Neutrino Mass, Coupling Unification, Verifiable Proton Decay, Vacuum Stability and WIMP Dark Matter in SU(5)

Nonsupersymmetric minimal SU(5) with Higgs representations ${24}_H$ and $5_H$ and standard fermions in ${\bar 5}_F\oplus {10}_F$ is well known for its failure in unification of gauge couplings and lack of predicting neutrino masses. Like standard model, it is also affected by the instability of the Higgs scalar potential. We note that extending the Higgs sector by ${75}_H$ and ${15}_H$ not only leads to the popular type-II seesaw ansatz for neutrino masses with a lower bound on the triplet mass $M_{\Delta} > 2\times 10^9$ GeV, but also achieves precision unification of gauge couplings without proliferation of non-standard light Higgs scalars or fermions near the TeV scale. Consistent with recent LUX-2016 lower bound, the model easily accommodates a singlet scalar WIMP dark matter near the TeV scale which resolves the vacuum stability issue even after inclusion of heavy triplet threshold effect. We estimate proton lifetime predictions for $p\to e^+\pi^0$ including uncertainties due to input parameters and threshold effects due to superheavy Higgs scalars and superheavy $X^{\pm 4/3},Y^{\pm 1/3}$ gauge bosons. The predicted lifetime is noted to be verifiable at Super Kamiokande and Hyper Kamiokande experiments.Comment: 36 pages, 9 figures (Accepted for publication in Advances in High Energy Physics

Scaling ansatz, four zero Yukawa textures and large θ13\theta_{13}

We investigate 'Scaling ansatz' in the neutrino sector within the framework of type I seesaw mechanism with diagonal charged lepton and right handed Majorana neutrino mass matrices ($M_R$). We also assume four zero texture of Dirac neutrino mass matrices ($m_D$) which severely constrain the phenomenological outcomes of such scheme. Scaling ansatz and the present neutrino data allow only Six such matrices out of 126 four zero Yukawa matrices. In this scheme, in order to generate large $\theta_{13}$ we break scaling ansatz in $m_D$ through a perturbation parameter and we also show our breaking scheme is radiatively stable. We further investigate CP violation and baryogenesis via leptogenesis in those surviving textures.Comment: 25 pages, 8 figures, Accepted for publication in Phys. Rev.

An integrated and open-ended experiment: study of chemical waves in time and space

In this article we discuss an exciting experiment in non-linear dynamics. This provides an imaginative platform for bringing in chemical, physical, biological, mathematical and computational sciences together. There are implications for earth sciences as well

Functional Diversity and Structural Disorder in the Human Ubiquitination Pathway

The ubiquitin-proteasome system plays a central role in cellular regulation and protein quality control (PQC). The system is built as a pyramid of increasing complexity, with two E1 (ubiquitin activating), few dozen E2 (ubiquitin conjugating) and several hundred E3 (ubiquitin ligase) enzymes. By collecting and analyzing E3 sequences from the KEGG BRITE database and literature, we assembled a coherent dataset of 563 human E3s and analyzed their various physical features. We found an increase in structural disorder of the system with multiple disorder predictors (IUPred - E1: 5.97%, E2: 17.74%, E3: 20.03%). E3s that can bind E2 and substrate simultaneously (single subunit E3, ssE3) have significantly higher disorder (22.98%) than E3s in which E2 binding (multi RING-finger, mRF, 0.62%), scaffolding (6.01%) and substrate binding (adaptor/substrate recognition subunits, 17.33%) functions are separated. In ssE3s, the disorder was localized in the substrate/adaptor binding domains, whereas the E2-binding RING/HECT-domains were structured. To demonstrate the involvement of disorder in E3 function, we applied normal modes and molecular dynamics analyses to show how a disordered and highly flexible linker in human CBL (an E3 that acts as a regulator of several tyrosine kinase-mediated signalling pathways) facilitates long-range conformational changes bringing substrate and E2-binding domains towards each other and thus assisting in ubiquitin transfer. E3s with multiple interaction partners (as evidenced by data in STRING) also possess elevated levels of disorder (hubs, 22.90% vs. non-hubs, 18.36%). Furthermore, a search in PDB uncovered 21 distinct human E3 interactions, in 7 of which the disordered region of E3s undergoes induced folding (or mutual induced folding) in the presence of the partner. In conclusion, our data highlights the primary role of structural disorder in the functions of E3 ligases that manifests itself in the substrate/adaptor binding functions as well as the mechanism of ubiquitin transfer by long-range conformational transitions. © 2013 Bhowmick et al

Exploring health care disparities in genetic testing and research for hereditary cardiomyopathy: current state and future perspectives

Background Hereditary cardiomyopathies are commonly occurring myocardial conditions affecting heart structure and function with a genetic or familial association, but the etiology is often unknown. Cardiomyopathies are linked to significant mortality, requiring robust risk stratification with genetic testing and early diagnosis. Hypothesis We hypothesized that health care disparities exist in genetic testing for hereditary cardiomyopathies within clinical practice and research studies. Methods In a narrative fashion, we conducted a literature search with online databases such as PubMed/MEDLINE, Google Scholar, EMBASE, and Science Direct on papers related to hereditary cardiomyopathies. A comprehensive analysis of findings from articles in English on disparities in diagnostics and treatment was grouped into four categories. Results Racial and ethnic disparities in research study enrollment and health care delivery favor White populations and higher socioeconomic status, resulting in differences in the development and implementation of effective genetic screening. Such disparities have shown to be detrimental, as minorities often suffer from disease progression to heart failure and sudden cardiac death. Barriers related to clinical genetic testing included insurance-related issues and health illiteracy. The underrepresentation of minority populations extends to research methodologies, as testing in ethnic minorities resulted in a significantly lower detection rate and diagnostic yield, as well as a higher likelihood of misclassification of variants. Conclusions Prioritizing minority-based participatory research programs and screening protocols can address systemic disparities. Diversifying research studies can improve risk stratification strategies and impact clinical practice