Sponsoring the Next Generation: Parental Willingness to Pay for Higher Education

Although sociologists and economists have been widely concerned with parental investment in children, that investment has rarely been examined directly. The Parent Survey of the High School and Beyond data set provides material for examining the traits of parents and children that shape parental payment for higher education. Parents\u27 reported willingness and ability to pay, along with savings for children\u27s future education, are shaped first by total income and the number of children who must share that income. Moreover, parental investment in higher education is increased when the parents themselves received parental financial support, which suggests continuity over generations. Gender of parent and child, academic achievement of child, marital status, education, and educational aspirations have more mixed and weaker effects. These findings cause a rethinking of the mechanisms of intergenerational influence as seen by status-attainment, human capital, and resource-dilution perspectives

Laboratory and Field Evaluation of Candidate Tick Repellent Materials to Be Used in the Formulation of Aerosol Bombs

Entomolog

Mechanistic Studies on Selective Trimerization of Linear α-Olefins over a Supported Titanium Catalyst

The supported titanium catalyst s(FI)Ti, generated by adding (FI)TiCl3 to MAO-treated SiO2 (FI = (N-(5-methyl-3-(1-adamantyl)salicylidene)-2’-(2”-methoxyphenyl)anilinato)], effects the selective trimerization of the linear α-olefins (LAOs) propene, 1-pentene, 1-hexene, 1-decene, with >95% selectivity for trimers and ~85% selectivity to a single isomer thereof (2,3,5-trialkyl-1-hexene). Mechanistic interpretations are offered for the high regioselectivity as well as for some unusual kinetics behavior, including third-order dependence on LAO concentration and nearly identical initial rates at 0 and 25 °C

Exploring the Future of Human Factors Education; Online Learning, MOOCs, Next Generation Standards, and the Technological Skills We Need to Impart

The objective of this panel was to examine how the future of human factors education is changing given the influx of technology, a push for online learning, and adapting to the changing market. The panel will begin by Heather Lum briefly giving an overview and the precipice for this discussion panel. The panelists then provided their views and experiences regarding this topic. Kelly Steelman will discuss the potential for MOOCs and other online formats to create faster and more flexible postgraduate programs. Christina Frederick will discuss her perspectives on the technological skills we should be equipping our human factors graduates with to be successful. Nathan Sonnenfeld will give his unique take on this as an undergraduate student currently obtaining a human factors education. Susan Amato-Henderson will discuss the Next Generation Science Standards and the ramifications for educators. Lastly, Thomas Smith will focus on the advantages and disadvantages of online learning at the K-12 level. Dr. Lum will foster discussion among the panelists and questions from the general audience. Discussion time: 90 minutes

Public expectations of disaster information provided by critical infrastructure operators: lessons learned from Barreiro, Portugal

© Springer International Publishing AG 2017. Previous research into the role of social media in crisis communication has tended to focus on how sites such as Twitter are used by emergency managers and the public rather than other key stakeholders, such as critical infrastructure (CI) operators. This paper sets out to address this gap by examining Barreiro residents’ expectations of disaster communication from CI operators through the use of an online questionnaire and comparing the results to the current practices of the Barreiro Municipal Water Network, which were examined via an in person interview. The findings suggest that the public expect CI operators to communicate via traditional and social media and that the Barreiro Municipal Water Network should expand their current practices to include digital media

High Erk-1 activation and Gadd45a expression as prognostic markers in high risk pediatric haemolymphoproliferative diseases

