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harshitatyagi

Penile Yeast Infection in Men, Causes, Symptoms and Treatment - 0 views

vocal.media/...-causes-symptoms-and-treatment

Yeast Infection in Men Penile Yeast Infection in Men Penile Yeast Infection Causes Penile Yeast Infection Symptoms Penile Yeast Infection Treatment

shared by harshitatyagi on 31 Oct 22 - No Cached
  • harshitatyagi on 31 Oct 22
     
    Penile Yeast infections in men are generally not known due to their lack of awareness. This severe illness can cause a range of infections that will affect hygiene and the fertility rate. And due to increasing cases of infertility in men, it becomes significant to acknowledge cautious infections in men to combat the rising infertility cases.
Nathan Goodyear

Red yeast rice induces less muscle fatigue symptom than simvastatin in dyslipidemic pat... - 0 views

bmccardiovascdisord.biomedcentral.com/...s12872-017-0560-z

cancer red yeast rice simvastatin

shared by Nathan Goodyear on 01 Sep 23 - No Cached
  • Nathan Goodyear on 01 Sep 23
     
    Less side effects with red yeast rice.
Nathan Goodyear

Candida albicans Is an Immunogen for Anti-Saccharomyces cerevisiae Antibody Markers of ... - 0 views

www.gastrojournal.org/...abstract

candida albicans yeast crohn's disease

shared by Nathan Goodyear on 29 Jun 11 - No Cached
  • Nathan Goodyear on 29 Jun 11
     
    Yeast species appears to play role in abnormal immune response in Crohn's disease
Nathan Goodyear

Antimicrobial activity of essential oils from plan... [J Food Prot. 2001] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...11456186

Oregano antimicrobial activity essential oils

shared by Nathan Goodyear on 15 Apr 11 - No Cached
  • Oregano essential oil showed the greatest inhibition (zone, > or = 70 to 80 mm) (MLC, approximately 8 ppm). Coriander and basil were also highly inhibitory (MLC, approximately 25 to 50 ppm) to E. coli O:157:H7 and to the other bacteria and fungi tested
  • Nathan Goodyear on 15 Apr 11
     
    oregano essential oil is effective in killing bacteria and yeast
Nathan Goodyear

Telomerase at the intersection of cancer and aging - 0 views

www.ncbi.nlm.nih.gov/...PMC3896987

telomere telomeres telomerase telomerase activator aging disease cancer

shared by Nathan Goodyear on 18 May 16 - No Cached
  • The anti-aging role of telomerase has been demonstrated to be largely mediated by its canonical role in elongating telomeres, which prevents the accumulation of critically short telomeres and loss of tissue homeostasis
  • Short telomeres, and subsequent DDR activation, could occur both in cancer and aging
  • increased abundance of short telomeres correlates with higher genomic instability and decreased longevity in various organisms, including mice, zebrafish, and yeast
  • ...15 more annotations...
  • mice deficient for telomerase or for telomere binding proteins are characterized by accelerated age-related defects
  • In humans, short telomeres are considered good indicators of an individual’s health status and correlate with both genetic and environmental factors
  • Although recent findings strongly support the idea that short telomeres drive several age-related diseases 38 we cannot exclude the possibility that in some situations short telomeres may be a consequence of the disease itself.
  • the current view is that telomerase deficiency may contribute to the early steps of cancer development by fueling chromosomal instability, while subsequent activation of telomerase may be necessary to allow tumor growth and tumor progression towards more malignant states
  • telomerase activation can be an early event in cancer, it is not necessary for cancer initiation
  • telomerase can stimulate tumor progression by ensuring maintenance of telomeres above a critically short length, thus preventing induction of cellular senescence or apoptosis
  • Almost all human cancers present activation of telomerase as a hallmark, most likely as a mechanism to allow unlimited cell proliferation of tumor cells
  • recent evidence demonstrated that short telomeres alone could lead to genomic instability and cancer
  • Getting rid of telomerase can also be problematic; the lack of telomerase could lead to increased chromosomal instability, which in turn could be at the basis for cancer initiation when tumor suppressor barriers are bypassed
  • telomerase activation is a potential therapeutic strategy for the treatment of age-related diseases
  • telomerase activation in adult or old mice by means of a gene therapy strategy was shown to be sufficient to improve metabolic fitness, neuromuscular capacity, and prevent bone loss, as well as significantly increase both median and maximum longevity, without increased cancer incidence
  • These studies suggest that telomerase expression could be considered a feasible approach to reverse tissue dysfunction and extend healthy lifespan without increasing cancer incidence
  • humans almost completely lose telomerase activity from somatic tissues in the adulthood
  • a change of paradigm seems to be occurring in telomerase biology, with a switch from viewing telomerase as fueling cancer to reversing aging
  • Telomerase expression in a background of high levels of tumor suppressors or in aged organisms seems to prevent its expected pro-cancer activity and yet it still functions as an anti-aging factor
  • Nathan Goodyear on 18 May 16
     
