PMID: Eur J Cancer. 2013 Jul ;49(10):2411-23. Epub 2013 Apr 3. PMID: 23562551 Abstract Title: Diabetes mellitus as an independent risk factor for lung cancer: a meta-analysis of observational studies. Abstract: BACKGROUND: Epidemiologic studies have demonstrated inconsistent associations between diabetes mellitus and the risk of lung cancer. To determine whether diabetes mellitus is associated with an increased risk of lung cancer, we performed a meta-analysis of observational studies.METHODS: PubMed, EMBASE and the Cochrane Library were searched for observational studies conducted prior to September 2012. We included prospective cohort studies that reported relative risks and case-control studies that showed odds ratios in the analysis. The pooled relative risk (RR) with 95% confidence intervals (CIs) was calculated with a random effects model. Sensitivity analysis was performed with studies which controlled for smoking status. Associations were assessed in several subgroups representing different participant and study characteristics.RESULTS: A total of 34 studies from 24 manuscripts (10 case-control studies and 24 cohort studies) were included in the analyses. Diabetes was significantly associated with the increased risk of lung cancer compared with non-diabetic controls when limiting the analysis to studies adjusting for smoking status (RR, 1.11; 95% CI, 1.02-1.20; I(2)=46.1%). By contrast, this association disappeared when the analysis was restricted to studies not adjusting for smoking status (RR, 0.99; 95% CI, 0.88-1.11; I(2)=96.7%). When stratifying by sex, an increased risk of lung cancer was prominent in diabetic women (RR, 1.14; 95% CI, 1.09-1.20; I(2)=0%), while there was no association in diabetic men (RR, 1.07; 95% CI, 0.89-1.28; I(2)=96.6%). Among diabetic women, significantly increased risks of lung cancer were found in the following subgroups: cohort studies (RR, 1.14; 95% CI, 1.08-1.20; I(2)=0%), studies controlling for major confounding variables such as age, smoking and alcohol (RR, 1.19; 95% CI, 1.00-1.43; I(2)=23.1%), studies with long-term follow-up (RR, 1.14; 95% CI, 1.08-1.20; I(2)=0%), and high-quality studies assessed by the Newcastle-Ottawa Scale (RR, 1.14; 95% CI, 1.08-1.20; I(2)=0%).INTERPRETATION: Preexisting diabetes mellitus may increase the risk of lung cancer, especially among female diabetic patients. Further large-scale prospective studies are needed to test specifically the effect of diabetes mellitus on lung cancer risk.
Aspartame may induce redox and lipid imbalance in rats via mechanism that involves oxidative stress and depletion of glutathione-dependent system.
PMID: J Basic Clin Physiol Pharmacol. 2015 Aug 6. Epub 2015 Aug 6. PMID: 26247507 Abstract Title: Effects of long-term administration of aspartame on biochemical indices, lipid profile and redox status of cellular system of male rats. Abstract: BACKGROUND: Aspartame (N-L-α-aspartyl-L-phenylalanine-1-methyl ester) (ASP) is a synthetic sweetener used in foods and its safety remains controversial. The study was designed to investigate the effects of long-term administration of aspartame on redox status, lipid profile and biochemical indices in tissues of male Wistar rats.METHODS: Rats were assigned into four groups and given distilled water (control), aspartame at doses of 15 mg/kg (ASP 1), 35 mg/kg (ASP 2) and 70 mg/kg (ASP 3) daily by oral gavage for consecutive 9 weeks.RESULTS: Administration of ASP 2 and ASP 3 significantly increased the weight of liver and brain, and relative weight of liver of rats. Lipid peroxidation products significantly increased in the kidney, liver and brain of rats at all doses of ASP with concomitant depletion of antioxidant parameters, viz. glutathione-s-transferase, glutathione peroxidase, superoxide dismutase, catalase and reduced glutathione. Furthermore, ASP 2 and ASP 3 significantly increased the levels of gamma glutamyl transferase by 70% and 85%; alanine aminotransferase by 66% and 117%; aspartate aminotransferase by 21% and 48%; urea by 72% and 58% and conjugated bilirubin by 63% and 64%, respectively. Also, ASP 2 and ASP 3 significantly increased the levels of total cholesterol, triglycerides and low-density lipoprotein cholesterol in the rats. Histological findings showed that ASP 2 and ASP 3 caused cyto-architectural changes such as degeneration, monocytes infiltration and necrotic lesions in brain, kidney and liver of rats.CONCLUSIONS: Aspartame may induce redox and lipid imbalance in rats via mechanism that involves oxidative stress and depletion of glutathione-dependent system.
