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Nathan Goodyear

SVCT1 and SVCT2: key proteins for vitamin C uptake. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...17541511

SVCTs SVCT "sodium-ascorbate co-transporters " "vitamin C"

shared by Nathan Goodyear on 25 Jan 19 - No Cached
  • Nathan Goodyear on 25 Jan 19
     
    Good review of sodium ascorbate co-transporters SVCT.
felipp windsor

Toothache Taken Care Of - 1 views

I would like to say a warm and big thanks to The Dental Co. for helping my daughter. She was terribly in pain for 3 days due to extreme toothache. I was already worried because her gums were alread...

dental care windsor

started by felipp windsor on 02 Jul 13 no follow-up yet
Management Health Solutions Inc

Webinar: Focusing on the Big Picture of Your Supply Chain Yields Compelling Financial R... - 0 views

upcoming.yahoo.com/...fairfield

mhs events

shared by Management Health Solutions Inc on 24 Oct 12 - No Cached
  • Management Health Solutions Inc on 24 Oct 12
     
    Continuous changes in the healthcare reimbursement criteria require executives across the industry to focus on enterprise-wide changes that have a positive effect on supply chain savings. It's a complex problem and it's easy to get distracted on one issue when having the ability to see a clear BIG picture of your entire supply chain is what can lead to the most dramatic results and return on investments. Register for MHS' webinar on November 01 (2:00pm EST) to learn about how their customers experience an average 4:1 ROI with continual savings into the millions and a positive financial impact to their bottom line through inventory reduction, avoidance of obsolete and expired inventory, improved charge capture for each patient, and physician preference card optimization. Click on http://bit.ly/UvD3nq Presenters *Michael Ferris: Co-Founder, MHS with over 30 years of supply chain management experience *Steve Basiliere: Former Director of Supply Chain Services at Saints Medical Center, Lowell, MA *Art Kozyrovicius: Finance and Procurement Systems Support at New York-Presbyterian Hospital, New York, NY WHY ATTEND? Join a unique discussion with healthcare supply chain thought leaders and understand how to drive significant and sustainable supply chain operational improvements. Get a jump on making an immediate and positive impact on your bottom line as you head into 2013. Register by clicking on http://bit.ly/UvD3nq Note: Event will be online, through WebEx Please Register at http://bit.ly/UvD3nq
Nathan Goodyear

Hyponatremia and the Thyroid: Causality or Association? - 0 views

www.ncbi.nlm.nih.gov/...PMC4470237

hypothyroid hypothyroidism hyponatremia sodium thyroid

shared by Nathan Goodyear on 23 May 16 - No Cached
  • Nathan Goodyear on 23 May 16
     
    hypothyroidism and hyponatremia is a rare finding; more commonly associated with severe hypothyroidism.  Co-exisitng medical complications need to be considered.
Windows Customer Support Number

1-800-485-4057 Windows technical support number - 0 views

www.vendanything.com/...-technical-support-number.html

Windows tech support customer services

shared by Windows Customer Support Number on 25 May 16 - No Cached
  • Windows Customer Support Number on 25 May 16
     
    With the help of Windows technical support service you can never facing any issues or queries with your Windows software. Our services are of excellence in nature! We provides our services by well-trained and experienced specialists who are good at what they do. You need to do it just dial our Windows technical support nnmber 1-800-485-4057 and get excellent help, you can also visit our websites as http://technicalsupportnumberforwindows.co m/
Nathan Goodyear

http://www.curcumin.co.nz/pdf/Curcumin_Getting_Back_To_The_Roots.pdf - 0 views

www.curcumin.co.nz/..._Getting_Back_To_The_Roots.pdf

curcumin turmeric disease natural therapy treatment

shared by Nathan Goodyear on 22 Jan 14 - No Cached
  • Nathan Goodyear on 22 Jan 14
     
