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Nathan Goodyear

Molecular Control of Immune/Inflammatory Responses: Interactions Between Nuclear Factor-κB and Steroid Receptor-Signaling Pathways - 0 views

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    Benefits of progesterone, are in part, due to its function on the immune system.  Progesterone shown to decrease T cell activity, macrophage activity and NK cell activity.  Aside, NK cell activity has been found to be increased in those with recurrent first trimester miscarriages and progesterone defects.  So, low progesterone allows for a rise in NK cell activity and inflammation that is detrimental to a developing pregnancy.  If that is the case in pregnancy, what about the rest of the body?
Nathan Goodyear

Vitamin D inhibits monocyte/macrophage proinflamma... [J Immunol. 2012] - PubMed - NCBI - 0 views

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    Vitamin D inhibits inflammatory signaling through the LPS stimulated macrophages through the up regulation of MKP-1.
Nathan Goodyear

Adipose Tissue Recruitment of Leukocytes - 0 views

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    good discussion on how adipose tissue recruits macrophages and increases inflammatory signaling initiating insulin resistance.  This reveals how adipose tissue is extremely active.
Nathan Goodyear

Autoimmunity following Hepatitis B vaccine as part of the spectrum of 'Autoimmune (Auto-inflammatory) Syndrome induced by Adjuvants' (ASIA): analysis of 93 cases - 0 views

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    large case study of Autoimmune Syndrome Induced by Adjuvants; also known as ASIA.  Think of Aluminum as the perfect example and think of macrophages myofasciitis.
Nathan Goodyear

Mechanisms of aluminum adjuvant toxicity and autoimmunity in pediatric populations - 0 views

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    Adjuvants in vaccines are dangerous.  ASIA and macrophages myofasciitis are implicated in the damage caused by adjuvants, of which aluminum is the most widely known.  I love what the author says here: "safe assessments for vaccines have often not included appropriate toxicity studies because vaccines have not been viewed as inherently toxic".  This is not political but scientific.
Nathan Goodyear

Aluminum vaccine adjuvants: are they safe? - PubMed - NCBI - 0 views

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    Aluminum as an adjuvant in vaccines is associated with macrophages myofasciitis and ASIA.
Nathan Goodyear

Cordycepin Suppresses Expression of Diabetes Regulating Genes by Inhibition of Lipopolysaccharide-induced Inflammation in Macrophages - 0 views

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    cordyceps shown to decrease LPS stimulated macrophage inflammation.  Specifically, IL-1Beta, IL-6, TNF-alpha were shown to be inhibited.  Also, NF-kappaB inhibition was found with cordyceps
Nathan Goodyear

ingentaconnect Adipose Tissue Macrophages, Low Grade Inflammation and Insulin Re... - 0 views

  • “M1” or “classically activated” macrophages
  • PPAR-gamma agonists
  • “M2” or an “alternatively activated” anti-inflammatory phenotype
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    ATMs and obesity induced inflammation initiates insulin resistance and thus type II diabetes. The bodies reaction to a fat cell is no different than a bacterial, viral, or parasitic infection.  The body recognizes something (fat) that shouldn't be there and it attempts to destroy it and remove it.
Nathan Goodyear

ARS | Publication request: Sex hormone modulation of proinflammatory cytokine and CRP expression in macrophages from older men and postmenopausal women - 0 views

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    Study finds that Testosterone provided a small anti-inflammatory effect in post-menopausal women and men, whereas Estrogen increased macrophage cytokine production in post-menopausal women with elevated LDL.  Now, this study did not differentiate PCOS versus non-PCOS, nor did it look at the effects of adiposity in these hormonal effects in women.  Both of which, will effect the outcome.
Nathan Goodyear

http://www.2ndchance.info/onesize4all-Perricone2013.pdf - 0 views

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    Absolute must read!  Science. That is what physicians are.  Eliminate politics and bias.  Aluminum, common adjuvant in vaccines and well known neurotoxin, has been linked to post vaccine macrophagic myofascitis.  Now, world experts have placed it at the forefront of a new created syndrome "ASIA" which is autoimmune/inflammatory syndrome induced by adjuvants.  
Nathan Goodyear

A review on the association between inflammato... [Autoimmun Rev. 2014] - PubMed - NCBI - 0 views

