A5060331724- Virus-based gene therapy research
- Herpesvirus Infections and Treatments
- Alzheimer's disease research and treatments
- CAR-T cell therapy research
- Nerve injury and regeneration
- RNA Interference and Gene Delivery
- Neuroinflammation and Neurodegeneration Mechanisms
- Immunotherapy and Immune Responses
- Neurogenesis and neuroplasticity mechanisms
- Criminal Justice and Corrections Analysis
- Axon Guidance and Neuronal Signaling
- Immune Cell Function and Interaction
- Jury Decision Making Processes
- CRISPR and Genetic Engineering
- Cytomegalovirus and herpesvirus research
- Viral Infectious Diseases and Gene Expression in Insects
- Angiogenesis and VEGF in Cancer
- Immune Response and Inflammation
- Computational Drug Discovery Methods
- T-cell and B-cell Immunology
- interferon and immune responses
- Tryptophan and brain disorders
- Cholinesterase and Neurodegenerative Diseases
- Apelin-related biomedical research
- Nuclear Receptors and Signaling
University of Florida
2025
University of Rochester
2005-2023
University of Washington
2022
Vaccinex (United States)
2014-2015
University of Rochester Medical Center
2003-2014
Union Theological Seminary
2008
Stanford University
2008
Princeton Theological Seminary
2008
Wacker (United States)
2008
Pittsburgh Theological Seminary
2008
Poly(ADP-ribose) polymerase-1 (PARP-1) protects the genome by functioning in DNA damage surveillance network. PARP-1 is also a mediator of cell death after ischemia-reperfusion injury, glutamate excitotoxicity, and various inflammatory processes. We show that activation required for translocation apoptosis-inducing factor (AIF) from mitochondria to nucleus AIF necessary PARP-1-dependent death. N-methyl-N'-nitro-N-nitrosoguanidine, H2O2, N-methyl-d-aspartate induce death, which prevented PARP...
Mitochondrial dysfunction has been reported in both familial and sporadic Parkinson's disease (PD). However, effective therapy targeting this pathway is currently inadequate. Recent studies suggest that manipulating the processes of mitochondrial fission fusion considerable potential for treating human diseases. To determine therapeutic impact these pathways on PD, we used two complementary mouse models impairments as seen PD. We show here blocking neuroprotective PTEN-induced putative...
The profound neuroprotection observed in poly(ADP-ribose) polymerase-1 (PARP-1) null mice to ischemic and excitotoxic injury positions PARP-1 as a major mediator of neuronal cell death. We report here that apoptosis-inducing factor (AIF) mediates PARP-1-dependent glutamate excitotoxicity caspase-independent manner after translocation from the mitochondria nucleus. In primary murine cortical cultures, neurotoxic NMDA exposure triggers AIF translocation, mitochondrial membrane depolarization,...
Alzheimer's disease (AD) is a progressively debilitating brain disorder pathologically defined by extracellular amyloid plaques, intraneuronal neurofibrillary tangles, and synaptic disintegrity. AD has not been widely considered of white matter, but more recent evidence suggests the existence abnormalities in myelination patterns myelin attrition AD-afflicted human brains. Herein, we demonstrate that triple-transgenic (3xTg-AD) mice, which harbor precursor protein Swedish mutant transgene,...
Alzheimer's disease is a complex neurodegenerative disorder characterized pathologically by temporal and spatial progression of beta-amyloid (Abeta) deposition, neurofibrillary tangle formation, synaptic degeneration. Inflammatory processes have been implicated in initiating and/or propagating AD-associated pathology within the brain, as inflammatory cytokine expression other markers inflammation are pronounced individuals with AD pathology. The current study examines whether evident early...
Several transgenic animal models genetically predisposed to develop Alzheimer's disease (AD)-like pathology have been engineered facilitate the study of pathophysiology and vetting potential disease-modifying therapeutics. The triple mouse model AD (3xTg-AD) harbors three AD-related genetic loci: human PS1M146V, APPswe, tauP301L. These mice both amyloid plaques neurofibrillary tangle-like in a progressive age-dependent manner, while these pathological hallmarks are predominantly restricted...
Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are associated with late-onset, autosomal-dominant, familial Parkinson's disease (PD) and also contribute to sporadic disease. The LRRK2 encodes a large protein multiple domains, including functional Roc GTPase domains. most likely cause through toxic gain-of-function mechanism. expression of human variants cultured primary neurons induces toxicity that is dependent on intact GTP binding or activities. However, mechanism(s)...
In this critique of Professor Ehrlich's recent research on capital punishment,' we conclude that he has failed to provide any reliable evidence the death penalty deters murder.His data are inadequate for purposes his analysis and misapplies highly sophisticated statistical techniques employs.We begin with an evaluation uses measure critical variables in theoretical formulation then consider flaws which would invalidate conclusions even if were adequate.We by explaining how produces results...
Drawing on a wide variety of data sources, this study examines arbi trariness and discrimination under capital statutes in Florida, Georgia, Texas, Ohio, which are responsible for roughly 70 percent the. death sentences imposed nationwide the five years following United States Supreme Court's Furman decision. It finds that there gross dif ferences treatment potentially offenders by race fender victim judicial circuits within states. These (1) inde pendent aggravating felony-related...
Clinical studies to date have failed establish therapeutic benefit of glial cell-derived neurotrophic factor (GDNF) in Parkinson's disease (PD). In contrast previous nonclinical neuroprotective reports, this study shows clinically relevant and long-lasting regeneration the dopaminergic system rhesus macaques lesioned with 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine 3-6 months before GDNF gene delivery (AAV2-GDNF). The observed progressive amelioration functional deficits, recovery dopamine,...
Multiple sclerosis (MS) is a chronic neuroinflammatory disease characterized by immune cell infiltration of CNS, blood-brain barrier (BBB) breakdown, localized myelin destruction, and progressive neuronal degeneration. There exists significant need to identify novel therapeutic targets strategies that effectively safely disrupt even reverse pathophysiology. Signaling cascades initiated semaphorin 4D (SEMA4D) induce glial activation, process collapse, inhibit migration differentiation...
Abstract Semaphorin 4D (SEMA4D, CD100) and its receptor plexin-B1 (PLXNB1) are broadly expressed in murine human tumors, their expression has been shown to correlate with invasive disease several tumors. SEMA4D normally functions regulate the motility differentiation of multiple cell types, including those immune, vascular, nervous systems. In setting cancer, SEMA4D–PLXNB1 interactions have reported affect vascular stabilization transactivation ERBB2, but effects on immune-cell trafficking...
Huntington disease (HD) is an inherited, fatal neurodegenerative with no disease-modifying therapy currently available. In addition to characteristic motor deficits and atrophy of the caudate nucleus, signature hallmarks HD include behavioral abnormalities, immune activation, cortical white matter loss. The identification validation novel therapeutic targets that contribute these degenerative cellular processes may lead new interventions slow or even halt course this insidious disease....
In mice, Brn3 POU domain transcription factors play essential roles in the differentiation and survival of projection neurons within retina, inner ear, dorsal root trigeminal ganglia. During retinal ganglion cell differentiation, Brn3b is expressed first, followed by Brn3a Brn3c. Targeted deletion Brn3b, but not or Brn3c, leads to a loss most cells before birth. However, as few are still present Brn3b–/– Brn3c may partially compensate for Brn3b. To examine role development, we generated...
In this study, we find that in New York State over the period 1907-63 there were, on average, two additional homicides month after an execution. Controls for time trends, seasonality, effects of war, and adjustments autocorrelation tend to confirm finding. Such a "brutalizing" effect executions is consistent with research violent events such as publicized suicides, mass murders, assassinations; previous studies long-term availability use capital punishment; small number investigations...