    Great, exhaustive review of turmeric and disease.
Nathan Goodyear

Testosterone and glucose metabolism in men: current concepts and controversies - 0 views

joe.endocrinology-journals.org/...R37.full

Low T Testosterone metabolic syndrome MetS Diabetes men male glucose hormone hormones g

shared by Nathan Goodyear on 04 Feb 14 - No Cached
  • Around 50% of ageing, obese men presenting to the diabetes clinic have lowered testosterone levels relative to reference ranges based on healthy young men
  • The absence of high-level evidence in this area is illustrated by the Endocrine Society testosterone therapy in men with androgen deficiency clinical practice guidelines (Bhasin et al. 2010), which are appropriate for, but not specific to men with metabolic disorders. All 32 recommendations made in these guidelines are based on either very low or low quality evidence.
  • A key concept relates to making a distinction between replacement and pharmacological testosterone therapy
  • ...59 more annotations...
  • The presence of symptoms was more closely linked to increasing age than to testosterone levels
  • Findings similar to type 2 diabetes were reported for men with the metabolic syndrome, which were associated with reductions in total testosterone of −2.2 nmol/l (95% CI −2.41 to 1.94) and in free testosterone
  • low testosterone is more predictive of the metabolic syndrome in lean men
  • Cross-sectional studies uniformly show that 30–50% of men with type 2 diabetes have lowered circulating testosterone levels, relative to references based on healthy young men
  • In a recent cross-sectional study of 240 middle-aged men (mean age 54 years) with either type 2 diabetes, type 1 diabetes or without diabetes (Ng Tang Fui et al. 2013b), increasing BMI and age were dominant drivers of low total and free testosterone respectively.
  • both diabetes and the metabolic syndrome are associated with a modest reduction in testosterone, in magnitude comparable with the effect of 10 years of ageing
  • In a cross-sectional study of 490 men with type 2 diabetes, there was a strong independent association of low testosterone with anaemia
  • In men, low testosterone is a marker of poor health, and may improve our ability to predict risk
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      probably the most important point made in this article
  • low testosterone identifies men with an adverse metabolic phenotype
  • Diabetic men with low testosterone are significantly more likely to be obese or insulin resistant
  • increased inflammation, evidenced by higher CRP levels
  • Bioavailable but not free testosterone was independently predictive of mortality
  • It remains possible that low testosterone is a consequence of insulin resistance, or simply a biomarker, co-existing because of in-common risk factors.
  • In prospective studies, reviewed in detail elsewhere (Grossmann et al. 2010) the inverse association of low testosterone with metabolic syndrome or diabetes is less consistent for free testosterone compared with total testosterone
  • In a study from the Framingham cohort, SHBG but not testosterone was prospectively and independently associated with incident metabolic syndrome
  • low SHBG (Ding et al. 2009) but not testosterone (Haring et al. 2013) with an increased risk of future diabetes
  • In cross-sectional studies of men with (Grossmann et al. 2008) and without (Bonnet et al. 2013) diabetes, SHBG but not testosterone was inversely associated with worse glycaemic control
  • SHBG may have biological actions beyond serving as a carrier protein for and regulator of circulating sex steroids
  • In men with diabetes, free testosterone, if measured by gold standard equilibrium dialysis (Dhindsa et al. 2004), is reduced
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      expensive, laborious process filled with variables
  • Low free testosterone remains inversely associated with insulin resistance, independent of SHBG (Grossmann et al. 2008). This suggests that the low testosterone–dysglycaemia association is not solely a consequence of low SHBG.
  • Experimental evidence reviewed below suggests that visceral adipose tissue is an important intermediate (rather than a confounder) in the inverse association of testosterone with insulin resistance and metabolic disorders.
  • testosterone promotes the commitment of pluripotent stem cells into the myogenic lineage and inhibits their differentiation into adipocytes
  • testosterone regulates the metabolic functions of mature adipocytes (Xu et al. 1991, Marin et al. 1995) and myocytes (Pitteloud et al. 2005) in ways that reduce insulin resistance.
  • Pre-clinical evidence (reviewed in Rao et al. (2013)) suggests that at the cellular level, testosterone may improve glucose metabolism by modulating the expression of the glucose-transported Glut4 and the insulin receptor, as well as by regulating key enzymes involved in glycolysis.
  • More recently testosterone has been shown to protect murine pancreatic β cells against glucotoxicity-induced apoptosis
