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finchloe121

5 Things You Need To Understand If You are Having Chronic Pain! - 0 views

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    Chronic pain is a type of pain that usually lasts for weeks to months. This pain can come and go, and it can be anywhere in the body. Chronic pain can lead to anxiety, depression, and insomnia. Chronic pain is quite different from acute pain and there are some differences between the two types. People usually experience severe pain, when it is injured by a broken bone or a cut on the skin. This pain does not last long. Pain is not something that can be ignored. If it grows, it should be fixed. As fear and pain persist, one begins to think negatively. Long-term negative thoughts begin to form in his mind, a process called fear conditioning. This factor causes an increase in blood pressure and anxiety disorders. Chronic pain is difficult to treat, and results in increased pain, fear, and negative thoughts. Extreme levels of fear lead to more pain, and the cycle of pain threats can be difficult to break. One of the best pills used to treat body pain symptoms is Hydrocodone 325mg, which you can easily buy from any trusted online pharmacy, such as Pharma Health Online.
wheelchairindia9

Karman Ergo Lite S-2501 Wheelchair - 0 views

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    Karma Ergo Lite 2501 Wheelchair The extremely lightweight Ergo Lite 2501 Transport Wheelchair weighs only 8.16 kg. and features an ergonomically-designed seat and backrest, making it one of the most comfortable transport chairs on the market. The folding seat and backrest make the S-Ergo ideal for storage or travel, and the built in AEGIS anti-bacterial cushion provides added comfort and support. Despite its light weight, the S-Ergo features a 115 kg. weight capacity along with large, 14" flat-free polyurethane rear tires. Karma Ergo Lite 2501 Wheelchair Features Lightest transporter on the market! Patented S-Style Ergonomic Seat Frame 6061 T-6 Aircraft-grade Aluminum Only 18 lb . (w/ footrests) Built in Silver Aegis Anti-bacterial Cushion Fixed Armrests w/Concaved Armpads Pocket Behind Backrest & Small Carry Pouch on Each Armrest 6" x 1" Polyurethane Front Casters 16" x 17" or 18" x 17" Seat Width S-Style Ergonomic Seat 14" Rear Polyurethane, High Tread, Flat Free Wheels 3-Stage handle brake: allows light to firm grip for lock Folding Backrest/ Folding Seat for Transporting in Vehicle or Travel Fixed Footrests w/ Extra Wide Footplates Frame Color: Pearl Silver Weight Capacity of 100 kg Ergonomic Transporter w/ handle brakes Karma Ergo Lite 2501 Wheelchair Measurements Seat Width 16 inch., 18 inch. Seat Depth 17 inch. Armrest Height 8 inch. Seat Height 19 inch. Back Height 17 inch. Overall Height 36 inch. Overall Open Width 23 inch., 25 inch. Folded Width 12 inch. Overall Length 39 inch. Weight Without Riggings 8 kg. Weight Cap 100 kg. Shipping Dimensions 35" L x 30" H x 12" W
Nathan Goodyear

PLOS ONE: Increased Risk of Non-Fatal Myocardial Infarction Following Testosterone Ther... - 0 views

  • For all TT prescription subjects combined, the post/pre prescription rate ratio for MI (RR)was 1.36
  • In men aged 65 years and older the RR was 2.19 (1.27, 3.77), while in men under age 65 years the RR was 1.17
  • increasing RR with increasing age.
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  • The RRs were 0.95 (0.54, 1.67) under 55 years
  • 1.35 (0.77, 2.38) at 55–59
  • 1.29 (0.71, 2.35) at 60–64,
  • 1.35 (0.44, 4.18) at 65–69, 1.62
  • 3.43 (1.54, 7.66) at 75 years and older
  • The adjusted post/pre RR for PDE5I across all ages was 1.08
  • For TT prescription, in men under age 65 years, the RR was 2.90 (1.49, 5.62) for those with a history of heart disease and 0.90 (0.61, 1.34) for those without
  • In men aged 65 year and older, the RR was 2.16 (0.92, 5.10) for those with a history of heart disease and 2.21 (1.09, 4.45) for those without.
  • Among men aged 65 years and older, we observed a two-fold increase in the risk of MI in the 90 days after filling an initial TT prescription
  • Among younger men with a history of heart disease, we observed a two to three-fold increased risk of MI in the 90 days following an initial TT prescription and no excess risk in younger men without such a history
  • Among older men, the two-fold increased risk was associated with TT prescription regardless of cardiovascular disease history
  • our own findings appear consistent with a higher frequency of thrombotic events following TT prescription among men with more extensive coronary vascular disease.
  • Our findings are consistent with a recent meta-analysis of placebo-controlled randomized trials of testosterone therapy lasting 12 or more weeks among mainly older men, which reported that testosterone therapy increased the risk of adverse cardiovascular-related events (OR = 1.54, 95%CI:1.09, 2.18), as well as serious adverse cardiovascular-related events (OR = 1.61, 95%CI:1.01, 2.56) which included myocardial infarction along with other conditions
  • This association appeared unrelated to average baseline testosterone level (p = 0.70) but varied by source of funding (p = 0.03), with a stronger summary effect in a meta-analysis of studies not funded by the pharmaceutical industry (OR = 2.06, 95%CI:1.34, 3.17) compared with studies funded by the pharmaceutical industry
    • Nathan Goodyear
       
