Probing gauge-phobic heavy Higgs bosons at high energy hadron colliders

We study the probe of the gauge-phobic (or nearly gauge-phobic) heavy Higgs bosons (GPHB) at high energy hadron colliders including the 14 TeV LHC and the 50 TeV Super Proton-Proton Collider (SppC). We take the process $pp\to t\bar t t\bar t$, and study it at the hadron level including simulating the jet formation and top quark tagging (with jet substructure). We show that, for a GPHB with $M^{}_H<800$ GeV, $M^{}_H$ can be determined by adjusting the value of $M^{}_H$ in the theoretical $p^{}_T(b_1)$ distribution to fit the observed $p^{}_T(b_1)$ distribution, and the resonance peak can be seen at the SppC for $M^{}_H$=800 GeV and 1 TeV.Comment: 6 pages, with 7 eps files for 7 figure

Deciphering the Structural Evolution and Electronic Properties of Magnesium Clusters: An Aromatic Homonuclear Metal Mg17 Cluster

The structures and electronic properties of low-energy neutral and anionic Mg_<i>n</i> (<i>n</i> = 3–20) clusters have been studied by utilizing a widely adopted CALYPSO structure searching method coupled with density functional theory calculations. A large number of low-energy isomers are optimized at the B3PW91 functional with the 6-311+G­(d) basis set. The optimized geometries clearly indicate that a structural transition from hollow three-dimensional configurations to filled-cage-like structures occurs at <i>n</i> = 16 for both neutral and anionic clusters. Based on the anionic ground state structures, photoelectron spectra are simulated using time-dependent density functional theory (TD-DFT) and compared with experimental results. The good agreement validates that the current ground state structures, obtained from the symmetry-unconstrained searches, are true global minima. A detailed chemical bonding analysis distinctly indicates that the Mg₁₇ cluster is the first neutral locally π-aromatic homonuclear all-metal cluster, which perfectly satisfies Hückel’s well-known 4<i>N</i> + 2 rule

Proteomic Profile of Carbonylated Proteins Screen Regulation of Apoptosis via CaMK Signaling in Response to Regular Aerobic Exercise

To research carbonylated proteins and screen molecular targets in the rat striatum on regular aerobic exercise, male SpragueDawley rats (13 months old, n = 24) were randomly divided into middle-aged sedentary control (M-SED) and aerobic exercise (M-EX) groups (n = 12 each). Maximum oxygen consumption (VO2max) gradually increased from 50%–55% to 65%–70% for a total of 10 weeks. A total of 36 carbonylated proteins with modifed oxidative sites were identifed by Electrospray IonizationQuadrupole-Time of Flight-Mass Spectrometer (ESI-Q-TOF-MS), including 17 carbonylated proteins unique to the M-SED group, calcium/calmodulin-dependent protein kinase type II subunit beta (CaMKII�), and heterogeneous nuclear ribonucleoprotein A2/B1 (Hnrnpa2b1), among others, and 19 specifc to the M-EX group, ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1), and malic enzyme, among others. Regular aerobic exercise improved behavioral and stereological indicators, promoted normal apoptosis (P \u3c 0.01), alleviated carbonylation of the CaMKII� and Hnrnpa2b1, but induced carbonylation of the UCH-L1, and signifcantly upregulated the expression levels of CaMKII�, CaMKII�, and Vdac1 (p \u3c 0.01) and Hnrnpa2b1 and UCH-L1 (p \u3c 0.01), as well as the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways (PI3K/Akt/mTOR) pathway-related genes Akt and mTOR. Regular aerobic exercise for 10 weeks (incremental for the frst 6 weeks followed by constant loading for 4 weeks) enhanced carbonylation of CaMKII�, Hnrnpa2b1, and modulated apoptosis via activation of CaMK and phosphoinositide 3-kinase/protein kinase B/mTOR signaling. It also promoted normal apoptosis in the rat striatum, which may have protective efects in neurons

MicroRNA Expression Profiling Screen miR-3557/324-targeted CaMK/mTOR in the Rat Striatum of Parkinson\u27s Disease in Regular Aerobic Exercise

This study aimed to screen the target miRNAs and to investigate the differential miR-3557/324-targeted signal mechanisms in the rats’ model of Parkinson’s disease (PD) with regular aerobic exercise. Rats were divided into sedentary control PD group (SED-PD, n = 18) and aerobic exercise PD group (EX-PD, n = 22). After 8 weeks of regular aerobic exercise, a 6-hydroxydopamine- (6-OHDA-) induced PD lesion model was constructed. Preregular aerobic exercises enhanced the injury resistance of rats with 6-OHDA-induced PD. The rotational behavior after injection of apomorphine hydrochloride was alleviated. Under the scanning electron microscopy, we found the neurons, axons, and villi of the striatum were clearly and tightly arranged, and neurons and axons significantly becoming larger. Tyrosine hydroxylase (TH) was increased significantly and α-synuclein protein expression was reduced in the EX-PD group compared to the SED-PD group. Screening from miRNA microarray chip, we further found upregulation of miR-3557 and downregulation of miR-324 were closely related to the calcium-modulating signaling pathway, remitting the progress of Parkinson’s disease on aerobic exercise. Compared to the SED-PD group, Ca2+/calmodulin dependent protein kinase II (CaMK2α) was upregulated, but CaMKV and voltage-dependent anion-selective channel protein 1 (Vdac1) were significantly downregulated in the EX-PD group. Additionally, phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) expression were activated, and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) expression was upregulated in the EX-PD group. Conclusions: the adaptive mechanism of regular aerobic exercise delaying neurodegenerative diseases and lesions was that miR-3557/324 was activated to regulate one of its targets CaMKs signaling pathways. CaMKs, coordinated with mTOR pathway-related gene expression, improved UCH-L1 level to favor for delaying neurodegeneration or improving the pathogenesis of PD lesions