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Nathan Goodyear

Acute Effects of Triiodothyronine (T3) Replacement Therapy in Patients with Chronic Hea... - 0 views

jcem.endojournals.org/...1351

T3 hypothyroid hypothyroidism cardiac disease

shared by Nathan Goodyear on 01 Feb 11 - No Cached
  • In DC patients, short-term synthetic L-T3 replacement therapy significantly improved neuroendocrine profile and ventricular performance
  • Nathan Goodyear on 01 Feb 11
     
    T3 provides significant improvement in cardiac function in those with dilated cardiomyopathy
Nathan Goodyear

Acute Effects of Triiodothyronine (T3) Replacement Therapy in Patients with Chronic Hea... - 0 views

jcem.endojournals.org/...1351.long

T3 fT3 thyroid disease low T3 syndrome T3 syndrome cardiomyopathy CHF congestive heart failure

shared by Nathan Goodyear on 03 Jul 12 - No Cached
  • Nathan Goodyear on 03 Jul 12
     
    IV T3 was given to patients with chronic heart failure.  What the study found may surprise you: improved heart function (ventricular), improved BNP, decrease heart rate, no side effects.  T3 has been shown to be more predictive of cardiac death in those with cardiac disease, than elevated lipids or decreased ejection fraction.
Nathan Goodyear

The development of mitochondrial medicine - 0 views

www.pnas.org/...8731.short

mitochondrial mitochondria disease Parkinson Alzheimer Huntington ALS

shared by Nathan Goodyear on 03 Mar 11 - No Cached
  • n addition to being a primary cause of disease, mitochondrial DNA mutations and impaired oxidation have now been found to occur as secondary phenomena in aging as well as in age-related degenerative diseases such as Parkinson, Alzheimer, and Huntington diseases, amyotrophic lateral sclerosis and cardiomyopathies, atherosclerosis, and diabetes mellitus.
  • Nathan Goodyear on 03 Mar 11
     
    good discussion on primary and secondary mitochondrial diseases.  Aging and age-related disease are the result of secondary mitochondrial dysfunction
Nathan Goodyear

Thyroid Replacement Therapy and Heart Failure - 0 views

circ.ahajournals.org/...385.full

thyroid T3 hormone hormones cardiovascular disease heart health failure CHF MI myocardial infarction heart attack heart disease

shared by Nathan Goodyear on 24 Sep 14 - No Cached
  • A good biomarker of intracardiac TH signaling would be helpful but has not been identified. In the absence of such a marker, a rational, cautious therapeutic approach might be to restore and maintain over time biochemical euthyroidism as documented by normal circulating levels of TSH, FT4, and FT3.
  • a low-T3 state resulting from altered peripheral TH metabolism secondary to caloric restriction is associated with impaired cardiac contractility
  • Low-T3 syndrome is the central finding and defines the illness in a variety of acute and chronic severe nonthyroidal illnesses with cardiac origin, including MI, HF, and surgically treated cardiac disease.1 Low circulating levels of T3 in the absence of primary thyroid hypofunction have been found in 20% to 30% of patients with dilated cardiomyopathy.
  • ...1 more annotation...
  • FT3 levels were inversely correlated to coronary artery disease
  • Nathan Goodyear on 24 Sep 14
     
    Great review of the current understanding of thyroid hormone metabolism in cardiac tissue.  Low T3 and increased rT3 (via increased D3 activity) is CLEARLY associated with poor cardiac performance and post MI and CHF is associated with poor outcomes.  T3 is critical in cardiac remodeling and recovery post MI.  T3 is actually a vasodilatory in the coronary arteries.   Why a endocrinologist would call rT3 useless only points to their ignorance of the literature.
Nathan Goodyear

Repurposing Drugs in Oncology (ReDO)-chloroquine and hydroxychloroquine as anti-cancer ... - 0 views

www.ncbi.nlm.nih.gov/...PMC5718030

chloroquine hydroxychloroquine cancer repurposed drugs

shared by Nathan Goodyear on 03 May 21 - No Cached
  • HCQ, doses for long-term use range between 200 and 400 mg per day.
  • Short-term administration of CQ or HCQ rarely causes severe side effects
  • Short-term administration of CQ or HCQ rarely causes severe side effects
  • ...24 more annotations...
  • bone marrow suppression
  • cardiomyopathy
  • irreversible retinal toxicity
  • hypoglycaemia
  • daily doses up to 400 mg of HCQ or 250 mg CQ for several years are considered to carry an acceptable risk for CQ-induced retinopathies, with the exception of individuals of short stature
  • chronic CQ or HCQ therapy be monitored through regular ophthalmic examinations (3–6 month intervals), full blood counts and blood glucose level checks
  • long-term HCQ exposure, skeletal muscle function and tendon reflexes should be monitored for weakness
  • both CQ and HCQ, specific caution is advised in patients suffering from impaired hepatic function (especially when associated with cirrhosis), porphyria, renal disease, epilepsy, psoriasis, glucose-6-phosphate dehydrogenase deficiency and known hypersensitivity to 4-aminoquinoline compounds
  • CQ and HCQ can effectively increase the efficacy of various anti-cancer drugs
  • CQ can prevent the entrapment of protonated chemotherapeutic drugs by buffering the extracellular tumour environment and intracellular acidic spaces
  • This study recommends an adjuvant HCQ dose of 600 mg, twice daily.
  • HCQ addition was shown to produce metabolic stress in the tumours
  • HCQ (400 mg/day)
  • important effects of CQ and HCQ on the tumour microenvironment
  • The main and most studied anti-cancer effect of CQ and HCQ is the inhibition of autophagy
  • the expression levels of TLR9 are higher in hepatocellular carcinoma, oesophageal, lung, breast, gastric and prostate cancer cells as compared with adjacent noncancerous cells, and high expression is often linked with poor prognosis
  • TLR9-mediated activation of the NF-κB signalling pathway and the associated enhanced expression of matrix metalloproteinase-2 (MMP-2), MMP-7 and cyclo-oxygenase 2 mRNA
  • HCQ can activate caspase-3 and modulate the Bcl-2/Bax ratio inducing apoptosis in CLL, B-cell CLL and glioblastoma cells
  • In triple-negative breast cancer, CQ was shown to eliminate cancer stem cells through reduction of the expression of Janus-activated kinase 2 and DNA methyl transferase 1 [106] or through induction of mitochondrial dysfunction, subsequently causing oxidative DNA damage and impaired repair of double-stranded DNA breaks
  • CQ or HCQ would be considered for use in combination with immunomodulation anti-cancer therapies
  • Therapies used in combination with CQ or HCQ include chemotherapeutic drugs, tyrosine kinase inhibitors, various monoclonal antibodies, hormone therapies and radiotherapy
  • Most studies hypothesise that CQ and HCQ could increase the efficacy of other anti-cancer drugs by blocking pro-survival autophagy.
  • daily doses between 400 and 1200 mg for HCQ are safe and well tolerated, but two studies identified 600-mg HCQ daily as the MTD
  • HCQ is often administered twice daily to limit plasma fluctuations and toxicity
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