PMID: 

Amino Acids. 2019 Jan ;51(1):73-81. Epub 2018 Aug 22. PMID: 30136029

Abstract Title: 

Carnosine supplementation reduces plasma soluble transferrin receptor in healthy overweight or obese individuals: a pilot randomised trial.

Abstract: 

Abnormalities of iron homeostasis have been linked to insulin resistance, type 2 diabetes and cardiovascular disease. Carnosine, an over-the-counter food supplement with chelating properties, has been shown to decrease serum iron and improve glucose metabolism in diabetic rodents. We have previously demonstrated that carnosine supplementation prevented worsening of glucose metabolism in healthy overweight and obese middle-aged adults. Yet, the impact of carnosine on markers of iron metabolism in humans has not been investigated. We aimed to determine whether carnosine supplementation has an effect on iron parameters in overweight and obese, otherwise healthy adults. We included 26 participants, who were randomly allocated to receive 1 g carnosine (n = 14) or identical placebo (n = 12) twice daily for 12 weeks. Iron parameters including iron, ferritin, transferrin, soluble transferrin receptor, total iron binding capacity and iron saturation were measured in serum or plasma by standard commercial assays. Carnosine supplementation decreased plasma soluble transferrin receptor compared to placebo (mean change difference ± standard error: - 0.07 ± 0.03 mg/l, p = 0.04). None of the other iron parameters were different between carnosine and placebo groups. At follow-up, soluble transferrin receptor wasassociated inversely with urinary carnosine concentrations and positively with serum carnosinase-1 activity (both p 

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PMID: 

Curr Med Chem. 2019 Jul 12. Epub 2019 Jul 12. PMID: 31309876

Abstract Title: 

Carnosine and Lung Disease.

Abstract: 

Carnosine (b-alanyl-L-histidine) is a small dipeptide with numerous activities, including antioxidant effects, metal ion chelation, proton buffering capacity, and inhibitory effects on protein carbonylation and glycation. Carnosine has been mostly studied in organs where it is abundant, including skeletal muscle, cerebral cortex, kidney, spleen, and plasma. Recently, the effect of supplementation with carnosine has been studied in organs with low levels of carnosine, such as the lung, in animal models of influenza virus- or lipopolysaccharide-induced acute lung injury and pulmonary fibrosis. Among the known protective effects of carnosine, its antioxidant effect has attracted increasing attention for potential use in treating lung disease. In this review, we describe the in vitro and in vivo biological and physiological actions of carnosine. We also report our recent study and discuss the roles of carnosine or its related compounds in organs where carnosine is present in only small amounts (especially the lung) and its protective mechanisms.

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PMID: 

Future Oncol. 2019 Oct 30. Epub 2019 Oct 30. PMID: 31664860

Abstract Title: 

Carnosine increases efficiency of temozolomide and irradiation treatment of isocitrate dehydrogenase-wildtype glioblastoma cells in culture.

Abstract: 

The naturally occurring dipeptide carnosine (CAR) has been considered for glioblastoma therapy. As CAR also protects against ionizing irradiation (IR), we investigated whether it may counteract standard therapy consisting of postsurgery IR and treatment with temozolomide (TMZ).Four isocitrate dehydrogenase-wildtype primary cell cultures were exposed to different doses of IR and different concentrations of TMZ and CAR. After exposure, viability under the different conditions and combinations of them was determined.All cultures responded to treatment with TMZ and IR with reduced viability. CAR further decreased viability when TMZ and IR were combined.Treatment with CAR does not counteract glioblastoma standard therapy. As the dipeptide also protects nontumor cells from IR, it may reduce deleterious side effects of treatment.

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PMID: 

Amino Acids. 2019 May ;51(5):761-772. Epub 2019 Mar 12. PMID: 30863889

Abstract Title: 

Carnosine's inhibitory effect on glioblastoma cell growth is independent of its cleavage.