THC may provide a protective effect against oxidative damage induced by diabetes.
PMID: Cell Biochem Funct. 2014 Oct ;32(7):612-9. Epub 2014 Sep 3. PMID: 25187240 Abstract Title: Oxidative stress and cannabinoid receptor expression in type-2 diabetic rat pancreas following treatment withΔ⁹-THC. Abstract: The objectives of study were (a) to determine alteration of feeding, glucose level and oxidative stress and (b) to investigate expression and localization of cannabinoid receptors in type-2 diabetic rat pancreas treated withΔ(9)-tetrahydrocannabinol (Δ(9)-THC). Rats were randomly divided into four groups: control, Δ(9)-THC, diabetes and diabetes + Δ(9)-THC groups. Diabetic rats were treated with a single dose of nicotinamide (85 mg/kg) 15 min before injection of streptozotocin (65 mg/kg). Δ(9)-THC was administered intraperitoneally at 3 mg/kg/day for 7 days. Body weights and blood glucose level of rats in all groups were measured on days 0, 7, 14 and 21. On day 15 after the Δ(9)-THC injections, pancreatic tissues were removed. Blood glucose levels and body weights of diabetic rats treatedwith Δ(9)-THC did not show statistically significant changes when compared with the diabetic animals on days 7, 14 and 21. Treatment with Δ(9)-THC significantly increased pancreas glutathione levels, enzyme activities of superoxide dismutase and catalase in diabetes compared with non-treatment diabetes group. The cannabinoid 1 receptor was found in islets, whereas the cannabinoid 2 receptor was found in pancreatic ducts. Their localization in cells was both nuclear and cytoplasmic. We can suggest that Δ(9) -THC may be an important agent for the treatment of oxidative damages induced by diabetes. However, it must be supported with anti-hyperglycaemic agents. Furthermore, the present study for the first time emphasizes that Δ(9)-THC may improve pancreatic cells via cannabinoid receptors in diabetes. The aim of present study was to elucidate the effects of Δ(9)-THC, a natural cannabinoid receptor agonist, on the expression and localization of cannabinoid receptors, and oxidative stress statue in type-2 diabetic rat pancreas. Results demonstrate that the cannabinoid receptors are presented in both Langerhans islets and duct regions. The curative effects of Δ(9)-THC can be occurred via activation of cannabinoid receptors in diabetic rat pancreas. Moreover, it may provide a protective effect against oxidative damage induced by diabetes. Thus, it is suggested that Δ(9)-THC can be a candidate for therapeutic alternatives of diabetes symptoms.
These results suggested that curcumin inhibit lung cancer invasion and metastasis by attenuating GLUT1/MT1-MMP/MMP2 pathway.
PMID: Int J Clin Exp Med. 2015;8(6):8948-8957. Epub 2015 Jun 15. PMID: 26309547 Abstract Title: Curcumin inhibits lung cancer invasion and metastasis by attenuating GLUT1/MT1-MMP/MMP2 pathway. Abstract: Glucose transporter (GLUT) 1 is found highly expressed in malignant tumors and considered a mediator inducing cancer metastasis. Curcumin is a natural product which exerts anti-invasion and metastasis effects in cancer. This study aimed at evaluating whether attenuating GLUT1 was involved in curcumin’s anti-invasion and metastasis effects. In the in vitro part, constricted pcDNA3.1-GLUT1 vector was transfected into A549 cells. MTT assay was used to assess the curcumin’s effects on proliferation in lung cancer A549 cells. Transwell assay was used to evaluate the anti-invasion effect of curcumin on A549 cells. Real-time PCR and Western-blotting were employed to examine the expression levels of GLUT1, membrane type 1-MMP (MT1-MMP) and matrix metalloproteinase (MMP) 2 in curcumin- incubated A549 cells. In the in vivo part, tumor weight and metastatic rate were assessed in nude mice bearing untransfected, empty vector transfected and pcDNA3.1-GLUT1 transfected A549 cells originated tumors. In this study, we found that curcumin began to show significant cytotoxicity against proliferation effect at 45μmol/L. Curcumin inhibited invasion and expressions of GLUT1, MT1-MMP and MMP2 untransfected A549 cells in a concentration-dependent manner. pcDNA3.1-GLUT1 transfected A549 cells exhibited resistance to curcumin’s anti-invasion effect by up-regulating expressions of GLUT2, MT1-MMP and MMP2. Furthermore, curcumin failed to decrease the metastatic rate in nude mice bearing pcDNA3.1-GLUT1 transfected A549 cells originated tumors. These results suggested that curcumin inhibit lung cancer invasion and metastasis by attenuating GLUT1/MT1-MMP/MMP2 pathway.
