An examination of persistence in charitable giving to education through the 2002 economic downturn

Using three waves of the Center on Philanthropy Panel Study, a module of the Panel Study of Income Dynamics, fi elded by the Institute for Social Research at the University of Michigan, we examine characteristics of donors who gave to any level of education in each of the years studied (2000, 2002 and 2004). We fi nd that these persistent donors to education are more likely to have higher income (average of US $ 142 603 in 2000) and higher levels of education (bachelor ’ s degree or above) than are less frequent education donors and non-donors to education. There is some support for a positive association between persistent giving to education and the number and age of children in the household. There is strong support for positive association between educational attainment and persistence in giving to education and in giving to other secular causes. Implications for fundraising practice and further research topics are discussed

Use of Reversible Contraceptive Methods Among U.S. Women with Physical or Sensory Disabilities

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138241/1/psrh12031.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138241/2/psrh12031_am.pd

Role of A20 in cIAP-2 Protection against Tumor Necrosis Factor α (TNF-α)-Mediated Apoptosis in Endothelial Cells

Tumor necrosis factor α (TNF-α) influences endothelial cell viability by altering the regulatory molecules involved in induction or suppression of apoptosis. However, the underlying mechanisms are still not completely understood. In this study, we demonstrated that A20 (also known as TNFAIP3, tumor necrosis factor α-induced protein 3, and an anti-apoptotic protein) regulates the inhibitor of apoptosis protein-2 (cIAP-2) expression upon TNF-α induction in endothelial cells. Inhibition of A20 expression by its siRNA resulted in attenuating expression of TNF-α-induced cIAP-2, yet not cIAP-1 or XIAP. A20-induced cIAP-2 expression can be blocked by the inhibition of phosphatidyl inositol-3 kinase (PI3-K), but not nuclear factor (NF)-κB, while concomitantly increasing the number of endothelial apoptotic cells and caspase 3 activation. Moreover, TNF-α-mediated induction of apoptosis was enhanced by A20 inhibition, which could be rescued by cIAP-2. Taken together, these results identify A20 as a cytoprotective factor involved in cIAP-2 inhibitory pathway of TNF-α-induced apoptosis. This is consistent with the idea that endothelial cell viability is dependent on interactions between inducers and suppressors of apoptosis, susceptible to modulation by TNF-α

Software Citation Implementation Challenges

The main output of the FORCE11 Software Citation working group (https://www.force11.org/group/software-citation-working-group) was a paper on software citation principles (https://doi.org/10.7717/peerj-cs.86) published in September 2016. This paper laid out a set of six high-level principles for software citation (importance, credit and attribution, unique identification, persistence, accessibility, and specificity) and discussed how they could be used to implement software citation in the scholarly community. In a series of talks and other activities, we have promoted software citation using these increasingly accepted principles. At the time the initial paper was published, we also provided guidance and examples on how to make software citable, though we now realize there are unresolved problems with that guidance. The purpose of this document is to provide an explanation of current issues impacting scholarly attribution of research software, organize updated implementation guidance, and identify where best practices and solutions are still needed

Cell adhesion molecule CD166 drives malignant progression and osteolytic disease in multiple myeloma

Multiple myeloma (MM) is incurable once osteolytic lesions have seeded at skeletal sites, but factors mediating this deadly pathogenic advance remain poorly understood. Here we report evidence of a major role for the cell adhesion molecule CD166, which we discovered to be highly expressed in MM cell lines and primary bone marrow (BM) cells from patients. CD166+ MM cells homed more efficiently than CD166− cells to the BM of engrafted immunodeficient NSG mice. CD166 silencing in MM cells enabled longer survival, a smaller tumor burden and less osteolytic lesions, as compared to mice bearing control cells. CD166 deficiency in MM cell lines or CD138+ BM cells from MM patients compromised their ability to induce bone resorption in an ex vivo organ culture system. Further, CD166 deficiency in MM cells also reduced formation of osteolytic disease in vivo after intra-tibial engraftment. Mechanistic investigation revealed that CD166 expression in MM cells inhibited osteoblastogenesis of BM-derived osteoblast progenitors by suppressing RUNX2 gene expression. Conversely, CD166 expression in MM cells promoted osteoclastogenesis by activating TRAF6-dependent signaling pathways in osteoclast progenitors. Overall, our results define CD166 as a pivotal director in MM cell homing to the BM and MM progression, rationalizing its further study as a candidate therapeutic target for MM treatment