Abstract: 

The naturally occurring dipeptide carnosine (β-alanyl-L-histidine) inhibits the growth of tumor cells. As its component L-histidine mimics the effect, we investigated whether cleavage of carnosine is required for its antineoplastic effect. Using ten glioblastoma cell lines and cell cultures derived from 21 patients suffering from this malignant brain tumor, we determined cell viability under the influence of carnosine and L-histidine. Moreover, we determined expression of carnosinases, the intracellular release of L-histidine from carnosine, and whether inhibition of carnosine cleavage attenuates carnosine's antineoplastic effect. We observed a significantly higher response of the cells to L-histidine than to carnosine with regard to cell viability in all cultures. In addition, we detected protein and mRNA expression of carnosinases and a low but significant release of L-histidine in cells incubated in the presence of 50 mM carnosine (p 

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PMID: 

Am J Chin Med. 2019 ;47(2):477-494. PMID: 30909731

Abstract Title: 

Carnosine Suppresses Human Colorectal Cell Migration and Intravasation by Regulating EMT and MMP Expression.

Abstract: 

Carnosine is an endogenous dipeptide found in the vertebrate skeletal muscles that is usually obtained through the diet. To investigate the mechanism by which carnosine regulates the migration and intravasation of human colorectal cancer (CRC) cells, we used cultured HCT-116 cells as an experimental model in this study. We examined HCT-116 cell migratory and intravasive abilities and expression of epithelial-mesenchymal transition (EMT)-associated molecules and matrix metalloproteinases (MMPs) after carnosine treatment. The results showed that both migration and invasion were inhibited in cells treated with carnosine. We found significant decreases in Twist-1 protein levels and increases in E-cadherin protein levels in HCT-116 cells after carnosine exposure. Although plasminogen activator (uPA) and MMP-9 mRNA and protein levels were decreased, TIMP-1 mRNA and protein levels were increased. Furthermore, the cytosolic levels of phosphorylated IB (p-IB) and NF-B DNA-binding activity were reduced after carnosine treatment. These results indicate that carnosine inhibits the migration and intravasation of human CRC cells. The regulatory mechanism may occur by suppressing NF-B activity and modulating MMP and EMT-related gene expression in HCT-116 cells.

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PMID: 

N Z Med J. 2018 12 14 ;131(1487):97-107. Epub 2018 Dec 14. PMID: 30543616

Abstract Title: 

Public health and the radio frequency radiation emitted by cellphone technology, smart meters and WiFi.

Abstract: 

This paper argues that the prevailing official narrative in New Zealand concerning the relationship between public health and the radio frequency emissions (RF) from cellphone technology, WiFi and electricity smart meters is scientifically and ethically flawed. The main regulatory document in the area, NZS2772.1:1999, is 20 years out of date and ignores existing laboratory evidence disproving its core assumption that the only biological effect of non-ionising radiation is tissue heating. This and further laboratory evidence for harmful effects of RF continues to be ignored, nominally on the contradictory grounds that (a) cellphone manufacturers say their products now emit less RF than early models, so early lab studies exposed tissue to RF levels higher than those now relevant (b) given the lack of actual data on population exposures either then or now, all laboratory evidence is unconvincing anyway. The offical narrative further opines that since there exist both laboratory and epidemiological studies concluding that RF is not biologically harmful, as well as studies concluding that RF is harmful, the appropriate response is to count up the number on each side, declare the"weight of evidence"to be such that"causation is not proven"and, pending unspecified further studies, continue exposing to unmonitored levels of RF the entire population of the country, none of whom has given informed consent to participate in the experiment. This approach is obviously unethical. It is also unacceptable scientifically. First, the algebraic model is flawed: studies that do find a harmful effect of RF are not invalidated by differently constructed studies that fail to find an effect. Secondly, while causation is relatively easy to study in the laboratory, it is difficult if not impossible to prove epidemiologically, given that (1) the very narrative under discussion has ensured that there is now no unexposed control group and (2) interpretation of timeline correlation studies is hampered by changes in the way new cancer registrations have been recorded over the years and the perennial problem of multiple possible causal factors. The present paper concludes that a precautionary approach is justified, and ends with a number of specific suggestions on how to start implementing such an approach.

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PMID: 

Exp Ther Med. 2019 Apr ;17(4):2641-2647. Epub 2019 Jan 30. PMID: 30930967

Abstract Title: 

Carnosine improves diabetic retinopathy via the MAPK/ERK pathway.

