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Enfermedad de Riñón con Nivel de Creatinina 3.5 Hay Algún Medicina Natural Pu... - 0 views

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    Enfermedad de Riñón con Nivel de Creatinina 3.5 Hay Algún Medicina Natural Puede TratarTengo un amigo que tiene un alto nivel de creatinina y en la actualidad en torno a 3.5. Existe algún medicamento a base de hierbas puede controlar el alto nivel de creatinina y tratar esta enfermedad?Como todos sabemos el nivel de creatinina es uno de los indicadores de la enfermedad renal, generalmente el más alto es el nivel de creatinina es la más grave es la enfermedad.En la clínica, creatinina 3.5 debe ser en la etapa 3, que se conoce como la etapa muy crucial.
wheelchairindia9

Pride Go Chair - 0 views

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    Pride Go Chair The Go-Chair is the first travel chair that combines super portability, maneuverability and style at a low cost. Pride Go Chair Features Easy to remove battery pack and compact, lightweight frame. Twin motors for traction and precision handling. Conveniently disassembles into four manageable pieces. Fits in most vehicle trunks. Top speed of 3.5 mph and enough power to get you where you want to go. Pride Go Chair Specifications Weight Capacity 250 lbs. Turning Radius 26.87" with foot platform Width: 19" Length 27" without foot platform Maximum Speed up to 3.5 mph Ground Clearance: 1.37" Front Wheels 3x5" solid casters Drive Wheels 3x8" solid Rear Wheels 3" solid anti-tips Drivetrain One-motor, rear-wheel drive Braking System Regenerative Suspension Type Limited Standard Electronics: 40A, PG GC3 Battery Size: 12 volt, 12 amp (2 required) Standard Battery Charger: 2A, off-board Per-Charge Range Up to 8 miles Battery Weight 20 lbs. Base Weight 57 LBS. (rear section 34.5 lbs.; front section 22.5 lbs.) Standard Seat Weight 25 lbs. (foldable, compact, lightweight)
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Es Diálisis Único Tratamiento para la Creatinina 3.5 a 4 en la Enfermedad Renal - 0 views

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    Es la diálisis el único tratamiento para la creatinina 3.5 a 4 en la enfermedad renal?La diálisis es el más común para aliviar los síntomas de la insuficiencia renal , como la presión arterial alta.Pero sabe usted que no es la única manera de tratar la enfermedad renal.
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Si Tengo la Enfermedad Renal con la Creatinina 3.5 Puedo Ser Revertida - 0 views

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    Si tengo la enfermedad renal con la creatinina 3.5 puedo ser revertida ?Soy un paciente de la enfermedad renal ,y el médico me dijo que ahora tengo el nivel de creatinina 3.5.Ade más, tengo un poco proteína ,también la sangre en mi orina ,quiero saber si puedo ser revertida?
Nathan Goodyear

Dietary supplement adverse events: Report of a one-year poison center surveillance project - 0 views

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    Context, context, context.   In the year 2006, there were 1.5 million adverse events reported directly related to prescription drugs at a cost of 3.5$ billion.  One often hears of the dangers of supplements.  This analysis from 2008 found 275 adverse events reported.  Contrast 1.5 million versus 275 and it really puts into context where the dangers lie.
Nathan Goodyear

Age Trends in the Level of Serum Testosterone and Other Hormones in Middle-Aged Men: Lo... - 0 views

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    MMAS study finds an age associated decline in Total Testosterone and free Testosterone levels. This study focus on the % decline based on other variables i.e. age, BMI...IN contrast, a 3.5% rise in DHT levels were observed. There is debate about the correlation of serum DHT and intra-tissue DHT. In fact, studies suggest there is little correlation.
Nathan Goodyear

Lower low density lipid cholesterol levels are associated with Parkinson's disease - 0 views

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    Lower LDL levels associated with increased risk of Parkinson's disease.  LDL levels < 113 were associated with a 3.5 fold increase in Parkinson's disease compared to LDL of 138.
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El Paciente de la Enfermedad Renal con la Creatinina 3.5 y la Hipertensión Pu... - 0 views

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    FIL es de 68 años de edad y su nivel de creattinina es 3.5, tiene hipertensión durante más de 10 años y diabetes por unos 5 años, mi pregunta es hay alguna oportunidad para reducir el alto nivel de creatinina y revertir esta enfermedad?
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Cómo Tratar la Enfermedad Renal Poliquística con la Creatinina 3.5 - 0 views

