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Está Dirigido por la Insuficiencia Renal Si Sufre la PKD - 0 views

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    ¿ Está dirigido por la insuficiencia renal si sufre la PKD? La respuesta es sí. Así que hay que prestar atención una vez que fue diagnosticado con PKD, y lo que necesita saber que cómo detener la progresión de PKD y prevenir la insuficiencia renal.
star yu

Cómo Prevenir el Riñon a Reducir Más - 0 views

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    Como todos sabemos, una vez que el riñón va a reducirse es difícil de revertir, pero el paciente puede prevenir el riñón va a reducirse más si se puede obtener el tratamiento adecuado a tiempo. La atrofia del riñón significa que su riñón es menor u obviamente encoge relativamente.
star yu

Cómo Tratar la Enfermedad Renal en la Diabetes y la Hipertensión - 0 views

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    Mi madre es un paciente con enfermedad renal de creatinina 4.3.Y ella también sufrió la diabetes y la hipertensión.¿Quiero saber cómo tratar su enfermedad?
star yu

Cómo Evitar que la Función Renal Disminuye en la Enfermedad Renal - 0 views

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    Usted sabe la enfermedad renal es una enfermedad progresiva, como se desarrolló la voluntad de la función renal disminuye por lo tanto inducir más síntomas. Así que si el paciente desea evitar que su función renal disminuye, deben tomar algunos tratamientos oportunos.
star yu

Mejor Medicamento para Bajar Su Creatinina en la Nefropatía por IgA - 0 views

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    Nefropatía por IgA es un tipo de enfermedad sistema inmune .Cuando el sistema inmune se vuelve anormal ,no puede eliminar el complejo inmune IgA,por lo tanto algunos estancia en la sangre ,mientera algunos depósitos están en los riñónes .
star yu

Los Medicamentos Chinos para Curar la Nefropatía por IgA - 0 views

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    Nefropatía por IgA se caracteriza por sus complejos inmunes nombrado Inmunoglobulina.A depositado en membrana basilar glomerular. La enfermedad es una de las principales causas que representa (enfermedad renal terminal) hoy en día. No hay causas claras y su patología han conocido hasta ahora.
star yu

Cómo Prevenir la PKD con la Creatinina 4.7 Entra en Uremia - 0 views

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    En la clínica ,PKD es un tipo de enfermedad genetica ,no se puede curar totalmente ,porque nadie puede cambiar os genes,sin embargo ,los expertos han encontrado los tratamiento s adecuados y efectivos que puede controlar bien esta enfermedad . ¿Qué consejos son utilies para curar la PKD? 1.
star yu

La Diálisis es Util para el Paciente del Nefritis Lúpica con la Creatinina 5.5 - 0 views

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    Soy un paciente del nefritis lúpica y recientemente mi nivel de creatinina aumentó a 5.5, excepto que no tengo síntomas mucho. Creo que sólo necesito hacer unos pequeños cambios en mi dieta, pero mi doctor dijo que tengo que tomar diálisis. Quiero saber es la diálisis es una elección obligada para mí?
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Nefropatía Diabética :Usted Necesita Prestar Más Atención en 4 Factores - 0 views

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    La nefropatía diabética se refiere a una enfermedad renal común, que es causada por la larga historia de la diabetes. Una vez que fue diagnosticado con nefropatía diabética, un tratamiento rápido y eficaz es lo más importante para prevenir la insuficiencia renal .
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Los Pacientes de la Diálisis Pueden Sobrevivir con la Medicina China tradicional - 0 views

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    Los pacientes en diálisis pueden sobrevivir con lla medicina china tradicional, que necesitan para responder en diálisis para filtrar la sangre para eliminar los desechos y toxinas en el cuerpo. Pero la diálisis no puede hacer nada para r Los pacientes en diálisis pueden sobrevivir con lla medicina china tradicional, que necesitan para responder en diálisis para filtrar la sangre para eliminar los desechos y toxinas en el cuerpo.
star yu

La Acupurura :el Tratamiento para Curar la Insuficiencia Renal - 0 views

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    Acupuntura: Es una terapia que se utiliza para tratar la insuficiencia renal, y pertenece al tratamiento sistemático de la medicina china tradicional.
Nathan Goodyear

