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Nathan Goodyear

Lead exposure, polymorphisms in genes related to oxidative stress and risk of adult bra... - 0 views

www.ncbi.nlm.nih.gov/...PMC2750838

meningioma CNS tumor tumors glioblastoma brain oxidative damage oxidative stress

shared by Nathan Goodyear on 04 Mar 13 - No Cached
  • Nathan Goodyear on 04 Mar 13
     
    another study that showed that lead exposure in susceptible individuals increased risk of CNS tumors, including menngiomas, and gliomas.  The apparent mechanism in this study was proposed through oxidative damage.  
Nathan Goodyear

EDTA chelation therapy, without added vitamin C, decreases oxidative DNA damage and lip... - 0 views

www.altmedrev.com/...56.pdf

EDTA EDTA chelation vitamin C IV vitamin C CVD cardiovascular disease Diabetes

shared by Nathan Goodyear on 05 Jun 13 - No Cached
  • Nathan Goodyear on 05 Jun 13
     
    This study found that the elimination of hight dose vitamin C in EDTA chelation removed the pro oxidant effect. This provided an antioxidant effect only from EDTA chelation, which is beneficial in the oxidative damage diseases like CVD and Diabetes
Nathan Goodyear

Metabolic management of brain cancer - 0 views

www.sciencedirect.com/...S0005272810006857

brain cancer

shared by Nathan Goodyear on 17 Jun 13 - No Cached
  • Glutamine is a major metabolic fuel for both brain tumor cells and tumor-associated macrophages (TAMs)
  • the malignant phenotype of brain tumor cells that survive radiotherapy is often greater than that of the cells from the original tumor.
  • Conventional chemotherapy has faired little better than radiation therapy for the long-term management of malignant brain cancer
  • ...37 more annotations...
  • most conventional radiation and brain cancer chemotherapies can enhance glioma energy metabolism and invasive properties, which would contribute to tumor recurrence and reduced patient survival [34].
  • We contend that all cancer regardless of tissue or cellular origin is a disease of abnormal energy metabolism
  • complex disease phenotypes can be managed through self-organizing networks that display system wide dynamics involving oxidative and non-oxidative (substrate level) phosphorylation
  • As long as brain tumors are provided a physiological environment conducive for their energy needs they will survive; when this environment is restricted or abruptly changed they will either grow slower, growth arrest, or perish [8] and [19]
  • New information also suggests that ketones are toxic to some human tumor cells and that ketones and ketogenic diets might restrict availability of glutamine to tumor cells [68], [69] and [70].
  • The success in dealing with environmental stress and disease is therefore dependent on the integrated action of all cells in the organism
  • Tumor cells survive in hypoxic environments not because they have inherited genes making them more fit or adaptable than normal cells, but because they have damaged mitochondria and have thus acquired the ability to derive energy largely through substrate level phosphorylation
  • Cancer cells survive and multiply only in physiological environments that provide fuels (mostly glucose and glutamine) subserving their requirement for substrate level phosphorylation
  • Integrity of the inner mitochondrial membrane is necessary for ketone body metabolism since β-hydroxybutyrate dehydrogenase, which catalyzes the first step in the metabolism of β-OHB to acetoacetate, interacts with cardiolipin and other phospholipids in the inner membrane
  • the mitochondria of many gliomas and most tumors for that matter are dysfunctional
  • Cardiolipin is essential for efficient oxidative energy production and mitochondrial function
  • Any genetic or environmental alteration in the content or composition of cardiolipin will compromise energy production through oxidative phosphorylation
  • The Crabtree effect involves the inhibition of respiration by high levels of glucose
  • the Warburg effect involves elevated glycolysis from impaired oxidative phosphorylation
  • the Crabtree effect can be reversible, the Warburg effect is largely irreversible because its origin is with permanently damaged mitochondria
  • The continued production of lactic acid in the presence of oxygen is the metabolic hallmark of most cancers and is referred to as aerobic glycolysis or the Warburg effect
  • We recently described how the retrograde signaling system could induce changes in oncogenes and tumor suppressor genes to facilitate tumor cell survival following mitochondrial damage [48].
  • In addition to glycolysis, glutamine can also increase ATP production under hypoxic conditions through substrate level phosphorylation in the TCA cycle after its metabolism to α-ketoglutarate
  • mitochondrial lipid abnormalities, which alter electron transport activities, can account in large part for the Warburg effect
  • targeting both glucose and glutamine metabolism could be effective for managing most cancers including brain cancer
  • The bulk of experimental evidence indicates that mitochondria are dysfunctional in tumors and incapable of generating sufficient ATP through oxidative phosphorylation
  • Cardiolipin defects in tumor cells are also associated with reduced activities of several enzymes of the mitochondrial electron transport chain making it unlikely that tumor cells with cardiolipin abnormalities can generate adequate energy through oxidative phosphorylation
  • The Crabtree effect involves the inhibition of respiration by high levels of glucose
  • Warburg effect involves elevated glycolysis from impaired oxidative phosphorylation
  • TCA cycle substrate level phosphorylation could therefore become another source of ATP production in tumor cells with impairments in oxidative phosphorylation
  • Caloric restriction, which lowers glucose and elevates ketone bodies [63] and [64], improves mitochondrial respiratory function and glutathione redox state in normal cells
  • DR naturally inhibits glycolysis and tumor growth by lowering circulating glucose levels, while at the same time, enhancing the health and vitality of normal cells and tissues through ketone body metabolism
  • DR is anti-angiogenic
  • DR also reduces angiogenesis in prostate and breast cancer
  • We suggest that apoptosis resistance arises largely from enhanced substrate level phosphorylation of tumor cells and to the genes associated with elevated glycolysis and glutaminolysis, e.g., c-Myc, Hif-1a, etc, which inhibit apoptosis
  • Modern medicine has not looked favorably on diet therapies for managing complex diseases especially when well-established procedures for acceptable clinical practice are available, regardless of how ineffective these procedures might be in managing the disease
  • More than 60 years of clinical research indicates that such approaches are largely ineffective in extending survival or improving quality of life
  • The process is rooted in the well-established scientific principle that tumor cells are largely dependent on substrate level phosphorylation for their survival and growth
  • Glucose and glutamine drive substrate level phosphorylation
  • targeting the glycolytically active tumor cells that produce pro-cachexia molecules, restricted diet therapies can potentially reduce tumor cachexia
  • It is important to recognize, however, that “more is not better” with respect to the ketogenic diet
  • Blood glucose ranges between 3.0 and 3.5 mM (55–65 mg/dl) and β-OHB ranges between 4 and 7 mM should be effective for tumor management
  • Nathan Goodyear on 17 Jun 13
     
