Statistical Eigenmode Transmission for the MU-MIMO Downlink in Rician Fading

In this paper, we study the achievable ergodic sum-rate of multiuser multiple-input multiple-output downlink systems in Rician fading channels. We first derive a lower bound on the average signal-to-leakage-and-noise ratio by using the Mullen’s inequality, and then use it to analyze the effect of channel mean information on the achievable ergodic sum-rate. A novel statistical-eigenmode space-division multiple-access (SESDMA) downlink transmission scheme is then proposed. For this scheme, we derive an exact analytical closed-form expression for the achievable ergodic rate and present tractable tight upper and lower bounds. Based on our analysis, we gain valuable insights into the system parameters, such as the number of transmit antennas, the signal-to-noise ratio (SNR) and Rician K-factor on the system sum-rate. Results show that the sum-rate converges to a saturation value in the high SNR regime and tends to a lower limit for the low Rician K-factor case. In addition, we compare the achievable ergodic sum-rate between SE-SDMA and zeroforcing beamforming with perfect channel state information at the base station. Our results reveal that the rate gap tends to zero in the high Rician K-factor regime. Finally, numerical results are presented to validate our analysis.

Cathepsin S Cleavage of Protease-Activated Receptor-2 on Endothelial Cells Promotes Microvascular Diabetes Complications

Endothelial dysfunction is a central pathomechanism in diabetes-associated complications. We hypothesized a pathogenic role in this dysfunction of cathepsin S (Cat-S), a cysteine protease that degrades elastic fibers and activates the protease-activated receptor-2 (PAR2) on endothelial cells. We found that injection of mice with recombinant Cat-S induced albuminuria and glomerular endothelial cell injury in a PAR2-dependent manner. In vivo microscopy confirmed a role for intrinsic Cat-S/PAR2 in ischemia-induced microvascular permeability. In vitro transcriptome analysis and experiments using siRNA or specific Cat-S and PAR2 antagonists revealed that Cat-S specifically impaired the integrity and barrier function of glomerular endothelial cells selectively through PAR2. In human and mouse type 2 diabetic nephropathy, only CD68(+) intrarenal monocytes expressed Cat-S mRNA, whereas Cat-S protein was present along endothelial cells and inside proximal tubular epithelial cells also. In contrast, the cysteine protease inhibitor cystatin C was expressed only in tubules. Delayed treatment of type 2 diabetic db/db mice with Cat-S or PAR2 inhibitors attenuated albuminuria and glomerulosclerosis (indicators of diabetic nephropathy) and attenuated albumin leakage into the retina and other structural markers of diabetic retinopathy. These data identify Cat-S as a monocyte/macrophage-derived circulating PAR2 agonist and mediator of endothelial dysfunction-related microvascular diabetes complications. Thus, Cat-S or PAR2 inhibition might be a novel strategy to prevent microvascular disease in diabetes and other diseases.

Sustained intraocular VEGF neutralization results in retinal neurodegeneration in the Ins2Akita diabetic mouse

Current therapies that target vascular endothelial growth factor (VEGF) have become a mainstream therapy for the management of diabetic macular oedema. The treatment involves monthly repeated intravitreal injections of VEGF inhibitors. VEGF is an important growth factor for many retinal cells, including different types of neurons. In this study, we investigated the adverse effect of multiple intravitreal anti-VEGF injections (200 ng/μl/eye anti-mouse VEGF164, once every 2 weeks totalling 5-6 injections) to retinal neurons in Ins2(Akita) diabetic mice. Funduscopic examination revealed the development of cotton wool spot-like lesions in anti-VEGF treated Ins2(Akita) mice after 5 injections. Histological investigation showed focal swellings of retinal nerve fibres with neurofilament disruption. Furthermore, anti-VEGF-treated Ins2(Akita) mice exhibited impaired electroretinographic responses, characterized by reduced scotopic a- and b-wave and oscillatory potentials. Immunofluorescent staining revealed impairment of photoreceptors, disruptions of synaptic structures and loss of amacrine and retinal ganglion cells in anti-VEGF treated Ins2(Akita) mice. Anti-VEGF-treated WT mice also presented mild amacrine and ganglion cell death, but no overt abnormalities in photoreceptors and synaptic structures. At the vascular level, exacerbated albumin leakage was observed in anti-VEGF injected diabetic mice. Our results suggest that sustained intraocular VEGF neutralization induces retinal neurodegeneration and vascular damage in the diabetic eye.

