Signature Of Parity Research Articles

Half quantized Hall effect

Here we report a half-quantized Hall effect in a metal or semimetal. The Hall conductance is half quantized and the longitudinal conductance is nonzero. Consequently, the Hall resistivity is not quantized. The half quantization occurs when the parity symmetry or time reversal symmetry emerges near the Fermi surface or Fermi level while the symmetry is broken in the whole system. A recent experiment reports the observation of the half-quantized Hall conductance in a magnetically-doped topological insulator. We discover that a single gapless Dirac cone exists in the band structure and has half-quantized conductance when the Fermi level intercepts the gapless surface states in which the parity symmetry is invariant. As there are no localized chiral edge states in the gapless and metallic system, we find that the chiral edge current is carried by the gapless surface states. The current density peaks at the edge and decays in a power law rather than the exponential decay as in the conventional quantum anomalous Hall effect. The half quantized Hall conductance is a signature of parity anomaly in a single gapless Dirac cone on a lattice. We term the nontrivial quantum phase as “parity anomalous semimetal”. The work opens the door to exploring novel topological states of matter with fractional topological invariants.

Signature of parity anomaly: Crossover from one half to integer quantized Hall conductance in a finite magnetic field

Signature of parity anomaly: Crossover from one half to integer quantized Hall conductance in a finite magnetic field

Cellular and molecular signatures of motherhood in the adult and ageing rat brain.

Pregnancy is marked by robust changes, including brain changes to volume, structure, connectivity and neuroplasticity. Although some brain changes are restricted to pregnancy and the postpartum, others are long-lasting. Few studies have examined possible mechanisms of these changes or the effects of multiple pregnancies. We characterized various cellular and molecular signatures of parity (nulliparous, primiparous, biparous) in the rat hippocampus. We investigated density of neural stems cells (Sox2), microglia (Iba-1) and levels of a synaptic protein (PSD-95), cell signalling pathways, neuroinflammation, and the tryptophan-kynurenine (TRP-KYN) pathway, one week after weaning their pups from the last pregnancy (age of dam: seven months) and in middle-age (age of dam: 13 months). Parity increased PSD-95 levels in both age groups and prevented the age-related decrease in neural stem cell density observed in nulliparous rats. Biparity increased cell signalling phosphoproteins (pp70S6K, S6RP) and number of microglia in the dentate gyrus, regardless of age. Parity resulted in transient changes to the TRP-KYN system. Thus, previous parity has lasting effects on synaptic plasticity with fewer lasting effects on inflammation and cell signalling phosphoproteins in the whole hippocampus.

Signature of parity anomaly in the measurement of optical Hall conductivity in quantum anomalous Hall systems

Parity anomaly is a quantum mechanical effect that the parity symmetry in a two-dimensional classical action is failed to be restored in any regularization of the full quantum theory and is characterized by a half-quantized Hall conductivity. Here we propose a scheme to explore the experimental signature from parity anomaly in the measurement of optical Hall conductivity, in which the optical Hall conductivity is nearly half quantized for a proper range of frequency. The behaviors of optical Hall conductivity are studied for several models, which reveal the appearance of half-quantized Hall conductivity in low or high-frequency regimes. The optical Hall conductivity can be extracted from the measurement of Kerr and Faraday rotations and the absorption rate of the circularly polarized light. This proposal provides a practical method to explore the signature of parity anomaly in topological quantum materials.

Electron Electric Dipole Moment Searches Using Clock Transitions in Ultracold Molecules.

Permanent electric dipole moments (EDMs) of fundamental particles such as the electron are signatures of parity and time-reversal violation occurring in physics beyond the standard model. EDM measurements probe new physics at energy scales well beyond the reach of present-day colliders. Recent advances in assembling molecules from ultracold atoms have opened up new opportunities for improving the reach of EDM experiments. However, the magnetic field sensitivity of such ultracold molecules means that new measurement techniques are needed before these opportunities can be fully exploited. We present a technique that takes advantage of magnetically insensitive hyperfine clock transitions in polar molecules, offering a way to improve both the precision and accuracy of EDM searches with ultracold assembled molecules.

