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Nathan Goodyear

'Spikeopathy': COVID-19 Spike Protein Is Pathogenic, from Both Virus and Vaccine mRNA - Abstract - Europe PMC - 0 views

europepmc.org/...PMC10452662

COVID COVID19 COVID-19 spike proteins spikeopathy cancer SARS-CoV-2

shared by Nathan Goodyear on 01 Sep 23 - No Cached
  • toxicity of the spike protein—both from the virus and also when produced by gene codes in the novel COVID-19 mRNA and adenovectorDNA vaccines
  • ‘spikeopathy’;
  • A central issue has been growing evidence of pathogenic effects of the SARS-CoV-2 spike protein—whether as part of the virus or produced by genetic codes in the mRNA and adenovectorDNA vaccines
  • ...10 more annotations...
  • It is apparent that the original Wuhan strain and early variants of SARS-CoV-2 in 2020 were more pathogenic than later variants. This is consistent with typical viral adaptive evolution to more infectious but less pathogenic strains, a natural phenomenon
  • SARS-CoV-2 spike protein is pathogenic, whether from the virus or created from genetic code in mRNA and adenovectorDNA vaccines.
  • Evidence suggests reverse transcription of mRNA into a DNA copy is possible
  • further suggests the possibility of intergenerational transmission if germline cells incorporate the DNA copy into the host genome
    • Nathan Goodyear
      Nathan Goodyear on 01 Sep 23
       
      Intergenerational and transgenerational!
  • (‘spikeopathy’) via several mechanisms that lead to inflammation, thrombogenesis, and endotheliitis-related tissue damage
  • Interaction of the vaccine-encoded spike protein with ACE-2, P53 and BRCA1 suggests a wide range of possible biological interference with oncological potential
  • Repeated COVID-19 vaccine booster doses appear to induce tolerance and may contribute to recurrent COVID-19 infection and ‘long COVID’.
  • spike protein is not only toxic through binding of ACE-2 receptors
  • interaction with cancer suppressor genes BRCA and P53
  • mitochondrial damage
Nathan Goodyear

http://www.trjfas.org/pdf/issue_12_01/0121.pdf - 0 views

www.trjfas.org/...0121.pdf

probiotics

shared by Nathan Goodyear on 01 Apr 15 - No Cached
  • Nathan Goodyear on 01 Apr 15
     
    Non-medical study finds that probiotics can be used to eliminate pathogenic bacteria.  These probiotics release bactericidal and/or bacteriostatic chemicals that can eradicate/control pathogenic and opportunistic bacteria in aquaculture.  This same logic should be applied to the Gut as well.
Nathan Goodyear

Toll-like receptor signaling links dietary fatty acids to the metabolic syndrome - 0 views

www.ncbi.nlm.nih.gov/...PMC3099529

TLR toll-like receptors toll-like receptors fatty acids fat metabolic syndrome obesity overweight inflammation dietary

