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Nathan Goodyear

Rebuilding the post-infarcted myocardium by a... [Heart Fail Rev. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...18773293

thyroid MI myocardial infarction heart attack hormone hormones post-MI heart cardiac remodeling

shared by Nathan Goodyear on 03 Jul 12 - No Cached
  • Nathan Goodyear on 03 Jul 12
     
    Wow, thyroid hormones play a significant role in cardiac remodeling post MI.  Thyroid hormones, "promotes tissue growth and differentiation and favorably remodels cardiac cell while increases cellular survival..."  How many people post-MI are having their thyroid evaluated, let alone correctly evaluated?
Nathan Goodyear

Exercise-induced right ventricular dysfunction and structural remodelling in endurance ... - 0 views

eurheartj.oxfordjournals.org/...998

endurance athletes training heart health injury

shared by Nathan Goodyear on 09 Jan 15 - No Cached
  • In a cohort of well-trained athletes, we demonstrated that intense endurance exercise causes an acute reduction in RV function that increases with race duration and correlates with increases in biomarkers of myocardial injury
  • no relationship between LV function and biomarker levels
  • focal gadolinium enhancement and increased RV remodelling were more prevalent in those athletes with a longer history of competitive sport, suggesting that repetitive ultra-endurance exercise may lead to more extensive RV change and possible myocardial fibrosis
  • ...22 more annotations...
  • he cardiac impact of both acute and cumulative exercise is greatest on the RV.
  • Greater reductions in RV function occurred in those athletes competing for a longer duration, suggesting that the heart has a finite capacity to maintain the increased work demands of exercise
  • We enrolled elite and subelite athletes and found a significant association between fitness (VO2max) and the reduction in post-race RVEF
  • Previous investigators have documented reductions in RV function in less trained subjects over the marathon distance
  • cardiac injury is greatest in the least trained
  • Even after many years of detraining, cardiac dilation may not completely regress in elite athletes
  • The focus on well-trained athletes may be of particular relevance, given that they perform exercise of highest intensity and duration most frequently, and, thus, may be at a greater risk of cumulative injury.
  • The lack of correlation between increases in troponin and changes in LV function seen in this study has been previously interpreted as evidence that post-exercise elevations in cardiac biomarkers are benign.
  • a significant correlation between changes in RVEF and post-race biomarker levels and this relationship was even stronger in the athletes who completed the race of longest duration, the ultra-triathlon
  • It has been demonstrated that ventricular load increases with exercise intensity and is greater for the RV than the LV,29 thus potentially explaining why the RV is more susceptible to fatigue after prolonged exercise.
  • BNP release during intense exercise is associated with greater relative increases in RV systolic pressures, but not LV pressures
  • BNP may provide a measure of both acute RV load and the resultant fatigue which occurs when this load is sustained
  • The correlations with RVEF, but not LVEF, provide further evidence of the differential effects of intense exercise on RV and LV function
  • This study demonstrates, for the first time, an association between endurance exercise of increasing duration and structural, functional, and biochemical markers of cardiac dysfunction in highly trained athletes
  • Functional abnormalities were confined to the RV and were largely reversible 1 week following the event
  • there remained a significant minority of athletes in whom there was evidence of myocardial fibrosis in the interventricular septum
  • RV abnormalities may be acquired through cumulative bouts of intense exercise and provides direction for prospective investigations aimed at elucidating whether extreme exercise may promote arrhythmias in some athletes.
  • the acute injury and chronic remodelling of the myocardium both disproportionately affect the RV and it remains possible that the two are linked.
  • focal DGE was confined to the interventricular septum and commonly at the site of RV attachment
  • emerging evidence that intense endurance exercise may be associated with an excess in arrhythmic disorders, the mechanisms for which remain unexplained
  • RVEF (and not LVEF) was reduced in athletes with complex ventricular arrhythmias when compared with healthy athletes and non-athletes without arrhythmias
  • it is premature to conclude that these changes may represent a proarrhythmic substrate
  • Nathan Goodyear on 09 Jan 15
     
