Cadmium is widely utilized in nickel-cadmium batteries, stabilizers, and coating applications due to its versatile physico-chemical properties. The aim of present study was to evaluate the impact of biofield treatment on atomic, thermal, and physical properties of cadmium powder. The cadmium powder was divided into two groups, one group as control and another group as treated. The treated group received Mr. Trivedi’s biofield treatment. Control and treated samples were characterized using X-ray diffraction (XRD), differential scanning calorimetry (DSC), particle size analyzer, surface area analyzer, and scanning electron microscopy (SEM). XRD results showed significant alteration in lattice parameter, unit cell volume, densities, nuclear charge per unit volume, and atomic weight in treated cadmium powder as compared to control. Furthermore, crystallite size was significantly reduced upto 66.69% in treated cadmium as compared to control. DSC analysis results showed that the latent heat of fusion of the treated cadmium powder was considerably reduced by 16.45% as compared to control. Particle size data revealed that average particle size (d50) of treated cadmium powder was significantly reduced by 47.79 % as compared to the control. In addition, the surface area of treated cadmium powder was substantially enhanced by 156.36% as compared to control. Surface morphology observed by SEM showed the more facets and fractured surface with satellite boundaries in treated cadmium powder as compared to control. These findings suggest that biofield treatment has significantly altered the atomic, thermal and physical properties of cadmium.
Authors: Rohit seth
Comments: 5 Pages.
Previous studies have shown that zinc deficiency leads to apoptosis of neuronal precursor cells in vivo and in vitro. In addition to the role of p53 as a nuclear transcription factor in zinc deficient cultured human neuronal precursors (NT-2), we have now identified the translocation of phosphorylated p53 to the mitochondria and p53-dependent increases in the pro-apoptotic mitochondrial protein BAX leading to a loss of mitochondrial membrane potential as demonstrated by a 25% decrease in JC-1 red:green fluorescence ratio. Disruption of mitochondrial membrane integrity was accompanied by efflux of the apoptosis inducing factor (AIF) from the mitochondria and translocation to the nucleus with a significant increase in reactive oxygen species (ROS) after 24 h of zinc deficiency. Measurement of caspase cleavage, mRNA, and treatment with caspase inhibitors revealed the involvement of caspases 2, 3, 6, and 7 in zinc deficiency-mediated apoptosis. Down-stream targets of caspase activation, including the nuclear structure protein lamin and polyADP ribose polymerase (PARP), which participates in DNA repair, were also cleaved. Transfection with a dominant-negative p53 construct and use of the p53 inhibitor, pifithrin- , established that these alterations were largely dependent on p53. Together these data identify a cascade of events involving mitochondrial p53 as well as p53-dependent caspase-mediated mechanisms leading to apoptosis during zinc deficiency.