Understanding the Overrepresentation of Minorities in One State's Juvenile Justice System

The University Archives has determined that this item is of continuing value to OSU's history.McCarter, Susan A., Ph.D., Ph.D., Virginia Commonwealth University, 1997, Adjunct Faculty, Virginia Commonwealth University - "Understanding the Overrepresentation of Minorities in One State's Juvenile Justice System"The Ohio State University College of Social Wor

Bringing Racial Justice to the Courtroom and Community: Race Matters for Juvenile Justice and the Charlotte Model

This article describes regional institutional organizing efforts to bring racial justice to the Charlotte courts and community through a collaborative called Race Matters for Juvenile Justice (RMJJ). The authors explain community and institutional organizing in-depth using the example of minority overrepresentation in the juvenile justice system, but recognize the pervasiveness of racial and ethnic disparities. Moreover, as the Race Matters for Juvenile Justice-Charlotte Model has gained national prominence, many jurisdictions seek to replicate the collaborative and the authors, therefore, provide RMJJ’s history as well as strategies for changing the narrative through communication and education, workforce development, data and research, community collaboration, practice change, and legislation reform

31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016) : part two

Background The immunological escape of tumors represents one of the main ob- stacles to the treatment of malignancies. The blockade of PD-1 or CTLA-4 receptors represented a milestone in the history of immunotherapy. However, immune checkpoint inhibitors seem to be effective in specific cohorts of patients. It has been proposed that their efficacy relies on the presence of an immunological response. Thus, we hypothesized that disruption of the PD-L1/PD-1 axis would synergize with our oncolytic vaccine platform PeptiCRAd. Methods We used murine B16OVA in vivo tumor models and flow cytometry analysis to investigate the immunological background. Results First, we found that high-burden B16OVA tumors were refractory to combination immunotherapy. However, with a more aggressive schedule, tumors with a lower burden were more susceptible to the combination of PeptiCRAd and PD-L1 blockade. The therapy signifi- cantly increased the median survival of mice (Fig. 7). Interestingly, the reduced growth of contralaterally injected B16F10 cells sug- gested the presence of a long lasting immunological memory also against non-targeted antigens. Concerning the functional state of tumor infiltrating lymphocytes (TILs), we found that all the immune therapies would enhance the percentage of activated (PD-1pos TIM- 3neg) T lymphocytes and reduce the amount of exhausted (PD-1pos TIM-3pos) cells compared to placebo. As expected, we found that PeptiCRAd monotherapy could increase the number of antigen spe- cific CD8+ T cells compared to other treatments. However, only the combination with PD-L1 blockade could significantly increase the ra- tio between activated and exhausted pentamer positive cells (p= 0.0058), suggesting that by disrupting the PD-1/PD-L1 axis we could decrease the amount of dysfunctional antigen specific T cells. We ob- served that the anatomical location deeply influenced the state of CD4+ and CD8+ T lymphocytes. In fact, TIM-3 expression was in- creased by 2 fold on TILs compared to splenic and lymphoid T cells. In the CD8+ compartment, the expression of PD-1 on the surface seemed to be restricted to the tumor micro-environment, while CD4 + T cells had a high expression of PD-1 also in lymphoid organs. Interestingly, we found that the levels of PD-1 were significantly higher on CD8+ T cells than on CD4+ T cells into the tumor micro- environment (p < 0.0001). Conclusions In conclusion, we demonstrated that the efficacy of immune check- point inhibitors might be strongly enhanced by their combination with cancer vaccines. PeptiCRAd was able to increase the number of antigen-specific T cells and PD-L1 blockade prevented their exhaus- tion, resulting in long-lasting immunological memory and increased median survival

Developing interactions with industry in rare diseases: lessons learned and continuing challenges.

The National Institutes of Health (NIH) established the Rare Diseases Clinical Research Network to address the unique challenges of performing research on rare diseases. The Urea Cycle Disorders Consortium (UCDC) was one of the original ten consortia established. The UCDC represents a unique partnership among clinicians, patients, and the NIH with a primary goal of increasing the development of therapeutics that improve patient outcomes for persons affected with a UCD. Based in part on financial incentives associated with the Orphan Drug Act biopharmaceutical and investment entities have an intense interest in engaging with research consortia like the UCDC, which have compiled potentially valuable longitudinal data characterizing outcomes in a relatively large number of affected individuals. We describe the UCDC experience and the bases for evaluating partnerships with such private entities. We review early industry interactions, the development of policies and procedures, and describe the establishment of an Industry Relations Committee, including guiding principles. Challenges encountered, particularly in the transition when products are approved, and potential solutions are discussed. By building a framework for industry partnerships that guides us in resolving inevitable challenges, we can enthusiastically pursue novel and promising collaborations that can lead to breakthroughs in therapeutic interventions for patients

Promote Smart Decarceration and Eliminate Racism Grand Challenges for Social Work: Reimagining Marijuana Policy