    Telomerase activity and longer telomere length is shown to correlated inversely with many chronic diseases of aging.  In contrast, telomerase activity is found to be involved in carcinogenesis.  Increased carcinogenic potential of telomerase activity has not borne out in studies.  In addition, increased CD8 cell activity as a result of telomerase activation will actually decrease carcinogenic potential via NK activation.
Nathan Goodyear

Invasive fungal infection in systemic ... [Rheumatology (Oxford). 2007] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...17043051

Lupus SLE fungal infection infections yeast candida

shared by Nathan Goodyear on 30 Oct 13 - No Cached
  • Nathan Goodyear on 30 Oct 13
     
    Lupus associated with increased fungal infections.
Nathan Goodyear

Candida dubliniensis: Characteristics and Identification - 0 views

jcm.asm.org/329

candida dubliniensis candida yeast

shared by Nathan Goodyear on 01 Oct 14 - No Cached
  • Nathan Goodyear on 01 Oct 14
     
    candida dublniensis.
Nathan Goodyear

A Review of the Rationale for Additional Therapeutic Interventions to Attain Lower LDL-... - 0 views

www.ncbi.nlm.nih.gov/...PMC3252497

natural cholesterol red yeast rice diet nutrition fiber niacin plant sterols

shared by Nathan Goodyear on 28 Aug 15 - No Cached
  • Nathan Goodyear on 28 Aug 15
     
    review of a few natural therapies to manage cholesterol.
Nathan Goodyear

Differential pathways regulating innate and adaptive antitumor immune respons... - 0 views

www.ncbi.nlm.nih.gov/...PMC3128477

beta-glucan immune system cancer cells

shared by Nathan Goodyear on 22 May 14 - No Cached
  • Nathan Goodyear on 22 May 14
     
    beta glucans stimulate both innate and adaptive immune system to attack tumor cells.
Nathan Goodyear

Zearalenone, an Estrogenic Mycotoxin, Is an Immunotoxic Compound - 0 views

www.ncbi.nlm.nih.gov/...PMC3968378

mycotoxin mycotoxins yeast fungi zearalenone inflammation immune system immunoexcitotoxicity immunotoxic

shared by Nathan Goodyear on 26 Jul 14 - No Cached
  • Nathan Goodyear on 26 Jul 14
     
    The mycotoxin, Zearalenone, proves to be immunotoxic.
Nathan Goodyear

Evaluation of candidal colonization and specific humoral responses against Candida albi... - 0 views

onlinelibrary.wiley.com/...abstract

candida candida albicans candidiasis yeast psoriasis dermatology

shared by Nathan Goodyear on 03 Dec 15 - No Cached
  • Nathan Goodyear on 03 Dec 15
     
    higher colonization of candida albicans found in people with psoriasis vs controls.  Higher in oral cultures vs skin.
Nathan Goodyear