    Dr Seyfriend presents his metabolic approach to the treatment of brain cancer.
Nathan Goodyear

Uptake, recycling, and antioxidant actio... [Free Radic Biol Med. 2002] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...12086686

alpha lipoic acid oxidative damage oxidative stress antioxidant

shared by Nathan Goodyear on 20 Feb 13 - No Cached
  • Nathan Goodyear on 20 Feb 13
     
    Alpha lipoic acid is shown to protect the vascular endothelium against oxidative damage.
Nathan Goodyear

Oxidative stress and neurodegeneration: where are we now? - Halliwell - 2006 - Journal ... - 0 views

onlinelibrary.wiley.com/...full

oxidative damage oxidative stress detoxification CNS neurodegeneration neurodegenerative disease Free radicals Alzheimer's Parkinson's disease ALS MS

shared by Nathan Goodyear on 29 Oct 12 - No Cached
  • Nathan Goodyear on 29 Oct 12
     
    Fantastic review of oxidative damage and the CNS.  This is a 2006 review of our understanding of how neurodegeneration occurs through oxidative stress and of course poor detoxification.
Nathan Goodyear

Statin-associated muscle-related adverse eff... [Pharmacotherapy. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20500044

statin statins muscle damage CoQ10

shared by Nathan Goodyear on 16 Mar 12 - No Cached
  • Nathan Goodyear on 16 Mar 12
     
    study showing statin associated muscle damage and the associated symptoms
Nathan Goodyear

