CBD may have therapeutic effects on gastric cancer.

PMID: 

Biomolecules. 2019 Jul 25 ;9(8). Epub 2019 Jul 25. PMID: 31349651

Abstract Title: 

Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells.

Abstract: 

The main chemical component of cannabis, cannabidiol (CBD), has been shown to have antitumor properties. The present study examined the in vitro effects of CBD on human gastric cancer SGC-7901 cells. We found that CBD significantly inhibited the proliferation and colony formation of SGC-7901 cells. Further investigation showed that CBD significantly upregulated ataxia telangiectasia-mutated gene (ATM) and p53 protein expression and downregulated p21 protein expression in SGC-7901 cells, which subsequently inhibited the levels of CDK2 and cyclin E, thereby resulting in cell cycle arrest at the G0-G1 phase. In addition, CBD significantly increased Bax expression levels, decreased Bcl-2 expression levels and mitochondrial membrane potential, and then upregulated the levels of cleaved caspase-3 and cleaved caspase-9, thereby inducing apoptosis in SGC-7901 cells. Finally, we found that intracellular reactive oxygen species (ROS) increased after CBD treatment. These results indicated that CBD could induce G0-G1 phase cell cycle arrest and apoptosis by increasing ROS production, leading to the inhibition of SGC-7901 cell proliferation, thereby suggesting that CBD may have therapeutic effects on gastric cancer.

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The adverse effects of electromagnetic fields may be mediated by activation of voltage-gated calcium channels.

PMID: 

J Cell Mol Med. 2013 Aug ;17(8):958-65. Epub 2013 Jun 26. PMID: 23802593

Abstract Title: 

Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects.

Abstract: 

The direct targets of extremely low and microwave frequency range electromagnetic fields (EMFs) in producing non-thermal effects have not been clearly established. However, studies in the literature, reviewed here, provide substantial support for such direct targets. Twenty-three studies have shown that voltage-gated calcium channels (VGCCs) produce these and other EMF effects, such that the L-type or other VGCC blockers block or greatly lower diverse EMF effects. Furthermore, the voltage-gated properties of these channels may provide biophysically plausible mechanisms for EMF biological effects. Downstream responses of such EMF exposures may be mediated through Ca(2+) /calmodulin stimulation of nitric oxide synthesis. Potentially, physiological/therapeutic responses may be largely as a result of nitric oxide-cGMP-protein kinase G pathway stimulation. A well-studied example of such an apparent therapeutic response, EMF stimulation of bone growth, appears to work along this pathway. However, pathophysiological responses to EMFs may be as a result of nitric oxide-peroxynitrite-oxidative stress pathway of action. A single such well-documented example, EMF induction of DNA single-strand breaks in cells, as measured by alkaline comet assays, is reviewed here. Such single-strand breaks are known to be produced through the action of this pathway. Data on the mechanism of EMF induction of such breaks are limited; what data are available support this proposed mechanism. Other Ca(2+) -mediated regulatory changes, independent of nitric oxide, may also have roles. This article reviews, then, a substantially supported set of targets, VGCCs, whose stimulation produces non-thermal EMF responses by humans/higher animals with downstream effects involving Ca(2+) /calmodulin-dependent nitric oxide increases, which may explain therapeutic and pathophysiological effects.

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Role of the gut microbiota in the development of various neurological diseases.

PMID: 

Neurologia. 2019 Jul 21. Epub 2019 Jul 21. PMID: 31340904

Abstract Title: 

Role of the gut microbiota in the development of various neurological diseases.

Abstract: 

INTRODUCTION: In recent years, the scientific evidence supporting a relationship between the microbiota and various diseases has increased significantly; this trend has also been observed for neurological diseases. This has given rise to the concept of the gut-brain axis and the idea of a relationship between the gut microbiota and several neurological diseases whose aetiopathogenesis is yet to be clearly defined.DEVELOPMENT: We review the role of the gut microbiota in the gut-brain axis and analyse those neurological diseases in which alterations in the gut microbiota have been described as a result of human studies: specifically, Parkinson's disease, Alzheimer disease, amyotrophic lateral sclerosis, neuromyelitis optica, and multiple sclerosis.CONCLUSIONS: The body of evidence linking the gut microbiota to various neurological diseases has grown considerably. Several interesting studies show a relationship between the gut microbiota and Parkinson's disease, Alzheimer disease, neuromyelitis optica, and multiple sclerosis, whereas other controversial studies implicate it in amyotrophic lateral sclerosis. Many of these studies place considerable emphasis on modulation of inflammation, particularly by bacteria capable of producing short-chain fatty acids. Despite these encouraging results, many questions remain, and there is a need to demonstrate causality, determine the role of fungi or viruses, and research possible treatment through diet, probiotics, or faecal microbiota transplantation.

