747 research outputs found

    BD-22 3467, a DAO-type star exciting the nebula Abell 35

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    Spectral analyses of hot, compact stars with NLTE (non-local thermodynamical equilibrium) model-atmosphere techniques allow the precise determination of photospheric parameters. The derived photospheric metal abundances are crucial constraints for stellar evolutionary theory. Previous spectral analyses of the exciting star of the nebula A 35, BD-22 3467, were based on He+C+N+O+Si+Fe models only. For our analysis, we use state-of-the-art fully metal-line blanketed NLTE model atmospheres that consider opacities of 23 elements from hydrogen to nickel. For the analysis of high-resolution and high-S/N (signal-to-noise) FUV (far ultraviolet, FUSE) and UV (HST/STIS) observations, we combined stellar-atmosphere models and interstellar line-absorption models to fully reproduce the entire observed UV spectrum. The best agreement with the UV observation of BD-22 3467 is achieved at Teff = 80 +/- 10 kK and log g =7.2 +/- 0.3. While Teff of previous analyses is verified, log g is significantly lower. We re-analyzed lines of silicon and iron (1/100 and about solar abundances, respectively) and for the first time in this star identified argon, chromium, manganese, cobalt, and nickel and determined abundances of 12, 70, 35, 150, and 5 times solar, respectively. Our results partially agree with predictions of diffusion models for DA-type white dwarfs. A combination of photospheric and interstellar line-absorption models reproduces more than 90 % of the observed absorption features. The stellar mass is M ~ 0.48 Msun. BD-22 3467 may not have been massive enough to ascend the asymptotic giant branch and may have evolved directly from the extended horizontal branch to the white dwarf state. This would explain why it is not surrounded by a planetary nebula. However, the star, ionizes the ambient interstellar matter, mimicking a planetary nebula.Comment: 13 pages, 17 figure

    Selective Deletion of the A1 Adenosine Receptor Abolishes Heart-Rate Slowing Effects of Intravascular Adenosine In Vivo

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    OBJECTIVE:Intravenous adenosine induces temporary bradycardia. This is due to the activation of extracellular adenosine receptors (ARs). While adenosine can signal through any of four ARs (A1AR, A2AAR, A2BAR, A3AR), previous ex vivo studies implicated the A1AR in the heart-rate slowing effects. Here, we used comparative genetic in vivo studies to address the contribution of individual ARs to the heart-rate slowing effects of intravascular adenosine. METHODS AND RESULTS:We studied gene-targeted mice for individual ARs to define their in vivo contribution to the heart-rate slowing effects of adenosine. Anesthetized mice were treated with a bolus of intravascular adenosine, followed by measurements of heart-rate and blood pressure via a carotid artery catheter. These studies demonstrated dose-dependent slowing of the heart rate with adenosine treatment in wild-type, A2AAR(-/-), A2BAR(-/-), or A3AR(-/-) mice. In contrast, adenosine-dependent slowing of the heart-rate was completely abolished in A1AR(-/-) mice. Moreover, pre-treatment with a specific A1AR antagonist (DPCPX) attenuated the heart-rate slowing effects of adenosine in wild-type, A2AAR(-/-), or A2BAR(-/-) mice, but did not alter hemodynamic responses of A1AR(-/-) mice. CONCLUSIONS:The present studies combine pharmacological and genetic in vivo evidence for a selective role of the A1AR in slowing the heart rate during adenosine bolus injection

