The Impact of Disability Benefits on Labor Supply: Evidence from the VA's Disability Compensation Program

Combining administrative data from the US Army, Department of Veterans Affairs, and Social Security Administration, we analyze the effect of the VA's Disability Compensation (DC) program on veterans' labor force participation and earnings. We study the 2001 Agent Orange decision, a unique policy change that expanded DC eligibility for Vietnam veterans who served in theater but did not expand eligibility to other veterans of this era, to assess the causal effects of DC enrollment. We estimate that benefits receipt reduced veterans' labor force participation by 18 percentage points, though measured income net of transfer income rose on average.United States. Social Security Administration (grant #10-P-98363-1-05 to the National Bureau of Economic Research as part of the SSA Retirement Research Consortium

Müller cell activation, proliferation and migration following laser injury.

PurposeMüller cells are well known for their critical role in normal retinal structure and function, but their reaction to retinal injury and subsequent role in retinal remodeling is less well characterized. In this study we used a mouse model of retinal laser photocoagulation to examine injury-induced Müller glial reaction, and determine how this reaction was related to injury-induced retinal regeneration and cellular repopulation.MethodsExperiments were performed on 3-4-week-old C57BL/6 mice. Retinal laser photocoagulation was used to induce small, circumscribed injuries; these were principally confined to the outer nuclear layer, and surrounded by apparently healthy retinal tissue. Western blotting and immunohistochemical analyses were used to determine the level and location of protein expression. Live cell imaging of green fluorescent protein (GFP)-infected Müller cells (AAV-GFAP-GFP) were used to identify the rate and location of retinal Müller cell nuclear migration.ResultsUpon injury, Müller cells directly at the burn site become reactive, as evidenced by increased expression of the intermediate filament proteins glial fibrillary acidic protein (GFAP) and nestin. These reactive cells re-enter the cell cycle as shown by expression of the markers Cyclin D1 and D3, and their nuclei begin to migrate toward the injury site at a rate of approximately 12 microm/hr. However, unlike other reports, evidence for Müller cell transdifferentiation was not identified in this model.ConclusionsRetinal laser photocoagulation is capable of stimulating a significant glial reaction, marked by activation of cell cycle progression and retinal reorganization, but is not capable of stimulating cellular transdifferentiation or neurogenesis

The Second Conference on Lunar Bases and Space Activities of the 21st Century, volume 1

These papers comprise a peer-review selection of presentations by authors from NASA, LPI industry, and academia at the Second Conference (April 1988) on Lunar Bases and Space Activities of the 21st Century, sponsored by the NASA Office of Exploration and the Lunar Planetary Institute. These papers go into more technical depth than did those published from the first NASA-sponsored symposium on the topic, held in 1984. Session topics covered by this volume include (1) design and operation of transportation systems to, in orbit around, and on the Moon, (2) lunar base site selection, (3) design, architecture, construction, and operation of lunar bases and human habitats, and (4) lunar-based scientific research and experimentation in astronomy, exobiology, and lunar geology

The Second Conference on Lunar Bases and Space Activities of the 21st Century, volume 2

These 92 papers comprise a peer-reviewed selection of presentations by authors from NASA, the Lunar and Planetary Institute (LPI), industry, and academia at the Second Conference on Lunar Bases and Space Activities of the 21st Century. These papers go into more technical depth than did those published from the first NASA-sponsored symposium on the topic, held in 1984. Session topics included the following: (1) design and operation of transportation systems to, in orbit around, and on the Moon; (2) lunar base site selection; (3) design, architecture, construction, and operation of lunar bases and human habitats; (4) lunar-based scientific research and experimentation in astronomy, exobiology, and lunar geology; (5) recovery and use of lunar resources; (6) environmental and human factors of and life support technology for human presence on the Moon; and (7) program management of human exploration of the Moon and space

Endothelial cell-surface tissue transglutaminase inhibits neutrophil adhesion by binding and releasing nitric oxide

Nitric oxide (NO) produced by endothelial cells in response to cytokines displays anti-inflammatory activity by preventing the adherence, migration and activation of neutrophils. The molecular mechanism by which NO operates at the blood-endothelium interface to exert anti-inflammatory properties is largely unknown. Here we show that on endothelial surfaces, NO is associated with the sulfhydryl-rich protein tissue transglutaminase (TG2), thereby endowing the membrane surfaces with anti-inflammatory properties. We find that tumor necrosis factor-α-stimulated neutrophil adherence is opposed by TG2 molecules that are bound to the endothelial surface. Alkylation of cysteine residues in TG2 or inhibition of endothelial NO synthesis renders the surface-bound TG2 inactive, whereas specific, high affinity binding of S-nitrosylated TG2 (SNO-TG2) to endothelial surfaces restores the anti-inflammatory properties of the endothelium, and reconstitutes the activity of endothelial-derived NO. We also show that SNO-TG2 is present in healthy tissues and that it forms on the membranes of shear-activated endothelial cells. Thus, the anti-inflammatory mechanism that prevents neutrophils from adhering to endothelial cells is identified with TG2 S-nitrosylation at the endothelial cell-blood interface