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    Author states that there may be a link between vaccine adjuvants and post-vaccine myopathies as in macrophagic myofasciitis.  He concludes with "the concept of a possible causal link between immunization and inflammatory myopathies should not be totally rejected".  Not associated, but causal.
Nathan Goodyear

Diet-induced obesity and low testosterone increase neuroinflammation and impair neural function - 0 views

  • both obesity and low testosterone are also risk factors for neural dysfunction, including cognitive impairment [58–61] and development of AD
  • Levels of obesity and testosterone are often inversely correlated
  • diet-induced obesity causes significant metabolic disturbances and impairs central and peripheral nervous systems.
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  • both obesity and low testosterone are linked with promotion of inflammatory pathways [70–72] and exert harmful actions on the central [73–75] and peripheral [29,76] nervous systems
  • In general, obesity-related changes were worsened by low testosterone and improved by testosterone treatment; however, this relationship was not statistically significant in several instances. Further, our data suggest that a common pathway that may contribute to obesity and testosterone effects is regulation of inflammation
  • fasting blood glucose levels were independently and additively increased by GDX-induced testosterone depletion and high-fat diet
  • testosterone treatment significantly reduced fasting glucose under both the normal and high-fat diets, demonstrating potential therapeutic efficacy of testosterone supplementation
  • fasting insulin, insulin resistance (HOMA index), and glucose tolerance, low testosterone tended to exacerbate and or testosterone treatment improved outcomes.
  • testosterone status did not significantly affect body weight
  • testosterone’s effects likely do not indicate an indirect result on adiposity but rather regulatory action(s) on other aspects of metabolic homeostasis
  • Prior work in rodents has shown diet-induced obesity induces insulin resistance in rat brain [63] and that testosterone replacement improves insulin sensitivity in obese rats [64]. Our findings are consistent with the human literature, which indicates that (i) testosterone levels are inversely correlated to insulin resistance and T2D in healthy [30,65] as well as obese men [66], and (ii) androgen therapy can improve some metabolic measures in overweight men with low testosterone
  • it has been shown that TNFα has inhibitory effects on neuron survival, differentiation, and neurite outgrowth
  • Our data demonstrate that low testosterone and obesity independently increased cerebrocortical mRNA levels of both TNFα and IL-1β
  • Testosterone status also affected metabolic and neural measures
  • many beneficial effects of testosterone, including inhibition of proinflammatory cytokine expression
  • neuroprotection [80,81], are dependent upon androgen receptors, the observed effects of testosterone in this study may involve androgen receptor activation
  • testosterone can be converted by the enzyme aromatase into estradiol, which is also known to exert anti-inflammatory [82] and neuroprotective [83] actions
  • glia are the primary sources of proinflammatory molecules in the CNS
  • poorer survival of neurons grown on glia from mice maintained on high-fat diet
  • Since testosterone can affect glial function [86] and improve neuronal growth and survival [87–89], it was unexpected that testosterone status exhibited rather modest effects on neural health indices with the only significant response being an increase in survival in the testosterone-treated, high-fat diet group
  • significantly increased expression of TNFα and IL-1β in glia cultures derived from obese mice
  • testosterone treatment significantly lowered TNFα and IL-1β expression to near basal levels even in obese mice, indicating a protective benefit of testosterone across diet conditions
  • IL-1β treatment has been shown to induce synapse loss and inhibit differentiation of neurons
  • Testosterone status and diet-induced obesity were associated with significant regulation of macrophage infiltration
  • testosterone prevented and/or restored thermal nociception in both diet groups
  • a possible mechanism by which obesity and testosterone levels may affect the health of both CNS and PNS
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    Study points to obesity and low Testosterone contribution of neuroinflammation.  No effect of body weight was seen with TRT.  This animal model found similar positive effects of TRT in insulin sensitivity.  Obesity and low T increase inflammatory cytokine production: this study found an increase in TNF-alpha and IL-1beta and TRT reduced TNF-alpha and IL-1beta to near base-line.  Testosterone is neuroprotective and this study reviewed the small volume of evaded that pointed to benefit from estradiol.  Testosterone's effect on glial survival was positive but not significant.  Obesity and low T were found to be associated with increased macrophage infiltration in the PNS with increased TNF-alpha and IL-1beta.   Testosterone therapy improved peripheral neuropathy via its positive effects on nocicieption.
Nathan Goodyear

