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Nathan Goodyear

Hypothalamo-Pituitary-Adrenal Axis Dysfunction in Chronic Fatigue Syndrome, and the Eff... - 0 views

jcem.endojournals.org/...3545.long

CFS chronic fatigue syndrome hydrocortisone cortisol fatigue adrenal fatigue hypoadrenia HPA adrenal insufficiency adrenal adrenals

shared by Nathan Goodyear on 01 May 12 - No Cached
  • We conclude that the improvement in fatigue seen in some patients with chronic fatigue syndrome during hydrocortisone treatment is accompanied by a reversal of the blunted cortisol responses to human CRH
  • These data further suggest that the hypocortisolism found in chronic fatigue syndrome may be secondary to reduced adrenal gland output.
  • 5-mg replacement dose of hydrocortisone, and the remainder 10 mg
  • Nathan Goodyear on 01 May 12
     
    low dose hydrocortisone therapy (defined as 5-10 mg), in this study, was used to treat CFS.  This study found an improvement in symptoms in these patients.  Additionally, low cortisol was found in these patients with CFS.  Their conclusion, was that low adrenal function is a component of CFS and low dose hydrocortisone therapy is an effective treatment.   Now, is the low cortisol as the result of increased metabolism as well?
Nathan Goodyear

High Progesterone Receptor Expression in Prostate Cancer Is Associated with Clinical Fa... - 0 views

www.ncbi.nlm.nih.gov/...PMC4344236

prostate cancer progesterone progesterone receptor hormones cancer prostate

shared by Nathan Goodyear on 03 Jun 18 - No Cached
  • Currently, there is a general agreement of PGR presence in the stromal cells of PCa
  • expressed in both stromal and tumor cells of the PCa tissue
  • In univariate analysis, a high density level of PGR in both TE and TS was associated with CF
  • ...17 more annotations...
  • High density level of PGR in the TE was an independent prognostic factor for CF.
  • Our large-sized study demonstrates a wide distribution of PGR in stromal and epithelial cells of both benign and malignant prostate tissue
  • there seems to be a general agreement of PGR presence in the stromal cells of PCa
  • In line with our findings, several have also reported a high PGR expression in TE of PCa [9,10,23,25]. In contrast, others have demonstrated a total lack of PGR expression in TE
  • the actions of progesterone are tissue specific
  • In our work univariate analysis demonstrated a high PGR expression in TS to be associated with clinical failure in PCa patients. So far we have not yet demonstrated the mechanism underlying this association
  • Several non-genomic proliferative actions of progesterone have been proposed in tumor cells of other organs, including breast [35–37], astrocytoma [38] and osteosarcoma [39] cell lines. However, such results are contradicted by suggestions of anti-proliferative actions of progesterone in endometrial cancer
  • Yu et al. found PGR to be negatively regulating stromal cell proliferation in vitro
  • high PGR density level in TE was associated with CF in patients with Gleason score ≥ 7
  • Bonkhoff et al. have suggested progressive emergence of PGR during PCa progression and metastasis
  • Latil and co-workers found a decreased PGR expression in clinically localized tumors and increased PGR expression in hormone-refractory tumors, when compared with normal prostate tissue
  • Our findings provide further support to these findings, indicating that PGR plays a role in the pathogenesis of PCa
  • Ki67 and PGR in TE were correlated with CF (S3 Text), indicating an association between PGR and proliferative activity
  • The mechanism behind the PGR up-regulation in PCa has not yet been elucidated
  • The PGR is, like the glucocorticoid receptor, similar to androgen receptor with 88% sequence homology in the ligand-binding domain
  • progesterone induced expression of androgen receptor-regulated genes could be a potential mechanism contributing to the development of castrate resistant PCa
  • A possibility of different roles by the two PGR isoforms in normal prostate tissue and PCa, as is suggested for the estrogen receptors [13], must also be taken into account
  • Nathan Goodyear on 03 Jun 18
     