shared by Nathan Goodyear on 08 Oct 12 - No Cached
  • Activation of the innate immune system controls macronutrient metabolism
  • the innate immune response is the first line of defense against invading pathogens, wherein highly conserved pathogen-associated molecular patterns (PAMPs) are recognized by cognate pattern recognition receptors (PRRs
  • many studies have supported the idea that cytokine signaling directly promotes insulin resistance
  • ...10 more annotations...
  • innate immune system may be causally linked to obesity
  • adipose tissue contains a substantial population of macrophages, and macrophage-driven adipose inflammation contributes significantly to the pathogenesis of obesity
  • Collectively, activation of the innate immune system is strongly associated with ASCVD, insulin resistance, and obesity, and recent evidence suggests that much of this association can be traced to a unique family of PRRs known as TLRs
  • TLRs are a family of type I transmembrane receptors, currently thought to comprise at least 13 members in mammals, that specifically recognize a variety of microbial PAMPs and trigger host cellular responses
  • Free SFAs have indeed been demonstrated to elicit TLR4-dependent and TLR2-dependent responses in several cell types.
  • Endogenous SFAs released from adipocytes activate cocultured macrophages via TLR4 [18], indicating the potential for cellular crosstalk in adipose tissue. Collectively, there is a growing body of evidence that SFAs promote, whereas long chain PUFA antagonize, TLR4-dependent and TLR2-dependent signaling in multiple cell models
  • In an elegant study, Shi et al. [16] demonstrated that SFAs activate TLR4-dependent signaling in both macrophages and adipocytes, and mice lacking TLR4 are protected against insulin resistance driven by intravenous lipid infusion
  • In addition to effects in macrophages and adipocytes, SFAs can activate TLR4 in the hypothalamus, which triggers a central inflammatory response that results in resistance to anorexigenic signals
  • endogenous SFAs can indeed promote innate immunity and inflammatory disease
  • This finding strongly supports the work of Hwang and coworkers [19–22] demonstrating that ω-3 PUFAs can effectively counteract SFA-induced TLR4 activation in cultured macrophages and dendritic cells.
  • Nathan Goodyear on 08 Oct 12
     
    high dietary fatty acids linked to metabolic syndrome through TLR.
George Thomas

TPE kills pathogens without toxins - 0 views

www.plasticsinfomart.com/kills-pathogens-without-toxins

Industry Portal News Plastic Marketplace Products Jobs Community Business Directory Machineries & Machines Polymer Raw Material Chemical Prices Companies HDPE PVC LDPE Injection Molding Extrusion Fillers Masterbatches Additives Granules plastics Trade

shared by George Thomas on 01 Apr 13 - No Cached
  • George Thomas on 01 Apr 13
     
    Plastics News Portal, Plastics Jobs, Plastics Directory And Trade Website for World and India - Plasticsinfomart.com
Nathan Goodyear

Update on the pathogenic potential and treatment options for Blastocystis sp | Gut Pathogens | Full Text - 0 views

gutpathogens.biomedcentral.com/...1757-4749-6-17

blastocystis hominis gut

shared by Nathan Goodyear on 28 Jun 16 - No Cached
  • Nathan Goodyear on 28 Jun 16
     
    Blastocystis hominis.  A more recent review of the data.
Nathan Goodyear

BACTERIAL INTERACTIONS WITH CELLS OF THE INTESTINAL MUCOSA: TOLL-LIKE RECEPTORS AND NOD2 -- Cario 54 (8): 1182 -- Gut - 0 views

gut.bmj.com/...1182.long

gut bacteria microbiota dysbiosis health GI TLRs NODs

shared by Nathan Goodyear on 08 Mar 12 - No Cached
  • Nathan Goodyear on 08 Mar 12
     
    How interactions between the bacteria, both commensal and pathogenic, occur.  This can precipitate disease or promote health.  This occurs through TLRs and Nods
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
  • ...56 more annotations...
  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Update on the treatment of Pseudomonas aeruginosa pneumonia - 0 views

jac.oxfordjournals.org/...229.full

P aeuroginosa Pseudomas aeuroginosa Pseudomas aeuroginosa

shared by Nathan Goodyear on 22 Jul 14 - No Cached
  • Nathan Goodyear on 22 Jul 14
     
    pseudomonas aeruginosa is an opportunistic pathogen that requires treatment, especially in the immunocompromised.
Nathan Goodyear

Chronic Inflammation and Cytokines in the Tumor Microenvironment - 0 views

www.hindawi.com/...149185

inflammation cytokines tumor cancer inflammatory IL-6 IL-10 TNF-alpha

shared by Nathan Goodyear on 26 Jun 15 - No Cached
  • Nathan Goodyear on 26 Jun 15
     