Genomic signature of parity in the breast of premenopausal women

BackgroundFull-term pregnancy (FTP) at an early age confers long-term protection against breast cancer. Previously, we reported that a FTP imprints a specific gene expression profile in the breast of postmenopausal women. Herein, we evaluated gene expression changes induced by parity in the breast of premenopausal women.MethodsGene expression profiling of normal breast tissue from 30 nulliparous (NP) and 79 parous (P) premenopausal volunteers was performed using Affymetrix microarrays. In addition to a discovery/validation analysis, we conducted an analysis of gene expression differences in P vs. NP women as a function of time since last FTP. Finally, a laser capture microdissection substudy was performed to compare the gene expression profile in the whole breast biopsy with that in the epithelial and stromal tissues.ResultsDiscovery/validation analysis identified 43 differentially expressed genes in P vs. NP breast. Analysis of expression as a function of time since FTP revealed 286 differentially expressed genes (238 up- and 48 downregulated) comparing all P vs. all NP, and/or P women whose last FTP was less than 5 years before biopsy vs. all NP women. The upregulated genes showed three expression patterns: (1) transient: genes upregulated after FTP but whose expression levels returned to NP levels. These genes were mainly related to immune response, specifically activation of T cells. (2) Long-term changing: genes upregulated following FTP, whose expression levels decreased with increasing time since FTP but did not return to NP levels. These were related to immune response and development. (3) Long-term constant: genes that remained upregulated in parous compared to nulliparous breast, independently of time since FTP. These were mainly involved in development/cell differentiation processes, and also chromatin remodeling. Lastly, we found that the gene expression in whole tissue was a weighted average of the expression in epithelial and stromal tissues.ConclusionsGenes transiently activated by FTP may have a role in protecting the mammary gland against neoplastically transformed cells through activation of T cells. Furthermore, chromatin remodeling and cell differentiation, represented by the genes that are maintained upregulated long after the FTP, may be responsible for the lasting preventive effect against breast cancer.

Shell-model-like approach based on cranking covariant density functional theory: Band crossing and shape evolution in Fe60

The shell-model-like approach is implemented to treat the cranking many-body Hamiltonian based on the covariant density functional theory including pairing correlations with exact particle number conservation. The self-consistency is achieved by iterating the single-particle occupation probabilities back to the densities and currents. As an example, the rotational structures observed in the neutron-rich nucleus $^{60}$Fe are investigated and analyzed. Without introducing any \emph{ad hoc} parameters, the bandheads, the rotational spectra, and the relations between the angular momentum and rotational frequency for the positive parity band A, and negative parity bands B and C are well reproduced. The essential role of the pairing correlations is revealed. It is found that for band A, the bandcrossing is due to the change of the last two occupied neutrons from the $1f_{5/2}$ signature partners to the $1g_{9/2}$ signature partners. For the two negative parity signature partner bands B and C, the bandcrossings are due to the pseudo-crossing between the $1f_{7/2,~5/2}$ and the $1f_{5/2,~1/2}$ orbitals. Generally speaking, the deformation parameters $\beta$ for bands A, B, and C decrease with rotational frequency. For band A, the deformation jumps from $\beta\sim0.19$ to $\beta\sim0.29$ around the bandcrossing. In comparison with its signature partner band C, band B exhibits appreciable triaxial deformation.

Optical signatures of parity anomaly in a gapped graphene-like system

Parity anomaly refers to the violation of coordinate reflection symmetry induced by the quantum fluctuations. It is proposed to exist in a graphene-like system with a finite bare mass for Dirac fermions, and manifests itself as a parity-violating quantum correction to the current of each species of fermions. Coulomb interaction greatly increases the fermion mass, and produces various types of excitons. Of particular interest is the ρ-exciton, which is directly connected to parity anomaly and can be generated by absorbing a specific photon. The exciton is a particle-hole bound state, and can be regarded as condensed-matter analogue of meson composed of quark-anti-quark pair. By virtue of this correspondence, we analyze the optical conductivity and calculate the mass of ρ-exciton by employing the Shifman–Vainshtein–Zakharov sum rule method that is widely used in the studies of hadron phenomenology. We show that ρ-exciton leads to a sharp peak in the optical conductivity, which is observable in optical experiments. Moreover, we study the impact of scalar-like excitons on two-photon processes by computing the decay amplitude, and also find peaks in the Raman spectra.