Studies on activated cell-signaling pathways responsible for neoplastic transformation are numerous in solid tumors and in adult leukemias. Despite of positive results in the evolution of pediatric hematopoietic neoplasias, there are some high-risk subtypes at worse prognosis. The aim of this study was to asses the expression and activation status of crucial proteins involved in cell-signaling pathways in order to identify molecular alterations responsible for the proliferation and/or escape from apoptosis of leukemic blasts. The quantitative and qualitative expression and activation of Erk-1, c-Jun, Caspase8, and Gadd45a was analyzed, by immunocytochemical (ICC) and western blotting methods, in bone marrow blasts of 72 patients affected by acute myeloid leukemia (AML), T-cell acute lymphoblastic leukemia (ALL) and stage IV non-Hodgkin Lymphoma (NHL). We found an upregulation of Erk-1, Caspase8, c-Jun, and Gadd45a proteins with a constitutive activation in 95.8%, 91.7%, 86.2%, 83.4% of analyzed specimens, respectively. It is worth noting that all AML patients showed an upregulation of all proteins studied and the high expression of GADD45a was associated to the lowest DFS median (p = 0.04). On univariate analysis, only Erk-1 phosphorylation status was found to be correlated with a significantly shorter 5-years DFS in all disease subgroups (p = 0.033) and the lowest DFS median in ALL/NHL subgroup (p = 0.04). Moreover, the simultaneous activation of multiple kinases, as we found for c-Jun and Erk-1 (r = 0.26; p = 0.025), might synergistically enhance survival and proliferation potential of leukemic cells. These results demonstrate an involvement of these proteins in survival of blast cells and, consequently, on relapse percentages of the different subgroups of patients

The immune cell landscape in kidneys of patients with lupus nephritis.

Lupus nephritis is a potentially fatal autoimmune disease for which the current treatment is ineffective and often toxic. To develop mechanistic hypotheses of disease, we analyzed kidney samples from patients with lupus nephritis and from healthy control subjects using single-cell RNA sequencing. Our analysis revealed 21 subsets of leukocytes active in disease, including multiple populations of myeloid cells, T cells, natural killer cells and B cells that demonstrated both pro-inflammatory responses and inflammation-resolving responses. We found evidence of local activation of B cells correlated with an age-associated B-cell signature and evidence of progressive stages of monocyte differentiation within the kidney. A clear interferon response was observed in most cells. Two chemokine receptors, CXCR4 and CX3CR1, were broadly expressed, implying a potentially central role in cell trafficking. Gene expression of immune cells in urine and kidney was highly correlated, which would suggest that urine might serve as a surrogate for kidney biopsies

Regulation of cell survival by sphingosine-1-phosphate receptor S1P1 via reciprocal ERK-dependent suppression of bim and PI-3-kinase/protein kinase C-mediated upregulation of Mcl-1

Although the ability of bioactive lipid sphingosine-1-phosphate (S1P) to positively regulate anti-apoptotic/pro-survival responses by binding to S1P1 is well known, the molecular mechanisms remain unclear. Here we demonstrate that expression of S1P1 renders CCL39 lung fibroblasts resistant to apoptosis following growth factor withdrawal. Resistance to apoptosis was associated with attenuated accumulation of pro-apoptotic BH3-only protein Bim. However, although blockade of extracellular signal-regulated kinase (ERK) activation could reverse S1P1-mediated suppression of Bim accumulation, inhibition of caspase-3 cleavage was unaffected. Instead S1P1-mediated inhibition of caspase-3 cleavage was reversed by inhibition of phosphatidylinositol-3-kinase (PI3K) and protein kinase C (PKC), which had no effect on S1P1 regulation of Bim. However, S1P1 suppression of caspase-3 was associated with increased expression of anti-apoptotic protein Mcl-1, the expression of which was also reduced by inhibition of PI3K and PKC. A role for the induction of Mcl-1 in regulating endogenous S1P receptor-dependent pro-survival responses in human umbilical vein endothelial cells was confirmed using S1P receptor agonist FTY720-phosphate (FTY720P). FTY720P induced a transient accumulation of Mcl-1 that was associated with a delayed onset of caspase-3 cleavage following growth factor withdrawal, whereas Mcl-1 knockdown was sufficient to enhance caspase-3 cleavage even in the presence of FTY720P. Consistent with a pro-survival role of S1P1 in disease, analysis of tissue microarrays from ER+ breast cancer patients revealed a significant correlation between S1P1 expression and tumour cell survival. In these tumours, S1P1 expression and cancer cell survival were correlated with increased activation of ERK, but not the PI3K/PKB pathway. In summary, pro-survival/anti-apoptotic signalling from S1P1 is intimately linked to its ability to promote the accumulation of pro-survival protein Mcl-1 and downregulation of pro-apoptotic BH3-only protein Bim via distinct signalling pathways. However, the functional importance of each pathway is dependent on the specific cellular context