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Nathan Goodyear

Lipoprotein(a), Hormone Replacement Therapy and Risk of Future Cardiovascular Events - 0 views

www.ncbi.nlm.nih.gov/...PMC2958092

hormone replacement therapy cardiovascular disease events risk Lp(a) lipoprotein(a) lipoproteins CVD women HT HRT hormones

shared by Nathan Goodyear on 26 Aug 14 - No Cached
  • Nathan Goodyear on 26 Aug 14
     
    study finds HT reduced Lp(a) in women and reduced the Lp(a) association with CVD.  Women not on HT in this study had higher Lp(a) versus those on HT.
Nathan Goodyear

Therapeutic hyperthermia: The old, the new, and the upcoming - Critical Reviews in Onco... - 1 views

www.croh-online.com/...fulltext

hyperthermia hyperthermic therapy cancer oncology

shared by Nathan Goodyear on 30 Aug 18 - No Cached
  • not well understood, but it is felt to be a combination of both heat-induced necrosis and of protein inactivation (e.g., repair enzymes) as opposed to DNA damage
  • alterations in tumor cytoskeletal and membrane structures, which disrupt cell motility and intracellular signal transduction
  • A common explanation for HT-enhancement of RT and CT involves inhibition of homologous recombination repair of double-strand DNA breaks, preventing cells from repairing sub-lethal damage
  • ...15 more annotations...
  • it does appear to inhibit rejoining of RT-induced DNA breaks more than is commonly observed after RT alone
  • HT damages cells and enhances RT and CT sensitivity as a function of both temperature and duration of treatment
  • as temperature or duration increase, the rate of cell killing also increases
  • At temperatures above 42 °C, tumor vasculature is damaged, resulting in decreased blood flow
  • Cancer cells are particularly vulnerable to heating; in vivo studies have shown that temperatures in the range of 40–44 °C cause more selective damage to tumor cells
  • cancerous blood vessels are chaotic, leaky, and inefficient
  • selective cytotoxic effect on tumor cells include inhibition of key cancer cell-signaling pathways such as AKT, inducing apoptosis, suppression of cancer stem cell proliferation, and others
  • increase in immunological attacks against tumors after HT, which were believed to be achieved through activation of HSPs and subsequent modulation of the innate and adaptive immune responses against tumor cells
  • HT does lead to activation of the immune system and HSP-induced cell death through modification of the tumor cell surface
  • These HSPs and tumor antigens are taken up by dendritic cells and macrophages and go on to induce specific anti-tumor immunity
  • In vivo studies demonstrate HT-enhancement of NK cell activity, and HT has been shown to increase neutrophilic granulocytes with anti-tumor activity
  • it has become increasingly clear that HT results in immune stimulation, through both direct heat-mediated cell killing as well as innate and adaptive immune system modulation
  • The term hyperthermia is used in this review to refer to heating within the clinically accepted range of 40–45 °C
  • temperatures above 42.5–43 °C the exposure time can be halved with each 1 °C increase while maintaining equivalent cell killing
  • gradual heating at 43 °C for 1 h worked through an apoptotic pathway
  • Nathan Goodyear on 30 Aug 18
     
    Comprehensive review of hyperthemic therapy.
Nathan Goodyear

Hormone Therapy, Estrogen Metabolism, and Risk of Breast Cancer in the Women's Health I... - 0 views

www.ncbi.nlm.nih.gov/...PMC3493689

breast cancer estrogen metabolites 2-OH-estrone 2:16 cancer hormones estrogen

shared by Nathan Goodyear on 11 Sep 15 - No Cached
  • These results demonstrate that although 16α-OHE1 was increased more by E+P than by E-alone, the increase in the 2:16 ratio was similar for both HT regimens, due to ~4-fold greater increase in 2OHE-1 than 16α-OHE1 for both HT regimens
  • baseline and 1 year change in 16α-OHE1 showed little relationship to incident breast cancer
  • higher baseline 2-OHE1 and the 2:16 ratio were modestly associated with higher odds of incident breast cancer, but larger 1 year increase in 2-OHE-1 and the 2:16 ratio were also weakly associated with lower odds of breast cancer
  • Nathan Goodyear on 11 Sep 15
     
    Good review of the data from the WHI-HT on estrogen metabolites and breast cancer risk.  Increased 2-OHestrone and 2:16 ratio without statistical significance reached.
Nathan Goodyear

