Energy Options for Future Humans on Titan

We review the possibilities for in situ energy resources on Titan for use by future humans, including chemical, nuclear, wind, solar, geothermal and hydropower. All of these options, with the possible exception of geothermal, represent effective sources of power. Combustion of methane (after electrolysis of the native water), in combination with another source of power such as nuclear, is a viable option; another chemical source of energy is the hydrogenation of acetylene. The large seas Kraken and Ligeia potentially represent effective sources of hydropower. Wind power, particularly at altitudes ~40 km, is expected to be productive. Despite the distance from the sun and the absorbing atmosphere, solar power is (as on Earth) an extremely efficient source of power on Titan

Experience Corps: Pathway to New Engagement

Experience Corps: Pathway to New Engagemen

IL-4/IL-13-Dependent and Independent Expression of miR-124 and Its Contribution to M2 Phenotype of Monocytic Cells in Normal Conditions and during Allergic Inflammation

Monocytic cells exhibit a high level of heterogeneity and have two distinct modes of their activation: 1) classical M1 path associated with inflammation and tissue damage, and 2) alternative M2 path. Although it has been demonstrated that M2 macrophages play an important role in the regulation of the allergic immune responses, tissue maintenance and repair, little is known about the mechanisms that determine the M2 phenotype. We have previously shown that miR-124 is expressed in microglia that exhibit the M2 phenotype and overexpression of miR-124 in macrophages resulted in downregulation of a number of M1 markers (MHC class II, CD86) and up-regulation of several M2 markers (Fizz1, Arg1). We further investigated whether the polarization of macrophages towards the M2 phenotype induced miR-124 expression. We found that exposure of cells to IL-4 and IL-13 resulted in the upregulation of miR-124 in macrophages. We also demonstrated that IL-4 induced expression of three miR-124 precursor transcripts with predominant expression of pri-miR-124.3, suggesting regulation of miR-124 expression by IL-4 on a transcriptional level. Expression of miR-124 in microglia did not depend on IL-4 and/or IL-13, whereas expression of miR-124 in lung resident macrophages was IL-4 and IL-13-dependent and was upregulated by systemic administration of IL-4 or during allergic inflammation. Upregulation of several M2 markers (CD206, Ym1) and downregulation of the M1 markers (CD86, iNOS, TNF) in M2-polarized macrophages was abrogated by a miR-124 inhibitor, suggesting that this microRNA contributed to the M2 phenotype development and maintenance. Finally we showed that human CD14+CD16+ intermediate monocytes, which are found in increased numbers in patients with allergies and bronchial asthma, expressed high levels of miR-124 and exhibited other properties of M2-like cells. Thus, our study suggests that miR-124 serves as a regulator of the M2 polarization in various subsets of monocytic cells both in vitro and in vivo

Glatiramer Acetate (Copaxone) Modulates Platelet Activation and Inhibits Thrombin-Induced Calcium Influx: Possible Role of Copaxone in Targeting Platelets during Autoimmune Neuroinflammation

Background: Glatiramer acetate (GA, Copaxone, Copolymer-1) is an FDA approved drug for the treatment of MS and it is very effective in suppressing neuroinflammation in experimental autoimmune encephalitis (EAE), an animal model of MS. Although this drug was designed to inhibit pathogenic T cells, the exact mechanism of EAE/MS suppression by GA is still not well understood. Previously we presented evidence that platelets become activated and promote neuroinflammation in EAE, suggesting a possible pathogenic role of platelets in MS and EAE. We hypothesized that GA could inhibit neuroinflammation by affecting not only immune cells but also platelets. Methodology/Principal Findings We investigated the effect of GA on the activation of human platelets in vitro: calcium influx, platelet aggregation and expression of activation markers. Our results in human platelets were confirmed by in-vitro and in-vivo studies of modulation of functions of platelets in mouse model. We found that GA inhibited thrombin-induced calcium influx in human and mouse platelets. GA also decreased thrombin-induced CD31, CD62P, CD63, and active form of αIIbβ3 integrin surface expression and formation of platelet aggregates for both mouse and human platelets, and prolonged the bleeding time in mice by 2.7-fold. In addition, we found that GA decreased the extent of macrophage activation induced by co-culture of macrophages with platelets. Conclusions: GA inhibited the activation of platelets, which suggests a new mechanism of GA action in suppression of EAE/MS by targeting platelets and possibly preventing their interaction with immune cells such as macrophages. Furthermore, the reduction in platelet activation by GA may have additional cardiovascular benefits to prevent thrombosis

Analysis of a Standardized Suicide Intervention Training for Counselor Trainees

The present study evaluates the impact of an evidence-based suicide intervention model and how pedagogical practices of counselor education programs may prepare counselors-in-training (CIT) to respond to clients who are considering suicide. Using content analysis to explore pre and post-training data, the researchers examined the impact of the 14-hour evidence-based Applied Suicide Intervention Skills Training (ASIST) on 54 CITs (76% female, 24% male; 58% White, 20% African American, 11% Latinx/Hispanic, 11% Other), with a mean age of 30 years (SD =8.6). Further data were collected 6 months later, after CITs had the opportunity to utilize suicide intervention skills during their clinical experiences. Content analysis yielded several changes between pre- and post-training data which elucidate the process of suicide intervention skill acquisition. CITs also reported having frequently applied their skills during clinical internship with clients considering suicide. Findings support the use of ASIST in the preparation of future counselors

Self-Management Strategies Mediate Self-Efficacy and Physical Activity

Self-efficacy theory proposes that girls who have confidence in their capability to be physically active will perceive fewer barriers to physical activity or be less influenced by them, be more likely to pursue perceived benefits of being physically active, and be more likely to enjoy physical activity. Self-efficacy is theorized also to influence physical activity through self-management strategies (e.g., thoughts, goals, plans, and acts) that support physical activity, but this idea has not been empirically tested

Neuronal extracellular microRNAs miR-124 and miR-9 mediate cell-cell communication between neurons and microglia

In contrast to peripheral macrophages, microglia in the central nervous system (CNS) exhibit a specific deactivated phenotype; however, it is not clear how this phenotype is maintained. Two alternative hypotheses were postulated recently: (a) microglia differ from peripheral macrophages being derived from the yolk sac (YS), whereas peripheral macrophages originate from bone marrow (BM); (b) microglia acquire a specific phenotype under the influence of the CNS microenvironment. We have previously shown that microglia express miR-124, which was also induced in BM-derived macrophages co-cultured with a neurons. We here investigated the possibility of horizontal transfer of the neuron-specific microRNAs miR-124 and miR-9 from primary neurons to microglia/macrophages. We found that after incubation with neuronal conditioned media (NCM), macrophages downregulated activation markers MHC class II and CD45. Neither cultured adult microglia nor YS- and BM-derived macrophages demonstrated intrinsic levels of miR-124 expression. However, after incubation with NCM, miR-124 was induced in both YS- and BM-derived macrophages. Biochemical analysis demonstrated that the NCM contained miR-124 and miR-9 in complex with small proteins, large high-density lipoproteins (HDLs), and exosomes. MiR-124 and miR-9 were promptly released from neurons, and this process was inhibited by tetrodotoxin, indicating an important role of neuronal electric activity in secretion of these microRNAs. Incubation of macrophages with exogenous miR-124 resulted in efficient translocation of miR-124 into the cytoplasm. This study demonstrates an important role of neuronal miRNAs in communication of neurons with microglia, which favors the hypothesis that microglia acquire a specific phenotype under the influence of the CNS microenvironment