This study indicates that extracts from M. oleifera may be developed as an adjuvant therapy for the treatment of leishmaniasis.
PMID: Z Naturforsch C. 2014 Mar-Apr;69(3-4):110-6. PMID: 24873031 Abstract Title: Antileishmanial compounds from Moringa oleifera Lam. Abstract: The antileishmanial activity of extracts and phytoconstituents of Moringa oleifera Lam. was investigated in vitro against promastigotes of Leishmania donavani. The 70% ethanolic extract of roots and the methanolic extract of leaves showed moderate inhibitory activity with IC50 values of 83.0 microg/ml and 47.5 microg/ml, respectively. Antileishmanial activity of the methanolic extract of leaves increased upon fractionation, as its ethyl acetate fraction was found to be more active with an IC50 value of 27.5 microg/ml. The most active antileishmanial compound niazinin, a thiocarbamate glycoside isolated from this fraction, showed an IC50 value of 5.25 microM. Results presented in this study indicate that extracts from M. oleifera may be developed as an adjuvant therapy for the treatment of leishmaniasis.
MSHE and MCF were both effective to treat experimental colitis and this might be attributed to their similar major components, biophenols and flavonoids.
PMID: Avicenna J Phytomed. 2014 Mar ;4(2):127-36. PMID: 25050310 Abstract Title: Anti-inflammatory effect of Moringa oleifera Lam. seeds on acetic acid-induced acute colitis in rats. Abstract: OBJECTIVE: Anti-inflammatory, immuno-modulatory, and antioxidant properties of Moringa oleifera Lam. suggest that it might have beneficial effects on colitis. The present study was performed to investigate the anticolitis effect of Moringa oleifera seeds hydro-alcoholic extract (MSHE) and its chloroform fraction (MCF) on acetic acid-induced colitis in rats.MATERIALS AND METHODS: Both MSHE and MCF with three increasing doses (50, 100, and 200 mg/kg) were administered orally to separate groups of male Wistar rats, 2 h before ulcer induction (using acetic acid 4%) and continued for 5 days. Prednisolone (4 mg/kg) and normal saline (1 ml/kg) were used in reference and control groups, respectively. All rats were sacrificed 24 h after the last dose (at day 6) and tissue injuries were assessed macroscopically and pathologically.RESULTS: Extracts with three doses mentioned before were effective to reduce weight of distal colon (8 cm) as a marker for inflammation and tissue edema. Three doses of MSHE and two greater doses of MCF (100 and 200 mg/kg) were effective to reduce ulcer severity, area, and index as well as mucosal inflammation severity and extent, crypt damage, invasion involvement, total colitis index, and MPO activity compared with controls. MCF (50 mg/kg) was not significantly effective in reducing evaluated parameters of colitis compared with controls.CONCLUSION: It is concluded that MSHE and MCF were both effective to treat experimental colitis and this might be attributed to their similar major components, biophenols and flavonoids. Since the efficacy was evident even in low doses of MSHE, presence of active constituents with high potency in seeds is persuasive.
A Critique Of Scientific Literature: Pesticides and Polio
This article by Jim West was first published in The Townsend Letter for Doctors and Patients, June 2000, then republished as a 2nd edition in 2002 by The Weston A. Price Foundation, with additional material and the editorship of Sally Fallon. The article summarizes his book, “DDT/Polio”, which he had attempted to publish in 1998. This is a 3rd edition, August 14, 2015.