Renin-angiotensin system and cancer: A review - 0 views

  • crucial role of the RAS in the development and maintenance of cancer
  • kidneys, which produce renin in response to decreased arterial pressure, reduced sodium in the distal tubule, or sympathetic nervous system activity via the β-adrenergic receptors
  • Renin is secreted from the juxtaglomerular cells into the bloodstream where it encounters angiotensinogen (AGN), normally produced by the liver
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  • Renin catalyses the conversion of AGN to angiotensin I (ATI), which is quickly cleaved by angiotensin converting enzyme (ACE) to form angiotensin II (ATII)
  • ATII triggers the release of aldosterone from the adrenal glands, which stimulates reabsorption of sodium and water and thereby increases blood volume and blood pressure
  • ATII also acts on smooth muscle to cause vasoconstriction of the arterioles
  • ATII promotes the release of antidiuretic hormone from the posterior pituitary gland, which results in water retention and triggers the thirst reflex
  • ability of non-CSCs to ‘de-differentiate’ into CSCs due to epigenetic or environmental factors, which further increases the complexity of tumour biology and treatment
  • efficacy of RAS modulators on cancer in both cancer models and cancer patients
  • A localised (‘paracrine’) RAS mechanism has been identified in many types of cancers, and interruption of the control of the RAS is thought to be the basis for its role in cancer
  • Components of the RAS are expressed by these CSCs, supporting the hypothesis of the presence of a ‘paracrine RAS’ in regulating these CSCs
  • Renin is an enzyme normally released by the kidneys in response to falling arterial pressure
  • a study of GBM demonstrating overexpression of PRR coupled with the observation that inhibition of renin reduces cellular proliferation and promotes apoptosis
  • PRR has been found to be vital for normal Wnt signalling
  • A major focus of PRR research is its relationship with Wnt signalling
  • suggest a crucial role for PRR activation on the proliferation of CSCs, possibly via Wnt/β-catenin signalling, leading to carcinogenesis.
  • Angiotensin converting enzyme (ACE), also known as CD143, is the endothelial-bound peptidase which physiologically converts ATI to ATII
  • ACE is crucial in the regulation of blood pressure, angiogenesis and inflammation
  • results suggest that an overactive ACE promotes cancer growth and progression, and an inhibited or low-activity ACE may have cancer-protective effects
  • When bound to ATII or ATIII it causes vasoconstriction by stimulating the release of vasopressin, reabsorption of water and sodium by promoting secretion of aldosterone and insulin, fibrosis, cellular growth and migration, pro-inflammation, glucose release from the liver, increased plasma triglyceride concentration, and reduced gluconeogenesis
  • ATIIR1 is a G-protein-coupled receptor, with downstream signalling involved in vasodilation, hypertrophy and NF-κB activation leading to TNF-α and PAI-1 expression
  • ATIIR1 has well-documented links with cancer, with one study demonstrating its overexpression in ~20% of breast cancer patients
  • the effect of RAS dysregulation has been associated with increased VEGF expression and angiogenesis in cancers
  • In ovarian and cervical cancer, ATIIR1 overexpression has been shown to be an indicator of tumour invasiveness
  • administration of ATIIR1 blockers (ARBs) have been associated with reduced tumour size, reduction in tumour vascularisation, lower occurrence of metastases, and lower VEGF levels
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    Great review on RAS in cancer.
Nathan Goodyear

The current state and future perspectives of cannabinoids in cancer biology - 0 views

  • The activation of each of them leads to an inhibition of adenylyl cyclase via G proteins (Gi/o), which in turn activates many metabolic pathways such as mitogen‐activated protein kinase pathway (MAPK), phosphoinositide 3‐kinase pathway (PI3K), cyclooxygenase‐2 pathway (COX‐2), accumulation of ceramide, modulation of protein kinase B (Akt), and ion channels
  • phytocannabinoids, endocannabinoids, and synthetic cannabinoids
  • Action of THC in human organism relies on mimicking endogenous agonists of CB receptors—endocannabinoids
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  • The upregulated expression of CB receptors and the elevated levels of endocannabinoids have been observed in a variety of cancer cells (skin, prostate, and colon cancer, hepatocellular carcinoma, endometrial sarcoma, glioblastoma multiforme, meningioma and pituitary adenoma, Hodgkin lymphoma, chemically induced hepatocarcinoma, mantel cell lymphoma)
  • concentration of endocannabinoids, expression level of their receptors, and the enzymes involved in their metabolism frequently are associated with an aggressiveness of cancer
  • CB2 receptor contributes to human epidermal growth factor receptor (HER2) pro‐oncogenic signaling and an overexpression of CB2 increases susceptibility for leukemia development after leukemia viral infection
  • endocannabinoid‐degrading enzymes are upregulated in cancer cell lines and in human tumors
  • Many cannabinoids, ranging from phytocannabinoids (THC, CBD), endocannabinoids (2‐arachidonoylglycerol, anandamide), to synthetic cannabinoids (JWH‐133, WIN‐55,212‐2), have shown ability to inhibit proliferation, metastasis, and angiogenesis in a variety of models of cancer
  • Despite some inconsistent data, the main effect of cannabinoids in a tumor is the inhibition of cancer cells’ proliferation and induction of cancer cell death by apoptosis
  • CB1 and CB2 receptor agonists stimulate apoptotic cell death in glioma cells by induction of de novo synthesis of ceramide, sphingolipid with proapoptotic activity
  • process of autophagy is upstream of apoptosis in mechanism of cell death induced by cannabinoids
hohanbogdan

