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Nathan Goodyear

Reversal of fatigue during prolonged exercise by c... [J Appl Physiol. 1987] - PubMed r... - 0 views

www.ncbi.nlm.nih.gov/...3325488

prolonged exercise fatigue

shared by Nathan Goodyear on 08 Mar 11 - No Cached
  • Nathan Goodyear on 08 Mar 11
     
    prolonged interval to fatigue in those with glucose infusion/ngestion during exercise
Nathan Goodyear

The effect of metformin on survival of patients with pancreatic cancer: a meta-analysis... - 0 views

www.nature.com/...s41598-017-06207-x

"Pancreatic cancer" metformin

shared by Nathan Goodyear on 27 Nov 18 - No Cached
  • Nathan Goodyear on 27 Nov 18
     
    Metformin prolongs survival in pancreatic cancer. Though, the evidence for prolonging survival decreased with advancing disease i.e. metastatic disease.
Nathan Goodyear

PLOS ONE: The Ketogenic Diet and Hyperbaric Oxygen Therapy Prolong Survival in Mice wit... - 0 views

journals.plos.org/...article

ketogenic ketogenic diet ketones ketone bodies cancer nutrition diet hyperbaric oxygen hyperbaric therapy hyperbaric

shared by Nathan Goodyear on 17 Nov 16 - No Cached
  • This finding strongly supports the efficacy of the KD and HBO2T as therapies to inhibit tumor progression and prolong survival in animals with metastatic cancer.
  • We found that the KD fed ad libitum significantly increased mean survival time in mice with metastatic cancer
  • Ketogenic diets are also known to have an appetite suppressing effect which may contribute to body weight loss
  • ...5 more annotations...
  • the ketogenic diet may inhibit cancer progression in part by indirect dietary energy restriction
  • KD with HBO2T. Combining these therapies nearly doubled survival time in mice with metastatic cancer,
  • low carbohydrate or ketogenic diets promote weight loss in overweight individuals, they are also known to spare muscle wasting during conditions of energy restriction and starvation
  • dietary-induced therapeutic ketosis in a cancer patient would prevent muscle wasting similarly as it does with athletes undergoing intense exercise
  • when given as an adjuvant treatment to advanced cancer patients, the KD improves quality of life and enhances the efficacy of chemotherapy treatment in the clinic
  • Nathan Goodyear on 17 Nov 16
     
    mouse study finds that ketogenic diet plus hyperbaric O2 treatment prolongs survival.
  • Open TeleShop on 17 May 17
     
    Hey Dear Check Out Our Online Shopping store in all Over Pakistan.As Seen as On Tv Products Like as Health Beauty,Fitness,Homeware,Kitchenware,And Other Electronic Products in Pakistan Check Out Now| www.openTeleshop.Com
fitspresso

https://www.thefastleanpro.us/ - 0 views

www.thefastleanpro.us

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shared by fitspresso on 27 Sep 23 - No Cached
  • fitspresso on 27 Sep 23
     
    Fast Lean Pro™ (official) | weight lose Formula thefastleanpro.us · by Fast Lean Pro Fast Lean Pro Only $49/Bottle Limited Time Offer! Fast Lean Pro Special Deal + Special 51% Discount Save $300 + 180 Days Money Back Guarantee FastLeanPro The #1 Solution To natural metabolism booster helps you lose weight quickly without starving yourself. Fast Lean Pro is a natural powder supplement for weight loss that has recently been developed by Japanese scientists. Regular Price: $99/per bottle Only for: $49/per bottle What Is Fast Lean Pro? Fast Lean Pro is a powdered dietary powdery supplement designed to aid in weight loss. It contains a unique combination of ingredients that are believed to activate the body's "fasting switch" to optimize results. This product focuses not only on weight loss but also on promoting cellular rejuvenation, fasting, and a healthy metabolism. The concept behind Fast Lean Pro is that incorporating fasting into one's lifestyle can lead to positive outcomes irrespective of individual food choices and eating habits. To comprehend the mechanism of the Fast Lean Pro process, it is necessary to delve into its specific details. One of the few weight loss pills on the market that contains Fibersol is Fast Lean Pro. This safe, specialized fiber adds bulk to its weight when combined with water, curbing your appetite before it throws off your meal plan. If you're trying to lose weight or curb your appetite, Fast Lean Pro can help. Supporting substances such as niacin and chromium contribute to this. The body can further benefit from these nutrients, such as through improved metabolic regulation. Fast lean Pro is non-GMO, vegan friendly, and contains no artificial ingredients or stimulants. Fast Lean Pro is a weight loss product that promotes the body's natural self-feeding process. The body naturally removes old, damaged cells through a process known as autophagy to encourage cell regeneration and repair. Recent studies by a group
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
  • ...56 more annotations...
  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Comparisons of normal saline and lactated Ringer's resuscitation on hemodynamics, metab... - 0 views