Abstract: 

Diabetic retinopathy (DR) is one of the most common causes of blindness in developed countries. Due to its asymptomatic onset and progressive disease course, DR is typically diagnosed at a late stage when treatment options are limited and therefore often results in irreversible blindness. Studies have demonstrated that carnosine may prevent and treat DR. In a previous study, the positive effect of carnosine on DR was determined and it was revealed that there may be an association between carnosine and the mitogen-activated protein kinase (MAPK)/extracellular signal related kinase (ERK) signaling pathway. To assess the interaction between carnosine and the MAPK/ERK signaling pathway, changes in PKC, ERK and p-ERK expression was assessed in diabetic rats following treatment with carnosine, PD98059 or U46619 via reverse transcription-quantitative polymerase chain reaction and western blotting. The results demonstrated that the expression of ERK and p-ERK were significantly suppressed following treatment with carnosine, but no significant effect on the expression of PKC was identified, which indicates that suppressing the activation of the MAPK/ERK signaling pathway may serve an important role in carnosine-induced DR prevention and treatment.

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PMID: 

J Biomed Phys Eng. 2018 Dec ;8(4):403-408. Epub 2018 Dec 1. PMID: 30568930

Abstract Title: 

Electromagnetic Fields of Mobile Phone Jammer Exposure on Blood Factors in Rats.

Abstract: 

Background: The increasing demand for using mobile phones has led to increasing mobile phone jammers as well. On the other hand, reports show that exposure to electromagnetic field causes an increase in the incidence of diseases such as leukemia, cancer, depression and failure in pregnancy outcomes; therefore, the aim of this study is to investigate the effects of exposure to electromagnetic fields of mobile phone jammers on blood factors.Materials and Methods: Thirty male Wistar immature and thirty mature rats were selected randomly and each one was divided into three groups of ten. The control group did not receive any radiation; the sham group was exposed to a switched-off jammer device and the experimental group was exposed to electromagnetic fields (EMF) radiated by Mobile Phone Jammer daily eight hours for five days a week during forty days. Blood sample was taken from heart and blood factors including PLT, MCHC and RDWCV were measured. The data were analyzed by ANOVA which was followed by Duncan's test.Results: The data from mature rats revealed that jammer usage led to a significant difference in blood factors including RBC, platelet, hemoglobin, hematocrit, MCV and RDWCV (P≤0.05); however, the number of lymphocytes, WBC and MCVH in the blood was the same in all groups. In immature rats, the exposure to jammer did not change RBC, lymphocyte and WBC count, hemoglobin and hematocrit; while, the platelet count along with MCHC, MVC and RDWCV changed by jammer radiation.Conclusion: The results exhibited that mobile phone jammer caused frequent changes in blood cell factors.

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PMID: 

Bioelectromagnetics. 2019 Sep ;40(6):375-390. Epub 2019 Jun 3. PMID: 31157927

Abstract Title: 

Morphological Changes Induced By Extremely Low-Frequency Electric Fields.

Abstract: 

In this paper, morphological effects of electric fields on avian erythrocytes (nucleated red blood cells) have been studied in detail. Morphological changes include rounding and cytoplasm transparency. It has been shown that the effect is non-thermal. Careful imaging and image analyses have been carried out to show that the degree of this effect is frequency-dependent, and has a higher conversion rate at higher temperatures. Furthermore, to better understand the mechanisms behind the morphological changes, we investigated the dedifferentiation hypothesis and performed a series of tests on avian erythrocytes including fluorescence spectroscopy for hemoglobin, and tests on human umbilical cord blood, mesenchymal stem cells, and bone marrow mesenchymal stem cells including flow-cytometry analysis for expression of certain markers and calcium staining. Bioelectromagnetics. 2019;40:375-390.© 2019 Bioelectromagnetics Society.

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PMID: 

Genes (Basel). 2019 06 25 ;10(6). Epub 2019 Jun 25. PMID: 31242701

Abstract Title: 

Electromagnetic Fields, Genomic Instability and Cancer: A Systems Biological View.

Abstract: 

This review discusses the use of systems biology in understanding the biological effectsof electromagnetic fields, with particular focus on induction of genomic instability and cancer. Weintroduce basic concepts of the dynamical systems theory such as the state space and attractors andthe use of these concepts in understanding the behavior of complex biological systems. We thendiscuss genomic instability in the framework of the dynamical systems theory, and describe thehypothesis that environmentally induced genomic instability corresponds to abnormal attractorstates; large enough environmental perturbations can force the biological system to leave normalevolutionarily optimized attractors (corresponding to normal cell phenotypes) and migrate to lessstable variant attractors. We discuss experimental approaches that can be coupled with theoreticalsystems biology such as testable predictions, derived from the theory and experimental methods,that can be used for measuring the state of the complex biological system. We also reviewpotentially informative studies and make recommendations for further studies.

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