Making Judicial Recusal More Rigorous

The right to an impartial arbiter is the bedrock of due process. Yet litigants in most state courts face judges subject to election and reelection – and therefore to majoritarian political pressures that would appear to undermine the judges\u27 impartiality. This tension has existed for as long as judges have been elected (and, to some extent, for as long as they have been appointed, in which case campaigns often take a less public but equally politicized form). In recent years, however, this tension has become more acute. Today, state courts around the country increasingly resemble – and are increasingly perceived to resemble – interest group battlegrounds in which judges represent particular constituencies in addition to, or even instead of, the rule of law. Two key developments are driving this transformation: the role of money in judicial elections is growing while the canons of conduct are shrinking. These trends are creating dramatic new threats to judicial impartiality and due process. Taking our cue from Justice Anthony Kennedy\u27s concurrence in Republican Party of Minnesota v. White, we explore in this article a possible solution: making judicial recusal rules more rigorous

Making Judicial Recusal More Rigorous

The right to an impartial arbiter is the bedrock of due process. Yet litigants in most state courts face judges subject to election and reelection – and therefore to majoritarian political pressures that would appear to undermine the judges\u27 impartiality. This tension has existed for as long as judges have been elected (and, to some extent, for as long as they have been appointed, in which case campaigns often take a less public but equally politicized form). In recent years, however, this tension has become more acute. Today, state courts around the country increasingly resemble – and are increasingly perceived to resemble – interest group battlegrounds in which judges represent particular constituencies in addition to, or even instead of, the rule of law. Two key developments are driving this transformation: the role of money in judicial elections is growing while the canons of conduct are shrinking. These trends are creating dramatic new threats to judicial impartiality and due process. Taking our cue from Justice Anthony Kennedy\u27s concurrence in Republican Party of Minnesota v. White, we explore in this article a possible solution: making judicial recusal rules more rigorous

Integrated water resources management in North Georgia implications of wastewater management policy

Water management in the southeast, and particularly in Georgia, has become increasingly more complex due to rapid population growth, dwindling water supplies, water quality and instream flow concerns, and allocation disputes with neighboring states. The Georgia state legislature responded with two key initiatives: SB 130, passed in 2001, which formed the Metropolitan North Georgia Water Planning District (MNGWPD), and HB 237, passed in 2004, which requires the development of a Comprehensive Statewide Water Plan (CSWP). In 2003, the MNGWPD adopted wastewater management, watershed protection, and water supply and conservation plans that will guide water resources in metropolitan Atlanta for the next 30 years. Implementation costs of the MNGWPD water and wastewater plans through 2030 has been estimated to total $60B. To conserve financial resources and encourage a sustainable development pattern, it is necessary to prioritize these investments, i.e., focus investments upon areas have the ability to increase population density due to the proximity of existing services. Currently, growth management policies in some jurisdictions encourage septic system development, increasing overall wastewater treatment costs and interfering with water management goals.Sponsored by: Georgia Environmental Protection Division U.S. Geological Survey, Georgia Water Science Center U.S. Department of Agriculture, Natural Resources Conservation Service Georgia Institute of Technology, Georgia Water Resources Institute The University of Georgia, Water Resources Facult

Recommendations to improve wildlife exposure estimation for development of soil screening and cleanup values