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    La PKD es una complicada enfermedad renal con numerosos quistes.Con los numerosos quistes, la función renal disminuye cada vez más.La creatinina es un índice de las restantes funciónes, también está de pie para un datos serios para la PKD. ¿La creatinina 3.5 en PKD significa qué?
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Los Aumentos de Creatinina desde 3.5 hasta 8.7 en la Nefropatía Diabética Cóm... - 0 views

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    Como todos sabemos, la nefropatía diaética es causada por largos términos de la diabetes, con el desarrollo de esta enfermedad , el nivel de creatinina también aumenta gradualmente. ¿Por qué la creatinina aumenta de 3.5 a 8.7 nivel?
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10.5 M LFD Test Kits : UKSHA Plans To Distribute It Per Week - 0 views

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    As an unprecedented demand for Lateral Flow Device (LFD) test kits continues through the Pharmacy Collect service, the UK Health Security Agency (UKHSA) is planning to distribute 10.5 million tests per week via Alliance Healthcare this month. By the end of this week (January 8), the UKHSA aims to distribute more than 8 million tests to Alliance Healthcare - sole distributor to pharmacies. The announcement comes after many in the pharmacy sector voiced concerns over shortage of test kits. Earlier this week, it emerged that Alliance Healthcare closed for four days shortly after receiving around 2.5 million tests on Christmas Eve. Meanwhile, the UKHSA indicated that Alliance Healthcare has been delivering 86 per cent of its orders within 24 hours of the pharmacy order, nearly half of that on the same day. Besides, a plan to switch on a Parcel Force delivery contingency is being finalised by UKHSA, which would enable supply of a further 3.5 million test kits.
Nathan Goodyear

Metabolic management of brain cancer - 0 views

  • Glutamine is a major metabolic fuel for both brain tumor cells and tumor-associated macrophages (TAMs)
  • the malignant phenotype of brain tumor cells that survive radiotherapy is often greater than that of the cells from the original tumor.
  • Conventional chemotherapy has faired little better than radiation therapy for the long-term management of malignant brain cancer
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  • most conventional radiation and brain cancer chemotherapies can enhance glioma energy metabolism and invasive properties, which would contribute to tumor recurrence and reduced patient survival [34].
  • We contend that all cancer regardless of tissue or cellular origin is a disease of abnormal energy metabolism
  • complex disease phenotypes can be managed through self-organizing networks that display system wide dynamics involving oxidative and non-oxidative (substrate level) phosphorylation
  • As long as brain tumors are provided a physiological environment conducive for their energy needs they will survive; when this environment is restricted or abruptly changed they will either grow slower, growth arrest, or perish [8]&nbsp;and&nbsp;[19]
  • New information also suggests that ketones are toxic to some human tumor cells and that ketones and ketogenic diets might restrict availability of glutamine to tumor cells [68], [69]&nbsp;and&nbsp;[70].
  • The success in dealing with environmental stress and disease is therefore dependent on the integrated action of all cells in the organism
  • Tumor cells survive in hypoxic environments not because they have inherited genes making them more fit or adaptable than normal cells, but because they have damaged mitochondria and have thus acquired the ability to derive energy largely through substrate level phosphorylation
  • Cancer cells survive and multiply only in physiological environments that provide fuels (mostly glucose and glutamine) subserving their requirement for substrate level phosphorylation
  • Integrity of the inner mitochondrial membrane is necessary for ketone body metabolism since β-hydroxybutyrate dehydrogenase, which catalyzes the first step in the metabolism of β-OHB to acetoacetate, interacts with cardiolipin and other phospholipids in the inner membrane
  • the mitochondria of many gliomas and most tumors for that matter are dysfunctional
  • Cardiolipin is essential for efficient oxidative energy production and mitochondrial function
  • Any genetic or environmental alteration in the content or composition of cardiolipin will compromise energy production through oxidative phosphorylation
  • The Crabtree effect involves the inhibition of respiration by high levels of glucose
  • the Warburg effect involves elevated glycolysis from impaired oxidative phosphorylation
  • the Crabtree effect can be reversible, the Warburg effect is largely irreversible because its origin is with permanently damaged mitochondria
  • The continued production of lactic acid in the presence of oxygen is the metabolic hallmark of most cancers and is referred to as aerobic glycolysis or the Warburg effect
  • We recently described how the retrograde signaling system could induce changes in oncogenes and tumor suppressor genes to facilitate tumor cell survival following mitochondrial damage [48].
  • In addition to glycolysis, glutamine can also increase ATP production under hypoxic conditions through substrate level phosphorylation in the TCA cycle after its metabolism to α-ketoglutarate
  • mitochondrial lipid abnormalities, which alter electron transport activities, can account in large part for the Warburg effect
  • targeting both glucose and glutamine metabolism could be effective for managing most cancers including brain cancer
  • The bulk of experimental evidence indicates that mitochondria are dysfunctional in tumors and incapable of generating sufficient ATP through oxidative phosphorylation
  • Cardiolipin defects in tumor cells are also associated with reduced activities of several enzymes of the mitochondrial electron transport chain making it unlikely that tumor cells with cardiolipin abnormalities can generate adequate energy through oxidative phosphorylation
  • The Crabtree effect involves the inhibition of respiration by high levels of glucose
  • Warburg effect involves elevated glycolysis from impaired oxidative phosphorylation
  • TCA cycle substrate level phosphorylation could therefore become another source of ATP production in tumor cells with impairments in oxidative phosphorylation
  • Caloric restriction, which lowers glucose and elevates ketone bodies [63]&nbsp;and&nbsp;[64], improves mitochondrial respiratory function and glutathione redox state in normal cells
  • DR naturally inhibits glycolysis and tumor growth by lowering circulating glucose levels, while at the same time, enhancing the health and vitality of normal cells and tissues through ketone body metabolism
  • DR is anti-angiogenic
  • DR also reduces angiogenesis in prostate and breast cancer
  • We suggest that apoptosis resistance arises largely from enhanced substrate level phosphorylation of tumor cells and to the genes associated with elevated glycolysis and glutaminolysis, e.g., c-Myc, Hif-1a, etc, which inhibit apoptosis
  • Modern medicine has not looked favorably on diet therapies for managing complex diseases especially when well-established procedures for acceptable clinical practice are available, regardless of how ineffective these procedures might be in managing the disease
  • More than 60&nbsp;years of clinical research indicates that such approaches are largely ineffective in extending survival or improving quality of life
  • The process is rooted in the well-established scientific principle that tumor cells are largely dependent on substrate level phosphorylation for their survival and growth
  • Glucose and glutamine drive substrate level phosphorylation
  • targeting the glycolytically active tumor cells that produce pro-cachexia molecules, restricted diet therapies can potentially reduce tumor cachexia
  • It is important to recognize, however, that “more is not better” with respect to the ketogenic diet
  • Blood glucose ranges between 3.0 and 3.5&nbsp;mM (55–65&nbsp;mg/dl) and β-OHB ranges between 4 and 7&nbsp;mM should be effective for tumor management
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    Dr Seyfriend presents his metabolic approach to the treatment of brain cancer.
Nathan Goodyear

