A Bohr's Semiclassical Model of the Black Hole Thermodynamics

We propose a simple procedure for evaluating the main thermodynamical attributes of a Schwarzschild's black hole: Bekenstein-Hawking entropy, Hawking's temperature and Bekenstein's quantization of the surface area. We make use of the condition that the circumference of a great circle on the black hole horizon contains finite number of the corresponding reduced Compton's wavelength. It is essentially analogous to Bohr's quantization postulate in Bohr's atomic model interpreted by de Broglie's relation. We present black hole radiation in the form conceptually analogous to Bohr's postulate on the photon emission by discrete quantum jump of the electron within the Old quantum theory. It enables us, in accordance with Heisenberg's uncertainty relation and Bohr's correspondence principle, to make a rough estimate of the time interval for black hole evaporation, which turns out very close to time interval predicted by the standard Hawking's theory. Our calculations confirm Bekenstein's semiclassical result for the energy quantization, in variance with Frasca's (2005) calculations. Finally we speculate about the possible source-energy distribution within the black hole horizon.Comment: no figure

Study of Nd-Fe-B Alloys with Nonstoichiometric Nd Content in Optimal Magnetic State

Characterization of two rapid-quenched Nd-Fe-B alloys with nonstoichiometric Nd content in the optimized magnetic state was carried out using the X-ray diffractometry (XRD), (57)Fe Mossbauer spectroscopic phase analysis (MS), electron microscopy (TEM), high resolution TEM (HREM) and Superconducting Quantum Interference Device (SQUID) magnetometer. The experimental results demonstrate the fundamental difference in the structure and magnetic properties of the two investigated alloys in the optimized magnetic state. The Nd-Fe-B alloy with the reduced Nd content (Nd(4.5)Fe(77)B(18.5)) was found to have the nanocomposite structure of Fe(3)B/Nd(2)Fe(14)B and partly alpha-Fe/Nd(2)Fe(14)B, with mean grain size below 30 nm. On the other side, the overstoichiometric Nd(14)Fe(79)B(7) alloy has almost a monophase structure with the dominant content of the hard magnetic phase Nd(2)Fe(14)B (up to 95 wt. %) and a mean crystallite size about 60 nm, as determined by XRD and TEM analysis. The results of magnetic measurements on SQUID magnetometer also suggest the nanocomposite structure of the Nd-low alloy and nanocrystalline decoupled structure of the Nd-rich alloy after the optimal heat treatment.open

Non-equilibrium supercurrent through mesoscopic ferromagnetic weak links

We consider a mesoscopic normal metal, where the spin degeneracy is lifted by a ferromagnetic exchange field or Zeeman splitting, coupled to two superconducting reservoirs. As a function of the exchange field or the distance between the reservoirs, the supercurrent through this device oscillates with an exponentially decreasing envelope. This phenomenon is similar to the tuning of a supercurrent by a non-equilibrium quasiparticle distribution between two voltage-biased reservoirs. We propose a device combining the exchange field and non-equilibrium effects, which allows us to observe a range of novel phenomena. For instance, part of the field-suppressed supercurrent can be recovered by a voltage between the additional probes.Comment: 7 pages, 8 figures, Europhys. Lett., to be published, corrected two reference

Threshold detachment of negative ions by electron impact

The description of threshold fragmentation under long range repulsive forces is presented. The dominant energy dependence near threshold is isolated by decomposing the cross section into a product of a back ground part and a barrier penetration probability resulting from the repulsive Coulomb interaction. This tunneling probability contains the dominant energy variation and it can be calculated analytically based on the same principles as Wannier's description for threshold ionization under attractive forces. Good agreement is found with the available experimental cross sections on detachment by electron impact from $D^{-}$, $O^{-}$ and $B^{-}$.Comment: 4 pages, 4 figures (EPS), to appear in Phys.Rev.Lett, Feb. 22nd, 199

