A5061201724- Tryptophan and brain disorders
- Reproductive tract infections research
- Alzheimer's disease research and treatments
- Gut microbiota and health
- Urinary Tract Infections Management
- Glioma Diagnosis and Treatment
- Phytoestrogen effects and research
- Blood properties and coagulation
- Stress Responses and Cortisol
- Innovations in Medical Education
- Neuroinflammation and Neurodegeneration Mechanisms
- Reproductive System and Pregnancy
- Barrier Structure and Function Studies
- Drug Transport and Resistance Mechanisms
- Prion Diseases and Protein Misfolding
- Ion channel regulation and function
- Pelvic floor disorders treatments
- Health, Environment, Cognitive Aging
- Cardiac Arrest and Resuscitation
- Nanoplatforms for cancer theranostics
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Cardiomyopathy and Myosin Studies
- Medical Education and Admissions
- Traumatic Brain Injury Research
- Autophagy in Disease and Therapy
Philadelphia College of Osteopathic Medicine
2013-2022
SciencePharma (Poland)
2007
Drexel University
1993-1999
Allegheny College
1996-1998
University of Pennsylvania
1987-1992
Utilizing β-amyloid precursor protein (βAPP) as a substrate, α-, β-, and γ-secretases are responsible for sequential cleavage events leading to the formation of β-amyloid, classic pathologic hallmark Alzheimer’s Disease. Members this class proteases also catalyze activation numerous other membrane-localized proteins implicated in cell growth neuroinflammation such NOTCH Interleukin/TNF-receptor family, respectively. This investigation addresses if an vitro Chlamydia pneumoniae infection...
Sporadic late-onset Alzheimer's disease (AD) appears to evolve from an interplay between genetic and environmental factors. One factor that continues be of great interest is Chlamydia pneumoniae infection its association with disease. Detection this organism in clinical autopsy samples has proved challenging using a variety molecular histological techniques. Our current investigation utilized immunohistochemistry battery commercially available anti-C. antibodies determine whether C. was...
Pathology consistent with that observed in Alzheimer's disease (AD) has previously been documented following intranasal infection of normal wild-type mice Chlamydia pneumoniae (Cpn) isolated from an AD brain (96-41). In the current study, BALB/c were intranasally infected a laboratory strain Cpn, AR-39, and olfactory bulbs obtained at 1-4 months post-infection (pi). Immunohistochemistry for amyloid beta or Cpn antigens was performed on sections brains mock-infected mice. Chlamydia-specific...
We have investigated the effects of Chlamydia pneumoniae on human brain endothelial cells (HBMECs) and monocytes as a mechanism for breaching blood-brain barrier (BBB) in Alzheimer's disease (AD). HBMECs peripheral blood may be key components controlling entry C. into brain. Our results indicate that infects vessels AD tissues compared with normal tissue. infection stimulates transendothelial through HBMECs. This is facilitated by up-regulation VCAM-1 ICAM-1 corresponding increase LFA-1,...
The purpose of this investigation was to identify and localize tissue transglutaminase (TGase) within neurons from the hippocampi normal aged individuals those with confirmed Alzheimer's disease (AD). This enzyme may be a factor in molecular mechanisms neurodegeneration formation insoluble macromolecular complexes found AD brain tissue. An antibody made extracellular TGase, coagulation XIIIa, specific for purified intracellular guinea pig liver TGase. specificity TGase has enabled us...
Chlamydia pneumoniae has been identified and associated with multiple sclerosis (MS) Alzheimer's disease (AD) pathogenesis, although the relationship of this organism in these diseases remains controversial. We have hypothesized that one potential avenue infection is through junctional complexes between blood–brain barrier (BBB) endothelia. C. characteristically a respiratory pathogen, but implicated atherosclerosis, coronary artery disease, neuroinflammatory conditions. may lead to...
Epidemiologic studies strongly suggest that the pathophysiology of late-onset Alzheimer disease (AD) versus early-onset AD has environmental rather than genetic causes, thus revealing potentially novel therapeutic targets to limit progression. Several supporting “pathogen hypothesis” demonstrate a strong association between pathogens and production β-amyloid, pathologic hallmark AD. Although mechanism pathogen-induced neurodegeneration remains unclear, astrocytes, key player CNS innate...
Chlamydophila (Chlamydia) pneumoniae is an intracellular bacterium that has been identified within cells in areas of neuropathology found Alzheimer disease (AD), including endothelia, glia, and neurons. Depending on the cell type host, infection by C. shown to influence apoptotic pathways both pro- anti-apoptotic fashions. We have hypothesized persistent chlamydial neurons may be important mediator characteristic observed AD brains. Chronic and/or neuronal with brain affect apoptosis...
We describe the molecular mode of action and pharmacodynamics a new entity (NME) that induces NLRP3 inflammasome-mediated innate immune response. This response reduces pathogen load in an experimentally induced methicillin-resistant Staphylococcos aureus infection, enhances survival Gram-negative bacteremia, overrides escape mechanism obligate intracellular pathogen, viz. Chlamydia pneumoniae. Furthermore, NME is more effective than standard-of-care antibiotic therapy clinically established...
ABSTRACT We previously identified a protein that was stimulatory for malignant Sézary T cells, termed T-cell activating factor (SAF). However, the identity of this has not been fully elucidated, nor it’s role determined in pathogenesis cutaneous lymphoma (CTCL). The basis epidermotropism and proliferation cells skin patients with CTCL is unknown. Using monoclonal antibody inhibitory SAF activity, we demonstrated present 16 27 samples from mycosis fungoides, predominant form CTCL. In report,...