    Study finds endurance racing results in reduce Right ventricle ejection fraction even in elite athletes.  This post-race RVEF reduction is associated with VO2max.
Nathan Goodyear

Testosterone suppresses ventricular remodeling and improves left ventricular function i... - 0 views

www.ncbi.nlm.nih.gov/...PMC4353801

Testosterone therapy heart heart health myocardial infarction heart attack male hormone hormones CVD cardiovascular disease

shared by Nathan Goodyear on 24 Mar 15 - No Cached
  • Nathan Goodyear on 24 Mar 15
     
    Animal model finds that Testosterone improves ventricular remodeling and function following myocardial infarction in male rats.  This similar finding has been found in human studies as well.   Testosterone therapy was found to lower BNP in this rat study.
Nathan Goodyear

T Cells Promote Metastasis by Regulating Extracellular Matrix Remodeling following Chem... - 0 views

aacrjournals.org/...omote-Metastasis-by-Regulating

chemotherapy metastasis

shared by Nathan Goodyear on 04 Oct 22 - No Cached
  • Nathan Goodyear on 04 Oct 22
     
    "…chemotherapy-induced, host-mediated mechanism that promotes remodeling of the extracellular matrix (ECM), ultimately facilitating cancer cell seeding and metastasis."
Nathan Goodyear

Low-T3 Syndrome - 0 views

circ.ahajournals.org/...708.long

T3 low T3 cardiac heart disease CVD cardiovascular thyroid hormone hormones hypothyroid hypothyroidism

shared by Nathan Goodyear on 03 Jul 12 - No Cached
  • More than 80% of the biologically active hormone triiodothyronine (T3) derives from peripheral conversion of prohormone thyroxine (T4) secreted by the thyroid gland
  • Low thyroid hormone concentrations, in particular low serum T3 concentrations, are a common finding in patients with nonthyroidal illnesses, including cardiac disorders
  • a direct relationship between low circulating levels of T3 and adverse prognosis of cardiac patients
  • ...4 more annotations...
  • The present study clearly shows the existence of a strong association between the reduction of biologically active T3 and mortality in a large population of cardiac hospitalized patients
  • highly significant increase in the incidence of cardiac and cumulative deaths in patients with low T3 compared with patients with normal T3 levels
  • the relevance of the low T3 state as a strong, independent predictor of mortality in cardiac patients
  • low T3 concentrations are a strong independent predictive marker of poor prognosis in cardiac patients
  • Nathan Goodyear on 03 Jul 12
     
    low T3 associated with poor prognosis in cardiac patients.   Poor prognosis = death.  T3 is important in cardiac remodeling, which is inherently important with cardiac disease.
Nathan Goodyear

Thyroid Hormone and Cardiac Disease: From Basic Concepts to Clinical Application - 0 views

www.ncbi.nlm.nih.gov/...PMC3134399

T3 cardiovascular death disease heart health MI myocardial infarction CHF heart failure thyroid hormone hormones hypothyroid hypothyroidism CVD

shared by Nathan Goodyear on 24 Sep 14 - No Cached
  • Nathan Goodyear on 24 Sep 14
     
    Low T3 post MI is associated with increased CHF, morbidity and mortality.  Article discusses thyroid hormones and cardiac function/remodeling post infarct.  The article also lays the ground work for a new study of T3 in patients post MI to be followed for 6 months.
Nathan Goodyear

Acute myocardial infarction and thyroid function: New pathophysiological and therapeuti... - 0 views

informahealthcare.com/...07853890.2011.573501

thyroid hormone hormones T3 heart attack heart health myocardial infarction MI

shared by Nathan Goodyear on 24 Sep 14 - No Cached
  • Nathan Goodyear on 24 Sep 14
     
    Thyroid hormone plays significant role in cardiac remodeling after acute myocardial infarction.  Thyroid hormone, particularly T3 as the vast majority of T3 is produced in heart tissue via D1 enzymatic activity, improves cardiac contractility, reduces systemic vascular resistance, reduces cardiac work load, decreases blood pressure, improves cardiac metabolism, and thus improves outcomes post MI.
Nathan Goodyear

