A5037373175- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Gut microbiota and health
- Complement system in diseases
- Advanced Drug Delivery Systems
- Barrier Structure and Function Studies
- COVID-19 Impact on Reproduction
- Neuropeptides and Animal Physiology
- Immune cells in cancer
- S100 Proteins and Annexins
- Neurological Disease Mechanisms and Treatments
- Neuroscience and Neuropharmacology Research
- Piperaceae Chemical and Biological Studies
- Phagocytosis and Immune Regulation
- Medicinal Plants and Bioactive Compounds
- Antimicrobial Peptides and Activities
- Software-Defined Networks and 5G
- Plant responses to water stress
- Single-cell and spatial transcriptomics
- Cancer therapeutics and mechanisms
- Graphene and Nanomaterials Applications
- Agricultural Practices and Plant Genetics
- 14-3-3 protein interactions
- Biological Activity of Diterpenoids and Biflavonoids
- Cell Adhesion Molecules Research
University of California, Irvine
2010-2024
World Vegetable Center
2021
University of Macau
2021
Irvine Valley College
2017
The complement cascade not only provides protection from infection but can also mediate destructive inflammation. Complement is involved in elimination of neuronal synapses which essential for proper development, be detrimental during aging and disease. C1q, required several these complement-mediated activities, present the neuropil, microglia, a subset interneurons brain.To identify source(s) C1q brain, C1qa gene was selectively inactivated microglia or Thy-1+ neurons both wild type mice...
ABSTRACT Alternative splicing is widely acknowledged to be a crucial regulator of gene expression and key contributor both normal developmental processes disease states. While cost-effective accurate for quantification, short-read RNA-seq lacks the ability resolve full-length transcript isoforms despite increasingly sophisticated computational methods. Long-read sequencing platforms such as Pacific Biosciences (PacBio) Oxford Nanopore (ONT) bypass reconstruction challenges short reads. Here...
Abstract Background Complement proteins and activation products have been found associated with neuropathology in Alzheimer's disease (AD). Recently, a C5a receptor antagonist was shown to suppress two murine models of AD, Tg2576 3xTg. Previously, genetic deficiency C1q the mouse model showed an accumulation fibrillar plaques similar complement sufficient Tg2576, but reactive glia were significantly decreased neuronal integrity improved suggesting detrimental consequences for AD. The goal...
Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). Recent large genome wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) C3b/C4b receptor (CR1 or CD35) that late onset AD. Here, anti-CR1 antibodies (Abs) directed against different epitopes receptor, were used to localize CR1 brain, relative binding affinities ligands, C1q C3b, assessed by ELISA. Most Abs tested stained red...
The complement system is part of the innate immune that clears pathogens and cellular debris. In healthy brain, influences neurodevelopment neurogenesis, synaptic pruning, clearance neuronal blebs, recruitment phagocytes, protects from pathogens. However, excessive downstream activation leads to generation C5a, C5a engagement with its receptor C5aR1, instigates a feed-forward loop inflammation, injury, death, making C5aR1 potential therapeutic target for neuroinflammatory disorders. ablation...
Abstract Multiple studies have recognized the involvement of complement cascade during Alzheimer’s disease pathogenesis. However, specific role C5a-C5aR1 signaling in progression this neurodegenerative is still not clear. Furthermore, its potential as a therapeutic target to treat AD remains be elucidated. Canonically, generation anaphylatoxin C5a result activation and interaction with receptor C5aR1 triggers potent inflammatory response. Previously, genetic ablation mouse model exerted...
Alzheimer's disease (AD) is the leading cause of dementia in older adults, and need for effective, sustainable therapeutic targets imperative. The complement pathway has been proposed as a target. C5aR1 inhibition reduces plaque load, gliosis, memory deficits animal models, however, cellular bases underlying this neuroprotection were unclear. Here, we show that antagonist PMX205 improves outcomes Arctic48 mouse model AD. A combination single cell nucleus RNA-seq analysis hippocampi derived...
Alzheimer's disease (AD), a progressive neurodegenerative characterized by the accumulation of amyloid-beta protein and neuronal loss, is leading cause age-related dementia in world today. The also associated with neuroinflammation, robust activation astrocytes microglia, evidence complement system, localized both fibrillar (fAbeta) plaques tangles. observations are consistent complement-dependent component AD progression. We have previously shown that inhibition major receptor for C5a...