An integral component in the development of media-specific values for the ecological risk assessment of chemicals is the derivation of safe levels of exposure for wildlife. Although the derivation and subsequent application of these values can be used for screening purposes, there is a need to identify the threshold for effects when making remedial decisions during site-specific assessments. Methods for evaluation of wildlife exposure are included in the US Environmental Protection Agency (USEPA) ecological soil screening levels (Eco-SSLs), registration, evaluation, authorization, and restriction of chemicals (REACH), and other risk-based soil assessment approaches. The goal of these approaches is to ensure that soil-associated contaminants do not pose a risk to wildlife that directly ingest soil, or to species that may be exposed to contaminants that persist in the food chain. These approaches incorporate broad assumptions in the exposure and effects assessments and in the risk characterization process. Consequently, thresholds for concluding risk are frequently very low with conclusions of risk possible when soil metal concentrations fall in the range of natural background. A workshop held in September, 2012 evaluated existing methods and explored recent science about factors to consider when establishing appropriate remedial goals for concentrations of metals in soils. A Foodweb Exposure Workgroup was organized to evaluate methods for quantifying exposure of wildlife to soil-associated metals through soil and food consumption and to provide recommendations for the development of ecological soil cleanup values (Eco-SCVs) that are both practical and scientifically defensible. The specific goals of this article are to review the current practices for quantifying exposure of wildlife to soil-associated contaminants via bioaccumulation and trophic transfer, to identify potential opportunities for refining and improving these exposure estimates, and finally, to make recommendations for application of these improved models to the development of site-specific remedial goals protective of wildlife. Although the focus is on metals contamination, many of the methods and tools discussed are also applicable to organic contaminants. The conclusion of this workgroup was that existing exposure estimation models are generally appropriate when fully expanded and that methods are generally available to develop more robust site-specific exposure estimates. Improved realism in site-specific wildlife Eco-SCVs could be achieved by obtaining more realistic estimates for diet composition, bioaccumulation, bioavailability and/or bioaccessibility, soil ingestion, spatial aspects of exposure, and target organ exposure. These components of wildlife exposure estimation should be developed on a site-, species-, and analyte-specific basis to the extent that the expense for their derivation is justified by the value they add to Eco-SCV development

The BHLF1 locus of Epstein-Barr virus contributes to viral latency and B-cell immortalization

Funding: U.S. Public Health Service grant AI110328 to J.T.S. and in part by Commonwealth Universal Research Enhancement (CURE) funds. L.N.L. received support from National Cancer Institute training grant T32 CA060395, and is a Lymphoma Research Foundation Grantee.The Epstein-Barr virus (EBV) BHLF1 gene encodes an abundant linear and several circular RNAs believed to perform non-coding functions during virus replication, though an open reading frame is retained among an unknown percentage of EBV isolates. Evidence suggests that BHLF1 is also transcribed during latent infection, which prompted us to investigate the contribution of this locus to latency. Analysis of transcripts transiting BHLF1 revealed its transcription is widespread among B-cell lines supporting the latency I or III program of EBV protein expression, and to be more complex than originally presumed. EBV-negative Burkitt lymphoma cell lines infected with either wild-type or two different BHLF1 mutant EBVs were initially indistinguishable in supporting latency III. However, cells infected with BHLF1- virus ultimately transitioned to the more restrictive latency I, whereas cells infected with wild-type virus either sustained latency III or transitioned more slowly to latency I. Upon infection of primary B cells, which require latency III for growth in vitro, both BHLF1- viruses exhibited variably reduced immortalization potential relative to wild-type virus. Finally, in transfection experiments, efficient protein expression from an intact BHLF1 ORF required the EBV post-transcriptional regulator protein SM, whose expression is limited to the replicative cycle. Thus, one way in which BHLF1 may contribute to latency is through a mechanism, possibly mediated or regulated by a long non-coding RNA, that supports latency III critical for the establishment of EBV latency and lifelong persistence within its host, whereas any retained protein-dependent function of BHLF1 may be restricted to the replication cycle. Importance. Epstein-Barr virus (EBV) has significant oncogenic potential that is linked to its latent infection of B lymphocytes, during which virus replication is not supported. Establishment of latent infection, which is life long and can precede tumor development by years, requires the concerted actions of nearly a dozen EBV proteins and numerous small non-protein-coding RNAs. Elucidation of how these EBV products contribute to latency is crucial to understanding EBV's role in specific malignancies, and ultimately to clinical intervention. Historically, EBV genes that contribute to virus replication have been excluded from consideration of a role in latency, primarily because of the general incompatibility between virus production and cell survival. However, here we provide evidence that the genetic locus containing one such gene, BHLF1, indeed contributes to key aspects of EBV latency, including its ability to promote continuous growth of B lymphocytes, thus providing significant new insight into EBV biology and oncogenic potential.PostprintPeer reviewe

Illness Mapping: A time and cost effective method to estimate healthcare data needed to establish community-based health insurance

