Motion Compensated Video Compression with 3D Wavelet Transform and SPIHT

The following paper introduces a low bitrate video coding method on the basis of 3D motion compensated wavelet transform and SPIHT algorithm. In contrast to the conventional algorithms applying motion compensation and differential coding, here wavelet transform is used to exploit the opportunities of time redundancy. For coefficient collection, the 3D version of SPIHT algorithm was selected from the various procedures developed for wavelet transform. Motion vectors are compressed, too (also by wavelet transform), therefore the time and spatial redundancy of coding is exploited here as well. These procedures result in effective video compressing and can easily be aligned to the MPEG4 standard

Cyclic AMP-dependent protein kinase and Ca2+-calmodulin stimulate the formation of polyphosphoinositjdes in a sarcoplasmic reticulum preparation of rabbit heart

AbstractA rabbit heart membrane fraction enriched in sarcoplasmic reticulum was incubated in a reaction mixture containing [γ-32P]ATP. The catalytic subunit of cyclic AMP-dependent protein kinase enhanced the 32P-labelling of both phosphatidylinositol-4-phosphate and phosphatidylinositol-4,5-bisphosphate. Ca2+-calmodulin also increased the 32P-incorporation into both polyphosphoinositides. Upon SDS gel-electrophoretic analysis of the membrane proteins, phospholamban was found to be concurrently phosphorylated by the exogenous catalytic subunit as well as by an endogenous Ca2+-calmodulm-dependent protein kinase

It’s been mostly about money!: a multi-method research approach to the sources of institutionalization

Although much has been written about the process of party system insti- tutionalization in different regions, the reasons why some party systems institutionalize while others do not still remain a mystery. Seeking to fill this lacuna in the literature, and using a mixed-methods research approach, this article constitutes a first attempt to answer simultaneously the following three questions: (1) What specific factors help party systems to institutio- nalize (or not)? (2) What are the links (in terms of time and degree) as well as the causal mechanisms behind such relationships? and (3) how do they affect a particular party system? In order to do so, this article focuses on the study of party system development and institutionalization in 13 postcommunist democracies between 1990 and 2010. Methodologically, the article innovates in five respects. First, it continues the debate on the importance of ‘‘mixed methods’’ when trying to answer different research questions. Second, it adds to the as yet brief literature on the combination of process tracing and qualitative comparative analysis. Third, it constitutes the first attempt to date to use a most similar different outcome/most different same outcome pro- cedure in order to reduce causal complexity before undertaking a crisp-set qualitative comparative analysis. Third, it also shows the merits of combining both congruence and process tracing in the same comparative study. Finally, it also develops a novel ‘‘bipolar comparative method’’ to explain the extent to which opposite outcomes are determined by reverse conditions and conflicting intervening causal forces

Postoperative infection following strabismus surgery: case series and increased incidence in a single large referral center

Purpose To identify and analyze cases of postoperative infection following strabismus surgery at a large referral center and to report the incidence, risk factors, and outcomes. Methods An electronic database search identified strabismus procedures at Duke Eye Center from July 1996 to October 2017. Diagnosis codes for periocular infections were used to further identify patients with possible infections following strabismus surgery. Results Of 9,111 strabismus surgeries, 13 (0.14%) met criteria for probable infection, all occurring since October 2012 (0/6580 before vs 13/2531 [0.51%] after; P < 0.0001). Mean age of infection cases was 11.4 years; 11 patients (85%) were under 18 years of age. Associated previous diagnoses were genetic abnormalities with associated developmental delay (n = 5 [38%]), previous skin or ear infection (n = 4 [31%]), and acute or chronic rhinitis (n = 3 [23%]). Infection site cultures revealed methicillin-resistant Staphylococcus aureus (n = 3 [23%]), methicillin-sensitive S. aureus (n = 3 [23%]), and Streptococcus pyogenes/group-A Streptococcus (n = 2 [15%]). Only 1 case had bilateral infection. Infection remained extraocular in all cases, but one eye lost light perception secondary to optic atrophy. No common surgeon/procedure/preparation-related risks were identified. Conclusions A unifying explanation for the increase in post–strabismus surgery infections at Duke Eye Center was not identified. Potential risk factors include age <18 years, developmental delay, immune compromise, preceding nonocular infection, and bacterial colonization

