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Tynor Ankle Brace - 0 views

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    Tynor Ankle Brace Ankle brace is designed to support, stabilize, and limit the range-of-motion of the ankle joint. In injury, or offer protection to people who are prone to ankle injuries. It uses the triple action of straps, laces and rigid lateral natomical splints to provide optimal ankle stabilization. Rigid Splinting Fits left & right. Easy to wear Controlled compression. Comfortable sung fit. Tynor Ankle Brace Features Triple stabilization Splint ensure strong immobilization Lace offers regional tightening, firm grip and good fitting. "Figure of eight Tynor Ankle Brace Measurements Measure circumference approx 2 inches above the ankle joint. Size Chart- Size Inches CM Small 7.2-8.4 18-21 Medium 8.4-9.6 21-24 Large 9.6-10.8 24-27 XL 10.8-12 27-30
wheelchairindia9

Golden Motor Electric Wheelchair - 0 views

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    Powerchairs are generally four-wheeled or six-wheeled and non-folding, however some folding designs exist and other designs may have some ability to partially dismantle for transit. Four general styles of powerchair drive systems exist: front, centre or rear wheel drive and all-wheel drive. Powered wheels are typically somewhat larger than the trailing/castoring wheels, while castoring wheels are typically larger than the castors on a manual chair. Centre wheel drive powerchairs have castors at both front and rear for a six-wheel layout. Angel Wheelchair Electric standing wheelchair Standing up, driving function by power. Head and signal light (controlled by joystick). Adjustable headrest. Adjustable footplate. Detachable backrest Rigid steel framework W/liquid coating Flip-backward armrest Max speed: 9.15KM/H Front castor: 2.80/2.50-4 pneumatic castor (9") Rear wheels: 3.00-8 pneumatic tire (14") Available seat width: A (46 cm), D (42 cm) Max loading: A size: 135 kg Net weight w/o battery: 62.7 kg A powerchairs is a wheelchair that is propelled by means of an electric motor rather than manual power. Power wheelchairs are useful for those unable to propel a manual wheelchair or who may need to use a wheelchair for distances or over terrain which would be fatiguing in a manual wheelchair. They may also be used not just by people with 'traditional' mobility impairments, but also by people with cardiovascular and fatigue based condition. An powerwheelchair powers more than just chair. It gives the power to safely travel long distances on own. It empowers to navigate through home, backyard, school, workplace or local park. It gives power to do the things,want to do. It gives power. When accidents occur that leave permanent leg injuries, or as age sets in and joint pain becomes unbearable, the power chair acts as a gateway to continue living life to the fullest. The powerwheelchairs in our lineup are all battery powered, yet each device fills
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La Creatinina 3.9 en la Enfermedad Renal es Puede Reversible - 0 views

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    La creatinia 3.9 en la enfermedad renal es puede reversible?De hecho, el alto nivel de creatinina es uno de los síntomas más comunes de la enfermedad renal, casi todos los pacientes de la enfermedad de riñón experimentará él, por lo que el tratamiento de la misma está preocupada por muchas personas.Entonces es creatinina 3.9 en la enfermedad renal crónica reversible?En caso afirmativo, cómo revertirla?
wheelchairindia9

Ultra Lightweight Wheelchairs - 0 views

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    Selection of portable travel wheelchairs, utilizing small caster wheel and lightweight materials, can tip the scale at as little as 13 lbs! Like transport chairs, travel chairs are geared towards storability and portability, but they're even more convenient for those on-the-go. These chairs feature four smaller wheels, rather than the large rear-mounted wheels that characterize standard wheelchairs, and their design ensures that they're always foldable and convenient to carry. Whether it's a family vacation, or a good ol' fashioned road trip, these lightweight wheelchairs are best bet. Lightweight travel wheelchairs give the most independence of movement with the least amount of effort. This type of wheelchair is recommended for someone who cannot self-propel in a standard wheelchair. The weight of this type wheelchair ranges from 28-34 pounds. Lightweight wheelchair is for the highly active individual as they are more easily maneuverable and durable. This type wheelchair weighs in as low as 14 pounds. This helps with ease of use and transport. Travel wheelchair assists people to become more mobile and independent. There are many different types of wheelchairs that are used for various reasons. It is important to understand the limitations and safe operation of whatever wheelchair choose or need. The travel chair seat size (width and depth), seat-to-floor height, footrests/leg rests, front caster outriggers, adjustable backrests, controls, and many other features can be customized on, or added to, many basic models, while some users, often those with specialised needs, may have wheelchairs custom-built. A single-arm drive enables the user to turn either left or right while the two-armed drive enables user to move forward or backward on a straight line. Another type of wheelchair commonly used is a lever-drive wheelchair. This type of chair enables the user to move forward by pumping the lever back and forth. Travel Wheelchairs are usually designed fo
wheelchairindia9