Background: Most healthcare spending in developing countries is private out-of-pocket. One explanation for low penetration of health insurance is that poorer individuals doubt their ability to enforce insurance contracts. Community-based health insurance schemes (CBHI) are a solution, but launching CBHI requires obtaining accurate local data on morbidity, healthcare utilization and other details to inform package design and pricing. We developed the "Illness Mapping" method (IM) for data collection (faster and cheaper than household surveys). Methods. IM is a modification of two non-interactive consensus group methods (Delphi and Nominal Group Technique) to operate as interactive methods. We elicited estimates from "Experts" in the target community on morbidity and healthcare utilization. Interaction between facilitator and experts became essential to bridge literacy constraints and to reach consensus.The study was conducted in Gaya District, Bihar (India) during April-June 2010. The intervention included the IM and a household survey (HHS). IM included 18 women's and 17 men's groups. The HHS was conducted in 50 villages with1,000 randomly selected households (6,656 individuals). Results: We found good agreement between the two methods on overall prevalence of illness (IM: 25.9% ±3.6; HHS: 31.4%) and on prevalence of acute (IM: 76.9%; HHS: 69.2%) and chronic illnesses (IM: 20.1%; HHS: 16.6%). We also found good agreement on incidence of deliveries (IM: 3.9% ±0.4; HHS: 3.9%), and on hospital deliveries (IM: 61.0%. ± 5.4; HHS: 51.4%). For hospitalizations, we obtained a lower estimate from the IM (1.1%) than from the HHS (2.6%). The IM required less time and less person-power than a household survey, which translate into reduced costs. Conclusions: We have shown that our Illness Mapping method can be carried out at lower financial and human cost for sourcing essential local data, at acceptably accurate levels. In view of the good fit of results obtained, we assume that the method could work elsewhere as well

The Effect of Epstein-Barr Virus Latent Membrane Protein 2 Expression on the Kinetics of Early B Cell Infection

Infection of human B cells with wild-type Epstein-Barr virus (EBV) in vitro leads to activation and proliferation that result in efficient production of lymphoblastoid cell lines (LCLs). Latent Membrane Protein 2 (LMP2) is expressed early after infection and previous research has suggested a possible role in this process. Therefore, we generated recombinant EBV with knockouts of either or both protein isoforms, LMP2A and LMP2B (Δ2A, Δ2B, Δ2A/Δ2B) to study the effect of LMP2 in early B cell infection. Infection of B cells with Δ2A and Δ2A/Δ2B viruses led to a marked decrease in activation and proliferation relative to wild-type (wt) viruses, and resulted in higher percentages of apoptotic B cells. Δ2B virus infection showed activation levels comparable to wt, but fewer numbers of proliferating B cells. Early B cell infection with wt, Δ2A and Δ2B viruses did not result in changes in latent gene expression, with the exception of elevated LMP2B transcript in Δ2A virus infection. Infection with Δ2A and Δ2B viruses did not affect viral latency, determined by changes in LMP1/Zebra expression following BCR stimulation. However, BCR stimulation of Δ2A/Δ2B cells resulted in decreased LMP1 expression, which suggests loss of stability in viral latency. Long-term outgrowth assays revealed that LMP2A, but not LMP2B, is critical for efficient long-term growth of B cells in vitro. The lowest levels of activation, proliferation, and LCL formation were observed when both isoforms were deleted. These results suggest that LMP2A appears to be critical for efficient activation, proliferation and survival of EBV-infected B cells at early times after infection, which impacts the efficient long-term growth of B cells in culture. In contrast, LMP2B did not appear to play a significant role in these processes, and long-term growth of infected B cells was not affected by the absence of this protein. © 2013 Wasil et al

Genetically inferred birthweight, height, and puberty timing and risk of osteosarcoma

