Gravitational Wave Signatures from Domain Wall and Strong First-Order Phase Transitions in a Two Complex Scalar extension of the Standard Model

We consider a simple extension of Standard Model by adding two complex singlet scalars with a $\rm{U}\left(1\right)$ symmetry. A discrete $\mathcal{Z}_2 \times \mathcal{Z}^{\prime}_2$ symmetry is imposed in the model and the added scalars acquire a non zero vacuum expectation value (VEV) when the imposed symmetry is broken spontaneously. The real (CP even) parts of the complex scalars mix with the SM Higgs and give three physical mass eigenstates. One of these physical mass eigenstates is attributed to the SM like Higgs boson with mass 125.09 GeV. In the present scenario, domain walls are formed in the early Universe due to the breaking of discrete $\mathcal{Z}_2 \times \mathcal{Z}^{\prime}_2$ symmetry. In order to ensure the unstability of the domain wall this discrete symmetry is also explicitly broken by adding a bias potential to the Lagrangian. The unstable annihilating domain walls produce a significant amount of gravitational waves (GWs). In addition, we also explore the possibility of the production of GW emission from the strong first-order phase transition. We calculate the intensities and frequencies of each of such gravitational waves originating from two different phenomena of the early Universe namely annihilating domain walls and strong first-order phase transition. Finally, we investigate the observational signatures from these GWs at the future GW detectors such as ALIA, BBO, DECIGO, LISA, TianQin, Taiji, aLIGO, aLIGO+ and pulsar timing arrays such as SKA, IPTA, EPTA, PPTA, NANOGrav11 and NANOGrav12.5.Comment: 30 pages, 3 figures and 5 table

Scotogenic U(1)Lμ−LτU(1)_{L_{\mu}-L_{\tau}} origin of (g−2)μ(g-2)_\mu, W-mass anomaly and 95 GeV excess

We study a scotogenic extension of the minimal gauged $L_{\mu}-L_{\tau}$ model, including three right-handed singlet fermions and a scalar doublet all odd under an in-built $Z_2$ symmetry to explain the anomalous magnetic moments of the muon, CDF-II W-mass anomaly, and the 95 GeV excess reported by the CMS collaboration. While the minimal model can successfully explain the muon $(g-2)$ and CDF-II W-mass anomalies, the required diphoton signal strength for the 95 GeV scalar, together with that of the SM Higgs, can not be obtained in the minimal model. The same can, however, be explained by incorporating two additional scalar doublets whose only role is to contribute radiatively to diphoton decay modes of the light, neutral scalars. Due to the scotogenic extension, the model remains consistent with the observed properties of light neutrinos and dark matter in the Universe.Comment: 13 pages, 9 captioned figure

AQUEOUS BARK EXTRACT OF TERMINALIA ARJUNA PROTECTS AGAINST PHENYLHYDRAZINE INDUCED OXIDATIVE DAMAGE IN GOAT RED BLOOD CELL MEMBRANE BOUND AND METABOLIC ENZYMES

Objective: The objective of the present study is to determine the phenylhydrazine (PHZ) induced oxidative stress mediated alteration in the metabolic status and morphology of the red blood cells (RBC) and amelioration of the same by aqueous bark extract of Terminalia arjuna (TA).Methods: Fresh goat blood collected from local Kolkata Corporation approved slaughter house, was used for the present study. Packed cells were prepared from the freshly collected goat blood and were divided into four groups as follows for further studies i. e Group I: Control (CON), Group II: TA bark extract treated, named T5C (5 mg/ml, incubation mixture; positive control), Group III: PHZ treated (1 mM), Group IV: PHZ treated+TA bark extract at a dose of 5 mg/ml, named as P+T5. ROS, superoxide anion radical, and hydroxyl radical scavenging activity were determined. Intracellular iron and intracellular nitrate concentration were estimated. Activities of various membrane-bound enzymes like Na+/K+-ATPase, Mg2+-ATPase and Ca2+-ATPase and Ach-E were determined. Moreover, the activities of some metabolic enzymes like glucose 6-phosphate dehydrogenase (G6PDH), hexokinase, aldolase, lactase dehydrogenase were also studied. In addition, the morphological structure of RBCs was also determined.Results: PHZ treatment caused significant alterations in RBC morphology as well as altered the activities of membrane-bound as well as metabolic enzymes. All these changes following oxidative stress were found to be ameliorated when the RBCs were co-treated with PHZ and aqueous bark extract of TA. However, aqueous bark extract of TA alone did not exhibit any such changes in RBC.Conclusion: The aqueous bark extract of TA ameliorates PHZ-induced oxidative damages in goat RBC possibly by an antioxidant mechanism(s). The aqueous bark extract of TA may have future therapeutic relevance in oxidative stress-induced damages in RBCs.Keywords: Antioxidant enzymes, Aqueous bark extract, Oxidative stress, Phenylhydrazine, Red blood cells, Terminalia arjun