Fat-free mass index and fat mass index percentiles in Caucasians aged 1898 y - 0 views

  • BMI is the sum of FFMI+FMI
  • FMI were significantly higher in elderly subjects as compared to younger ones
  • During menopause and aging39,40 changes in FFM and FM are not adequately picked up by changes in BMI
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  • One advantage of FMI, as compared to the BMI concept, is that it amplifies the relative effect of aging on body fat
  • We believe that the definition of obesity based on relative body fat (ie percentage) remains of great value for the definition of obesity. However, in a situation in which a patient is losing weight without substantially changing his/her relative body fat (as is the case with crash diets), the calculation of FMI will quantitatively reveal the amount of body fat store lost.
  • high sensitivity of FMI (respectively FFMI) to a slight change of body fat stores
  • Sarcopenic obesity has been defined as a low FFM associated with a high body fat
  • relative FFM lower than 73% (ie a relative body fat greater than 27%) in men and a FFM lower than 62% (ie a body fat greater than 38%) in women.
  • FMIs greater than 8.2 kg/m2 in men and 11.8 kg/m2 in women would define the 'overfat' status (rather than the overweight range) in terms of fat mass
  • In young women, FMI averaged 5.5 kg/m2 (range 5th-95th percentile: 3.5-8.7 kg/m2) ie 38% higher than in males
  • the average FMI for young men was 4.0 kg/m2
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    good review of FMI, FFMI, and BMI.
Nathan Goodyear

Review of health risks of low testosterone and testosterone administration - 0 views

