Combining Planck with Large Scale Structure gives strong neutrino mass constraint

We present the strongest current cosmological upper limit on the sum of neutrino masses of < 0.18 (95% confidence). It is obtained by adding observations of the large-scale matter power spectrum from the WiggleZ Dark Energy Survey to observations of the cosmic microwave background data from the Planck surveyor, and measurements of the baryon acoustic oscillation scale. The limit is highly sensitive to the priors and assumptions about the neutrino scenario. We explore scenarios with neutrino masses close to the upper limit (degenerate masses), neutrino masses close to the lower limit where the hierarchy plays a role, and addition of massive or massless sterile species.Comment: 7 pages, 4 figures. Found bug in analysis which is fixed in v2. The resulting constraints on M_nu remain very strong. Additional info added on hierarch

Nuclear Factor-κB-Independent Anti-Inflammatory Action of Salicylate in Human Endothelial Cells

In contrast to aspirin, salicylate, its active metabolite, possesses profound anti-inflammatory properties without blocking cyclooxygenase. Inhibition of the transcription factor nuclear factor-κB (NF-κB) has been discussed to play a role in the anti-inflammatory profile of salicylate. However, NF-κB-independent effects of salicylate have been assumed but have up to now been poorly investigated. Therefore, the aim of the present study was to investigate NF-κB-independent anti-inflammatory mechanisms of salicylate in human umbilical vein endothelial cells using interleukin-4 (IL-4) as NF-κB-independent proinflammatory stimulus and P-selectin as inflammatory read-out parameter. Using quantitative real-time reverse transcriptionpolymerase chain reaction, we found that salicylate decreases IL-4-induced P-selectin expression. As judged by Western blot analysis, salicylate increased endothelial heme oxygenase-1 (HO-1) protein levels. Using both the HO-1 inhibitor tin(II) protoporphyrin IX and HO-1 antisense oligonucleotides, we causally linked the induction of HO-1 to the decrease of P-selectin. Moreover, we were interested in the signaling mechanisms leading to the up-regulation of HO-1 by salicylate. c-Jun NH2-terminal kinase (JNK) was found to be activated by salicylate, and we could causally link this activation to the induction of HO-1 by using the JNK inhibitor 1,9-pyrazoloanthrone. By applying activator protein-1 (AP-1) decoys, it was shown that the transcription factor AP-1 is crucially involved in the up-regulation of HO-1 downstream of JNK. In summary, our study introduces HO-1 as novel NF-κB-independent anti-inflammatory target of salicylate in human endothelial cells. Moreover, we elucidated the JNK/AP-1 pathway as crucial for the induction of HO-1 by salicylate

EQUIPARTITION OF FORCES: REVIEW OF A NEW PRINCIPLE FOR PROCESS DESIGN AND OPTIMIZATION

We present a general proof for a design principle developed during the last two years: The principle of equipartition of forces. The principle is derived for parallel, coupled transport processes without restrictions on the phenomenological coefficients. Minimum entropy production is obtained for the total system, when the thermodynamic forces of transport are the same over all parallel paths in the system. We review some of the results obtained so far by application of the principle to distillation columns

Impact of public release of performance data on the behaviour of healthcare consumers and providers.

BACKGROUND: It is becoming increasingly common to publish information about the quality and performance of healthcare organisations and individual professionals. However, we do not know how this information is used, or the extent to which such reporting leads to quality improvement by changing the behaviour of healthcare consumers, providers, and purchasers. OBJECTIVES: To estimate the effects of public release of performance data, from any source, on changing the healthcare utilisation behaviour of healthcare consumers, providers (professionals and organisations), and purchasers of care. In addition, we sought to estimate the effects on healthcare provider performance, patient outcomes, and staff morale. SEARCH METHODS: We searched CENTRAL, MEDLINE, Embase, and two trials registers on 26 June 2017. We checked reference lists of all included studies to identify additional studies. SELECTION CRITERIA: We searched for randomised or non-randomised trials, interrupted time series, and controlled before-after studies of the effects of publicly releasing data regarding any aspect of the performance of healthcare organisations or professionals. Each study had to report at least one main outcome related to selecting or changing care. DATA COLLECTION AND ANALYSIS: Two review authors independently screened studies for eligibility and extracted data. For each study, we extracted data about the target groups (healthcare consumers, healthcare providers, and healthcare purchasers), performance data, main outcomes (choice of healthcare provider, and improvement by means of changes in care), and other outcomes (awareness, attitude, knowledge of performance data, and costs). Given the substantial degree of clinical and methodological heterogeneity between the studies, we presented the findings for each policy in a structured format, but did not undertake a meta-analysis. MAIN RESULTS: We included 12 studies that analysed data from more than 7570 providers (e.g. professionals and organisations), and a further 3,333,386 clinical encounters (e.g. patient referrals, prescriptions). We included four cluster-randomised trials, one cluster-non-randomised trial, six interrupted time series studies, and one controlled before-after study. Eight studies were undertaken in the USA, and one each in Canada, Korea, China, and The Netherlands. Four studies examined the effect of public release of performance data on consumer healthcare choices, and four on improving quality.There was low-certainty evidence that public release of performance data may make little or no difference to long-term healthcare utilisation by healthcare consumers (3 studies; 18,294 insurance plan beneficiaries), or providers (4 studies; 3,000,000 births, and 67 healthcare providers), or to provider performance (1 study; 82 providers). However, there was also low-certainty evidence to suggest that public release of performance data may slightly improve some patient outcomes (5 studies, 315,092 hospitalisations, and 7502 providers). There was low-certainty evidence from a single study to suggest that public release of performance data may have differential effects on disadvantaged populations. There was no evidence about effects on healthcare utilisation decisions by purchasers, or adverse effects. AUTHORS\u27 CONCLUSIONS: The existing evidence base is inadequate to directly inform policy and practice. Further studies should consider whether public release of performance data can improve patient outcomes, as well as healthcare processes

Metalloporphyrins inactivate caspase-3 and -8

Activation of caspases represents one of the earliest biochemical indicators for apoptotic cell death. Therefore, measurement of caspase activity is a widely used and generally accepted method to determine apoptosis in a wide range of in vivo and in vitro settings. Numerous publications characterize the role of the heme-catabolizing enzyme heme oxygenase-1 (HO-1) in regulating apoptotic processes. Different metalloporphyrins representing inducers and inhibitors of this enzyme are often used, followed by assessment of apoptotic cell death. In the present work, we found that caspase-3-like activity, as well as activity of caspase-8 measured in either Fas (CD95) ligand-treated Jurkat T-lymphocytes or by the use of recombinant caspase-3 or -8, was inhibited by different metalloporphyrins (cobalt(III) protoporphyrin IX, tin and zinc II) protoporphyrin-IX). Moreover, employing the mouse model of Fas-induced liver apoptosis these properties of porphyrins could also be demonstrated in vivo. The metalloporphyrins were shown to inhibit caspase-3-mediated PARP cleavage. Molecular modeling studies demonstrated that porphyrins can occupy the active site of caspase-3 in an energetically favorable manner and in a binding mode similar to that of known inhibitors. The data shown here introduce metalloporphyrins as direct inhibitors of caspase activity. This finding points to the need for careful employment of metalloporphyrins as modulators of HO-1