Implications of the Ticket to Work and Self-Sufficiency Program for Young Adults

On December 17, 1999, President Clinton signed the Ticket to Work and Work Incentives Improvement Act (P.L. 106-170) into law establishing in section 101(a) the Ticket to Work and Self-Sufficiency Program (Ticket to Work Program) as well as several other provisions to support the movement of beneficiaries with disabilities who receive Supplemental Security Income (SSI) and Social Security Disability Insurance (SSDI) into employment. The Ticket to Work Program was established to expand the universe of providers available to beneficiaries with disabilities as they are afforded the opportunity to choose from whom they access their needed employment services and supports. The Ticket to Work Program also increased provider incentives to serve these individuals. The Social Security Administration (SSA) administers this new program with the support of Maximus, Inc, the entity contracted with by the SSA to serve as the program manager. The SSA is currently contracting with agencies to serve as Employment Networks (EN). These ENs perform an array of duties under the law, including providing employment services, vocational rehabilitation (VR) services, and other support services to assist individuals with disabilities to obtain and maintain employment. Under this program, the SSA is directed to provide to beneficiaries with disabilities who meet certain eligibility criteria a Ticket they may use to obtain employment services, VR services and/or other support services from an EN of their choice. “A Ticket under the Ticket to Work and Self-Sufficiency Program is a document that provides evidence of SSA’s agreement to pay an EN or a State VR agency for providing employment services, VR services and/or other support services to a Ticket recipient who requests such services.” (SSA 2001, p. 12) The Ticket to Work Program will be phased in nationally over a three-year period beginning in January, 2002, with beneficiaries in 13 states: Arizona, Colorado, Delaware, Florida, Illinois, Iowa, Massachusetts, New York, Oklahoma, Oregon, South Carolina, Vermont and Wisconsin. The remaining states will be included by January, 2004

Mental Health And The Role Of The States

Researchers from the State Health Care Spending Project -- a collaboration between The Pew Charitable Trusts and the John D. and Catherine T. MacArthur Foundation -- sought to better understand the country's mental health challenges and, in particular, the states' role in addressing them. The project found that:In 2013, approximately 44 million adults -- 18.5 percent of the population 18 and older -- were classified as having a mental illness. Of these, 10 million had a serious mental illness. The rate of serious mental illness varied from state to state.In 2009, the most recent year for which national mental health data are available, $147 billion was spent on mental health treatment in the United States. A majority of the spending, 60 percent, came from public sources such as Medicaid, state and local governments, Medicare, and federal grants. Private sources, including health insurance and individual out-of-pocket spending, made up the difference.Funding from states and localities totaled$22 billion (15 percent) in 2009. This total does not include state and local Medicaid expenditures. Counting those contributions brings total state and local spending up to $35.5 billion (24 percent).This report is intended to help federal, state, and local policymakers working to address the country's mental health challenges to better understand their prevalence, treatment, and funding trends

Fructose Alters Cell Survival and Gene Expression in Microglia and Neuronal Cells Lines

Purpose: Microglia are macrophages that are found primarily in the CNS and play a crucial role in maintaining a healthy brain by engulfing invading microorganisms, releasing inflammatory mediators, and pruning dead cells. Microglia can become activated in response to certain stimuli which causes them to transition into a pro-inflammatory state, and can sometimes become chronically activated which can result in neuronal damage. Studies have shown a causal relationship between this activation and sugars such as fructose and glucose. We sought to understand the role of sugars in microglial activation and the subsequent effects on neuron health. Methods: Rat microglia (HAPI) and neuronal (B35) cell lines were treated with varying concentrations of fructose (25 mM, 12.5 mM, and 6.25 mM) or glucose (25 mM and 12.5 mM)as a positive control to determine their effects on the cells. Following treatment and incubation for 3 or 24 hours, the cells were analyzed using an MTT assay to measure cell survival or real-time polymerase chain reaction (RT-PCR) to measure gene expression levels. Effects of fructose were measured in HAPI microglia after direct treatment with the sugar. The genes investigated by the RT-PCR in the HAPI cells included: glucose transporter 5 (GLUT5), and the inflammatory markers high mobility group box 1 (HMGB1), and prostaglandin E receptor 2 (Ptger2). To evaluate the effects of microglial activation on neuronal function, the B35 neurons were treated either directly with sugars or with the supernatant collected from fructose-treated HAPI microglia. This allows examination of the effects of soluble neuron-injury factors released by microglia. The genes investigated by RT-PCR in B35 neurons included nuclear factor-κB (NFκB) and enolase 2 (Eno2). Results: Cell survival assays showed that 24-hour direct fructose treatment increased B35 cell survival by up to 13%, while groups treated with microglia supernatant increased cell survival by up to 33%. In HAPI microglia, 3 hours of treatment with fructose caused GLUT5 expression to be suppressed by up to 32% in all treatment groups except for 6.25 mM fructose, while Ptger2 and HMGB1 expression was increased by as much as 65% and 15%, respectively. After 24-hours of treatment with fructose, the HAPI microglia showed a maximum of 80% increased expression of HMGB1, while Ptger2 expression was mostly unchanged. In B35 neurons, 3 hours of treatment with fructose caused a decrease of up to 26% in NFκB and an increase of up to 46% in Eno2 expression. Conclusion: Cell survival results indicate that the microglia may provide a short term protective effect on the B35 neurons. However, data from the gene expression assays show evidence of cellular dysfunction in neurons and pro-inflammatory activity in microglia which may lead to neuronal death on a longer timeline. As seen in the gene expression results, microglia had increased expression of pro-inflammatory genes and B35 neuronal cells had increased expression of markers of cellular damage. Future studies will further explore the effects of fructose on expression of other genes and examine the effects on neuron survival at later time points

