Dynamics of the pedestal transport during edge localized mode cycles at ASDEX Upgrade

The dynamic behaviour of the ion and electron energy, particle and momentum transport measured during type-I edge localized mode (ELM) cycles at ASDEX Upgrade is presented. Fast measurements of the ion and electron temperature profiles revelead that the ion and electron energy transport recover on different timescales, with the electrons recovering on a slower timescale (Cavedon et al 2017 Plasma Phys. Control. Fusion 59 105007). The dominant mechanism for the additional energy transport in the electron channel that could cause the delay in the electron temperature gradient (VTe) recovery is attributed to the depletion of energy caused by the ELM. The local sources and sinks for the electron channel in the steep gradient region are much smaller compared to the energy flux arriving from the pedestal top, indicating that the core plasma may dictate the local dynamics of the VTe recovery during the ELM cycle. A model for the edge momentum transport based on toroidal torque balance that takes into account the existence of poloidal impurity asymmetries has been developed. The analysis of the profile evolution during the ELM cycle shows that the model captures the dynamics of the rotation both before the ELM crash and during the recovery phase.European Commission (Euratom) Grant agreement No. 633053H2020 Marie-Sklodowska Curie programme (grant agreement No. 708257)European Union’s Horizon 2020 (grant agreement No. 805162

Interferon γ–Induced Human Guanylate Binding Protein 1 Inhibits Mammary Tumor Growth in Mice

Interferon γ (IFN-γ) has recently been implicated in cancer immunosurveillance. Among the most abundant proteins induced by IFN-γ are guanylate binding proteins (GBPs), which belong to the superfamily of large GTPases and are widely expressed in various species. Here, we investigated whether the well-known human GBP-1 (hGBP-1), which has been shown to exert antiangiogenic activities and was described as a prognostic marker in colorectal carcinomas, may contribute to an IFN-γ–mediated tumor defense. To this end, an IFN-independent, inducible hGBP-1 expression system was established in murine mammary carcinoma (TS/A) cells, which were then transplanted into syngeneic immune-competent Balb/c mice. Animals carrying TS/A cells that had been given doxycycline for induction of hGBP-1 expression revealed a significantly reduced tumor growth compared with mock-treated mice. Immunohistochemical analysis of the respective tumors demonstrated a tightly regulated, high-level expression of hGBP-1. No signs of an enhanced immunosurveillance were observed by investigating the number of infiltrating B and T cells. However, hemoglobin levels as well as the number of proliferating tumor cells were shown to be significantly reduced in hGBP-1–expressing tumors. This finding corresponded to reduced amounts of vascular endothelial growth factor A (VEGF-A) released by hGBP-1–expressing TS/A cells in vitro and reduced VEGF-A protein levels in the corresponding mammary tumors in vivo. The results suggest that hGBP-1 may contribute to IFN-γ–mediated antitumorigenic activities by inhibiting paracrine effects of tumor cells on angiogenesis. Consequently, owing to these activities GBPs might be considered as potent members in an innate, IFN-γ–induced antitumoral defense system

Limitation of life support techniques at admission to the intensive care unit: a multicenter prospective cohort study

Purpose: To determine the frequency of limitations on life support techniques (LLSTs) on admission to intensive care units (ICU), factors associated, and 30-day survival in patients with LLST on ICU admission. Methods: This prospective observational study included all patients admitted to 39 ICUs in a 45-day period in 2011. We recorded hospitals’ characteristics (availability of intermediate care units, usual availability of ICU beds, and financial model) and patients’ characteristics (demographics, reason for admission, functional status, risk of death, and LLST on ICU admission (withholding/withdrawing; specific techniques affected)). The primary outcome was 30-day survival for patients with LLST on ICU admission. Statistical analysis included multilevel logistic regression models. Results: We recruited 3042 patients (age 62.5 ± 16.1 years). Most ICUs (94.8%) admitted patients with LLST, but only 238 (7.8% [95% CI 7.0–8.8]) patients had LLST on ICU admission; this group had higher ICU mortality (44.5 vs. 9.4% in patients without LLST; p < 0.001). Multilevel logistic regression showed a contextual effect of the hospital in LLST on ICU admission (median OR = 2.30 [95% CI 1.59–2.96]) and identified the following patient-related variables as independent factors associated with LLST on ICU admission: age, reason for admission, risk of death, and functional status. In patients with LLST on ICU admission, 30-day survival was 38% (95% CI 31.7–44.5). Factors associated with survival were age, reason for admission, risk of death, and number of reasons for LLST on ICU admission. Conclusions: The frequency of ICU admission with LLST is low but probably increasing; nearly one third of these patients survive for ≥ 30 days

Copernicus Marine Service Ocean State Report, Issue 3 Introduction

International audienc

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field