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Nathan Goodyear

Regulation of Cyclooxygenase-2 Expression in Monocytes by Ligation of the Receptor for ... - 0 views

www.jbc.org/...34834.full

COX2 AGE advanced glycation end products RAGE inflammation

shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • Nathan Goodyear on 11 Jun 12
     
    good article on the biochemistry of COX2 in inflammation.  Particularily with AGE and it the receptors RAGE.  COX2 has been shown to decrease insulin secretion through inhibition of islet cell production, but in the presence of disease level inflammation, COX2 can be a part of a very dangerous autocrine/paracrine loop.
Nathan Goodyear

INAUGURAL ARTICLE by a Recently Elected Academy Member:COX-2 mediates tumor-stromal pro... - 0 views

www.ncbi.nlm.nih.gov/...PMC6431196

COX-2 prolactin cancer

shared by Nathan Goodyear on 19 Aug 19 - No Cached
  • Nathan Goodyear on 19 Aug 19
     
    Cox-2 found to increase prolactin expression to increase metastatic spread of cancer cells. Cox-2 may work here more in the autocrine/paracrine prolactin signaling. This is an animal study.
Nathan Goodyear

Carvacrol, a component of thyme oil, activates PPARα and γ and suppresses COX... - 0 views

www.ncbi.nlm.nih.gov/...PMC2789773

essential oil essential oils LPS COX2 cox-2 cyclooxygenase inflammation thyme natural

shared by Nathan Goodyear on 29 Sep 14 - No Cached
  • Nathan Goodyear on 29 Sep 14
     
    essential oils inhibit LPS induced COX-2 activity.
Nathan Goodyear

Suppression of chemotherapy-induced cytokine/lipid mediator surge and ovarian cancer by... - 0 views

www.researchgate.net/...r_by_a_dual_COX-2sEH_inhibitor

chemotherapy COX2 ovarian cancer COX-2 cytokine storm

shared by Nathan Goodyear on 06 Apr 20 - No Cached
  • Nathan Goodyear on 06 Apr 20
     
    COX2 inhibition used to counter chemotherapy induced cytokine storm metastasis.
Nathan Goodyear

Surgically induced accelerated local and distant tumor growth is significantly attenuat... - 0 views

pubmed.ncbi.nlm.nih.gov/15734421

cancer metastasis surgery

shared by Nathan Goodyear on 13 Aug 20 - No Cached
  • Nathan Goodyear on 13 Aug 20
     
    Cox II inhibition helps to slow surgical induced metastatic and local recurrence of cancer. Surgery does cause metastasis and local recurrence and cox II inhibition stops spread.
Nathan Goodyear

The COX-2 inhibitor celecoxib and its use in the management of prostate cancer. | Cance... - 0 views

cancerres.aacrjournals.org/...1239.4

cox-2 cancer prostate cancer Celebrex

shared by Nathan Goodyear on 07 Aug 18 - No Cached
  • Nathan Goodyear on 07 Aug 18
     
    COX-2 inhibition therapy useful in the treatment of prostate cancer?
Nathan Goodyear

Selective Association of Peroxiredoxin 1 with Genomic DNA and COX-2 Upstream Promoter E... - 0 views

www.ncbi.nlm.nih.gov/...PMC2929992

COX-2 metastasis chemotherapy cancer

shared by Nathan Goodyear on 16 Feb 21 - No Cached
  • Nathan Goodyear on 16 Feb 21
     
    the chemotherapy, cisplatin, found to increase COX-2 expression in breast cancer cell lines that is required for metastasis.
Nathan Goodyear

Cyclooxygenase-2 Induces EP1- and HER-2/Neu-Dependent Vascular Endothelial Growth Facto... - 0 views

cancerres.aacrjournals.org/...554

COX-2 cancer HER-2 Celebrex VEGF metastasis prostate cancer lung cancer colorectal cancer

shared by Nathan Goodyear on 07 Aug 18 - No Cached
  • Nathan Goodyear on 07 Aug 18
     
    COX-2 is overexpressed in a variety of human cancers i.e. colorectal, prostate, lung adenocarcinoma.  This study hightlights the increased tumor metastatic potential via upregulation of VEGF-C via EP1 and HER-2 dependent pathways.  This upregulation was correlated with survival and mets.
Nathan Goodyear

Suppression of chemotherapy-induced cytokine/lipid mediator surge and ovarian cancer by... - 0 views

www.pnas.org/...1698

metastasis chemotherapy COX2

shared by Nathan Goodyear on 08 Apr 20 - No Cached
  • Nathan Goodyear on 08 Apr 20
     
    COX2 inhibition to slow/block chemotherapy induced metastasis.
Nathan Goodyear

Artesunate inhibits the growth and induces apoptosis of human gastric cancer cells by d... - 0 views

www.ncbi.nlm.nih.gov/...PMC4406257

gastric cancer COX2 artesunate

shared by Nathan Goodyear on 07 May 20 - No Cached
  • Nathan Goodyear on 07 May 20
     
