The use of non-invasive salivary sampling and a cost-effective, direct enzymeimmunoassay showed a considerable advantage in the present study, compared with previous ones.
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Buy Verified PayPal Account - Old/New USA, UK, CA Countriest - 0 views
verifiedcashapp.hashnode.dev/-accounts-a-step-by-step-guide
bitcoin enabled cash app account buy a verified cashapp accounts usa old reddit how do i get is my
shared by erickjhonkdkk72 on 20 Jul 23
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Are you looking to buy verified cashapp accounts with BTC enable? We are able to provide you btc enable cashapp account at a reasonable price
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Testosterone Treatment and Mortality in Men with Low Testosterone Levels - 1 views
jcem.endojournals.org/...jc.2011-2591.abstract
testosterone therapy treatment low T men hormone hormones BHRT
shared by Nathan Goodyear on 18 Jun 12
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Testosterone therapy shown to reduce male mortality rate. Another study verifies testosterone in men with low T.
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Assessment of bioavailability of oral micronized p... [Gynecol Endocrinol. 1993] - PubM... - 0 views
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saliva testing verified as cost effective and with considerable advantage
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shared by Nathan Goodyear on 27 Jan 14
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Androgen deprivation promotes intratumoral synthesis of dihydrotestosterone from androg... - 0 views
www.nature.com/...srep01528.html
prostate cancer 3-alpha androstanediol 3-beta androstanediol DHT metabolite metabolites
shared by Nathan Goodyear on 27 Jan 14
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PSA levels in media were increased by 3α-diol
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Similarly to 3α-diol, 3β-diol also increased PSA levels in media in a concentration-dependent manner
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intracellular DHT is synthesized from inactive androgen 3α- and 3β-diol via different pathways in prostate cancer cells
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error in statement: DHT metabolites are not inactive, they just don't activate AR.
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3β-diol can be a precursor of DHT in prostate cancer cells.
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serum 3α-diol G levels reflect the androgen milieu in localized prostate cancer patients receiving ADT
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A few studies reported that 3β-diol is a potential ligand of estrogen receptor β (ERβ) and has an antiproliferative effect
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our results revealed that 3β-diol is potentially a precursor of DHT in prostate cancer cells
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Bauman et al. showed that 3α-diol is inactive at AR, but induces prostate growth
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Prostate cancer cells promoted synthesis from the DHT metabolite 3α-diol during the long duration of ADT
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the authors highlight the suggestion is that 3alpha-diol's activity is via 3alpha-HSD, but fail to mention that it is known that 3alpha-diol interacts with the ER-alpha in the prostate.
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verified the synthesis of DHT from 3α- or 3β-diol via different pathways in prostate cancer cells in this study
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HSD17B6 expression levels in prostate cancer can be useful for the diagnosis of high-risk prostate cancer
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serum 3α-diol G levels reflect the adrenal androgen milieu in localized prostate cancer patients
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3α- and 3β-diol has a much more significant role in intratumoral androgen metabolism during ADT
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DHT metabolites play an important role of intra-prostate DHT synthesis in those following ADT. This is a proposed mechanism for the failure rate and aggressive nature of prostate cancer that fails ADT. 3-alpha androstanediol is converted via 3 alpha HSD back to DHT. In contrast, 3-beta androstanediol cannot.
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Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside - 0 views
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MAF precursor activity has also been lost or reduced after Gc-globulin treatment in some cancer cell lines
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This appears to result from the deglycosylated ɑ-N-acetylgalactosaminidase (nagalase) secreted from cancerous cells
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Nagalase has been detected in many cancer patients, but not in healthy individuals
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Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
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It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
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The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
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It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
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The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
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Administration of Gc-MAF stimulates immune-cell progenitors for extensive mitogenesis, activates macrophages and produces antibodies. “This indicates that Gc-MAF is a powerful adjuvant for immunization.”
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Cancer cell lines do not develop into tumor genes in mouse models after Gc-MAF-primed immunization (29-31) and the effect of Gc-MAF has been approved for macrophage stimulation for angiogenesis, proliferation, migration and metastatic inhibition on tumors induced by MCF-7 human breast cancer cell line
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The protocol included: "a high dose of second-generation Gc-MAF (0.5 ml) administered twice a week intramuscularly for a total of 21 injections.”
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Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
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Inui et al. reported that a 74-year-old man diagnosed with prostate cancer with multiple bone metastases was in complete remission nine months after initiation of GcMAF therapy simultaneously with hyper T/NK cell, high-dose vitamin C and alpha lipoic acid therapy
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It has also been approved for non-neoplastic diseases such as autism (41), multiple sclerosis (42, 43), chronic fatigue syndrome (CFS) (40), juvenile osteoporosis (44) and systemic lupus erythematous (45).