www.ncbi.nlm.nih.gov/...PMC4029282

IV fluids lactated ringers normal saline LR NS

shared by Nathan Goodyear on 03 Jul 18 - No Cached
  • NS contains 154 mM Na+ and Cl-, with an average pH of 5.0 and osmolarity of 308 mOsm/L.
  • LR solution has an average pH of 6.5, is hypo-osmolar (272 mOsm/L), and has similar electrolytes (130 mM Na+, 109 mM Cl-, 28 mM lactate, etc.) to plasma
  • hyperchloremic acidosis
  • ...26 more annotations...
  • LR’s acid base balance is superior to that of NS’s
  • There were no significant differences between LR and NS groups in fibrinogen concentrations or platelet count
  • Total protein dropped
  • no significant differences in Hct (Table  1) or total protein between LR and NS groups
  • Bicarbonate HCO3- levels were decreased by hemorrhage but returned to pre-hemorrhage values by 3 h after LR resuscitation, whereas no return was observed with NS resuscitation
  • Na+ was increased after NS resuscitation
  • No changes in Na+ or K+ were observed
  • K+ did not change initially after NS resuscitation but was elevated at 6 h afterwards
  • Ca++ was similarly decreased
  • Cl- was elevated for 6 h after NS resuscitation, with no changes shown after LR resuscitation
  • PT was similarly prolonged by resuscitation with LR (from 11.2 ± 0.2 sec at baseline to 12.1 ± 0.2 sec at 6 h) and NS
  • Plasma aPTT was also similarly prolonged by resuscitation with LR (from 17.1 ± 0.5 sec baseline to 20.1 ± 1.2 sec at 6 h) or NS
  • NS resuscitation resulted in better oxygen delivery and oxygen delivery-to-oxygen demand ratio as an index of oxygen debt
  • NS had better tissue perfusion and oxygen metabolism than LR
  • LR resuscitation returned BE and bicarbonate to pre-hemorrhage levels within 3 h, but no return of BE or bicarbonate was observed for 6 hr with NS resuscitation
  • current blood bank guidelines state that LR should not be mixed with blood to prevent the risk of clot formation from calcium included in LR
  • LR resuscitation should not be given with blood through the same iv-line and crystalloids should be avoided in patients with blood transfusion
  • PT and aPTT were prolonged for 6 h after hemorrhage and resuscitation, suggesting a hypocoagulable states
  • potential thrombotic risk from LR resuscitation is unlikely.
  • we suspected that the blood pressure after NS resuscitation would be lower than that of LR due to its vasodilator effects
  • NS required a larger resuscitation volume and was associated with poor acid base status and elevated serum potassium in this model
  • NS required 50% more volume and was associated with a higher cardiac output and lower peripheral resistance, as compared to LR resuscitation
  • These differences are possibly due to the vasodilator effects from NS
  • an elevation of K+ was observed at 6 h post NS resuscitation, while no change of K+ was observed after LR resuscitation
  • The mechanism for the increase of K+ from NS is not fully known
  • NS is associated with vasodilator effects and the risks of metabolic acidosis and hyperkalemia
  • Nathan Goodyear on 03 Jul 18
     
    LR vs NS crystalloid.
Nathan Goodyear

Assessment of the safety of supplementation with different amounts of vitamin E in heal... - 0 views

ajcn.nutrition.org/...311.abstract

vitamins vitamin E alternative medicine safety

shared by Nathan Goodyear on 13 Jun 16 - No Cached
  • Nathan Goodyear on 13 Jun 16
     
    Vitamin E supplementation in individuals >65 for 4 months on dosing up to 800 IU not found to have adverse events as described as decreased platelets, prolonged bleeding time, lower hemoglobin/hematocrit...
wheelchairindia9