Incidence of Candida in psoriasis--a study on the fungal flora of psoriatic patients. -... - 0 views

www.ncbi.nlm.nih.gov/...11413927

candida candida albicans candidiasis psoriasis dermatology yeast

shared by Nathan Goodyear on 03 Dec 15 - No Cached
  • Nathan Goodyear on 03 Dec 15
     
    statistically higher candida detected in those with psoriasis vs controls.
Nathan Goodyear

Increased prevalence of onychomycosis among psoriatic patients in Israel. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...18176747

candida yeast fungus psoriasis

shared by Nathan Goodyear on 03 Dec 15 - No Cached
  • Nathan Goodyear on 03 Dec 15
     
    higher prevalence of toe nail fungus in those with psoriasis vs controls.
Nathan Goodyear

Candida parapsilosis, an Emerging Fungal Pathogen - 0 views

www.ncbi.nlm.nih.gov/...PMC2570155

Candida yeast candida parapsilosis

shared by Nathan Goodyear on 03 Mar 15 - No Cached
  • Nathan Goodyear on 03 Mar 15
     
    review of Candida parapsilosis
Nathan Goodyear

http://www.life-worldwide.org/assets/uploads/files/Candida%20parapsilosis2009.pdf - 0 views

www.life-worldwide.org/...Candida%20parapsilosis2009.pdf

Candida yeast candida parapsilosis

shared by Nathan Goodyear on 12 Jan 16 - No Cached
  • Nathan Goodyear on 12 Jan 16
     
    Candida parapsilosis review
Nathan Goodyear

Press-pulse: a novel therapeutic strategy for the metabolic management of cancer | Nutr... - 0 views

nutritionandmetabolism.biomedcentral.com/...s12986-017-0178-2

ketogenic diet ketogenic press-pulse hyperbaric oxygen therapy HBOTnutrition diet cancer HBOT IVC IV vitamin C DCA dichloracetic acid cancer therapy cancer treatment alternative cancer treatment

