Foreground removal from WMAP 7yr polarization maps using an MLP neural network

One of the fundamental problems in extracting the cosmic microwave background signal (CMB) from millimeter/submillimeter observations is the pollution by emission from the Milky Way: synchrotron, free-free, and thermal dust emission. To extract the fundamental cosmological parameters from CMB signal, it is mandatory to minimize this pollution since it will create systematic errors in the CMB power spectra. In previous investigations, it has been demonstrated that the neural network method provide high quality CMB maps from temperature data. Here the analysis is extended to polarization maps. As a concrete example, the WMAP 7-year polarization data, the most reliable determination of the polarization properties of the CMB, has been analysed. The analysis has adopted the frequency maps, noise models, window functions and the foreground models as provided by the WMAP Team, and no auxiliary data is included. Within this framework it is demonstrated that the network can extract the CMB polarization signal with no sign of pollution by the polarized foregrounds. The errors in the derived polarization power spectra are improved compared to the errors derived by the WMAP Team.Comment: Accepted for publication in Astrophysics & Space Scienc

Deep rest-frame far-UV spectroscopy of the giant Lyman-alpha emitter 'Himiko'

We present deep 10h VLT/XSHOOTER spectroscopy for an extraordinarily luminous and extended Lya emitter at z=6.595 referred to as Himiko and first discussed by Ouchi et al. (2009), with the purpose of constraining the mechanisms powering its strong emission. Complementary to the spectrum, we discuss NIR imaging data from the CANDELS survey. We find neither for HeII nor any metal line a significant excess, with 3 sigma upper limits of 6.8, 3.1, and 5.8x10^{-18} erg/s/cm^2 for CIV $\lambda$1549, HeII $\lambda$1640, CIII] $\lambda$1909, respectively, assuming apertures with 200 km/s widths and offset by -250 km/s w.r.t to the peak Lya redshift. These limits provide strong evidence that an AGN is not a major contribution to Himiko's Lya flux. Strong conclusions about the presence of PopIII star-formation or gravitational cooling radiation are not possible based on the obtained HeII upper limit. Our Lya spectrum confirms both spatial extent and flux (8.8+/-0.5x10^{-17} erg/s/cm^2) of previous measurements. In addition, we can unambiguously exclude any remaining chance of it being a lower redshift interloper by significantly detecting a continuum redwards of Lya, while being undetected bluewards

Effects of pre- or postoperative morphine and of preoperative ketamine in experimental surgery in rats, evaluated by pain scoring and c-fos expression

Since Wall (1988) hypothesised a beneficial post surgical effect of preoperative analgesic treatment (so-called pre-emptive analgesic treatment) as a supplement to postoperative analgesic treatment, the concept has been subject to many scientific debates. According to the hypothesis, applying analgesics before the nociceptive stimulus is beneficial due to reduced wind-up and reduced central sensitisation resulting in diminished risk of postoperative hyperalgesia and allodynia (Woolf and Chong, 1993). The scientific literature provides conflicting evidence for this theory. Beneficial effect of preemptive analgesic treatment has been reported after pre-emptive treatment with local analgesics, opioids and NSAID´s compared with placebo (Woolf and Chong, 1993). Some clinical settings have showed beneficial analgesic effect of preemptive analgesia, when the same pre-emptive and postoperative treatments with lidocaine (Ejlersen et al., 1992; Doyle and Bowler, 1998) or opioids (Katz et al., 1992) were compared. However, Dahl et al. (1992) and Elhakim et al. (1995) did not obtained supportive results in their clinical studies.In the majority of studies using animal models addressing this concept, the nociceptive stimulus has been obtained by injection of irritating chemicals, in particular formalin. When somatic tissue is damaged or irritated, nociceptive receptors are activated by peripheral release of extracellular inflammatory mediators. The activated receptors lead the signal to the synapses in the dorsal horn of the spinal cord as a 2-phased signal. In the acute first phase, nociceptive stimuli are mediated centrally through Aä fibres fibres. During the slower and long-lasting second phase, the nociceptive stimuli are mediated mainly through C-fibres (Cross et al., 1994). The release of extracellular inflammatory mediators increases the peripheral excitability, which leads to hyperalgesia (Woolf, 1995). Repetitive peripheral nociceptive impulses mediated through C-fibres result in an increased central excitability of dorsal appears to be in part mediated through N-methylhorn neurones. This state is called wind-up and appears to be in part mediated through N-methyl- D-aspartate (NMDA) receptors on dorsal horn secondary nociceptive neurones. Transmission of multiple slow stimuli leads to release of glutamate, which removes the Mg++-block in the NMDA receptor and allows substantial Ca++-inflow (Urban et al., 1994). NMDA receptor antagonists bind to the same site as Mg++ and prevents Ca++- inflow (Hirota and Lambert, 1996; Kress, 1997). NMDA-receptor antagonists can prevent wind-up but not the initial responses of the neurones, whereas the reverse is true for opioids (Chapman and Dickenson, 1992). NMDA-antagonists have no effect on pain of the acute first phase, but may act synergistic to the analgesic effect of opioids (Chapman and Dickenson, 1992; Honoré et al., 1996). Only few studies deal with a postoperative experimental model in animals and those available are conflicting. Brennan et al. (1996) developed an elegant postoperative model in rats with surgical intervention on the plantar surface of the hind foot. In this study a relationship was found between behavioural pain observation scores and mechanical hyperalgesia. Ovariohysterectomized rats have also been used as animal models of postoperative pain (Lascelles et al. 1995). A commonly used method of determining the nociceptive activity caused by a peripheral stimulus is to identify and quantify the nuclear protein Fos expressed in secondary nociceptive neurones in the spinal cord. c-fos is an immediate early gene (IEG), that encodes for Fos. IEG’s are rapidly and transiently induced in neuronal cells within minutes of extracellular stimulation (Sheng and Greenberg, 1990). The c-fos mRNA accumulates, and reaches its peak after 30 to 40 minutes. The Fos level peaks approximately two hours after induction of c-fos (Harris, 1998). Since Hunt (1987) reported, that peripheral inflammation induced c-fos in neurones in the dorsal horn of the spinal cord, many studies have shown the relationship between nociception and cfos expression.The aim of the present investigation was to study the effect of pre-emptive versus postoperative opioid analgesic treatment by use of the surgical model of Brennan et al. (1996) and combine the pre-emptive and postoperative opioid treatment with pre-emptive ketamine. The effects were quantified by stereological estimation of the number of dorsal horn neurones expressing c-fos and pain scoring from the operated hind foot