    Acute inflammation is a response to an alteration induced by a pathogen or a physical or chemical insult, which functions to eliminate the source of the damage and restore homeostasis to the affected tissue. However, chronic inflammation triggers cellular events that can promote malignant transformation of cells and carcinogenesis. Several inflammatory mediators, such as TNF-α, IL-6, TGF-β, and IL-10, have been shown to participate in both the initiation and progression of cancer. In this review, we explore the role of these cytokines in important events of carcinogenesis, such as their capacity to generate reactive oxygen and nitrogen species, their potential mutagenic effect, and their involvement in mechanisms for epithelial mesenchymal transition, angiogenesis, and metastasis. Finally, we will provide an in-depth analysis of the participation of these cytokines in two types of cancer attributable to chronic inflammatory disease: colitis-associated colorectal cancer and cholangiocarcinoma.
Nathan Goodyear

Bactericidal activities of plant essential oils an... [J Food Prot. 2002] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...12380738

essential oils bactericidal activity antibacterial

shared by Nathan Goodyear on 15 Apr 11 - No Cached
  • Nathan Goodyear on 15 Apr 11
     
    essential oils have broad spectrum activity against pathogenic bacteria
Nathan Goodyear

Toll-like Receptor Status in Obesity and Metabolic Syndrome: A Translational Perspective: The Journal of Clinical Endocrinology & Metabolism: Vol 99, No 1 - 0 views

press.endocrine.org/...jc.2013-3092

toll like receptors toll-like receptors TLRs TLR-4 TLR4 inflammation metabolic syndrome MetS insulin resistance IR Diabetes obesity

shared by Nathan Goodyear on 06 Jan 14 - No Cached
  • Nathan Goodyear on 06 Jan 14
     
    Only the abstract is available publicly.   Toll-like receptors, particularly TLR-4 has been shown to be associated with insulin resistance.  These TLRs have specific pathogen recognition sites.  TLRs are stimulated by fatty acids (FA) and endotoxemia from bacteria.  Thus, dietary intake of high trans fats, inflammation originating from the gut can be the source of insulin receptor dysfunction through TLRs.
Nathan Goodyear

Frontiers | Microbiome-Derived Lipopolysaccharide Enriched in the Perinuclear Region of Alzheimer's Disease Brain | Immunology - 0 views

journal.frontiersin.org/...full

LPS lipopolysaccharides Alzheimer's disease brain inflammation

shared by Nathan Goodyear on 23 Sep 17 - No Cached
  • lipopolysaccharides (LPS), either alone or in combination, have indicated that when compared, bacterial LPSs exhibit the strongest induction of pro-inflammatory signaling in human neuronal–glial cells in primary coculture of any single inducer, and different LPS extracts from different gastrointestinal (GI)-tract resident Gram-negative bacteria appeared to have different pro-inflammatory potential
  • powerful inducer of the NF-κB
  • In both neocortex and hippocampus, LPS has been detected to range from a ~7- to ~21-fold increase abundance in AD brain
  • ...15 more annotations...
  • Major Gram-negative bacilli of the human GI-tract, such as the abundant B. fragilis and Escherichia coli (E. coli), are capable of discharging a remarkably complex assortment of pro-inflammatory neurotoxins
  • (i) bacterial amyloids (10, 21); (ii) endotoxins and exotoxins (5, 12); (iii) LPS (12, 18); and (iv) small non-coding RNAs (sncRNAs)
  • integral components of the outer leaflet of the outer membrane of Gram-negative bacteria, LPS
  • LPS, the major molecular component of the outer membrane of Gram-negative bacteria normally serves as a physical barrier providing the bacteria protection from its surroundings
  • LPS is also recognized by the immune system as a marker for the detection of bacterial pathogen invasion and responsible for the development of inflammatory response is perhaps the most potent stimulator and trigger of inflammation known
  • AD-affected brains have remarkably large loads of bacterial-derived toxins compared to controls. The transfer of noxious, pro-inflammatory molecules from the GI-tract microbiome to the CNS may be increasingly important during the course of aging when both the GI-tract and blood–brain barriers become significantly more permeable
  • first evidence of a perinuclear association of LPS with AD brain cell nuclei
  • LPS-mediated stimulation of chronic inflammation, beta-amyloid accumulation, and episodic memory decline in murine models of AD (39, 40) and a biophysical association of LPS with amyloid deposits and blood vessels in human AD patients
  • Strong adherence of LPS to the nuclear periphery has recently been shown to inhibit nuclear maturation and function that may impair or block export of mRNA signals from brain cell nuclei, a highly active organelle with extremely high rates of transcription, mRNA processing, and export into the cytoplasm
  • LPS may be further injurious to the nuclear membrane just as LPS contributes to cerebrovascular endothelial cell membrane injury
  • high intake of dietary fiber is a strong inhibitor of B. fragilis abundance and proliferation in the intact human GI-tract and as such is a potent inhibitor of the neurotoxic B. fragilis-derived amyloids, LPS, enterotoxins, and sncRNAs.
  • GI-tract microbiome-derived LPS may be an important initiator and/or significant contributor to inflammatory degeneration in the AD CNS
  • LPS has been recently localized to the same anatomical regions involved in AD-type neuropathology
  • a known pro-inflammatory transcription factor complex that triggers the expression of pathogenic pathways involved in neurodegenerative inflammation
  • pro-inflammatory amyloids, endo- and exotoxins, LPSs, and sncRNAs but also serve as potent sources of membrane-disrupting agents
  • Nathan Goodyear on 23 Sep 17
     