Tynor Knee Cap Comfeel - 0 views

www.wheelchairindia.com/...Tynor-Knee-Cap-Comfeel

Tynor Knee Cap Comfeel Knee Cap Comfeel knee cap comfeel support tynor knee comfeel tynor knee cap comfeel brace knee caps comfeel

shared by wheelchairindia9 on 14 Mar 16 - No Cached
  • wheelchairindia9 on 14 Mar 16
     
    Tynor Knee Cap Comfeel Knee cap comfeel is a next generation tubular product knitted on a 3 dimensional computer controlled circular looms to provide mild compression, warmth and support to the knee joint. It is used to allay pain and inflammation, generally associated with old age, arthritis or injury. Soft Patella Fine grip at the edges Four way stretch Uniform compression Simple pull on application. Tynor Knee Cap Comfeel Features Anatomically shaped and reduced compression on patella No Chondromalacia on prolonged use Better compression and grip Easy knee movement Improved comfort Bi-layered, cotton on the inside , a dermophillic interphase Enhanced comfort Better sweat absorption Better patient compliance. Bilayered, nylon on the outside Ensures long life Excellent aesthetics Color fastness. Four-way stretchable fabric Effective compression Enhanced comfort. Two layered with interwoven air space Retains body heat effectively. Speeds up healing Allays pain. Tynor Knee Cap Comfeel Measurements Measure circumference around mid thigh - approx 6 inches above knee Size Chart - Size Inches CM Small 14.8-17.2 37-43 Medium 17.2-19.6 43-49 Large 19.6-22 49-55 XL 22-24.4 55-61
wheelchairindia9

Tynor Cervical Collar Soft - 0 views

www.wheelchairindia.com/...Tynor-Cervical-Collar-Soft

Tynor Cervical Collar Soft cervical collar neck braces soft cervical collar soft neck brace cervical soft collar cervical collar soft Cervical Collar Soft tynor tynor soft cervical collar

shared by wheelchairindia9 on 17 Mar 16 - No Cached
  • wheelchairindia9 on 17 Mar 16
     
    Tynor Cervical Collar Soft Cervical collar soft is used for supporting the neck and protecting it against jerks impacts and vibrations. Recommended where a partial or controlled immobilization of the cervical region is required. Ultimate comfort. Partial immobilization. Optimal support. Excellent aesthetics. Absorbs impact. Tynor Cervical Collar Soft Features Soft polyurethane Provides unmatched comfort, used as prophylactic collar, reduces pain and provides comfortable support during traveling. Covered with hypoallergenic cotton stockinet. Better patient comfort, no allergy or rash even to sensitive skin, better compliance No hard, bony reinforcement Improves patient comfort, particularly recommended for geriatric patients, excellent for prolonged use. Anatomical design Uniform support to the mandible, effective action and better fit, better comfort. Perforated collar body Improved ventilation, more patient comfort, better compliance.
Nathan Goodyear

Timing Protein Intake Increases Energy Expenditure 24 h afte... : Medicine & Science in... - 0 views

journals.lww.com/...ses_Energy_Expenditure.21.aspx

whey protein energy sports exercise

shared by Nathan Goodyear on 13 Apr 12 - No Cached
  • Nathan Goodyear on 13 Apr 12
     
    protein supplementation (compared to carbohydrates)  prior to heavy resistance training resulted in prolonged increase in resting energy expenditure at 24 hours.  The supplementation in this study was 18 grams of whey protein.  This study reveals the lingering effect of diet on benefits of exercise.
Nathan Goodyear

Exercise and Testosterone - 0 views

www.sast.org.tw/...FI1112060008_aO.pdf

testosterone training athletic performance athlete athletic muscle

shared by Nathan Goodyear on 26 Jun 12 - No Cached
  • Nathan Goodyear on 26 Jun 12
     
    type and length of training effects testosterone secretion. Testosterone plays an important role in muscle performance and mass. Prolonged training can result in a decrease in testosterone level. This has significance with highly trained athletes. One pitfall of this study was the assessment of testosterone via serum.
Nathan Goodyear

The effects of creatine supplementation o... [Eur J Appl Physiol. 2004] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...14685870

phosphocreatine athletic performance muscle training creatine

shared by Nathan Goodyear on 26 Jun 12 - No Cached
  • Nathan Goodyear on 26 Jun 12
     
    phosphocreatine helps to maintains muscular performance.  This appears to be an early benefit.  The question is does this help in prolonged performance requirements.
Nathan Goodyear

