643 research outputs found

    A 43-Gbps Lithium Niobate Modulator Driver Module

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    This paper describes the realization of a 43-Gbps Lithium Niobate modulator driver module. The NRZ driver module utilizes four stages of GaAs p-HEMT MMIC amplifiers integrated with an output level detector and feedback loop to provide thermal stability and external control of the output swing. The bias and loop control circuitry are contained in the housing on a PC board external to the sealed MIC section. The integrated module (50.8 x 73.4 x 9.5 mm 3) provides 6.0 Vp-p controllable single-ended output voltage while dissipating only 4 watt

    Electronic population transfer via impulsive stimulated x-ray Raman scattering with attosecond soft-x-ray pulses

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    Artículo escrito por un elevado número de autores, solo se referencian el que aparece en primer lugar, el nombre del grupo de colaboración, si le hubiere, y los autores pertenecientes a la UA

    Hypoxic pre-conditioning increases the infiltration of endothelial cells into scaffolds for dermal regeneration pre-seeded with mesenchymal stem cells.

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    Many therapies using mesenchymal stem cells (MSC) rely on their ability to produce and release paracrine signals with chemotactic and pro-angiogenic activity. These characteristics, however, are mostly studied under standard in vitro culture conditions. In contrast, various novel cell-based therapies imply pre-seeding MSC into bio-artificial scaffolds. Here we describe human bone marrow-derived MSC seeded in Integra matrices, a common type of scaffold for dermal regeneration (SDR). We show and measured the distribution of MSC within the SDR, where cells clearly establish physical interactions with the scaffold, exhibiting constant metabolic activity for at least 15 days. In the SDR, MSC secrete VEGF and SDF-1α and induce transwell migration of CD34(+) hematopoietic/endothelial progenitor cells, which is inhibited in the presence of a CXCR4/SDF-1α antagonist. MSC in SDR respond to hypoxia by altering levels of angiogenic signals such as Angiogenin, Serpin-1, uPA, and IL-8. Finally, we show that MSC-containing SDR that have been pre-incubated in hypoxia show higher infiltration of endothelial cells after implantation into immune deficient mice. Our data show that MSC are fully functional ex vivo when implanted into SDR. In addition, our results strongly support the notion of hypoxic pre-conditioning MSC-containing SDR, in order to promote angiogenesis in the wounds

    Systematic review and meta-analysis of mortality and digoxin use in atrial fibrillation

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    Background: There is growing controversy regarding the association between digoxin and mortality in atrial fibrillation (AF). The aim of this analysis was to systematically review digoxin use and risk of mortality in patients with AF. Methods: MEDLINE, EMBASE, GoogleScholar, CINAHL, meeting abstracts, presentations, and Cochrane central databases were searched from inception through December 2014, without language restrictions. For a study to be selected, it had to report the risk of mortality associated with digoxin use in AF patients as an outcome measure. Data were extracted by 2 independent authors. Evidence tables were created. Results: A total of 16 studies (6 post hoc analyses of randomized controlled trials) with 111,978 digoxin users and 389,643 non-digoxin users were included. In a random effects model, patients treated with digoxin had a 27% increased risk of all-cause mortality (pooled HR 1.27; 95% CI 1.19–1.36) and 21% increased risk of cardiovascular mortality (pooled HR 1.21; 95% CI 1.12–1.30) compared with those who did not use digoxin. In a random effects model, the association of digoxin with all-cause mortality was stronger for AF patients without heart failure (pooled HR 1.47; 95% CI 1.25–1.73) than AF patients with heart failure (pooled HR 1.21; 95% CI 1.07–1.36, interaction p = 0.06). Conclusions: Digoxin use in AF is associated with increased risk of all-cause and cardiovascular mortalities. The effect size was larger for AF patients without heart failure than AF patients with heart failure. The study suggests further directed analyses to study the effect that is suggested by this meta-analysis, especially in AF without heart failure.

    Racial Differences in Survival among Hemodialysis Patients after Coronary Artery Bypass Grafting

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    The aim of this study was to examine racial differences in long-term survival among hemodialysis patients after coronary artery bypass grafting (CABG). To our knowledge this has not been previously addressed in the literature. Black and white hemodialysis patients undergoing first-time, isolated CABG procedures between 1992 and 2011 were compared. Survival probabilities were computed using the Kaplan-Meier product-limit method and stratified by race. Hazard ratios (HR) and 95% confidence intervals (CI) were computed using a Cox regression model. A total of 207 (2%) patients were on hemodialysis at the time of CABG. White (n = 80) hemodialysis patients had significantly decreased 5-year survival compared with black (n = 127) patients (adjusted HR = 1.9, 95% CI = 1.2–2.8). Our finding provides useful outcome information for surgeons, primary care providers, and their patients

    Risk-Adjusted Survival after Coronary Artery Bypass Grafting: Implications for Quality Improvement

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    Mortality represents an important outcome measure following coronary artery bypass grafting. Shorter survival times may reflect poor surgical quality and an increased number of costly postoperative complications. Quality control efforts aimed at increasing survival times may be misleading if not properly adjusted for case-mix severity. This paper demonstrates how to construct and cross-validate efficiency-outcome plots for a specified time (e.g., 6-month and 1-year survival) after coronary artery bypass grafting, accounting for baseline cardiovascular risk factors. The application of this approach to regional centers allows for the localization of risk stratification rather than applying overly broad and non-specific models to their patient populations

