Four-colour photometry of eclipsing binaries. XLI uvby light curves for AD Bootis, HW Canis Majoris, SW Canis Majoris, V636 Centauri, VZ Hydrae, and WZ Ophiuchi

CONTEXT: Accurate mass, radius, and abundance determinations from binaries provide important information on stellar evolution, fundamental to central fields in modern astrophysics and cosmology. AIMS: Within the long-term Copenhagen Binary Project, we aim to obtain high-quality light curves and standard photometry for double-lined detached eclipsing binaries with late A, F, and G type main-sequence components, needed for the determination of accurate absolute dimensions and abundances, and for detailed comparisons with results from recent stellar evolutionary models. METHODS: Between March 1985 and July 2007, we carried out photometric observations of AD Boo, HW CMA, SW CMa, V636 Cen, VZ Hya, and WZ Oph at the Str"omgren Automatic Telescope at ESO, La Silla. RESULTS: We obtained complete uvby light curves, ephemerides, and standard uvby\beta indices for all six systems.For V636 Cen and HW CMa, we present the first modern light curves, whereas for AD Boo, SW CMa, VZ Hya, and WZ Oph, they are both more accurate and more complete than earlier data. Due to a high orbital eccentricity (e = 0.50), combined with a low orbital inclination (i = 84.7), only one eclipse, close to periastron, occurs for HW CMa. For the two other eccentric systems, V636 Cen (e = 0.134) and SW CMa (e = 0.316), apsidal motion has been detected with periods of 5270 +/- 335 and 14900 +/- 3600 years, respectively.Comment: Only change is: Bottom lines (hopefully) not truncated anymore. Accepted for publication in Astonomy & Astrophysic

Activin A Causes Muscle Atrophy through MEF2C-Dependent Impaired Myogenesis.

Activin A (ActA) is considered to play a major role in cancer-induced cachexia (CC). Indeed, circulating ActA levels are elevated and predict survival in patients with CC. However, the mechanisms by which ActA mediates CC development and in particular skeletal muscle (SM) atrophy in humans are not yet fully understood. In this work, we aimed to investigate the effects of ActA on human SM and in mouse models of CC. We used a model of human muscle cells in culture to explore how ActA acts towards human SM. In this model, recombinant ActA induced myotube atrophy associated with the decline of MyHC-β/slow, the main myosin isoform in human muscle cells studied. Moreover, ActA inhibited the expression and activity of MEF2C, the transcription factor regulating , the gene which codes for MyHC-β/slow. This decrease in MEF2C was involved in the decline of MyHC-β/slow expression, since inhibition of MEF2C by a siRNA leads to the decrease in MyHC-β/slow expression. The relevance of this ActA/MEF2C pathway in vivo was supported by the parallel decline of expression and SM mass, which are both blunted by ActA inhibition, in animal models of CC. In this work, we showed that ActA is a potent negative regulator of SM mass by inhibiting MyHC-β/slow synthesis through downregulation of MEF2C. This observation highlights a novel interaction between ActA signaling and MEF2C transcriptional activity which contributes to SM atrophy in CC models

Decreased Craniocervical CSF Flow in Patients with Normal Pressure Hydrocephalus: A Pilot Study

Normal pressure hydrocephalus is characterized by systolic peaks of raised intracranial pressure, possibly due to a reduced compliance of the spinal CSF spaces. This concept of a reduced spinal CSF buffer function may be reflected by a low cervical CSF outflow from the cranium. The aim of this study was to investigate craniospinal CSF flow rates by phase-contrast MR imaging in patients with normal pressure hydrocephalus. A total of 42 participants were included in this prospective study, consisting of 3 study groups: 1) 10 patients with normal pressure hydrocephalus (mean age, 74 [SD, 6] years, with proved normal pressure hydrocephalus according to current scientific criteria); 2) eighteen age-matched healthy controls (mean age, 71 [SD, 5] years); and 3) fourteen young healthy controls (mean age, 21 [SD, 2] years, for investigation of age-related effects). Axial phase-contrast MR imaging was performed, and the maximal systolic CSF and total arterial blood flow rates were measured at the level of the upper second cervical vertebra and compared among all study groups (2-sample unpaired test). The maximal systolic CSF flow rate was significantly decreased in patients with normal pressure hydrocephalus compared with age-matched and young healthy controls (53 [SD,  40] mL/m; 329 [SD,  175] mL/m; 472 [SD, 194] mL/m; each < .01), whereas there were no significant differences with regard to maximal systolic arterial blood flow (1160 [SD, 404] mL/m; 1470 [SD,  381] mL/m; 1400 [SD, 254] mL/m; each > .05). The reduced maximal systolic craniospinal CSF flow rate in patients with normal pressure hydrocephalus may be reflective of a reduced compliance of the spinal CSF spaces and an ineffective spinal CSF buffer function. Systolic craniospinal CSF flow rates are an easily obtainable MR imaging-based measure that may support the diagnosis of normal pressure hydrocephalus

Continuous administration of growth hormone does not prevent the decrease of IGF-I gene expression in zinc-deprived rats despite normalization of liver GH binding.