Obosit mereu - 0 views

De ce sunt obosit mereu? https://obosit-mereu.weebly.com/shop.html

Sanatate

started by hohanbogdan on 19 Jan 18 no follow-up yet
hohanbogdan

De ce sunt obosit ? - 1 views

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obesity

started by hohanbogdan on 19 Jan 18 no follow-up yet
trungtamnamkhoa

Learn More About Foreskin Disease - Men's Health Clinic In Viet Nam - 1 views

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    Semi-glans It is a situation in which the boy is still "open his eyes" but is either very difficult or painful or requires the help of slipping from the homeowner. Having opened the eyes is not necessarily good in this case because soon enough the foreskin will form a tightening ring just below, obstructing the healed blood, leading to edema, and when the penis is hard, everything even worse.
Nathan Goodyear

How is the Immune System Suppressed by Cancer - 1 views

  • nitric oxide (NO) released by tumor cells
  • Excellent work by Prof de Groot of Essen, indicated by adding exogenous xanthine oxidase ( XO) in hepatoma cells, hydrogen peroxide was produced to destroy the hepatoma cells
  • NO from eNOS in cancer cells can travel through membranes and over long distances in the body
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  • NO also is co linked to VEGF which in turn increases the antiapoptotic gene bcl-2
  • The other important influence of NO is in its inhibition of the proapoptoic caspases cascade. This in turn protects the cells from intracellular preprogrammed death.
  • nitric oxide in immune suppression in relation to oxygen radicals is its inhibitory effect on the binding of leukocytes (PMN) at the endothelial surface
  • Inhibition of inducible Nitric Oxide Synthase (iNOS)
  • NO from the tumor cells actually suppresses the iNOS, and in addition it reduces oxygen radicals to stop the formation of peroxynitrite in these cells. But NO is not the only inhibitor of iNOS in cancer.
  • Spermine and spermidine, from the rate limiting enzyme for DNA synthases, ODC, also inhibit iNOS
  • tolerance in the immune system that decreases the immune response to antigens on the tumors
  • Freund’s adjuvant
  • increase in kinases in these cells which phosphorylate serine, and tyrosine
  • responsible for activation of many growth factors and enzymes
  • phosphorylated amino acids suppress iNOS activity
  • Hexokinase II
  • Prostaglandin E2, released from tumor cells is also an inhibitor of iNOS, as well as suppressing the immune system
  • Th-1 subset of T-cells. These cells are responsible for anti-viral and anti-cancer activities, via their cytokine production including Interleukin-2, (IL-2), and Interleukin-12 which stimulates T-killer cell replication and further activation and release of tumor fighting cytokines.
    • Nathan Goodyear
       
      Th1 cells stimulate NK and other tumor fighting macrophages via IL-2 and IL-12; In contrast, Th2, which is stimulated in allergies and parasitic infections, produce IL-4 and IL-10.  IL-4 and IL-10 inhibit TH-1 activation and the histamine released from mast cell degranulation upregulates T suppressor cells to further immune suppression.
  • Th-2 subset of lymphocytes, on the other hand are activated in allergies and parasitic infections to release Interleukin-4 and Interleukin-10
  • These have respectively inhibitory effects on iNOS and lymphocyte Th-1 activation
  • Mast cells contain histamine which when released increases the T suppressor cells, to lower the immune system and also acts directly on many tumor Histamine receptors to stimulate tumor growth
  • Tumor cells release IL-10, and this is thought to be one of the important areas of Th-1 suppression in cancer patients
  • IL-10 is also increased in cancer causing viral diseases such as HIV, HBV, HCV, and EBV
  • IL-10 is also a central regulator of cyclooxygenase-2 expression and prostaglandin production in tumor cells stimulating their angiogenesis and NO production
  • nitric oxide in tumor cells even prevents the activation of caspases responsible for apoptosis
    • Nathan Goodyear
       
