155 research outputs found

    Possible canted antiferromagnetism in UCu9_9Sn4_4

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    We report on the new compound UCu9{}_9Sn4{}_4 which crystallizes in the tetragonal structure \emph{I}4/\emph{mcm} with lattice parameters a=8.600A˚a = 8.600{\rm\AA} and c=12.359A˚c = 12.359{\rm\AA}. This compound is isotyp to the ferromagnetic systems RECu9{}_9Sn4{}_4 (RE = Ce, Pr, Nd) with Curie temperatures TCT{}\rm_C = 5.5 K, 10.5 K and 15 K, respectively. UCu9{}_9Sn4{}_4 exhibits an uncommon magnetic behavior resulting in three different electronic phase transitions. Below 105 K the sample undergoes a valence transition accompanied by an entropy change of 0.5 Rln2. At 32 K a small hump in the specific heat and a flattening out in the susceptibility curve probably indicate the onset of helical spin order. To lower temperatures a second transition to antiferromagnetic ordering occurs which develops a small ferromagnetic contribution on lowering the temperature further. These results are strongly hinting for canted antiferromagnetism in UCu9{}_9Sn4{}_4.Comment: 2 pages, 3 figures, SCES0

    Alloimmunity and nonimmunologic risk factors in cardiac allograft vasculopathy

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    Graft vasculopathy is an accelerated form of coronary artery disease that occurs in transplanted hearts. Despite major advances in immunosuppression, the prevalence of the disease has remained substantially unchanged during the last two decades. According to the ‘response to injury' paradigm, graft vasculopathy is the result of a continuous inflammatory response to tissue injury initiated by both alloantigen-dependent and independent stress responses. Experimental evidence suggests that these responses may become self-sustaining, as allograft re-transplantation into the donor strain at a later stage fails to prevent disease progression. Histological evidence of endothelitis and arteritis, in association with intima fibrosis and atherosclerosis, reflects the central role of alloimmunity and inflammation in the development of arterial lesions. Experimental results in gene-targeted mouse models indicate that cellular and humoral immune responses are both involved in the pathogenesis of graft vasculopathy. Circulating antibodies against donor endothelium are found in a significant number of patients, but their pathogenic role is still controversial. Alloantigen-independent factors include donor-transmitted coronary artery disease, surgical trauma, ischaemia-reperfusion injury, viral infections, hyperlipidaemia, hypertension, and glucose intolerance. Recent therapeutic advances include the use of novel immunosuppressive agents such as sirolimus (rapamycin), HMG-CoA reductase inhibitors, calcium channel blockers, and angiotensin converting enzyme inhibitors. Optimal treatment of cardiovascular risk factors remains of paramount importanc

    The association of N-terminal pro-brain-type natriuretic peptide with hemodynamics and functional capacity in therapy-naive precapillary pulmonary hypertension: results from a cohort study

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    Background: N-terminal pro-brain-type natriuretic peptide (NT-proBNP) is currently used as a surrogate marker for disease severity in pulmonary hypertension (PH). However, NT-proBNP tends to have a high variability and may insufficiently correlate with hemodynamics and exercise capacity. Methods: To investigate the association of NT-proBNP with hemodynamics and cardio-pulmonary exercise testing (CPET) in 84 therapy-naive patients with precapillary PH. Results: NT-proBNP levels were significantly correlated with hemodynamics and CPET parameters except for cardiac index, diffusion capacity, PaO2 at peak exercise, and peak minute ventilation. NT-proBNP correlated best with hemodynamics and CPET in women and patients >65 years. NT-proBNP correlated better with CPET in pulmonary arterial hypertension compared to chronic thromboembolic PH (CTEPH). Conclusion: NT-proBNP is associated with disease severity in precapillary PH. The association might be age-and gender-dependent. NT-proBNP may insufficiently correlate with disease severity in CTEPH, possibly due to comorbidity

    Poly-MTO, {(CH_3)_{0.92} Re O_3}_\infty, a Conducting Two-Dimensional Organometallic Oxide

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    Polymeric methyltrioxorhenium, {(CH_{3})_{0.92}ReO_{3}}_{\infty} (poly-MTO), is the first member of a new class of organometallic hybrids which adopts the structural pattern and physical properties of classical perovskites in two dimensions (2D). We demonstrate how the electronic structure of poly-MTO can be tailored by intercalation of organic donor molecules, such as tetrathiafulvalene (TTF) or bis-(ethylendithio)-tetrathiafulvalene (BEDT-TTF), and by the inorganic acceptor SbF3_3. Integration of donor molecules leads to a more insulating behavior of poly-MTO, whereas SbF3_3 insertion does not cause any significant change in the resistivity. The resistivity data of pure poly-MTO is remarkably well described by a two-dimensional electron system. Below 38 K an unusual resistivity behavior, similar to that found in doped cuprates, is observed: The resistivity initially increases approximately as ρ\rho \sim ln(1/T(1/T) before it changes into a T\sqrt{T} dependence below 2 K. As an explanation we suggest a crossover from purely two-dimensional charge-carrier diffusion within the \{ReO2_2\}_{\infty} planes at high temperatures to three-dimensional diffusion at low temperatures in a disorder-enhanced electron-electron interaction scenario (Altshuler-Aronov correction). Furthermore, a linear positive magnetoresistance was found in the insulating regime, which is caused by spatial localization of itinerant electrons at some of the Re atoms, which formally adopt a 5d15d^1 electronic configuration. X-ray diffraction, IR- and ESR-studies, temperature dependent magnetization and specific heat measurements in various magnetic fields suggest that the electronic structure of poly-MTO can safely be approximated by a purely 2D conductor.Comment: 15 pages, 16 figures, 2 table

