Rabbit Anti-Human MAPT (Phospho-Ser396) polyclonal antibody

We discuss an experiment to investigate neutrino physics at the LHC, with emphasis on tau flavour. As described in our previous paper Beni et al (2019 J. Phys. G: Nucl. Part. Phys. 46 115008), the detector can be installed in the decommissioned TI18 tunnel, approximate to 480 m downstream the ATLAS cavern, after the first bending dipoles of the LHC arc. The detector intercepts the intense neutrino flux, generated by the LHC beams colliding in IP1, at large pseudorapidity eta, where neutrino energies can exceed a TeV. This paper focuses on exploring the neutrino pseudorapity versus energy phase space available in TI18 in order to optimize the detector location and acceptance for neutrinos originating at the pp interaction point, in contrast to neutrinos from pion and kaon decays. The studies are based on the comparison of simulated pp collisions at root s = 13 TeV: PYTHIA events of heavy quark (c and b) production, compared to DPMJET minimum bias events (including charm) with produced particles traced through realistic LHC optics with FLUKA. Our studies favour a configuration where the detector is positioned off the beam axis, slightly above the ideal prolongation of the LHC beam from the straight section, covering 7.4 < eta < 9.2. In this configuration, the flux at high energies (0.5-1.5 TeV and beyond) is found to be dominated by neutrinos originating directly from IP1, mostly from charm decays, of which approximate to 50% are electron neutrinos and approximate to 5% are tau neutrinos. The contribution of pion and kaon decays to the muon neutrino flux is found small at those high energies. With 150 fb(-1) of delivered LHC luminosity in Run 3 the experiment can record a few thousand very high energy neutrino charged current (CC) interactions and over 50 tau neutrino CC events. These events provide useful information in view of a high statistics experiment at HL-LHC. The electron and muon neutrino samples can extend the knowledge of the charm PDF to a new region of x, which is dominated by theory uncertainties. The tau neutrino sample can provide first experience on reconstruction of tau neutrino events in a very boosted regime.

Background: Thymoquinone (TQ), a biologically active ingredient of Nigella sativa, has anti-inflammatory, antioxidative and neuroprotective properties. Therefore, it could be a good candidate in the recovery of Alzheimer's disease (AD) pathology rather than current symptomatic reliefs. Purpose: In the present study, we examined the molecular healing effects of TQ in amyloid beta 1-42 (A beta(1-)(42)) peptide-infused AD rat hippocampus. Study design: A micro-osmotic pump containing aggregated A beta(1-)(42) was cannulated into the hippocampus of adult female rats. After two weeks infusion, the dose of TQ (10 mg/kg or 20 mg/kg) was determined according to the HPLC results of cerebrospinal fluid and TQ was given to rats intragastrically for 15 days. Methods: The memory performance of rats was determined by Morris water maze test. Afterwards, the acetylcholinesterase (AChE) level were measured by ELISA. Histopathological examinations of hippocampal tissue were performed for cell survival by Nissl staining, for detection of amyloid plaque deposits by Congo red staining and for determination of degenerating neurons by Fluoro Jade C staining. MicroRNA/mRNA levels and protein expressions of AD-related genes and proteins were analyzed by Real-Time Polymerase Chain Reaction and Western Blotting, respectively. Results: Administration of TQ enhanced the memory performance of A beta(1-)(42 )infused rats and it also ameliorated the neuronal loss in the cornu ammonis (CA1), but not in the dentate gyrus (DG). In addition, TQ treatment decreased the fibril deposition whose accumulation was significantly higher in the A beta(1-)(42)-infused animals compared to that of the control group. The expression profiles of mir29c and Box which significantly upregulated in the A beta(1-)(42)-infused animals were attenuated by TQ. Furthermore, administration of TQ decreased the expressions of A beta, phosphorylated-tau, and BACE-1 proteins. There was no significant therapeutic effect of TQ on the AKT/GSK3 beta or MAPK signaling pathways which were affected due to A beta(1-)(42) infusion. Conclusion: TQ has the capacity to recover the neuropathology by removing A beta plaques and by restoring neuron viability. All might have established the molecular basement of the consolidation in the memory observed by means of TQ treatment.