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At least 217 records · Page 12Linked to original sources
PubMed1994

The lack of evidence for ELF magnetic-field effects on bilayer membranes and reconstituted membrane channels.

The effects of low-frequency (10-500 Hz) magnetic fields on the electrical properties of channel-free bilayer membranes, and on the single-channel conductance and macroscopic gating characteristics of porin channels incorporated into membranes, have been studied for field strengths in the range 10-100 microT. The field conditions that could in theory give rise to 'cyclotron resonance' effects were also studied. No evidence has been found to support the concept that cyclotron resonance and membrane ion channel effects are involved in the reported biological effects of ELF magnetic fields.

Dose-Response Relationship, Radiation↗
PubMed2004

Influence of probe size on the measurement accuracy of non-uniform ELF magnetic fields.

The accuracy of extremely low frequency (ELF) magnetic field measurements can be sensitively varied by the meter probe size when the spatial distribution of the magnetic flux density is highly non-uniform, e.g. if the measurement point is close to the field source. The deviation between measured and actual field varies from point to point depending on the probe dimension and on the source configuration, once the other measurement conditions are fixed. The analysis of this effect is developed through a two-dimensional numerical model that enables the evaluation of the actual field value and of the corresponding probe indication. The error distribution, i.e. the deviation between actual and measured value, is computed for magnetic fields generated by industrial three-phase systems under both balanced and unbalanced supply conditions. The analysis shows how, for a given source, the error depends not simply on the distance from the source in relation to the probe size, but on its spatial distribution, which is complex and cannot be a priori predicted without using a computational tool such as the one proposed.

Algorithms↗
PubMed1989

A numerical method for the computation of induced currents inside 3-D heterogeneous biological bodies by ELF--LF electric fields.

A numerical technique, based on the combination of surface-charge integral equations (SCIE) and an impedance network method, has been developed to compute internal electric fields and currents inside 3-D heterogeneous biological bodies with arbitrary grounding impedances induced by ELF-LF electric fields. The method has been applied to a biological concentric-sphere and the numerical results agree well with an existing analytical solution. Numerical results of the induced current inside a simplified heterogeneous model of the human head computed by this method are also presented.

Body Surface Area↗
PubMed1993

ELF magnetic fields, breast cancer, and melatonin: 60 Hz fields block melatonin's oncostatic action on ER+ breast cancer cell proliferation.

In this study we investigated whether a 60 Hz magnetic field can act at the cellular level to influence the growth of human estrogen-dependent breast cancer cells. Our experimental design assessed cell proliferation of a human breast cancer cell line, MCF-7, in the absence or the presence of melatonin which inhibits growth at a physiological concentration of 10(-9) M. In three experiments, continuous exposure to average sinusoidal 60 Hz magnetic fields of 1.90 +/- 0.01, 2.40 +/- 0.70, and 2.53 +/- 0.50 mG, or simultaneous exposure in matched incubators to average 60 Hz magnetic fields of 10.4 +/- 2.12, 11.95 +/- 2.73, and 11.95 +/- 3.28 mG, respectively, had no effect on cell proliferation in the absence of melatonin. When MCF-7 cells were cultured in the presence of 10(-9) M melatonin, an 18% inhibition of growth was observed for cells in a 2.40 +/- 0.70 mG field. This effect was blocked by a 60 Hz magnetic field of 11.95 +/- 2.75 mG. In a second experiment, a 27% inhibition of MCF-7 cell growth was observed for cells in a 2.53 +/- 0.50 mG magnetic field, and this was blocked by a 60 Hz magnetic field of 11.95 +/- 3.28 mG. These results provide the first evidence that ELF frequency magnetic fields can act at the cellular levels to enhance breast cancer cell proliferation by blocking melatonin's natural oncostatic action. In addition, there appears to be a dose threshold between 2 and 12 mG. The mechanism(s) of action is unknown and may involve modulation of signal transduction events associated with melatonin's regulation of cell growth.

Adenocarcinoma↗
PubMed1994

Elf-1 binds to a critical element in a second CD4 enhancer.