    STudy finds that increased Progesterone receptor expression on epithelial and stromal cells is associated with increased clinical failure of therapy.  Several proposed mechanisms: 88% homologous with androgen receptor suggesting cross-stimulation and via progesterone induced increased androgen receptor gene stimulation i.e. epigenetics.
Nathan Goodyear

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4865785/ - 0 views

www.ncbi.nlm.nih.gov/...PMC4865785

CF cystic fibrosis

shared by Nathan Goodyear on 07 Feb 17 - No Cached
  • Nathan Goodyear on 07 Feb 17
     
    good review of CF
Nathan Goodyear

Alterations in diurnal salivary cortisol rhyth... [Psychosom Med. 2008] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...18378875

CFS chronic fatigue syndrome saliva salivary cortisol IL-6 inflammation fatigue cytokine

shared by Nathan Goodyear on 02 May 12 - No Cached
  • Nathan Goodyear on 02 May 12
     
    Individuals with CFS found to have flattened salivary cortisol 4-point pattern and elevated IL-6.
Nathan Goodyear

Salivary cortisol response to awakening in chronic fatigue syndrome - 0 views

bjp.rcpsych.org/...136.full.pdf

chronic fatigue syndrome CFS salivary saliva cortisol hormone hormones fatigue

shared by Nathan Goodyear on 02 May 12 - No Cached
  • Nathan Goodyear on 02 May 12
     
    This study found suppressed am salivary cortisol in those with CFS.
Nathan Goodyear

Diurnal variation of adrenocortical activ... [Neuropsychobiology. 1998] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...9813459

CFS chronic fatigue syndrome adrenal adrenals adrenocortical activity fatigue

shared by Nathan Goodyear on 02 May 12 - No Cached
  • Nathan Goodyear on 02 May 12
     
    adrenocortical dysfunction found to play a role in CFS
Nathan Goodyear

Low-Dose Hydrocortisone for Treatment of Chronic Fatigue Syndrome, September 23/30, 199... - 0 views

jama.ama-assn.org/...1061.long

CFS cortisol hydrocortisone adrenal adrenals fatigue chronic fatigue syndrome

shared by Nathan Goodyear on 02 May 12 - No Cached
  • Nathan Goodyear on 02 May 12
     
    this study revealed symptom improvement with hydrocortisone treatment in those with CFS. Pre/post treatment was with serum cortisol and not salivary cortisol.  This is a weakness of the study.  The starting dosage of 25-30 mg hydrocortisone is high and with inadequate evaluation, this high dosage could have resulted in high dosage and adrenal suppression.  
Nathan Goodyear

Hypothalamo-Pituitary-Adrenal Axis Dysfunction in Chronic Fatigue Syndrome, and the Eff... - 0 views

jcem.endojournals.org/...3545.full.pdf

CFS chronic fatigue syndrome adrenal fatigue cortisol therapy

shared by Nathan Goodyear on 12 May 12 - No Cached
  • Nathan Goodyear on 12 May 12
     
    This study reveals CFS to be low adrenal cortisol output problem. In this study, low dose cortisol (hydrocortisone) therapy improved symptoms of fatigue and improved the CRH adrenal stimulation of adrenal cortisol production.
Nathan Goodyear

Urinary Cortisol and Cortisol Metabolite Excretion in Chronic Fatigue Syndrome - 0 views

www.psychosomaticmedicine.org/...578.full.pdf

CFS chronic fatigue syndrome salivary saliva cortisol metabolism metabolization

shared by Nathan Goodyear on 13 Mar 12 - No Cached
  • Nathan Goodyear on 13 Mar 12
     
    It has been suggested in the literature that low salivary cortisol is a common finding in those with chronic fatigue. This study found no difference in the cortisol metabolite excretion. This would suggest that an increase metabolization of cortisol exists in those with CFS.
Nathan Goodyear

