Quantifying the Suitability of Reference Signals for the Video Streaming Analysis for IPTV, Journal of Telecommunications and Information Technology, 2016, nr 1

IP networks are indispensable nowadays and they are some of the most efficient platforms. The constantly growing number of users and new services in these networks – the largest being the Internet – require a satisfactory quality of service from any application they use. So, determining the QoS in real-time services is particularly important. This work shows how to quantify the suitability of reference signals for analyzing the quality of video streaming in IPTV. The assessment relies on two different algorithms: PEVQ and VQuad-HD. Three different reference signals – two real ones and an artificial one – are used in this study, and a numerical measurement system is used, which simulates mean network impairments. These measurements provide valuable information for determining the QoS of actual IPTV services in practice

Startle disease in Irish wolfhounds associated with a microdeletion in the glycine transporter GlyT2 gene

AbstractDefects in glycinergic synaptic transmission in humans, cattle, and rodents result in an exaggerated startle reflex and hypertonia in response to either acoustic or tactile stimuli. Molecular genetic studies have determined that mutations in the genes encoding the postsynaptic glycine receptor (GlyR) α1 and β subunits (GLRA1 and GLRB) and the presynaptic glycine transporter GlyT2 (SLC6A5) are the major cause of these disorders. Here, we report the first genetically confirmed canine cases of startle disease. A litter of seven Irish wolfhounds was identified in which two puppies developed muscle stiffness and tremor in response to handling. Although sequencing of GLRA1 and GLRB did not reveal any pathogenic mutations, analysis of SLC6A5 revealed a homozygous 4.2kb microdeletion encompassing exons 2 and 3 in both affected animals. This results in the loss of part of the large cytoplasmic N-terminus and all subsequent transmembrane domains due to a frameshift. This genetic lesion was confirmed by defining the deletion breakpoint, Southern blotting, and multiplex ligation-dependent probe amplification (MLPA). This analysis enabled the development of a rapid genotyping test that revealed heterozygosity for the deletion in the dam and sire and three other siblings, confirming recessive inheritance. Wider testing of related animals has identified a total of 13 carriers of the SLC6A5 deletion as well as non-carrier animals. These findings will inform future breeding strategies and enable a rational pharmacotherapy of this new canine disorder

Novel missense mutations in the glycine receptor β subunit gene (GLRB) in startle disease

Startle disease is a rare, potentially fatal neuromotor disorder characterized by exaggerated startle reflexes and hypertonia in response to sudden unexpected auditory, visual or tactile stimuli. Mutations in the GlyR alpha(1) subunit gene (GLRA1) are the major cause of this disorder, since remarkably few individuals with mutations in the GlyR beta subunit gene (GLRB) have been found to date. Systematic DNA sequencing of GLRB in individuals with hyperekplexia revealed new missense mutations in GLRB, resulting in M177R, L285R and W310C substitutions. The recessive mutation M177R results in the insertion of a positively-charged residue into a hydrophobic pocket in the extracellular domain, resulting in an increased EC50 and decreased maximal responses of alpha(1)beta GlyRs. The de novo mutation L285R results in the insertion of a positively-charged side chain into the pore-lining 9' position. Mutations at this site are known to destabilize the channel closed state and produce spontaneously active channels. Consistent with this, we identified a leak conductance associated with spontaneous GlyR activity in cells expressing alpha(1)beta(L285R) GlyRs. Peak currents were also reduced for alpha(1)beta(L285R) GlyRs although glycine sensitivity was normal. W310C was predicted to interfere with hydrophobic side-chain stacking between M1, M2 and M3. We found that W310C had no effect on glycine sensitivity, but reduced maximal currents in alpha(1)beta GlyRs in both homozygous (alpha(1)beta(W310C)) and heterozygous (alpha(1)beta beta(W310C)) stoichiometries. Since mild startle symptoms were reported in W310C carriers, this may represent an example of incomplete dominance in startle disease, providing a potential genetic explanation for the 'minor' form of hyperekplexia. (C) 2012 Elsevier Inc. All rights reserved

Acceleration of tissue phase mapping with sensitivity encoding at 3T

<p>Abstract</p> <p>Background</p> <p>The objective of this study was to investigate the impact of sensitivity encoding on the quantitative assessment of cardiac motion in black blood cine tissue phase mapping (TPM) sequences. Up to now whole volume coverage of the heart is still limited by the long acquisition times. Therefore, a significant increase in imaging speed without deterioration of quantitative motion information is indispensable.</p> <p>Methods</p> <p>20 volunteers were enrolled in this study. Each volunteer underwent myocardial short-axis TPM scans with different SENSE acceleration factors. The influence of SENSE acceleration on the measured motion curves was investigated.</p> <p>Results</p> <p>It is demonstrated that all TPM sequences with SENSE acceleration have only minimum influence on the motion curves. Even with a SENSE factor of four, the decrease in the amplitude of the motion curve was less than 3%. No significant difference was observed for the global correlation coefficient and deviation between the motion curves obtained by the reproducibility and the SENSE accelerated measurements.</p> <p>Conclusions</p> <p>It is feasible to accelerate myocardial TPM measurements with SENSE factors up to 4 without losing substantial information of the motion pattern.</p