    LPS links gut to inflammation in Alzheimer's disease
Nathan Goodyear

The effect of lipopolysaccharide-induced obesity and its chronic inflammation on influenza virus-related pathology - ScienceDirect - 0 views

www.sciencedirect.com/...S1382668915300983

obesity influenza lipopolysaccharides metabolic endotoxemia virus LPS

shared by Nathan Goodyear on 19 Sep 21 - No Cached
  • Nathan Goodyear on 19 Sep 21
     
    Study suggests LPS mediated obesity increases pathogenicity of influenza virus.
Nathan Goodyear

The ISME Journal - An opportunistic pathogen isolated from the gut of an obese human causes obesity in germfree mice - 0 views

www.nature.com/...ismej2012153a.html

obesity obese LPS endotoxin dysbiosis GI gut

shared by Nathan Goodyear on 20 Dec 12 - No Cached
  • Nathan Goodyear on 20 Dec 12
     
    LPS endotoxin found to increase obesity rates in mice.  The bacteria balance in the gut and the toxins they produce can contribute to the incidence of obesity.
Nathan Goodyear

Minireview: Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up - 0 views

endo.endojournals.org/...4109.full

inflammation obesity overweight hypothalamus HPA

shared by Nathan Goodyear on 04 Oct 12 - No Cached
  • Leptin, secreted by adipocytes in proportion to body fat mass
  • The saturated fatty acid palmitate (16:0) induces NF-κB signaling through a TLR4-dependent mechanism
  • 18:0 (stearic) and longer saturated fatty acids as well as linolenic acid (18:3) increased proinflammatory cytokines, ER stress markers, and TLR4 activation
  • ...6 more annotations...
  • (SOCS)-3. A member of a protein family originally characterized as negative feedback regulators of inflammation (13, 37), SOCS3 inhibits insulin and leptin signaling
  • IKKβ signaling in discrete neuronal subsets appears to be required for both hypothalamic inflammation and excess weight gain to occur during HF feeding
  • the paradoxical observation that hyperphagia and weight gain occur when hypothalamic inflammation is induced by HF feeding, yet when it occurs in response to systemic or local inflammatory processes (e.g. administration of endotoxin), anorexia and weight loss are the rule
  • , serves as a circulating signal of energy stores in part by providing feedback inhibition of hypothalamic orexigenic pathways [e.g. neurons that express neuropeptide Y and agouti-related peptide (AgRP)]
  • and stimulating anorexigenic neurons
  • signals from Toll-like receptors (TLRs), evolutionarily conserved pattern recognition molecules critical for detecting pathogens, amplified through signaling intermediates such as MyD88 activate the inhibitor of κB-kinase-β (IKKβ)/nuclear factor-κB (NF-κB), c-Jun N-terminal kinase (Jnk) and other intracellular inflammatory signals in response to stimulation by circulating saturated fatty acids
  • Nathan Goodyear on 04 Oct 12
     
    great read on the current understanding of how obesity and resultant inflammation disrupts hypothalamic function.
Nathan Goodyear