      This supports prior analysis that studies done by pharmaceutical corps will be more favorable to their product(s) than those independently funded.  This is called bias.
  • the evidence supports an association between testosterone therapy and risk of serious, adverse cardiovascular-related events–including non-fatal myocardial infarction–in men
  • there is some evidence that low endogenous testosterone levels may also be positively associated with cardiovascular events
  • effects of endogenous and exogenous testosterone may differ. Exogenous testosterone (TT) is associated with physiologic changes that predispose to clotting and thrombotic disorders including increased blood pressure [18], polycythemia [19], reductions in HDL cholesterol [18], [20], and hyperviscosity of the blood and platelet aggregation. [20]–[23]; TT also increases circulating estrogens [24], [25] which may play a role in the observed excess of adverse cardiovascular-related events, given that estrogen therapy has been associated with this excess in both men and women
  • did not include information on the serologic or diagnostic indications for treatment.
  • no association between PDE5I prescriptions and the risk of MI
  • Recently TT has been increasing extraordinarily rapidly, including among younger men and among those without hormone measurement
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    New cohort study finds increased risk of Testosterone in men > 65 and those : these are based in marketing-based medicine not evidence based medicine.
Nathan Goodyear

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

  • 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
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  • 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 [
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    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Nutrapharmacology of Tocotrienols for Metabol... [Curr Pharm Des. 2011] - PubMed - NCBI - 0 views

  • This review evaluates the effects of tocotrienols on the risk factors of metabolic syndrome using data from human, animal and in vitro studies. Tocotrienols improved lipid profiles and reduced atherosclerotic lesions, decreased blood glucose and glycated hemoglobin concentrations, normalized blood pressure, and inhibited adipogenesis.
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    Tocotrienols, vitamin E, shown to improve metabolic syndrome risk factors.
Nathan Goodyear

Association between Blood Pressure and Serum Thyroid-Stimulating Hormone Conc... - 0 views

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    subclinical hypothyroidism associated with elevated B/P and cardiovascular disease
wheelchairindia9

Functional Knee Support - 0 views

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    Tynor Functional Knee Support Functional knee Support is an anterior opening device, which offers the advantage of controlled compression around the knee and a rigid lateral support and immobilization. It allows normal flexion and free movement of the knee joint. Anterio Open able Easy application Controlled compression. Perfect lateral splinting. Anatomical design. Tynor Functional Knee Support Features Bi axial heavy duty aluminum hinge Mimics the natural knee joint Ensures full weight bearing. Allows free flexion movement Four way stretchable fabric Controlled and comfortable compression No buckling No vaso constriction Enhanced comfort Open patella design Release patellar pressure Hold the patella in position Can be used for Patellofemoral diseases Wrap design with anterior closing Easy application and removal on swollen or asymmetric knees Easy application and removal for weak or geriatric patients. Allows customized compression Offers flexibility in sizing Ergonomic design Anti tourniquet effect - ensures no constriction to blood flow Better grip of the product to the body. Anatomic construction- Better functionality and Snug fit.
Nathan Goodyear

Lifestyle modification increases serum testosterone level and decrease central blood pr... - 0 views

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    study finds aerobic exercise increased Testosterone levels in obese men.
Nathan Goodyear

Chronic antioxidant treatment improves arterial renovascular hypertension and oxidative... - 0 views

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    animal study finds vitamin C improves hypertension via renovascular source and oxidative stress.  The dosage was 150 mg/kg/day.  This would be equivalent to 10,800 grams daily for a 72 human.  But what about a 200 lb male or female?  That would be 13,650 grams of vitamin C daily.
Nathan Goodyear

Amino Acid Intake Is Inversely Associated with Arterial Stiffness and Central Blood Pre... - 0 views

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    Select amino acids found to be cardioprotective.
Nathan Goodyear

Hypertension - 0 views

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    low vitamin D levels have been shown to be associated with hypertension. 
Nathan Goodyear