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Gc-MAF has been verified for use in colon, thyroid (38), lung (39), liver, thymus (36), pancreatic (40), bladder and ovarian cancer and tongue squamous carcinoma
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Prostate, breast, colon, liver, stomach, lung (including mesothelioma), kidney, bladder, uterus, ovarian, head/neck and brain cancers, fibrosarcomas and melanomas are the types of cancer tested thus far
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weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
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this treatment has been suggested for non-anemic patients
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Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
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Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
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In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
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individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
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Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
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Gc-MAF supports humoral immunity by producing, developing and releasing large quantities of antibodies against cancer. Clinical evidence from a human model of breast cancer patients supports this hypothesis
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There is also evidence that confirms the tumoricidal role of Gc-MAF via Fc-receptor mediation
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It is likely that the best therapeutic responses will be observed when the nutritional and inflammatory aspects are taken together with stimulation of the immune system
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it should be noted that no harmful side effects of Gc-MAF treatment have been reported, even when it was successfully administered to autistic children
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The natural activation mechanism of macrophages by Gc-MAF is so natural and it should not have any side effects on humans or animal models even in cell culture
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Besides the Gc-MAF efficacy on macrophage activity, it can be a potential anti-angiogenic agent (28) and an inhibitor of the migration of cancerous cells in the absence of macrophages (47).
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Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
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It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
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inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
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macrophages highly-activated by the addition of Gc-MAF can show tumoricidal activity
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Previous clinical investigations have confirmed the efficacy of Gc-MAF. In addition to activating existing macrophages, Gc-MAF is a potent mitogenic factor that can stimulate the myeloid progenitor cells to increase systemic macrophage cell counts by 40-fold in four days
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great review on Gc-MAF in cancer. An increase in nagalase blocks Gc-protein to Gc-MAF activity leaving the host immune system compromised.
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shared by Nathan Goodyear on 30 Jan 18
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Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2... - 0 views
www.nature.com/...s41698-017-0044-8
cancer cancer stem cells liver cancer vitamin C IV vitamin C oncology
shared by Nathan Goodyear on 30 Jan 18
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Chen et al. have revealed that ascorbate at pharmacologic concentrations (0.3–20 mM) achieved only by intravenously (i.v.) administration selectively kills a variety of cancer cell lines in vitro, but has little cytotoxic effect on normal cells.
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Ascorbic acid (the reduced form of vitamin C) is specifically transported into cells by sodium-dependent vitamin C transporters (SVCTs)
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SVCT-1 is predominantly expressed in epithelial tissues
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whereas the expression of SVCT-2 is ubiquitous
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differential sensitivity to VC may result from variations in VC flow into cells, which is dependent on SVCT-2 expression.
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high-dose VC significantly impaired both the tumorspheres initiation (Fig. 4d, e) and the growth of established tumorspheres derived from HCC cells (Fig. 4f, g) in a time-dependent and dose-dependent manner.
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Hepatocellular carcinoma (HCC)
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The antioxidant, N-acetyl-L-cysteine (NAC), preventing VC-induced ROS production (a ROS scavenger), completely restored the viability and colony formation among VC-treated cells
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DNA double-strand damage was found following VC treatment
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DNA damage was prevented by NAC
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Interestingly, the combination of VC and cisplatin was even more effective in reducing tumor growth and weight
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Consistent with the in vitro results, stemness-related genes expressions in tumor xenograft were remarkably reduced after VC or VC+cisplatin treatment, whereas conventional cisplatin therapy alone led to the increase of CSCs
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VC is one of the numerous common hepatoprotectants.
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Interestingly, at extracellular concentrations greater than 1 mM, VC induces strong cytotoxicity to cancer cells including liver cancer cells
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we hypothesized that intravenous VC might reduce the risk of recurrence in HCC patients after curative liver resection.
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Intriguingly, the 5-year disease-free survival (DFS) for patients who received intravenous VC was 24%, as opposed to 15% for no intravenous VC-treated patients
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Median DFS time for VC users was 25.2 vs. 18 months for VC non-users
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intravenous VC use is linked to improved DFS in HCC patients.
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In this study, based on the elevated expression of SVCT-2, which is responsible for VC uptake, in liver CSCs, we revealed that clinically achievable concentrations of VC preferentially eradicated liver CSCs in vitro and in vivo
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the authors here made similar mistakes to the Mayo authors i.e. under doses here in this study. They dosed at only 2 grams IVC. A woefully low dose of IVC.
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Additionally, we found that intravenous VC reduced the risk of post-surgical HCC progression in a retrospective cohort study.