S-adenosylmethionine in alcoholic liver cirrhosis:... [J Hepatol. 1999] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...10406187

SAMe NAFLD GSH glutathione liver cirrhosis cirrhosis liver

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe, at doses of 1200 mg, shown to decrease mortality rate and prolong transplantation in those with cirrhosis.  Very likely, these individuals, if tested, had low SAMe and methyl donors as well as depleted glutathione. This is a set up for low phosphotidyl choline/ethanolamine levels resulting in fat accumulation.
Nathan Goodyear

Sleep Duration and Biomarkers of Inflammation - 0 views

www.ncbi.nlm.nih.gov/...PMC2635584

sleep TNF-alpha IL-6 CRP inflammation

shared by Nathan Goodyear on 24 Jan 12 - No Cached
  • Nathan Goodyear on 24 Jan 12
     
    shortened sleep interval increased TNF-alpha levels and prolonged sleep intervals increased IL-6 and CRP.  It appears that sleep duration has a direct effect on inflammation
Nathan Goodyear

Long-term benefits of testosterone replacement therapy on angina threshold and atheroma... - 0 views

eje-online.org/...443.long

low Testosterone low T heart myocardium ischemia men male testosterone hormone hormones

shared by Nathan Goodyear on 17 Jul 12 - No Cached
  • Nathan Goodyear on 17 Jul 12
     
    Testosterone therapy in men prolongs time to myocardial ischemia.  The follow of this study was 12 months and the number of men was small (15 men).  This was continually therapy during the duration of 12 months.
Nathan Goodyear

[Effects of testosterone on insulin r... [Zhonghua Yi Xue Za Zhi. 2006] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...16842700

low T testosterone GLUT4 insulin IRS-1

shared by Nathan Goodyear on 12 Feb 12 - No Cached
  • Nathan Goodyear on 12 Feb 12
     
    Testosterone shown to improve GLUT 4 and IRS-1 expression with low dose short term therapy; in contrast, high dose, prolonged therapy shown to down regulate IRS-1 and GLUT 4 expression.  This shows the importance of using saliva for evaluation versus serum.  Serum testing routinely leads to over treatment with high dosages of testosterone.
Nathan Goodyear

Reproductive History and risk of colorectal cancer in postmenopausal women - 0 views

jnci.oxfordjournals.org/...jnci.djr101.full.pdf

colon cancer colorectal estrogen post-menopause

shared by Nathan Goodyear on 19 Nov 13 - No Cached
  • Nathan Goodyear on 19 Nov 13
     
    study finds prolonged exposure to estrogen associated with increased colorectal cancer risk in postmenopausal women. So many unanswered questions. What was the ER status of these patients? What was the weight of these patients? One cannot simply compare estrogen exposure to colorectal cancer risk and say aha! What is the environment of the individual(s)?!
Nathan Goodyear

Testosterone and the Cardiovascular System: A Comprehensive Review of the Clinical Lite... - 0 views

jaha.ahajournals.org/...e000272

low T Testosterone cardiovascular disease CAD CHF insulin resistance type II diabetes diabetes obesity men male hormone hormones therapy

shared by Nathan Goodyear on 13 May 14 - No Cached
  • Nathan Goodyear on 13 May 14
     
    Some startling statistics in this 2013 review on Testosterone in men.  Studies reflect an inverse relationship between Testosterone and CAD severity.  That is, the lower the Testosterone levels, the increase in severity of CAD. This same association was also found with CHF.  Low Testosterone is common in those with CAD, CHF, type II diabetes, increased IMT in carotids and aorta, and obesity when compared to "healthy" individuals.  Testosterone therapy in those with CAD found benefits: prolongation of ST segment depression, coronary vasodilation, improved exercise capacity in those with CHF, shift to type I muscle fibers, shorten the QTc interval.  Testosterone therapy has been shown to improve insulin resistance, improve HgbA1c and decrease waist circumference and fat loss in obese individuals.  Otherwise, a good review of the association between a declining Testosterone and cardiovascular disease.
wheelchairindia9