Marijuana decriminalization and legalization policies are being passed in many state and local jurisdictions throughout the United States (U.S.). In this process, many lawmakers have used the argument that these policies and associated practices will redress racial disparities in the criminal punishment system. Yet, the evidence suggests this is not the case. We, therefore, use Critical Race Theory (CRT) to interrogate how marijuana-related policies and practices perpetuate collateral consequences and racial disparities in mass incarceration and recidivism to uncover the ways in which they challenge efforts to promote smart decarceration and eliminate racism. We argue that in order to effectively promote smart decarceration and eliminate racism, we must move beyond the limits of current social equity programs to a race-conscious approach to marijuana policy reform. And to that end, we offer evidence-supported policy and practice recommendations

Long-Term Experimental Manipulation of Atmospheric Sulfate Deposition to a Peatland: Response of Methylmercury and Related Solute Export in Streamwater

Changes in sulfate (SO42–) deposition have been linked to changes in mercury (Hg) methylation in peatlands and water quality in freshwater catchments. There is little empirical evidence, however, of how quickly methyl-Hg (MeHg, a bioaccumulative neurotoxin) export from catchments might change with declining SO42– deposition. Here, we present responses in total Hg (THg), MeHg, total organic carbon, pH, and SO42– export from a peatland-dominated catchment as a function of changing SO42– deposition in a long-term (1998–2011), whole-ecosystem, control-impact experiment. Annual SO42– deposition to half of a 2-ha peatland was experimentally increased 6-fold over natural levels and then returned to ambient levels in two phases. Sulfate additions led to a 5-fold increase in monthly flow-weighted MeHg concentrations and yields relative to a reference catchment. Once SO42– additions ceased, MeHg concentrations in the outflow streamwater returned to pre-SO42– addition levels within 2 years. The decline in streamwater MeHg was proportional to the change in the peatland area no longer receiving experimental SO42– inputs. Importantly, net demethylation and increased sorption to peat hastened the return of MeHg to baseline levels beyond purely hydrological flushing. Overall, we present clear empirical evidence of rapid and proportionate declines in MeHg export from a peatland-dominated catchment when SO42– deposition declines

Long-Term Experimental Manipulation of Atmospheric Sulfate Deposition to a Peatland: Response of Methylmercury and Related Solute Export in Streamwater

Changes in sulfate (SO42–) deposition have been linked to changes in mercury (Hg) methylation in peatlands and water quality in freshwater catchments. There is little empirical evidence, however, of how quickly methyl-Hg (MeHg, a bioaccumulative neurotoxin) export from catchments might change with declining SO42– deposition. Here, we present responses in total Hg (THg), MeHg, total organic carbon, pH, and SO42– export from a peatland-dominated catchment as a function of changing SO42– deposition in a long-term (1998–2011), whole-ecosystem, control-impact experiment. Annual SO42– deposition to half of a 2-ha peatland was experimentally increased 6-fold over natural levels and then returned to ambient levels in two phases. Sulfate additions led to a 5-fold increase in monthly flow-weighted MeHg concentrations and yields relative to a reference catchment. Once SO42– additions ceased, MeHg concentrations in the outflow streamwater returned to pre-SO42– addition levels within 2 years. The decline in streamwater MeHg was proportional to the change in the peatland area no longer receiving experimental SO42– inputs. Importantly, net demethylation and increased sorption to peat hastened the return of MeHg to baseline levels beyond purely hydrological flushing. Overall, we present clear empirical evidence of rapid and proportionate declines in MeHg export from a peatland-dominated catchment when SO42– deposition declines

Long-Term Experimental Manipulation of Atmospheric Sulfate Deposition to a Peatland: Response of Methylmercury and Related Solute Export in Streamwater

Changes in sulfate (SO42–) deposition have been linked to changes in mercury (Hg) methylation in peatlands and water quality in freshwater catchments. There is little empirical evidence, however, of how quickly methyl-Hg (MeHg, a bioaccumulative neurotoxin) export from catchments might change with declining SO42– deposition. Here, we present responses in total Hg (THg), MeHg, total organic carbon, pH, and SO42– export from a peatland-dominated catchment as a function of changing SO42– deposition in a long-term (1998–2011), whole-ecosystem, control-impact experiment. Annual SO42– deposition to half of a 2-ha peatland was experimentally increased 6-fold over natural levels and then returned to ambient levels in two phases. Sulfate additions led to a 5-fold increase in monthly flow-weighted MeHg concentrations and yields relative to a reference catchment. Once SO42– additions ceased, MeHg concentrations in the outflow streamwater returned to pre-SO42– addition levels within 2 years. The decline in streamwater MeHg was proportional to the change in the peatland area no longer receiving experimental SO42– inputs. Importantly, net demethylation and increased sorption to peat hastened the return of MeHg to baseline levels beyond purely hydrological flushing. Overall, we present clear empirical evidence of rapid and proportionate declines in MeHg export from a peatland-dominated catchment when SO42– deposition declines