The SPS Individual Bunch Measurement System

The Individual Bunch Measurement System (IBMS) allows the intensity of each bunch in an LHC batch to be the measured both in the PS to SPS transfer lines and in the SPS ring itself. The method is vased on measuring the peak and valley of the analogue signal supplied by a Fast Beam Current Transformer at a frequency of 40 MHz. A 12 bit acquisition system is required to obtain a 1% resolution for the intensity range of 5X10`9 to 1.7X10`11 protons per bunch, corresponding to the pilot and ultimate LHC bunch intensities. The acquisition selection and external trigger adjustment system is driven by the 200MHz RF, which is distributed using a single-mode fibre-optic link. A local oscilloscope, controlled via a GPIB interface, allows the remote adjustment of the timing signals. The low-level software consists of a real-time task and a communication server run on a VME Power PC, which is accessed using a graphical user interface. This paper describes the system as a whole and presents some recent uses and results from the SPS run in 2000

Remote control of a streak camera for real time bunch size measurement in LEP

A double sweep streak camera, built by industry according to CERN specifications, has been used for a number of years to provide real time three-dimensional measurements of bunches in LEP, by means of a dedicated synchrotron light source. Originally requiring local manipulation in an underground lab close to the LEP tunnel, the camera can now be fully operated via the control system network. Control functions, such as the adjustment of lens and mirror positions, the selection of camera weep speeds, and the setting of 12 ps resolution trigger timing, are handled by various networked VME systems, as is real time image processing. Bunch dimension averages are transferred every few seconds via the control system to the LEP measurement database, and a dedicated high bandwidth video transmission allows the streak camera images and processed results to be viewed in real time (at 25 Hz) in the LEP control room. Feedback control loops for light intensity, trigger timing and image tracking allow the setup to provide useful bunch images and logged measurements over extended periods, without human intervention. An X-Window based control application (GUI) will allow LEP machine operators to select different bunches for display and measurement. The same application allows the specialists to control all parameters of the system

The Vitamin A Derivative All-Trans Retinoic Acid Repairs Amyloid-β-Induced Double-Strand Breaks in Neural Cells and in the Murine Neocortex.

The amyloid-β peptide or Aβ is the key player in the amyloid-cascade hypothesis of Alzheimer's disease. Aβ appears to trigger cell death but also production of double-strand breaks (DSBs) in aging and Alzheimer's disease. All-trans retinoic acid (RA), a derivative of vitamin A, was already known for its neuroprotective effects against the amyloid cascade. It diminishes, for instance, the production of Aβ peptides and their oligomerisation. In the present work we investigated the possible implication of RA receptor (RAR) in repair of Aβ-induced DSBs. We demonstrated that RA, as well as RAR agonist Am80, but not AGN 193109 antagonist, repair Aβ-induced DSBs in SH-SY5Y cells and an astrocytic cell line as well as in the murine cortical tissue of young and aged mice. The nonhomologous end joining pathway and the Ataxia Telangiectasia Mutated kinase were shown to be involved in RA-mediated DSBs repair in the SH-SY5Y cells. Our data suggest that RA, besides increasing cell viability in the cortex of young and even of aged mice, might also result in targeted DNA repair of genes important for cell or synaptic maintenance. This phenomenon would remain functional up to a point when Aβ increase and RA decrease probably lead to a pathological state

Nanoscale structure of amyloid-β plaques in Alzheimer’s disease

Abstract Soluble amyloid-β (Aβ) is considered to be a critical component in the pathogenesis of Alzheimer’s disease (AD). Evidence suggests that these non-fibrillar Aβ assemblies are implicated in synaptic dysfunction, neurodegeneration and cell death. However, characterization of these species comes mainly from studies in cellular or animal models, and there is little data in intact human samples due to the lack of adequate optical microscopic resolution to study these small structures. Here, to achieve super-resolution in all three dimensions, we applied Array Tomography (AT) and Stimulated Emission Depletion microscopy (STED), to characterize in postmortem human brain tissue non-fibrillar Aβ structures in amyloid plaques of cases with autosomal dominant and sporadic AD. Ultrathin sections scanned with super-resolution STED microscopy allowed the detection of small Aβ structures of the order of 100 nm. We reconstructed a whole human amyloid plaque and established that plaques are formed by a dense core of higher order Aβ species (~0.022 µm3) and a peripheral halo of smaller Aβ structures (~0.003 µm3). This work highlights the potential of AT-STED for human neuropathological studies

