PSA levels in media were increased by 3α-diol
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Errors in Health Care: A Leading Cause of Death and Injury - To Err is Human - NCBI Boo... - 0 views
Voluntary Electronic Reporting of Medical Errors and Adverse Events - 0 views
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shared by Nathan Goodyear on 02 Jun 13
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The effect of combined estrogen and progester... [Ann Intern Med. 2005] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...15968009
HRT lupus SLE hormone hormones women estrogen progesterone medroxyprogesterone acetate
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shared by Nathan Goodyear on 27 Jan 14
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Androgen deprivation promotes intratumoral synthesis of dihydrotestosterone from androg... - 0 views
www.nature.com/...srep01528.html
prostate cancer 3-alpha androstanediol 3-beta androstanediol DHT metabolite metabolites
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Similarly to 3α-diol, 3β-diol also increased PSA levels in media in a concentration-dependent manner
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intracellular DHT is synthesized from inactive androgen 3α- and 3β-diol via different pathways in prostate cancer cells
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serum 3α-diol G levels reflect the androgen milieu in localized prostate cancer patients receiving ADT
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A few studies reported that 3β-diol is a potential ligand of estrogen receptor β (ERβ) and has an antiproliferative effect
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Prostate cancer cells promoted synthesis from the DHT metabolite 3α-diol during the long duration of ADT
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verified the synthesis of DHT from 3α- or 3β-diol via different pathways in prostate cancer cells in this study
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HSD17B6 expression levels in prostate cancer can be useful for the diagnosis of high-risk prostate cancer
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DHT metabolites play an important role of intra-prostate DHT synthesis in those following ADT. This is a proposed mechanism for the failure rate and aggressive nature of prostate cancer that fails ADT. 3-alpha androstanediol is converted via 3 alpha HSD back to DHT. In contrast, 3-beta androstanediol cannot.
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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
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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
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shared by Nathan Goodyear on 14 Oct 13
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Estrogen Metabolism and Risk of Breast Cancer in Postmenopausal Women - 0 views
www.ncbi.nlm.nih.gov/...PMC3283536
estrogen metabolism estrogen metabolism breast cancer breast cancer
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The ratio of the 2-hydroxylation pathway to parent estrogens was associated with a statistically significantly decreased risk of breast cancer
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In this study, this ratio was more strongly associated with the risk of breast cancer compared with the ratio of 2-hydroxylation pathway to 16-hydroxylation pathway or unconjugated estradiol alone
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2-hydroxylation pathway catechols have relatively low affinities for estrogen receptors (4) and are rapidly cleared from circulation
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In this study, the ratio of the 2-hydroxylation pathway to the 16-hydroxylation pathway was associated with a non-statistically significantly decreased risk of breast cancer
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In this study, the ratio of catechols to methylated catechols in the 4-hydroxylation pathway was associated with statistically significantly increased risk of breast cancer.
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This result is consistent with the hypothesis that mutagenic quinones derived from 4-hydroxylation pathway catechols contribute to pathogenesis of postmenopausal breast cancer.
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Catechols in both the 2- and 4-hydroxylation pathways can be oxidized to form quinones; these reactive electrophiles can then react with DNA to form a variety of adducts
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the most common DNA adducts derived from 4-hydroxylation pathway catechols are depurinating and highly mutagenic (7,40), most of those derived from 2-hydroxylation pathway catechols are stable and can be repaired with little error
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shared by Nathan Goodyear on 24 Sep 18
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Inborn-like errors of metabolism are determinants of breast cancer risk, clinical respo... - 0 views
www.ncbi.nlm.nih.gov/...PMC6114970
cancer metabolism breast cancer glutamine glutamate aspartate oncogenes
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We now recognize that human cancers evolve in an environment of metabolic stress. Rapidly proliferating tumor cells deprived of adequate oxygen, nutrients, hormones and growth factors up-regulate pathways that address these deficiencies to overcome hypoxia (HIF), vascular insufficiency (VEGF), growth factor deprivation (EGFR, HER2) and the loss of hormonal support (ER, PR, AR) all to enhance survival and proliferation
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The results suggest that breast cancer could be preceded by systemic subclinical disturbances in glucose-insulin homeostasis characterized by mild, likely asymptomatic, IEM-like biochemical changes
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The process would include variable periods of hyperinsulinemia with the consequent systemic MYC activation of glycolysis, glutaminolysis, structural lipidogenesis and further exacerbation of hypoglycemia, the result of MYC's known role as an inhibitor of liver gluconeogenesis