Transport Chair - 0 views

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    Lightweight wheelchairs provide convenience and comfort to the user and caregiver alike and are often built using materials like aluminum and titanium alloy, while foldable wheelchairs allow for easy storage and transport. Merge the two styles, and got a great mobility aid that isn't a pain to lug around. Utilizing small wheels and lighter materials, transport wheelchairs can tip the scale at as little as 19 lbs, ideal for those looking for a highly portable option. Transport chairs also tend to be more affordable and offer the benefit of increased mobility without breaking the bank. Transport wheelchairs or companion chairs are companion wheelchairs where the purpose is for a companion to push the user. Most transporters have swing-away leg rests, fixed armrests, and side panels. Instead of the usual large back - small front wheels typical of most wheelchairs, light travel chairs have four small wheels providing much easier maneuverability of the chair. Karma KM 2500 Small Wheel Wheelchair: Karma KM 2500 Small Wheel Wheelchair Specifications: Width 18" Front/Rear Wheels 6" to 14" Seat Width 47cm Seat Depth 40cm Overall Width 66cm Overall Collapsed Width 36cm Armrest Height 21cm Overall Length 90cm Seat Height 47cm Backrest Height 38cm Overall Height 86cm Weight 9.2 k.g. Karma KM 2500 Small Wheel Wheelchair Seat and Back: AEGIS Microbe Shield Approved by the FDA, EPA, EU, etc., bonded anti-microbial barrier upholstery protects from odor, staining and deterioration from bacteria, fungus and other microorganisms. It is a shield for your health. Karma KM 2500 Small Wheel Wheelchair Extended Armrest: By simulating the natural position of arms, the extended armrest design is ergonomic and creates bigger seating space. An Ultra lightweight wheelchair (9.2 kg) with a compact design for either attendant assisted or self propelling users. The use of aircraft-grade aluminium alloy and double cross brace provide this model
wheelchairindia9

Pediatric Wheelchair KM 7501 - 0 views

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    Ergonomically designed wheelchair not only for the patients but also for the assistants, both of them are considered users of this wheelchair. WheelCare has been designed to prevent work injury to the assistants by redesigned the handle, seat, hanger, rear pedals and front pedals, make them adjustable and easier to use. Tube-shaped structure allows the users to install extensional gears depends on the different needs. Ergonomic Wheelchairs with a body contouring S-Shaped seat frame and contoured armrests provides the user with all day comfort and ultimate mobility. And since this wheelchair is designed around the human body, less likely to need a seat cushion or other device to help make the wheelchair more comfortable. Ergonomics is really about using bodies safely and efficiently, in a way which doesn't strain the tissues. A way which is comfortable, While working, cooking, driving, creating or other work. Karma Wheelchair KM 7501: Karma Healthcare KM 7501 Pediatric Wheelchair is a manual wheelchair for children. It's ergonomically antelope horn-shaped handle makes it easy to steer and push the chair, and vertical footrest allow legs to be placed in the correct position. One-piece footplate increases stability. The wheelchair has a great look with a bright color and modern style. Karma Healthcare Wheelchair KM 7501 Features: Karma Healthcare Wheelchair KM-7501 Paediatric Wheelchair offers here-we-go handle Caring footrest Seat width: 11" or 13.5" Ultra lightweight and compact Outward extended front wheels 6" solid caster and 14" solid rear wheel Maximum user weight: 60Kg One Year Warranty Karma Wheelchair KM 7501 Measurements: Width 11" 13.5" Front/Rear Wheels 6" to 14" 6" to 14" Seat Width 28cm 34cm Seat Depth 30cm 30cm Overall Width 45cm 51cm Overall Collapsed Width 34cm 34cm Armrest Height 18cm 18cm Overall Length 70W 70W Seat Height 39cm 39cm Backrest Height 36cm 36cm Overall Height 102cm 102cm Weight 9.3kg 9.3kg Karma Ergo
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Cómo Reducir el Nivel Alto de Creatinina 9 - 0 views

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    Cuando nivel de creatinina sérica es más de 9, se necesitan medidas médicas para limpiar la sangre,de lo contrario, se causaron más problemas de salud. Bueno,¿cómo reducir el alto nivel de creatinina 9? Cuando nivel de creatinina sérica es más de 9, se necesitan medidas médicas para limpiar la sangre,de lo contrario, se causaron más problemas de salud.
wheelchairindia9

Pristine Flex Ostrich Mobility Wheelchair - 0 views

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    Pristine Flex Ostrich Mobility Wheelchair Pristine is the most stylish powered wheelchair with revolutionary Split Frame Chassis (SFC). This indoor outdoor mobility equipment gives great comfort, stability and safety even in the toughest outdoor conditions. The body panels and the shopping basket make this equipment best suited for your kind of lifestyle. Pristine Flex Ostrich Mobility Wheelchair Features Split Frame Chassis (SFC). Call alarm, fault alarm, reverse alarm (on request). Low voltage alarm. Key pad locking. Mobility cut-off while charging. Auto shut-off after 3 minutes. Five speed selector. Length adjustable joystick control unit (can be changed from left to right and vice versa). Foldable, height adjustable and angle adjustable foot rest. Wide arm rest with height and width adjustment. Bucket seat with headrest and lap belt. Seat can be folded for transportation. Seat reclines 25 degrees in 6 steps. Removable and width adjustable calf support. Reflectors as per standards. Head lamp. Tail lamp. Pristine Flex Ostrich Mobility Wheelchair Specifications Load capacity: 110 Kg Speed: 9.5 Kmph max Speed selection: 5 speeds, Speed 1- 1.5Kmph, Speed 2-2.5 Kmph, speed 3- 4.8 Kmph, Speed 4- 7.2 Kmph, Speed 5- 9.5 Kmph Power: 320W Motor speed: 5300 rpm Gear ratio: 32:1 Brake: Electromagnetic Permissible Gradeability: 12 Degrees Drive range: 32-35 Km Ground clearance:2.5 inches Turn circle radius: 620mm Tire: Puncture free foam filled rubber tires Front- Tire diameter: 220X55 mm, Rear- Tire diameter: 320X72mm, Anti tippers-1 inch solid Battery: 24 Volt 48 Ah Sealed Maintenance Free VRLA Charger Input-230/240 Volts AC Single phase, Output-24 Volts-4 Amps DC Overall length with footrest (at 90 degree):1180mm, Overall width:640mm, Overall height: 1250mm, Overall height after folding the seat: 690mm, Overall weight: 102 Kg Seat depth: 500mm, Seat width:480mm, Backrest height: 540mm (without head rest), Backrest width: 440mm, Se
Nathan Goodyear

