Technology development for a low-cost, roll-to-roll chip embedding solution based on PET foils

The aim of the research described in this paper is to develop a low-cost, roll-to-roll compatible process for the realization of electronic systems in foil using chip embedding. The small cost makes these systems suitable for disposable applications as food labels, medicine packages or smart bandages. Surface mount attaching of components on foils is a well-known process for building systems-in-foil. When using low-cost films like PEN and PET, there are serious restrictions on the maximum temperatures that can be used for the surface mounting process (soldering, adhesive bonding). Surface mounting has the additional disadvantage that the components are on the surface of the foil and are therefore not well protected mechanically and physically. The proposed process flow for embedding thin chips in PET foils overcomes these limitations. A key aspect of this technology is the application of a suitable adhesive to encapsulate the chips. The resulting product is based on full-metal copper which has a good thermal and electrical conductivity and allows for fine pitches. The process is compatible with several metal foils (Cu, Al …), offering further possibilities in cost reduction, and does not rely on bumping of the chips or plating of the interconnections to the chips

Constraining the Milky Way potential with a 6-D phase-space map of the GD-1 stellar stream

The narrow GD-1 stream of stars, spanning 60 deg on the sky at a distance of ~10 kpc from the Sun and ~15 kpc from the Galactic center, is presumed to be debris from a tidally disrupted star cluster that traces out a test-particle orbit in the Milky Way halo. We combine SDSS photometry, USNO-B astrometry, and SDSS and Calar Alto spectroscopy to construct a complete, empirical 6-dimensional phase-space map of the stream. We find that an eccentric orbit in a flattened isothermal potential describes this phase-space map well. Even after marginalizing over the stream orbital parameters and the distance from the Sun to the Galactic center, the orbital fit to GD-1 places strong constraints on the circular velocity at the Sun's radius V_c=224 \pm 13 km/s and total potential flattening q_\Phi=0.87^{+0.07}_{-0.04}. When we drop any informative priors on V_c the GD-1 constraint becomes V_c=221 \pm 18 km/s. Our 6-D map of GD-1 therefore yields the best current constraint on V_c and the only strong constraint on q_\Phi at Galactocentric radii near R~15 kpc. Much, if not all, of the total potential flattening may be attributed to the mass in the stellar disk, so the GD-1 constraints on the flattening of the halo itself are weak: q_{\Phi,halo}>0.89 at 90% confidence. The greatest uncertainty in the 6-D map and the orbital analysis stems from the photometric distances, which will be obviated by Gaia.Comment: 16 pages, 18 figures; accepted to ApJ; full resolution version is available at http://www.ast.cam.ac.uk/~koposov/files/gd1_fullres.pd

POPDC1 scaffolds a complex of adenylyl cyclase 9 and the potassium channel TREK-1 in heart

The establishment of macromolecular complexes by scaffolding proteins is key to the local production of cAMP by anchored adenylyl cyclase (AC) and the subsequent cAMP signaling necessary for cardiac functions. We identify a novel AC scaffold, the Popeye domain-containing (POPDC) protein. The POPDC family of proteins is important for cardiac pacemaking and conduction, due in part to their cAMP-dependent binding and regulation of TREK-1 potassium channels. We show that TREK-1 binds the AC9:POPDC1 complex and copurifies in a POPDC1-dependent manner with AC9 activity in heart. Although the AC9:POPDC1 interaction is cAMP-independent, TREK-1 association with AC9 and POPDC1 is reduced upon stimulation of the β-adrenergic receptor (βAR). AC9 activity is required for βAR reduction of TREK-1 complex formation with AC9:POPDC1 and in reversing POPDC1 enhancement of TREK-1 currents. Finally, deletion of the gene-encoding AC9 (Adcy9) gives rise to bradycardia at rest and stress-induced heart rate variability, a milder phenotype than the loss of Popdc1 but similar to the loss of Kcnk2 (TREK-1). Thus, POPDC1 represents a novel adaptor for AC9 interactions with TREK-1 to regulate heart rate control