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Radiofrequency-induced stress can damage mitochondria and induce elimination of damaged organelles via autophagy.

PMID: 

Cancer. 2014 Nov 1 ;120(21):3418-25. Epub 2014 Jul 1. PMID: 24986120

Abstract Title: 

Noninvasive radiofrequency treatment effect on mitochondria in pancreatic cancer cells.

Abstract: 

BACKGROUND: The development of novel therapeutic approaches for cancer therapy is important, especially for tumors that have poor response or develop resistance to standard chemotherapy and radiation. We discovered that noninvasive radiofrequency (RF) fields can affect cancer cells but not normal cells, inhibit progression of tumors in mice, and enhance the anticancer effects of chemotherapy. However, it remains unclear what physiological and molecular mechanisms this treatment induces inside cells. Here, we studied the effect of RF treatment on mitochondria in human pancreatic cancer cells.METHODS: The morphology of mitochondria in cells was studied via electron microscopy. The alteration of mitochondrial membrane potential (Δψ) was accessed using a Mitotracker probe. The respiratory activity of mitochondria was evaluated by analyzing changes in oxygen consumption rates determined with a Mito Stress Test Kit. The production of intracellular reactive oxygen species was performed using flow cytometry. The colocalizationof mitochondria and autophagosome markers in cells was performed using fluorescence immunostaining and confocal microscopy analysis.RESULTS: RF fields treatment changed the morphology of mitochondria in cancer cells, altered polarization of the mitochondrial membrane, substantially impaired mitochondrial respiration, and increased reactive oxygen species production, indicating RF-induced stress on the mitochondria. We also observed frequent colocalization of the autophagosome marker LC3B with the mitochondrial marker Tom20 inside cancer cells after RF exposure, indicating the presence of mitochondria in the autophagosomes. This suggests that RF-induced stress can damage mitochondria and induce elimination of damaged organelles via autophagy.CONCLUSION: RF treatment impaired the function of mitochondria in cancer cells. Therefore, mitochondria can represent one of the targets of the RF treatment.

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This review outlines the overlooked mechanisms of electromagnetic field damage and the critical role Earth’s natural electromagnetic signaling plays in the biology of the human body.

PMID: 

Rev Environ Health. 2015 ;30(4):293-303. PMID: 26368042

Abstract Title: 

The implications of non-linear biological oscillations on human electrophysiology for electrohypersensitivity (EHS) and multiple chemical sensitivity (MCS).

Abstract: 

The 'informational content' of Earth's electromagnetic signaling is like a set of operating instructions for human life. These environmental cues are dynamic and involve exquisitely low inputs (intensities) of critical frequencies with which all life on Earth evolved. Circadian and other temporal biological rhythms depend on these fluctuating electromagnetic inputs to direct gene expression, cell communication and metabolism, neural development, brainwave activity, neural synchrony, a diversity of immune functions, sleep and wake cycles, behavior and cognition. Oscillation is also a universal phenomenon, and biological systems of the heart, brain and gut are dependent on the cooperative actions of cells that function according to principles of non-linear, coupled biological oscillations for their synchrony. They are dependent on exquisitely timed cues from the environment at vanishingly small levels. Altered 'informational content' of environmental cues can swamp natural electromagnetic cues and result in dysregulation of normal biological rhythms that direct growth, development, metabolism and repair mechanisms. Pulsed electromagnetic fields (PEMF) and radiofrequency radiation (RFR) can have the devastating biological effects of disrupting homeostasis and desynchronizing normal biological rhythms that maintain health. Non-linear, weak field biological oscillations govern body electrophysiology, organize cell and tissue functions and maintain organ systems. Artificial bioelectrical interference can give false information (disruptive signaling) sufficient to affect critical pacemaker cells (of the heart, gut and brain) and desynchronize functions of these important cells that orchestrate function and maintain health. Chronic physiological stress undermines homeostasis whether it is chemically induced or electromagnetically induced (or both exposures are simultaneous contributors). This can eventually break down adaptive biological responses critical to health maintenance; and resilience can be compromised. Electrohypersensitivity can be caused by successive assaults on human bioelectrochemical dynamics from exogenous electromagnetic fields (EMF) and RFR or a single acute exposure. Once sensitized, further exposures are widely reported to cause reactivity to lower and lower intensities of EMF/RFR, at which point thousand-fold lower levels can cause adverse health impacts to the electrosensitive person. Electrohypersensitivity (EHS) can be a precursor to, or linked with, multiple chemical sensitivity (MCS) based on reports of individuals who first develop one condition, then rapidly develop the other. Similarity of chemical biomarkers is seen in both conditions [histamines, markers of oxidative stress, auto-antibodies, heat shock protein (HSP), melatonin markers and leakage of the blood-brain barrier]. Low intensity pulsed microwave activation of voltage-gated calcium channels (VGCCs) is postulated as a mechanism of action for non-thermal health effects.

