Effect of nano-size on magnetostriction of BiFeO3 and exceptional magnetoelectric coupling properties of BiFeO3_P(VDF-TrFE) polymer composite films for magnetic field sensor application

The existence of magnetostriction in bulk BiFeO3 is still a matter of investigation and it is also an issue to investigate the magnetostriction effect in nano BiFeO3. Present work demonstrates the existence of magnetostrictive strain in superparamagnetic BiFeO3 nanoparticles at room temperature and the magnetoelectric coupling properties in composite form with P(VDFTrFE). Despite few reports on the magnetostriction effect in bulk BiFeO3 evidenced by the indirect method, the direct method (strain gauge) was employed in this work to examine the magnetostriction of superparamagnetic BiFeO3. In addition, a high magnetoelectric coupling coefficient was observed by the lock-in technique for optimized BiFeO3_P(VDF-TrFE) nanocomposite film. These nanocomposite films also exhibit room-temperature multiferroic properties. These results provide aspects of material with immense potential for practical applications in spintronics and magneto-electronics applications. We report a magnetoelectric sensor using superparamagnetic BiFeO3_P(VDF-TrFE) nanocomposite film for detection of ac magnetic field

Anomalous behavior of depolarization of light in a turbid medium

Depolarization of polarized light transmitting through a turbid medium is known to decrease with increasing value of anisotropy parameter g of the medium. We have observed that for turbid media comprised of scatterers having size parameter (X) and relative refractive index ratio (m) in the range [0.05≤(m-1)X≤2.5], although for a given value of X, a decrease in the value of m leads to higher g, depolarization also increases. This anomalous behavior arises because the depolarization characteristics of anisotropic scattering media (g≥0.7) comprised of low refractive index scatterers [(m-1)≤1,(m-1)X≤1] are much similar to that for Rayleigh scatterers

Therapeutic influence of simvastatin on MCF-7 and MDA-MB-231 breast cancer cells via mitochondrial depletion and improvement in chemosensitivity of cytotoxic drugs

Background: Breast cancer is the most commonly diagnosed cancer worldwide with 2.26 million cases in 2020. Cancer heterogeneity is the major challenge before existing therapeutic modalities due to metabolic variability of the cells as Warburg and anti-Warburg both type of metabolic phenotypes has been reported as a major contributing factors for cancer progression, invasion, metastasis and relapse. Also, this metabolic variability is associated with chemo and radio-resistance and poor therapeutic outcomes. Therefore, in present study we put an attempt to understand how simvastatin exert its effects on two metabolically different cell types and second how this drug can affect mitochondrial biomass, mt-DNA and glycolysis in both the cell types. Methods: We have observed effects of simvastatin on MCF-7 (dependent more on OXPHOS) and MDA-MB-231 (TNBC; more glycolytic with defected mitochondria) cells alone and after simvastatin pre-treatment followed by cytotoxic drugs including cisplatin, doxorubicin, gemcitabine, vincristine. We have conducted MTT assay for viability, cell death detection assay, apoptotic morphology study, scratch assay, transwell migration assay, lactate estimation in media (glycolysis parameter), mt-DNA to n-DNA ratio, mitotracker red (for mitochondrial membrane potential) and mitotracker green staining (for mitochondrial biomass) and qPCR to study expression of mitochondrial transcription factors and apoptotic genes including PGC-1α, NRF-1, NRF-2, TFAM, Bcl-2 and Bax. Results: We observed that 20 μM simvastatin (SIM) was most efficient dose for MCF-7, whereas 12.5 μM for MDA-MB-231 cells. Simvastatin itself caused a significant decrease in viability, increased cell death, and diminished wound closure in scratch assay as well as inhibited transwell migration. Also, the cells pre-treated with simvastatin for 72 h followed by treatment with cytotoxic drugs for 48 h increased chemo-sensitivity of cisplatin (CIS), doxorubicin (DOX), gemcitabine (GEM) and vincristine (VIN). SIM alone and in pre-treatment followed by cytotoxic drug treatment studies, there was a significant decrease in mitochondrial biomass and mitochondrial membrane potential (MMP), but also decreased glycolysis as evidenced by decrease in lactate levels in culture media. For inhibition of migratory potential, it was in the following order: CIS ˃ VIN ˃DOX˃ GEM, which was in the same order to diminish mitochondrial functionality (mt-DNA/n-DNA ratio, mitotracker green staining and a significant decrease in the expression of transcriptional factors of mitochondrial biogenesis). Contrastingly a decrease in the same order was observed in lactate concentration independent to the mitochondrial loss, but probably via inherent ability of the drugs to reduce lactate and glycolysis. However, for cell death, apoptotic phenotype, diminished expression of Bcl-2 along with increase in Bax and loss of viability, the efficiency of simvastatin alone and in pre-treatment studies was in the following order: VIN ˃ DOX˃GEM˃CIS, which was supported by loss of fluorescence of mitotracker red, suggested decrease in MMP; marker of cell death. Conclusion: We conclude that by using different doses simvastatin can target different metabolic phenotypes of breast cancer cells and can also increase the chemo-sensitivity of cytotoxic drugs, so that they can work efficiently at lower doses which will ultimately diminish the cost and toxicity issues