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hohanbogdan

Obosit mereu - 0 views

De ce sunt obosit mereu? https://obosit-mereu.weebly.com/shop.html

Sanatate

started by hohanbogdan on 19 Jan 18 no follow-up yet
Nathan Goodyear

Transgenerational Epigenetic Inheritance: myths and mechanisms - 0 views

www.ncbi.nlm.nih.gov/...PMC4020004

epigenetics transgenerational inheritance

shared by Nathan Goodyear on 09 Oct 17 - No Cached
  • Nathan Goodyear on 09 Oct 17
     
    epigenetics can be inheritable transgenerationally via maternal and paternal epigenetic alterations.
fnfdoc

Stroke Genetics And Risk Factors | Your Health Our Priority - 0 views

www.fnfdoc.com/...stroke-genetics-risk-factors

Genetics Ischemic Stroke

shared by fnfdoc on 03 May 18 - No Cached
  • fnfdoc on 03 May 18
     
    Stroke is a cerebrovascular syndrome that involves the blockage and bursting of blood vessels in the brain. It shows a multifactorial pattern of inheritance. High cholesterol levels, high blood pressure, hypertension and obesity are the key causes of stroke besides inherited genes.
Nathan Goodyear

A critical view on transgenerational epigenetic inheritance in humans | Nature Communic... - 0 views

www.nature.com/...s41467-018-05445-5

intergenerational inheritance epigenetics fetal programming

shared by Nathan Goodyear on 29 Jul 23 - No Cached
  • Nathan Goodyear on 29 Jul 23
     
    Is there something here missed on the authors. If one had ill intentions, could one not recommend a pregnant mother as the ideal candidate to program, or reprogram the offspring. Changes induced to F2 are called inter generational inheritance.
Nathan Goodyear

Inter- and transgenerational epigenetic inheritance: evidence in asthma and COPD? | Cli... - 0 views

clinicalepigeneticsjournal.biomedcentral.com/...s13148-015-0085-1

epigenetic transgenerational inheritance intergenerational inheritance transgenerational inheritance epigenetics

shared by Nathan Goodyear on 29 Jul 23 - No Cached
  • Nathan Goodyear on 29 Jul 23
     
    "The effects of developmental programming can be induced by the intrauterine environment (cigarette smoke, nutrition, and stress) which not only affect the fetus (F1) but also the germ line of the fetus (F2), leading to so-called intergenerational epigenetic effects. When developmental programming is transmitted across generations beyond F3, it is considered to be transgenerational and can not be explained by direct environmental exposure anymore."
Nathan Goodyear

Chemotherapy-Induced Late Transgenerational Effects in Mice | PLOS ONE - 0 views

journals.plos.org/...article

transgenerational inheritance chemotherapy doxorubicin

shared by Nathan Goodyear on 19 Dec 22 - No Cached
  • Nathan Goodyear on 19 Dec 22
     
    Animal model finds doxorubicin chemotherapy induces epigenetic transgenerational inheritence
Nathan Goodyear

http://ac.els-cdn.com/S0303720713002426/1-s2.0-S0303720713002426-main.pdf?_tid=360bb0b2... - 0 views

ac.els-cdn.com/...2.0-S0303720713002426-main.pdf

endocrine disorders mitochondria disease biochemistry diabetes aging hypoparathyroidism hypothyroidism hypogonadism hormones

shared by Nathan Goodyear on 30 Apr 14 - No Cached
  • Nathan Goodyear on 30 Apr 14
     
    Very well done article that discusses the relationship between mitochondria and endocrine disorders.  Mitochondrial disorders cannot just include inherited mitochondriopathies, but acquired mitochondriopathies as well.
Nathan Goodyear

Transgenerational Epigenetic Inheritance | Annual Review of Genetics - 0 views

www.annualreviews.org/...annurev-genet-120417-031404

epigenetics Transgenerational inheritance

shared by Nathan Goodyear on 16 Jun 20 - No Cached
  • Nathan Goodyear on 16 Jun 20
     
    Great read
Nathan Goodyear

Chemotherapy-Induced Late Transgenerational Effects in Mice - PMC - 0 views

www.ncbi.nlm.nih.gov/...PMC3060098

transgenerational inheritance chemotherapy transgenerational inheritance of pathology pathology cancer

shared by Nathan Goodyear on 17 Jul 23 - No Cached
  • Nathan Goodyear on 17 Jul 23
     
    Peaks in 4-6th generation
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.
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