Availability of evidence of benefits on overall survival and quality of life of cancer ... - 0 views

  • Although the goal of cancer treatment is to improve the quantity and quality of life,123 clinical trials designed to gain regulatory approval for new drugs often evaluate indirect or “surrogate” measures of drug efficacy. These endpoints show that an agent has biological activity, but they are not reliable surrogates for improved survival4567891011 or quality of life46111213
  • two recent systematic reviews suggest that the strength of association between surrogates in cancer clinical trials and life extension is generally low
  • Available data from the US show that only a small proportion of cancer treatments approved by the US Food and Drug Administration (FDA) unequivocally show benefits on survival or quality of life.30
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  • We sought to systematically evaluate the evidence base for all new drugs and new indications for the treatment of solid tumours and haematological malignancies approved by the EMA in the five year period 2009-13
  • Three investigators (AP, EP, and EG) independently extracted data on and descriptively analysed the following trial features: characteristics of the participant population, study design (randomisation, crossover from experimental to control group, and blinding of investigators and participants), experimental and control groups, enrolment, primary and secondary endpoints, magnitude of benefit on survival and quality of life, and narrative interpretation of the findings
  • Only 18 of the 68 (26%) were supported by a pivotal study powered to evaluate overall survival as the primary outcome
  • From 2009 to 2013, the EMA approved use of 48 oncology drugs
  • Seventeen drugs were approved for treatment of haematological malignancies and 51 for treatment of solid tumours
  • Overall, 72 clinical trials supported the approval of 68 novel drug uses
  • Our scoring was limited to drugs for solid tumours
  • Among 68 cancer drug indications approved by the EMA in the period 2009-13, and with a median of 5.4 years’ follow-up, only 35 (51%) were associated with a significant improvement in survival (26/35) or quality of life (9/35) over existing treatment options, placebo, or as add on treatment
  • Only two of the 26 drugs shown to extend life also showed benefits on quality of life
  • 33 (49%) had not shown any improvement on survival or quality of life
  • This systematic evaluation of oncology drug approvals by the EMA in 2009-13 shows that most of the drugs (39/68, 57%) entered the market without evidence of improved survival or quality of life
  • At a minimum 3.3 years after market entry, there was still no conclusive evidence that 33 of these 39 cancer drugs either extended or improved life
  • What are potential reasons for the paucity of drug approvals with demonstrable survival advantages over existing treatments?
  • Firstly, only 18 (26%) indications for use in our cohort were supported by trials in which extension of life was the primary outcome
  • None of the pivotal studies supporting oncology drug approvals from 2009 to 2013 included quality of life as a primary outcome measure
  • Most new oncology drugs authorised by the EMA in 2009-13 came onto the market without clear evidence that they improved the quality or quantity of patients’ lives
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    New study from European Medicines Agency questions alot of the new cancer drugs brought to the market 2009-2013.  57% of the new drugs (39/68) were brought to the market without evidence of improved survival or quality of life.
fitspresso

LeanBiome™ (Official) | Get Save UpTo $540 Today Only! - 0 views

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    LeanBiome™ (Official) | Get Save UpTo $540 Today Only! usleanbiome.com LeanBiome™ Hurry Up! Offer Expires in: 00 HOUR 29 MINUTE 59 SECOND LeanBiome Attention! Get Special 84% Discount Today Faster fat burning and weight loss Healthy cholesterol and sugar levels Higher energy levels Regular price: $129 Only for: 39$ What Is LeanBiome? LeanBiome Lean for Good is a weight loss dietary supplement derived from scientifically researched ingredients and comprehensively developed to help people achieve sustainable weight control. The formula comes in a capsule format that is easy to take and is made with natural ingredients from plants and other sources to achieve its goals. The main ingredient in LeanBiome is piperine, which has been found to affect the body's ability to absorb micronutrients and other compounds more effectively. LeanBiome is a dietary supplement that claims to help weight management. It contains 100% natural ingredients that support healthy weight loss. It does not interfere with any natural process making it safe for use. It ranks among the top weight loss supplements that claim to provide a permanent solution. LeanBiome is made by a company named Lean for Good. It is made with natural and research-backed ingredients that help you lose excess fat without hassles. It is sold in capsule form. The company assures the composition is GMO, gluten, and soy-free. As for manufacturing standards, you need not fret. The company makes the supplement in a facility certified by the FDA. How Does LeanBiome Work? The starting period of the LeanBiome program includes a detoxification process that effectively removes any accumulated ree radicals, toxins, fand oxidative stress. This cleansing enables improved blood circulation, setting the stage for the body to initiate its own fat-burning mechanisms. To enhance metabolic activity, introducing the lean bacteria contained in LeanBiome to your gut microbiome is a beneficial approach. This activation triggers r
vrocky

How to lose belly Fat 9 best ways | Health2day | vie2day.com - 0 views

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    Stubborn Belly fat can make your jeans feel extra snug, many can think how to lose belly fat, but really there is something way worse about in Health2day
wheelchairindia9