  • Hypogonadism may be defined either as serum concentration of T (either total T, bioavailable T or free T) or as low T plus symptoms of hypogonadism
  • The Baltimore Longitudinal Study on Aging reported the incidence of total serum T &lt; 325 ng/dL to be 20% for men in their 60s, 30% for men in their 70s and 50% for men over 80
  • The Massachusetts Aging Male Study reported that 12.3% of men aged 40 to 70 had a total serum T of &lt; 200 ng/dL with 3 or more symptoms of hypogonadism
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  • The Boston Area Community Health Study reported that 5.6% of men aged 30 to 70 were hypogonadal, as defined by total serum T &lt; 300 ng/dL; or, free serum T &lt; 5 ng/dL plus 3 or more symptoms of hypogonadism
  • In a health screening project among 819 men in Taiwan, the prevalence of hypogonadism (total serum T &lt; 300 ng/dL) ranged from 16.5% for men in their 40s, 23.0% for men in their 50s, 28.9% for men in their 60s, and 37.2% for men older than 70 years of age
  • The prevalence of hypogonadism among men in Taiwan is higher than the prevalence reported in the Massachusetts Male Aging Study
  • CAG repeat sequence, within the androgen receptor (AR). Rajender et al[12] reviewed over 30 studies on the AR trinucleotide repeat and infertility
  • suggestion that CAG repeat length may determine androgen responsiveness, this issue is not clearly settled
  • reported prevalence of low T in older men range from 5.6% to 50%
  • Those in the hypogonadal group (n = 4269) had direct health care costs, that exceeded the eugonadal group (n = 4269) by an average of $7100 over the course of the observation window
  • higher economic burden and presence of co-morbidities for hypogonadism
  • minor to moderate improvements in lean mass and muscle strength
  • increased bone mineral density
  • modest enhancement in sexual function
  • reduced adiposity
  • lessening of depressive symptoms
  • Meta-analyses of clinical TRT trials as of 2010 have identified three major adverse events resulting from TRT: (1) polycythemia; (2) an increase in prostate-related events; and (3) and a slight reduction in serum high-density lipoprotein (HDL) cholesterol
  • polycythemia (&gt; 3.5-fold increase in risk
  • TRT produced a 40% prostate enlargement in older hypogonadal male Veterans over 12 mo
  • no published analysis has reported measurable increases in prostate cancer risk or Gleason score in men undergoing TRT, or in hypogonadal men with a history of prostate cancer undergoing TRT
  • the prostate which highly expresses the type II 5α-reductase enzyme. Inhibition of this enzyme via finasteride (a type II 5α-reductase inhibitor) or dutasteride (a dual type I and II 5α-reductase inhibitor) reduces circulating DHT 50%-75% and &gt; 90%, respectively[47], and reduces prostate mass[48] and prostate cancer risk
  • Normally estradiol partially regulates testosterone levels, at the hypothalamus, blunting LH and FSH release from the pituitary. As a selective estrogen receptor modulator, CC interrupts this pathway, and consequently there is a greater stimulation for the production of testosterone in Leydig cells
    • Nathan Goodyear
       
      this would only apply if E1 and/or E2 levels were elevated, which the authors make no mention of.
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    to be read
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Por qué Hiperpotasemia Aparecen en la Insuficiencia Renal y Cómo Curarla - 0 views

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    Por qué La hiperpotasemia se produce en la insuficiencia renal ?Niveles de potasio sérico normales van de 3.5 a 5.0 mEq / litro en la sangre. Ingesta diaria normal de potasio es 70-100 mEq (270-390 mg / dl), y requiere de los riñones para eliminar la misma cantidad cada día.Una vez que los riñones dañados, no pueden eliminar el potasio oportuna que conduzca a la hiperpotasemia.
Nathan Goodyear

Genetic Determinants of Serum Testosterone Concentrations in Men - 0 views

  • mean serum testosterone concentrations were found to be lower in men with GG than in those with TT genotype for rs12150660
  • men with the CT genotype for rs6258 had lower serum testosterone concentrations than those with CC genotype.
  • The two autosomal SNPs identified by GWAS had a significant influence on the risk of having low serum testosterone (serum testosterone &lt;300 ng/dl) in both the discovery and the replication cohorts with a combined odds ratio (OR) per minor allele of 0.72 (95% CI, 0.65 – 0.79) and 2.7 (95% CI, 2.1 – 3.5) for rs12150660 and rs6258, respectively
  • ...3 more annotations...
  • The risk of having low serum testosterone concentrations increased by the number of risk alleles with an OR of 1.62 (95% CI, 1.41 – 1.86) for each risk allele (Figure S4). Low serum testosterone concentrations were 6.5-times more prevalent in men with ≥3 risk alleles (30.1% prevalence of low serum testosterone) compared to men without any risk allele (4.6% prevalence of low serum testosterone;
  • SNP rs5934505 was associated with serum testosterone without SHBG-adjustment (combined p-value of 1.7×10−9) and with free testosterone (combined p-value of 6.7×10−15), but not with SHBG
  • The mean serum testosterone and calculated free testosterone but not SHBG concentrations were lower in men with T genotype than in those with C genotype for rs5934505
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    Genetic SNP rs5934505 associated with lower total Testosterone and lower calculated free Testosterone.  No effects on SHBG.
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