The coordinated expression of CD4 and CD8 during T-cell development is tightly coupled with the maturation state of the T cell. Additionally, the mutually exclusive expression of these receptors in mature T cells is representative of the functional T-cell subclasses (CD4+ helper T cells versus CD8+ cytotoxic T cells). We have studied the regulation CD4 gene transcription during T-cell development in an attempt to gain an understanding of the molecular mechanisms involved in T-cell development and differentiation. Here we present the identification of a second transcriptional enhancer in the murine CD4 locus 24 kb upstream of the CD4 promoter. This enhancer is active in mature T cells and is especially active in CD4+ helper T cells. A number of nuclear proteins bind to elements in the minimal CD4 enhancer that includes consensus sites for AP-1, Sp1, Gata, and Ets transcription factor families. We find that the Ets consensus site is crucial for enhancer activity and that the recently identified Ets factor, Elf-1, which is expressed at high levels in T cells and involved in the regulation of several other T-cell-specific genes, is a dominant protein in T-cell nuclear extracts that binds to this site.

Animals↗
PubMed1994

Activation of the granulocyte-macrophage colony-stimulating factor promoter in T cells requires cooperative binding of Elf-1 and AP-1 transcription factors.

The granulocyte-macrophage colony-stimulating factor (GM-CSF) gene has been studied extensively as a model system of transcriptional induction during T-lymphocyte activation. The GM-CSF gene is not expressed in resting peripheral blood T cells but is rapidly induced at the transcriptional level following activation through the cell surface T-cell receptor. A highly conserved 19-bp element located immediately 5' of the human GM-CSF TATA box (bp -34 to -52), herein called purine box 1 (PB1), has been shown to bind a T-cell nuclear protein complex and to be required for transcriptional induction of the GM-CSF gene following T-cell activation. The PB1 sequence motif is highly conserved in both human and murine GM-CSF genes. In this report, we demonstrate that the PB1 element alone confers inducibility on a heterologous promoter following transfection into human Jurkat T cells. In addition, we identify a major PB1 nuclear protein-binding complex that is not present in resting peripheral blood T cells but is rapidly induced following T-cell activation. Sequence analysis revealed that PB1 is composed of adjacent binding sites for Ets and AP-1 transcription factors. In vitro mutagenesis experiments demonstrated that both the Ets and AP-1 sites are required for binding of the inducible PB1 nuclear protein complex and for the transcriptional activity of this element and the GM-CSF promoter in activated T cells. Using antibodies specific for different Ets and AP-1 family members, we demonstrate that the major inducible PB1-binding activity present in activated T-cell nuclear extracts is composed of the Elf-1, c-Fos, and JunB transcription factors. Taken together, these results suggest that cooperative interactions between specific Ets and AP-1 family members are important in regulating inducible gene expression following T-cell activation.

Adult↗
PubMed2004

The scl +18/19 stem cell enhancer is not required for hematopoiesis: identification of a 5' bifunctional hematopoietic-endothelial enhancer bound by Fli-1 and Elf-1.

Analysis of cis-regulatory elements is central to understanding the genomic program for development. The scl/tal-1 transcription factor is essential for lineage commitment to blood cell formation and previous studies identified an scl enhancer (the +18/19 element) which was sufficient to target the vast majority of hematopoietic stem cells, together with hematopoietic progenitors and endothelium. Moreover, expression of scl under control of the +18/19 enhancer rescued blood progenitor formation in scl(-/-) embryos. However, here we demonstrate by using a knockout approach that, within the endogenous scl locus, the +18/19 enhancer is not necessary for the initiation of scl transcription or for the formation of hematopoietic cells. These results led to the identification of a bifunctional 5' enhancer (-3.8 element), which targets expression to hematopoietic progenitors and endothelium, contains conserved critical Ets sites, and is bound by Ets family transcription factors, including Fli-1 and Elf-1. These data demonstrate that two geographically distinct but functionally related enhancers regulate scl transcription in hematopoietic progenitors and endothelial cells and suggest that enhancers with dual hematopoietic-endothelial activity may represent a general strategy for regulating blood and endothelial development.

Animals↗
PubMed2006

Endoglin expression in the endothelium is regulated by Fli-1, Erg, and Elf-1 acting on the promoter and a -8-kb enhancer.