Abdominal Support Belt - 0 views

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    Tynor Hot and Cold Pack is a convenient device to provide hot fomentation or cold compress. Tynor Hot and Cold Pack is of multipurpose advantage. It is a convenient and effective approach for both hot as well as a cold therapy. Hot pack can be used for body ache, joint pain, etc., whereas a cold pack can be used for fever, sprains, fever, bleeding, etc. It is easy to use and maintains the temperature for a long period of time. It is available in 11.22 x 7.67 inch universal sizes. Hot fomentation of the injured or inflamed area enhances the threshold of pain and thus reduces the perception of pain. It has a synergistic effect along with pain relieving drugs. Raising temperature of the injured tissue also enhances the blood profusion and the healing process. Hot fomentation has a relaxing effect. Cold compress helps in reduction of inflammation in injuries, protects by slowing the metabolic rate around the tissue, reduce oedema and bleeding. Cold compress helps in immediately lowering fever, in very high fever conditions. It can be used after an acute injury or surgical procedure. No heat or cryo burns. Requires no holding. Reusable. Easy application. Appealing aesthetics. Tynor Hot and Cold Pack Features Multi functionality Reduce swelling and odema at the site of injury. Muscles spasm and pain. Headache and minor injuries. Versatile design Can be used as either cold or hot pack. Reusable in either hot & cold condition. Temperature range - Can be used from 0 Cº to 75Cº. Longer temperature retention time. Fabric cover ensures no cryo burns or hot skin burns. Physical features Non-toxic, and biodegradable. Gel remains soft and flexible upto 0 degree. Durable, and puncture resistant. Soft, "frost free" PVC cover. Flexible conforms to the body contours. Easy to clean and maintain. Excellent workmanship. Good aesthetics. Elastic belt Holds the pack against the body, No need to hold by hand. Enhances convenience. Tynor
Nathan Goodyear

The Androgen Derivative 5α-Androstane-3β,17β-Diol Inhibits Prostate Cancer Ce... - 0 views

  • In the early stages, prostate cancer growth is dependent on circulating androgens
    • Nathan Goodyear
       
      This is in contrast to studies that show poor prognosis with Lower T at time of diagnosis of prostate cancer
  • 5α-reductase not only provides a potent amplification of the androgenic signal ( 4– 6), but it also prevents estrogen formation by subtracting testosterone from the action of aromatase ( 7, 8), thus blocking activation of the estrogen receptor subtypes (ERα and ERβ; refs. 9, 10)
  • ERβ is the prevailing subtype ( 11), and a growing body of evidence points to the protective role of this receptor in prostate cancer
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  • It has been shown that the transformation of the dihydrotestosterone to 5α-androstane-3α,17β-diol (3α-diol) and 5α-androstane-3β,17β-diol (3β-Adiol), generates two metabolites unable to bind the androgen receptor, but possessing a very high affinity for the estrogen receptors
  • the effects of testosterone may result from the balance between the androgenic and the estrogenic molecules originating from its catabolism.
  • Recent data have been published postulating a direct estrogenic role of the 3β-hydroxylated derivatives of dihydrotestosterone in the prostate development and homeostasis
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    Here is the full article.
Nathan Goodyear

Testosterone Deficiency, Cardiac Health, and Older Men - 0 views

  • Studies have shown pharmacological doses of testosterone to relax coronary arteries when injected intraluminally [39] and to produce modest but consistent improvement in exercise-induced angina and reverse associated ECG changes [40]. The mechanism of action is via blockade of calcium channels with effect of similar magnitude to nifedipine
    • Nathan Goodyear
       
      This directly refutes the recent studies (3) that Testosterone therapy increases cardiovascular events.
    • Nathan Goodyear
       
      Testosterone acts as a calcium channel blocker inducing vasodilation.
  • men with chronic stable angina pectoris, the ischaemic threshold increased after 4 weeks of TRT and a recent study demonstrates improvement continuing beyond 12 months [
  • Exercise capacity in men with chronic heart failure increased after 12 weeks
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  • Studies have shown an inverse relationship between serum testosterone and fasting blood glucose and insulin levels
  • Medications such as chronic analgesics, anticonvulsants, 5ARIs, and androgen ablation therapy are associated with increased risk of testosterone deficiency and insulin resistance
  • Women with T2D or metabolic syndrome characteristically have low SHBG and high free testosterone
    • Nathan Goodyear
       
      This stands in polar opposite of that with men.
  • Hypogonadism is a common feature of the metabolic syndrome
  • The precise interaction between insulin resistance, visceral adiposity, and hypogonadism is, as yet, unclear but the important mechanisms are through increased aromatase production, raised leptin levels, and increase in inflammatory kinins
  • levels of testosterone are reduced in proportion to degree of obesity
  • Men should be encouraged to combine aerobic exercise with strength training. As muscle increases, glucose will be burned more efficiently and insulin levels will fall. A minimum of 30 minutes exercise three times weekly should be advised
  • Testosterone increases levels of fast-twitch muscle fibres
  • By increasing testosterone, levels of type 2 fibres increase and glucose burning improves
  • Weight loss will increase levels of testosterone
  • studies now clearly show that low testosterone leads to visceral obesity and metabolic syndrome and is also a consequence of obesity
  • In the case of MMAS [43], a baseline total testosterone of less than 10.4 nmol/L was associated with a greater than 4-fold incidence of type 2 diabetes over the next 9 years
  • There is high level evidence that TRT improves insulin resistance
  • Low testosterone predicts increased mortality and testosterone therapy improves survival in 587 men with type 2 diabetes
  • A similar retrospective US study involved 1031 men with 372 on TRT. The cumulative mortality was 21% in the untreated group versus 10% ( ) in the treated group with the greatest effect in younger men and those with type 2 diabetes
  • the presence of ED has been shown to be an independent risk factor, particularly in hypogonadal men, increasing the risk of cardiac events by over 50%
  • A recent online publication on ischaemic heart disease mortality in men concluded optimal androgen levels are a biomarker for survival
  • inverse associations between low TT or FT (Table 2) and the severity of CAD
  • A recent 10 year study from Western Australia involving 3690 men followed up from 2001–2010 concluded that TT and FT levels in the normal range were associated with decreased all-cause and cardiovascular mortality, for the first time suggesting that both low and DHT are associated with all-cause mortality and higher levels of DHT reduced cardiovascular risk
  • TDS is associated with increased cardiovascular and all-cause mortality
  • The effect of treatment with TRT reduced the mortality rate of treated cohort (8.4%) to that of the eugonadal group whereas the mortality for the untreated remained high at 19.2%
  • hypogonadal men had slightly increased triglycerides and HDL
  • Men with angiographically proven CAD (coronary artery disease) have significantly lower testosterone levels [29] compared to controls ( ) and there was a significant inverse relationship between the degree of CAD and TT (total testosterone) levels
  • TRT has also been shown to reduce fibrinogen to levels similar to fibrates
  • men treated with long acting testosterone showed highly significant reductions in TC, LDL, and triglycerides with increase in HDL, associated with significant reduction in weight, BMI, and visceral fat
  • Low androgen levels are associated with an increase in inflammatory markers
  • In the Moscow study, C-reactive protein was reduced by TRT at 30 weeks versus placebo
  • In some studies, a decline in diastolic blood pressure has been observed, after 3–9 months [24, 26] and in systolic blood pressure
  • A decline was noted in IL6 and TNF-alpha
  • No studies to date show an increase in LUTS/BPH symptoms with higher serum testosterone levels
  • TRT has been shown to upregulate PDE5 [65] and enhance the effect of PDE5Is (now an accepted therapy for both ED and LUTS), it no longer seems logical to advice avoidance of TRT in men with mild to moderate BPH.
    • Nathan Goodyear
       