What is the connection between pesticides and polio? Research shows a correlation between the use of DDT production and incidence of polio.
This review highlights specific biological processes that could be exploited as targets for the prevention and therapy of cancer.
PMID: Semin Cancer Biol. 2015 Apr 10. Epub 2015 Apr 10. PMID: 25865775 Abstract Title: Cancer prevention and therapy through the modulation of the tumor microenvironment. Abstract: Cancer arises in the context of an in vivo tumor microenvironment. This microenvironment is both a cause and consequence of tumorigenesis. Tumor and host cells co-evolve dynamically through indirect and direct cellular interactions, eliciting multiscale effects on many biological programs, including cellular proliferation, growth, and metabolism, as well as angiogenesis and hypoxia and innate and adaptive immunity. Here we highlight specific biological processes that could be exploited as targets for the prevention and therapy of cancer. Specifically, we describe how inhibition of targets such as cholesterol synthesis and metabolites, reactive oxygen species and hypoxia, macrophage activation and conversion, indoleamine 2,3-dioxygenase regulation of dendritic cells, vascular endothelial growth factor regulation of angiogenesis, fibrosis inhibition, endoglin, and Janus kinase signaling emerge as examples of important potential nexuses in the regulation of tumorigenesis and the tumor microenvironment that can be targeted. We have also identified therapeutic agents as approaches, in particular natural products such as berberine, resveratrol, onionin A, epigallocatechin gallate, genistein, curcumin, naringenin, desoxyrhapontigenin, piperine, and zerumbone, that may warrant further investigation to target the tumor microenvironment for the treatment and/or prevention of cancer.
Opuntia ficus-indica preparations are a rich source of minerals mainly potassium and calcium.
PMID: Plant Foods Hum Nutr. 2015 Aug 5. Epub 2015 Aug 5. PMID: 26243666 Abstract Title: Phenolic Profiles, Phytchemicals and Mineral Content of Decoction and Infusion of Opuntia ficus-indica Flowers. Abstract: Opuntia flowers are a natural source of biologically active compounds and they have been used as medicinal plant for a long time. Despite the various uses reported for the decoction and infusion of these flowers, their characterization has been discarded. In this study, the decoction and infusion prepared from Opuntia ficus-indica were analyzed with respect to their content in minerals and phytochemicals in order to evaluate its nutritional characteristics. The obtained data proved that these preparations are a rich source of minerals mainly K and Ca. Moreover, the phytochemical analysis revealed that they have important polyphenols, flavonoids and tannins contents with the infusion that presented the highest polyphenol levels. LC-MS analyses of decoction and infusion allowed the characterization of 20 phenolic compounds. It is mainly identified by the presence of flavonols glycosides.
X ray irradiation combined with AsA treatment resulted in increased suppression of cell growth of HT1080, SAS and A549 cells in vitro compared with X ray irradiation alone.
PMID: Mol Med Rep. 2015 Jul 22. Epub 2015 Jul 22. PMID: 26238154 Abstract Title: Effects of X‑ray irradiation in combination with ascorbic acid on tumor control. Abstract: Our previous studies demonstrated that the combination of treatment with ascorbic acid (AsA) and X‑ray irradiation results in increased apoptosis in HL60 cells. The present study was performed to investigate the effects of the combined use of AsA and X‑ray irradiation on epithelial cancer and sarcoma cells, and its potential use in future clinical treatment. X‑ray irradiation combined withAsA treatment resulted in increased suppression of cell growth of HT1080, SAS and A549 cells in vitro compared with X‑ray irradiation alone. The combined treatment also suppressed tumor growth in implanted HT‑1080 cells in vivo. Using annexin V/propidium iodide staining and the detection ofactivated caspase 3, it was found that X‑ray irradiation increased the apoptotic rate of HT1080 cells and resulted in G2/M arrest. However, apoptosis in the HT1080 cells treated with 5 mM AsA remained unchanged, and no changes were observed in the G2/M fraction. By contrast, AsA treatment caused increased suppression of proliferation compared with X‑ray irradiation. These results suggested that 5 mM AsA slowed the cell cycle and reduced tumor growth. Therefore, X‑ray irradiation combined with AsA treatment may be effective against epithelial cancer and sarcoma cells.
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