Tax Increment Financing in Missouri: An Analysis of Determinants, Competitive Dynamics, Equity, and Path Dependency

Tax increment financing (TIF) has been a popular and controversial economic development tool for several decades. This research considers the determinants of competitive dynamics, equity, and path dependency on TIF use. We use logistic and ordinary least squares regressions on the approval, number, and value of TIFs in Missouri to flesh out the way the determinants contribute to TIF approval, value, and frequency of use. This study finds that there are competitive dynamics that affect TIF use: being adjacent to another city that uses TIFs increases the likelihood that a city will approve a TIF. The study finds evidence that TIF adoption patterns contribute to intermunicipal inequality, and provides some support for the importance of path dependency on TIF use

Supporting Career Development and Employment: Benefits Planning, Assistance and Outreach (BPA&O) and Protection and Advocacy for Beneficiaries of Social Security (PABSS)

This training curriculum is dedicated to increasing knowledge and understanding of the Social Security Administration\u27s disability and return to work programs and work incentive provisions as prescribed in the Social Security Act and Ticket to Work and Work Incentives Improvement Act of 1999 as well as other federal benefit programs. These informational resources were compiled and edited to provide continuing education and print materials for benefits specialists and protection and advocacy personnel on the interplay of these benefit programs and impact or employment

Exploring Patterns of Tax Increment Financing Use and Structural Explanations in Missouri’s Major Metropolitan Regions

This article examines tax increment financing (TIF) in Kansas City and St. Louis, two heavy users of the tool under the same statutory authority. Based on a complete database of TIF projects through 2013 (2012 for Kansas City) and numerous interviews with local government officials in both metropolitan areas, we explore the TIF use of these two cities, which have different structural aspects and have gone through sharp policy changes, to examine if central cities that use different strategies beget different outcomes in their suburban areas. We document distinctly different patterns of use in the two central cities. When St. Louis dramatically increased its TIF use under Mayor Francis Slay, the number of projects per year in the suburbs increased. Kansas City suburbs appeared to fill the gap in TIF use when the city sharply decreased its use of TIF under Mayor Mark Funkhouser. More research is needed to determine the factors that drive these mixed effects and if they hold true by context and in other metropolitan areas

USE OF CHAMBERLAIN FIXED EFFECTS APPROACH TO ESTIMATE WILLINGNESS-TO-PAY FOR LITTLE TENNESSEE RIVER BASIN MANAGEMENT ALTERNATIVES

The paper discusses an application of Chamberlain's fixed effects model to contingent valuation method survey data obtained for eight management alternatives for the Little Tennessee River basin. The advantages of using this approach versus cross-sectional logit, pooled logit, and cross-sectional logit with lags are discussed and a technique to obtain willingness-to-pay estimates from estimated coefficients is offered. Drawbacks of using Chamberlain's fixed effects model, difficulties encountered, and directions for further research are presented.Environmental Economics and Policy,

Cloning of terminal transferase cDNA by antibody screening

A cDNA library was prepared from a terminal deoxynucleotidyltransferase-containing thymoma in the phage vector λgt11. By screening plaques with anti-terminal transferase antibody, positive clones were identified of which some had β-galactosidase-cDNA fusion proteins identifiable after electrophoretic fractionation by immunoblotting with anti-terminal transferase antibody. The predominant class of cross-hybridizing clones was determined to represent cDNA for terminal transferase by showing that one representative clone hybridized to a 2200-nucleotide mRNA in close-matched enzyme-positive but not to enzyme-negative cells and that the cDNA selected a mRNA that translated to give a protein of the size and antigenic characteristics of terminal transferase. Only a small amount of genomic DNA hybridized to the longest available clone, indicating that the sequence is virtually unique in the mouse genome

Emergence of a STAT3 mutated NK clone in LGL leukemia

AbstractLarge granular lymphocyte (LGL) leukemia is a chronic clonal lymphoproliferative disorder. Here, a T-LGL leukemia patient developed NK-LGL leukemia with residual leukemic T-LGL. TCRVβ usage and CDR3 sequence drifts were observed with disease progression. A STAT3 S614R mutation was identified in NK but not T-cells in the mixed leukemic stage. Multiple, non-dominant T-cell clones with distinct STAT3 mutations were present throughout. Our results suggest that T and NK-LGL leukemia may share common pathogenesis mechanisms and that STAT3 mutation alone is insufficient to bring about clonal expansion. Mutational and immunological monitoring may provide diagnostic and therapeutic significance in LGL leukemia