Thyroid hormone attenuates cardiac remodeling and ... [Eur J Cardiothorac Surg. 2007] -... - 0 views

www.ncbi.nlm.nih.gov/...17560116

thyroid hormone Cardiovascular disease

shared by Nathan Goodyear on 02 Feb 11 - No Cached
  • CONCLUSIONS: Thyroid hormone administration early after infarction attenuates cardiac remodeling and significantly improves myocardial performance.
  • Nathan Goodyear on 02 Feb 11
     
    Wow, Thyroid replacement after MI, improves heart function and reduces damage
Nathan Goodyear

Thyroid Hormone Treatment to Mend a Broken Heart -- Klein and Danzi 93 (4): 1172 -- Jou... - 0 views

jcem.endojournals.org/...1172

hormone thyroid T3 heart disease Cardiovascular

shared by Nathan Goodyear on 02 Feb 11 - No Cached
  • Nathan Goodyear on 02 Feb 11
     
    Incredible read on how T3 improves heart remodeling, healing,and function; sadly, most physicians are unaware
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

Exploring the basic science of prolapse meshes - 0 views

www.ncbi.nlm.nih.gov/...PMC5161092

vaginal mesh mesh immune system M1 M2 macrophages

shared by Nathan Goodyear on 24 Jan 19 - No Cached
  • Nathan Goodyear on 24 Jan 19
     
    Mesh implantation, here in the vaginal area, increases both M1 and M2 maturation migration. M1 increases pro-inflammatory signaling and processes and M2 promotes remodeling/healing... Both increase, but M1 increases more than M2 proportionally. M2 can increase the bridge scaring that can occur as well as the potential for immune suppression and autoimmune/cancer implications
Nathan Goodyear

An integrative analysis reveals coordinated reprogramming of the epigenome and the tran... - 0 views