To determine the role of reduced liver GH binding (GHR) in the decreased IGF-I observed in zinc-deficient (ZD) animals, we investigated the effects of GHR restoration on growth, insulin-like growth factor I (IGF-I) and its binding proteins (IGFBPs) in ZD rats. Rats were fed for 4 weeks a zinc-deficient diet (ZD Zn, 0 ppm) or a Zinc-normal diet (pair-fed or PF; Zn, 75 ppm). ZD rats received continuous s.c. infusion of bovine growth hormone (bGH) (100 microg/d) for the 4 weeks or for the last week of the study. Compared with pair-fed rats, zinc deficiency produced attenuated weight gain (-43%, P < 0.001), lower serum IGF-I and liver IGF-I mRNA (-52%, P < 0.001 and -44%, P < 0.05), lower serum IGFBPs (IGFBP-3 -66%, IGFBP-4 -48%, 34-29 kDa IGFBP cluster -53%, P < 0.05), lower liver GHR and its mRNA (-20 and -34%, P < 0.05) and lower serum growth hormone binding protein (GHBP) and its mRNA (-56 and -48%, P < 0.05; all comparisons vs PF rats). Exogenous bGH given continuously normalized the liver GHR, serum GHBP and their liver mRNAs, as well as circulating IGFBPs. Despite restoration of GHR and GHBP to normal, growth, serum IGF-I and its liver mRNA were not stimulated by GH infusion in ZD rats, indicating that IGF-I synthesis requires the presence of zinc in addition to GH, and that the lack of growth-promoting action of GH in zinc-deprived rats results from a defect beyond GH binding to its liver receptors

Verbmobil. AP 6.9: Szenariotests und Wizard-of-Oz Aufnahmen Schlussbericht

SIGLEAvailable from TIB Hannover: DtF QN1(88,42) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekBundesministerium fuer Bildung, Wissenschaft, Forschung und Technologie, Bonn (Germany)DEGerman

Early activation of cardiac and renal endothelin systems in experimental heart failure

peer reviewedaudience: researcher, professionalWe investigated the time course of the expression of cardiac and renal endothelin systems in tachycardia-induced heart failure in dogs. Eleven beagles underwent rapid pacing at a progressively increased rate over a period of 5 wk, with a weekly clinical examination, echocardiography, measurement of circulating and urinary endothelin-1 (ET-1), and myocardial and renal tissue biopsies. Real-time quantitative PCR was used for determinations of tissue prepro-ET-1 (ppET-1), ET-1-converting enzyme (ECE-1), and ETA and ETB receptor mRNA. Cardiac and renal tissue ET-1 contents were evaluated by immunostaining and measured by radioimmunoassay at autopsy. Rapid pacing caused a progressive increase in end-systolic and end-diastolic ventricular volumes (P<0.05) from week 2 together with a decrease in ejection fraction and in mean velocity of circumferential shortening (P<0.05) from week 1. These changes were tightly correlated to myocardial ppET-1 and renal ETA receptor mRNA and less so to myocardial ECE-1 mRNA, and they occurred before any increase in plasma and urinary ET-1 (P<0.05 from week 4) and clinical signs of heart failure. Renal ppET-1 did not change. Both cardiac and renal ET-1 peptide contents were increased at autopsy. We conclude that tachycardia-induced heart failure in dogs is characterized by an early activation of the cardiac and renal tissue endothelin systems, which occurs before any changes in circulating and urinary ET-1 and is closely related to altered ventricular function

Marked Increased Production of Acute Phase Reactants by Skeletal Muscle during Cancer Cachexia

Loss of skeletal muscle mass in cancer cachexia is recognized as a predictor of mortality. This study aimed to characterize the changes in the muscle secretome associated with cancer cachexia to gain a better understanding of the mechanisms involved and to identify secreted proteins which may reflect this wasting process. The changes in the muscle proteome of the C26 model were investigated by label-free proteomic analysis followed by a bioinformatic analysis in order to identify potentially secreted proteins. Multiple reaction monitoring and Western blotting were used to verify the presence of candidate proteins in the circulation. Our results revealed a marked increased muscular production of several acute phase reactants (APR: Haptoglobin, Serine protease inhibitor A3N, Complement C3, Serum amyloid A-1 protein) which are released in the circulation during C26 cancer cachexia. This was confirmed in other models of cancer cachexia as well as in cancer patients. Glucocorticoids and proinflammatory cytokines are responsible for an increased production of APR by muscle cells. Finally, their muscular expressions are strongly positively correlated with body weight loss as well as the muscular induction of atrogens. Our study demonstrates therefore a marked increased production of APR by the muscle in cancer cachexia