shared by Nathan Goodyear on 09 Jul 17 - No Cached
mamdouh_hfz liked it
  • A “press” disturbance was considered a chronic environmental stress on all organisms in an ecological community
  • “pulse” disturbances were considered acute events that disrupted biological communities to produce high mortality
  • Neoplasia involving dysregulated cell growth is the biological endpoint of the disease
  • ...84 more annotations...
  • Data from the American Cancer Society show that the rate of increase in cancer deaths/year (3.4%) was two-fold greater than the rate of increase in new cases/year (1.7%) from 2013 to 2017
  • cancer is predicted to overtake heart disease as the leading cause of death in Western societies
  • cancer can also be recognized as a metabolic disease.
  • glucose is first split into two molecules of pyruvate through the Embden–Meyerhof–Parnas glycolytic pathway in the cytosol
  • Aerobic fermentation, on the other hand, involves the production of lactic acid under normoxic conditions
  • persistent lactic acid production in the presence of adequate oxygen is indicative of abnormal respiration
  • Otto Warburg first proposed that all cancers arise from damage to cellular respiration
  • The Crabtree effect is an artifact of the in vitro environment and involves the glucose-induced suppression of respiration with a corresponding elevation of lactic acid production even under hyperoxic (pO2 = 120–160 mmHg) conditions associated with cell culture
  • the Warburg theory of insufficient aerobic respiration remains as the most credible explanation for the origin of tumor cells [2, 37, 51, 52, 53, 54, 55, 56, 57].
  • The main points of Warburg’s theory are; 1) insufficient respiration is the predisposing initiator of tumorigenesis and ultimately cancer, 2) energy through glycolysis gradually compensates for insufficient energy through respiration, 3) cancer cells continue to produce lactic acid in the presence of oxygen, and 4) respiratory insufficiency eventually becomes irreversible
  • Efraim Racker coined the term “Warburg effect”, which refers to the aerobic glycolysis that occurs in cancer cells
  • Warburg clearly demonstrated that aerobic fermentation (aerobic glycolysis) is an effect, and not the cause, of insufficient respiration
  • all tumor cells that have been examined to date contain abnormalities in the content or composition of cardiolipin
  • The evidence supporting Warburg’s original theory comes from a broad range of cancers and is now overwhelming
  • respiratory insufficiency, arising from any number mitochondrial defects, can contribute to the fermentation metabolism seen in tumor cells.
  • data from the nuclear and mitochondrial transfer experiments suggest that oncogene changes are effects, rather than causes, of tumorigenesis
  • Normal mitochondria can suppress tumorigenesis, whereas abnormal mitochondria can enhance tumorigenesis
  • In addition to glucose, cancer cells also rely heavily on glutamine for growth and survival
  • Glutamine is anapleurotic and can be rapidly metabolized to glutamate and then to α-ketoglutarate for entry into the TCA cycle
  • Glucose and glutamine act synergistically for driving rapid tumor cell growth
  • Glutamine metabolism can produce ATP from the TCA cycle under aerobic conditions
  • Amino acid fermentation can generate energy through TCA cycle substrate level phosphorylation under hypoxic conditions
  • Hif-1α stabilization enhances aerobic fermentation
  • targeting glucose and glutamine will deprive the microenvironment of fermentable fuels
  • Although Warburg’s hypothesis on the origin of cancer has created confusion and controversy [37, 38, 39, 40], his hypothesis has never been disproved
  • Warburg referred to the phenomenon of enhanced glycolysis in cancer cells as “aerobic fermentation” to highlight the abnormal production of lactic acid in the presence of oxygen
  • Emerging evidence indicates that macrophages, or their fusion hybridization with neoplastic stem cells, are the origin of metastatic cancer cells
  • Radiation therapy can enhance fusion hybridization that could increase risk for invasive and metastatic tumor cells
  • Kamphorst et al. in showing that pancreatic ductal adenocarcinoma cells could obtain glutamine under nutrient poor conditions through lysosomal digestion of extracellular proteins
  • It will therefore become necessary to also target lysosomal digestion, under reduced glucose and glutamine conditions, to effectively manage those invasive and metastatic cancers that express cannibalism and phagocytosis.
  • Previous studies in yeast and mammalian cells show that disruption of aerobic respiration can cause mutations (loss of heterozygosity, chromosome instability, and epigenetic modifications etc.) in the nuclear genome
  • The somatic mutations and genomic instability seen in tumor cells thus arise from a protracted reliance on fermentation energy metabolism and a disruption of redox balance through excess oxidative stress.
  • According to the mitochondrial metabolic theory of cancer, the large genomic heterogeneity seen in tumor cells arises as a consequence, rather than as a cause, of mitochondrial dysfunction
  • A therapeutic strategy targeting the metabolic abnormality common to most tumor cells should therefore be more effective in managing cancer than would a strategy targeting genetic mutations that vary widely between tumors of the same histological grade and even within the same tumor
  • Tumor cells are more fit than normal cells to survive in the hypoxic niche of the tumor microenvironment
  • Hypoxic adaptation of tumor cells allows for them to avoid apoptosis due to their metabolic reprograming following a gradual loss of respiratory function
  • The high rates of tumor cell glycolysis and glutaminolysis will also make them resistant to apoptosis, ROS, and chemotherapy drugs
  • Despite having high levels of ROS, glutamate-derived from glutamine contributes to glutathione production that can protect tumor cells from ROS
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      reason to eliminate glutamine in cancer patients and even GSH with cancer patients
  • It is clear that adaptability to environmental stress is greater in normal cells than in tumor cells, as normal cells can transition from the metabolism of glucose to the metabolism of ketone bodies when glucose becomes limiting
  • Mitochondrial respiratory chain defects will prevent tumor cells from using ketone bodies for energy
  • glycolysis-dependent tumor cells are less adaptable to metabolic stress than are the normal cells. This vulnerability can be exploited for targeting tumor cell energy metabolism