Angiogenesis is critical to the growth and regeneration of tissue but is also a key component of tumor growth and chronic inflammatory disorders. Endoglin plays a key role in angiogenesis by modulating cellular responses to transforming growth factor-beta (TGF-beta) signaling and is upregulated in proliferating endothelial cells. To gain insights into the transcriptional hierarchies that govern endoglin expression, we used a combination of comparative genomic, biochemical, and transgenic approaches. Both the promoter and a region 8 kb upstream of exon 1 were active in transfection assays in endothelial cells. In transgenic mice, the promoter directed low-level expression to a subset of endothelial cells. By contrast, inclusion of the -8 enhancer resulted in robust endothelial activity with additional staining in developing ear mesenchyme. Subsequent molecular analysis demonstrated that both the -8 enhancer and the promoter depend on conserved Ets sites, which were bound in endothelial cells in vivo by Fli-1, Erg, and Elf-1. This study therefore establishes the transcriptional framework within which endoglin functions during angiogenesis.

Animals↗
PubMed2004

The regulation of human beta-defensin 2 by the ETS transcription factor MEF (myeloid Elf-1-like factor) is enhanced by promyelocytic leukemia protein.

The human beta-defensin 2 (HBD 2) is a potent anti-bacterial peptide with a wide spectrum of activity. MEF (myeloid elf-1-like factor) or Elf4, a member of the ETS transcription factor family, has been shown to up-regulate the basal expression of the HBD 2 gene in epithelial cells. The mammalian cell nucleus is organized into distinct nuclear domains, one of which is the PML (promyelocytic leukemia) nuclear body involved in the regulation of transcription. Here, we show that PML stimulated MEF transcriptional activity, resulting in the up-regulation of endogenous HBD 2 expression.

Anti-Infective Agents↗
PubMed1999

The transcription factors Elf-1 and GATA-1 bind to cell-specific enhancer elements of human high-affinity IgE receptor alpha-chain gene.

Key regulatory regions necessary for the expression of the gene encoding FcepsilonRI alpha-chain, a component of the high-affinity IgE receptor primarily responsible for IgE-dependent allergic response, were investigated. Two regions, -74/-69 and -55/-47, which contained binding motifs for proteins belonging to the Ets family and the GATA family, respectively, were shown to be necessary for the activation of the alpha-chain promoter. Both the regulatory elements enhanced the promoter activity only in alpha-chain-producing cells PT18 and RBL-2H3 (mast cell lines), indicating that the elements required specific trans-acting proteins present in the alpha-chain-producing cells. EMSA using nuclear extracts and in vitro-translated proteins revealed that Elf-1 and GATA-1 bound to the enhancer elements. This is the first report describing the regulation in the expression of the FcepsilonRI alpha-chain.

Animals↗
PubMed2000

[The role of melatonin in the molecular mechanism of weak, static and extremely low frequency (50 Hz) magnetic fields (ELF)].

Melatonin is a neurohormone produced by the pineal gland. It has been recently found that it is also an antioxidant and a free radical scavenger. Melatonin was documented to be a direct trap of hydroxyl and peroxyl radicals. Therefore, this hormone could protect cells, tissues and organs against oxidative (free radicals) damage (DNA, protein, lipids). It has been suggested that noxious effects of ELF exposure (cancer or immunological disturbances) could be due to increased the concentration of free radicals induced by magnetic field. This is also leading to a hypothesis that melatonin suppression (by electromagnetic fields) in humans may increase the probability of mutagenic and carcinogenic risks. The future experiments, in vitro and in vivo, should provide an answer to the question on what is the real role of melatonin in the molecular (free radicals) mechanisms of weak magnetic fields.

Humans↗
PubMed2000

Human health consequences of environmentally-modulated gene expression: potential roles of ELF-EMF induced epigenetic versus mutagenic mechanisms of disease.

