Adaptive resource allocation for QoE-aware mobile communication networks

A real-time adaptive resource allocation algorithm considering the end user's Quality of Experience (QoE) in the context of video streaming service is presented in this work. An objective no-reference quality metric, namely Pause Intensity (PI), is used to control the priority of resource allocation to users during the scheduling process. An online adjustment has been introduced to adaptively set the scheduler's parameter and maintain a desired trade-off between fairness and efficiency. The correlation between the data rates (i.e. video code rates) demanded by users and the data rates allocated by the scheduler is taken into account as well. The final allocated rates are determined based on the channel status, the distribution of PI values among users, and the scheduling policy adopted. Furthermore, since the user's capability varies as the environment conditions change, the rate adaptation mechanism for video streaming is considered and its interaction with the scheduling process under the same PI metric is studied. The feasibility of implementing this algorithm is examined and the result is compared with the most commonly existing scheduling methods.

Optimal packing for cascaded regenerative transmission based on phase sensitive amplifiers

We investigate the transmission performance of advanced modulation formats in nonlinear regenerative channels based on cascaded phase sensitive amplifiers. We identify the impact of amplitude and phase noise dynamics along the transmission line and show that after a cascade of regenerators, densely packed single ring PSK constellations outperform multi-ring constellations. The results of this study will greatly simplify the design of future nonlinear regenerative channels for ultra-high capacity transmission. © 2013 Optical Society of America.

Light propagation in biaxial crystals

We present a formalism able to predict the transformation of light beams passing through biaxial crystals. We use this formalism to show both theoretically and experimentally the transition from double refraction to conical refraction, which is found when light propagates along one of the optic axes of a biaxial crystal. Additionally, we demonstrate that the theory is applicable both to non-cylindrically symmetric and non-homogeneously polarized beams by predicting the transformation of input beams passing through a cascade of biaxial crystals.

The amyloid precursor protein (APP) binds the PIKfyve complex and modulates its function

Phosphoinositides are important components of eukaryotic membranes that are required for multiple forms of membrane dynamics. Phosphoinositides are involved in defining membrane identity, mediate cell signalling and control membrane trafficking events. Due to their pivotal role in membrane dynamics, phosphoinositide de-regulation contributes to various human diseases. In this review, we will focus on the newly emerging regulation of the PIKfyve complex, a phosphoinositide kinase that converts the endosomal phosphatidylinositol-3-phosphate [PI(3)P] to phosphatidylinositol-3,5-bisphosphate [PI(3,5)P2)], a low abundance phosphoinositide of outstanding importance for neuronal integrity and function. Loss of PIKfyve function is well known to result in neurodegeneration in both mousemodels and human patients. Our recent work has surprisingly identified the amyloid precursor protein (APP), the central molecule in Alzheimer s disease aetiology, as a novel interaction partner of a subunit of the PIKfyve complex, Vac14. Furthermore, it has been shown that APP modulates PIKfyve function and PI(3,5)P2 dynamics, suggesting that the APP gene family functions as regulator of PI(3,5)P2 metabolism. The recent advances discussed in this review suggest a novel, unexpected, â-amyloid-independent mechanism for neurodegeneration in Alzheimer s disease.

Optical wave turbulence and wave condensation in a nonlinear optical experiment

We present theory, numerical simulations and experimental observations of a 1D optical wave system. We show that this system is of a dual cascade type, namely, the energy cascading directly to small scales, and the photons or wave action cascading to large scales. In the optical context the inverse cascade is particularly interesting because it means the condensation of photons. We show that the cascades are induced by a six-wave resonant interaction process described by weak turbulence theory. We show that by starting with weakly nonlinear randomized waves as an initial condition, there exists an inverse cascade of photons towards the lowest wavenumbers. During the cascade nonlinearity becomes strong at low wavenumbers and, due to the focusing nature of the nonlinearity, it leads to modulational instability resulting in the formation of solitons. Further interaction of the solitons among themselves and with incoherent waves leads to the final condensate state dominated by a single strong soliton. In addition, we show the existence of the direct energy cascade numerically and that it agrees with the wave turbulence prediction.

Radial growth of Rhizocarpon section Rhizocarpon lichen thalli over six years at snoqualmie pass in the Cascade Range, Washington State

This article describes a 6-yr study of the radial growth rates (RGR, mm yr-1) of Rhizocarpon section Rhizocarpon thalli on a talus slope at Snoqualmie Pass in the Cascade Range, Washington State, United States (47°27'N; 121°26'W). At the end of the growth period, 32 of a total of 39 thalli had exhibited a positive RGR, and 7 of a total of 39 thalli showed no measurable growth. Mean RGR of all thalli was 0.07 mm yr-1 (range, 0-0.19 mm, SD = 0.06). Analysis of variance suggested no significant variation in RGR in successive growth periods, but significant differences were present both within and between thalli. The slope of a boulder facet did not influence RGR, but growth was affected by aspect, the least growth being observed on north-northwest facets. A plot of RGR against thallus diameter revealed a wide scatter of data points with little evidence for a significant change in growth with thallus size. Hence, the study showed that the RGR of Rhizocarpon thalli at Snoqualmie is extremely slow and highly variable and significantly less than estimates based on lichenometry. To determine the growth curve of a yellow-green Rhizocarpon by direct measurement at such a site would require a large sample of thalli and careful standardization of the species studied, the aspect conditions under which the thalli were measured, and the initial hypothallus width of the thalli. © 2005 Regents of the University of Colorado.

