains....

10.1038/jcbfm.1993.87 article EN Journal of Cerebral Blood Flow & Metabolism 1993-07-01

Sublethal insults can induce tolerance to subsequent stressors in neurons. As cell death activators such as ROS generation and decreased ATP initiate tolerance, we tested whether other cellular elements normally associated with neuronal injury could add this process. In an vivo model of ischemic were surprised observe widespread caspase 3 cleavage, without death, preconditioned tissue. To dissect the preconditioning pathways activating caspases, mechanisms by which these proteases are held...

10.1073/pnas.0232966100 article EN Proceedings of the National Academy of Sciences 2003-01-09

A number of studies have provided evidence that neuronal cell loss after stroke involves programmed death or apoptosis. In particular, recent biochemical and immunohistochemical demonstrated the expression activation intracellular proteases, notably caspase-3, which act as both initiators executors apoptotic process. To further elucidate involvement caspases in induced by focal we developed a panel antibodies investigated spatial temporal pattern caspase-8 caspase-3 expression. Our efforts...

10.1523/jneurosci.19-14-05932.1999 article EN cc-by-nc-sa Journal of Neuroscience 1999-07-15

In the present study, we examined expression of tumor necrosis factor-α (TNF-α) mRNA in specific regions following experimental lateral fluid percussion traumatic brain injury (TBI) rats. Adult Sprague-Dawley rats (n = 42) were anesthetized with sodium pentobarbital (60 mg/kg, i.p.) and subjected to moderate severity (2.4 atm.) centered over left temporoparietal cortex, or 'sham' treatment (anesthesia surgery without injury). Animals killed by decapitation at 1, 6 24 h post injury, brains...

10.1016/0169-328x(95)00274-v article EN cc-by-nc-nd Molecular Brain Research 1996-03-01

The stress-activated mitogen-activated protein kinase (MAPK) p38 has been linked to the production of inflammatory cytokines/mediators/inflammation and death/apoptosis following cell stress. In these studies, a second-generation MAPK inhibitor, SB 239063 (IC(50) = 44 nM), was found exhibit improved selectivity increased cellular (3-fold) in vivo (3- 10-fold) activity over first-generation inhibitors. Oral inhibited lipopolysaccharide-induced plasma tumor necrosis factor 2.6 mg/kg) reduced...

10.1016/s0022-3565(24)38747-6 article EN Journal of Pharmacology and Experimental Therapeutics 2001-02-01

Cytokines have been shown to be induced following a variety of central nervous system (CNS) insults, and may play role in the pathophysiological sequelae CNS injury. In present study, we characterized regional expression interleukin-1β (IL-1β) mRNA specific brain regions experimental lateral fluid-percussion traumatic injury (TBI) rats. Adult Sprague-Dawley rats (n = 42) were anesthetized with sodium pentobarbital (60 mg/kg, i.p.) subjected moderate severity (2.4 atm.) centered over left...

10.1016/0169-328x(94)00287-o article EN cc-by-nc-nd Molecular Brain Research 1995-05-01

Previously we demonstrated that focal cerebral ischemia results in an increased expression of several cytokines/chemokines precede the infiltration leukocytes into ischemic cortex after stroke induced by occlusion middle artery (MCAO). Monocyte chemoattractant protein-1 (MCP-1) is a potent specific for monocytes. The aim present study was to examine whether MCP-1 messenger RNA (mRNA) expressed brain tissue MCAO.The mRNA first identified means sensitive reverse transcription and polymerase...

10.1161/01.str.26.4.661 article EN Stroke 1995-04-01
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