Hypercalcemia of malignancy and new treatment options - 0 views

  • Hypercalcemia of malignancy occurs as the result of direct bone metastasis and via humoral mechanisms such as parathyroid hormone-related protein (PTHrP) or 1,25-dihydroxyvitamin D mediated pathways
  • ectopic secretion of parathyroid hormone (PTH) has been implicated
  • Hypercalcemia due to osteolytic bone lesions is common in multiple myeloma, leukemia, and breast cancer
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  • Humoral hypercalcemia is predominant in squamous cell, renal cell and ovarian cancers, and lymphomas are associated with 1,25-dihydroxyvitamin D mediated hypercalcemia
  • 20% of cases of hypercalcemia of malignancy and is frequently encountered in multiple myeloma, metastatic breast cancer, and to a lesser extent in leukemia and lymphoma
  • Physiologic bone turnover requires the complementary activity of osteoblasts – mesenchymal stem cell-derived bone-forming cells – and bone-resorbing cells of monocyte and macrophage lineage known as osteoclasts
  • In local osteolytic hypercalcemia, the RANKL/RANK interaction results in excessive osteoclast activation leading to enhanced bone resorption and thus hypercalcemia
  • In addition, osteoclast activation is also mediated by malignancy secreted cytokines, including interleukin-1, initially termed “osteoclast stimulating factor”
  • Macrophage inflammation protein 1-alpha (MIP 1-alpha)
  • hypercalcemia is through extra-renal 1,25-dihydroxyvitamin D (calcitriol) production
  • 1% of cases
  • increased production of 1,25-dihydroxyvitamin D occurs nearly exclusively in Hodgkin and non-Hodgkin lymphoma with case reports of the same in ovarian dysgerminoma
  • 1-α-hydroxylase in the kidney, a process regulated by PTH
  • in 1,25-dihydroxyvitamin D induced hypercalcemia, malignant cells likely recruit and induce adjacent macrophages to express 1-α-hydroxylase, converting endogenous calcidiol into calcitriol.31 Calcitriol then binds to receptors in the intestine leading to heightened enteric calcium reabsorption with resultant hypercalcemia
  • this mechanism of disease is best conceptualized as an absorptive form of hypercalcemia
  • Ectopic production of PTH by malignant cells has been described in a handful of cases involving cancer of the ovary and lung, as well as neuroendocrine tumors and sarcoma
  • primary hyperparathyroidism and malignancy comprising nearly 90% of cases of hypercalcemia
  • an initial panel consisting of PTH, PTHrP, phosphorus, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D should be obtained
  • Lymphoma, a hypercalcemia due to 1,25-dihydroxyvitamin D mediated pathways, is implied by elevations in 1,25-dihydroxyvitamin D without concomitant elevations in 25-hydroxyvitamin D. In such cases, PTH is low and PTHrP undetectable
  • Treatment of hypercalcemia of malignancy is aimed at lowering the serum calcium concentration by targeting the underlying disease, specifically by inhibiting bone resorption, increasing urinary calcium excretion, and to a lesser extent by decreasing intestinal calcium absorption
  • mildly symptomatic disease
  • marked symptoms
  • hydration with isotonic fluid (if admitted), avoidance of thiazide diuretics, and a low-calcium diet
  • denosumab
  • Denosumab is an RANKL antibody that inhibits osteoclast maturation, activation, and function
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    hypercalcemia in cancer and treatments.
Nathan Goodyear

KoreaMed Synapse - 0 views

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    macrophages
Nathan Goodyear

Induction of interferon and activation of NK cells and macrophages in mice by oral administration of Ge-132, an organic germanium compound. - PubMed - NCBI - 0 views

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    Orally administered Germanium, at 300 mg/kg) found to increase NK activity and activation of macrophages via Interferon in mouse animal model.
Nathan Goodyear

Vitamin C Inhibits Metastasis of Peritoneal Tumors By Preventing Spheroid Formation in ID8 Murine Epithelial Peritoneal Cancer Model - 0 views

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    Vitamin C inhibits M2 macrophages in the TME and inhibits EMT.
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