On the Security of Balanced Encoding Countermeasures

Most cryptographic devices should inevitably have a resistance against the threat of side channel attacks. For this, masking and hiding schemes have been proposed since 1999. The security validation of these countermeasures is an ongoing research topic, as a wider range of new and existing attack techniques are tested against these countermeasures. This paper examines the side channel security of the balanced encoding countermeasure, whose aim is to process the secret key-related data under a constant Hamming weight and/or Hamming distance leakage. Unlike previous works, we assume that the leakage model coefficients conform to a normal distribution, producing a model with closer fidelity to real-world implementations. We perform analysis on the balanced encoded PRINCE block cipher with simulated leakage model and also an implementation on an AVR board. We consider both standard correlation power analysis (CPA) and bit-wise CPA. We confirm the resistance of the countermeasure against standard CPA, however, we find with a bit-wise CPA that we can reveal the key with only a few thousands traces.

Passive Intermodulation in Distributed Circuits with Cascaded Discrete Nonlinearities

The principle aspects of passive intermodulation (PIM) characterisation in distributed printed circuits with cascaded lumped nonlinearities are presented. Mechanisms of PIM generations have been investigated experimentally and modelled using the formalism of X-parameters. The devised equivalent circuit models are applied to the analysis of microstrip lines with distributed and cascaded lumped sources of nonlinearity. The dynamic measurements have revealed that PIM generation rates in straight and meandered microstrip lines differ and significantly deviate from those expected for the respective discrete sources of nonlinearity. The obtained results indicate that multiple physical sources of nonlinearity contribute to PIM generation in printed circuits. Finally, it is demonstrated that the electrical discontinuities can have significant effect on the overall PIM response of the distributed passive circuits and cause PIM product leakage and parasitic coupling between isolated circuit elements.

On the Privacy of Encrypted Skype Communications

The privacy of voice over IP (VoIP) systems is achieved by compressing and encrypting the sampled data. This paper investigates in detail the leakage of information from Skype, a widely used VoIP application. In this research, it has been demonstrated by using the dynamic time warping (DTW) algorithm, that sentences can be identified with an accuracy of 60%. The results can be further improved by choosing specific training data. An approach involving the Kalman filter is proposed to extract the kernel of all training signals.

Extravascular modified lipoproteins: a role in the propagation of diabetic retinopathy in a mouse model of type 1 diabetes

Aims/hypothesis: We aimed to determine whether plasma lipoproteins, after leakage into the retina and modification by glycation and oxidation, contribute to the development of diabetic retinopathy in a mouse model of type 1 diabetes.

Methods: To simulate permeation of plasma lipoproteins intoretinal tissues, streptozotocin-induced mouse models of diabetes and non-diabetic mice were challenged with intravitreal injection of human ‘highly-oxidised glycated’ low-density lipoprotein (HOG-LDL), native- (N-) LDL, or the vehicle PBS.Retinal histology, electroretinography (ERG) and biochemical markers were assessed over the subsequent 14 days.

Results: Intravitreal administration of N-LDL and PBS had noeffect on retinal structure or function in either diabetic or non-diabetic animals. In non-diabetic mice, HOG-LDL elicited a transient inflammatory response without altering retinal function,but in diabetic mice it caused severe, progressive retinal injury, with abnormal morphology, ERG changes, vascular leakage, vascular endothelial growth factor overexpression, gliosis, endoplasmic reticulum stress, and propensity to apoptosis.

Conclusions/interpretation: Diabetes confers susceptibility to retinal injury imposed by intravitreal injection of modified LDL. The data add to the existing evidence that extravasated, modified plasma lipoproteins contribute to the propagation of diabetic retinopathy. Intravitreal delivery of HOG-LDL simulates a stress known to be present, in addition to hyperglycaemia, in human diabetic retinopathy once blood retinal barriers are compromised.