High Availability in the Future Internet

With the evolution of the Internet, a huge number of real- time applications, like Voice over IP, has started to use IP as primary transmission medium. These services require high availability, which is not amongst the main features of today’s heterogeneous Internet where fail- ures occur frequently. Unfortunately, the primary fast resilience scheme implemented in IP routers, Loop-Free Alternates (LFA), usually does not provide full protection against failures. Consequently, there has been a growing interest in LFA-based network optimization methods, aimed at tuning some aspect of the underlying IP topology to maximize the ratio of failure cases covered by LFA. The main goal of this chapter is to give a comprehensive overview of LFA and survey the related LFA network op- timization methods, pointing out that these optimization tools can turn LFA into an easy-to-deploy yet highly effective IP fast resilience scheme

Molecular Background of Leak K+ Currents: Two-Pore Domain Potassium Channels

Enyedi P, Czirjak G. Molecular Background of Leak K+ Currents: Two-Pore Domain Potassium Channels. Physiol Rev 90: 559-605, 2010; doi:10.1152/physrev.00029.2009.-Two-pore domain K+ (K-2P) channels give rise to leak (also called background) K+ currents. The well-known role of background K+ currents is to stabilize the negative resting membrane potential and counterbalance depolarization. However, it has become apparent in the past decade (during the detailed examination of the cloned and corresponding native K-2P channel types) that this primary hyperpolarizing action is not performed passively. The K-2P channels are regulated by a wide variety of voltage-independent factors. Basic physicochemical parameters (e. g., pH, temperature, membrane stretch) and also several intracellular signaling pathways substantially and specifically modulate the different members of the six K-2P channel subfamilies (TWIK, TREK, TASK, TALK, THIK, and TRESK). The deep implication in diverse physiological processes, the circumscribed expression pattern of the different channels, and the interesting pharmacological profile brought the K-2P channel family into the spotlight. In this review, we focus on the physiological roles of K-2P channels in the most extensively investigated cell types, with special emphasis on the molecular mechanisms of channel regulation

PKC in platelet Ca²⁺ signalling

Rises in cytosolic Ca(2+) concentration ([Ca(2+)]cyt) are central in platelet activation, yet many aspects of the underlying mechanisms are poorly understood. Most studies examine how experimental manipulations affect agonist-evoked rises in [Ca(2+)]cyt, but these only monitor the net effect of manipulations on the processes controlling [Ca(2+)]cyt (Ca(2+) buffering, sequestration, release, entry and removal), and cannot resolve the source of the Ca(2+) or the transporters or channels affected. To investigate the effects of protein kinase C (PKC) on platelet Ca(2+) signalling, we here monitor Ca(2+) flux around the platelet by measuring net Ca(2+) fluxes to or from the extracellular space and the intracellular Ca(2+) stores, which act as the major sources and sinks for Ca(2+) influx into and efflux from the cytosol, as well as monitoring the cytosolic Na(+) concentration ([Na(+)]cyt), which influences platelet Ca(2+) fluxes via Na(+)/Ca(2+) exchange. The intracellular store Ca(2+) concentration ([Ca(2+)]st) was monitored using Fluo-5N, the extracellular Ca(2+) concentration ([Ca(2+)]ext) was monitored using Fluo-4 whilst [Ca(2+)]cyt and [Na(+)]cyt were monitored using Fura-2 and SFBI, respectively. PKC inhibition using Ro-31-8220 or bisindolylmaleimide I potentiated ADP- and thrombin-evoked rises in [Ca(2+)]cyt in the absence of extracellular Ca(2+). PKC inhibition potentiated ADP-evoked but reduced thrombin-evoked intracellular Ca(2+) release and Ca(2+) removal into the extracellular medium. SERCA inhibition using thapsigargin and 2,5-di(tert-butyl) l,4-benzohydroquinone abolished the effect of PKC inhibitors on ADP-evoked changes in [Ca(2+)]cyt but only reduced the effect on thrombin-evoked responses. Thrombin evokes substantial rises in [Na(+)]cyt which would be expected to reduce Ca(2+) removal via the Na(+)/Ca(2+) exchanger (NCX). Thrombin-evoked rises in [Na(+)]cyt were potentiated by PKC inhibition, an effect which was not due to altered changes in non-selective cation permeability of the plasma membrane as assessed by Mn(2+) quench of Fura-2 fluorescence. PKC inhibition was without effect on thrombin-evoked rises in [Ca(2+)]cyt following SERCA inhibition and either removal of extracellular Na(+) or inhibition of Na(+)/K(+)-ATPase activity by removal of extracellular K(+) or treatment with digoxin. These data suggest that PKC limits ADP-evoked rises in [Ca(2+)]cyt by acceleration of SERCA activity, whilst rises in [Ca(2+)]cyt evoked by the stronger platelet activator thrombin are limited by PKC through acceleration of both SERCA and Na(+)/K(+)-ATPase activity, with the latter limiting the effect of thrombin on rises in [Na(+)]cyt and so forward mode NCX activity. The use of selective PKC inhibitors indicated that conventional and not novel PKC isoforms are responsible for the inhibition of agonist-evoked Ca(2+) signalling.This work was funded by the British Heart Foundation (PG/07/100/23759). AGSH was supported by a Research Fellowship from St Catharine’s College, University of Cambridge. RAL was supported by a Wellcome Trust Summer Studentship and BBS by a Browning Summer Bursary from Magdalene College, Cambridge.This is the author accepted manuscript. The final version is available from Cell Calcium via http://dx.doi.org/10.1016/j.ceca.2015.09.00