JAMA Network | JAMA Psychiatry | Mineralocorticoid Receptor Function in Major Depression - 0 views

archpsyc.jamanetwork.com/article.aspx

depression cortisol serotonin 5-HT1A receptors

shared by Nathan Goodyear on 03 Feb 14 - No Cached
  • Nathan Goodyear on 03 Feb 14
     
    High cortisol reduce 5-HT1A receptors in major depression.
Nathan Goodyear

Interferon-[alpha] reduces the density of monoaminergic axon... : NeuroReport - 0 views

journals.lww.com/..._reduces_the_density_of.7.aspx

depression inflammation IFN-gamma 5-HT serotnin noradrenergic neurotransmitter

shared by Nathan Goodyear on 14 Sep 11 - No Cached
  • Nathan Goodyear on 14 Sep 11
     
    inflammation, IFN-gamma, shown to lead to 5-HT and noradrenergic axon degeneration.  This reveals another inflammatory contribution to depression
Nathan Goodyear

Risk of Breast Cancer in Relation to Combined Effects of Hormone Th... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25695354

breast cancer cancer women hormones hormone Testosterone Estrogen Estradiol ER+ estrogen receptors obesity overweight hormone therapy

shared by Nathan Goodyear on 23 Feb 15 - No Cached
  • Nathan Goodyear on 23 Feb 15
     
    Study finds increases serum Estradiol and Testosterone levels associated with increased risk of breast cancer.  Increased risk was also found associated with being overweight/obese, increased alcohol intake, alcohol combined with HT.  This was found in estrogen receptor + cases of breast cancer.
Nathan Goodyear

Sex hormones affect neurotransmitters and shape the adult female brain during hormonal ... - 0 views

www.ncbi.nlm.nih.gov/...PMC4335177

hormones neurotransmitters serotonin GABA dopamine estradiol progesterone glutamate

shared by Nathan Goodyear on 11 Jul 17 - No Cached
  • estrogen administration has been found to increase tryptophan hydroxylase
  • 5-HT2A mRNA levels in brain areas relevant for the control of mood, mental state and cognition (Sumner and Fink, 1998) and 5-HTT mRNA when administered for a longer period
  • n the other hand, estrogen treatment has also been observed to decrease mRNA related to serotonergic neurotransmission
  • ...4 more annotations...
  • Furthermore, acute estrogen administration decreases 5-HTT mRNA levels (Pecins-Thompson et al., 1998) and 5-HT1A mRNA levels and binding
  • assigning the effects of estrogen on serotonin to a homogenous functional class of stimulation or inhibition seems not to be feasible
  • Progesterone has been suggested to increase serotonergic neurotransmission via the regulation of the expression of serotonin-related genes and proteins
  • menopausal women gain less benefit from antidepressant treatments compared to women during their reproductive years
  • Nathan Goodyear on 11 Jul 17
     
    good review of the relationship of the sex hormones and neurotransmitters.
Nathan Goodyear

Hyperthermia and Chemotherapy - Holland-Frei Cancer Medicine - NCBI Bookshelf - 0 views

www.ncbi.nlm.nih.gov/...NBK13550

Hyperthermia Cancer Chemotherapy hyperthermic therapy

shared by Nathan Goodyear on 18 Dec 18 - No Cached
  • Nathan Goodyear on 18 Dec 18
     
    Brief review from book on severe hyperthermia and chemotherapy: The mechanisms that underlie the synergy may include (1) increased cellular uptake of drug, (2) increased oxygen radical production, and (3) increased DNA damage and inhibition of repair; potential use of HT with many drugs is its ability to reverse, at least partially, drug resistance
Nathan Goodyear

Effects of hyperthermia on normal and tumor microenvironment. | Radiology - 0 views

pubs.rsna.org/...radiology.137.2.7433686

TME hyperthermia tumor microenvironment

shared by Nathan Goodyear on 13 Feb 21 - No Cached
  • Nathan Goodyear on 13 Feb 21
     
    The effect of HT in the TME is dictated but the temperature.
Nathan Goodyear

Potential enhancement of host immunity and anti-tumor efficacy of nanoscale curcumin an... - 0 views

bmccancer.biomedcentral.com/...s12885-020-07072-0

heat shock proteins curcumin HSP70 resveratrol hyperthermia colon cancer

shared by Nathan Goodyear on 25 Feb 21 - No Cached
  • Nathan Goodyear on 25 Feb 21
     
