Simulating the effects of mid- to upper-tropospheric clouds on microwave emissions in EC-Earth using COSP

In this work, the Cloud Feedback Model Intercomparison (CFMIP) Observation Simulation Package (COSP) is expanded to include scattering and emission effects of clouds and precipitation at passive microwave frequencies. This represents an advancement over the official version of COSP (version 1.4.0) in which only clear-sky brightness temperatures are simulated. To highlight the potential utility of this new microwave simulator, COSP results generated using the climate model EC-Earth's version 3 atmosphere as input are compared with Microwave Humidity Sounder (MHS) channel (190.311 GHz) observations. Specifically, simulated seasonal brightness temperatures (TB) are contrasted with MHS observations for the period December 2005 to November 2006 to identify possible biases in EC-Earth's cloud and atmosphere fields. The EC-Earth's atmosphere closely reproduces the microwave signature of many of the major large-scale and regional scale features of the atmosphere and surface. Moreover, greater than 60 % of the simulated TB are within 3 K of the NOAA-18 observations. However, COSP is unable to simulate sufficiently low TB in areas of frequent deep convection. Within the Tropics, the model's atmosphere can yield an underestimation of TB by nearly 30 K for cloudy areas in the ITCZ. Possible reasons for this discrepancy include both incorrect amount of cloud ice water in the model simulations and incorrect ice particle scattering assumptions used in the COSP microwave forward model. These multiple sources of error highlight the non-unique nature of the simulated satellite measurements, a problem exacerbated by the fact that EC-Earth lacks detailed micro-physical parameters necessary for accurate forward model calculations. Such issues limit the robustness of our evaluation and suggest a general note of caution when making COSP-satellite observation evaluations.

Non-genomic actions of estrogens and their interaction with genomic actions in the brain

Ligands for the nuclear receptor superfamily have at least two mechanisms of action: (a) classical transcriptional regulation of target genes (genomic mechanisms); and (b) non-genomic actions, which are initiated at the cell membrane, which could also impact transcription. Though transcriptional mechanisms are increasingly well understood, membrane-initiated actions of these ligands are incompletely understood. This has led to considerable debate over the physiological relevance of membrane-initiated actions of hormones versus genomic actions of hormones, with genomic actions predominating in the endocrine field. There is good evidence that the membrane-limited actions of hormones, particularly estrogens, involve the rapid activation of kinases and the release of calcium and that these are linked to physiologically relevant scenarios in the brain. We show evidence in this review, that membrane actions of estrogens, which activate these rapid signaling cascades, can also potentiate nuclear transcription in both the central nervous system and in non-neuronal cell lines. We present a theoretical scenario which can be used to understand this phenomenon. These signaling cascades may occur in parallel or in series but subsequently, converge at the modification of transcriptionally relevant molecules such as nuclear receptors and/or coactivators. In addition, other non-cognate hormones or neurotransmitters may also activate cascades to crosstalk with estrogen receptor-mediated transcription, though the relevance of this is less clear. The idea that coupling between membrane-initiated and genomic actions of hormones is a novel idea in neuroendocrinology and provides us with a unified view of hormone action in the central nervous system.