      NO produced by cancer cells inhibits proapoptotic pathways such as the caspases.
  • early stages of carcinogenesis, which we call tumor promotion, one needs a strong immune system, and fewer oxygen radicals to prevent mutations but still enough to destroy the tumor cells should they develop
  • later stages of cancer development, the oxygen radicals are decreased around the tumors and in the tumor cells themselves, and the entire cancer fighting Th-1 cell replication and movement are suppressed. The results are a decrease in direct toxicity and apoptosis, which is prevented by NO, a suppression of the macrophage and leukocyte toxicity and finally, a suppression of the T-cell induced tumor toxicity
  • cGMP is increased by NO
  • NO in cancer is its ability to increase platelet-tumor cell aggregates, which enhances metastases
  • the greater the malignancies and the greater the metastatic potential of these tumors
  • The greater the NO production in many types of tumors,
  • gynecological
  • elevated lactic acid which neutralizes the toxicity and activity of Lymphocyte immune response and mobility
  • The lactic acid is also feeding fungi around tumors and that leads to elevated histamine which increases T-suppressor cells.  Histamine alone stimulates many tumor cells.
    • Nathan Goodyear
       
      The warburg effect in cancer cells results in the increase in local lactic acid production which suppresses lymphocyte activity and toxicity as well as stimulates histamine production with further stimulates tumor cell growth.
  • T-regulatory cells (formerly,T suppressor cells) down regulate the activity of Natural killer cells
  • last but not least, the Lactic acid from tumor cells and acidic diets shifts the lymphocyte activity to reduce its efficacy against cancer cells and pathogens in addition to altering the bacteria of the intestinal tract.
  • intestinal tract bacteria in cancer cells release sterols that suppress the immune system and down regulate anticancer activity from lymphocytes.
  • In addition to the lactic acid, adenosine is also released from tumors. Through IL-10, adenosine and other molecules secreted by regulatory T cells, the CD8+ cells can be inactivated to an anergic state
  • Adenosine up regulates the PD1 receptor in T-1 Lymphocytes and inhibits their activity
  • Adenosine is a purine nucleoside found within the interstitial fluid of solid tumors at concentrations that are able to inhibit cell-mediated immune responses to tumor cells
  • Adenosine appears to up-regulate the PD1 receptor in T-1 Lymphocytes and inhibits the immune system further
  • Mast cells with their release of histamine lower the immune system and also stimulate tumor growth and activate the metalloproteinases involved in angiogenesis and metastases
  • COX 2 inhibitors or all trans-retinoic acid
  • Cimetidine, an antihistamine has been actually shown to increase in apoptosis in MDSC via a separate mechanism than the antihistamine effect
    • Nathan Goodyear
       
      cimetidine is an H2 blocker
  • interleukin-8 (IL-8), a chemokine related to invasion and angiogenesis
  • In vitro analyses revealed a striking induction of IL-8 expression in CAFs and LFs by tumor necrosis factor-alpha (TNF-alpha)
  • these data raise the possibility that the majority of CAFs in CLM originate from resident LFs. TNF-alpha-induced up-regulation of IL-8 via nuclear factor-kappaB in CAFs is an inflammatory pathway, potentially permissive for cancer invasion that may represent a novel therapeutic target
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    Great review of the immunosuppression in cancer driven by the likes of NO.
Nathan Goodyear

Thieme E-Journals - International Journal of Sports Medicine / Abstract - 0 views

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    Only abstract available here: compound resistance treaining in highly trained young men found to increase GH and Testosterone over isolation exercises. Those that trained > 2 years had significnt increase in Testosterone pre/post exercise compared to no statistical change in those traing < 2 years.
Nathan Goodyear

Effects of short-term high-fat overfeeding on genome-wide DNA methylation in the skelet... - 0 views

  • short-term HFO introduces DNA methylation changes on a genome-wide scale in human skeletal muscle
  • These changes were only partly reversed after 6–8&nbsp;weeks
  • The induction of DNA methylation changes after 5&nbsp;days of HFO supports the growing awareness of DNA methylation as a dynamic signal that is possibly relevant to short-term day-to-day metabolic adaptations, including acute exercise
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  • Diverging DNA methylation levels between elderly, but not young, genetically identical twins indicate that environmental exposures throughout life may permanently influence DNA methylation, suggesting some preservation of de novo DNA methylation in adults
  • our finding of a slow reversibility rate indicates the demethylation process may be somewhat impeded compared with the induction of methylation changes by diet, which could have implications for the preservation or build-up of CpG methylation over time
  • A slow reversibility of DNA methylation induced by carcinogenic agents has likewise been observed due to ingestion of high-fat diets in rodents
  • the relationship between DNA methylation and gene expression is not always straightforward
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    Study finds variability of methylation and some genetic expression alteration with high fat diet.  Restated, what you eat interacts with your DNA to alter genetic expression.  This has implications on initiation of therapy as well as response to therapy.
Nathan Goodyear

Chemotherapy-Induced Metastasis: Molecular Mechanisms, Clinical Manifestations, Therape... - 0 views

  • recent evidence has linked the cytotoxic effects of chemotherapy with the de novo elicitation of a prometastatic tumor microenvironment
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    Full dose chemotherapy induces cytokine storm to induce metastasis.
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