A Process Similar to Autophagy is Associated with Cytocidal Chloroquine Resistance in Plasmodium Falciparum

Resistance to the cytostatic activity of the antimalarial drug chloroquine (CQ) is becoming well understood, however, resistance to cytocidal effects of CQ is largely unexplored. We find that PfCRT mutations that almost fully recapitulate P. falciparum cytostatic CQ resistance (CQR(CS)) as quantified by CQ IC50 shift, account for only 10-20% of cytocidal CQR (CQR(CC)) as quantified by CQ LD50 shift. Quantitative trait loci (QTL) analysis of the progeny of a chloroquine sensitive (CQS; strain HB3)×chloroquine resistant (CQR; strain Dd2) genetic cross identifies distinct genetic architectures for CQR(CS) vs CQR(CC) phenotypes, including identification of novel interacting chromosomal loci that influence CQ LD50. Candidate genes in these loci are consistent with a role for autophagy in CQR(CC), leading us to directly examine the autophagy pathway in intraerythrocytic CQR parasites. Indirect immunofluorescence of RBC infected with synchronized CQS vs CQR trophozoite stage parasites reveals differences in the distribution of the autophagy marker protein PfATG8 coinciding with CQR(CC). Taken together, the data show that an unusual autophagy-like process is either activated or inhibited for intraerythrocytic trophozoite parasites at LD50 doses (but not IC50 doses) of CQ, that the pathway is altered in CQR P. falciparum, and that it may contribute along with mutations in PfCRT to confer the CQR(CC) phenotype

A Process Similar to Autophagy is Associated with Cytocidal Chloroquine Resistance in Plasmodium Falciparum

Resistance to the cytostatic activity of the antimalarial drug chloroquine (CQ) is becoming well understood, however, resistance to cytocidal effects of CQ is largely unexplored. We find that PfCRT mutations that almost fully recapitulate P. falciparum cytostatic CQ resistance (CQR(CS)) as quantified by CQ IC50 shift, account for only 10-20% of cytocidal CQR (CQR(CC)) as quantified by CQ LD50 shift. Quantitative trait loci (QTL) analysis of the progeny of a chloroquine sensitive (CQS; strain HB3)×chloroquine resistant (CQR; strain Dd2) genetic cross identifies distinct genetic architectures for CQR(CS) vs CQR(CC) phenotypes, including identification of novel interacting chromosomal loci that influence CQ LD50. Candidate genes in these loci are consistent with a role for autophagy in CQR(CC), leading us to directly examine the autophagy pathway in intraerythrocytic CQR parasites. Indirect immunofluorescence of RBC infected with synchronized CQS vs CQR trophozoite stage parasites reveals differences in the distribution of the autophagy marker protein PfATG8 coinciding with CQR(CC). Taken together, the data show that an unusual autophagy-like process is either activated or inhibited for intraerythrocytic trophozoite parasites at LD50 doses (but not IC50 doses) of CQ, that the pathway is altered in CQR P. falciparum, and that it may contribute along with mutations in PfCRT to confer the CQR(CC) phenotype

F-box protein FBXO16 functions as a tumor suppressor by attenuating nuclear beta-catenin function

Aberrant activation of beta-catenin has been implicated in a variety of human diseases, including cancer. In spite of significant progress, the regulation of active Wnt/beta-catenin-signaling pathways is still poorly understood. In this study, we show that F-box protein 16 (FBXO16) is a putative tumor suppressor. It is a component of the SCF (SKP1-Cullin1-F-box protein) complex, which targets the nuclear beta-catenin protein to facilitate proteasomal degradation through the 26S proteasome. FBXO16 interacts physically with the C-terminal domain of beta-catenin and promotes its lysine 48-linked polyubiquitination. In addition, it inhibits epithelial-to-mesenchymal transition (EMT) by attenuating the level of beta-catenin. Therefore, depletion of FBXO16 leads to increased levels of beta-catenin, which then promotes cell invasion, tumor growth, and EMT of cancer cells. Furthermore, FBXO16 and beta-catenin share an inverse correlation of cellular expression in clinical breast cancer patient samples. In summary, we propose that FBXO16 functions as a putative tumor suppressor by forming an SCF(FBXO16) complex that targets nuclear beta-catenin in a unique manner for ubiquitination and subsequent proteasomal degradation to prevent malignancy. This work suggests a novel therapeutic strategy against human cancers related to aberrant beta-catenin activation