Transitions from AFDC to SSI Prior to Welfare Reform – Policy Brief

The Supplemental Security Income (SSI) and Temporary Assistance for Needy Families (TANF) programs serve overlapping target groups. SSI serves adults and children with disabilities from low-income families, while TANF serves low-income families with children. Consequently, policy changes in one program can affect the other. The target group for Aid to Families with Dependent Children (AFDC), TANF’s predecessor, also overlapped with SSI’s target group. Many have anticipated that the replacement of AFDC with TANF in August 1996 would eventually increase SSI participation as TANF recipients with disabilities sought SSI benefits to avoid TANF work requirements and time limits

Impacts of Expanding Health Care Coverage on the Employment and Earnings of Participants in the SSI Work Incentive Program - Policy Brief

While people with disabilities often say that a loss of public health insurance is a deterrent to work, it is rare to find situations in which they might actually exhibit such a behavioral response to a change in access. Expansions in the income threshold for SSI work incentives program (Sections 1619(a) and (b)) provide an opportunity to observe such a response. Section 1619(b) allows SSI recipients to maintain Medicaid eligibility even if their income is above the level that makes them ineligible for SSI payments. If earnings increase beyond the 1619(b) threshold, however, the person loses their SSI and Medicaid eligibility. Section 1619(b) income thresholds vary significantly across states and over time. Stapleton and Tucker (2000) use the variation in Section 1619(b) income thresholds to examine the employment, earnings and program participation patterns of SSI recipients who have incomes near the threshold level for their state. They find strong evidence that many SSI recipients restrain their earnings to stay below the 1619(b) threshold. It is important to note, however, that the findings only provide evidence on the behavior of a small portion of the population with disabilities (i.e., SSI recipients who work). Nonetheless, this evidence seems to provide strong empirical support for the hypothesis that lack of access to health insurance is an important work disincentive for people with disabilities. They also find that 1619(b) participation varies significantly from month to month. Consequently, cross-sectional estimates on the share of SSI recipients participating in 1619(b) significantly understate the share of SSI recipients who ever participate. These findings are consistent with previous findings that cross-sectional estimates of employment tend to understate multi-period employment patterns for the broader population with disabilities

Regulation of mitochondrial permeability transition pore by PINK1

Background: Loss-of-function mutations in PTEN-induced kinase 1 (PINK1) have been linked to familial Parkinson’s disease, but the underlying pathogenic mechanism remains unclear. We previously reported that loss of PINK1 impairs mitochondrial respiratory activity in mouse brains. Results: In this study, we investigate how loss of PINK1 impairs mitochondrial respiration using cultured primary fibroblasts and neurons. We found that intact mitochondria in PINK1−/− cells recapitulate the respiratory defect in isolated mitochondria from PINK1−/− mouse brains, suggesting that these PINK1−/− cells are a valid experimental system to study the underlying mechanisms. Enzymatic activities of the electron transport system complexes are normal in PINK1−/− cells, but mitochondrial transmembrane potential is reduced. Interestingly, the opening of the mitochondrial permeability transition pore (mPTP) is increased in PINK1−/− cells, and this genotypic difference between PINK1−/− and control cells is eliminated by agonists or inhibitors of the mPTP. Furthermore, inhibition of mPTP opening rescues the defects in transmembrane potential and respiration in PINK1−/− cells. Consistent with our earlier findings in mouse brains, mitochondrial morphology is similar between PINK1−/− and wild-type cells, indicating that the observed mitochondrial functional defects are not due to morphological changes. Following FCCP treatment, calcium increases in the cytosol are higher in PINK1−/− compared to wild-type cells, suggesting that intra-mitochondrial calcium concentration is higher in the absence of PINK1. Conclusions: Our findings show that loss of PINK1 causes selective increases in mPTP opening and mitochondrial calcium, and that the excessive mPTP opening may underlie the mitochondrial functional defects observed in PINK1−/− cells

Metadata Librarians for Open Access: A Path Towards Sustainable Discovery and Impact for Open Access Resources

Support by academic libraries for open access (OA) over the past three-plus decades has largely focused on the development of digital infrastructure, promotion of open access publishing, support of policy-driven access mandates, and more recently, adoption of transformative agreements. Libraries have correspondingly created a broad array of scholarly communication roles to support these varied approaches. Surprisingly, one area of open access support that has received less attention from libraries is the facilitation of description and discovery of open access resources through the creation of robust original metadata. Expertise in Organization of Recorded Knowledge and Information represents a core competency of librarianship, yet the current academic library landscape shows few positions that specifically apply this expertise towards support for OA resources. Efforts to describe OA resources typically fall below those dedicated to licensed resources and pale in comparison to OA advocacy work, repository, publishing and other services. This case study offers an example of how one large academic library has introduced a metadata librarian position focused on description of open access resources into its activities supporting open access.  For decades, commercially licensed resources have benefitted from metadata enhanced layer by layer by commercial and library professionals alike. With increased focus and funding being devoted to open access driven by governmental, institutional, and private funders, attention is critically needed to ensure that these new resources obtain the description necessary to allow them to be useful. Metadata librarians focused on open access resources can work with array of positions, such as repository managers and other digital asset management professionals, to ensure that open access resources are properly ingested and managed, and that metadata practices are aligned with best practices for preservation and long-term access. OA metadata librarians could be responsible for developing and implementing metadata standards and practices for open access resources like scholarly articles, data sets, and other digital objects. These standards would help ensure that open access resources are accurately described and discoverable alongside purchased resources, making them more accessible to researchers and other users.   In addition to their technical responsibilities, OA metadata librarians can also play key roles in advocating for open access resources and educating library staff and users about the importance of metadata in supporting discoverability and accessibility. Through participation in professional organizations and initiatives focused on open access and metadata, OA metadata librarians can help raise awareness of the importance of metadata in supporting open access resources, their sustainability, and ultimately, their impact

