Sex-Based Discrimination in Healthcare Under Section 1557: The New Final Rule and Supreme Court Developments

One of the primary goals of the Patient Protection and Affordable Care Act (PPACA) has been the reduction and elimination of health disparities, generally defined as population-level health differences that adversely affect disadvantaged groups, including disparities associated with sex and gender. Many of PPACA’s general provisions — expanded access to public and private insurance coverage, guarantee issue and pricing reforms, and coverage mandates — were expected to reduce barriers and eliminate discriminatory practices targeting or disproportionately impacting women and transgender individuals. Provisions like the Women’s Health Amendment, which mandated women’s preventive healthcare to be covered without cost sharing, and the even broader prohibition of discrimination on the basis of race, color, national origin, disability, age, and sex in Section 1557 of PPACA also promote gender equity. Prior to PPACA, a patchwork of federal laws targeted only certain areas for sex nondiscrimination protections and enforcement, notably employment (Title VII of the Civil Rights Act of 1964) and education (Title IX of the Education Amendments of 1972). Such laws had been used to address healthcare access to some degree, but their scope has been limited. For example, Title VII has been used to eliminate coverage exclusions that uniquely harm women, such as pregnancy-related care, but only in employment-based plans. Section 1557 filled this critical gap by creating a new healthcare-specific prohibition of sex discrimination. Prohibiting sex and gender discrimination was a dominant focus of the May 2016 Final Rule implementing Section 1557 (2016 Final Rule) issued by the U.S. Department of Health and Human Services (HHS) Office for Civil Rights (OCR). Notably, the 2016 Final Rule clarified that Section 1557’s sex discrimination provision would protect transgender individuals from discrimination on the basis of gender identity in healthcare delivery and insurance. By contrast, in June 2020, OCR issued new regulations that dramatically narrowed Section 1557’s scope, including interpreting the prohibition on sex discrimination to not include discrimination on the basis of gender identity or transgender status (2020 Final Rule). In addition, the 2020 Final Rule significantly expanded the grounds for providers of care or insurance to obtain exemptions from nondiscrimination mandates. The battle over the scope of sex discrimination protection is also playing out in the courts. Indeed, the United States Supreme Court recently weighed in on this issue, though not in the healthcare context. In Bostock v. Clayton County, Georgia, a consolidation of three high-profile cases involving claims of sex discrimination in employment under Title VII, the Supreme Court affirmed a definition of sex discrimination consistent with the 2016 Final Rule. In a 6-3 decision, the Court held that an employer that fires an individual merely for being transgender or gay violates the sex discrimination prohibition under Title VII. Bostock’s implications for Section 1557 are significant, but the fact that it is a non-healthcare case means the battle over the scope of sex discrimination protections under Section 1557 will continue. This article examines the current regulatory and litigation landscape for defining and enforcing PPACA’s prohibition on sex discrimination in healthcare. It considers three key questions engaging regulators and courts at this time, which are discussed below: Who is protected? What kind of activity is prohibited or required? How should religious objections to these requirements be balanced against the health and equity interests advanced by nondiscrimination protections

Reversible DNA micro-patterning using the fluorous effect

We describe a new method for the immobilisation of DNA into defined patterns with sub-micron resolution, using the fluorous effect. The method is fully reversible via a simple solvent wash, allowing the patterning, regeneration and re-patterning of surfaces with no degradation in binding efficiency following multiple removal/attachment cycles of different DNA sequences

The Pafah1b Complex Interacts with the Reelin Receptor VLDLR

Reelin is an extracellular protein that directs the organization of cortical structures of the brain through the activation of two receptors, the very low-density lipoprotein receptor (VLDLR) and the apolipoprotein E receptor 2 (ApoER2), and the phosphorylation of Disabled-1 (Dab1). Lis1, the product of the Pafah1b1 gene, is a component of the brain platelet-activating factor acetylhydrolase 1b (Pafah1b) complex, and binds to phosphorylated Dab1 in response to Reelin. Here we investigated the involvement of the whole Pafah1b complex in Reelin signaling and cortical layer formation and found that catalytic subunits of the Pafah1b complex, Pafah1b2 and Pafah1b3, specifically bind to the NPxYL sequence of VLDLR, but not to ApoER2. Compound Pafah1b1(+/−);Apoer2(−/−) mutant mice exhibit a reeler-like phenotype in the forebrain consisting of the inversion of cortical layers and hippocampal disorganization, whereas double Pafah1b1(+/−);Vldlr(−/−) mutants do not. These results suggest that a cross-talk between the Pafah1b complex and Reelin occurs downstream of the VLDLR receptor

A Graphical Null Model for Scaling Biodiversity–Ecosystem Functioning Relationships

