A5032954959- Neuroinflammation and Neurodegeneration Mechanisms
- Semiconductor materials and devices
- Alzheimer's disease research and treatments
- Dental Implant Techniques and Outcomes
- Mast cells and histamine
- Immune Cell Function and Interaction
- Semiconductor materials and interfaces
- Immune Response and Inflammation
- Inflammasome and immune disorders
- Organizational and Employee Performance
- Blockchain Technology Applications and Security
- Advancements in Semiconductor Devices and Circuit Design
- Silicon and Solar Cell Technologies
- interferon and immune responses
- Dental Radiography and Imaging
- Thin-Film Transistor Technologies
- Tryptophan and brain disorders
- T-cell and B-cell Immunology
- Traumatic Brain Injury and Neurovascular Disturbances
- Copper Interconnects and Reliability
- Silicon Nanostructures and Photoluminescence
- CRISPR and Genetic Engineering
- Blockchain Technology in Education and Learning
- Calcium signaling and nucleotide metabolism
- Cardiac electrophysiology and arrhythmias
Menlo School
2024
Rutgers, The State University of New Jersey
2022-2023
Smile Train
2022-2023
Kokilaben Dhirubhai Ambani Hospital
2023
Synergy University Dubai
2020-2022
S P Jain School of Global Management
2020-2022
University of California, Los Angeles
2010-2021
Harry S. Truman Memorial Veterans' Hospital
2017-2020
University of Missouri
2017-2020
United States Department of Veterans Affairs
2017-2020
Inhalation of crystalline silica and asbestos is known to cause the progressive pulmonary fibrotic disorders silicosis asbestosis, respectively. Although alveolar macrophages are believed initiate these inflammatory responses, mechanism by which this occurs has been unclear. Here we show that response subsequent development fibrosis after inhalation dependent on Nalp3 inflammasome. Stimulation with results in activation caspase-1 a Nalp3-dependent manner. Macrophages deficient components...
Dying cells are capable of activating the innate immune system and inducing a sterile inflammatory response. Here, we show that necrotic sensed by Nlrp3 inflammasome resulting in subsequent release proinflammatory cytokine IL-1β. Necrotic produced pressure disruption, hypoxic injury, or complement-mediated damage were inflammasome. activation was triggered part through ATP mitochondria released from damaged cells. Neutrophilic influx into peritoneum response to vivo also markedly diminished...
Control of tuberculosis worldwide depends on our understanding human immune mechanisms, which combat the infection. Acquired T cell responses are critical for host defense against microbial pathogens, yet mechanisms by they act in humans remain unclear. We report that cells, release interferon-γ (IFN-γ), induce autophagy, phagosomal maturation, production antimicrobial peptides such as cathelicidin, and activity Mycobacterium macrophages via a vitamin D-dependent pathway. IFN-γ induced...
Macrophage activation/polarization to distinct functional states is critically supported by metabolic shifts. How polarizing signals coordinate and reprogramming, the potential implications for control of macrophage activation, remains poorly understood. Here we show that IL-4 signaling co-opts Akt-mTORC1 pathway regulate Acly, a key enzyme in Ac-CoA synthesis, leading increased histone acetylation M2 gene induction. Only subset genes controlled this way, including those regulating cellular...
Interfering with Interferons Infections Mycobacteria, including Mycobacterium leprae or M. tuberculosis , vary substantially in their clinical presentation. For instance, some cases of the infection is self-healing very few lesions. In contrast, people experience disseminated form, where skin lesions abound and bacteria are abundant. patients infected Teles et al. (p. 1448 published online 28 February) found that disease associates a type I interferon gene signature, whereas form II...
Abstract One-third of the world’s population is infected with Mycobacterium tuberculosis (Mtb), and three million people die each year. Following its ingestion by macrophages (MPs), Mtb inhibits maturation phagosome, preventing progression to a bactericidal phagolysosome. Phagocytosis uncoupled from elevation in MP cytosolic Ca2+ that normally accompanies microbial ingestion, resulting inhibition phagosome-lysosome fusion increased intracellular viability. This study demonstrates mechanism...
IL-10 is a potent anti-inflammatory molecule that regulates excessive production of inflammatory cytokines during an infection or tissue damage. Dysregulation associated with number autoimmune diseases, and so, understanding the mechanisms by which gene expression regulated remains important area study. Macrophages represent major source IL-10, generated in response to TLR signaling as feedback mechanism curtail response. In this study, we identify pathway murine bone marrow-derived...
Abstract The NLRP3 inflammasome is activated in response to microbial and danger signals, resulting caspase-1–dependent secretion of the proinflammatory cytokines IL-1β IL-18. Canonical activation a two-step process requiring both priming signals. During activation, associates with mitochondria; however, role for this interaction unclear. In article, we show that mouse caspase-1 independently interact mitochondrial lipid cardiolipin, which externalized outer membrane at reactive oxygen...
Abstract Rapid and robust induction of type I IFN (IFN-I) is a critical event in host antiviral innate immune response. It has been well demonstrated that cyclic GMP-AMP (cGAMP) synthase (cGAS) plays an important role sensing cytosolic DNA triggering STING dependent signaling to induce IFN-I. However, it largely unknown how cGAS itself regulated during pathogen infection IFN-I production. In this study, we show pattern recognition receptor (PRR) ligands, including lipid A, LPS, poly(I:C),...
Mast cell activation plays an important role in stress-mediated disease pathogenesis. Chronic stress cause or exacerbate aging and age-dependent neurodegenerative diseases. The severity of inflammatory diseases is worsened by the stress. activation-dependent mediators augment associated pain neuroinflammation. Stress second most common trigger headache due to mast activation. Alzheimer's (AD) a progressive irreversible that affects more women than men woman's increased susceptibility chronic...
Alzheimer's disease (AD) is a progressive neurodegenerative characterized by the presence of intracellular neurofibrillary tangles (NFTs) containing hyperphosphorylated tau, and extracellular deposition amyloid plaques (APs) with misfolded amyloid-β (Aβ) peptide. Glia maturation factor (GMF), highly conserved pro-inflammatory protein, isolated cloned in our laboratory, has been shown to activate glial cells leading neuroinflammation neurodegeneration AD. We hypothesized that inflammatory...
Abstract Mycobacterium tuberculosis successfully parasitizes macrophages by disrupting the maturation of its phagosome, creating an intracellular compartment with endosomal rather than lysosomal characteristics. We have recently demonstrated that live M. infect human in absence increase cytosolic Ca2+ ([Ca2+]c), which correlates inhibition phagosome-lysosome fusion and viability. In contrast, killed induces elevation [Ca2+]c is coupled to fusion. tested hypothesis defective activation...
For the first time we describe a positive application of electromigration, as an electrically programmable fuse device (eFUSE). Upon programming, eFUSE's show large increase in resistance that enable easy sensing. The transient characteristics eFUSE stays low state during programming due to local heating link. is enhanced by design uses cathode which increases temperature gradient and minimizes effect microstructural variations.