  • In contrast to dietary energy reduction, radiation and toxic drugs can damage the microenvironment and transform normal cells into tumor cells while also creating tumor cells that become highly resistant to drugs and radiation
  • Drug-resistant tumor cells arise in large part from the damage to respiration in bystander pre-cancerous cells
  • Because energy generated through substrate level phosphorylation is greater in tumor cells than in normal cells, tumor cells are more dependent than normal cells on the availability of fermentable fuels (glucose and glutamine)
  • Ketone bodies and fats are non-fermentable fuels
  • Although some tumor cells might appear to oxidize ketone bodies by the presence of ketolytic enzymes [181], it is not clear if ketone bodies and fats can provide sufficient energy for cell viability in the absence of glucose and glutamine
  • Apoptosis under energy stress is greater in tumor cells than in normal cells
  • A calorie restricted ketogenic diet or dietary energy reduction creates chronic metabolic stress in the body
  • . This energy stress acts as a press disturbance
  • Drugs that target availability of glucose and glutamine would act as pulse disturbances
  • Hyperbaric oxygen therapy can also be considered another pulse disturbance
  • The KD can more effectively reduce glucose and elevate blood ketone bodies than can CR alone making the KD potentially more therapeutic against tumors than CR
  • Campbell showed that tumor growth in rats is greater under high protein (>20%) than under low protein content (<10%) in the diet
  • Protein amino acids can be metabolized to glucose through the Cori cycle
  • The fats in KDs used clinically also contain more medium chain triglycerides
  • Calorie restriction, fasting, and restricted KDs are anti-angiogenic, anti-inflammatory, and pro-apoptotic and thus can target and eliminate tumor cells through multiple mechanisms
  • Ketogenic diets can also spare muscle protein, enhance immunity, and delay cancer cachexia, which is a major problem in managing metastatic cancer
  • GKI values of 1.0 or below are considered therapeutic
  • The GKI can therefore serve as a biomarker to assess the therapeutic efficacy of various diets in a broad range of cancers.
  • It is important to remember that insulin drives glycolysis through stimulation of the pyruvate dehydrogenase complex
  • The water-soluble ketone bodies (D-β-hydroxybutyrate and acetoacetate) are produced largely in the liver from adipocyte-derived fatty acids and ketogenic dietary fat. Ketone bodies bypass glycolysis and directly enter the mitochondria for metabolism to acetyl-CoA
  • Due to mitochondrial defects, tumor cells cannot exploit the therapeutic benefits of burning ketone bodies as normal cells would
  • Therapeutic ketosis with racemic ketone esters can also make it feasible to safely sustain hypoglycemia for inducing metabolic stress on cancer cells
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      Ketones are much more than energy adaptabilit, but actually are therapeutic.
  • ketone bodies can inhibit histone deacetylases (HDAC) [229]. HDAC inhibitors play a role in targeting the cancer epigenome
  • Therapeutic ketosis reduces circulating inflammatory markers, and ketones directly inhibit the NLRP3 inflammasome, an important pro-inflammatory pathway linked to carcinogenesis and an important target for cancer treatment response
  • Chronic psychological stress is known to promote tumorigenesis through elevations of blood glucose, glucocorticoids, catecholamines, and insulin-like growth factor (IGF-1)
  • In addition to calorie-restricted ketogenic diets, psychological stress management involving exercise, yoga, music etc. also act as press disturbances that can help reduce fatigue, depression, and anxiety in cancer patients and in animal models
  • Ketone supplementation has also been shown to reduce anxiety behavior in animal models
  • This physiological state also enhances the efficacy of chemotherapy and radiation therapy, while reducing the side effects
  • lower dosages of chemotherapeutic drugs can be used when administered together with calorie restriction or restricted ketogenic diets (KD-R)
  • Besides 2-DG, a range of other glycolysis inhibitors might also produce similar therapeutic effects when combined with the KD-R including 3-bromopyruvate, oxaloacetate, and lonidamine
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      oxaloacetate is a glycolytic inhibitor, as is doxycycline, and IVC.
  • A synergistic interaction of the KD diet plus radiation was seen
  • It is important to recognize, however, that the radiotherapy used in glioma patients can damage the respiration of normal cells and increase availability of glutamine in the microenvironment, which can increase risk of tumor recurrence especially when used together with the steroid drug dexamethasone
  • Poff and colleagues demonstrated that hyperbaric oxygen therapy (HBOT) enhanced the ability of the KD to reduce tumor growth and metastasis
  • HBOT also increases oxidative stress and membrane lipid peroxidation of GBM cells in vitro
  • The effects of the KD and HBOT can be enhanced with administration of exogenous ketones, which further suppressed tumor growth and metastasis
  • Besides HBOT, intravenous vitamin C and dichloroacetate (DCA) can also be used with the KD to selectively increase oxidative stress in tumor cells
  • Recent evidence also shows that ketone supplementation may enhance or preserve overall physical and mental health
  • Some tumors use glucose as a prime fuel for growth, whereas other tumors use glutamine as a prime fuel [102, 186, 262, 263, 264]. Glutamine-dependent tumors are generally less detectable than glucose-dependent under FDG-PET imaging, but could be detected under glutamine-based PET imaging
  • GBM and use glutamine as a major fuel
  • Many of the current treatments used for cancer management are based on the view that cancer is a genetic disease
  • Emerging evidence indicates that cancer is a mitochondrial metabolic disease that depends on availability of fermentable fuels for tumor cell growth and survival
  • Glucose and glutamine are the most abundant fermentable fuels present in the circulation and in the tumor microenvironment
  • Low-carbohydrate, high fat-ketogenic diets coupled with glycolysis inhibitors will reduce metabolic flux through the glycolytic and pentose phosphate pathways needed for synthesis of ATP, lipids, glutathione, and nucleotides
  • Nathan Goodyear on 09 Jul 17
     