  • Interestingly, a reciprocal feedback also appears to exist, given that not only chronic (Cameron et al. 1990, Allan 2013) but also, as shown more recently (Iranmanesh et al. 2012, Caronia et al. 2013), acute hyperglycaemia can lower testosterone levels.
  • There is also evidence that testosterone regulates insulin sensitivity directly and acutely
  • In men with prostate cancer commencing androgen deprivation therapy, both total as well as, although not in all studies (Smith 2004), visceral fat mass increases (Hamilton et al. 2011) within 3 months
  • More prolonged (>12 months) androgen deprivation therapy has been associated with increased risk of diabetes in several large observational registry studies
  • Testosterone has also been shown to reduce the concentration of pro-inflammatory cytokines in some, but not all studies, reviewed recently in Kelly & Jones (2013). It is not know whether this effect is independent of testosterone-induced changes in body composition.
  • the observations discussed in this section suggest that it is the decrease in testosterone that causes insulin resistance and diabetes. One important caveat remains: the strongest evidence that low testosterone is the cause rather than consequence of insulin resistance comes from men with prostate cancer (Grossmann & Zajac 2011a) or biochemical castration, and from mice lacking the androgen receptor.
  • Several large prospective studies have shown that weight gain or development of type 2 diabetes is major drivers of the age-related decline in testosterone levels
  • there is increasing evidence that healthy ageing by itself is generally not associated with marked reductions in testosterone
  • Circulating testosterone, on an average 30%, is lower in obese compared with lean men
  • increased visceral fat is an important component in the association of low testosterone and insulin resistance
  • The vast majority of men with metabolic disorders have functional gonadal axis suppression with modest reductions in testosterone levels
  • obesity is a dominant risk factor
  • men with Klinefelter syndrome have an increased risk of metabolic disorders. Interestingly, greater body fat mass is already present before puberty
  • Only 5% of men with type 2 diabetes have elevated LH levels
  • inhibition of the gonadal axis predominantly takes place in the hypothalamus, especially with more severe obesity
  • Metabolic factors, such as leptin, insulin (via deficiency or resistance) and ghrelin are believed to act at the ventromedial and arcuate nuclei of the hypothalamus to inhibit gonadotropin-releasing hormone (GNRH) secretion from GNRH neurons situated in the preoptic area
  • kisspeptin has emerged as one of the most potent secretagogues of GNRH release
  • hypothesis that obesity-mediated inhibition of kisspeptin signalling contributes to the suppression of the HPT axis, infusion of a bioactive kisspeptin fragment has been recently shown to robustly increase LH pulsatility, LH levels and circulating testosterone in hypotestosteronaemic men with type 2 diabetes
  • A smaller study with a similar experimental design found that acute testosterone withdrawal reduced insulin sensitivity independent of body weight, whereas oestradiol withdrawal had no effects
  • suppression of the diabesity-associated HPT axis is functional, and may hence be reversible
  • Obesity and dysglycaemia and associated comorbidities such as obstructive sleep apnoea (Hoyos et al. 2012b) are important contributors to the suppression of the HPT axis
  • weight gain and development of diabetes accelerate the age-related decline in testosterone
  • Modifiable risk factors such as obesity and co-morbidities are more strongly associated with a decline in circulating testosterone levels than age alone
  • 55% of symptomatic androgen deficiency reverted to a normal testosterone or an asymptomatic state after 8-year follow-up, suggesting that androgen deficiency is not a stable state
  • Weight loss can reactivate the hypothalamic–pituitary–testicular axis
  • Leptin treatment resolves hypogonadism in leptin-deficient men
  • The hypothalamic–pituitary–testicular axis remains responsive to treatment with aromatase inhibitors or selective oestrogen receptor modulators in obese men
  • Kisspeptin treatment increases LH secretion, pulse frequency and circulating testosterone levels in hypotestosteronaemic men with type 2 diabetes
  • change in BMI was associated with the change in testosterone (Corona et al. 2013a,b).
  • weight loss can lead to genuine reactivation of the gonadal axis by reversal of obesity-associated hypothalamic suppression
  • There is pre-clinical and observational evidence that chronic hyperglycaemia can inhibit the HPT axis
  • in men who improved their glycaemic control over time, testosterone levels increased. By contrast, in those men in whom glycaemic control worsened, testosterone decreased
  • testosterone levels should be measured after successful weight loss to identify men with an insufficient rise in their testosterone levels. Such men may have HPT axis pathology unrelated to their obesity, which will require appropriate evaluation and management.
  • Nathan Goodyear on 04 Feb 14
     