Biologically relevant oxidants and terminology, classification and nomenclature of oxidatively generated damage to nucleobases and 2-deoxyribose in nucleic acids

A broad scientific community is involved in investigations aimed at delineating the mechanisms of formation and cellular processing of oxidatively generated damage to nucleic acids. Perhaps as a consequence of this breadth of research expertise, there are nomenclature problems for several of the oxidized bases including 8-oxo-7,8-dihydroguanine (8-oxoGua), a ubiquitous marker of almost every type of oxidative stress in cells. Efforts to standardize the nomenclature and abbreviations of the main DNA degradation products that arise from oxidative pathways are reported. Information is also provided on the main oxidative radicals, non-radical oxygen species, one-electron agents and enzymes involved in DNA degradation pathways as well in their targets and reactivity. A brief classification of oxidatively generated damage to DNA that may involve single modifications, tandem base modifications, intrastrand and interstrand cross-links together with DNA-protein cross-links and base adducts arising from the addition of lipid peroxides breakdown products is also included

Contemplative Practices and Mental Training: Prospects for American Education

This article draws on research in neuroscience, cognitive science, developmental psychology, and education, as well as scholarship from contemplative traditions concerning the cultivation of positive development, to highlight a set of mental skills and socioemotional dispositions that are central to the aims of education in the 21st century. These include self‐regulatory skills associated with emotion and attention, self‐representations, and prosocial dispositions such as empathy and compassion. It should be possible to strengthen these positive qualities and dispositions through systematic contemplative practices, which induce plastic changes in brain function and structure, supporting prosocial behavior and academic success in young people. These putative beneficial consequences call for focused programmatic research to better characterize which forms and frequencies of practice are most effective for which types of children and adolescents. Results from such research may help refine training programs to maximize their effectiveness at different ages and to document the changes in neural function and structure that might be induced.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/92125/1/cdep240.pd

Dissociable Genetic Contributions to Error Processing: A Multimodal Neuroimaging Study

Background: Neuroimaging studies reliably identify two markers of error commission: the error-related negativity (ERN), an event-related potential, and functional MRI activation of the dorsal anterior cingulate cortex (dACC). While theorized to reflect the same neural process, recent evidence suggests that the ERN arises from the posterior cingulate cortex not the dACC. Here, we tested the hypothesis that these two error markers also have different genetic mediation. Methods: We measured both error markers in a sample of 92 comprised of healthy individuals and those with diagnoses of schizophrenia, obsessive-compulsive disorder or autism spectrum disorder. Participants performed the same task during functional MRI and simultaneously acquired magnetoencephalography and electroencephalography. We examined the mediation of the error markers by two single nucleotide polymorphisms: dopamine D4 receptor (DRD4) C-521T (rs1800955), which has been associated with the ERN and methylenetetrahydrofolate reductase (MTHFR) C677T (rs1801133), which has been associated with error-related dACC activation. We then compared the effects of each polymorphism on the two error markers modeled as a bivariate response. Results: We replicated our previous report of a posterior cingulate source of the ERN in healthy participants in the schizophrenia and obsessive-compulsive disorder groups. The effect of genotype on error markers did not differ significantly by diagnostic group. DRD4 C-521T allele load had a significant linear effect on ERN amplitude, but not on dACC activation, and this difference was significant. MTHFR C677T allele load had a significant linear effect on dACC activation but not ERN amplitude, but the difference in effects on the two error markers was not significant. Conclusions: DRD4 C-521T, but not MTHFR C677T, had a significant differential effect on two canonical error markers. Together with the anatomical dissociation between the ERN and error-related dACC activation, these findings suggest that these error markers have different neural and genetic mediation

β-cell metabolic alterations under chronic nutrient overload in rat and human islets

The aim of this study was to assess multifactorial β-cell responses to metabolic perturbations in primary rat and human islets. Treatment of dispersed rat islet cells with elevated glucose and free fatty acids (FFAs, oleate:palmitate = 1:1 v/v) resulted in increases in the size and the number of lipid droplets in β-cells in a time- and concentration-dependent manner. Glucose and FFAs synergistically stimulated the nutrient sensor mammalian target of rapamycin complex 1 (mTORC1). A potent mTORC1 inhibitor, rapamycin (25 nM), significantly reduced triglyceride accumulation in rat islets. Importantly, lipid droplets accumulated only in β-cells but not in α-cells in an mTORC1-dependent manner. Nutrient activation of mTORC1 upregulated the expression of adipose differentiation related protein (ADRP), known to stabilize lipid droplets. Rat islet size and new DNA synthesis also increased under nutrient overload. Insulin secretion into the culture medium increased steadily over a 4-day period without any significant difference between glucose (10 mM) alone and the combination of glucose (10 mM) and FFAs (240 μM). Insulin content and insulin biosynthesis, however, were significantly reduced under the combination of nutrients compared with glucose alone. Elevated nutrients also stimulated lipid droplet formation in human islets in an mTORC1-dependent manner. Unlike rat islets, however, human islets did not increase in size under nutrient overload despite a normal response to nutrients in releasing insulin. The different responses of islet cell growth under nutrient overload appear to impact insulin biosynthesis and storage differently in rat and human islets