INTRODUCTION: Several studies have linked increased risk of osteosarcoma with tall stature, high birthweight, and early puberty, although evidence is inconsistent. We used genetic risk scores (GRS) based on established genetic loci for these traits and evaluated associations between genetically inferred birthweight, height, and puberty timing with osteosarcoma. METHODS: Using genotype data from two genome-wide association studies, totaling 1039 cases and 2923 controls of European ancestry, association analyses were conducted using logistic regression for each study and meta-analyzed to estimate pooled odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup analyses were conducted by case diagnosis age, metastasis status, tumor location, tumor histology, and presence of a known pathogenic variant in a cancer susceptibility gene. RESULTS: Genetically inferred higher birthweight was associated with an increased risk of osteosarcoma (OR =1.59, 95% CI 1.07-2.38, P = 0.02). This association was strongest in cases without metastatic disease (OR =2.46, 95% CI 1.44-4.19, P = 9.5 ×10-04). Although there was no overall association between osteosarcoma and genetically inferred taller stature (OR=1.06, 95% CI 0.96-1.17, P = 0.28), the GRS for taller stature was associated with an increased risk of osteosarcoma in 154 cases with a known pathogenic cancer susceptibility gene variant (OR=1.29, 95% CI 1.03-1.63, P = 0.03). There were no significant associations between the GRS for puberty timing and osteosarcoma. CONCLUSION: A genetic propensity to higher birthweight was associated with increased osteosarcoma risk, suggesting that shared genetic factors or biological pathways that affect birthweight may contribute to osteosarcoma pathogenesis

Hardship financing of healthcare among rural poor in Orissa, India

<p>Abstract</p> <p>Background</p> <p>This study examines health-related "hardship financing" in order to get better insights on how poor households finance their out-of-pocket healthcare costs. We define hardship financing as having to borrow money with interest or to sell assets to pay out-of-pocket healthcare costs.</p> <p>Methods</p> <p>Using survey data of 5,383 low-income households in Orissa, one of the poorest states of India, we investigate factors influencing the risk of hardship financing with the use of a logistic regression.</p> <p>Results</p> <p>Overall, about 25% of the households (that had any healthcare cost) reported hardship financing during the year preceding the survey. Among households that experienced a hospitalization, this percentage was nearly 40%, but even among households with outpatient or maternity-related care around 25% experienced hardship financing.</p> <p>Hardship financing is explained not merely by the wealth of the household (measured by assets) or how much is spent out-of-pocket on healthcare costs, but also by when the payment occurs, its frequency and its duration (e.g. more severe in cases of chronic illnesses). The location where a household resides remains a major predictor of the likelihood to have hardship financing despite all other household features included in the model.</p> <p>Conclusions</p> <p>Rural poor households are subjected to considerable and protracted financial hardship due to the indirect and longer-term deleterious effects of how they cope with out-of-pocket healthcare costs. The social network that households can access influences exposure to hardship financing. Our findings point to the need to develop a policy solution that would limit that exposure both in quantum and in time. We therefore conclude that policy interventions aiming to ensure health-related financial protection would have to demonstrate that they have reduced the frequency and the volume of hardship financing.</p

Updated Guidance Regarding The Risk ofAllergic Reactions to COVID-19 Vaccines and Recommended Evaluation and Management: A GRADE Assessment, and International Consensus Approach

This guidance updates 2021 GRADE (Grading of Recommendations Assessment, Development and Evaluation) recommendations regarding immediate allergic reactions following coronavirus disease 2019 (COVID-19) vaccines and addresses revaccinating individuals with first-dose allergic reactions and allergy testing to determine revaccination outcomes. Recent meta-analyses assessed the incidence of severe allergic reactions to initial COVID-19 vaccination, risk of mRNA-COVID-19 revaccination after an initial reaction, and diagnostic accuracy of COVID-19 vaccine and vaccine excipient testing in predicting reactions. GRADE methods informed rating the certainty of evidence and strength of recommendations. A modified Delphi panel consisting of experts in allergy, anaphylaxis, vaccinology, infectious diseases, emergency medicine, and primary care from Australia, Canada, Europe, Japan, South Africa, the United Kingdom, and the United States formed the recommendations. We recommend vaccination for persons without COVID-19 vaccine excipient allergy and revaccination after a prior immediate allergic reaction. We suggest against \u3e 15-minute postvaccination observation. We recommend against mRNA vaccine or excipient skin testing to predict outcomes. We suggest revaccination of persons with an immediate allergic reaction to the mRNA vaccine or excipients be performed by a person with vaccine allergy expertise in a properly equipped setting. We suggest against premedication, split-dosing, or special precautions because of a comorbid allergic history