www.ncbi.nlm.nih.gov/...PMC4622000

exercise epigenetics muscle

shared by Nathan Goodyear on 03 Oct 17 - No Cached
  • contribution to the training response of the epigenome as a mediator between genes and environment
  • Differential DNA methylation was predominantly observed in enhancers, gene bodies and intergenic regions and less in CpG islands or promoters
  • highly consistent and associated modifications in methylation and expression, concordant with observed health-enhancing phenotypic adaptations, are induced by a physiological stimulus
  • ...34 more annotations...
  • The health benefits following exercise training are elicited by gene expression changes in skeletal muscle, which are fundamental to the remodeling process
  • there is increasing evidence that more short-term environmental factors can influence DNA methylation
  • dietary factors have the potency to alter the degree of DNA methylation in different tissues, 9,10 including skeletal muscle
  • In one study, a single bout of endurance-type exercise was shown to affect methylation at a few promoter CpG sites
  • In the context of diabetes, exercise training has been shown to affect genome-wide methylation pattern in skeletal muscle,13 as well as in adipose tissue.
  • physiological stressors can indeed affect DNA methylation
  • training intervention reshapes the epigenome and induces significant changes in DNA methylation
  • the findings from this tightly controlled human study strongly suggest that the regulation and maintenance of exercise training adaptation is to a large degree associated to epigenetic changes, especially in regulatory enhancer regions
  • Endurance training [after training (T2) vs. before training (T1)] induced significant (false discovery rate, FDR< 0.05) methylation changes at 4919 sites across the genome in the trained leg
  • identified 4076 differentially expressed genes
  • a complementary approach revealed that over 600 CpG sites correlated to the increase in citrate synthase activity, an objective measure of training response (Figure S4 and Dataset S14). This might imply that some of these sites could influence the degree of training response.
  • As expected by a physiological environmental trigger on adult tissue, the observed effect size on DNA methylation was small in comparison to disease states such as cancer
  • a preferential localization outside of CpG Islands/Shelves/Shores
  • endurance training especially influences enhancers
  • negative correlation was more prominent for probes in promoter/5′UTR/1st exon regions, while gene bodies had a stronger peak of positive correlation
  • The significant changes in DNA methylation, that primarily occurred in enhancer regions, were to a large extent associated with relevant changes in gene expression
  • The main findings of this study were that 3 months of endurance training in healthy human volunteers induced significant methylation changes at almost 5000 sites across the genome and significant differential expression of approximately 4000 genes
  • DMPs that increased in methylation were mainly associated to structural remodeling of the muscle and glucose metabolism, while the DMPs with decreased methylation were associated to inflammatory/immunological processes and transcriptional regulation
  • This suggests that the changes in methylation seen with training were not a random effect across the genome but rather a controlled process that likely contributes to skeletal muscle adaptation to endurance training
  • Correlation of the changes in DNA methylation to the changes in gene expression showed that the majority of significant methylation/expression pairs were found in the groups representing either increases in expression with a concomitant decrease in methylation or vice versa
  • The fraction of genes showing both significant decrease in methylation and upregulation was 7.5% of the DEGs or 2.3% of all genes detected in muscle tissue with at least one measured DNA methylation position. Correspondingly, 7.0% of the DEGs or 2.1% of all genes showed both significant increase in methylation and downregulation
  • we show that DNA methylation changes are associated to gene expression changes in roughly 20% of unique genes that significantly changed with training
  • Examples of structural genes include COL4A1, COL4A2 and LAMA4. These genes have also been identified as important for differences in responsiveness to endurance training
  • methylation status could be part of the mechanism behind variable training response
  • Among the metabolic genes, MDH1 catalyzes the reversible oxidation of malate to oxaloacetate, utilizing the NAD/NADH cofactor system in the citric acid cycle and NDUFA8 plays an important role in transferring electrons from NADH to the respiratory chain
  • PPP1R12A,
  • In the present study, methylation predominantly changed in enhancer regions with enrichment for binding motifs for different transcription factors suggesting that enhancer methylation may be highly relevant also in exercise biology
  • Of special interest in the biology of endurance training may be that MRFs, through binding to the PGC-1α core promoter, can regulate this well-studied co-factor for mitochondrial biogenesis
  • That endurance training led to an increased methylation in enhancer regions containing motifs for the MRFs and MEFs is somewhat counterintuitive since it should lead to the repression of the action of the above discussed transcription factors
  • decrease with training in this study, including CDCH15, MYH3, TNNT2, RYR1 and SH3GLB1
  • expression of MEF2A itself decreased with training
  • this study demonstrates that the transcriptional alterations in skeletal muscle in response to a long-term endurance exercise intervention are coupled to DNA methylation changes
  • We suggest that the training-induced coordinated epigenetic reprogramming mainly targets enhancer regions, thus contributing to differences in individual response to lifestyle interventions
  • a physiological health-enhancing stimulus can induce highly consistent modifications in DNA methylation that are associated to gene expression changes concordant with observed phenotypic adaptations
  • Nathan Goodyear on 03 Oct 17
     
    Exercise alters gene expression via methylation--the power of epigenetics.  Interestingly, the majority of the methylation was outside the CPG island regions.  This 3 month study found methylation of 5,000 sites across the genome resulting in altered expression of apps 4,000 genes.  The altered muscle changes of the endurance training was linked to DNA methylation changes.
Nathan Goodyear

Total testosterone levels, metabolic parameters, cardiac remodeling and exercise capaci... - 0 views

informahealthcare.com/...07853890.2012.711951

low T low testosterone Low T testosterone Diabetes DM exercise men male

shared by Nathan Goodyear on 23 Apr 13 - No Cached
  • Nathan Goodyear on 23 Apr 13
     
    Low Total testosterone associated with poor exercise capacity, increased obesity, poor glucose control including diabetes, increased cardiac hypertrophy in those with CAD.  Simply put, low T in men is associated with metabolic dysregulation.
Nathan Goodyear