Oral antibiotics for treating infection with Pseudomonas aeruginosa in people with cyst... - 0 views

www.ncbi.nlm.nih.gov/...PMH0013450

P aeruginosa treatment pseudomonas aeruginosa

shared by Nathan Goodyear on 30 Sep 14 - No Cached
  • Nathan Goodyear on 30 Sep 14
     
    Oral Antibiotics, no less effective than IV therapy.  This is a cochrane review of the treatment of p aeruginosa in those with CF.
Nathan Goodyear

Hypothalamic-pituitary-adrenal axis, neuroendorine factors and stress - 0 views

cfids-cab.org/...tsigos.chrousos02.pdf

stress cortisol HPA

shared by Nathan Goodyear on 01 Feb 13 - No Cached
  • Nathan Goodyear on 01 Feb 13
     
    Great review on how stress effects the neuroimmunoendocrine systems.
Nathan Goodyear

Alterations in Diurnal Salivary Cortisol Rhythm in a Population-Based Sample of Cases W... - 0 views

www.psychosomaticmedicine.org/...298.full

cortisol salivary saliva testing CFS chronic fatigue syndrome IL-6 inflammation

shared by Nathan Goodyear on 24 Apr 12 - No Cached
  • Nathan Goodyear on 24 Apr 12
     
    low flattened cortisol diurnal salivary pattern and elevated IL-6 found in chronic fatigue patients.  
Nathan Goodyear

Low-dose hydrocortisone in chronic fatigue syndrome: a randomised crossover trial : The... - 0 views

www.thelancet.com/...fulltext

CFS chronic fatigue syndrome hydrocortisone cortisol fatigue adrenal fatigue hypoadrenia adrenal insufficiency

shared by Nathan Goodyear on 01 May 12 - No Cached
  • Nathan Goodyear on 01 May 12
     
    low dose hydrocortisone therapy, 5-10 mg, shown to be effective short-term therapy in patients with chronic fatigue syndrome.  Additionally, and very important, this study found no adrenal function suppression at these doses.
Nathan Goodyear

Salivary cortisol response to awakening in chronic fatigue syndrome - 0 views

bjp.rcpsych.org/...136.long

saliva salivary cortisol chronic fatigue syndrome CFS testing morning cortisol

shared by Nathan Goodyear on 12 May 12 - No Cached
  • Nathan Goodyear on 12 May 12
     
    Low morning cortisol found in those with chronic fatigue syndrome.
Nathan Goodyear

Urinary Cortisol and Cortisol Metabolite Excretion in Chronic Fatigue Syndrome - 0 views

www.psychosomaticmedicine.org/...578.full

urinary cortisol metabolite metabolites saliva salivary hormone hormones CFS chronic fatigue syndrome

shared by Nathan Goodyear on 20 Feb 12 - No Cached
  • Nathan Goodyear on 20 Feb 12
     
    low cortisol is a frequent finding in chronic fatigue syndrome.  However, in the urine, the cortisol levels may be normal.  This is a reflection of increased metabolism of cortisol.  This is not a contradiction, but a metabolic effect.
Nathan Goodyear

Low Dehydroepiandrosterone Sulfate is Associated With Increased Risk of Ischemic Stroke... - 0 views

stroke.ahajournals.org/...1784.full

DHEA DHEAS DHEA-S dehydroepiandrosterone stroke women female hormone hormones cardiovascular disease

shared by Nathan Goodyear on 22 Jul 14 - No Cached
  • Nathan Goodyear on 22 Jul 14
     
    Lower DHEAS, not below normal, levels associated with increased risk of ischemic stroke in women when compared to higher DHEAS levels.
Nathan Goodyear

Chronic fatigue syndrome and mitochondrial dysfunction - 0 views

www.ncbi.nlm.nih.gov/...PMC2680051

mitochondria CFS fatigue chronic fatigues syndrome

shared by Nathan Goodyear on 18 Aug 14 - No Cached
  • Nathan Goodyear on 18 Aug 14
     
