Multiphoton processes and higher resonances in the quantum regime of the free-electron laser

Despite exhibiting novel radiation features, the operation of the proposed quantum free-electron laser would have the drawback that the number of emitted photons is limited by one per electron, significantly reducing the output power of such a device. We show that relying on different resonances of the initial momentum of the electrons increases the number of emitted photons, but also increases the required length of the undulator impeding an experimetal realization. Moreover, we investigate how multiphoton processes influence the dynamics in the deep quantum regime

A high-gain Quantum free-electron laser: emergence & exponential gain

We derive an effective Dicke model in momentum space to describe collective effects in the quantum regime of a free-electron laser (FEL). The resulting exponential gain from a single passage of electrons allows the operation of a Quantum FEL in the high-gain mode and avoids the experimental challenges of an X-ray FEL oscillator. Moreover, we study the intensity fluctuations of the emitted radiation which turn out to be super-Poissonian

Crosstalk between Cdk5 and GSK3β: Implications for Alzheimer's Disease

GSK3β and Cdk5 are the two kinases in the center of research on Alzheimer's disease (AD), involved in the pathological symptoms of AD, Aβ plaque formation, tau hyperphosphorylation and neurodegeneration. So far, both kinases have mostly been examined in isolation, leading to a schism of the research field into defenders of the GSK3β-versus the Cdk5 hypotheses of AD. However, in this debate the fact that activities of GSK3β and Cdk5 can influence each other deserves more attention. Recent evidence from p25 transgenic mice suggests that there is a dynamic crosstalk: during aging or prolonged overactivation of Cdk5, GSK3β activity may alter in favor of AD pathogenesis. In this review we summarize the connections between GSK3β and Cdk5 and discuss implications for AD hypotheses

Epithelial-to-Mesenchymal Transition in Pancreatic Ductal Adenocarcinoma and Pancreatic Tumor Cell Lines: The Role of Neutrophils and Neutrophil-Derived Elastase

Pancreatic ductal adenocarcinoma (PDAC) is frequently associated with fibrosis and a prominent inflammatory infiltrate in the desmoplastic stroma. Moreover, in PDAC, an epithelial-to-mesenchymal transition (EMT) is observed. To explore a possible connection between the infiltrating cells, particularly the polymorphonuclear neutrophils (PMN) and the tumor cell transition, biopsies of patients with PDAC (n=115) were analysed with regard to PMN infiltration and nuclear expression of β-catenin and of ZEB1, well-established indicators of EMT. In biopsies with a dense PMN infiltrate, a nuclear accumulation of β-catenin and of ZEB1 was observed. To address the question whether PMN could induce EMT, they were isolated from healthy donors and were cocultivated with pancreatic tumor cells grown as monolayers. Rapid dyshesion of the tumor cells was seen, most likely due to an elastase-mediated degradation of E-cadherin. In parallel, the transcription factor TWIST was upregulated, β-catenin translocated into the nucleus, ZEB1 appeared in the nucleus, and keratins were downregulated. EMT was also induced when the tumor cells were grown under conditions preventing attachment to the culture plates. Here, also in the absence of elastase, E-cadherin was downmodulated. PMN as well as prevention of adhesion induced EMT also in liver cancer cell line. In conclusion, PMN via elastase induce EMT in vitro, most likely due to the loss of cell-to-cell contact. Because in pancreatic cancers the transition to a mesenchymal phenotype coincides with the PMN infiltrate, a contribution of the inflammatory response to the induction of EMT and—by implication—to tumor progression is possible

lim+, delta+, and Non-Permutability of beta-Steps

Using a human-oriented formal example proof of the (lim+) theorem, i.e. that the sum of limits is the limit of the sum, which is of value for reference on its own, we exhibit a non-permutability of beta-steps and delta+-steps (according to Smullyan's classification), which is not visible with non-liberalized delta-rules and not serious with further liberalized delta-rules, such as the delta++-rule. Besides a careful presentation of the search for a proof of (lim+) with several pedagogical intentions, the main subject is to explain why the order of beta-steps plays such a practically important role in some calculi.Comment: ii + 36 page