Early long-term L-T3 replacement rescues mitochondria and prevents ischemic cardiac rem... - 0 views

onlinelibrary.wiley.com/...abstract

T3 thyroid hormone hormones MI mitochondria HIF-1alpha

shared by Nathan Goodyear on 29 Jun 13 - No Cached
  • Nathan Goodyear on 29 Jun 13
     
    T3 in the post MI individual decreases the MI infarct size and the progression to heart failure. What is really  interesting about this study is that the T3 induced mitochondrial biogenesis and activity which is a great thing in recovery of MI and also in disease i.e. cancer.  However, it appears to increase HIF-1alpha and angiogenesis which is stimulated by retrograde signaling.  There is a muddied picture here.  Because T3 stimulates oxidative phosphorylation and mitochondria biogenesis which is favorable for health.  However, in this study of rats, it induced HIF-1alpha and angiogenesis in post MI, which is favorable to recovery, yet this is unfavorable for cancer.    Yet oxidative phosphorylation is favorable to cancer prevention/elimination and MI recovery.
Nathan Goodyear

Exercise-induced right ventricular dysfunction and structural remodelling in endurance ... - 0 views

eurheartj.oxfordjournals.org/...eurheartj.ehr397.abstract

endurance training athletes cardiac heart right ventricular function

shared by Nathan Goodyear on 28 Jan 12 - No Cached
  • Nathan Goodyear on 28 Jan 12
     
    endurance training found to induce heart dysfunction.  This was all in the right ventricular function, but significant dysfunction was found.
Nathan Goodyear

Thyroid hormone and "cardiac metamorphosis": poten... [Pharmacol Ther. 2008] - PubMed r... - 0 views

www.ncbi.nlm.nih.gov/...18455802

thyroid hormone heart cardiac

shared by Nathan Goodyear on 02 Feb 11 - No Cached
  • Nathan Goodyear on 02 Feb 11
     
    thyroid hormone plays important role in heart failure and heart repair; thyroid balance critical
Nathan Goodyear

http://www.msma.org/docs/communications/momed/Excessive_Endurance_Exercise_and_Heart_Di... - 0 views

www.msma.org/..._Disease_MOMED_JulyAug2012.pdf

heart disease endurance exercise exercise marathons triathlon endurance athletes heart health disease

shared by Nathan Goodyear on 10 Jan 15 - No Cached
  • Nathan Goodyear on 10 Jan 15
     
    great review of data on cardiac damage associated with extreme endurance training.  These EEEs, that they are called, are rare in those < 40 and usually involved genetic defects.  This article points to aggressive preventive testing in those > 50.
Nathan Goodyear

Adenoid cystic carcinoma: current therapy and potential therapeutic advances based on g... - 0 views