    Article discusses the expanding evidence of low T and Metabolic syndrome.
Nathan Goodyear

http://www.nutri-online1.co.uk/LinkClick.aspx?fileticket=t2zR1kIHuCA%3D&tabid=101&mid=1260 - 0 views

www.nutri-online1.co.uk/LinkClick.aspx

detoxification disease

shared by Nathan Goodyear on 02 Mar 14 - No Cached
  • Nathan Goodyear on 02 Mar 14
     
    Detoxification and chronic disease.
felipp windsor

Thank You The Dental Co. - 1 views

I really got worried when I found out that I got some tooth problems. For one thing, I have low tolerance to pain and I do not want to lose any of my teeth. That is why I looked for the best dentis...

teeth whitening windsor

started by felipp windsor on 03 Dec 13 no follow-up yet
Nathan Goodyear

Estrogen receptor acts as a dominant regulator of estrogen signaling - 0 views

www.nature.com/...1203828a.html

ER beta ER-beta ER alpha ER-alpha ER estrogen receptor estrogen receptors estrogen

shared by Nathan Goodyear on 09 Jun 14 - No Cached
  • Nathan Goodyear on 09 Jun 14
     
    ER-beta expression appears to regulate estrogenic activity through ER-alpha expression.  Co-expression of ER-alpha and ER-beta is associated with reduced estrogenic signaling, indicating a significant counter regulatory role for ER-beta.
Willow O'Donnell

Sell you infusion pumps -Willomed - angel.co - 0 views

angel.co/willow-odonnell

Sell you infusion pumps

shared by Willow O'Donnell on 20 Oct 14 - No Cached
  • Willow O'Donnell on 20 Oct 14
     
    Willow Medical provides Medical/Safety Supplies, IV pumps & Refurbished Medical Equipment to various market segments.
wheelchairindia9

Net Neutrality: Battle to 'save the Internet' - 0 views

onlywheelchair.blogspot.in/...y-battle-to-save-internet.html

Net Neutrality: Battle to 'save the Internet' Internet service providers Net Neutrality KP 80 power standing wheelchair control the traffic

shared by wheelchairindia9 on 15 Apr 15 - No Cached
  • wheelchairindia9 on 15 Apr 15
     
    Net neutrality is one of the biggest issue debated globally by the telecom regulators and it is also in the process of finalising what will be a landmark recommendation for Indian telecom. The important aspects of Net neutrality are: Internet service providers should enable access to all content and applications regardless of the source. The Internet service provider from whom buy internet pack, should not under any circumstance be able to control how exactly use it and it's upto how you use the data. All websites can co-exist without hampering others and all websites are accessible at the same speed and no particular website of application is favoured. All web sites and content creators are treated equal, and it don't have to pay extra for faster Internet speed to a particular site/service. The concept of net neutrality doesn't exist legally but most companies have Net Neutrality is simply the Internet Freedom - Free, Fast and Open Internet for all. Net Neutrality is the principle that Internet service providers (ISPs) should give consumers access to all and every contents and application on an equal basis, treating all Internet traffic equally. Today, if there's something that makes everyone across the world "Equal" is nothing but the Internet. Equality over the Internet means, the richest man in the world has the same rights to access the Internet as the poorer. And this is what "Net Neutrality" aims at adhered to it until now. With the Internet taking the world into its folds, Internet Service Providers across the world are trying to encash this potent commodity and trying to control the traffic. Karma Healthcare KP-80 Standing Wheelchair is a compact and fully powered wheelchair designed for budget. The front-wheel drive provides agile control for the chair to negotiate various indoors and out. It comes with the innovative seat and wide range of power backrest angle adjustment (80~120 degree).
wheelchairindia9

Cervical Collar Hard Adjustable With Chin - 0 views

www.wheelchairindia.com/...llar-Hard-Adjustable-With-Chin

Is Applying Or Removing a Cervical Collar Dangerous convenient hook and loop closure completely restrict motion immobilizing or adjusting the neck muscular atrophy and patients neck injuries and strains

shared by wheelchairindia9 on 02 Apr 16 - No Cached
  • wheelchairindia9 on 02 Apr 16
     
