Enhanced thjthj signal at the LHC with h→γγh\rightarrow \gamma\gamma decay and CP\mathcal{CP}-violating top-Higgs coupling

We study the observability of non-standard top Yukawa couplings in the $pp\rightarrow t(\rightarrow \ell \nu_\ell b ) h(\rightarrow \gamma\gamma)j$ channel at 14 TeV high-luminosity LHC (HL-LHC). The small diphoton branching ratio is enhanced when the $\mathcal{CP}$-violating phase, $\xi$, of the top-Higgs interaction is non-zero. When the modulus of the top-Higgs interaction assumes the SM value, $y_t=y_t^{SM}$, we find that the signal significance reaches $2.7\sigma$ $( 7.7\sigma)$ when $\xi= 0.25\pi$ $(0.5\pi)$. Furthermore, the different couplings modify the polarisation of the top quark, and can subsequently be distinguished via asymmetries in spin correlations with the final state leptons. The diphoton decay mode is found to be significantly more promising than the previously considered $pp\rightarrow t(\rightarrow \ell \nu_\ell b ) h(\rightarrow b\overline{b})j$ channel.Comment: 14 pages, 3 figures and 2 tables; minor corrections to match published versio

Gravitational waves from a supercooled electroweak phase transition and their detection with pulsar timing arrays

We investigate the properties of a stochastic gravitational wave background produced by a first-order electroweak phase transition in the regime of extreme supercooling. We study a scenario whereby the percolation temperature that signifies the completion of the transition, $T_p$, can be as low as a few MeV (nucleosynthesis temperature), while most of the true vacuum bubbles are formed much earlier at the nucleation temperature, $T_n\sim 50$ GeV. This implies that the gravitational wave spectrum is mainly produced by the collisions of large bubbles and characterised by a large amplitude and a peak frequency as low as $f \sim 10^{-9}-10^{-7}$ Hz. We show that such a scenario can occur in (but not limited to) a model based on a non-linear realisation of the electroweak gauge group, such that the Higgs vacuum configuration is altered by a cubic coupling. In order to carefully quantify the evolution of the phase transition of this model over such a wide temperature range, we go beyond the usual fast transition approximation, taking into account the expansion of the Universe as well as the behaviour of the nucleation probability at low temperatures. Our computation shows that there exists a range of parameters for which the gravitational wave spectrum lies at the edge between the exclusion limits of current pulsar timing array experiments and the detection band of the future Square Kilometre Array observatory.Comment: 20 pages, 3 figures. V2: references added and corrections to match published versio

Central-edge asymmetry as a probe of Higgs-top coupling in ttˉht\bar{t}h production at LHC

The Higgs-top coupling plays a central role in the hierarchy problem and the vacuum stability of the Standard Model (SM). We propose a central-edge asymmetry ($A_{CE}$) to probe the CP violating Higgs-top coupling in dileptonic channel of $t\bar{t}h(\to b\bar{b})$ production at the LHC. We demonstrate that the CP-violating Higgs-top coupling can affect the central-edge asymmetry through distorting $\Delta y_{\ell^+\ell^-}$ distribution because of the contribution of new top charge asymmetric term. Since $\Delta y_{\ell^+\ell^-}$ distribution is frame-independent and has a good discrimination even in boosted regime, we use the jet substructure technique to enhance the observability of the dileptonic channel of $t\bar{t}h$ production. We find that (1) the significance of dileptonic channel of $t\bar{t}h$ production can reach $5\sigma$ for CP phase $\xi=0,\pi/4,\pi/2$ when the luminosity ${\cal L}=795,993,1276$ fb$^{-1}$ at 14 TeV LHC. (2) the central-edge asymmetry $A_{CE}$ show a good discrimination power of CP phase of $t\bar{t}h$ interaction, which are -40.26\%, -26.60\%, -9.47\% for $\xi=0$, $\pi/4$, $\pi/2$ respectively and are hardly affected by the event selections. Besides, by performing the binned-$\chi^2$ analysis of $\Delta y_{\ell^+\ell^-}$ distribution, we find that the scalar and pseudo-scalar interactions can be distinguished at 95\% C.L. level at 14 TeV HL-LHC.Comment: minor changes, version accepted by PL

Subacute Sclerosing Panencephalitis of the Brainstem as a Clinical Entity.