JCI - Hotspot autoimmune T cell receptor binding underlies pathogen and insulin peptide cross-reactivity - 0 views

www.jci.org/...85679

diabetes autoimmune autoimmune disease gut flora gut gut microbiome gut microbiota

shared by Nathan Goodyear on 18 May 16 - No Cached
  • Nathan Goodyear on 18 May 16
     
    Type I diabetes can be caused by Tcell autoimmunity against beta cells induced by gut flora and MCH/TCR cross reactivity.
Nathan Goodyear

The role of androgens and estrogens in the pathogenes... [J Urol. 1988] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...3172358

prostatitis E2 estradiol testosterone T:E2 testosterone:Estradiol aromatase inhibitors

shared by Nathan Goodyear on 01 May 12 - No Cached
  • Testosterone can block the effect of estradiol on prostatitis, however treatment with an anti-estrogen or an aromatase inhibitor to block estrogen action does not improve prostatitis in the rat
  • Nathan Goodyear on 01 May 12
     
    Estradiol and imbalanced Testosterone:Estradiol ratio contributes to prostatitis.  In this study, with rats, aromatase inhibitors did not improve prostatitis.
Nathan Goodyear

ScienceDirect - Toxicology and Applied Pharmacology : The potential biological mechanisms of arsenic-induced diabetes mellitus - 0 views

www.sciencedirect.com/...S0041008X04001309

arsenic exposure diabetes potential pharmacology

shared by Nathan Goodyear on 06 Dec 11 - No Cached
  • Recent studies have shown that, in subjects with chronic arsenic exposure, oxidative stress is increased and the expression of tumor necrosis factor α (TNFα) and interleukin-6 (IL-6) is upregulated
  • these two cytokines have been well known for their effect on the induction of insulin resistance
  • Oxidative stress has been suggested as a major pathogenic link to both insulin resistance and β cell dysfunction through mechanisms involving activation of nuclear factor-κB (NF-κB), which is also activated by low levels of arsenic
  • Nathan Goodyear on 06 Dec 11
     
    discussion of possible mechanisms of arsenic induced diabetes
Nathan Goodyear

Obesity - Inducible Toll-like Receptor and NF-[kappa]B Regulatory Pathway Expression in Human Adipose Tissue - 0 views

www.nature.com/...oby200825a.html

TLR-4 TLR Toll-like receptors NF-kapppB inflammation obesity

shared by Nathan Goodyear on 19 Jan 12 - No Cached
  • TLRs are functionally inducible and associated with downstream NF-B activation and proinflammatory cytokine production.
  • TLRs represent a family of receptors that are critical to the innate immune response against foreign pathogens and microorganisms
  • LPS has been shown to induce proinflammatory chemokine gene expression in differentiated human adipocytes through TLR and NF-B action
  • ...2 more annotations...
  • Stimulation of TLRs initiates intracellular signaling cascades resulting in downstream NF-B and mitogen-activated protein kinase activation and production of proinflammatory chemokines associated with mechanisms of metabolic dysfunction and cardiovascular disease progression.
  • Elevated fatty acids levels associated with obesity activate TLR4 signaling in fat cells and macrophages, and induce insulin resistance in murine models
  • Nathan Goodyear on 19 Jan 12
     
    TLR, especially TLR-4, is directly involved in NF-KappaB activation and release of inflammatory cytokines
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