Majorana Phase And Matter Effects In Neutrino Chiral Oscillation

Due to finite masses and mixing, for neutrinos propagation in space-time, there is a chiral oscillation between left- and right- chiral neutrinos, besides the usual oscillation between different generations. The probability of chiral oscillation is suppressed by a factor of $m^2/E^2$ making the effect small for relativistic neutrinos. However, for non-relativistic neutrinos, this effects can be significant. In matter, the equation of motion is modified. When neutrinos produced in weak interaction pass through the matter, the effective energies are split into two different ones depending on the helicity of the neutrino. This results in different oscillation behavior for neutrinos with different helicity, in particular there is a new resonant effect related to the helicity state of neutrino different than the usual MSW effect. For Majorana neutrinos, chiral oscillation also depends on Majorana phases

Methyl N′-[(E)-2-methoxy­benzyl­idene]­hydrazinecarboxyl­ate

The title compound, C10H12N2O3, crystallizes with two independent mol­ecules in the asymmetric unit. The side chains in the two independent mol­ecules have slightly different orientations, with the C=N—N—C torsion angle being 169.19 (14)° in one of the mol­ecules and −179.86 (14)° in the other. Each independent mol­ecule adopts a trans configuration with respect to the C=N bond. In the crystal structure, mol­ecules are linked into chains running along [001] by N—H⋯O, N—H⋯N and C—H⋯O hydrogen bonds. In addition, an inter­molecular C—H⋯π inter­action is observed

Ultrastructural Changes, Nuclear Factor-κB Activation, and Tumor Necrosis Factor-α Expression in Brain after Acute Normovolemic Hemodilution and Controlled Hypotension in Rats

Cilj Ispitati moždana oštećenja u štakora nakon različitih stupnjeva akutne normovolemične hemodilucije i kontrolirane hipotenzije s pomoću morfološke analize neurona i provjeriti aktivaciju jezgrenog faktora-κB (NF- κB) i izražaj čimbenika nekroze tumora-α (TNF-α). Postupci Četrdeset štakora nasumično je raspoređeno u one lažno operirane i one s normovolemičnom hemodilucijom i kontroliranom hipotenzijom (s hematokritom od 30%, 25%, 20%, and 15%). Normovolemična hemodilucija i kontrolirana hipotenzija izazvane su nakon što su osnovni fiziološki parametri praćeni 20 minuta. Kontrolirana hipotenzija izazvana je nakon 30 minuta s pomoću natrijeva nitroprusida, a srednji arterijski tlak održavao se sljedeći sat vremena na 50-60 mmHg. Tri i pol sata nakon operacije životinje su eutanazirane. Razina TNF-α i aktivnost NF-κB određene su u temporalnoj moždanoj kori. Ultrastrukturna oštećenja ocijenjena su u području CA1 u hipokampusu. Promjene mitohondrija ocijenjene su polukvantitativno. Rezultati U skupinama s hematokritom od 20% i 15% nađena su izražena ultrastrukturna oštećenja, poput denaturacije mitohondrija i izobličenja jezgara. Izražaj TNF-α i aktivnost NF-κB bila je značajno povišena u svim skupinama s normovolemičnom hemodilucijom i kontroliranom hipotenzijom, a najviše su bile u skupini s hematokritom od 25%. Zaključak Izražena normovolemična hemodilucija i kontrolirana hipotenzija s hematokritom ≤20% mogu izazvati moždana oštećenja pa ih treba izbjegavati. U stanju ishemije, aktivacija NF-κB i izražaj TNF-α mogu predstavljati funkcionalne korelate. Bolje upoznavanje uloge NF-κB i TNF-α u mozgu može otvoriti nove pristupe prevenciji i liječenju neuroloških bolesti.Aim To examine brain damage following different degrees of acute normovolemic hemodilution combined with controlled hypotension (ANH-CH) by neuronal morphological analysis and investigate the expression of nuclear factor-kappa B (NF-κB) activity and tumor necrosis factor-alpha (TNF-α) in the rat. Methods Forty rats were randomly assigned to receive a sham operation or ANH-CH (with hematocrit 30%, 25%, 20%, and 15%). ANH was performed after baseline physiological parameters had been monitored for 20 minutes. CH was induced 30 minutes later using sodium nitroprusside and mean arterial pressure was maintained at 50-60 mm Hg for 1 hour. Rats were euthanatized 3 and a half hours after operation. TNF-α levels and NF-κB activities in cerebral temporal cortex were measured. Ultrastructural alterations in the CA1 region of the rat hippocampi were observed. Changes in mitochondria were evaluated semiquantitatively. Results Marked ultrastructural alterations, such as mitochondrial denaturalization and nucleus distortion, were observed in the CA1 region of the hippocampus in the ANH-CH hematocrit 20% group and ANH-CH hematocrit 15% group. TNF-α expression and NF-κB activity in the cerebral temporal cortex significantly increased in all ANHCH groups and peaked in the ANH-CH hematocrit 25% group. Conclusion Severe ANH-CH with hematocrit ≤20% may induce cerebral damage and should be avoided. NF-κB activation and TNF-α expression may play a functional role under the ischemic condition. A better understanding of the role of NF-κB and TNF-α in the brain may lead to a novel approach for preventing and treating various neurological disorders