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The metabolic changes we describe in breast cancer arise in concert with IEM-like changes in oxidative phosphorylation as detected by increased values of the ratio lactate/pyruvate (Supplementary Table 2A, 2B) characteristic of Ox/Phos deficiency [25]. In our study, 76% (70/92) of the European breast cancer patients had lactate/pyruvate ratios values higher than the normal value of 25.8
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four-fold higher frequency of cancer (including breast) in patients with energy metabolism disorders
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growing recognition that cancer cells differ from their normal counterparts in their use of nutrients, synthesis of biomolecules and generation of energy
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glutamine concentrations in the cancer patients were reduced to nearly 1/8 of the levels observed in the normal population
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blood concentrations of aspartate (p = 1.7e-67, FDR = 8.3e-67) (Figure (Figure1E)1E) and glutamate (p = 6.4e-96, FDR = 6.2e-95) (Figure (Figure1F)1F) were nearly 10 fold higher than the normal ranges of 0–5 μM/L and 40 μM/L, respectively
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glutamine consumption associated with parallel increases in glutamate and aspartate (Figure (Figure1A1A red arrows) is considered a hallmark of MYC-driven “glutaminolysis”
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Gln/Glu ratio inversely correlates with i- late stage metabolic syndrome and with ii- increased chance of death
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changes in glutamine consumption, reflected by the Gln/Glu ratio could provide a metabolic link between breast cancer initiation and diabetes, reflective of a systemic metabolic reprogramming from glucose to glutamine as the preferred source of precursors for biosynthetic reactions and cellular energy
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the metabolic dependencies of cancer characterized by excessive glycolysis, glutaminolysis and malignant lipidogenesis, previously considered a consequence of local tumor DNA aberration [23] could, instead, represent a systemic biochemical aberration that predates and very likely promotes tumorigenesis
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accumulation of very long chain acylcarnitines such as C14:1-OH (p = 0.0, FDR = 0.0), C16 (p = 0.0, FDR = 0.0), C18 (p = 0.0, FDR = 0.0) and C18:1 (p = 1.73e-322, FDR = 1.16-321) and lipids containing VLCFA (lysoPC a C28:0) (p = 1.14-e95, FDR = 1.65e-95) in the blood of breast and colon cancer patients
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Among the most powerful metabolic equations for MYC-activation is that which links the widely used MYC-driven desaturation marker ratio of SFA/MUFA to the MYC glutaminolysis-associated ratio of (Asp/Gln)
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liver dysfunction shares many features with both IEM and cancer suggesting a role for hepatic dysfunction in carcinogenesis
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cancer “conscripts” the human genome to meet its needs under conditions of systemic metabolic stress
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Substantial contribution of extrinsic risk factors to cancer development - 0 views
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Here we provide evidence that intrinsic risk factors contribute only modestly (<10~30%) to cancer development
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we conclude that cancer risk is heavily influenced by extrinsic factors. These results carry immense consequences for strategizing cancer prevention
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cancers are proposed to originate from the malignant transformation of normal tissue progenitor and stem cells
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“Intrinsic processes” include those that result in mutations due to random errors in DNA replication whereas “extrinsic factors” are environmental factors that affect mutagenesis rates (such as UV radiation, ionizing radiation, and carcinogens
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intrinsic cancer risk should be determined by the cancer incidence for those cancers with the least risk in the entire group controlling for total stem cell divisions
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if one or more cancers would feature a much higher cancer incidence, for example, lung cancer among smokers vs. non-smokers, then this most likely reflects additional (and probably extrinsic) risk factors (smoking in this case)
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Particularly, for breast and prostate cancers, it has long been observed that large international geographical variations exist in their incidences (5-fold for breast cancer, 25-fold for prostate cancer)14, and immigrants moving from countries with lower cancer incidence to countries with higher cancer rates soon acquire the higher risk of their new country
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Colorectal cancer is another high-incidence cancer that is widely considered to be an environmental disease17, with an estimated 75% or more colorectal cancer risk attributable to diet
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HPV may cause ~90% cases in cervical cancer23, ~90% cases in anal cancer24, and ~70% in oropharyngeal cancer
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While a few cancers have relatively large proportions of intrinsic mutations (>50%), the majority of cancers have large proportions of extrinsic mutations, for example, ~100% for Myeloma, Lung and Thyroid cancers and ~80–90% for Bladder, Colorectal and Uterine cancers, indicating substantial contributions of carcinogen exposures in the development of most cancers
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onsistent estimate of contribution of extrinsic factors of >70–90% in most common cancer types. This concordance lends significant credibility to the overall conclusion on the role of extrinsic factors in cancer development
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