    Spin and orbital frustration in MnSc_2S_4 and FeSc_2S_4

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    Crystal structure, magnetic susceptibility, and specific heat were measured in the normal cubic spinel compounds MnSc_2S_4 and FeSc_2S_4. Down to the lowest temperatures, both compounds remain cubic and reveal strong magnetic frustration. Specifically the Fe compound is characterized by a Curie-Weiss temperature \Theta_{CW}= -45 K and does not show any indications of order down to 50 mK. In addition, the Jahn-Teller ion Fe^{2+} is orbitally frustrated. Hence, FeSc_2S_4 belongs to the rare class of spin-orbital liquids. MnSc_2S_4 is a spin liquid for temperatures T > T_N \approx 2 K.Comment: 4 pages, to be published in Physical Review Letter

    PGE1 nebulisation during caesarean section for Eisenmenger's syndrome: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>Eisenmenger's syndrome in pregnancy can lead to death in 50% to 65% of parturients. Expensive invasive monitoring and medication have improved management and outcomes. Cheaper alternatives for the management of high-risk patients who present with no prenatal care are still not available.</p> <p>Case presentation</p> <p>We describe the obstetric anaesthesia management of a 34-year-old, 34-weeks pregnant woman who presented with a recent diagnosis of severe Eisenmenger's syndrome. A combined spinal epidural anaesthesia was used together with invasive cardiac monitoring as well as PGE1 nebulisation after delivery of the baby. This helped achieve a reduction of shunt, improvement of hypoxia and reduction of pulmonary pressures.</p> <p>Conclusion</p> <p>We found this to be a cheaper and safe alternative in the management of such patients who present with no adequate prior management.</p

    IL-23 suppresses innate immune response independently of IL-17A during carcinogenesis and metastasis

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    IL-23 is an important molecular driver of Th17 cells and has strong tumor-promoting proinflammatory activity postulated to occur via adaptive immunity. Conversely, more recently it has been reported that IL-17A elicits a protective inflammation that promotes the activation of tumor-specific CD8(+) T cells. Here we show the much broader impact of IL-23 in antagonizing antitumor immune responses primarily mediated by innate immunity. Furthermore, the majority of this impact was independent of IL-17A, which did not appear critical for many host responses to tumor initiation or metastases. IL-23-deficient mice were resistant to experimental tumor metastases in three models where host NK cells controlled disease. Immunotherapy with IL-2 was more effective in mice lacking IL-23, and again the protection afforded was NK cell mediated and independent of IL-17A. Further investigation revealed that loss of IL-23 promoted perforin and IFN-gamma antitumor effector function in both metastasis models examined. IL-23-deficiency also strikingly protected mice from tumor formation in two distinct mouse models of carcinogenesis where the dependence on host IL-12p40 and IL-17A was quite different. Notably, in the 3'-methylcholanthrene (MCA) induction of fibrosarcoma model, this protection was completely lost in the absence of NK cells. Overall, these data indicate the general role that IL-23 plays in suppressing natural or cytokine-induced innate immunity, promoting tumor development and metastases independently of IL-17A

    Improving Metabolic Health Through Precision Dietetics in Mice

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    The incidence of diet-induced metabolic disease has soared over the last half-century, despite national efforts to improve health through universal dietary recommendations. Studies comparing dietary patterns of populations with health outcomes have historically provided the basis for healthy diet recommendations. However, evidence that population-level diet responses are reliable indicators of responses across individuals is lacking. This study investigated how genetic differences influence health responses to several popular diets in mice, which are similar to humans in genetic composition and the propensity to develop metabolic disease, but enable precise genetic and environmental control. We designed four human-comparable mouse diets that are representative of those eaten by historical human populations. Across four genetically distinct inbred mouse strains, we compared the American diet’s impact on metabolic health to three alternative diets (Mediterranean, Japanese, and Maasai/ketogenic). Furthermore, we investigated metabolomic and epigenetic alterations associated with diet response. Health effects of the diets were highly dependent on genetic background, demonstrating that individualized diet strategies improve health outcomes in mice. If similar genetic-dependent diet responses exist in humans, then a personalized, or “precision dietetics,” approach to dietary recommendations may yield better health outcomes than the traditional one-size-fits-all approach
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