www.ncbi.nlm.nih.gov/...PMC4741919

adenoid cystic carcinoma

shared by Nathan Goodyear on 03 Oct 18 - No Cached
  • Cisplatin and 5-FU or CAP (cisplatin, doxorubicin, and cyclophosphamide) regimens can be used for combination chemotherapy
  • patients with advanced salivary gland malignancy treated with the CAP regimen achieved partial response (PR) or stable disease (SD) rates of 67% (8 out of 12 patients)
  • Agents commonly given as monotherapy for treating ACC are cisplatin, mitoxantrone, epirubicin, vinorelbine, paclitaxel, and gemcitabine. However, few of these agents have shown efficacy
  • ...23 more annotations...
  • single agent mitoxantrone or vinorelbine were recommended as reasonable choices
  • ACC is subdivided into 3 histological groups based on solid components of the tumor including cribriform, tubular, and solid
  • Cribriform and tubular ACCs usually exhibit a more indolent course, whereas the solid subtype is associated with worse prognosis
  • ACC consists of two different cell types: inner luminal epithelial cells and outer myoepithelial cells
  • epithelial cells express c-kit, cox-2 and Bcl-2
  • myoepithelial cells express EGFR and MYB
  • a balanced translocation of the v-myb avian myeloblastosis viral oncogene homolog-nuclear factor I/B (MYB-NFIB) is considered to be a signature molecular event of ACC oncogenesis
  • As a transcription factor, MYB is known to modulate multiple genetic downstream targets involved in oncogenesis, such as cox-2, c-kit, Bcl-2 and BclX
  • Various signaling cascades are essential for cancer cells to survive and grow. The PI3K/Akt/mTOR pathway is one of them
  • This pathway regulates cell survival and growth and is upregulated in many cancers
  • Mutations in genes associated with DNA repair are frequently found in familial cancer syndromes, such as hereditary breast-ovarian cancer syndrome (HBOC), hereditary non-polyposis colorectal cancer (HNPCC, also called Lynch syndrome) and Li-Fraumeni syndrome [30, 31]. These mutations were also reported in non-hereditary cancers
  • 70% of ACC samples (58 of 84) were found to have genetic alterations in the MYB/MYC pathway, indicating that changes in this pathway are crucial in ACC pathogenesis
  • The second most frequently mutated pathway was involved in chromatin remodeling (epigenetic modification), a pathway that includes multiple histone related proteins, and was altered in 44% of samples
  • C-kit
  • VEGF, iNOS and NF-κB were noted to be highly expressed in ACC cells as compared to normal salivary gland cells
  • members of the SOX family, such as SOX 4 and SOX10, are overexpressed in ACC
  • FABP7 (Fatty acid binding protein 7) and AQP1 (Aquaporin 1) tend to be overexpressed in ACC cell lines
  • considerable variability in HER2 overexpression ranging from 0–58% in patients with ACC
  • the study with cetuximab and concurrent chemoradiation or chemotherapy showed the highest ORR (total 43%, 9.5% CR and 33% PR), but this regimen was only given to the EGFR positive patients
  • Cancer immunotherapy can be classified into 3 major groups. Active immunization using anti-tumor vaccines to induce and recruit T cells, passive immunization based on monoclonal antibodies, and adoptive cell transfer to expand tumor-reactive autologous T cells ex vivo and then reintroduce these cells into the same individual
  • LAK cells showed cytotoxicity against ACC cells
  • cytokine-induced cell apoptosis and the cytotoxic effect of the LAK cells contributed to tumor regression
  • molecular finding of the MYB-NFIB fusion gene has the greatest potential to target what appears to be a fundamental event in disease pathogenesis
  • Nathan Goodyear on 03 Oct 18
     
    good review of adenoid cystic carcinoma
Nathan Goodyear

Quercetin Remodels the Tumor Microenvironment To Improve the Permeation, Retention, and... - 0 views

www.ncbi.nlm.nih.gov/...PMC5961944

quercetin cancer

shared by Nathan Goodyear on 09 May 19 - No Cached
  • Nathan Goodyear on 09 May 19
     
    Quercetin inhibits Wnt16 to induce apoptosis.
Nathan Goodyear

Doxycycline Decreases Tumor Burden in a Bone Metastasis Model of Human Breast Cancer | ... - 0 views

cancerres.aacrjournals.org/...1588

doxycycline cancer breast cancer

shared by Nathan Goodyear on 08 May 18 - No Cached
  • it appears more likely that the effectiveness relies on the properties of doxycycline as an inhibitor of tumor cell proliferation and less on its effect as a MMP inhibitor
  • Our results suggest that doxycycline may be useful not only for the treatment of osteolytic but also for the treatment of osteoblastic bone metastasis
  • A prominent feature of bone metastasis of breast cancer is the uncoupling of bone remodeling
  • ...3 more annotations...
  • doxycycline can improve this to some extent by increasing bone formation
  • the current study clearly demonstrates the benefit of doxycycline when administered from the time of the development of the tumor
  • In conclusion, doxycycline greatly reduced tumor burden and could also compensate for the increased bone resorption frequently associated with bone metastasis from breast cancer
  • Nathan Goodyear on 08 May 18
     
    doxycycline useful in breast cancer animal model to reduce tumor burden through inhibition of tumor cell proliferation and inhibition of MMP.
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