    Discussion of the mitochondrial role in chronic fatigue syndrome.  As the authors conclude, there is dysfunction, but whether the cause is primary or secondary or likely varies from individual to individual is yet undetermined.
  • Blu Electronic Cigarettes on 20 Aug 14
     
    very helpful post!
Nathan Goodyear

Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside - 0 views

www.ncbi.nlm.nih.gov/...PMC5686300

nagalase Gc-MAF cancer

shared by Nathan Goodyear on 29 Jan 18 - No Cached
  • MAF precursor activity has also been lost or reduced after Gc-globulin treatment in some cancer cell lines
  • This appears to result from the deglycosylated ɑ-N-acetylgalactosaminidase (nagalase) secreted from cancerous cells
  • Nagalase has been detected in many cancer patients, but not in healthy individuals
  • ...31 more annotations...
  • Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
  • It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
  • The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
  • It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
  • The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
  • Administration of Gc-MAF stimulates immune-cell progenitors for extensive mitogenesis, activates macrophages and produces antibodies. “This indicates that Gc-MAF is a powerful adjuvant for immunization.”
  • Cancer cell lines do not develop into tumor genes in mouse models after Gc-MAF-primed immunization (29-31) and the effect of Gc-MAF has been approved for macrophage stimulation for angiogenesis, proliferation, migration and metastatic inhibition on tumors induced by MCF-7 human breast cancer cell line
  • The protocol included: "a high dose of second-generation Gc-MAF (0.5 ml) administered twice a week intramuscularly for a total of 21 injections.”
  • Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
  • Inui et al. reported that a 74-year-old man diagnosed with prostate cancer with multiple bone metastases was in complete remission nine months after initiation of GcMAF therapy simultaneously with hyper T/NK cell, high-dose vitamin C and alpha lipoic acid therapy
  • It has also been approved for non-neoplastic diseases such as autism (41), multiple sclerosis (42, 43), chronic fatigue syndrome (CFS) (40), juvenile osteoporosis (44) and systemic lupus erythematous (45).
  • Gc-MAF has been verified for use in colon, thyroid (38), lung (39), liver, thymus (36), pancreatic (40), bladder and ovarian cancer and tongue squamous carcinoma
  • Prostate, breast, colon, liver, stomach, lung (including mesothelioma), kidney, bladder, uterus, ovarian, head/neck and brain cancers, fibrosarcomas and melanomas are the types of cancer tested thus far
  • weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
  • this treatment has been suggested for non-anemic patients
  • Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
  • Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
  • In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
  • individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
  • Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
  • Gc-MAF supports humoral immunity by producing, developing and releasing large quantities of antibodies against cancer. Clinical evidence from a human model of breast cancer patients supports this hypothesis
  • There is also evidence that confirms the tumoricidal role of Gc-MAF via Fc-receptor mediation
  • It is likely that the best therapeutic responses will be observed when the nutritional and inflammatory aspects are taken together with stimulation of the immune system
  • it should be noted that no harmful side effects of Gc-MAF treatment have been reported, even when it was successfully administered to autistic children
  • The natural activation mechanism of macrophages by Gc-MAF is so natural and it should not have any side effects on humans or animal models even in cell culture
  • Besides the Gc-MAF efficacy on macrophage activity, it can be a potential anti-angiogenic agent (28) and an inhibitor of the migration of cancerous cells in the absence of macrophages (47).
  • Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
  • It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
  • inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
  • macrophages highly-activated by the addition of Gc-MAF can show tumoricidal activity
  • Previous clinical investigations have confirmed the efficacy of Gc-MAF. In addition to activating existing macrophages, Gc-MAF is a potent mitogenic factor that can stimulate the myeloid progenitor cells to increase systemic macrophage cell counts by 40-fold in four days
  • Nathan Goodyear on 29 Jan 18
     
    great review on Gc-MAF in cancer.  An increase in nagalase blocks Gc-protein to Gc-MAF activity leaving the host immune system compromised.
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