    Local HT augments anti-cancer effects of curcumin and resveratrol.
Nathan Goodyear

Targeted near infrared hyperthermia combined with immune stimulation for optimized ther... - 0 views

www.ncbi.nlm.nih.gov/...PMC4872755

HSP70 thyroid cancer quercetin hyperthermia

shared by Nathan Goodyear on 05 Nov 21 - No Cached
  • Nathan Goodyear on 05 Nov 21
     
    Quercetin inhibits HSP70 and improves efficacy of HT in thyroid cancer in vitro and in vivo studies.
Nathan Goodyear

Effects of the flavonoid drug quercetin on the response of human prostate tumours to hy... - 0 views

pubmed.ncbi.nlm.nih.gov/11471985

quercetin hyperthermia

shared by Nathan Goodyear on 19 Jul 23 - No Cached
  • Nathan Goodyear on 19 Jul 23
     
    Quercetin in vitro and in vivo serves as a HT sensitizer.
Nathan Goodyear

Acute changes in 5-HT metabolism after S-adeno... [Gen Pharmacol. 1989] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...2473938

SAMe methylation depression serotonin

shared by Nathan Goodyear on 26 Jun 12 - No Cached
  • Nathan Goodyear on 26 Jun 12
     
    SAMe increased hippocampal serotonin levels by 300% in rat brain model.  Methylation is known to play a major role in serotonin, dopamine, and norepinephrine.
Nathan Goodyear

JAMA Network | JAMA | Conjugated Equine Estrogens and Incidence of Probable D... - 0 views

jama.jamanetwork.com/article.aspx

premarin memory dementia HRT HT hormone therapy hormone hormones women brain WHI MPA medroxyprogesterone acetate

shared by Nathan Goodyear on 06 Aug 13 - No Cached
  • Nathan Goodyear on 06 Aug 13
     
    This was the WHI review of data as it pertains to dementia and cognitive decline in women.  The take home here is that the data provides little evidence for premarin with or without medroxyprogesterone acetate in > 65 for prevention of dementia.  However, this is in women > 65 and studies show that younger women do indeed receive benefit, especially in those with early ovary removal.  Another point here, MPA (medroxyprogesterone acetate) increases cognitive decline.  Just don't take MPA, it is a bad drug all the way around!
Nathan Goodyear

Increased risk of cognitive impairment or dementia in women who underwent oophorectomy ... - 0 views

www.neurology.org/...1074

dementia cognitive decline menopause Estrogen women HRT HT BHRT hormone hormones

shared by Nathan Goodyear on 06 Aug 13 - No Cached
  • Nathan Goodyear on 06 Aug 13
     
    Untold risk of early ovary removal appears to be cognitive decline and increased risk of dementia.  The earlier the age of removal, the more the increased risk of cognitive decline.  
Nathan Goodyear

JAMA Network | JAMA | Estrogen Plus Progestin and the Incidence of Dementia a... - 0 views

jama.jamanetwork.com/article.aspx

estrogen dementia memory WHI HRT HT BHRT hormone therapy hormone hormones women MPA medroxyprogesterone acetate

shared by Nathan Goodyear on 06 Aug 13 - No Cached
  • Nathan Goodyear on 06 Aug 13
     
    Estrogen with progestin worsens cognitive decline in women >65.  Little can be taken from this study other than, medroxyprogesterone acetate is a bad drug and should not be given to women for any purpose, especially in those >65.  One wonders if bioidentical, physiologic hormone replacement would have the same effect?  I doubt it.  The likely negative impact of hormones on the brain in women >65 is due to the negative effects of MPA, the change in inflammatory cytokines, and the change in receptors.
Nathan Goodyear

Study Finds Estrogen Therapy Improves Depression and Anxiety in Recently Menopausal Wom... - 0 views

www.prnewswire.com/...gnitive-effects-172536101.html

estrogen therapy HT BHRT HRT depression anxiety

shared by Nathan Goodyear on 29 Oct 13 - No Cached
  • Nathan Goodyear on 29 Oct 13
     
    Estrogen therapy in women recently postmenopausal, found to improve symptoms of depression and anxiety.  The mean age of women in this study was 52.7.  Average age of menopause is 51, so apprx 1 year postmenopausal in this study.  Both premarin and bioidentical estradiol was used in different arms of the study.  Bioidentical progesterone was used in all 3 arms.
Nathan Goodyear