A high fat diet increases mitochondrial fatty acid oxidation and uncoupling to decrease efficiency in rat heart

Elevated levels of cardiac mitochondrial uncoupling protein 3 (UCP3) and decreased cardiac efficiency (hydraulic power/oxygen consumption) with abnormal cardiac function occur in obese, diabetic mice. To determine whether cardiac mitochondrial uncoupling occurs in non-genetic obesity, we fed rats a high fat diet (55% kcal from fat) or standard laboratory chow (7% kcal from fat) for 3 weeks, after which we measured cardiac function in vivo using cine MRI, efficiency in isolated working hearts and respiration rates and ADP/O ratios in isolated interfibrillar mitochondria; also, measured were medium chain acyl-CoA dehydrogenase (MCAD) and citrate synthase activities plus uncoupling protein 3 (UCP3), mitochondrial thioesterase 1 (MTE-1), adenine nucleotide translocase (ANT) and ATP synthase protein levels. We found that in vivo cardiac function was the same for all rats, yet oxygen consumption was 19% higher in high fat-fed rat hearts, therefore, efficiency was 21% lower than in controls. We found that mitochondrial fatty acid oxidation rates were 25% higher, and MCAD activity was 23% higher, in hearts from rats fed the high fat diet when compared with controls. Mitochondria from high fat-fed rat hearts had lower ADP/O ratios than controls, indicating increased respiratory uncoupling, which was ameliorated by GDP, a UCP3 inhibitor. Mitochondrial UCP3 and MTE-1 levels were both increased by 20% in high fat-fed rat hearts when compared with controls, with no significant change in ATP synthase or ANT levels, or citrate synthase activity. We conclude that increased cardiac oxygen utilisation, and thereby decreased cardiac efficiency, occurs in non-genetic obesity, which is associated with increased mitochondrial uncoupling due to elevated UCP3 and MTE-1 levels

Turbulence and galactic structure

Interstellar turbulence is driven over a wide range of scales by processes including spiral arm instabilities and supernovae, and it affects the rate and morphology of star formation, energy dissipation, and angular momentum transfer in galaxy disks. Star formation is initiated on large scales by gravitational instabilities which control the overall rate through the long dynamical time corresponding to the average ISM density. Stars form at much higher densities than average, however, and at much faster rates locally, so the slow average rate arises because the fraction of the gas mass that forms stars at any one time is low, ~10^{-4}. This low fraction is determined by turbulence compression, and is apparently independent of specific cloud formation processes which all operate at lower densities. Turbulence compression also accounts for the formation of most stars in clusters, along with the cluster mass spectrum, and it gives a hierarchical distribution to the positions of these clusters and to star-forming regions in general. Turbulent motions appear to be very fast in irregular galaxies at high redshift, possibly having speeds equal to several tenths of the rotation speed in view of the morphology of chain galaxies and their face-on counterparts. The origin of this turbulence is not evident, but some of it could come from accretion onto the disk. Such high turbulence could help drive an early epoch of gas inflow through viscous torques in galaxies where spiral arms and bars are weak. Such evolution may lead to bulge or bar formation, or to bar re-formation if a previous bar dissolved. We show evidence that the bar fraction is about constant with redshift out to z~1, and model the formation and destruction rates of bars required to achieve this constancy.Comment: in: Penetrating Bars through Masks of Cosmic Dust: The Hubble Tuning Fork strikes a New Note, Eds., K. Freeman, D. Block, I. Puerari, R. Groess, Dordrecht: Kluwer, in press (presented at a conference in South Africa, June 7-12, 2004). 19 pgs, 5 figure