Parity-related molecular signatures and breast cancer subtypes by estrogen receptor status.

IntroductionRelationships of parity with breast cancer risk are complex. Parity is associated with decreased risk of postmenopausal hormone receptor–positive breast tumors, but may increase risk for basal-like breast cancers and early-onset tumors. Characterizing parity-related gene expression patterns in normal breast and breast tumor tissues may improve understanding of the biological mechanisms underlying this complex pattern of risk.MethodsWe developed a parity signature by analyzing microRNA microarray data from 130 reduction mammoplasty (RM) patients (54 nulliparous and 76 parous). This parity signature, together with published parity signatures, was evaluated in gene expression data from 150 paired tumors and adjacent benign breast tissues from the Polish Breast Cancer Study, both overall and by tumor estrogen receptor (ER) status.ResultsWe identified 251 genes significantly upregulated by parity status in RM patients (parous versus nulliparous; false discovery rate = 0.008), including genes in immune, inflammation and wound response pathways. This parity signature was significantly enriched in normal and tumor tissues of parous breast cancer patients, specifically in ER-positive tumors.ConclusionsOur data corroborate epidemiologic data, suggesting that the etiology and pathogenesis of breast cancers vary by ER status, which may have implications for developing prevention strategies for these tumors.

Abstract 3651: Parity-related molecular signatures and breast cancer heterogeneity.

Abstract Background. Parity is an established protective factor for ER-positive but not ER-negative breast cancer and it may increase the risk of triple-negative (negative for ER, PR, and HER2) tumors. Characterizing parity-related gene expression patterns in normal breast and breast tumor tissues may improve our understanding of the biological mechanisms underlying the subtype-specific associations between parity and breast cancer risk. Method. Gene expression changes associated with parity were identified in microarray data (4x44 K Agilent) from breast tissue of 74 non-diseased reduction mammoplasty (RM) patients. This parity signature, together with published parity signatures, were compared by GSEA method with gene expression (4x44 K Agilent and Illumina arrays) from both normal (N=150) and tumor (N=208) tissues of breast cancer patients from the Polish Breast Cancer Study (PBCS), overall and by tumor ER status. Results. We identified 908 genes significantly up-regulated by parity status (parous vs. nulliparous, FDR = 0.047), including genes in inflammatory pathways. Parity-related signatures identified by us and by previously published studies were significantly enriched in normal and tumor tissue of parous PBCS patients, specifically in ER-positive tumors (FWER<0.1). Conclusions. Our analysis identified a novel parity-related gene signature in normal breast tissue from healthy women, which is also detected in normal and tumor tissues in breast cancer patients with ER-positive tumors. The lack of parity-associated signatures in ER-negative tumors may reflect the disruption of parity-associated pathways (pro-inflammatory) in ER-negative tumors. Citation Format: Melissa Rotunno, Xuezheng Sun, Jonine Figueroa, Mark Sherman, Montserrat Garcia-Closas, Paul Meltzer, Tyisha Williams, Sallie Smith Schneider, Joseph Jerry, Rose Yang, Melissa Troester. Parity-related molecular signatures and breast cancer heterogeneity. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3651. doi:10.1158/1538-7445.AM2013-3651

Abstract 1818: Gene expression profiling to understand stages in breast cancer development and progression: importance of tissue sampling and context .