    Artesunate inhibits gastric cancer cells via COX2 inhibition.
Nathan Goodyear

Effects of garlic on platelet biochemistry and physiology - PubMed - 0 views

pubmed.ncbi.nlm.nih.gov/17966136

allicin COX2 cyclooxygenase garlic platelets COX-2

shared by Nathan Goodyear on 08 Jun 23 - No Cached
  • Nathan Goodyear on 08 Jun 23
     
    Allicin inhibits platelet aggregation via COX2 inhibition.
Nathan Goodyear

JAMA Network | Archives of Neurology | Neuronal Cyclooxygenase 2 Expression in the Hipp... - 0 views

archneur.jamanetwork.com/article.aspx

COX-2 inflammation dementia AD Alzheimer's disease neurology brain

shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • Nathan Goodyear on 11 Jun 12
     
    COX-2 expression associated with increasing dementia in AD.
Nathan Goodyear

3-Phosphoinositide-Dependent Protein Kinase-1/Akt Signaling Represents a Major Cyclooxy... - 0 views

cancerres.aacrjournals.org/...1444

cox-2 Celebrex cancer prostate cancer

shared by Nathan Goodyear on 07 Aug 18 - No Cached
  • Nathan Goodyear on 07 Aug 18
     
    COX-2 therapy can inhibit tumor growth and even promote apoptosis in prostate cell model.
Nathan Goodyear

Progesterone receptor plays a major antiinfla... [Mol Endocrinol. 2006] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...16772530

progesterone receptor progesterone receptors PR inflammation NF-KappaB progesterone receptor receptors COX-2

shared by Nathan Goodyear on 26 Nov 12 - No Cached
  • Nathan Goodyear on 26 Nov 12
     
    progesterone receptor inhibits inflammation through NF-kappaB inhibition and through lack of activation of COX-2.
Nathan Goodyear

ScienceDirect.com - Free Radical Biology and Medicine - Anti-inflammatory effects of be... - 1 views

www.sciencedirect.com/...S0891584911011087

benfotiamine inflammation arachidonic acid LOX-5 COX-2

shared by Nathan Goodyear on 13 Jul 12 - No Cached
  • Nathan Goodyear on 13 Jul 12
     
    Benfotiamine's anti-inflammatory effect is through the inhibition of LOX-5 and COX-2.
Nathan Goodyear

Ginsenoside Rg3 Alleviates Lipopolysaccharide-Induced Learning and Memory Impairments b... - 0 views

www.ncbi.nlm.nih.gov/...PMC3825202

RG3 inflammation brain memory learning ginsenoside panax ginseng panax ginseng TNF-alpha IL-1beta cox-2 cognition

shared by Nathan Goodyear on 10 Apr 14 - No Cached
  • Nathan Goodyear on 10 Apr 14
     
    Rat model induced inflammatory reaction in brain via LPS injection.  The result was impaired memory.  RG3 from panax ginseng was shown to reduce inflammation, TNF-alpha, IL-1beta, cox-2, thus improving memory and cognitive function.
Nathan Goodyear

Intraperitoneal Oxidative Stress in Rabbits with Papillomavirus-Associated Head and Nec... - 0 views

clincancerres.aacrjournals.org/...4289.long

Ozone cancer COX-2 immunotherapy NK cells NK

shared by Nathan Goodyear on 02 Nov 18 - No Cached
  • Nathan Goodyear on 02 Nov 18
     
    O2-O3 triggers tumoricidal immune response after application of a repetitive highly oxidative stimulus by insufflation of a medical O3/O2 gas mixture into the peritoneal cavity in animal model. O3/O2-PP treatment, indicates an enhanced activation of the innate and adaptive arms of the immune system, implicating a role of activated TILs In the anti cancer effects of the O3. Interestingly, COX2 expression was decreased.
Nathan Goodyear

