A Thermodynamics Analysis for Improvement of Carbon Dioxide Removal Technologies for Space

The carbon dioxide removal assembly (CDRA) has been used for the past two decades to continually remove carbon dioxide (CO2) as part of the air revitalization system onboard the international space station (ISS). The CDRA is an adsorption-based system that relies on sorbent materials that require a significant energy input to be thermally regenerated. Additionally, the system faces challenges in reliability and size/weight, so it is being re-evaluated for viability beyond-lowearth-orbit missions. The CDRA removes CO2 from the cabin air through a cyclical adsorption-desorption process that uses four molecular sieve beds. The main components include two desiccant beds to remove H2O, two CO2 zeolite sorbent beds, an air blower, two resistive heaters, and a cooling heat exchanger. Past studies on the CDRA primarily focus on predictive physics-based modeling of the sorbent beds to understand reliability, performance, and sorbent kinetics, with very few performing a thermodynamic analysis of the entire system. This study aims to improve the understanding of component-level losses of the CDRA using exergy destruction analysis and to quantify the losses. We developed a thermodynamics black-box model using a first and second law balances over each individual component over one operational cycle. The results indicate that the molecular sieve sorbent beds are major contributors to lost work within the CDRA. However, the total exergy destruction in the desiccant beds is greater than the sorbent beds. This indicates that the desiccant beds are the largest contributor of losses. Removing water prior to the removal of CO2 from the flow stream is a necessary step because the zeolite sorbent will preferentially adsorb water. Our findings motivate the use of alternative components that may offer direct separation of water at higher efficiencies

Public perceptions of forests across Italy: An exploratory national survey

In a context of progressive expansion of the Italian forest area, we present the results of a national survey exploring public perception of forests across different geographical scales in Italy. Perceptions of forests are assessed in rela-tion to popular beliefs on relevant environmental issues such as countering climate change, protecting biodiversity, and promoting social cohesion and environmental education. Participants (N = 1059) living in five different regions of Northern (Trentino-Alto Adige/Südtirol, Piemonte), Central (Lazio, Molise) and Southern Italy (Puglia), were recruited in the survey and completed a paper-and-pencil questionnaire. Survey questions regarded the estimated percentage of forest cover, the perceived importance of different environmental issues and of different material and non-material forest products, as well as partici-pants’ perceptions regarding connectedness to nature. Results revealed a gen-eralized tendency to overestimate the extension of forest surface area in the participants’ region, in Italy, and in the European Union. Results also showed high scores for participants’ perceived importance of environmental issues, such as climate change and biodiversity protection, and in their belief that forests could play a positive role in addressing these issues and providing im-portant outcomes and benefits for the quality of human life, such as health and well-being or social cohesion

A saturated consensus linkage map of Picea abies including AFLP, SSR, STS, 5S rDNA and morphological markers

International audienc

A novel mitochondrial Kv1.3-caveolin axis controls cell survival and apoptosis

The voltage-gated potassium channel Kv1.3 plays an apparent dual physiological role by participating in activation and proliferation of leukocytes as well as promoting apoptosis in several types of tumor cells. Therefore, Kv1.3 is considered a potential pharmacological target for immunodeficiency and cancer. Different cellular locations of Kv1.3, at the plasma membrane or the mitochondria, could be responsible for such duality. While plasma membrane Kv1.3 facilitates proliferation, the mitochondrial channel modulates apoptotic signaling. Several molecular determinants of Kv1.3 drive the channel to the cell surface, but no information is available about its mitochondrial targeting. Caveolins, which are able to modulate cell survival, participate in the plasma membrane targeting of Kv1.3. The channel, via a caveolin-binding domain (CDB), associates with caveolin 1 (Cav1), which localizes Kv1.3 to lipid raft membrane microdomains. The aim of our study was to understand the role of such interactions not only for channel targeting but also for cell survival in mammalian cells. By using a caveolin association-deficient channel (Kv1.3 CDBless), we demonstrate here that while the Kv1.3-Cav1 interaction is responsible for the channel localization in the plasma membrane, a lack of such interaction accumulates Kv1.3 in the mitochondria. Kv1.3 CDBless severely affects mitochondrial physiology and cell survival, indicating that a functional link of Kv1.3 with Cav1 within the mitochondria modulates the pro-apoptotic effects of the channel. Therefore, the balance exerted by these two complementary mechanisms fine-tune the physiological role of Kv1.3 during cell survival or apoptosis. Our data highlight an unexpected role for the mitochondrial caveolin-Kv1.3 axis during cell survival and apoptosis

LAT-1 and GLUT-1 Carrier Expression and Its Prognostic Value in Gastroenteropancreatic Neuroendocrine Tumors

Cancer cells develop mechanisms that increase nutrient uptake, including key nutrient carriers, such as amino acid transporter 1 (LAT-1) and glucose transporter 1 (GLUT-1), regulated by the oxygen-sensing Von Hippel Lindau-hypoxia-inducible factor (VHL-HIF) transcriptional pathway. We aimed to analyze these metabolic players in gastroenteropancreatic neuroendocrine tumors (GEP-NET) and correlate them with tumor malignancy and progression. LAT-1, GLUT-1, and pVHL expression was analyzed in 116 GEP-NETs and 48 peritumoral tissue samples by immunohistochemistry. LAT-1 was stably silenced using specific shRNA in the human NET BON cell line. LAT-1 expression was significantly increased in tumor tissue compared to non-tumor tissue in both gastrointestinal (67% vs. 44%) and pancreatic NETs (54% vs. 31%). Similarly, GLUT-1 was substantially elevated in gastrointestinal (74% vs. 19%) and pancreatic (58% vs. 4%) NETs. In contrast, pVHL expression was decreased (85% vs. 58%) in pancreatic NETs. Tumors with metastases at diagnosis displayed increased LAT-1 and GLUT-1 and decreased pVHL expression (p < 0.001). In accordance with these data, silencing LAT-1 curtailed cell proliferation in BON cells. These findings suggest that specific mechanisms that increase nutrient uptake, such as LAT-1 and GLUT-1, are increased in GEP-NETs, whereas pVHL is decreased. These markers might be related to the proliferation and metastatic capacity of these tumors