Reclining Commode Wheelchair - 0 views

disabilityproduct.in/...Reclining-Wheelchair-609-GC

Disability Seating And Tilt-In-Space Wheelchair adjustable seat height and depth systems provide added comfort neck and trunk a much-needed break wheelchair provides a sole pivot point movable armrest and elevating footrest

shared by wheelchairindia9 on 25 Aug 15 - No Cached
  • wheelchairindia9 on 25 Aug 15
     
    Reclining Wheelchair 609 GC Reclining Wheelchair 609 GC is one of the multipurpose chairs which boast of features like reclining, inbuilt commode, customized armrest and footrest and foldable nature of the chair. Reclining Wheelchair 609 GC Features The wheelchair can be folded within very easily within seconds, making it easier during travels and outings. The backrest of the chair can be easily reclined, giving the user the freedom to relax by not moving up from the chair. The footrest can be inclined and adjusted so as to make the user comfortable during reclining or otherwise. A well paded thigh support is an add-on to the footrest. The front and rear wheels of the chair are designed and placed in such a way so as to support the reclining of the user, making it a very safe and friendly wheelchair. The inbuilt commode has its seat just underneath the main seat of the chair; it can be used by just removing the main seat. The Wheelchair can also be folded from between by just removing the commode and the chair's seat. This Wheelchair's functionality gives the user total freedom. Easy to fold and unfold within seconds. Reclining Wheelchair 609 GC Measurements Frame Style : Foldable Frame Material : MS Chrome Plated open position wheel to wheel width in : 26" (inches) Seat Width : 18" (inches) Total width in closing position : 11" (inches) Rear Wheel Size : 24" (inches) Front Wheel Size : 8" (inches) Seat to Floor Height in : 21" (inches) Seat Depth : 18" (inches) Total Height : 50" (inches) Max User Weight Capacity (kgs) : 110 Net Weight (kgs) : 23 Upholstery : Rexine Armrest : Detachable Leg rest : Detachable with elevated footrest Calf support for added comfort Wheel Quality : Rear Solid wheels Rear Wheel Lock : Yes Hand Brakes : No Drop back Handle : No Headrest Support Available Neck Support Available Plastic Commode seat with Pot. Cushioned Top Cover Rear tyer Solid tube less Round commode pan Removabl
Nathan Goodyear

PLOS ONE: Depletion of Brain Docosahexaenoic Acid Impairs Recovery from Traumatic Brain... - 0 views

journals.plos.org/...article

DHA TBI traumatic brain injury omega 3 brain injury brain omega-3

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • The polyunsaturated fatty acids linoleic (LA, 18:2n-6) and linolenic acid (LNA, 18:3n-3) are essential fatty acids that cannot be synthesized by the body.
  • LNA serves as the precursor for long chain omega-3 fatty acids such as docosahexaenoic acid (DHA) while LA is converted into long chain omega-6 fatty acids such as arachidonic acid (AA)
  • DHA and AA are abundantly found in the brain, where these are stored mainly in membrane phospholipids
  • ...10 more annotations...
  • DHA has been shown to increase neurite outgrowth and synaptogenesis, and promotes glutamatergic neurotransmission through increase in glutamate receptor subunit expression
  • DHA has been shown to be converted to anti-inflammatory, proresolving and neuroprotective mediators, such as resolvins [7] and protectins
  • AA is converted by cyclooxygenases into 2-series prostaglandins and 4-series leukotrienes, most of which exert pro-inflammatory effects
  • Supplementation of DHA exerts neuroprotective effects and has been reported to afford protection from diffuse axonal injury [11] and mixed brain injury [12] as well
  • severe depletion of membrane DHA in the brain renders mice significantly more susceptible to TBI and impairs recovery following the injury
  • Omega-3 fatty acids may serve as nutraceutical agents and precondition the brain to make it more resilient to injury
  • it can be suggested that enriching DHA in the brain may be prophylactic and protective against brain injury
  • severe DHA deficiency in the brain impairs functional recovery from TBI in terms of vestibulo-motor and cognitive deficits
  • DHA deficiency further elevates TBI-induced production of SBDPs
  • less neurons were found around the injury site of DHA deficient brain after TBI compared to the omega-3 fatty acid adequate group
  • Nathan Goodyear on 31 Aug 15
     
    mouse study finds prolonged recovery in DHA deficient mice compared to controls.
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