    The soft cervical collar is constructed of foam rubber and covered with a stockinette material. Normally, the closure is achieved with Velcro. Depending on the patient's pathology and body structure, physician and/or orthotist will determine the proper height of the collar. When worn, the soft cervical collar is a reminder to keep in head and neck in a restricted position. It is the mildest design of cervical immobilization. Cervical collars are applied to blunt trauma patients all the time. And most of the time, the neck is fine. It's just those few patients that have fracture or ligamentous injury that really need it. The Cervical Collar provides firm, comfortable support which helps to relieve neck discomfort while providing extra support. Cervical Collar has a convenient hook and loop closure which allows the unit to be adjusted for a proper fit. The Cervical Collar is constructed of soft, porous cotton cover for comfort which is over polyfoam for the best support. Cervical collars are an orthotic device used primarily in the treatment of neck injuries and strains. The most common use of cervical collars is during recovery after surgery on the cervical spine. They are also used in whiplash injuries and conditions like Cervical Radiculopathy, which is caused by the nerves in the neck compressing due to herniated disks in the spinal cord. The main function of the cervical collar is to immobilize the neck and hold it in a gravity-neutral position Tynor Cervical Collar Hard Adjustable is used for supporting, immobilizing or adjusting the neck in the flexion, extension, or hyperextension position. Recommended where a rigid immobilization of the cervical region is required. Anatomical shape. Comfortable edge padding. Adjustable height. Slight weight. Latex free. The soft cervical collar is not designed to completely restrict motion. It depends on providing resistance to movement, which tells the patient to restrict their movements. The soft collar i
Nathan Goodyear

https://onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%2819900501%2963%3A9%3C1700%3A... - 0 views

onlinelibrary.wiley.com/...NCR2820630910%3E3.0.CO%3B2-%23

Hodgkin's lymphoma non-hodgkin's lymphoma lymphoma sarcoidosis vitamin D calcitriol hypercalcemia calcium

shared by Nathan Goodyear on 21 Aug 18 - No Cached
  • Nathan Goodyear on 21 Aug 18
     
    Hodgkin's and non-Hodgkin's lymphoma increase calcitriol production (1,25) similar to sarcoidosis.  This can lead to hypercalcemia.  This is a case study.
Nathan Goodyear

https://doctorsonly.co.il/wp-content/uploads/2013/07/08_Epigenetic-Transmission.pdf - 0 views

doctorsonly.co.il/...08_Epigenetic-Transmission.pdf

PTSD epigenetics transgenerational transmission of trauma transgenerational inheritance

shared by Nathan Goodyear on 09 Oct 17 - No Cached
  • Nathan Goodyear on 09 Oct 17
     
    Study suggest the PTSD from the holocaust can be epigenetically transmitted to the offspring of the survivors.
Nathan Goodyear

The river blindness drug Ivermectin and related macrocyclic lactones inhibit WNT-TCF pa... - 0 views