      What about just starting with normalization of Testosterone levels first.
  • Several meta-analyses have failed to show a link between TRT and development of prostate cancer [66] but some studies have shown a tendency for more aggressive prostate cancer in men with low testosterone
    • Nathan Goodyear
       
      And if one would have looked at their estrogen levels, I guarantee they would have been found to be elevated.
  • low bioavailable testosterone and high SHBG were associated with a 4.9- and 3.2-fold risk of positive biopsy
  • Current EAU, ISSAM, and BSSM guidance [1, 2] is that there is “no evidence TRT is associated with increased risk of prostate cancer or activation of subclinical cancer.”
  • Men with prostate cancer, treated with androgen deprivation, develop an increase of fat mass with an altered lipid profile
  • Erectile dysfunction is an established marker for future cardiovascular risk and the major presenting symptom leading to a diagnosis of low testosterone
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Cuáles son las Posibilidades de Recuperar la Insuficiencia Renal con Creatini... - 0 views

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    "Soy un paciente con insuficiencia renal con creatinina de 5.9 y quiero saber cuáles son las posibilidades de recuperación de la misma."De hecho, para esta cuestión las posibilidades de recuperación depende principalmente en el tratamiento que el paciente elija.Con el tratamiento adecuado, la insuficiencia renal con creatinina 5.9 puede tener más de la mitad de posibilidades de conseguir la recuperación,a pesar de que no pueden revertir la enfermedad por completo, sino que también pueden vivir como una persona normal y vivir con esta enfermedad durante mucho tiempo.
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Tiene Creatinina 9.1 Significa Insuficiencia Renal - 0 views

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    Se sabe que el nivel de creatinina alta significa trastorno renal, y cuanto mayor sea el nivel de creatinina, la gravedad de la condición de enfermedad es.Sin embargo, para uno con nivel de creatinina sérica 9.1, es lo que significa la insuficiencia renal?
Nathan Goodyear

European Journal of Clinical Nutrition - Effect of maternal n-3 long-chain polyunsatura... - 0 views

  • It is estimated that approximately 30% of children and adolescents in the United States and about 15–30% of those in Europe can be classified as overweight or obese
  • An increasing body of evidence now suggests that the nutritional environment encountered in utero and the early postnatal life may elicit permanent alterations in adipose tissue structure or function and, thereby, programme the individual’s propensity to later obesity
  • The composition of fatty acids in the Western diets has shifted toward an increasing dominance of n-6 relative to n-3 LCPUFAs over the past decades.9,10 This shift is also reflected in the fatty acid composition of breast milk
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  • Evidence from animal studies suggests that the n-6 LCPUFA arachidonic acid promotes adipose tissue deposition, whereas the n-3 LCPUFAs eicosapentaenoic acid and docosahexaenoic acid seem to exert an opposite effect
  • Overall, no effect of supplementation was found on BMI in preschool (<5 years) and school-aged (6–12 years) children
  • increased adiposity, once established in childhood, tends to track into adulthood
  • Many studies have shown that even children <2 years with a high BMI are at increased risk of developing obesity later in life
  • The acquisition of fat cells early in life appears to be an irreversible process
  • Evidence from cell culture and animal studies suggests that early exposure to n-3 LCPUFAs has the potential to limit adipose tissue deposition mainly by attenuating the production of the arachidonic acid metabolite prostacyclin, which has been shown to enhance adipogenesis
  • In conclusion, there is currently no evidence to support that maternal n-3 LCPUFA supplementation during pregnancy and/or lactation exerts a favourable programming effect on adiposity status in childhood
  • our systematic review highlights that most of the trials reviewed were prone to methodological limitations
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    Literature review finds limited data (9 studies, only 6 RCTs) of omega-3 during pregnancy.  No data was found that supported reduced obesity in children by mothers taking n-3 during pregnancy.  No harm was found either.  Data was sparse.   Take home: not enough data, no harm to pregnancy, children, thus if indications are present for mother, then recommend n-3.  At this point not studies have pointed to reduced obesity in children.
Nathan Goodyear