Molecular interactions of the plasma membrane calcium ATPase 2 at pre- and post-synaptic sites in rat cerebellum.

The plasma membrane calcium extrusion mechanism, PMCA (plasma membrane calcium ATPase) isoform 2 is richly expressed in the brain and particularly the cerebellum. Whilst PMCA2 is known to interact with a variety of proteins to participate in important signalling events [Strehler EE, Filoteo AG, Penniston JT, Caride AJ (2007) Plasma-membrane Ca(2+) pumps: structural diversity as the basis for functional versatility. Biochem Soc Trans 35 (Pt 5):919-922], its molecular interactions in brain synapse tissue are not well understood. An initial proteomics screen and a biochemical fractionation approach identified PMCA2 and potential partners at both pre- and post-synaptic sites in synapse-enriched brain tissue from rat. Reciprocal immunoprecipitation and GST pull-down approaches confirmed that PMCA2 interacts with the post-synaptic proteins PSD95 and the NMDA glutamate receptor subunits NR1 and NR2a, via its C-terminal PDZ (PSD95/Dlg/ZO-1) binding domain. Since PSD95 is a well-known partner for the NMDA receptor this raises the exciting possibility that all three interactions occur within the same post-synaptic signalling complex. At the pre-synapse, where PMCA2 was present in the pre-synapse web, reciprocal immunoprecipitation and GST pull-down approaches identified the pre-synaptic membrane protein syntaxin-1A, a member of the SNARE complex, as a potential partner for PMCA2. Both PSD95-PMCA2 and syntaxin-1A-PMCA2 interactions were also detected in the molecular and granule cell layers of rat cerebellar sagittal slices by immunohistochemistry. These specific molecular interactions at cerebellar synapses may allow PMCA2 to closely control local calcium dynamics as part of pre- and post-synaptic signalling complexes

Functional analysis of missense variants in the TRESK (KCNK18) K+ channel

A loss of function mutation in the TRESK K2P potassium channel (KCNK18), has recently been linked with typical familial migraine with aura. We now report the functional characterisation of additional TRESK channel missense variants identified in unrelated patients. Several variants either had no apparent functional effect, or they caused a reduction in channel activity. However, the C110R variant was found to cause a complete loss of TRESK function, yet is present in both sporadic migraine and control cohorts, and no variation in KCNK18 copy number was found. Thus despite the previously identified association between loss of TRESK channel activity and migraine in a large multigenerational pedigree, this finding indicates that a single non-functional TRESK variant is not alone sufficient to cause typical migraine and highlights the genetic complexity of this disorder