www.ncbi.nlm.nih.gov/...PMC4287931

ivermectin cancer WTF Selamectin

shared by Nathan Goodyear on 19 Mar 18 - No Cached
  • WNT signaling
  • early colon cancers commonly display loss of function of the tumor suppressor Adenomatous polyposis coli (APC), a key component of the β-CATENIN destruction complex
  • Other cancers also show an active canonical WNT pathway; these include carcinomas of the lung, stomach, cervix, endometrium, and lung as well as melanomas and gliomas
  • ...31 more annotations...
  • In normal embryogenesis and homeostasis, the canonical WNT pathway is activated by secreted WNT ligands produced in highly controlled context-dependent manners and in precise amounts. WNT activity is transduced in the cytoplasm, inactivates the APC destruction complex, and results in the translocation of activate β-CATENIN to the nucleus, where it cooperates with DNA-binding TCF/LEF factors to regulate WNT-TCF targets and the ensuing genomic response
  • beyond the loss of activity of the APC destruction complex, for instance throughAPC mutation, phosphorylation of β-CATENIN at C-terminal sites is required for the full activation of WNT-TCF signaling and the ensuing WNT-TCF responses in cancer.
  • The WNT-TCF response blockade that we describe for low doses of Ivermectin suggests an action independent to the deregulation of chloride channels
  • involve the repression of the levels of C-terminally phosphorylated β-CATENIN forms and of CYCLIN D1, a critical target that is an oncogene and positive cell cycle regulator.
  • the Avermectin single-molecule derivative Selamectin, a drug widely used in veterinarian medicine (Nolan & Lok, 2012), is ten times more potent acting in the nanomolar range
  • Ivermectin also diminished the protein levels of CYCLIN D1, a direct TCF target and oncogene, in both HT29 and H358 tumor cells
  • Activated Caspase3 was used as a marker of apoptosis by immunohistochemistry 48 h after drug treatment. Selamectin and Ivermectin induced up to a sevenfold increase in the number of activated Caspase3+ cells in two primary (CC14 and CC36) and two cell line (DLD1 and Ls174T) colon cancer cell types (Fig​(Fig2C).2C). All changes were significative
  • The strong downregulation of the expression of the intestinal stem cell genesASCL2 andLGR5 (van der Flieret al, 2009; Scheperset al, 2012; Zhuet al, 2012b) by Ivermectin and Selamectin (Fig​(Fig2D)2D) raised the possibility that these drugs could affect WNT-TCF-dependent colon cancer stem cell behavior
  • Pre-established H358 tumors responded to Ivermectin showing a ˜ 50% repression of growth
  • Ivermectin hasin vivo efficacy against human colon cancer xenografts sensitive to TCF inhibition with no discernable side effects
  • Ivermectin (Campbellet al, 1983), an off-patent drug approved for human use, and related macrocyclic lactones, have WNT-TCF pathway response blocking and anti-cancer activities
  • these drugs block WNT-TCF pathway responses, likely acting at the level of β-CATENIN/TCF function, affecting β-CATENIN phosphorylation status.
  • anti-WNT-TCF activities of Ivermectin and Selamectin
  • Ivermectin has a well-known anti-parasitic activity mediated via the deregulation of chloride channels, leading to paralysis and death (Hibbs & Gouaux, 2011; Lynagh & Lynch, 2012). The same mode of action has been suggested to underlie the toxicity of Ivermectin for liquid tumor cells and the potentiation or sensitization effect of Avermectin B1 on classical chemotherapeutics
  • the specificity of the blockade of WNT-TCF responses we document, at low micromolar doses for Ivermectin and low nanomolar doses for Selamectin, indicate that the blockade of WNT-TCF responses and chloride channel deregulation are distinct modes of action
  • What is key then is to find a dose and a context where the use of Ivermectin has beneficial effects in patients, paralleling our results with xenografts in mice.
  • Cell toxicity appears at doses greater (> 10 μM for 12 h or longer or > 5 μM for 48 h or longer for Ivermectin) than those required to block TCF responses and induce apoptosis.
  • Our data point to a repression of WNT-β-CATENIN/TCF transcriptional responses by Ivermectin, Selamectin and related macrocylic lactones.
  • (i) The ability of Avermectin B1 to inhibit the activation of WNT-TCF reporter activity by N-terminal mutant (APC-insensitive) β-CATENIN as detected in our screen
  • (ii) The ability of Avermectin B1, Ivermectin, Doramectin, Moxidectin and Selamectin to parallel the modulation of WNT-TCF targets by dnTCF
  • (iii) The finding that the specific WNT-TCF response blockade by low doses of Ivermectin and Selamectin is reversed by constitutively active TCF
  • (iv) The repression of key C-terminal phospho-isoforms of β-CATENIN resulting in the repression of the TCF target and positive cell cycle regulator CYCLIN D1 by Ivermectin and Selamectin
  • (v) The specific inhibition ofin-vivo-TCF-dependent, but notin-vivo-TCF-independent cancer cells by Ivermectin in xenografts.
  • These results together with the reduction of the expression of the colon cancer stem cell markersASCL2 andLGR5 (e.g., Hirschet al, 2013; Ziskinet al, 2013) raise the possibility of an inhibitory effect of Ivermectin, Selamectin and related macrocyclic lactones on TCF-dependent cancer stem cells.
  • the capacity of cancer cells to form 3D spheroids in culture, as well as the growth of these, is also WNT-TCF-dependent (Kanwaret al, 2010) and they were also affected by Ivermectin treatment
  • If Ivermectin is specific, it should only block TCF-dependent tumor growth. Indeed, the sensitivity and insensitivity of DLD1 and CC14 xenografts to Ivermectin treatment, respectively, together with the desensitization to Ivermectin actionin vivo by constitutively active TCF provide evidence of the specificity of this drug to block an activated WNT-TCF pathway in human cancer.
  • Ivermectin has a good safety profile since onlyin-vivo-dnTCF-sensitive cancer xenografts are responsive to Ivermectin treatment, and we have not detected side effects in Ivermectin-treated mice at the doses used
  • previous work has shown that side effects from systemic treatments with clinically relevant doses in humans are rare (Yang, 2012), that birth defects were not observed after exposure of pregnant mothers (Pacquéet al, 1990) and that this drug does not cross the blood–brain barrier (Kokozet al, 1999). Similarly, only dogs with mutantABCB1 (MDR1) alleles leading to a broken blood–brain barrier show Ivermectin neurotoxicity (Mealeyet al, 2001; Orzechowskiet al, 2012)
  • Indications may include treatment for incurable β-CATENIN/TCF-dependent advanced and metastatic human tumors of the lung, colon, endometrium, and other organs.
  • Ivermectin, Selamectin, or related macrocyclic lactones could also serve as topical agents for WNT-TCF-dependent skin lesions and tumors such as basal cell carcinomas
  • they might also be useful as routine prophylactic agents, for instance against nascent TCF-dependent intestinal tumors in patients with familial polyposis and against nascent sporadic colon tumors in the general aging population
  • Nathan Goodyear on 19 Mar 18
     