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Three hundred thirty-nine participants (55.3%) received 2 g intravenous VC for 4 or more days after initial hepatectomy
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As the key protein responsible for VC uptake in the liver, SVCT-2 played crucial roles in regulating the sensitivity to ascorbate-induced cytotoxicity
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we also observed that SVCT-2 was highly expressed in human HCC samples and preferentially elevated in liver CSCs
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SVCT-2 might serve as a potential CSC marker and therapeutic target in HCC
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CSCs play critical roles in regulating tumor initiation, relapse, and chemoresistance
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we revealed that VC treatment dramatically reduced the self-renewal ability, expression levels of CSC-associated genes, and percentages of CSCs in HCC, indicating that CSCs were more susceptible to VC-induced cell death
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as a drug for eradicating CSCs, VC may represent a promising strategy for treatment of HCC, alone or particularly in combination with chemotherapeutic drugs
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In HCC, we found that VC-generated ROS caused genotoxic stress (DNA damage) and metabolic stress (ATP depletion), which further activated the cyclin-dependent kinase inhibitor p21, leading to G2/M phase cell cycle arrest and caspase-dependent apoptosis in HCC cells
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we demonstrated a synergistic effect of VC and chemotherapeutic drug cisplatin on killing HCC both in vitro and in vivo
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Intravenous VC has also been reported to reduce chemotherapy-associated toxicity of carboplatin and paclitaxel in patients,38 but the specific mechanism needs further investigation
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so, exclude the benefit to patients until the exact mechanism of action, which will never be fully elicited?!?!?
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Our retrospective cohort study also showed that intravenous VC use (2 g) was related to the improved DFS in HCC patients after initial hepatectomy
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Terribly inadequate dose. Target is 20-40 mM which other studies have found occur with 50-75 grams of IVC.
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several clinical trials of high-dose intravenous VC have been conducted in patients with advanced cancer and have revealed improved quality of life and prolonged OS
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high-dose VC was not toxic to immune cells and major immune cell subpopulations in vivo
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high recurrence rate and heterogeneity
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tumor progression, metastasis, and chemotherapy-resistance
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SVCT-2 was highly expressed in HCC samples in comparison to peri-tumor tissues
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high expression (grade 2+/3+) of SVCT-2 was in agreement with poorer overall survival (OS) of HCC patients (Fig. 1c) and more aggressive tumor behavior
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SVCT-2 is enriched in liver CSCs
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these data suggest that SVCT-2 is preferentially expressed in liver CSCs and is required for the maintenance of liver CSCs.
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pharmacologic concentrations of plasma VC higher than 0.3 mM are achievable only from i.v. administration
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The viabilities of HCC cells were dramatically decreased after exposure to VC in dose-dependent manner
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VC and cisplatin combination further caused cell apoptosis in tumor xenograft
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These results verify that VC inhibits tumor growth in HCC PDX models and SVCT-2 expression level is associated with VC response
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qPCR and IHC analysis demonstrated that expression levels of CSC-associated genes and percentages of CSCs in PDXs dramatically declined after VC treatment, confirming the inhibitory role of VC in liver CSCs
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IV vitamin C in vitro and in vivo found to "preferentially" eradicate cancer stem cells. In addition, IV vitamin C was found to be adjunctive to chemotherapy, found to be hepatoprotectant. This study also looked at SVCT-2, which is the transport protein important in liver C uptake.
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Intravenously administered vitamin C as cancer therapy: three cases - 0 views
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peak plasma concentrations obtained intravenously are estimated to reach 14 000 μmol/L, and concentrations above 2000 μmol/L may persist for several hours
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Emerging in vitro data show that extracellular ascorbic acid selectively kills some cancer but no normal cells by generating hydrogen peroxide
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Death is mediated exclusively by extracellular ascorbate, at pharmacologic concentrations that can be achieved only by intravenous administration
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Vitamin C may serve as a pro-drug for hydrogen peroxide delivery to extravascular tissues, but without the presence of hydrogen peroxide in blood
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not all cancer cells were killed by ascorbic acid in vitro
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Intravascular hemolysis was reported after massive vitamin C administration in people with glucose-6-phosphate dehydrogenase deficiency
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Administration of high-dose vitamin C to patients with systemic iron overload may increase iron absorption and represents a contraindication
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Ascorbic acid is metabolized to oxalate, and 2 cases of acute oxalate nephropathy were reported in patients with pre-existing renal insufficiency given massive intravenous doses of vitamin C
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Rare cases of acute tumour hemorrhage and necrosis were reported in patients with advanced cancer within a few days of starting high-dose intravenous vitamin C therapy, although this was not independently verified by pathologic review
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IV vitamin C associated with prolonged survival in 3 patients with different cancers. Peak serum levels reached 14,000 micromol/L, which levels above the 1,000 micro mol/L (cancer cell cytotoxic threshold) were maintained for hours