Anemia in cancer - 0 views

  • Anemia is a frequent finding in cancer patients, occurring in >40% of cases
  • chemotherapy, the incidence of anemia may rise to 90%
  • Anemia exerts a negative influence on the quality of life
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  • Anemia has also been identified as an adverse prognostic factor
  • mild (10 g/dl—normal), moderate (8–10 g/dl), severe (6.5–8 g/dl) and life threatening (<6.5 g/dl or unstable patient) anemia
  • anemia in cancer patients is often multifactorial.
  • Cancer itself can directly cause or exacerbate anemia either by suppressing hematopoiesis through bone marrow infiltration or production of cytokines that lead to iron sequestration, or by reduced red blood cell production
  • in inflammatory anemia, iron deficiency should be defined by a low transferrin saturation of <20%, ferritin levels of <100 ng/ml and a low reticulocyte hemoglobin concentration of <32 pg
  • anemia to thrombocytosis, as commonly seen in cancer patients
  • TNF-α inhibits hemoglobin production
  • treatment itself may be a major cause of anemia
  • Other cytokines, such as interleukin-6 (IL-6), IL-1 and interferon-γ, have also been shown to inhibit erythroid precursors in vitro [9], albeit to a lesser extent
  • In inflammation, from whatever cause, IL-6 induces the liver to produce hepcidin. Hepcidin decreases iron absorption from the bowel and blocks iron utilization in the bone marrow
  • Numerous in vitro studies have illustrated the central role of TNF-α in the pathogenesis of anemia
  • nephrotoxic effects of particular cytotoxic agents such as platinum salts can also lead to the persistence of anemia through reduced Epo production by the kidney
  • Currently two options are at the disposal of the clinician for the treatment of anemia in cancer patients: transfusion of packed red blood cells and the use of erythropoiesis-stimulating agents (ESAs)
  • The goal of the treatment is to relieve the symptoms of anemia such as fatigue and dyspnea.
  • Transfusion of 1 unit of packed red blood cells has been estimated to result in an increase in the hemoglobin level of 1 g/dl in a normal-sized adult
  • a higher mortality rate in patients receiving ESA treatment
  • Recent concerns regarding the risk of thromboembolism in patients treated with ESA have been corroborated by the meta-analyses conducted by Tonnelli and Bennett
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    Great review of anemia in Cancer:  1)  blood loss 2)  increased RBC loss 3)   decreased RBC production Cancer infiltration of marrow can reduce hematopoiesis.  Inflammatory cytokines can reduce hematopoiesis.  Inflammatory cytokines can block Fe absorption.  Chemo and radiation can cause anemia--particularily platinum based therapies.
Nathan Goodyear

Induction of metastasis, cancer stem cell phenotype, and oncogenic metabolism in cancer... - 0 views

  • More than half of cancer patients are treated with IR at some point during their treatment
  • fractionation schedule is the delivery of 1.8–2.0 Gy per day, five days per week
  • Nuclear DNA is the primary target of IR; it causes DNA damage (genotoxic stress) by direct DNA ionization
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  • IR also indirectly induces DNA damage by stimulating reactive oxygen species (ROS) production
  • IR is known to induce EMT in vitro
  • p53 is activated in response to IR-induced DNA damage
  • IR paradoxically also promotes tumour recurrence and metastasis
  • DNA double-strand breaks (DSBs)
  • cancer cells undergoing EMT acquire invasive and metastatic properties
  • changes in the tumour microenvironment (TME)
  • IR seems to induce EMT and CSC phenotypes by regulating cellular metabolism
  • EMT, stemness, and oncogenic metabolism are known to be associated with resistance to radiotherapy and chemotherapy
  • Hanahan and Weinberg proposed ten hallmarks of cancer that alter cell physiology to enhance malignant growth: 1) sustained proliferation, 2) evasion of growth suppression, 3) cell death resistance, 4) replicative immortality, 5) evasion of immune destruction, 6) tumour-promoting inflammation, 7) activation of invasion and metastasis, 8) induction of angiogenesis, 9) genome instability, and 10) alteration of metabolism
  • EMT is a developmental process that plays critical roles in embryogenesis, wound healing, and organ fibrosis
  • IR is known to induce stemness and metabolic alterations in cancer cells
  • transforming growth factor-β [TGF-β], epidermal growth factor [EGF]) and their associated signalling proteins (Wnt, Notch, Hedgehog, nuclear-factor kappa B [NF-κB], extracellular signal-regulated kinase [ERK], and phosphatidylinositol 3-kinase [PI3K]/Akt
  • activate EMT-inducing transcription factors, including Snail/Slug, ZEB1/δEF1, ZEB2/SIP1, Twist1/2, and E12/E47
  • Loss of E-cadherin is considered a hallmark of EMT
  • IR has been shown to induce EMT to enhance the motility and invasiveness of several cancer cells, including those of breast, lung, and liver cancer, and glioma cells
  • IR may increase metastasis in both the primary tumour site and in normal tissues under some circumstance
  • sublethal doses of IR have been shown to enhance the migratory and invasive behaviours of glioma cells
  • ROS are known to play an important role in IR-induced EMT
  • High levels of ROS trigger cell death by causing irreversible damage to cellular components such as proteins, nucleic acids, and lipids, whereas low levels of ROS have been shown to promote tumour progression—including tumour growth, invasion, and metastasis
  • hypoxia-inducible factor-1 (HIF-1) is involved in IR-induced EMT
  • Treatment with the N-acetylcysteine (NAC), a general ROS scavenger, prevents IR-induced EMT, adhesive affinity, and invasion of breast cancer cells
    • Nathan Goodyear
       