    Ivermectin, a common anti-parasitic, found to inhibit WTF-TCF pathway and decrease c-terminal phosophorylaiton of Beta-CATENIN all resulting in increased aptosis and inhibition of cancer growth in colon cancer cell lines and lung cancer cell lines.
Nathan Goodyear

Curcumin Down-Regulates DNA Methyltransferase 1 and Plays an Anti-Leukemic Role in Acut... - 0 views

www.ncbi.nlm.nih.gov/...PMC3572185

aml acute myeloid leukemia cancer leukemia curcumin NF-kappaB

shared by Nathan Goodyear on 12 May 18 - No Cached
  • In a variety of solid tumors and blood cancers, aberrant hypermethylation of CpG-rich regions (>55% CG content, 0.5-4 kb in length, the so-called “CpG islands”) in the promoters of tumor suppressor genes (TSGs) results in their transcriptional silencing
  • These agents have been reported to suppress tumor growth by reversing aberrantly hypermethylation in the promoters of inactivated TSGs (e.g. p15INK4B), allowing re-expression of TSGs, thereby restoring normal cell cycle regulation, proliferation, apoptosis, and differentiation
  • groups have reported that curcumin acts as a scavenger of free radicals [13], an inhibitor of NF-κB nuclear translocation [14], and a modulator of histone deacetylase (HDAC) and histone acetyltransferase (HAT)
  • ...9 more annotations...
  • In this study, we found that curcumin down-regulated DNMT1 expression in AML cells. This occurred, at least in part, through down-modulation of two positive regulators of DNMT1: Sp1 and the NF-κB component, p65. We also found that curcumin-mediated down-regulation of DNMT1 was associated with reactivation of TSGs and tumor suppression, both in vivo and in vitro.
  • curcumin may selectively downregulate DNMT1 expression in tumor cells, but not in normal cells
  • DNMT1 expression is positively regulated by Sp1 and the NF-κB signaling component
  • indicating that curcumin may have significant anti-tumor activity in AML
  • We found that, compared to the vehicle control, curcumin treatment reduced tumor weight by 70%
  • Surprisingly, although curcumin significantly inhibited tumor growth in these mice, we were unable to find any obvious toxicity associated with curcumin treatment
  • Consistent with our observations regarding curcumin’s ability to inhibit tumor growth in vivo (Figure 4) and down-regulate DNMT1 expression in vitro and ex vivo (Figure 1), we found that decreased levels of DNMT1 protein and mRNA were expressed by tumor cells isolated from curcumin-treated mice
  • we identified curcumin as a substance which acts as an inhibitor of DNA methyltransferase enzymatic activity and induces significant global DNA hypomethylation in AML cells
  • In this study, we first demonstrated that curcumin decreases DNMT1 mRNA and protein expression levels, most likely through inhibiting expression of positive regulators of DNMT1, such as Sp1 and the p65 component of NF-κB component, and/or altering their ability to bind to the promoter region of DNMT1
  • Nathan Goodyear on 12 May 18
     