Abstract Background: During the past decade, gene expression profiling has been widely employed to understand the heterogeneity of tumor biology. Novel biomarkers and signatures discovered using these techniques have impacted tumor diagnosis and prognosis, and have led to important insights into etiology. However, application of mRNA profiling to define mechanisms mediating breast cancer risk factor exposure remains underexplored. Identifying mediating pathways of breast carcinogenesis by tumor tissue profiling may be problematic because genomic instability may obscure causal changes. Methods: To evaluate how etiologically relevant signatures are expressed during different stages of carcinogenesis, we analyzed gene expression data from three types of whole tissue samples: benign tissues from non-diseased breasts (“normal”), benign tissues adjacent to cancer (“cancer-associated”), and tumors. We assessed three published signatures (Age, Obesity, and Parity, originally defined in “normal” breast tissues from healthy women) in 149 tumor tissues and paired cancer-adjacent benign tissues from the Polish Women's Breast Cancer Study. Associations of chronological age, body mass index and parity with their related mRNA signatures were evaluated. Results: The association between Obesity signature and actual obesity status showed a marked gradient from normal breast tissues (obese vs. non-obese: OR=5.78, p=0.0009) to cancer-adjacent and tumor tissues (cancer-adjacent: OR=1.85, p=0.09; tumor: OR=0.80, p=0.54). A similar pattern was also observed for Age signature (normal: OR [<40 y vs. ≥ 40y] =5.03, p<0.0001; cancer-adjacent: OR [<45 y vs. ≥ 45y] =6.97, p=0.005; tumor: OR=0.58 p=0.35) and Parity signature (parous vs. nulliparous, normal: OR =3.95, p=0.0002; cancer-adjacent: OR=1.38, p=0.44; tumor: OR=1.20, p=0.65). Simulation studies further demonstrated that the association strength was influenced by the proportion of risk factor-associated genes that were dysregulated during carcinogenesis. Differences in cellular composition between samples may also affect association strength. Conclusions: These results suggest that associations between risk factors and gene signatures are strongest in benign tissues from non-diseased breasts and may be weakened by the responses of cancer-adjacent issues to cancer progression, and by the effects of genomic instability in tumors. While tumor tissue is readily available in many epidemiologic studies, use of this tissue for studying etiologically relevant pathways may have important limitations. Identification of etiologically relevant pathways may rely on studies of well-annotated tissues from women without cancer. Citation Format: Xuezheng Sun, Alexandre Lockhart, Gretchen L. Gierach, Mark Sherman, Jonine D. Figueroa, Sallie S. Schneider, D. Joseph Jerry, Melissa A. Troester. Gene expression profiling to understand stages in breast cancer development and progression: importance of tissue sampling and context . [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1818. doi:10.1158/1538-7445.AM2013-1818 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.

Longitudinal atomic beam spin echo experiments: a possible way to study parity violation in hydrogen

We discuss the propagation of hydrogen atoms in static electric and magnetic fields in a longitudinal atomic beam spin echo (lABSE) apparatus. Depending on the choice of the external fields the atoms may acquire both dynamical and geometrical quantum mechanical phases. As an example of the former, we show first in-beam spin rotation measurements on atomic hydrogen, which are in excellent agreement with theory. Additional calculations of the behaviour of the metastable 2S states of hydrogen reveal that the geometrical phases may exhibit the signature of parity-(P-)violation. This invites for possible future lABSE experiments, focusing on P-violating geometrical phases in the lightest of all atoms.

Constrained parity testing

A generalized testing technique called constrained parity testing is presented for detecting multiple stuck-at faults in any single-output irredundant combinational network by verifying the subparities of the network. Implementation independent testability conditions are established for single- and multiple-input stuck-at faults. A spanning parity signature (SPS) is introduced to detect vacuous faults, which include all the input stuck-at faults and a majority of all other multiple stuck-at faults. The SPS is considered for testing all stuck-at faults in networks with small numbers of fanout lines, and a method of deriving tests for nonvacuous faults is proposed. For networks with large fanouts, a hybrid scheme by combining with syndrome testing is suggested to eliminate or reduce the need for expensive fault simulation. The proposed technique is a theoretical generalization of many existing methods and offers advantages such as versatility, flexibility, low test volume, low test time, high fault coverage, and reduced fault simulation and test generation costs.