    Brachial Flow-Mediated Dilation and Incident Atrial Fibrillation The Multi-Ethnic Study of Atherosclerosis

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    Objective—It is unknown whether endothelial dysfunction precedes atrial fibrillation (AF) development. The objective of this study was to examine the association of brachial flow-mediated dilation (FMD) with incident AF. Approach and Results—A total of 2936 participants (mean age, 61±9.9 years; 50% women; 66% nonwhites) from the Multi-Ethnic Study of Atherosclerosis with available ultrasound brachial FMD measurements who were free of baseline AF were included in this analysis. Baseline (2000–2002) FMD was computed from the percentage difference (%FMD) in brachial artery diameter and maximum diameter during measured vasodilator response. AF was ascertained from hospitalization data including Medicare claims during a median follow-up of 8.5 years. Probability-weighted Cox proportional-hazards regression was used to compute hazard ratios and 95% confidence intervals for the association between FMD as a continuous variable (%FMD values per 1-SD increase) and incident AF. Incident AF was detected in 137 (4.7%) participants. Those with %FMD values below the sex-specific median value (median %FMD; men, 3.6%; women, 4.2%; incidence rate per 1000 person-years, 7.3; 95% confidence interval, 5.9–9.0) were more likely to develop AF than people whose %FMD values were above the median value (incidence rate per 1000 person-years, 4.5; 95% confidence interval, 3.4–5.8; log-rank P=0.0043). In a multivariable Cox regression analysis, each 1-SD increase in %FMD values (SD, 2.8%) was associated with less incident AF (hazard ratio, 0.84; 95% confidence interval, 0.70–0.99). These results were consistent across subgroups stratified by age, sex, and race/ethnicity. Conclusions—Smaller brachial FMD values are associated with higher rates of AF, sugge

    A sensitive high performance liquid chromatography assay for the quantification of doxorubicin associated with DNA in tumor and tissues

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    A HPLC method was validated to quantify doxorubicin associated to DNA from tissue.Successfully applied to an in vivo mouse-based pharmacokinetic study.Important tool for future studies evaluating intracellular pharmacokinetics.Doxorubicin, a widely used anticancer agent, exhibits antitumor activity against a wide variety of malignancies. The drug exerts its cytotoxic effects by binding to and intercalating within the DNA of tumor and tissue cells. However, current assays are unable to accurately determine the concentration of the intracellular active form of doxorubicin. Thus, the development of a sample processing method and a high-performance liquid chromatography (HPLC) methodology was performed in order to quantify doxorubicin that is associated with DNA in tumors and tissues, which provided an intracellular cytotoxic measure of doxorubicin exposure after administration of small molecule and nanoparticle formulations of doxorubicin. The assay uses daunorubicin as an internal standard; liquid–liquid phase extraction to isolate drug associated with DNA; a Shimadzu HPLC with fluorescence detection equipped with a Phenomenex Luna C18 (2 μm, 2.0 × 100 mm) analytical column and a gradient mobile phase of 0.1% formic acid in water or acetonitrile for separation and quantification. The assay has a lower limit of detection (LLOQ) of 10 ng/mL and is shown to be linear up to 3000 ng/mL. The intra- and inter-day precision of the assay expressed as a coefficient of variation (CV%) ranged from 4.01 to 8.81%. Furthermore, the suitability of this assay for measuring doxorubicin associated with DNA in vivo was demonstrated by using it to quantify the doxorubicin concentration within tumor samples from SKOV3 and HEC1A mice obtained 72 h after administration of PEGylated liposomal doxorubicin (Doxil®; PLD) at 6 mg/kg IV x 1. This HPLC assay allows for sensitive intracellular quantification of doxorubicin and will be an important tool for future studies evaluating intracellular pharmacokinetics of doxorubicin and various nanoparticle formulations of doxorubicin

    A cool starspot or a second transiting planet in the TrES-1 system?

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    We investigate the origin of a flux increase found during a transit of TrES-1, observed with the HST. This feature in the HST light curve cannot be attributed to noise and is supposedly a dark area on the stellar surface of the host star eclipsed by TrES-1 during its transit. We investigate the likeliness of two possible hypothesis for its origin: A starspot or a second transiting planet. We made use of several transit observations of TrES-1 from space with the HST and from ground with the IAC-80 telescope. On the basis of these observations we did a statistical study of flux variations in each of the observed events, to investigate if similar flux increases are present in other parts of the data set. The HST observation presents a single clear flux rise during a transit whereas the ground observations led to the detection of two such events but with low significance. In the case of having observed a starspot in the HST data, assuming a central impact between the spot and TrES-1, we would obtain a lower limit for the spot radius of 42000 km. For this radius the spot temperature would be 4690 K, 560 K lower then the stellar surface of 5250 K. For a putative second transiting planet we can set a lower limit for its radius at 0.37 RJ_J and for periods of less than 10.5 days, we can set an upper limit at 0.72 RJ_J. Assuming a conventional interpretation, then this HST observation constitutes the detection of a starspot. Alternatively, this flux rise might also be caused by an additional transiting planet. The true nature of the origin can be revealed if a wavelength dependency of the flux rise can be shown or discarded with a higher certainty. Additionally, the presence of a second planet can also be detected by radial velocity measurements.Comment: 8 pages, 6 figures, accepted for publication in A&

    Materials Science

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/67251/2/10.1177_00220345830620051601.pd
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