Spatially orthogonal chemical functionalization of a hierarchical pore network for catalytic cascade reactions

The chemical functionality within porous architectures dictates their performance as heterogeneous catalysts; however, synthetic routes to control the spatial distribution of individual functions within porous solids are limited. Here we report the fabrication of spatially orthogonal bifunctional porous catalysts, through the stepwise template removal and chemical functionalization of an interconnected silica framework. Selective removal of polystyrene nanosphere templates from a lyotropic liquid crystal-templated silica sol–gel matrix, followed by extraction of the liquid crystal template, affords a hierarchical macroporous–mesoporous architecture. Decoupling of the individual template extractions allows independent functionalization of macropore and mesopore networks on the basis of chemical and/or size specificity. Spatial compartmentalization of, and directed molecular transport between, chemical functionalities affords control over the reaction sequence in catalytic cascades; herein illustrated by the Pd/Pt-catalysed oxidation of cinnamyl alcohol to cinnamic acid. We anticipate that our methodology will prompt further design of multifunctional materials comprising spatially compartmentalized functions.

The pathogenesis of Alzheimer's disease: a reevaluation of the "amyloid cascade hypothesis"

The most influential theory to explain the pathogenesis of Alzheimer's disease (AD) has been the "Amyloid Cascade Hypothesis" (ACH) first formulated in 1992. The ACH proposes that the deposition of ß-amyloid (Aß) is the initial pathological event in AD leading to the formation of senile plaques (SPs) and then to neurofibrillary tangles (NFTs) death of neurons, and ultimately dementia. This paper examines two questions regarding the ACH: (1) is there a relationship between the pathogenesis of SPs and NFTs, and (2) what is the relationship of these lesions to disease pathogenesis? These questions are examined in relation to studies of the morphology and molecular determinants of SPs and NFTs, the effects of gene mutation, degeneration induced by head injury, the effects of experimentally induced brain lesions, transgenic studies, and the degeneration of anatomical pathways. It was concluded that SPs and NFTs develop independently and may be the products rather than the causes of neurodegeneration in AD. A modification to the ACH is proposed which may better explain the pathogenesis of AD, especially of late-onset cases of the disease.

The spatial patterns of plaques and tangles in Alzheimer's disease do not support the 'cascade hypothesis'

In Alzheimer's disease (AD), the 'Cascade hypothesis' proposes that the formation of paired helical filaments (PHF) may be casually linked to the deposition of beta/A4 protein. Hence, there should be a close spatial relationship between senile plaques and cellular neurofibrillary tangles in a local region of the brain. In tissue from 6 AD patients, plaques and tangles occurred in clusters and individual clusters were often regularly spaced along the cortical strip. However, the clusters of plaques and tangles were in phase in only 4/32 cortical tissues examined. Hence, the data were not consistent with the 'Cascade hypothesis' that beta/A4 and PHF are directly linked in AD.

Q-switched induced gain switching of a twotransition cascade laser

A gain-switched laser transition, of a two-laser-transition cascade laser, that is driven by the adjacent laser transition which is Q-switched is demonstrated using a Ho3+ -doped fluoride fiber laser. Q-switching the 5|6 ? 5|7 transition at 3.002 µm produces stable gain-switched pulses from the 5|7 ? 5|8 transition at 2.074 µm; however, Q-switching the 5|7 ? 5|8 transition produced multiple gain switched pulses from the 5|6 ? 5|7 transition. The gain-switched pulses were measured to be of a similar duration to the Q-switched pulses suggesting that much shorter pulses of closer duration could be generated at pump power higher levels.

A critical analysis of the 'amyloid cascade hypothesis'

The 'amyloid cascade hypothesis' (ACH) is the most influential model of the pathogenesis of Alzheimer's disease (AD). The hypothesis proposes that the deposition of β-amyloid (Aβ) is the initial pathological event in AD, leading to the formation of extracellular senile plaques (SP), tau-immunoreactive neurofibrillary tangles (NFT), neuronal loss, and ultimately, clinical dementia. Ever since the formulation of the ACH, however, there have been questions regarding whether it completely describes AD pathogenesis. This review critically examines various aspects of the ACH including its origin and development, the role of amyloid precursor protein (APP), whether SP and NFT are related to the development of clinical dementia, whether Aβ and tau are 'reactive' proteins, and whether there is a pathogenic relationship between SP and NFT. The results of transgenic experiments and treatments for AD designed on the basis of the ACH are also reviewed. It was concluded: (1) Aβ and tau could be the products rather than the cause of neuro-degeneration in AD, (2) it is doubtful whether there is a direct causal link between Aβ and tau, and (3) SP and NFT may not be directly related to the development of dementia, (4) transgenic models involving APP alone do not completely replicate AD pathology, and (5) treatments based on the ACH have been unsuccessful. Hence, a modification of the ACH is proposed which may provide a more complete explanation of the pathogenesis of AD.