World J Gastroenterol - 0 views

www.wjgnet.com/...5996.asp

glycine liver injury cirrhosis damage

shared by Nathan Goodyear on 10 Feb 14 - No Cached
  • Nathan Goodyear on 10 Feb 14
     
    Animal model finds glycine reduces liver damage.
Nathan Goodyear

Curcumin prevents DNA damage and enhances ... [Eur J Cancer Prev. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21332098

curcumin tumeric Arsenic cancer

shared by Nathan Goodyear on 17 Sep 13 - No Cached
  • Nathan Goodyear on 17 Sep 13
     
    Interesting study.  Curcumin shown to prevent oxidative damage as a result of Arsenic exposure.  Good therapy choice for those living in areas with high Arsenic exposure.
Nathan Goodyear

Susceptibility of mitochondrial superoxide dismut... [Toxicology. 2009] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...19010380

SOD superoxide disumutase aluminum AL oxidative damage

shared by Nathan Goodyear on 09 Oct 13 - No Cached
  • Nathan Goodyear on 09 Oct 13
     
    Aluminum induces oxidative damage through a reduction in SOD.
Nathan Goodyear

Aluminium neurotoxicity: neurobehavioural and o... [Arch Toxicol. 2009] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...19568732

aluminum Neurodegeneration oxidative damage vaccine vaccinations

shared by Nathan Goodyear on 09 Oct 13 - No Cached
  • Nathan Goodyear on 09 Oct 13
     
    Neurobehavioral changes due to oxidative damage from aluminum toxicity.
Nathan Goodyear

Induction by estrogen metabolite 16 alpha-hydroxyestrone of genotoxic damage and aberra... - 0 views

www.ncbi.nlm.nih.gov/...1556774

estrogen estrogen metabolites 16-alpha-OH-estrone

shared by Nathan Goodyear on 25 Sep 15 - No Cached
  • Nathan Goodyear on 25 Sep 15
     
    16-alpha-hydroxyestrone induces dna damage.
Nathan Goodyear

Dietary Strategy to Repair Plasma Membrane After Brain Trauma - 0 views

nnr.sagepub.com/...75.long

curcumin DHA TBI traumatic brain injury brain injury neuroinflammation BDNF brain derived neurotrophic factor brain

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • concussive brain injury is a major cause of neuropsychological disability in spite of no obvious neuronal death
  • TBI elicits oxidative damage to plasma membrane phospholipids
  • DHA is the most abundant polyunsaturated fatty acid (PUFA) in the brain, where the DHA-containing phospholipids contribute to plasma membrane biogenesis and receptor signaling
  • ...10 more annotations...
  • curcumin has potent anti-inflammatory and antioxidant activities that can function to reduce oxidative damage and cognitive deficits associated with neurological disorders
  • Curcumin provided in the diet before TBI can reduce oxidative damage and counteract TBI-related cognitive dysfunction
  • Our previous study indicated that n-3 fatty acids supplemented in the diet counteracted learning disability after TBI
  • curcumin contributes to enhance the effects of DHA on TBI by promoting phosphorylation of the BDNF receptor TrkB in the hippocampus
  • previous evidence indicates that curcumin10 and DHA5 counteract TBI-related learning disability by involving BDNF
  • Our findings indicate that curcumin counteracted the TBI-related reduction in n-3 DPA.
  • curcumin may promote the conversion of n-3 DPA to DHA
  • the combination of both nutrients has been reported to produce anti-inflammatory action
  • the enhanced actions of curcumin and DHA in reducing cholesterol levels could be interpreted as preservation of levels of phospholipids in the plasma membrane
  • curcumin and DHA may contribute to reduce inflammation associated with the action of cholesterol in the pathology of TBI.
  • Nathan Goodyear on 31 Aug 15
     
    Curcumin and DHA shown to protect against TBI through a reduction in inflammation and maintenance of brain phospholipid membranes.  BDNF is increases also.
wheelchairindia9