Subacute sclerosing panencephalitis (SSPE) is a rare progressive neurological disorder of early adolescence caused by persistent infection of the measles virus, which remains prevalent worldwide despite an effective vaccine. SSPE is a devastating disease with a characteristic clinical course in subcortical white matter; however, atypical presentations of brainstem involvement may be seen in rare cases. This review summarizes reports to date on brainstem involvement in SSPE, including the clinical course of disease, neuroimaging presentations, and guidelines for treatment. A comprehensive literature search was performed for English-language publications with keywords "subacute sclerosing panencephalitis" and "brainstem" using the National Library of Medicine PubMed database (March 1981-September 2017). Eleven articles focusing on SSPE of the brainstem were included. Predominant brainstem involvement remains uncharacteristic of SSPE, which may lead to misdiagnosis and poor outcome. A number of case reports have demonstrated brainstem involvement associated with other intracranial lesions commonly presenting in later SSPE stages (III and IV). However, brainstem lesions can appear in all stages, independent of higher cortical structures. The varied clinical presentations complicate diagnosis from a neuroimaging perspective. SSPE of the brainstem is a rare but important clinical entity. It may present like canonical SSPE or with unique clinical features such as absence seizures and pronounced ataxia. While SSPE generally progresses to the brainstem, it can also begin with a primary focus of infection in the brainstem. Awareness of varied SSPE presentations can aid in early diagnosis as well as guide management and treatment

Genome-wide Integrative Analysis of Zika-Virus-Infected Neuronal Stem Cells Reveals Roles for MicroRNAs in Cell Cycle and Stemness.

Zika virus (ZIKV) infection is implicated in severe fetal developmental disorders, including microcephaly. MicroRNAs (miRNAs) post-transcriptionally regulate numerous processes associated with viral infection and neurodegeneration, but their contribution to ZIKV pathogenesis is unclear. We analyzed the mRNA and miRNA transcriptomes of human neuronal stem cells (hNSCs) during infection with ZIKV MR766 and Paraiba strains. Integration of the miRNA and mRNA expression data into regulatory interaction networks showed that ZIKV infection resulted in miRNA-mediated repression of genes regulating the cell cycle, stem cell maintenance, and neurogenesis. Bioinformatics analysis of Argonaute-bound RNAs in ZIKV-infected hNSCs identified a number of miRNAs with predicted involvement in microcephaly, including miR-124-3p, which dysregulates NSC maintenance through repression of the transferrin receptor (TFRC). Consistent with this, ZIKV infection upregulated miR-124-3p and downregulated TFRC mRNA in ZIKV-infected hNSCs and mouse brain tissue. These data provide insights into the roles of miRNAs in ZIKV pathogenesis, particularly the microcephaly phenotype

Zika virus infection reprograms global transcription of host cells to allow sustained infection.

Zika virus (ZIKV) is an emerging virus causally linked to neurological disorders, including congenital microcephaly and Guillain-Barré syndrome. There are currently no targeted therapies for ZIKV infection. To identify novel antiviral targets and to elucidate the mechanisms by which ZIKV exploits the host cell machinery to support sustained replication, we analyzed the transcriptomic landscape of human microglia, fibroblast, embryonic kidney and monocyte-derived macrophage cell lines before and after ZIKV infection. The four cell types differed in their susceptibility to ZIKV infection, consistent with differences in their expression of viral response genes before infection. Clustering and network analyses of genes differentially expressed after ZIKV infection revealed changes related to the adaptive immune system, angiogenesis and host metabolic processes that are conducive to sustained viral production. Genes related to the adaptive immune response were downregulated in microglia cells, suggesting that ZIKV effectively evades the immune response after reaching the central nervous system. Like other viruses, ZIKV diverts host cell resources and reprograms the metabolic machinery to support RNA metabolism, ATP production and glycolysis. Consistent with these transcriptomic analyses, nucleoside metabolic inhibitors abrogated ZIKV replication in microglia cells