Synaptic loss is a hallmark of Alzheimer's disease (AD) that correlates with cognitive decline in AD patients. Complement-mediated synaptic pruning has been associated this excessive synapses AD. Here, we investigated the effect C5aR1 inhibition on microglial and astroglial two mouse models
CD200 modified PLGA surfaces inhibits inflammatory cytokine (TNF-α) secretion, and enhances anti-inflammatory secretion (IL-10) phagocytosis by macrophages.
Okra (Abelmoschus esculentus) is a heat tolerant vegetable crop with high economic and nutritional importance in parts of Asia, Africa, America. The okra biodiversity held gene bank collections could be mined for traits breeding more stress cultivars. An core collection 166 accessions comprising A. esculentus, moschatus, caillei, manihot has been assembled from the World Vegetable Center germplasm (840 accessions) based on diversity analysis 20 microsatellite markers. A selection esculentus...
Leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) is an inhibitory receptor broadly expressed on immune cells, with its ligands residing within the extracellular matrix protein collagen. In this study, surfaces are modified a LAIR-1 ligand peptide (LP), and it observed that macrophages cultured LP-conjugated exhibit significantly reduced secretion of inflammatory cytokines in response to proinflammatory stimuli reflect injured environment. These downregulated mediators include...
Alzheimer's disease (AD) is the leading cause of dementia in older adults, and need for effective, sustainable therapeutic targets imperative. Pharmacologic inhibition C5aR1 reduces plaque load, gliosis memory deficits animal models. However, cellular basis underlying this neuroprotection which processes were consequence amyloid reduction vs alteration response to unclear. In Arctic model, antagonist PMX205 did not reduce but short-term female mice prevented. Hippocampal single cell nucleus...
The contribution of the gut microbiome to neuroinflammation, cognition, and Alzheimer's disease progression has been highlighted over past few years. Additionally, inhibition various components complement system repeatedly demonstrated reduce neuroinflammation improve cognitive performance in AD mouse models. Whether deletion these is associated with distinct composition, which could impact models not yet examined. Here, we provide a comprehensive analysis conditional constitutive knockouts,...
Flow scheduling and congestion control are two important techniques to reduce flow completion time in data center networks. While existing works largely treat them independently, the interactions between general overlooked which leads sub-optimal solutions, especially given that link capacity is increasing faster than switch port buffer size. In this paper, we present <italic xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">Flash</i> , a simple yet...
Synaptic loss is a hallmark of Alzheimer's disease (AD) that correlates with cognitive decline in AD patients. Complement-mediated synaptic pruning has been associated this excessive synapses AD. Here, we investigated the effect C5aR1 inhibition on microglial and astroglial two mouse models
Abstract Background The complement system contributes to enhanced inflammation and cognitive decline in Alzheimer’s disease (AD). Previous studies have demonstrated constitutive deletion of the classical initiator protein, C1q, reduces glial activity attenuates neuronal loss AD mouse models. As it is now known that microglia are primary producers C1q brain, objective this study was determine if microglial specific would reduce lysosome associated phagocytosis Vglut1, an excitatory synapse...
Abstract Background The complement system is part of the innate immune that clears pathogens and cellular debris. In healthy brain, influences neurodevelopment neurogenesis, synaptic pruning, clearance neuronal blebs, recruitment phagocytes, protects from pathogens. However, excessive downstream activation leads to generation C5a, C5a engagement with its receptor C5aR1, instigates a feed-forward loop inflammation, injury, death, making C5aR1 potential therapeutic target for neuroinflammatory...
Inflammatory elements are prominent pathological markers of Alzheimer's Disease (AD). Complement activation has long been known to produce a local inflammatory reaction including recruitment phagocytes, and thus association complement proteins reactive glia with fibrillar amyloid plaques in later stages development AD is consistent role for this system the acceleration or progression inflammation that disease. In vitro activates both classical alternative cascades. mouse model genetic...
Abstract Multiple studies have recognized the involvement of complement cascade during Alzheimer’s disease pathogenesis; however, specific role C5a-C5aR1 signaling in progression this neurodegenerative is still not clear. Furthermore, its potential as a therapeutic target to treat AD remains be elucidated. Canonically, generation anaphylatoxin C5a result activation and interaction with receptor C5aR1 triggers potent inflammatory response. Previously, genetic ablation mouse model exerted...
Abstract Background The complement (C’) system contributes to enhanced inflammation and cognitive decline in Alzheimer’s disease (AD). Previous studies have demonstrated constitutive deletion of the classical initiator protein, C1q, reduces pathology synaptic loss AD mouse model. As it is now known that microglia are primary producers C1q brain, main objective this study was determine if microglial specific would rescue impairment AD. Method C1qa FLlFL :CX3CR1Cre (designated ΔMG )mice, which...