Wheelchair Pediatric - 0 views

www.wheelchairindia.com/...CP-PEDIATRIC-WHEELCHAIR

Electric Wheelchair For Increased Independence foot rests and four wheels large wheels at the back strengths and environment propelled by a motor comfortable and functional stretching abdominal muscle

shared by wheelchairindia9 on 14 May 15 - No Cached
  • wheelchairindia9 on 14 May 15
     
    When it comes to wheelchairs, young children have a different set of needs than adults. Aesthetically, devices designed for kids are often sleek and colorful, and functionally, they are typically lightweight and adjustable. As any parent knows, young people don't stay the same size for long and since a wheelchair is a major purchase don't want a simple growth spurt to render it useless. That's why kids wheelchair category offers models that feature seat width and depth adjustability, elevating legrests, and other versatile features. Pediatric walkers differ from adult walkers in several ways. For one, walking aids for children are usually adjustable, taking growth patterns into account; but many models also provide gait training and postural correction. Those caring for kids in their formative years must be concerned about more than just the young person's mobility, they must also consider their development. Cerebral Palsy Wheelchair: Cerebral Palsy Wheelchair Description: The model designed for cerebral palsy child only. Ultra light weight aluminium alloy frame Seat Width 38 cms (15") Net Weight: 18.5 kgs Epoxy powder coated frame Detachable arm rest & foot rest provided Elevated and swinging foot rest Elevated foot rest provided to elevate leg angle Height adjustable and detachable head rest Hydraulic reclining high back for a comfortable posture Hydraulic adjustable seat angle Detachable back and seat pad Extra cushion upholstery provided to under arm, head & calg Foldable Lever and paddle brakes provided Safety belt provided Maintenance free rear solid wheels Cloth look like water proof upholstery Anti wheels for better safety and stability Extra cushion upholstery provided to under arm, head & leg Folding action Lever and paddle brakes provided Safety belt provided Maintenance free rear solid wheels Cerebral Palsy Wheelchair Recline system: Recline system provides kids with the most comfortable resting environme
Nathan Goodyear

Urinary Estrogens and Estrogen Metabolites and Subsequent Risk of Breast Cancer among P... - 0 views

cancerres.aacrjournals.org/...696.full

estrogen metabolites estrogen metabolism ER estrogen receptors ROS hormones cancer breast cancer

shared by Nathan Goodyear on 07 Oct 15 - No Cached
  • both 2- and 4-catechol estrogen metabolites bind to the ER with affinities comparable with estradiol, 4-catechol estrogen metabolites have lower dissociation rates than estradiol and an enhanced ability to upregulate ER-dependent processes
  • 2-catechol estrogen metabolites act as either weak mitogens (39) or weak inhibitors of cell proliferation
  • While 16α-hydroxyestrone binds to the ER with lower affinity than estradiol, it binds covalently (41) and leads to a constitutively activated ER
  • ...15 more annotations...
  • 4-hydroxyestradiol and 16α-hydroxyestrone increasing proliferation and decreasing apoptosis in a manner similar to estradiol; however, these effects were achieved only at concentrations 10-fold higher than estradiol (39). In contrast, 2-hydroxyestradiol did not have substantial proliferative or antiapoptotic effects
  • In our study, the associations with both 2-hydroxyestrone and 16α-hydroxyestrone were nonsignificantly inverse and we did not observe a consistent trend or significant associations between the 2-hydroxyestrone:16α-hydroxyestrone ratio and breast cancer risk
  • Ratios of the 3 hydroxylation pathways were not significantly associated with risk although the 2:16-pathway and 4:16-pathway ratios were suggestively inversely associated
  • a significant inverse association with the ratio of parent estrogens to estrogen metabolites
  • several potentially estrogenic and genotoxic mechanisms
  • Estrogen metabolites also can be genotoxic
  • Catechol estrogens can be oxidized into quinones and induce DNA damage directly through the formation of DNA adducts, or indirectly via redox cycling and generation of reactive oxygen species
  • the oxidized forms of the catechol estrogens differ in their ability to damage DNA through adducts, with oxidized 2-catechols forming stable and reversible DNA adducts and oxidized 4-catechols forming unstable adducts, which lead to depurination and mutations
  • 2- and 4-catechols have been shown to produce reactive oxygen species and induce oxidative DNA damage
  • act independently from the ER
  • 16α-Hydroxyestrone also may be genotoxic
  • While the catechol estrogens have estrogenic and genotoxic potential, the methylated catechol estrogens, which are catechol estrogens with one hydroxyl group methylated, have been hypothesized to lower the risk of breast cancer
  • The suggested mechanisms are indirect, by decreasing circulating levels of catechol estrogens and thereby the opportunity for catechols to exert genotoxic or proliferative effects, or direct, by inhibiting tumor growth and inducing apoptosis
  • the balance between phase I (oxidation) and phase II (methylation) metabolism of estrogen may be important in hormonally related cancer development.
  • Despite the estrogenic and genotoxic potential of many of the estrogen metabolites, we only observed a significantly increased breast cancer risk with one estrogen metabolite, 17-epiestriol, which has particularly strong estrogenic activity and binds to both ERα and ERβ with an affinity comparable with estradiol
  • Nathan Goodyear on 07 Oct 15
     