    Pressure Controlled Ventilation to Induce Acute Lung Injury in Mice

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    Murine models are extensively used to investigate acute injuries of different organs systems (1-34). Acute lung injury (ALI), which occurs with prolonged mechanical ventilation, contributes to morbidity and mortality of critical illness, and studies on novel genetic or pharmacological targets are areas of intense investigation (1-3, 5, 8, 26, 30, 33-36). ALI is defined by the acute onset of the disease, which leads to non-cardiac pulmonary edema and subsequent impairment of pulmonary gas exchange (36). We have developed a murine model of ALI by using a pressure-controlled ventilation to induce ventilator-induced lung injury (2). For this purpose, C57BL/6 mice are anesthetized and a tracheotomy is performed followed by induction of ALI via mechanical ventilation. Mice are ventilated in a pressure-controlled setting with an inspiratory peak pressure of 45 mbar over 1 - 3 hours. As outcome parameters, pulmonary edema (wet-to-dry ratio), bronchoalveolar fluid albumin content, bronchoalveolar fluid and pulmonary tissue myeloperoxidase content and pulmonary gas exchange are assessed (2). Using this technique we could show that it sufficiently induces acute lung inflammation and can distinguish between different treatment groups or genotypes (1-3, 5). Therefore this technique may be helpful for researchers who pursue molecular mechanisms involved in ALI using a genetic approach in mice with gene-targeted deletion

    Normalisierung des T3/T4-Quotienten im Serum bei Struma-Patienten unter Kaliumjodid

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    Bei 16 Patienten mit blander Struma kam es bereits nach 4-wöchentlicher Behandlung mit täglich nur 200 µg Kaliumjodid zu einer Normalisierung des zuvor erhöhten T3/T4-Quotienten. Die TSH-Spiegel zeigten unter dieser Kaliumjodidbehandlung dagegen keine meßbaren Veränderungen. Die Schilddrüse besitzt demnach offensichtlich auch beim Menschen die Fähigkeit, die Synthese und Sekretion der beiden Schilddrüsenhormone T3 und T4 unabhängig vom TSH der jeweiligen Jodzufuhr anzupassen (sog. Autoregulation der jeweiligen Jodzufuhr anzupassen (sog. Autoregulation der Schilddrüse)

    Myeloid Hypoxia-Inducible Factor HIF1A Provides Cardio-Protection During Ischemia and Reperfusion

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    The transcription factor hypoxia-inducible factor HIF1A induces cardioprotection from ischemia and reperfusion injury. Here, we investigate tissue-specific pathways that are critical for HIF1A-elicited tissue protection. Initial studies showed that mice with induced global Hif1a deletion (Hif1aloxP/loxP UbiquitinCre+) have exaggerated myocardial injury during in situ ischemia and reperfusion. Surprisingly, this phenotype was mirrored only in mice with myeloid-specific Hif1a deletion (Hif1aloxP/loxP LysM Cre+). In contrast, mice with myocardial specific (Hif1aloxP/loxP Myosin Cre+), or vascular Hif1a deletion (Hif1aloxP/loxP VEcadherin Cre+) experienced similar levels of injury as controls. Subsequent studies using adoptive transfer of Hif1a-deficient polymorphonuclear neutrophils (PMNs) prior to myocardial injury demonstrated increased reperfusion injury. On the contrary, the adoptive transfer of PMNs treated ex vivo with the hypoxia inducible factor (HIF) stabilizer dimethyloxalylglycine (DMOG) was associated with attenuated myocardial injury. Furthermore, DMOG-mediated cardioprotection was abolished in Hif1aloxP/loxP LysM Cre+ mice, but not in Hif2aloxP/loxP LysM Cre+ mice. Finally, studies of PMN-dependent HIF1A target genes implicated the neuronal guidance molecule netrin-1 in mediating the cardioprotective effects of myeloid HIF1A. Taken together, the present studies identified a functional role for myeloid-expressed HIF1A in providing cardioprotection during ischemia and reperfusion injury, which is mediated, at least in part, by the induction of the netrin-1 neuronal guidance molecule in neutrophils

    Detrended fluctuation analysis as a statistical tool to monitor the climate

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    Detrended fluctuation analysis is used to investigate power law relationship between the monthly averages of the maximum daily temperatures for different locations in the western US. On the map created by the power law exponents, we can distinguish different geographical regions with different power law exponents. When the power law exponents obtained from the detrended fluctuation analysis are plotted versus the standard deviation of the temperature fluctuations, we observe different data points belonging to the different climates, hence indicating that by observing the long-time trends in the fluctuations of temperature we can distinguish between different climates.Comment: 8 pages, 4 figures, submitted to JSTA
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