Probing the Intergalactic Medium with Lyα\mathrm{\alpha} and 21 cm Fluctuations

We study 21cm and Ly$\mathrm{\alpha}$ fluctuations, as well as H$\mathrm{\alpha}$, while distinguishing between Ly$\mathrm{\alpha}$ emission of galactic, diffuse, and scattered intergalactic medium (IGM) origin. Cross-correlation information about the state of the IGM is obtained, testing neutral versus ionized medium cases with different tracers in a seminumerical simulation setup. In order to pave the way toward constraints on reionization history and modeling beyond power spectrum information, we explore parameter dependencies of the cross-power signal between 21$\,$cm and Ly$\mathrm{\alpha}$, which displays a characteristic morphology and a turnover from negative to positive correlation at scales of a couple Mpc$^{-1}$. In a proof of concept for the extraction of further information on the state of the IGM using different tracers, we demonstrate the use of the 21$\,$cm and H$\mathrm{\alpha}$ cross-correlation signal to determine the relative strength of galactic and IGM emission in Ly$\mathrm{\alpha}$. We conclude by showing the detectability of the 21$\,$cm and Ly$\mathrm{\alpha}$ cross-correlation signal over more than one decade in scale at high signal-to-noise ratio for upcoming probes like SKA and the proposed all-sky intensity mapping satellites SPHEREx and CDIM, while also including the Ly$\mathrm{\alpha}$ damping tail and 21cm foreground avoidance in the modeling.Comment: 26 pages, 18 figures, 3 tables. Accepted for publication in Ap

Extensive search for bias in SNIa data

The use of advanced statistical analysis tools is crucial in order to improve cosmological parameter estimates via removal of systematic errors and identification of previously unaccounted for cosmological signals. Here we demonstrate the application of a new fully-Bayesian method, the internal robustness formalism, to scan for systematics and new signals in the recent supernova Ia Union compilations. Our analysis is tailored to maximize chances of detecting the anomalous subsets by means of a variety of sorting algorithms. We analyse supernova Ia distance moduli for effects depending on angular separation, redshift, surveys and hemispherical directions. The data have proven to be robust within 2 sigma, giving an independent confirmation of successful removal of systematics-contaminated supernovae. Hints of new cosmology, as for example the anisotropies reported by Planck, do not seem to be reflected in the supernova Ia data.Comment: 11 pages, 7 figures, matches version accepted for publication in MNRA

Identifying systems barriers that may prevent bereavement service access to bereaved carers: A report from an Australian specialist palliative care service

Background: Bereavement follow up is an integral element of palliative care. However, little is known about the systems that link bereavement services with bereaved carers. Aim: To map how effectively a specialist palliative care service linked bereavement service to bereaved carers. Methodology: A retrospective medical audit, using process mapping was undertaken within one Australian specialist palliative care service to identify the systems that linked bereavement services to a consecutive cohort of palliative care decedents (n=60) next of kin. Results: Bereavement records were located for 80% of decedents. Nearly all (98%) had a nominated next of kin, with just over half (54%) of those nominated contacted by bereavement services. Incomplete or missing contact details was the main reason (75%) that the bereavement service was unable to contact the decedents’ next of kin. Conclusion: Having access to a designated bereavement service can ensure that bereaved next of kin are contract routinely and in a timely way. However the effectiveness of this type of service is dependent upon the bereavement service having access to all relevant contact information. There are numerous opportunities to refine and strengthen the recording of palliative care next of kin details to optimize follow up

Neuroinflammation and Its Resolution: From Molecular Mechanisms to Therapeutic Perspectives

Neuroinflammation, the complex immune response of the central nervous system (CNS), when sustained, is a common denominator in the etiology and course of all major neurological diseases, including neurodevelopmental, neurodegenerative, and psychiatric disorders (e.g., Alzheimer's disease, AD; Parkinson's disease, PD; multiple sclerosis, MS; motor neuron disease; depression; autism spectrum disorder; and schizophrenia). Cellular (microglia and mast cells, two brain-resident immune cells, together with astrocytes) and molecular immune components (e.g., cytokines, complement and patternrecognition receptors) act as key regulators of neuroinflammation (Skaper et al., 2012). In response to pathological triggers or neuronal damage, immune cells start an innate immune response with the aim to eliminate the initial cause of injury. However, when the cellular activity becomes dysregulated, it results in an inappropriate immune response that can be injurious and affect CNS functions. Thus, limiting neuroinflammation and microglia activity represents a potential strategy to alleviate neuroinflammationrelated diseases. The Research Topic collects 20 manuscripts, divided into five sections, that include both original research articles and reviews of the emerging literature and explore the role of neuroinflammation in various neurological diseases. There is particular attention dedicated to the relevant research exploring the mechanisms and mediators involved in the resolution of neuroinflammation. Our aim was to generate a valuable discussion contributing to identify new therapeutic targets in brain damage and providing new drug development opportunities for the prevention and treatment of CNS diseases involving neuroinflammation

Winter storm risk of residential structures ? model development and application to the German state of Baden-Württemberg

International audienceThe derivation of probabilities of high wind speeds and the establishment of risk curves for storm damage is of prime importance in natural hazard risk analysis. Risk curves allow the assessment of damage being exceeded at a given level of probability. In this paper, a method for the assessment of winter storm damage risk is described in detail and applied to the German state of Baden-Württemberg. Based on meteorological observations of the years 1971?2000 and on damage information of 4 severe storm events, storm hazard and damage risk of residential buildings is calculated on the level of communities. For this purpose, highly resolved simulations of storm wind fields with the Karlsruher Atmospheric Mesoscale Model (KAMM) are performed and a storm damage model is developed. Risk curves including the quantification of the uncertainties are calculated for every community. Local differences of hazard and risk are presented in state-wide maps. An average annual winter storm damage to residential buildings of minimum 15 million Euro (reference year 2000) for Baden-Württemberg is expected