Testosterone: a vascular hormone in health and disease - 0 views

joe.endocrinology-journals.org/...R47.full

testosterone hormone health disease hormones men male cardiovascular disease CVD

shared by Nathan Goodyear on 13 May 13 - No Cached
  • Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
  • In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
  • testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
  • ...54 more annotations...
  • Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
  • there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
  • bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
  • Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
  • It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
  • no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
  • free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
  • Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
  • Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
  • Testosterone shares the same molecular binding site as nifedipine
  • Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
  • Testosterone also inhibited the Ca2+ influx response to PGF2α
  • one of the major actions of testosterone is on NO and its signalling pathways
  • In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
  • the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
  • Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
  • t long-term testosterone treatment reduced CIMT in men with low testosterone levels and angina
  • neither intracellular nor membrane-associated ARs are required for the rapid vasodilator effect
  • acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
  • Testosterone and DHT increased the expression of eNOS in HUVECs
  • oestrogens have been shown to activate eNOS and stimulate NO production in an ERα-dependent manner
  • Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
  • non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
  • increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
  • Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
  • Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
  • patients with the highest IL1β concentrations had lower endogenous testosterone levels
  • TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
  • testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
  • parenteral testosterone undecanoate, CRP decreased significantly in hypogonadal elderly men
  • Higher levels of serum adiponectin have been shown to lower cardiovascular risk
  • Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
  • Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
  • decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
  • The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
  • testosterone functions through the AR to modulate adhesion molecule expression
  • pre-treatment with DHT reduced the cytokine-stimulated inflammatory response
  • DHT inhibited NFκB activation
  • DHT could inhibit an LPS-induced upregulation of MCP1
  • Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
  • As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
  • prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
  • DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
  • (Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
  • TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
  • 3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
  • This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
  • The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
  • There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
  • The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
  • trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
  • Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
  • The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
  • the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
  • Nathan Goodyear on 13 May 13
     
    Good deep look into the testosterone and CVD link.
Nathan Goodyear

PPARs, Obesity, and Inflammation - 0 views

www.ncbi.nlm.nih.gov/...PMC1783744

obesity inflammation PPARs perioxisome proliferator-activated receptor

shared by Nathan Goodyear on 16 Jan 12 - No Cached
  • increase of 61% within 10 years
  • Many of the inflammatory markers found in plasma of obese individuals appear to originate from adipose tissue
  • obesity is a state of chronic low-grade inflammation that is initiated by morphological changes in the adipose tissue.
  • ...19 more annotations...
  • secretion of MCP-1, resistin, and other proinflammatory cytokines is increased by obesity, the adipose secretion of the anti-inflammatory protein adiponectin is decreased
  • the peroxisome proliferators- activated receptor (PPAR) family are involved in the regulation of inflammation and energy homestasis
  • natural agonists, including unsaturated fatty acids and eicosanoids
  • PPARα also regulates inflammatory processes, mainly by inhibiting inflammatory gene expression
  • upregulation of COX-2 is seen in alcoholic steatohepatitis and nonalcoholic steatohepatitis and has been directly linked to the progression of steatosis to steatohepatitis, the inhibitory effect of PPARα on COX-2 may reduce steatohepatitis
  • PPARα agonists have a clear anorexic effect resulting in decreased food intake, evidence is accumulating that PPARα may also directly influence adipose tissue function, including its inflammatory status.
  • PPARα may govern adipose tissue inflammation in three different ways: (1) by decreasing adipocyte hypertrophy, which is known to be connected with a higher inflammatory status of the tissue [3, 11, 59], (2) by direct regulation of inflammatory gene expression via locally expressed PPARα, or (3) by systemic events likely originating from liver
  • PPARγ is considered the master regulator of adipogenesis
  • Unsaturated fatty acids and several eicosanoids serve as endogenous agonists of PPARγ
  • PPARγ2, which is adipose-tissue specific
  • two different molecular mechanisms have been proposed by which anti-inflammatory actions of PPARγ are effectuated: (1) via interference with proinflammatory transcription factors including STAT, NF-κB, and AP-1
  • and (2) by preventing removal of corepressor complexes from gene promoter regions resulting in suppression of inflammatory gene transcription
  • diet-induced obesity is associated with increased inflammatory gene expression in adipose tissue via adipocyte hypertrophy and macrophage infiltration
  • PPARγ is able to reverse macrophage infiltration, and subsequently reduces inflammatory gene expression
  • Inflammatory adipokines mainly originate from macrophages which are part of the stromal vascular fraction of adipose tissue [18, 19], and accordingly, the downregulation of inflammatory adipokines in WAT by PPARγ probably occurs via effects on macrophages
  • By interfering with NF-κB signaling pathways, PPARγ is known to decrease inflammation in activated macrophages
  • Recent data suggest that activation of PPARγ in fatty liver may protect against inflammation
  • PPARs may influence the inflammatory response either by direct transcriptional downregulation of proinflammatory genes
  • anti-inflammatory properties of PPARs in human obesity
  • Nathan Goodyear on 16 Jan 12
     
    PPARs play pivotal in obesity.  PPARs appear to reduce the inflammatory cascade associated with obesity.  Downregulation of PPARs are associated with increased inflammation.  Natural PPARs include unsaturated fats and eicosanoids.
Nathan Goodyear

Progesterone Receptor Inhibits Aromatase and Inflammatory Response Pathways in Breast C... - 0 views

mend.endojournals.org/...1812.long

progesterone receptor receptors PR breast cancer anti-inflammatory

shared by Nathan Goodyear on 12 Nov 12 - No Cached
  • Nathan Goodyear on 12 Nov 12
     
    Progesterone receptor (PR) shown to provide an important anti-inflammatory role in breast cancer in this study.  PR shown to increase NF-kappaB inhibitor IkBalpha, shown to inhibit aromatase activity, shown to inhibit COX-2 expression and shown to inhibit HER-2/neu expression.
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