Elevated fetal steroidogenic activity in autism

Autism affects males more than females, giving rise to the idea that the influence of steroid hormones on early fetal brain development may be one important early biological risk factor. Utilizing the Danish Historic Birth Cohort and Danish Psychiatric Central Register, we identified all amniotic fluid samples of males born between 1993 and 1999 who later received ICD-10 (International Classification of Diseases, 10th Revision) diagnoses of autism, Asperger syndrome or PDD-NOS (pervasive developmental disorder not otherwise specified) (n=128) compared with matched typically developing controls. Concentration levels of Δ4 sex steroids (progesterone, 17α-hydroxy-progesterone, androstenedione and testosterone) and cortisol were measured with liquid chromatography tandem mass spectrometry. All hormones were positively associated with each other and principal component analysis confirmed that one generalized latent steroidogenic factor was driving much of the variation in the data. The autism group showed elevations across all hormones on this latent generalized steroidogenic factor (Cohen's d=0.37, P=0.0009) and this elevation was uniform across ICD-10 diagnostic label. These results provide the first direct evidence of elevated fetal steroidogenic activity in autism. Such elevations may be important as epigenetic fetal programming mechanisms and may interact with other important pathophysiological factors in autism

Expression and autoregulation of transforming growth factor beta receptor mRNA in small-cell lung cancer cell lines.

In small-cell lung cancer cell lines resistance to growth inhibition by transforming growth factor (TGF)-beta 1, was previously shown to correlate with lack of TGF-beta receptor I (RI) and II (RII) proteins. To further investigate the role of these receptors, the expression of mRNA for RI, RII and beta-glycan (RIII) was examined. The results showed that loss of RII mRNA correlated with TGF-beta 1 resistance. In contrast, RI-and beta-glycan mRNA was expressed by all cell lines, including those lacking expression of these proteins. According to Southern blot analysis, the loss of type II mRNA was not due to gross structural changes in the gene. The effect of TGF-beta 1 on expression of TGF-beta receptor mRNA (receptor autoregulation) was examined by quantitative Northern blotting in four cell lines with different expression of TGF-beta receptor proteins. In two cell lines expressing all three TGF-beta receptor proteins beta-glycan mRNA was rapidly down-regulated and this effect was sustained throughout the 24 h observation period. RI and RII mRNAs were slightly increased 24 h after treatment. In one cell line sensitive to growth inhibition by TGF-beta, 1 but lacking beta-glycan expression, and one cell line expressing only beta-glycan and thus TGF-beta 1 -resistant, no autoregulation of mRNA of either TGF-beta receptor was demonstrated. The results suggest that TGF-beta 1 regulates the expression of its receptors, in particular beta-glycan, and that this effect is dependent on co-expression of beta-glycan, RI and RII