Regulation of mitochondrial permeability transition pore by PINK1

Background: Loss-of-function mutations in PTEN-induced kinase 1 (PINK1) have been linked to familial Parkinson’s disease, but the underlying pathogenic mechanism remains unclear. We previously reported that loss of PINK1 impairs mitochondrial respiratory activity in mouse brains. Results: In this study, we investigate how loss of PINK1 impairs mitochondrial respiration using cultured primary fibroblasts and neurons. We found that intact mitochondria in PINK1−/− cells recapitulate the respiratory defect in isolated mitochondria from PINK1−/− mouse brains, suggesting that these PINK1−/− cells are a valid experimental system to study the underlying mechanisms. Enzymatic activities of the electron transport system complexes are normal in PINK1−/− cells, but mitochondrial transmembrane potential is reduced. Interestingly, the opening of the mitochondrial permeability transition pore (mPTP) is increased in PINK1−/− cells, and this genotypic difference between PINK1−/− and control cells is eliminated by agonists or inhibitors of the mPTP. Furthermore, inhibition of mPTP opening rescues the defects in transmembrane potential and respiration in PINK1−/− cells. Consistent with our earlier findings in mouse brains, mitochondrial morphology is similar between PINK1−/− and wild-type cells, indicating that the observed mitochondrial functional defects are not due to morphological changes. Following FCCP treatment, calcium increases in the cytosol are higher in PINK1−/− compared to wild-type cells, suggesting that intra-mitochondrial calcium concentration is higher in the absence of PINK1. Conclusions: Our findings show that loss of PINK1 causes selective increases in mPTP opening and mitochondrial calcium, and that the excessive mPTP opening may underlie the mitochondrial functional defects observed in PINK1−/− cells

A gut-to-brain signal of fluid osmolarity controls thirst satiation.

Satiation is the process by which eating and drinking reduce appetite. For thirst, oropharyngeal cues have a critical role in driving satiation by reporting to the brain the volume of fluid that has been ingested1-12. By contrast, the mechanisms that relay the osmolarity of ingested fluids remain poorly understood. Here we show that the water and salt content of the gastrointestinal tract are precisely measured and then rapidly communicated to the brain to control drinking behaviour in mice. We demonstrate that this osmosensory signal is necessary and sufficient for satiation during normal drinking, involves the vagus nerve and is transmitted to key forebrain neurons that control thirst and vasopressin secretion. Using microendoscopic imaging, we show that individual neurons compute homeostatic need by integrating this gastrointestinal osmosensory information with oropharyngeal and blood-borne signals. These findings reveal how the fluid homeostasis system monitors the osmolarity of ingested fluids to dynamically control drinking behaviour

First results from the VIRIAL survey: the stellar content of UVJUVJ-selected quiescent galaxies at 1.5<z<21.5 < z < 2 from KMOS

We investigate the stellar populations of 25 massive, galaxies ($\log[M_\ast/M_\odot] \geq 10.9$) at $1.5 < z < 2$ using data obtained with the K-band Multi-Object Spectrograph (KMOS) on the ESO VLT. Targets were selected to be quiescent based on their broadband colors and redshifts using data from the 3D-HST grism survey. The mean redshift of our sample is $\bar{z} = 1.75$, where KMOS YJ-band data probe age- and metallicity-sensitive absorption features in the rest-frame optical, including the $G$ band, Fe I, and high-order Balmer lines. Fitting simple stellar population models to a stack of our KMOS spectra, we derive a mean age of $1.03^{+0.13}_{-0.08}$ Gyr. We confirm previous results suggesting a correlation between color and age for quiescent galaxies, finding mean ages of $1.22^{+0.56}_{-0.19}$ Gyr and $0.85^{+0.08}_{-0.05}$ Gyr for the reddest and bluest galaxies in our sample. Combining our KMOS measurements with those obtained from previous studies at $0.2 < z < 2$ we find evidence for a $2-3$ Gyr spread in the formation epoch of massive galaxies. At $z < 1$ the measured stellar ages are consistent with passive evolution, while at $1 < z \lesssim2$ they appear to saturate at $\sim$1 Gyr, which likely reflects changing demographics of the (mean) progenitor population. By comparing to star-formation histories inferred for "normal" star-forming galaxies, we show that the timescales required to form massive galaxies at $z \gtrsim 1.5$ are consistent with the enhanced $\alpha$-element abundances found in massive local early-type galaxies.Comment: 6 pages, 5 figures, accepted for publication in ApJ

Living in a 2.2 World: ERA, Capacity Building and the Topography of Australian Educational Research

Early in 2011, the Australian Association for Research in Education (AARE) and the Australian Council of Deans of Education (ACDE) established a joint working party to create a strategic plan for strengthening national research capacity in the field of Education. This proposal followed the publication of Excellence of Research in Australia (ERA) 2010 results, which revealed that the national average weighting of Australian research in Field of Research 13 (FoR 13) - Education was well below the 'world standard' rating of 3.0. Moreover, the 2010 ERA data demonstrated that we had no up-to-date picture of who is involved in educational research, what their strengths are, or how they relate to one another. As an input into strategic research capacity building in Australian educational research, this project begins the process of documenting who 'we' are as educational researchers. The research described within the report used an ecological model to address the project's overarching question, which was: What is the topography of Australian educational research