Long-term neuromuscular sequelae of critical illness

In this observational study, we analyzed the long-term neuromuscular deficits of survivors of critical illness. Intensive care unit-acquired muscular weakness (ICU-AW) is a very common complication of critical illness. Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are two main contributors to ICU-AW. ICU-AW is associated with an increased mortality and leads to rehabilitation problems. However, the long-term outcome of ICU-AW and factors influencing it are not well known. We analyzed the medical records of 490 survivors of critical illness, aged 18-75years and located in the area of the study center. Intensive care unit (ICU) survivors with comorbidities that might influence neuromuscular follow-up examinations, muscle strength, or results of nerve conduction studies, such as renal or hepatic insufficiency, diabetes mellitus, or vitamin deficiency were excluded. A total of 51 patients were finally included in the study. Six to 24months after discharge from the ICU, we measured the Medical Research Council (MRC) sum score, the Overall Disability Sum score (ODSS), and also performed nerve conduction studies and EMG. For all ICU survivors, the median MRC sum score was 60 (range 47-60) and the median ODSS score was 0 (range 0-8). CIP was diagnosed in 21 patients (41%). No patient was diagnosed with CIM. Patients with diagnosis of CIP showed a higher median ODSS scores 1 (range 0-8) versus 0 (range 0-5); p<0.001 and lower median MRC sum scores 56 (range 47-60) versus 60 (range 58-60); p<0.001. The three main outcome variables MRC sum score, ODSS score and diagnosis of CIP were not related to age, gender, or diagnosis of sepsis. The MRC sum score (r=−0.33; p=0.02) and the ODSS score (r=0.31; p=0.029) were correlated with the APACHE score. There was a trend for an increased APACHE score in patients with diagnosis of CIP 19 (range 6-33) versus 16.5 (range 6-28); p=0.065. Patients with the diagnosis of CIP had more days of ICU treatment 11days (range 2-74) versus 4days (range 1-61); p=0.015, and had more days of ventilator support 8days (range 1-59) versus 2days (range 1-46); p=0.006. The MRC sum score and the ODSS score were correlated with the days of ICU treatment and with the days of ventilator support. The neuromuscular long-term consequences of critical illness were not severe in our study population. As patients with concomitant diseases and old patients were excluded from this study the result of an overall favorable prognosis of ICU-acquired weakness may not be true for other patient's case-mix. Risk factors for the development of long-term critical illness neuropathy are duration of ICU treatment, duration of ventilator support, and a high APACHE score, but not diagnosis of sepsis. Although ICU-AW can be serious complication of ICU treatment, this should not influence therapeutic decisions, given its favorable long-term prognosis, at least in relatively young patients with no concomitant disease

Effect of anti-inflammatory agents on transforming growth factor beta over-expressing mouse brains: a model revised.

BACKGROUND: The over-expression of transforming growth factor beta-1(TGF-beta1) has been reported to cause hydrocephalus, glia activation, and vascular amyloidbeta (Abeta) deposition in mouse brains. Since these phenomena partially mimic the cerebral amyloid angiopathy (CAA) concomitant to Alzheimer's disease, the findings in TGF-beta1 over-expressing mice prompted the hypothesis that CAA could be caused or enhanced by the abnormal production of TGF-beta1. This idea was in accordance with the view that chronic inflammation contributes to Alzheimer's disease, and drew attention to the therapeutic potential of anti-inflammatory drugs for the treatment of Abeta-elicited CAA. We thus studied the effect of anti-inflammatory drug administration in TGF-beta1-induced pathology. METHODS: Two-month-old TGF-beta1 mice and littermate controls were orally administered pioglitazone, a peroxisome proliferator-activated receptor-gamma agonist, or ibuprofen, a non steroidal anti-inflammatory agent, for two months. Glia activation was assessed by immunohistochemistry and western blot analysis; Abeta precursor protein (APP) by western blot analysis; Abeta deposition by immunohistochemistry, thioflavin-S staining and ELISA; and hydrocephalus by measurements of ventricle size on autoradiographies of brain sections. Results are expressed as means +/- SD. Data comparisons were carried with the Student's T test when two groups were compared, or ANOVA analysis when more than three groups were analyzed. RESULTS: Animals displayed glia activation, hydrocephalus and a robust thioflavin-S-positive vascular deposition. Unexpectedly, these deposits contained no Abeta or serum amyloid P component, a common constituent of amyloid deposits. The thioflavin-S-positive material thus remains to be identified. Pioglitazone decreased glia activation and basal levels of Abeta42- with no change in APP contents - while it increased hydrocephalus, and had no effect on the thioflavin-S deposits. Ibuprofen mimicked the reduction of glia activation caused by pioglitazone and the lack of effect on the thioflavin-S-labeled deposits. CONCLUSIONS: i) TGF-beta1 over-expressing mice may not be an appropriate model of Abeta-elicited CAA; and ii) pioglitazone has paradoxical effects on TGF-beta1-induced pathology suggesting that anti-inflammatory therapy may reduce the damage resulting from active glia, but not from vascular alterations or hydrocephalus. Identification of the thioflavin-S-positive material will facilitate the full appraisal of the clinical implication of the effects of anti-inflammatory drugs, and provide a more thorough understanding of TGF-beta1 actions in brain