Energy Metabolism in Uncoupling Protein 3 Gene Knockout Mice

Uncoupling protein 3 (UCP3) is a member of the mitochondrial anion carrier superfamily. Based upon its high homology with UCP1 and its restricted tissue distribution to skeletal muscle and brown adipose tissue, UCP3 has been suggested to play important roles in regulating energy expenditure, body weight, and thermoregulation. Other postulated roles for UCP3 include regulation of fatty acid metabolism, adaptive responses to acute exercise and starvation, and prevention of reactive oxygen species (ROS) formation. To address these questions, we have generated mice lacking UCP3 (UCP3 knockout (KO) mice). Here, we provide evidence that skeletal muscle mitochondria lacking UCP3 are more coupled (i.e. increased state 3/state 4 ratio), indicating that UCP3 has uncoupling activity. In addition, production of ROS is increased in mitochondria lacking UCP3. This study demonstrates that UCP3 has uncoupling activity and that its absence may lead to increased production of ROS. Despite these effects on mitochondrial function, UCP3 does not seem to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induced thermogenesis. The absence of such phenotypes in UCP3 KO mice could not be attributed to up-regulation of other UCP mRNAs. However, alternative compensatory mechanisms cannot be excluded. The consequence of increased mitochondrial coupling in UCP3 KO mice on metabolism and the possible role of yet unidentified compensatory mechanisms, remains to be determined

Energy Metabolism in Uncoupling Protein 3 Gene Knockout Mice

Uncoupling protein 3 (UCP3) is a member of the mitochondrial anion carrier superfamily. Based upon its high homology with UCP1 and its restricted tissue distribution to skeletal muscle and brown adipose tissue, UCP3 has been suggested to play important roles in regulating energy expenditure, body weight, and thermoregulation. Other postulated roles for UCP3 include regulation of fatty acid metabolism, adaptive responses to acute exercise and starvation, and prevention of reactive oxygen species (ROS) formation. To address these questions, we have generated mice lacking UCP3 (UCP3 knockout (KO) mice). Here, we provide evidence that skeletal muscle mitochondria lacking UCP3 are more coupled (i.e. increased state 3/state 4 ratio), indicating that UCP3 has uncoupling activity. In addition, production of ROS is increased in mitochondria lacking UCP3. This study demonstrates that UCP3 has uncoupling activity and that its absence may lead to increased production of ROS. Despite these effects on mitochondrial function, UCP3 does not seem to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induced thermogenesis. The absence of such phenotypes in UCP3 KO mice could not be attributed to up-regulation of other UCP mRNAs. However, alternative compensatory mechanisms cannot be excluded. The consequence of increased mitochondrial coupling in UCP3 KO mice on metabolism and the possible role of yet unidentified compensatory mechanisms, remains to be determined

Expression of Human α2-Adrenergic Receptors in Adipose Tissue of β3-Adrenergic Receptor-deficient Mice Promotes Diet-induced Obesity

Catecholamines play an important role in controlling white adipose tissue function and development. β- and α2-adrenergic receptors (ARs) couple positively and negatively, respectively, to adenylyl cyclase and are co-expressed in human adipocytes. Previous studies have demonstrated increased adipocyte α2/β-AR balance in obesity, and it has been proposed that increased α2-ARs in adipose tissue with or without decreased β-ARs may contribute mechanistically to the development of increased fat mass. To critically test this hypothesis, adipocyte α2/β-AR balance was genetically manipulated in mice. Human α2A-ARs were transgenically expressed in the adipose tissue of mice that were either homozygous (−/−) or heterozygous (+/−) for a disrupted β3-AR allele. Mice expressing α2-ARs in fat, in the absence of β3-ARs (β3-AR −/− background), developed high fat diet-induced obesity. Strikingly, this effect was due entirely to adipocyte hyperplasia and required the presence of α2-ARs, the absence of β3-ARs, and a high fat diet. Of note, obese α2-transgenic, β3 −/− mice failed to develop insulin resistance, which may reflect the fact that expanded fat mass was due to adipocyte hyperplasia and not adipocyte hypertrophy. In summary, we have demonstrated that increased α2/β-AR balance in adipocytes promotes obesity by stimulating adipocyte hyperplasia. This study also demonstrates one way in which two genes (α2 and β3-AR) and diet interact to influence fat mass