In order to determine if there might be biological and health consequences after exposures to extremely-low frequency electromagnetic fields (ELF-EMF), either experimentally or epidemiologically, mechanistic understanding of the potential means by which any environmental agent can affect cells in a multicellular organism has to be reviewed. The goal of this limited review is to demonstrate that, while the prevailing paradigm of the environmentally-induced acute and chronic diseases involves either cell killing (cytotoxicity) or gene/chromosome mutations (genotoxicity), alteration of the expression of genetic information at the transcriptional (turning genes "on" or "off"), translational (stabilizing or de-stabilizing the genetic message), or posttranslational (altering the gene product or protein) levels has the potential to contribute to various diseases. This latter mechanism, "epigenetic" toxicity, unlike the former two which are irreversible, is characterized by threshold-like action, multiple biochemical pathways and chronic, regular exposures to be effective. Ultimately, epigenetic toxicants affect one of four potential cell states, namely alteration of cell proliferation, cell differentiation, programmed cell death (apoptosis) or adaptive responses of differentiated cells.

DNA Damage↗
PubMed2003

Static and ELF magnetic fields enhance the in vivo anti-tumor efficacy of cis-platin against lewis lung carcinoma, but not of cyclophosphamide against B16 melanotic melanoma.

Previous works showed that exposure to static and extremely low frequency (ELF) magnetic fields (MF) over 3 mT slows down the growth kinetics of human tumors engrafted s.c. in immunodeficient mice, reducing their metastatizing power and prolonging mouse survival. In the experiments reported here, immunocompetent mice bearing murine Lewis Lung carcinomas (LLCs) or B16 melanotic melanomas were exposed to MF and treated respectively with two commonly used anti-cancer drugs: cis-diamminedichloroplatinum (cis-platin) and N,N-bis (2-chloroethyl)tetra-hydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide (cyclophosphamide). The experiment endpoint was survival time. The survival time of mice treated with cis-platin (3mg/kg i.p.) and exposed to MF was significantly (P<0.01) longer than that of mice treated only with cis-platin or only exposed to MF, superimposing that of mice treated with 10mg/kg i.p. of the drug, showing that MF act synergically with the pharmacological treatment. On the contrary, when mice treated with cyclophosphamide (50mg/kg i.p.) were exposed to MF no synergic effects were observed, the survival curve being exactly the same as that of mice treated with the drug alone. No clinical signs or toxicity were seen in any of the mice exposed to MF alone or along with cis-platin or cyclophosphamide treatment, compared to mice given only the two known drugs.A possible explanation for the synergic effect of MF being found in mice treated with cis-platin could be that the platinum ion stimulates radical production and that MF enhance active oxygen production bringing about changes in tumor cell membrane permeability, influencing positively the drug uptake. Alternatively, or in addition to this, it has been demonstrated that the rate of conversion of cis-platin to reactive species able to bind to DNA, is increased by localized production of free radicals by MF.

Animals↗
PubMedDate not supplied

[Experimental data on extremely low frequency (ELF) electromagnetic fields].

At the current state of knowledge, the biological effects both in vitro and in vivo connected to low frequency electromagnetic fields (ELF) are not univocally interpreted. Indeed a lot of literature seems strictly related to the particular experimental procedure depending both on the biological target and the exposure features under consideration. The best studied biological parameters in vitro are kinetics of cell proliferation, change in enzymatic activities, intramembrane ionic flux and integrity of chromosome complement. In general, the study on genotoxic effects induced by simultaneous exposure to electromagnetic fields and known chemical or physical mutagenes is based on the theory that electromagnetic fields may interfere with mutagenic substances rather than affect directly genetic material. In addition, studies in vivo confirm different results both in different animal species and in different (nervous, neuroendocrine, immunitary systems). Finally, in order to evaluate the wide research activity on this subject, we need to take into account the main standard criteria adopted by the world scientific community, such as the peer review process and the confirmation of experimental data by means of independent repetitions.

Animals↗
PubMed2004

Recent experimental data on Extremely Low Frequency (ELF) magnetic field carcinogenic risk: open questions.

