Magnetocaloric effect and improved relative cooling power in (La0.7Sr0.3MnO3/SrRuO3) superlattices

Magnetic properties of a series of (La0.7Sr0.3MnO3/SrRuO3) superlattices, where the SrRuO3 layer thickness is varying, are examined. A room-temperature magnetocaloric effect is obtained owing to the finite size effect which reduces the TC of La0.7Sr0.3MnO3 layers. While the working temperature ranges are enlarged,, -DeltaSmax values remains similar to the values in polycrystalline La0.7Sr0.3MnO3. Consequently, the relative cooling powers are significantly improved, the microscopic mechanism of which is related to the effect of the interfaces at La0.7Sr0.3MnO3/SrRuO3 and higher nanostructural disorder. This study indicates that artificial oxide superlattices/multilayers might provide an alternative pathway in searching for efficient room-temperature magnetic refrigerators for (nano)microscale systems.Comment: 14^pages, 3 figures, Submitted to J. Phys. Cond. Ma

Severe acute respiratory syndrome coronavirus Orf3a protein interacts with caveolin.

The orf3a (also called X1 or U274) gene is the largest unique open reading frame in the severe acute respiratory syndrome coronavirus genome and has been proposed to encode a protein with three transmembrane domains and a large cytoplasmic domain. Recent work has suggested that the 3a protein may play a structural role in the viral life cycle, although the mechanisms for this remain uncharacterized. Here, the expression of the 3a protein in various in vitro systems is shown, it has been localized to the Golgi region and its membrane topology in transfected cells has been confirmed. Three potential caveolin-1-binding sites were reported to be present in the 3a protein. By using various biochemical, biophysical and genetic techniques, interaction of the 3a protein with caveolin-1 is demonstrated. Any one of the potential sites in the 3a protein was sufficient for this interaction. These results are discussed with respect to the possible roles of the 3a protein in the viral life cycle

A generic scope actuation system for flexible endoscopes

Background: A scope actuation system assists a surgeon in steering a scope for navigating an operative field during an interventional or diagnostic procedure. Each system is tailored for a specific surgical procedure. The development of a generic scope actuation system could assist various laparoscopic and endoscopic procedures. This has the potential to reduce the deployment and maintenance costs for a hospital, making it more accessible for clinical usage. Methods: A modular actuation system (for maneuvering rigid laparoscopes) was adapted to enable incorporation of flexible endoscopes. The design simplifies the installation and disassembly processes. User studies were conducted to assess the ability of the system to focus onto a diagnostic area, and to navigate during a simulated esophagogastroduodenoscopy procedure. During the studies, the endoscope was maneuvered with (robotic mode) and without (manual mode) the actuation system to navigate the endoscope’s focus on a predefined track. Results: Results show that the robotic mode performed better than the manual mode on all the measured performance parameters including (a) the total duration to traverse a track, (b) the percentage of time spent outside a track while traversing, and (c) the number of times the scope focus shifts outside the track. Additionally, robotic mode also reduced the perceived workload based on the NASA-TLX scale. Conclusions: The proposed scope actuation system enhances the maneuverability of flexible endoscopes. It also lays the groundwork for future development of modular and generic scope assistant systems that can be used in both laparoscopic and endoscopic procedures

Bid Regulates the Pathogenesis of Neurotropic Reovirus

Reovirus infection leads to apoptosis in both cultured cells and the murine central nervous system (CNS). NF-κB-driven transcription of proapoptotic cellular genes is required for the effector phase of the apoptotic response. Although both extrinsic death-receptor signaling pathways and intrinsic pathways involving mitochondrial injury are implicated in reovirus-induced apoptosis, mechanisms by which either of these pathways are activated and their relationship to NF-κB signaling following reovirus infection are unknown. The proapoptotic Bcl-2 family member, Bid, is activated by proteolytic cleavage following reovirus infection. To understand how reovirus integrates host signaling circuits to induce apoptosis, we examined proapoptotic signaling following infection of Bid-deficient cells. Although reovirus growth was not affected by the absence of Bid, cells lacking Bid failed to undergo apoptosis. Furthermore, we found that NF-κB activation is required for Bid cleavage and subsequent proapoptotic signaling. To examine the functional significance of Bid-dependent apoptosis in reovirus disease, we monitored fatal encephalitis caused by reovirus in the presence and absence of Bid. Survival of Bid-deficient mice was significantly enhanced in comparison to wild-type mice following either peroral or intracranial inoculation of reovirus. Decreased reovirus virulence in Bid-null mice was accompanied by a reduction in viral yield. These findings define a role for NF-κB-dependent cleavage of Bid in the cell death program initiated by viral infection and link Bid to viral virulence

Z-boson production in p-Pb collisions at sNN=8.16 TeV and Pb-Pb collisions at sNN=5.02 TeV

Measurement of Z-boson production in p-Pb collisions at 8.16 TeV and Pb-Pb collisions at = 5.02 TeV is reported. It is performed in the dimuon decay channel, through the detection of muons with pseudorapidity -4 20 GeV/c in the laboratory frame. The invariant yield and nuclear modification factor are measured for opposite-sign dimuons with invariant mass 60 <m(mu)<120 GeV/c(2) and rapidity 2.5 deviation is seen in the integrated yield between the data and calculations based on the free-nucleon PDFs, while good agreement is found once nuclear modifications are considered.Peer reviewe