The UTfit Collaboration Average of D meson mixing data: Spring 2012

We derive constraints on the parameters $M_{12}$, $\Gamma_{12}$ and $\Phi_{12}$ that describe $D$ meson mixing using all available data, allowing for CP violation. We also provide posterior distributions and predictions for observable parameters appearing in $D$ physics.Comment: 5 pages, 3 figure

Quantum Gravity Effects in Black Holes at the LHC

We study possible back-reaction and quantum gravity effects in the evaporation of black holes which could be produced at the LHC through a modification of the Hawking emission. The corrections are phenomenologically taken into account by employing a modified relation between the black hole mass and temperature. The usual assumption that black holes explode around $1$TeV is also released, and the evaporation process is extended to (possibly much) smaller final masses. We show that these effects could be observable for black holes produced with a relatively large mass and should therefore be taken into account when simulating micro-black hole events for the experiments planned at the LHC.Comment: 14 pages, 8 figures, extended version of hep-ph/0601243 with new analysis of final products, final version accepted for publication in J. Phys.

Kinesin light chain-1 serine-460 phosphorylation is altered in Alzheimer's disease and regulates axonal transport and processing of the amyloid precursor protein

Damage to axonal transport is an early pathogenic event in Alzheimer's disease. The amyloid precursor protein (APP) is a key axonal transport cargo since disruption to APP transport promotes amyloidogenic processing of APP. Moreover, altered APP processing itself disrupts axonal transport. The mechanisms that regulate axonal transport of APP are therefore directly relevant to Alzheimer's disease pathogenesis. APP is transported anterogradely through axons on kinesin-1 motors and one route for this transport involves calsyntenin-1, a type-1 membrane spanning protein that acts as a direct ligand for kinesin-1 light chains (KLCs). Thus, loss of calsyntenin-1 disrupts APP axonal transport and promotes amyloidogenic processing of APP. Phosphorylation of KLC1 on serine-460 has been shown to reduce anterograde axonal transport of calsyntenin-1 by inhibiting the KLC1-calsyntenin-1 interaction. Here we demonstrate that in Alzheimer's disease frontal cortex, KLC1 levels are reduced and the relative levels of KLC1 serine-460 phosphorylation are increased; these changes occur relatively early in the disease process. We also show that a KLC1 serine-460 phosphomimetic mutant inhibits axonal transport of APP in both mammalian neurons in culture and in Drosophila neurons in vivo. Finally, we demonstrate that expression of the KLC1 serine-460 phosphomimetic mutant promotes amyloidogenic processing of APP. Together, these results suggest that increased KLC1 serine-460 phosphorylation contributes to Alzheimer's disease

Storage Infrastructure at the INFN LHC Tier-1

In this paper we will describe the Storage Infrastructure of the INFN-CNAF Tier-1, used to store data of High Energy Physics experiments, in particular those operating at the Large Hadron Collider

Sex-related penile fracture with complete urethral rupture: A case report and review of the literature

OBJECTIVE: To present the management of a patient with partial disruption of both cavernosal bodies and complete urethral rupture and to propose a non-systematic review of literature about complete urethral rupture. MATERIAL AND METHOD - CASE REPORT: A 46 years old man presented to our emergency department after a blunt injury of the penis during sexual intercourse. On physical examination there was subcutaneous hematoma extending over the proximal penile shaft with a dorsal-left sided deviation of the penis and urethral bleeding. Ultrasound investigation showed an hematoma in the ventral shaft of the penis with a discontinuity of the tunica albuginea of the right cavernosal corporum. The patient underwent immediate emergency surgery consisted on evacuation of the hematoma, reparation the partial defect of both two cavernosal bodies and end to end suture of the urethra that resulted completely disrupted. RESULTS: The urethral catheter was removed at the 12-th postoperative day without voiding symptoms after a retrograde urethrography. 6 months postoperatively the patients was evaluated with uroflowmetry demonstrating a max flow rate of 22 ml/s and optimal functional outcomes evaluated with validated questionnaires. 8 months after surgery the patients was evaluated by dynamic magnetic resonance (MRI) of the penis showing only a little curvature on the left side of the penile shaft. CONCLUSION: Penile fracture is an extremely uncommon urologic injury with approximately 1331 reported cases in the literature till the years 2001. To best of our knowledge from 2001 up today, 1839 more cases have been reported, only in 159 of them anterior urethral rupture was associated and in only 22 cases a complete urethral rupture was described. In our opinion, in order to prevent long term complications, in case of clinical suspicion of penile fracture, especially if it is associated to urethral disruption, emergency surgery should be the first choice of treatment