Generation of high-density high-polarization positrons via single-shot strong laser-foil interaction

We put forward a novel method for producing ultrarelativistic high-density high-polarization positrons through a single-shot interaction of a strong laser with a tilted solid foil. In our method, the driving laser ionizes the target, and the emitted electrons are accelerated and subsequently generate abundant $\gamma$ photons via the nonlinear Compton scattering, dominated by the laser. These $\gamma$ photons then generate polarized positrons via the nonlinear Breit-Wheeler process, dominated by a strong self-generated quasi-static magnetic field $\mathbf{B}^{\rm S}$. We find that placing the foil at an appropriate angle can result in a directional orientation of $\mathbf{B}^{\rm S}$, thereby polarizing positrons. Manipulating the laser polarization direction can control the angle between the $\gamma$ photon polarization and $\mathbf{B}^{\rm S}$, significantly enhancing the positron polarization degree. Our spin-resolved quantum electrodynamics particle-in-cell simulations demonstrate that employing a laser with a peak intensity of about $10^{23}$ W/cm$^2$ can obtain dense ($\gtrsim$ 10$^{18}$ cm$^{-3}$) polarized positrons with an average polarization degree of about 70\% and a yield of above 0.1 nC per shot. Moreover, our method is feasible using currently available or upcoming laser facilities and robust with respect to the laser and target parameters. Such high-density high-polarization positrons hold great significance in laboratory astrophysics, high-energy physics and new physics beyond the Standard Model

The association between ATM D1853N polymorphism and breast cancer susceptibility: a meta-analysis

BACKGROUND: Emerging evidence suggests that ataxia telangiectasia-mutated (ATM) is involved in numerous damage repair signaling pathways and cell-cycle checkpoints. Heterozygous carriers of ATM-mutations have an increased risk for the development of breast cancer. The purpose of this study is to evaluate the association between ATM exon39 5557G > A (D1853N, rs1801516) polymorphism and breast cancer susceptibility with the use of a meta-analysis. METHODS: By searching PubMed and Embase databases, a total of 9 epidemiological studies with 4,191 cases and 3,780 controls were identified. Crude odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) for ATM D1853N polymorphism and breast cancer risk were calculated using fixed- or random-effects model based on the degree of heterogeneity among studies. RESULTS: No significant association between the ATM D1853N polymorphism and breast cancer risk was observed in overall analysis (GA versus GG: OR = 1.18; 95% CI, 0.90-1.53; AA versus GG: OR = 0.77; 95% CI, 0.58-1.03; dominant model: OR = 1.16; 95% CI, 0.89-1.51; and recessive model: OR = 0.78; 95% CI, 0.59-1.04, respectively). CONCLUSION: Our results indicate that ATM D1853N polymorphism is not a risk factor for developing breast cancer