Bves Modulates Tight Junction Associated Signaling

Blood vessel epicardial substance (Bves) is a transmembrane adhesion protein that regulates tight junction (TJ) formation in a variety of epithelia. The role of TJs within epithelium extends beyond the mechanical properties. They have been shown to play a direct role in regulation of RhoA and ZONAB/DbpA, a y-box transcription factor. We hypothesize that Bves can modulate RhoA activation and ZONAB/DbpA activity through its regulatory effect on TJ formation. Immortalized human corneal epithelial (HCE) cells were stably transfected with Flag-tagged full length chicken Bves (w-Bves) or C-terminus truncated Bves (t-Bves). We found that stably transfected w-Bves and t-Bves were interacting with endogenous human Bves. However, interaction with t-Bves appeared to disrupt cell membrane localization of endogenous Bves and interaction with ZO-1. w-Bves cells exhibited increased TJ function reflected by increased trans-epithelial electrical resistance, while t-Bves cells lost TJ protein immunolocalization at cell-cell contacts and exhibited decreased trans-epithelial electrical resistance. In parental HCE and w-Bves cells ZONAB/DbpA and GEF-H1 were seen at cell borders in the same pattern as ZO-1. However, expression of t-Bves led to decreased membrane localization of both ZONAB/DbpA and GEF-H1. t-Bves cells had increased RhoA activity, as indicated by a significant 30% increase in FRET activity compared to parental HCE cells. ZONAB/DbpA transcriptional activity, assessed using a luciferase reporter probe, was increased in t-Bves cells. These studies demonstrate that Bves expression and localization can regulate RhoA and ZONAB/DbpA activity

High Throughput Microplate Respiratory Measurements Using Minimal Quantities Of Isolated Mitochondria

Recently developed technologies have enabled multi-well measurement of O2 consumption, facilitating the rate of mitochondrial research, particularly regarding the mechanism of action of drugs and proteins that modulate metabolism. Among these technologies, the Seahorse XF24 Analyzer was designed for use with intact cells attached in a monolayer to a multi-well tissue culture plate. In order to have a high throughput assay system in which both energy demand and substrate availability can be tightly controlled, we have developed a protocol to expand the application of the XF24 Analyzer to include isolated mitochondria. Acquisition of optimal rates requires assay conditions that are unexpectedly distinct from those of conventional polarography. The optimized conditions, derived from experiments with isolated mouse liver mitochondria, allow multi-well assessment of rates of respiration and proton production by mitochondria attached to the bottom of the XF assay plate, and require extremely small quantities of material (1–10 µg of mitochondrial protein per well). Sequential measurement of basal, State 3, State 4, and uncoupler-stimulated respiration can be made in each well through additions of reagents from the injection ports. We describe optimization and validation of this technique using isolated mouse liver and rat heart mitochondria, and apply the approach to discover that inclusion of phosphatase inhibitors in the preparation of the heart mitochondria results in a specific decrease in rates of Complex I-dependent respiration. We believe this new technique will be particularly useful for drug screening and for generating previously unobtainable respiratory data on small mitochondrial samples

First observation of Bs -> D_{s2}^{*+} X mu nu decays

Using data collected with the LHCb detector in proton-proton collisions at a centre-of-mass energy of 7 TeV, the semileptonic decays Bs -> Ds+ X mu nu and Bs -> D0 K+ X mu nu are detected. Two structures are observed in the D0 K+ mass spectrum at masses consistent with the known D^+_{s1}(2536) and $D^{*+}_{s2}(2573) mesons. The measured branching fractions relative to the total Bs semileptonic rate are B(Bs -> D_{s2}^{*+} X mu nu)/B(Bs -> X mu nu)= (3.3\pm 1.0\pm 0.4)%, and B(Bs -> D_{s1}^+ X munu)/B(Bs -> X mu nu)= (5.4\pm 1.2\pm 0.5)%, where the first uncertainty is statistical and the second is systematic. This is the first observation of the D_{s2}^{*+} state in Bs decays; we also measure its mass and width.Comment: 8 pages 2 figures. Published in Physics Letters