Neural theory for the perception of causal actions

The efficient prediction of the behavior of others requires the recognition of their actions and an understanding of their action goals. In humans, this process is fast and extremely robust, as demonstrated by classical experiments showing that human observers reliably judge causal relationships and attribute interactive social behavior to strongly simplified stimuli consisting of simple moving geometrical shapes. While psychophysical experiments have identified critical visual features that determine the perception of causality and agency from such stimuli, the underlying detailed neural mechanisms remain largely unclear, and it is an open question why humans developed this advanced visual capability at all. We created pairs of naturalistic and abstract stimuli of hand actions that were exactly matched in terms of their motion parameters. We show that varying critical stimulus parameters for both stimulus types leads to very similar modulations of the perception of causality. However, the additional form information about the hand shape and its relationship with the object supports more fine-grained distinctions for the naturalistic stimuli. Moreover, we show that a physiologically plausible model for the recognition of goal-directed hand actions reproduces the observed dependencies of causality perception on critical stimulus parameters. These results support the hypothesis that selectivity for abstract action stimuli might emerge from the same neural mechanisms that underlie the visual processing of natural goal-directed action stimuli. Furthermore, the model proposes specific detailed neural circuits underlying this visual function, which can be evaluated in future experiments.Seventh Framework Programme (European Commission) (Tango Grant FP7-249858-TP3 and AMARSi Grant FP7-ICT- 248311)Deutsche Forschungsgemeinschaft (Grant GI 305/4-1)Hermann and Lilly Schilling Foundation for Medical Researc

High-gain quantum free-electron laser: long-time dynamics and requirements

We solve the long-time dynamics of a high-gain free-electron laser in the quantum regime. In this regime each electron emits at most one photon on average, independently of the initial field. In contrast, the variance of the photon statistics shows a qualitatively different behavior for different initial states of the field. We find that the realization of a seeded Quantum FEL is more feasible than self-amplified spontaneous emission

The flow field of the upper hypoxic Eastern Tropical North Atlantic oxygen minimum zone

A subsurface low oxygen zone is located in the eastern tropical North Atlantic Ocean (ETNA) in the upper ocean with the core of the hypoxic (O2 ≤ 60 μmol kg−1) oxygen minimum zone (OMZ) at 400 to 500 m depth. The poorly known subsurface circulation in the OMZ region is derived from observations and data assimilation results. Measurements in the eastern tropical North Atlantic in November/December 2008, in November/December 2009 and October/November 2010 of velocity, oxygen and of a tracer (CF3SF5) that was released in April 2008 at ∼ 8° N, 23° W (at ∼ 330 m depth) show circulation in the upper part of the OMZ with spreading to the east in the North Equatorial Countercurrent (NECC) region and northwestward around the Guinea Dome. Three floats equipped with oxygen sensors deployed at ∼ 8° N, 23° W with parking depths at 330, 350 and 400 m depths were used to estimate velocity along the float trajectory at the surface and at the park depth. South of 9° N, the zonal surface velocity estimate from float data alternate seasonally. At the 350 m park depth north of 9° N a cyclonic northwestward flow across the OMZ was observed. The northward shift into the upper OMZ and the cyclonic flow around the Guinea Dome seem to be connected to a strong Atlantic Meridional Mode (AMM) event in 2009. A near-surface cyclonic circulation cell east of the Cape Verde Islands expands into the OMZ layer. The circulation of the upper OMZ mirrors the near surface circulation. Oxygen measurements from the cruises used here, as well as other recent cruises up to the year 2014 confirm the continuous deoxygenation trend in the upper OMZ since the 1960's near the Guinea Dome. The three floats deployed with the tracer show spreading paths consistent with the overall observed tracer spreading. Mesoscale eddies may modify the oxygen distribution in the OMZs. Oxygen sensors on the floats remained well calibrated for more than 20 months and so the oxygen profiles can be used to investigate mesoscale eddy signatures. However, in general eddies are less energetic in the ETNA south of the Cape Verde Islands compared to similar latitudes in the Eastern Tropical South Pacific

Generation of multi-innervated dendritic spines as a novel mechanism of long-term memory formation

NMDA receptor-dependent long-term potentiation (LTP) at hippocampal CA1 synapses is a well-accepted mechanism underlying long-term memory (LTM) formation. However, studies with mice that lack threonine-286 autophosphorylation of αCaMKII have shown that hippocampal LTM can be formed despite absence of NMDA receptor-dependent CA1 LTP. After multiple training trials, LTM formation in these mutants is linked to the generation of multi-innervated dendritic spines (MIS), a spine that receives typically two presynaptic inputs. PSD-95 overexpression is sufficient for MIS generation and depends on mTOR signaling. LTM that involves MIS generation appears less modifiable upon retrieval in comparison to LTM without MIS generation. Taken together, MIS generation appears to be a novel LTM mechanism after multiple training trials, which may occur in diseases with impaired LTP or conditions affecting negative feedback CaMKII signaling at the synapse