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Phaseolus vulgaris lower non-HDL cholesterol in animals

PMID: 

J Nutr. 2019 Jun 1 ;149(6):996-1003. PMID: 31006805

Abstract Title: 

Pinto Beans (Phaseolus vulgaris L.) Lower Non-HDL Cholesterol in Hamsters Fed a Diet Rich in Saturated Fat and Act on Genes Involved in Cholesterol Homeostasis.

Abstract: 

BACKGROUND: Pinto beans contain multiple active agents such as polyphenols, flavonoids, and saponins, and have been shown to lower cholesterol, but the mechanisms involved in this effect have not been explored.OBJECTIVE: This study was to investigate the changes in cholesterol metabolism in response to whole pinto beans (wPB) and their hulls (hPB) supplemented into a diet rich in saturated fat and the molecular mechanisms potentially responsible for these effects in hamsters.METHODS: Forty-four 9-wk-old male Golden Syrian hamsters were randomly assigned to 4 diet groups (n = 11), including a 5% (wt:wt) fat diet [normal-fat diet (NF)], a 15% (wt:wt) fat diet [diet rich in saturated fat (HSF), saturated fatty acids accounted for 70% of total fatty acids], or HSF supplemented with 5% (wt:wt) wPB or 0.5% (wt:wt) hPB for 4 wk. Plasma, liver, intestinal, and fecal samples were collected to evaluate multiple cholesterol markers and gene targets.RESULTS: The plasma non-high-density lipoprotein (non-HDL) concentration was significantly reduced in the wPB- and hPB-supplemented groups by 31.9 ± 3.5% and 53.6 ± 3.2%, respectively, compared with the HSF group (P 

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A diet including beans might represent health benefits and cancer-preventive effects.

PMID: 

J Food Biochem. 2019 Jun ;43(6):e12680. Epub 2018 Sep 16. PMID: 31353616

Abstract Title: 

Mechanisms associated to apoptosis of cancer cells by phenolic extracts from two canned common beans varieties (Phaseolus vulgaris L.).

Abstract: 

Two varieties of common beans (Phaseolus vulgaris L.), Bayo Victoria and Negro 8025, were evaluated to determine the effect on cellular viability and mechanisms involved in apoptosis pathways, using a cellular model with HT-29 cells. Aqueous methanolic (50:50) extracts from cooked beans were analyzed for phenolic composition, identifying greater diversity of phenolic compounds in Bayo Victoria extracts. However, Negro 8025 showed greater phenolic content and cytotoxicity effects at lower media inhibitory concentrations, and greater effectiveness to activate apoptotic pathways. Proteins related to the arrest of cell cycle were modulated by both bean cultivars. Qualitative analysis by HPLC-PAD and HPLC-MS systems of phenolic compounds in common bean extracts showed mainly hydroxybenzoic and hydroxycinnamic acids, flavonols, and monomeric flavan-3-ols. Bioactive phenolics such as catechin, kaempferol, and ferulic acid were found in both cultivars as well anticancer phytochemicals such as quercetin, protocatechuic acid, myricetin, naringenin and their derivatives, and procyanidins. PRACTICAL APPLICATIONS: Polyphenols in common beans (Phaseolus vulgaris L.) cultivars processed by canning display chemoprotective potential as they activate mechanisms involved in apoptosis pathways. Phenolics in common beans modulate 28 proteins related to apoptotic processes. Therefore, a diet including canned beans (particularly darker varieties) might represent health benefits and cancer-preventive effects.

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Frequent weekday technology use at bedtime was associated with significant adverse effects on multiple sleep parameters in adolescents.

PMID: 

Sleep Med. 2014 Feb ;15(2):240-7. Epub 2013 Dec 15. PMID: 24394730

Abstract Title: 

Associations between specific technologies and adolescent sleep quantity, sleep quality, and parasomnias.