Measurement invariance of the patient health questionnaire-9 (PHQ-9) depression screener in U.S. adults across sex, race/ethnicity, and education level: NHANES 2005–2016

Background: Despite its popularity, little is known about the measurement invariance of the Patient Health Questionnaire-9 (PHQ-9) across U.S. sociodemographic groups. Use of a screener shown not to possess measurement invariance could result in under-detection/treatment of depression, potentially exacerbating sociodemographic disparities in depression. Therefore, we assessed the factor structure and measurement invariance of the PHQ-9 across major U.S. sociodemographic groups. Methods: U.S. population representative data came from the 2005–2016 National Health and Nutrition Examination Survey (NHANES) cohorts We conducted a measurement invariance analysis of 31,366 respondents across sociodemographic factors of sex, race/ethnicity, and education level. Results: Considering results of single-group confirmatory factor analyses (CFAs), depression theory, and research utility, we justify a two-factor structure for the PHQ-9 consisting of a cognitive/affective factor and a somatic factor (RMSEA=0.034, TLI=0.985, CFI=0.989). Based on multiple-group CFAs testing configural, scalar, and strict factorial invariance, we determined that invariance held for sex, race/ethnicity, and education level groups, as all models demonstrated close model fit (RMSEA=0.025–0.025, TLI=0.985–0.992, CFI=0.986–0.991). Finally, for all steps ΔCFI was < −0.004, and ΔRMSEA was < 0.01. Conclusions: We demonstrate that the PHQ-9 is acceptable to use in major U.S. sociodemographic groups and allows for meaningful comparisons in total, cognitive/affective, and somatic depressive symptoms across these groups, extending its use to the community. This knowledge is timely as medicine moves towards alternative payment models emphasizing high-quality and cost-efficient care, which will likely incentivize behavioral and population health efforts. We also provide a consistent, evidence-based approach for calculating PHQ-9 subscale scores

Galectin-3 synergizes with CD47 to Suppress Phagocytosis and T cell immunity in Peritoneal Metastases of Gastric Adenocarcinoma

View full abstracthttps://openworks.mdanderson.org/leading-edge/1061/thumbnail.jp

Electrophysiological Properties of Motor Neurons in a Mouse Model of Severe Spinal Muscular Atrophy: In Vitro versus In Vivo Development

We examined the electrophysiological activity of motor neurons from the mouse model of severe spinal muscular atrophy (SMA) using two different methods: whole cell patch clamp of neurons cultured from day 13 embryos; and multi-electrode recording of ventral horns in spinal cord slices from pups on post-natal days 5 and 6. We used the MED64 multi-electrode array to record electrophysiological activity from motor neurons in slices from the lumbar spinal cord of SMA pups and their unaffected littermates. Recording simultaneously from up to 32 sites across the ventral horn, we observed a significant decrease in the number of active neurons in 5–6 day-old SMA pups compared to littermates. Ventral horn activity in control pups is significantly activated by serotonin and depressed by GABA, while these agents had much less effect on SMA slices. In contrast to the large differences observed in spinal cord, neurons cultured from SMA embryos for up to 21 days showed no significant differences in electrophysiological activity compared to littermates. No differences were observed in membrane potential, frequency of spiking and synaptic activity in cells from SMA embryos compared to controls. In addition, we observed no difference in cell survival between cells from SMA embryos and their unaffected littermates. Our results represent the first report on the electrophysiology of SMN-deficient motor neurons, and suggest that motor neuron development in vitro follows a different path than in vivo development, a path in which loss of SMN expression has little effect on motor neuron function and survival