Relationship between endogenous testosterone and cardiovascular risk in early postmenop... - 0 views

  • Body mass index and waist circumference were significantly higher in the group with testosterone levels
  • Median CRP levels were greater in the group with higher testosterone level
  • ET-1 levels were also higher in women with greater testosterone levels
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  • An association of testosterone with CRP (r = 0.416, P = .004) and ET-1 (r = 0.323, P = .031) was observed
  • Testosterone was also associated with waist circumference and blood pressure (P = .001)
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    testosterone associated with elevated CRP, increase BMI, and increased waist circumference in early, post-menopausal women.
Nathan Goodyear

Endogenous sex hormones and cardiovascular disease in men. A prospective population-bas... - 0 views

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    This study found that Testosterone levels were inversely associated with hypertension, fasting glucose, triglycerides, and BMI.
Nathan Goodyear

Sex hormones and hemostatic risk factors for cor... [J Hypertens. 1993] - PubMed - NCBI - 0 views

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    Testosterone inversely associated with increased cardiovascular risk in men--hypertension in this study.
Nathan Goodyear

Insulin and Sympathoexcitation: It Is Not All in Your Head - 0 views

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    Insulin has a stimulatory effect on the sympathetic system resulting in elevated B/P.  There is a movement by some to put every diabetic on insulin early.  This is seriously flawed and will only contribute to further complications.
Nathan Goodyear

Effects of Allium sativum (Garlic) on systol... [Pak J Pharm Sci. 2013] - PubMed - NCBI - 0 views

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    Head to head study of garlic versus atenolol shows that garlic is as good and better, depending on the dose, then atenolol.
Nathan Goodyear

Hypogonadism and Metabolic Syndrome in Nigerian Male Patients With Both Type 2 Diabetes... - 0 views

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    Asian study finds Testosterone is inversely associated with increased central obesity, increased dyslipidemia, and metabolic syndrome in me with new diagnosis of type II diabetes and hypertension.  Men with metabolic syndrome, type II diabetes, and CVD must have appropriate hormone evaluation.
Nathan Goodyear

Metabolic Effects of Liothyronine Therapy in Hypothyroidism: A Randomized, Double-Blind... - 0 views

  • tissue euthyroidism is the net result of multiple steps including conversion of the prohormone T4 into its active metabolite T3, which is ultimately responsible for signaling at the end-organ target level
  • The circulating and intracellular pools of T3 of treated hypothyroid patients (i.e. devoid of endogenous TH production) depend entirely on the conversion of exogenous l-T4 into T3
  • TH is the major regulator of basal metabolic rate
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  • The substitution of l-T3 for l-T4 caused a significant weight loss
  • The substitution of l-T3 for l-T4 caused a significant reduction in lipid parameters
  • TH action is increased in the liver, and the SHBG increase supports this hypothesis
  • The changes in serum lipid metabolism parameters are similar to the effects observed with drugs approved for the treatment of dyslipidemia
  • This differential response appears to be limited to the lipid metabolism and SHBG, whereas no differences in indices of insulin resistance were detected. This is remarkable because hyperthyroid states are associated with an increase in hepatic gluconeogenesis (37), and overt thyrotoxicosis is a known cause of secondary diabetes.
  • Despite the increase in serum T3, the l-T3 treatment did not cause major changes in cardiovascular or musculoskeletal function, as indicated by the echocardiographic and maximal exercise tolerance tests and DXA studies.
  • Similarly, no significant differences were observed in blood pressure, heart rate, or endothelial vascular function
  • In conclusion, the results of this pharmacology, proof-of-concept study indicate that replacement therapy of hypothyroidism with l-T3, compared with l-T4 causes weight loss and favorable changes in the lipid profile without appreciable side effects
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    Crossover study finds T3 versus T4 results in more weight loss, improved lipid management and increased SHBG without any adverse cardiovascular effects.   The T3 was dosed 3 x daily due to its short half life compared to T4.
Nathan Goodyear

The independent effects of eicosapentaenoic acid a... [Curr Opin Clin Nutr Metab Care. ... - 0 views

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    Omega-3, DHA, is equal or better than EPA in cardiovascular health
Nathan Goodyear

Effects of myo-inositol supplementation in postmen... [Menopause. 2011] - PubMed result - 0 views

  • Myo-inositol plus diet improved systolic and diastolic blood pressure, HOMA index, cholesterol, and triglyceride serum levels with highly significant differences,
  • Supplementation with myo-inositol may be considered a reliable option in the treatment of metabolic syndrome in postmenopausal women
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    myo-inositol proven to be a good treatment for those postmenopausal women with metabolic syndrome
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