Connecting the astronomical testbed community -- the CAOTIC project: Optimized teaching methods for software version control concepts

Laboratory testbeds are an integral part of conducting research and developing technology for high-contrast imaging and extreme adaptive optics. There are a number of laboratory groups around the world that use and develop resources that are imminently required for their operations, such as software and hardware controls. The CAOTIC (Community of Adaptive OpTics and hIgh Contrast testbeds) project is aimed to be a platform for this community to connect, share information, and exchange resources in order to conduct more efficient research in astronomical instrumentation, while also encouraging best practices and strengthening cross-team connections. In these proceedings, we present the goals of the CAOTIC project, our new website, and we focus in particular on a new approach to teaching version control to scientists, which is a cornerstone of successful collaborations in astronomical instrumentation.Comment: 15 pages, 6 figures, 2 tables; SPIE proceedings Astronomical Telescopes + Instrumentation 2022, 12185-11

Class Is Not Dead! It Has Been Buried Alive

By means of a reanalysis of the most relevant data source—the International Social Mobility and Politics File—this article criticizes the newly grown consensus in political sociology that class voting has declined since World War II. An increase in crosscutting cultural voting, rooted in educational differences rather than a decline in class voting, proves responsible for the decline of traditional class-party alignments. Moreover, income differences have not become less but more consequential for voting behavior during this period. It is concluded that the new consensus has been built on quicksand. Class is not dead—it has been buried alive under the increasing weight of cultural voting, systematically misinterpreted as a decline in class voting because of the widespread application of the so-called Alford index

Metabolism within the tumor microenvironment and its implication on cancer progression: an ongoing therapeutic target

Since reprogramming energy metabolism is considered a new hallmark of cancer, tumor metabolism is again in the spotlight of cancer research. Many studies have been carried out and many possible therapies have been developed in the last years. However, tumor cells are not alone. A series of extracellular components and stromal cells, such as endothelial cells, cancer-associated fibroblasts, tumor-associated macrophages and tumor-infiltrating T cells, surround tumor cells in the so-called tumor microenvironment. Metabolic features of these cells are being studied in deep in order to find relationships between metabolism within the tumor microenvironment and tumor progression. Moreover, it cannot be forgotten that tumor growth is able to modulate host metabolism and homeostasis, so that tumor microenvironment is not the whole story. Importantly, the metabolic switch in cancer is just a consequence of the flexibility and adaptability of metabolism and should not be surprising. Treatments of cancer patients with combined therapies including anti-tumor agents with those targeting stromal cell metabolism, anti-angiogenic drugs and/or immunotherapy are being developed as promising therapeutics.Mª Carmen Ocaña is recipient of a predoctoral FPU grant from the Spanish Ministry of Education, Culture and Sport. Supported by grants BIO2014-56092-R (MINECO and FEDER), P12-CTS-1507 (Andalusian Government and FEDER) and funds from group BIO-267 (Andalusian Government). The "CIBER de Enfermedades Raras" is an initiative from the ISCIII (Spain). The funders had no role in the study design, data collection and analysis, decision to publish or preparation of the manuscript

Evasion of anti-growth signaling: a key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds

The evasion of anti-growth signaling is an important characteristic of cancer cells. In order to continue to proliferate, cancer cells must somehow uncouple themselves from the many signals that exist to slow down cell growth. Here, we define the anti-growth signaling process, and review several important pathways involved in growth signaling: p53, phosphatase and tensin homolog (PTEN), retinoblastoma protein (Rb), Hippo, growth differentiation factor 15 (GDF15), AT-rich interactive domain 1A (ARID1A), Notch, insulin-like growth factor (IGF), and Krüppel-like factor 5 (KLF5) pathways. Aberrations in these processes in cancer cells involve mutations and thus the suppression of genes that prevent growth, as well as mutation and activation of genes involved in driving cell growth. Using these pathways as examples, we prioritize molecular targets that might be leveraged to promote anti-growth signaling in cancer cells. Interestingly, naturally-occurring phytochemicals found in human diets (either singly or as mixtures) may promote anti-growth signaling, and do so without the potentially adverse effects associated with synthetic chemicals. We review examples of naturally-occurring phytochemicals that may be applied to prevent cancer by antagonizing growth signaling, and propose one phytochemical for each pathway. These are: epigallocatechin-3-gallate (EGCG) for the Rb pathway, luteolin for p53, curcumin for PTEN, porphyrins for Hippo, genistein for GDF15, resveratrol for ARID1A, withaferin A for Notch and diguelin for the IGF1-receptor pathway. The coordination of anti-growth signaling and natural compound studies will provide insight into the future application of these compounds in the clinical setting

The co-receptor signaling model of HIV-1 pathogenesis in peripheral CD4 T cells

HIV-mediated CD4 depletion is the hallmark of AIDS and is the most reliable predictor of disease progression. While HIV replication is associated with CD4 depletion in general, plasma viremia by itself predicts the rate of CD4 loss only minimally in untreated patients. To resolve this paradox, I hypothesize the existence of a subpopulation of R5X4-signaling viruses. I also suggest that the gradual evolution and emergence of this subpopulation are largely responsible for the slow depletion of peripheral CD4 T cells

Inactivation of Effector Caspases through Nondegradative Polyubiquitylation

Ubiquitin-mediated inactivation of caspases has long been postulated to contribute to the regulation of apoptosis. However, detailed mechanisms and functional consequences of caspase ubiquitylation have not been demonstrated. Here we show that the Drosophila Inhibitor of Apoptosis 1, DIAP1, blocks effector caspases by targeting them for polyubiquitylation and nonproteasomal inactivation. We demonstrate that the conjugation of ubiquitin to drICE suppresses its catalytic potential in cleaving caspase substrates. Our data suggest that ubiquitin conjugation sterically interferes with substrate entry and reduces the caspase’s proteolytic velocity. Disruption of drICE ubiquitylation, either by mutation of DIAP1’s E3 activity or drICE’s ubiquitin-acceptor lysines, abrogates DIAP1’s ability to neutralize drICE and suppress apoptosis in vivo. We also show that DIAP1 rests in an “inactive” conformation that requires caspase-mediated cleavage to subsequently ubiquitylate caspases. Taken together, our findings demonstrate that effector caspases regulate their own inhibition through a negative feedback mechanism involving DIAP1 “activation” and nondegradative polyubiquitylation

On policy feedback: insights from survey experiments

In comparative social science, policy feedback has become a widely popular device with which to understand policy persistence and the impacts of state-making and political entrepreneurship on mass opinion. Although the existence of such effects is frequently taken for granted, recent work has challenged prevailing assumptions about the unproblematic nature of feedback from policy change to mass opinion. This is an opportune time to put policy feedback to further test. We do so by bringing to bear the two main theoretical perspectives that underlie established and recent scholarship, and applying for the first time survey experiments to evaluate key expectations. Focusing on the relatively novel domain of counter-terrorism policy, we analyze data drawn from a national survey conducted in 2009. Results from embedded experiments suggest new evidence for policy feedback effects. Analysis of mechanisms suggests limits in interest-centered explanations, and the relevance of some under-studied, cognitive factors. We discuss implications and limits of our study for policy feedback scholarship, and with further reference to the case of U.S. attitudes toward the war on terror.This research was supported by grants from the National Science Foundation (SES‐0830917), the Russell Sage Foundation (RSF-83-08-04), and the Spanish Ministry of Education (Juan dela Cierva program) from the research project "Welfare Attitudes in a Changing Europe" (CSO2008-02874- E/SOCI).Peer reviewe