      NAC for all patients receiving radiation therapy
  • Snail has been shown to play a crucial role in IR-induced EMT, migration, and invasion
  • IR activates the p38 MAPK pathway, which contributes to the induction of Snail expression to promote EMT and invasion
  • NF-κB signalling that promotes cell migration
  • ROS promote EMT to allow cancer cells to avoid hostile environments
  • HIF-1 is a heterodimer composed of an oxygen-sensitive α subunit and a constitutively expressed β subunit.
  • Under normoxia, HIF-1α is rapidly degraded, whereas hypoxia induces stabilisation and accumulation of HIF-1α
  • levels of HIF-1α mRNA are enhanced by activation of the PI3K/Akt/mammalian target of rapamycin (mTOR)
  • IR is known to increase stabilisation and nuclear accumulation of HIF-1α, since hypoxia is a major condition for HIF-1 activation
  • IR induces vascular damage that causes hypoxia
  • ROS is implicated in IR-induced HIF-1 activation
  • IR causes the reoxygenation of hypoxic cancer cells to increase ROS production, which leads to the stabilisation and nuclear accumulation of HIF-1
  • IR increases glucose availability under reoxygenated conditions that promote HIF-1α translation by activating the Akt/mTOR pathway
  • The stabilised HIF-1α then translocates to the nucleus, dimerizes with HIF-1β, and increases gene expression— including the expression of essential EMT regulators such as Snail—to induce EMT, migration, and invasion
  • TGF-β signalling has been shown to play a crucial role in IR-induced EMT
  • AP-1 transcription factor is involved in IR-induced TGF-β1 expression
  • Wnt/β-catenin signalling is also implicated in IR-induced EMT
  • Notch signalling is known to be involved in IR-induced EMT
  • IR also increases Notch-1 expression [99]. Notch-1 is known to induce EMT by upregulating Snail
  • PAI-1 signalling is also implicated in IR-induced Akt activation that increases Snail levels to induce EMT
  • EGFR activation is known to be associated with IR-induced EMT, cell migration, and invasion by activating two downstream pathways: PI3K/Akt and Raf/MEK/ERK
  • ROS and RNS are also implicated in IR-induced EGFR activation
  • IR has also been shown to activate Hedgehog (Hh) signalling to induce EMT
  • IR has been shown to induce Akt activation through several signalling pathways (EGFR, C-X-C chemokine receptor type 4 [CXCR4]/C-X-C motif chemokine 12 [CXCL12], plasminogen activator inhibitor 1 [PAI-1]) and upstream regulators (Bmi1, PTEN) that promote EMT and invasion
  • CSCs possess a capacity for self-renewal, and they can persistently proliferate to initiate tumours upon serial transplantation, thus enabling them to maintain the whole tumour
  • Conventional cancer treatments kill most cancer cells, but CSCs survive due to their resistance to therapy, eventually leading to tumour relapse and metastasis
  • identification of CSCs, three types of markers are utilised: cell surface molecules, transcription factors, and signalling pathway molecules
  • CSCs express distinct and specific surface markers; commonly used ones are CD24, CD34, CD38, CD44, CD90, CD133, and ALDH
  • Transcription factors, including Oct4, Sox2, Nanog, c-Myc, and Klf4,
  • signalling pathways, including those of TGF-β, Wnt, Hedgehog, Notch, platelet-derived growth factor receptor (PDGFR), and JAK/STAT
  • microRNAs (miRNAs), including let-7, miR-22, miR-34a, miR-128, the miR-200 family, and miR-451
  • Non-CSCs can be reprogrammed to become CSCs by epigenetic and genetic changes
  • EMT-inducing transcription factors, such as Snail, ZEB1, and Twist1, are known to confer CSC properties
  • Signalling pathways involved in EMT, including those of TGF-β, Wnt, and Notch, have been shown to play important roles in inducing the CSC phenotype
  • TGF-β1 not only increases EMT markers (Slug, Twist1, β-catenin, N-cadherin), but also upregulates CSC markers (Oct4, Sox2, Nanog, Klf4) in breast and lung cancer cells
  • some CSC subpopulations arise independently of EMT
  • IR has been shown to induce the CSC phenotype in many cancers, including breast, lung, and prostate cancers, as well as melanoma
  • Genotoxic stress due to IR or chemotherapy promotes a CSC-like phenotype by increasing ROS production
  • IR has been shown to induce reprogramming of differentiated cancer cells into CSCs
  • In prostate cancer patients, radiotherapy increases the CD44+ cell population that exhibit CSC properties
  • IR also induces the re-expression of stem cell regulators, such as Sox2, Oct4, Nanog, and Klf4, to promote stemness in cancer cells
  • EMT-inducing transcription factors and signalling pathways, including Snail, STAT3, Notch signalling, the PI3K/Akt pathway, and the MAPK cascade, have been shown to play important roles in IR-induced CSC properties
  • STAT3 directly binds to the Snail promoter and increases Snail transcription, which induces the EMT and CSC phenotypes, in cisplatin-selected resistant cells
  • Other oncogenic metabolic pathways, including glutamine metabolism, the pentose phosphate pathway (PPP), and synthesis of fatty acids and cholesterol, are also enhanced in many cancers
  • metabolic reprogramming
  • HIF-1α, p53, and c-Myc, are known to contribute to oncogenic metabolism
  • metabolic reprogramming
  • tumour cells exhibit high mitochondrial metabolism as well as aerobic glycolysis
  • occurring within the same tumour
  • CSCs can be highly glycolytic-dependent or oxidative phosphorylation (OXPHOS)-dependen
  • mitochondrial function is crucial for maintaining CSC functionality
  • cancer cells depend on mitochondrial metabolism and increase mitochondrial production of ROS that cause pseudo-hypoxia
  • HIF-1 then enhances glycolysis
  • CAFs have defective mitochondria that lead to the cells exhibiting the Warburg effect; the cells take up glucose, and then secrete lactate to 'feed' adjacent cancer cells