Opioid-induced nausea and vomiting - Smith - Annals of Palliative Medicine - 0 views

apm.amegroups.com/...1264

nausea

shared by Nathan Goodyear on 14 Aug 18 - No Cached
  • Some of the “emetogenic” receptors that have been proposed are dopamine-2 (D2), histamine-1 (H1), DOR, 5-hydroxytryptamine (serotonin) (5-HT3), acetylcholine (ACh), neurokinin-1 (NK-1), and cannabinoid receptor-1 (CB1)
  • Olanzapine decreased morphine-induced nausea and vomiting in a dose-dependent manner.
  • Nathan Goodyear on 14 Aug 18
     
    Good review of meds for nausea.
Nathan Goodyear

The river blindness drug Ivermectin and related macrocyclic lactones inhibit WNT-TCF pa... - 0 views

www.ncbi.nlm.nih.gov/...PMC4287931

ivermectin cancer WTF Selamectin

shared by Nathan Goodyear on 19 Mar 18 - No Cached
  • WNT signaling
  • early colon cancers commonly display loss of function of the tumor suppressor Adenomatous polyposis coli (APC), a key component of the β-CATENIN destruction complex
  • Other cancers also show an active canonical WNT pathway; these include carcinomas of the lung, stomach, cervix, endometrium, and lung as well as melanomas and gliomas
  • ...31 more annotations...
  • In normal embryogenesis and homeostasis, the canonical WNT pathway is activated by secreted WNT ligands produced in highly controlled context-dependent manners and in precise amounts. WNT activity is transduced in the cytoplasm, inactivates the APC destruction complex, and results in the translocation of activate β-CATENIN to the nucleus, where it cooperates with DNA-binding TCF/LEF factors to regulate WNT-TCF targets and the ensuing genomic response
  • beyond the loss of activity of the APC destruction complex, for instance throughAPC mutation, phosphorylation of β-CATENIN at C-terminal sites is required for the full activation of WNT-TCF signaling and the ensuing WNT-TCF responses in cancer.
  • The WNT-TCF response blockade that we describe for low doses of Ivermectin suggests an action independent to the deregulation of chloride channels
  • involve the repression of the levels of C-terminally phosphorylated β-CATENIN forms and of CYCLIN D1, a critical target that is an oncogene and positive cell cycle regulator.
  • the Avermectin single-molecule derivative Selamectin, a drug widely used in veterinarian medicine (Nolan & Lok, 2012), is ten times more potent acting in the nanomolar range
  • Ivermectin also diminished the protein levels of CYCLIN D1, a direct TCF target and oncogene, in both HT29 and H358 tumor cells
  • Activated Caspase3 was used as a marker of apoptosis by immunohistochemistry 48 h after drug treatment. Selamectin and Ivermectin induced up to a sevenfold increase in the number of activated Caspase3+ cells in two primary (CC14 and CC36) and two cell line (DLD1 and Ls174T) colon cancer cell types (Fig​(Fig2C).2C). All changes were significative
  • The strong downregulation of the expression of the intestinal stem cell genesASCL2 andLGR5 (van der Flieret al, 2009; Scheperset al, 2012; Zhuet al, 2012b) by Ivermectin and Selamectin (Fig​(Fig2D)2D) raised the possibility that these drugs could affect WNT-TCF-dependent colon cancer stem cell behavior
  • Pre-established H358 tumors responded to Ivermectin showing a ˜ 50% repression of growth
  • Ivermectin hasin vivo efficacy against human colon cancer xenografts sensitive to TCF inhibition with no discernable side effects
  • Ivermectin (Campbellet al, 1983), an off-patent drug approved for human use, and related macrocyclic lactones, have WNT-TCF pathway response blocking and anti-cancer activities
  • these drugs block WNT-TCF pathway responses, likely acting at the level of β-CATENIN/TCF function, affecting β-CATENIN phosphorylation status.
  • anti-WNT-TCF activities of Ivermectin and Selamectin
  • Ivermectin has a well-known anti-parasitic activity mediated via the deregulation of chloride channels, leading to paralysis and death (Hibbs & Gouaux, 2011; Lynagh & Lynch, 2012). The same mode of action has been suggested to underlie the toxicity of Ivermectin for liquid tumor cells and the potentiation or sensitization effect of Avermectin B1 on classical chemotherapeutics