Short-Term Enrichment Makes Male Rats More Attractive, More Defensive and Alters Hypothalamic Neurons

Innate behaviors are shaped by contingencies built during evolutionary history. On the other hand, environmental stimuli play a significant role in shaping behavior. In particular, a short period of environmental enrichment can enhance cognitive behavior, modify effects of stress on learned behaviors and induce brain plasticity. It is unclear if modulation by environment can extend to innate behaviors which are preserved by intense selection pressure. In the present report we investigate this issue by studying effects of relatively short (14-days) environmental enrichment on two prominent innate behaviors in rats, avoidance of predator odors and ability of males to attract mates. We show that enrichment has strong effects on both the innate behaviors: a) enriched males were more avoidant of a predator odor than non-enriched controls, and had a greater rise in corticosterone levels in response to the odor; and b) had higher testosterone levels and were more attractive to females. Additionally, we demonstrate decrease in dendritic length of neurons of ventrolateral nucleus of hypothalamus, important for reproductive mate-choice and increase in the same in dorsomedial nucleus, important for defensive behavior. Thus, behavioral and hormonal observations provide evidence that a short period of environmental manipulation can alter innate behaviors, providing a good example of gene-environment interaction

Deletion of aquaporin-4 in APP/PS1 mice exacerbates brain Aβ accumulation and memory deficits

BACKGROUND: Preventing or reducing amyloid-beta (Aβ) accumulation in the brain is an important therapeutic strategy for Alzheimer’s disease (AD). Recent studies showed that the water channel aquaporin-4 (AQP4) mediates soluble Aβ clearance from the brain parenchyma along the paravascular pathway. However the direct evidence for roles of AQP4 in the pathophysiology of AD remains absent. RESULTS: Here, we reported that the deletion of AQP4 exacerbated cognitive deficits of 12-moth old APP/PS1 mice, with increases in Aβ accumulation, cerebral amyloid angiopathy and loss of synaptic protein and brain-derived neurotrophic factor in the hippocampus and cortex. Furthermore, AQP4 deficiency increased atrophy of astrocytes with significant decreases in interleukin-1 beta and nonsignficant decreases in interleukin-6 and tumor necrosis factor-alpha in hippocampal and cerebral samples. CONCLUSIONS: These results suggest that AQP4 attenuates Aβ pathogenesis despite its potentially inflammatory side-effects, thus serving as a promising target for treating AD. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13024-015-0056-1) contains supplementary material, which is available to authorized users

Facteurs de risque dans la maladie d'Alzheimer

les facteurs de risque identifiés pour la maladie d'Alzheimer sont d'abord l'avancement en age, puis des facteurs génétiques. Dans les formes familiales précoces de la maladie, des mutations ont été mises en évidence sur trois gènes différents, les gènes du précurseur de la protéine amyloïde et des présénilines, tandis que la présence d'une forme particulière du gène de l'apolipoprotéine E, la forme E4, constitue un facteur de risque reconnu dans la population. Plusieurs facteurs non génétiques sont aussi mis en cause, parmi lesquels les traumatismes crâniens, la ménopause et son déficit en oestrogènes, le tabac, certains antécédents psychiatriques et le faible niveau éducatif. La responsabilité de l'aluminium est peu probable. D'autres facteurs pourraient jouer un rôle protecteur, notamment les anti-oxydants et les substances anti-inflammatoires

Reconnaître les démences fronto-temporales : une nouvelle classification

Les démences fronto-temporales correspondent à 20% des démences dégénératives préséniles. Elles se distinguent relativement facilement de la maladie d'Alzheimer. Aujourd'hui, le travail de consensus effectué par les groupes de Lund et de Manchester est communément admis. Il distingue trois formes principales: une démence fronto-temporale sans lésions histologiques spécifiques, une démence fronto-temporale avec corps de Pick et enfin une démence fronto-temporale associée à la maladie des motoneurones. Les progrès neuropathologiques apparaissent toutefois renforcer l'idée de types intermédiaires