Non-canonical role for Lpar1-EGFP subplate neurons in early postnatal mouse somatosensory cortex

Subplate neurons (SPNs) are thought to play a role in nascent sensory processing in neocortex. To better understand how heterogeneity within this population relates to emergent function, we investigated the synaptic connectivity of Lpar1-EGFP SPNs through the first postnatal week in whisker somatosensory cortex (S1BF). These SPNs comprise of two morphological subtypes: fusiform SPNs with local axons and pyramidal SPNs with axons that extend through the marginal zone. The former receive translaminar synaptic input up until the emergence of the whisker barrels, a timepoint coincident with significant cell death. In contrast, pyramidal SPNs receive local input from the subplate at early ages but then – during the later time window – acquire input from overlying cortex. Combined electrical and optogenetic activation of thalamic afferents identified that Lpar1-EGFP SPNs receive sparse thalamic innervation. These data reveal components of the postnatal network that interpret sparse thalamic input to direct the emergent columnar structure of S1BF

Mini Black Holes in the first year of the LHC

The experimental signatures of TeV-mass black hole (BH) formation in heavy ion collisions at the LHC is examined. We find that the black hole production results in a complete disappearance of all very high $p_T$ ({$> 500$} GeV) back-to-back correlated di-jets of total mass {$M > M_f \sim 1$}TeV. We show that the subsequent Hawking-decay produces multiple hard mono-jets and discuss their detection. We study the possibility of cold black hole remnant (BHR) formation of mass $\sim M_f$ and the experimental distinguishability of scenarios with BHRs and those with complete black hole decay. Due to the rather moderate luminosity in the first year of LHC running the least chance for the observation of BHs or BHRs at this early stage will be by ionizing tracks in the ALICE TPC. Finally we point out that stable BHRs would be interesting candidates for energy production by conversion of mass to Hawking radiation.Comment: 10 pages, 2 figure

ASPM and CITK regulate spindle orientation by affecting the dynamics of astral microtubules.

Correct orientation of cell division is considered an important factor for the achievement of normal brain size, as mutations in genes that affect this process are among the leading causes of microcephaly. Abnormal spindle orientation is associated with reduction of the neuronal progenitor symmetric divisions, premature cell cycle exit, and reduced neurogenesis. This mechanism has been involved in microcephaly resulting from mutation of ASPM, the most frequently affected gene in autosomal recessive human primary microcephaly (MCPH), but it is presently unknown how ASPM regulates spindle orientation. In this report, we show that ASPM may control spindle positioning by interacting with citron kinase (CITK), a protein whose loss is also responsible for severe microcephaly in mammals. We show that the absence of CITK leads to abnormal spindle orientation in mammals and insects. In mouse cortical development, this phenotype correlates with increased production of basal progenitors. ASPM is required to recruit CITK at the spindle, and CITK overexpression rescues ASPM phenotype. ASPM and CITK affect the organization of astral microtubules (MT), and low doses of MT-stabilizing drug revert the spindle orientation phenotype produced by their knockdown. Finally, CITK regulates both astral-MT nucleation and stability. Our results provide a functional link between two established microcephaly proteins

Measurements of the reaction pˉp→ϕη\bar{p}p \to \phi \eta of antiproton annihilation at rest at three hydrogen target densities

The proton-antiproton annihilation at rest into the $\phi\eta$ final state was measured for three different target densities: liquid hydrogen, gaseous hydrogen at NTP and at a low pressure of 5 mbar. The yield of this reaction in the liquid hydrogen target is smaller than in the low-pressure gas target. The branching ratios of the $\phi\eta$ channel were calculated on the basis of simultaneous analysis of the three data samples. The branching ratio for annihilation into $\phi\eta$ from the $^3S_1$ protonium state turns out to be about ten times smaller as compared to the one from the $^1P_1$ state.Comment: 10 pages, 3 Postscript figures. Accepted by Physics Letters