    review of estrogen metabolites and breast cancer risk in premenopausal women.
Nathan Goodyear

Oxidative damage to mitochondria and aging. [Exp Gerontol. 2001] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...11404044

mitochondria damage aging oxidative

shared by Nathan Goodyear on 08 Feb 11 - No Cached
  • Oxidative damage to mitochondria and aging.
  • Nathan Goodyear on 08 Feb 11
     
    mitochondria and aging
Nathan Goodyear

YouTube - How Mercury Destroys the Brain - University of Calgary - 0 views

www.youtube.com/watch

mercury brain damage

shared by Nathan Goodyear on 25 Feb 11 - No Cached
  • Nathan Goodyear on 25 Feb 11
     
    Great video from University of Calgary on how Mercury causes brain damage
Nathan Goodyear

5-Hydroxytrytophan Inhibits tert-Butylhydroperoxide (t-BHP)-Induced Oxidative... - 0 views

pubs.acs.org/...jf904201h

5 hydroxytrytophan 5-HTP glutathione NF-kappaB

shared by Nathan Goodyear on 27 May 11 - No Cached
  • Nathan Goodyear on 27 May 11
     
    5-HTP, precursor to serotonin, shows anti-oxidant activity, reduces oxidative damage, suppressed pro-inflammatory p38MAPK and NF-kappaB, and helps to prevent glutathione depletion
Nathan Goodyear

Mary Ann Liebert, Inc. - Journal of Neurotrauma - 0(ja): - 0 views

www.liebertonline.com/...neu.2011.1922

sulphoraphane Nrf2 glutathione inflammation neuroinflammation oxidative damage cytokines

shared by Nathan Goodyear on 24 Aug 11 - No Cached
  • Nathan Goodyear on 24 Aug 11
     
    sulphoraphane activates Nrf2 pathway, which promotes Glutathione production, plays role in reducing oxidative damage and neuroinflammation
Nathan Goodyear

Marathons damage the hearts of less fit runners for up to three months - - Heart and St... - 0 views

www.heartandstroke.nb.ca/...content2.aspx

endurance training running runners marathon marathons heart health CVD exercise

shared by Nathan Goodyear on 09 Jan 15 - No Cached
  • Nathan Goodyear on 09 Jan 15
     
    Summary of 2010 report on marathons and the heart.  Less fit runners can do significant damage to the heart i.e. fibrosis compared to fit runners.  V02 max is a good way to assess aerobic endurance and differentiate between the two.  Dr Larose showed via MRI that it can take 3 months for the heart to recover.
Nathan Goodyear

Liver damage from long-term methyltestosterone. - PubMed - NCBI - 1 views

www.ncbi.nlm.nih.gov/69876

liver Testosterone male hormones

shared by Nathan Goodyear on 22 Aug 16 - No Cached
  • Nathan Goodyear on 22 Aug 16
     
    oral methyl Testosterone associated with liver dysfunction and damage. This does not appear to apply to topical or IM Testosterone.  This risk is unique to oral methyl Testosterone.
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