The NTP experimental studies on Extremely Low Frequency (ELF) magnetic fields (two-year studies in rats and mice and magnetic field promotion/DMBA initiation in female rats studies, NTP 1999) are of main interest because of the value and completeness of the information produced on neoplastic and non-neoplastic effects. Ajoint evaluation of the two-year study data indicates a thyroid C-cell focal hyperplasia increase in female rats at the same exposures at which the neoplasm increment of the same cells has been observed only in male rats (on which the "equivocal evidence" NTP classification is based). The significant exposure-related trichoepithelioma and trichoepithelioma plus other skin neoplasms reported for male rats in the two year studies finds some support in the female rat data relative to trichoepithelioma reported in incidence summary of the NTP 26-week initiation/promotion study, even if the experimental designs of the two studies are different. An indication of exposure-related increase of single mammary carcinomas emerges from the summary of neoplasm incidence, together with a dose-related decrease of mammary gland multiple carcinomas. A significant decrease of lung alveolar/bronchiolar adenoma incidence was observed in exposed groups in both mouse genders. It seems improbable to attribute the above effects only to chance. The present debate, dividing science in two opposite fields: one of them denying any appreciable carcinogenic effect of magnetic fields, and the other one hypothesising their dramatic effects, are presently devoid of reliable and exhaustive scientific support, which could only be provided by further research.

Animals↗
PubMed2004

[Raman analysis of conformation changes of insulin solvent after being exposed to ELF pulsed electric field].

Raman spectra of insulin solvents are presented before and after being exposed to the pulsed electric field with extremely low frequency 50 Hz (ELF). The covalences of the molecule were not affected and the changes of some secondary bonds such as hydrogen bonds and salt bonds were observed. Detailed analysis of these spectra indicates that the alpha-helix of insulin molecule was destroyed after the exposure, which is proved by the shift of the peak of the amide I region toward higher wave number and by the appearance of several new peaks: 1561 and 1594 cm(-1). The disulfides were affected by the weaken alpha-helix, and their vibrational modes were changed. Meanwhile the hydrogen bonding between the dimer are broken down which leads to the increase in the peak intensities at 1002 and at 1602 cm(-1).

Electricity↗
PubMed2006

Some non neoplastic effects of ELF magnetic fields in experimental animals.

This study has been addressed to the non neoplastic effects observed in experimental animals exposed to the ELF magnetic fields exposure, giving particular attention to the large and comprehensive data of the two-year NTP (National Toxicology Program) studies. The statistical analysis of non neoplastic incidences, whenever not presented by the study authors, has been carried out in the present study. Only the effects coherently emerging for both the animal genders have been considered; gender specific effects have obviously been separately analysed. The trend analysis has been carried out over the 4 exposure levels (0, 2, 200 microT, and 1000 microT -microTesla) and on the first 3 ones. For 28 dose-response relationships, non neoplastic effects significantly emerged (6 for hyperplasia, 4 for cyst, 4 for inflammation, 3 for focus, 3 for atrophy, 2 for cellular infiltration, and 1 for each of other 6 effects). This number is much higher than the one of neoplastic effects indicated by the NTP as significant. For many of these dose-response relationships, the trend was significant only over the first 3 treatment levels (excluding the highest one, 1000 microT/1 mT), in agreement with the results of some other studies indicating a response reduction, or even a possible anticarcinogenic effects, at considerably high exposures (mT range). The obtained results suggest a complex effect modulation pattern.

Animals↗
PubMed1996

An IL-2 response element in the human IL-2 receptor alpha chain promoter is a composite element that binds Stat5, Elf-1, HMG-I(Y) and a GATA family protein.

Expression of the human interleukin-2 (IL-2) receptor alpha chain gene is potently upregulated by its own ligand, IL-2. In this study, we characterize an essential upstream IL-2 response element that contains both consensus and non-consensus GAS motifs, two putative Ets binding sites (EBS), one of which overlaps the consensus GAS motif, and a GATA motif, which overlaps the non-consensus GAS motif. We demonstrate that although the individual components of this element do not respond to IL-2, together they form a composite element capable of conferring IL-2 responsiveness to a heterologous promoter. Multiple factors including Stat5, Elf-1, HMG-I(Y) and GATA family proteins bind to the IL-2 response element and mutation of any one of these binding sites diminishes the activity of this element. An unidentified Ets family protein binds to the EBS overlapping the consensus GAS motif and appears to negatively regulate the human IL-2R alpha promoter. Thus, IL-2-induced IL-2R alpha promoter activity requires a complex upstream element, which appears to contain binding sites for both positive and negative regulatory factors.

Base Sequence↗