  • lactate transporter, monocarboxylate transporter (MCT)
  • nutrient microenvironment
  • Epithelial cancer cells express MCT1, while CAFs express MCT4. MCT4-positive, hypoxic CAFs secrete lactate by aerobic glycolysis, and MCT1-expressing epithelial cancer cells then uptake and use that lactate as a substrate for the tricarboxylic acid (TCA) cycle
  • MCT4-positive cancer cells depend on glycolysis and then efflux lactate, while MCT1-positive cells uptake lactate and rely on OXPHOS
  • metabolic heterogeneity induces a lactate shuttle between hypoxic/glycolytic cells and oxidative/aerobic tumour cells
  • bulk tumour cells exhibit a glycolytic phenotype, with increased conversion of glucose to lactate (and enhanced lactate efflux through MCT4), CSC subsets depend on oxidative phosphorylation; most of the glucose entering the cells is converted to pyruvate to fuel the TCA cycle and the electron transport chain (ETC), thereby increasing mitochondrial ROS production
  • the major fraction of glucose is directed into the pentose phosphate pathway, to produce redox power through the generation of NADPH and ROS scavengers
  • HIF-1α, p53, and c-Myc, are known to contribute to oncogenic metabolism
  • regulatory molecules involved in EMT and CSCs, including Snail, Dlx-2, HIF-1, STAT3, TGF-β, Wnt, and Akt, are implicated in the metabolic reprogramming of cancer cells
  • HIF-1 induces the expression of glycolytic enzymes, including the glucose transporter GLUT, hexokinase, lactate dehydrogenase (LDH), and MCT, resulting in the glycolytic switch
  • HIF-1 represses the expression of pyruvate dehydrogenase kinase (PDK), which inhibits pyruvate dehydrogenase (PDH), thereby inhibiting mitochondrial activity
  • STAT3 has been implicated in EMT-induced metabolic changes as well
  • TGF-β and Wnt play important roles in the metabolic alteration of cancer cells
  • Akt is also implicated in the glycolytic switch and in promoting cancer cell invasiveness
  • EMT, invasion, metastasis, and stemness
  • pyruvate kinase M2 (PKM2), LDH, and pyruvate carboxylase (PC), are implicated in the induction of the EMT and CSC phenotypes
  • decreased activity of PKM2 is known to promote an overall shift in metabolism to aerobic glycolysis
  • LDH catalyses the bidirectional conversion of lactate to pyruvate
  • High levels of LDHA are positively correlated with the expression of EMT and CSC markers
  • IR has been shown to induce metabolic changes in cancer cells
  • IR enhances glycolysis by upregulating GAPDH (a glycolysis enzyme), and it increases lactate production by activating LDHA, which converts pyruvate to lactate
  • IR enhances glycolysis by upregulating GAPDH (a glycolysis enzyme), and it increases lactate production by activating LDHA, which converts pyruvate to lactate
  • IR also elevates MCT1 expression that exports lactate into the extracellular environment, leading to acidification of the tumour microenvironment
  • IR increases intracellular glucose, glucose 6-phosphate, fructose, and products of pyruvate (lactate and alanine), suggesting a role for IR in the upregulation of cytosolic aerobic glycolysis
  • Lactate can activate latent TGF-
  • lactate stimulates cell migration and enhances secretion of hyaluronan from CAF that promote tumour metastasis
  • promote tumour survival, growth, invasion, and metastasis; enhance the stiffness of the ECM; contribute to angiogenesis; and induce inflammation by releasing several growth factors and cytokines (TGF-β, VEGF, hepatocyte growth factor [HGF], PDGF, and stromal cell-derived factor 1 [SDF1]), as well as MMP
  • tumours recruit the host tissue’s blood vessel network to perform four mechanisms: angiogenesis (formation of new vessels), vasculogenesis (de novo formation of blood vessels from endothelial precursor cells), co-option, and modification of existing vessels within tissues.
  • immunosuppressive cells such as tumour-associated macrophages (TAM), MDSCs, and regulatory T cells, and the immunosuppressive cytokines, TGF-β and interleukin-10 (IL-10)
  • immunosuppressive cells such as tumour-associated macrophages (TAM), MDSCs, and regulatory T cells, and the immunosuppressive cytokines, TGF-β and interleukin-10 (IL-10)
  • intrinsic immunogenicity or induce tolerance
  • cancer immunoediting’
  • three phases: 1) elimination, 2) equilibrium, and 3) escape.
  • The third phase, tumour escape, is mediated by antigen loss, immunosuppressive cells (TAM, MDSCs, and regulatory T cells), and immunosuppressive cytokines (TGF-β and IL-10).
  • IR can elicit various changes in the TME, such as CAF activity-mediated ECM remodelling and fibrosis, cycling hypoxia, and an inflammatory response
  • IR activates CAFs to promote the release of growth factors and ECM modulators, including TGF-β and MMP
  • TGF-β directly influences tumour cells and CAFs, promotes tumour immune escape, and activates HIF-1 signalling
    • Nathan Goodyear
       
      And now the receipts
  • MMPs degrade ECM that facilitates angiogenesis, tumour cell invasion, and metastasis
    • Nathan Goodyear
       
      Receipts and mechanisms
  • IR also promotes MMP-2/9 activation in cancer cells to promote EMT, invasion, and metastasis
  • IR-induced Snail increases MMP-2 expression to promote EMT
  • Radiotherapy has the paradoxical side-effect of increasing tumour aggressiveness
  • IR promotes ROS production in cancer cells, which may induce the activation of oncogenes and the inactivation of tumour suppressors, which further promote oncogenic metabolism
  • Metabolic alterations
  • oncogenic metabolism
  • elicit various changes in the TME
  • Although IR activates an antitumour immune response, this signalling is frequently suppressed by tumour escape mechanisms
  •  
    Important review article.
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