  • the specificity of the blockade of WNT-TCF responses we document, at low micromolar doses for Ivermectin and low nanomolar doses for Selamectin, indicate that the blockade of WNT-TCF responses and chloride channel deregulation are distinct modes of action
  • What is key then is to find a dose and a context where the use of Ivermectin has beneficial effects in patients, paralleling our results with xenografts in mice.
  • Cell toxicity appears at doses greater (> 10 μM for 12 h or longer or > 5 μM for 48 h or longer for Ivermectin) than those required to block TCF responses and induce apoptosis.
  • Our data point to a repression of WNT-β-CATENIN/TCF transcriptional responses by Ivermectin, Selamectin and related macrocylic lactones.
  • (i) The ability of Avermectin B1 to inhibit the activation of WNT-TCF reporter activity by N-terminal mutant (APC-insensitive) β-CATENIN as detected in our screen
  • (ii) The ability of Avermectin B1, Ivermectin, Doramectin, Moxidectin and Selamectin to parallel the modulation of WNT-TCF targets by dnTCF
  • (iii) The finding that the specific WNT-TCF response blockade by low doses of Ivermectin and Selamectin is reversed by constitutively active TCF
  • (iv) The repression of key C-terminal phospho-isoforms of β-CATENIN resulting in the repression of the TCF target and positive cell cycle regulator CYCLIN D1 by Ivermectin and Selamectin
  • (v) The specific inhibition ofin-vivo-TCF-dependent, but notin-vivo-TCF-independent cancer cells by Ivermectin in xenografts.
  • These results together with the reduction of the expression of the colon cancer stem cell markersASCL2 andLGR5 (e.g., Hirschet al, 2013; Ziskinet al, 2013) raise the possibility of an inhibitory effect of Ivermectin, Selamectin and related macrocyclic lactones on TCF-dependent cancer stem cells.
  • the capacity of cancer cells to form 3D spheroids in culture, as well as the growth of these, is also WNT-TCF-dependent (Kanwaret al, 2010) and they were also affected by Ivermectin treatment
  • If Ivermectin is specific, it should only block TCF-dependent tumor growth. Indeed, the sensitivity and insensitivity of DLD1 and CC14 xenografts to Ivermectin treatment, respectively, together with the desensitization to Ivermectin actionin vivo by constitutively active TCF provide evidence of the specificity of this drug to block an activated WNT-TCF pathway in human cancer.
  • Ivermectin has a good safety profile since onlyin-vivo-dnTCF-sensitive cancer xenografts are responsive to Ivermectin treatment, and we have not detected side effects in Ivermectin-treated mice at the doses used
  • previous work has shown that side effects from systemic treatments with clinically relevant doses in humans are rare (Yang, 2012), that birth defects were not observed after exposure of pregnant mothers (Pacquéet al, 1990) and that this drug does not cross the blood–brain barrier (Kokozet al, 1999). Similarly, only dogs with mutantABCB1 (MDR1) alleles leading to a broken blood–brain barrier show Ivermectin neurotoxicity (Mealeyet al, 2001; Orzechowskiet al, 2012)
  • Indications may include treatment for incurable β-CATENIN/TCF-dependent advanced and metastatic human tumors of the lung, colon, endometrium, and other organs.
  • Ivermectin, Selamectin, or related macrocyclic lactones could also serve as topical agents for WNT-TCF-dependent skin lesions and tumors such as basal cell carcinomas
  • they might also be useful as routine prophylactic agents, for instance against nascent TCF-dependent intestinal tumors in patients with familial polyposis and against nascent sporadic colon tumors in the general aging population
  • Nathan Goodyear on 19 Mar 18
     
    Ivermectin, a common anti-parasitic, found to inhibit WTF-TCF pathway and decrease c-terminal phosophorylaiton of Beta-CATENIN all resulting in increased aptosis and inhibition of cancer growth in colon cancer cell lines and lung cancer cell lines.
Nathan Goodyear

Cannabidiol inhibits paclitaxel-induced neuropathic pain through 5-HT1A receptors witho... - 0 views

www.ncbi.nlm.nih.gov/...PMC3969077

CBD hemp oil cannabinoids chemotherapy cancer pain neuropathy Paclitaxel

shared by Nathan Goodyear on 11 Aug 17 - No Cached
  • Nathan Goodyear on 11 Aug 17
     
    Animal study finds that CBD reduces chemotherapy induced neuropathy and pain.
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