    Cancer is a mitochondrial disease? So says the well published Dr Seyfried. Glucose and glutamine drive cancer growth.
Nathan Goodyear

Fructose-1,6-bisphosphate couples glycolytic flux to activation of Ras | Nature Communi... - 0 views

www.nature.com/...s41467-017-01019-z

cancer glucose sugar nutrition genetics vitamin C RAS

shared by Nathan Goodyear on 20 Oct 17 - No Cached
  • glucose deprivation triggers apoptosis47 and vitamin C treatment kills RAS-oncogene expressing tumor cells, but not wild-type RAS containing cells, by inhibition of GAPDH
  • Nathan Goodyear on 20 Oct 17
     
    New study out of the UK supports the role of glucose in cancer growth and aggressiveness.  This research found that high influx of glucose into the glycolysis pathway upregulated the RAS oncogene via accumulation of the Fructose 1,6 bisphosphonate through the enzyme phosphofructokinase..
Nathan Goodyear

Ozone therapy: A clinical review - 0 views

www.ncbi.nlm.nih.gov/...PMC3312702

cancer Ozone

shared by Nathan Goodyear on 13 Apr 20 - No Cached
  • Its basic function is to protect humans from harmful effects of UV radiation
  • Its effects are proven, consistent and with minimal side effects
  • Medical O3, used to disinfect and treat disease, has been around for over 150 years
  • ...11 more annotations...
  • O3 not only remedied infection, but also had hemodynamic and anti-inflammatory properties
  • Stimulation of oxygen metabolism
  • In fungi, O3 inhibits cell growth at certain stages
  • With viruses, the O3 damages the viral capsid and upsets the reproductive cycle by disrupting the virus-to-cell contact with peroxidation.
  • Inactivation of bacteria, viruses, fungi, yeast and protozoa: Ozone therapy disrupts the integrity of the bacterial cell envelope through oxidation of the phospholipids and lipoproteins
  • Activation of the immune system
  • 30 and 55 μg/cc
  • production of interferon and the greatest output of tumor necrosis factor and interleukin-2
  • Mechanism of action of O3 on the human lung
  • cascade of reactions like peroxidation of lipids leading to changes in membrane permeability,[41] lipid ozonation products (LOP) act as signal transducer molecules
  • Dietary antioxidants or free radical scavengers like vitamin E, C, etc., can prevent aforementioned effects of O3
  • Nathan Goodyear on 13 Apr 20
     
    Ozone therapy review
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