    Curcumin beneficial in AML
Nathan Goodyear

Interleukin‐2 enhances the natural killer cell response to Herceptin‐coated H... - 1 views

onlinelibrary.wiley.com/...%3AAID-IMMU3016%3E3.0.CO%3B2-J

IL-2 breast cancer cancer NK cells HER-2 immunotherapy

shared by Nathan Goodyear on 18 Jun 18 - No Cached
  • administration of low‐dose IL‐2 results in expansion of a CD3– / CD56+ NK cell population in patients with advanced cancer
  • approximately 20 % will overexpress theHer2 / neu proto‐oncogene
  • In breast cancer, Her2 / neu overexpression is associated with a worse histologicalgrade, decreased relapse‐free and overall survival periods, and altered sensitivity to chemotherapeutic regimens
  • ...17 more annotations...
  • NK cells are large granular lymphocytes that comprise approximately 10 % of circulating lymphocytes
  • all human NK cells express the CD56 antigen
  • treatment with various concentrations of IL‐2 in vivo may induce distinct functions within the NK cell compartment and, therefore, may have profound effects on NK cell‐mediated cytotoxicity
  • CD56bright
  • CD56dim
  • We show here that ADCC conducted by NK cells in vitro is enhanced by IL‐2 activation and is critically dependent on interactions between FcγRIII on NK cells and Herceptin‐coated tumor targets
  • administration of low‐dose IL‐2 to patients results in the marked expansion of a CD56+ population of immune effectors with the ability to lyse antibody‐coated cancer targets
  • NK cells represented only 7 % of lymphocytes prior to therapy but comprised over 50 % of the population after 10 weeks of low‐dose IL‐2
  • These data suggest that the enhanced ADCC seen following the expansion of NK cells with low‐dose IL‐2 is likely due to an increase in the overall number of NK cells
  • co‐administration of IL‐2 with rhu4D5 mAb will enhance activation of NK cell effector functions
  • Stimulation of NK cells with IL‐2 resulted in a significant increase in the lysis of rhu4D5‐coated targets
  • We have shown that costimulation with IL‐2 plus rhu4D5 results in significant production of IFN‐γ by NK cells with concomitant up‐regulation of cell‐surface activation and adhesion molecules
  • It has been previously demonstrated that continuous low‐dose IL‐2 can expand a CD56+ lymphocyte population, and we have now shown that this cell population is a potent mediator of ADCC against rhu4D5 mAb‐coated Her2 / neu+ targets
  • These results suggest that administration of low‐dose IL‐2 can be used to expand NK cell numbers, while higher doses may be used to enhance their cytolytic capacity in the setting of mAb therapy
  • we have demonstrated that NK cell lysis of Her2 / neu+ breast cancer cell lines in the presence of rhu4D5 mAb is markedly enhanced following stimulation with IL‐2
  • we have presented evidence that administration of low‐dose IL‐2 in vivo results in the expansion of a potent NK cell effector population
  • Our experiments suggest that NK cells costimulated with IL‐2 and immobilized IgG can secrete potent immunomodulatory cytokines which may serve to potentiate the anti‐tumor immune response.
  • Nathan Goodyear on 18 Jun 18
     
    low dose IL-2 found to expand NK levels in conjuction in with herceptin in HER-2 positive breast cancer cell lines.
Nathan Goodyear

http://www.imperialendo.co.uk/mohr.pdf - 0 views

www.imperialendo.co.uk/mohr.pdf

MMAS Massachusetts Male Aging Study low T low Testosterone Testosterone

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  • Nathan Goodyear on 07 May 17
     
    Massachusetts Male Aging Study (MMAS).
spineneuro

Health Articles - Brain Tumor Surgery Cost in India Is As Good As Anywhere Else in the... - 0 views

www.amazines.com/...6262353

Brain Tumor Surgery in India Brain Tumor Surgery Cost India Cost of Brain Tumor Surgery India Top Brain Tumor Surgeons India Best Brain Tumor Surgeons of India List of Top Brain Tumor Surgeons India

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  • spineneuro on 23 Aug 21
     
    Brain tumor surgery cost India, it is extraordinarily affordable and when compared to the developed countries comes out to be extraordinarily low cost, which is nearly one third the price in evaluation to US & UK.Top brain tumor surgeon India have gained reputation all across the world, all thanks to the high end specialists giving the best of the healthcare service at affordable cost.Spine and neuro surgery service India is right here that will help you with the high-quality low cost medical neurology procedure. Please Call +91-98604-32255 Email id:- enquiry@spineandneurosurgeryhospitalindia.co
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