Abstract: 

OBJECTIVE: We tested the hypothesis that weekday bedtime use of six technologies would be significantly associated with eight sleep parameters studied relating to sleep quantity, sleep quality, and parasomnias.METHODS: In our cross-sectional study, we previously administered validated age-appropriate questionnaires (School Sleep Habits Survey, Technology Use Questionnaire). Participating adolescents (n=738; 54.5% boys) were aged 11-13 years and were from the Midlands region of the United Kingdom in 2010.RESULTS: Frequent use of all technology types was significantly inversely associated with weekday sleep duration (hours). Frequent music listeners and video gamers had significantly prolonged sleep onset (β=7.03 [standard error {SE}, 2.66]; P

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Phaseolus vulgaris extract: Alpha-amylase inhibition against metabolic syndrome in mice.

n/a

PMID: 

Nutrients. 2019 Aug 1 ;11(8). Epub 2019 Aug 1. PMID: 31374931

Abstract Title: 

L. Extract: Alpha-Amylase Inhibition against Metabolic Syndrome in Mice.

Abstract: 

To examine the effects of the alpha-amylase inhibitor isoform 1 called phaseolamin, a standardized extract from white kidney beans (L) was tested against the hallmarks of metabolic syndrome. The efficacy of arepeated treatment withextract (500 mg/kg) was compared with metformin (100 mg/kg) and atorvastatin (10 mg/kg) in a model of metabolic syndrome evoked by prolonged high fat diet (HFD; week 1 to week 19) in C57BL/6 mice. Bean extract and compounds administration started after metabolic syndrome establishment (week 11).extract reduced the body weight overtime, as well as effectively lowered glycaemia, triglycerides, and cholesterol. On week 19, bean extract normalized the HFD-evoked tolerance to glucose and insulin. According to the phytochemical characterization, it inhibited the alpha-amylase activity. Animals treated with the extract were rescued from motor impairments and nociceptive threshold alterations induced by HFD. Specific organs analysis revealed thatextract decreased hepatic steatosis and lipid peroxidation in liver. It protected the heart from HFD oxidative alterations increasing the expression of the detoxifying enzymes catalase and glutathione reductase, and normalizing NADH dehydrogenase level. The histological analysis of aorta showed a protection about the development of fatty streaks in the muscular layers. In conclusion, a prolonged treatment with the standardized extract ofsignificantly reduced several pathological features related to a metabolic syndrome-like condition; a multifactorial approach that candidates this vegetal product as a possible therapeutic option against metabolic syndrome.

Baseline microbiota composition modulates antibiotic-mediated effects on the gut microbiota and host.

PMID: 

Microbiome. 2019 Aug 2 ;7(1):111. Epub 2019 Aug 2. PMID: 31375137

Abstract Title: 

Baseline microbiota composition modulates antibiotic-mediated effects on the gut microbiota and host.

Abstract: 

BACKGROUND: Normal mammalian development and homeostasis are dependent upon the gut microbiota. Antibiotics, essential for the treatment and prophylaxis of bacterial infections, can have collateral effects on the gut microbiota composition, which can in turn have far-reaching and potentially deleterious consequences for the host. However, the magnitude and duration of such collateral effects appear to vary between individuals. Furthermore, the degree to which such perturbations affect the host response is currently unclear. We aimed to test the hypothesis that different human microbiomes have different responses to a commonly prescribed antibiotic and that these differences may impact the host response.METHODS: Germ-free mice (n = 30) humanized with the microbiota of two unrelated donors (A and B) were subjected to a 7-day antibiotic challenge with amoxicillin-clavulanate ("co-amoxiclav"). Microbiome and colonic transcriptome analysis was performed, pre (day 0) and post antibiotics (day 8) and subsequently into recovery (days 11 and 18).RESULTS: Unique community profiles were evident depending upon the donor, with donor A recipient mice being dominated by Prevotella and Faecalibacterium and donor B recipient mice dominated by Bacteroides and Parabacteroides. Donor A mice underwent a marked destabilization of their microbiota following antibiotic treatment, while donor B mice maintained a more stable profile. Dramatic and overlapping alterations in the host transcriptome were apparent following antibiotic challenge in both groups. Despite this overlap, donor A mice experienced a more significant alteration in gene expression and uniquely showed correlations between host pathways and key microbial genera.CONCLUSIONS: Germ-free mice humanized by different donor microbiotas maintain distinct microbiome profiles, which respond in distinct ways to antibiotic challenge and evince host responses that parallel microbiome disequilibrium. These results suggest that inter-individual variation in the gut microbiota may contribute to personalized host responses following microbiota perturbation.

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