Global biodiversity is declining at rates faster than at any other point in human history. Experimental manipulations at small spatial scales have demonstrated that communities with fewer species consistently produce less biomass than higher diversity communities. Understanding the consequences of the global extinction crisis for ecosystem functioning requires understanding how local experimental results are likely to change with increasing spatial and temporal scales and from experiments to naturally assembled systems. Scaling across time and space in a changing world requires baseline predictions. Here, we provide a graphical null model for area scaling of biodiversity–ecosystem functioning relationships using observed macroecological patterns: the species–area curve and the biomass–area curve. We use species–area and biomass–area curves to predict how species richness–biomass relationships are likely to change with increasing sampling extent. We then validate these predictions with data from two naturally assembled ecosystems: a Minnesota savanna and a Panamanian tropical dry forest. Our graphical null model predicts that biodiversity–ecosystem functioning relationships are scale-dependent. However, we note two important caveats. First, our results indicate an apparent contradiction between predictions based on measurements in biodiversity–ecosystem functioning experiments and from scaling theory. When ecosystem functioning is measured as per unit area (e.g. biomass per m2), as is common in biodiversity–ecosystem functioning experiments, the slope of the biodiversity ecosystem functioning relationship should decrease with increasing scale. Alternatively, when ecosystem functioning is not measured per unit area (e.g. summed total biomass), as is common in scaling studies, the slope of the biodiversity–ecosystem functioning relationship should increase with increasing spatial scale. Second, the underlying macroecological patterns of biodiversity experiments are predictably different from some naturally assembled systems. These differences between the underlying patterns of experiments and naturally assembled systems may enable us to better understand when patterns from biodiversity–ecosystem functioning experiments will be valid in naturally assembled systems. Synthesis. This paper provides a simple graphical null model that can be extended to any relationship between biodiversity and any ecosystem functioning across space or time. Furthermore, these predictions provide crucial insights into how and when we may be able to extend results from small-scale biodiversity experiments to naturally assembled regional and global ecosystems where biodiversity is changing

Managing design and designers for strategic renewal

For producers of traditional or high-tech consumer durables seeking to differentiate themselves from their competitors, the role of the product designer is increasingly taking a key role. In fact design and designers can contribute to corporate strategic renewal, and this paper proposes a framework for understanding how this can be achieved. Building on a study of outstanding innovators in product design – names such as Apple, Alessi and Bang & Olufsen – the authors describe design-driven renewal as a four-phase process stimulated and supported by design, combining continuous product innovation with the periodic revision of the strategic course of the company. For each phase, it discusses the specific role of managers and the most common pitfalls that arise from poor management of the process

Can we use the pharmacy data to estimate the prevalence of chronic conditions? a comparison of multiple data sources

<p>Abstract</p> <p>Background</p> <p>The estimate of the prevalence of the most common chronic conditions (CCs) is calculated using direct methods such as prevalence surveys but also indirect methods using health administrative databases.</p> <p>The aim of this study is to provide estimates prevalence of CCs in Lazio region of Italy (including Rome), using the drug prescription's database and to compare these estimates with those obtained using other health administrative databases.</p> <p>Methods</p> <p>Prevalence of CCs was estimated using pharmacy data (PD) using the Anathomical Therapeutic Chemical Classification System (ATC).</p> <p>Prevalences estimate were compared with those estimated by hospital information system (HIS) using list of ICD9-CM diagnosis coding, registry of exempt patients from health care cost for pathology (REP) and national health survey performed by the Italian bureau of census (ISTAT).</p> <p>Results</p> <p>From the PD we identified 20 CCs. About one fourth of the population received a drug for treating a cardiovascular disease, 9% for treating a rheumatologic conditions.</p> <p>The estimated prevalences using the PD were usually higher that those obtained with one of the other sources. Regarding the comparison with the ISTAT survey there was a good agreement for cardiovascular disease, diabetes and thyroid disorder whereas for rheumatologic conditions, chronic respiratory illnesses, migraine and Alzheimer's disease, the prevalence estimates were lower than those estimated by ISTAT survey. Estimates of prevalences derived by the HIS and by the REP were usually lower than those of the PD (but malignancies, chronic renal diseases).</p> <p>Conclusion</p> <p>Our study showed that PD can be used to provide reliable prevalence estimates of several CCs in the general population.</p

IL28B and IL10R -1087 polymorphisms are protective for chronic genotype 1 HCV infection and predictors of response to interferon-based therapy in an East-Central European cohort.

BACKGROUND: Previous studies have shown that single nucleotide polymorphisms (SNP) in IL28B and IL10R are associated with sustained virological response (SVR) in chronic hepatitis C patients treated with pegilated interferon plus ribavirin (P/R). The present study extends our earlier investigations on a large East-Central European cohort. The allele frequencies of IL28B and IL10R in genotype 1 HCV infection were compared with that of healthy controls for the purpose of examining the relationship between the polymorphisms and the SVR to P/R treatment. METHODS: A total of 748 chronic HCV1 infected patients (365 male, 383 female; 18-82 years) and 105 voluntary blood donors as controls were enrolled. Four hundred and twenty HCV patients were treated with P/R for 24-72 weeks, out of them 195 (46.4%) achieved SVR. The IL28 rs12979860 SNP was determined using Custom Taqman SNP Genotyping Assays. The IL10R -1087 (also known as IL10R -1082 (rs1800896) promoter region SNP was determined by RT-PCR and restriction fragment length polymorphism analysis. RESULTS: The IL28B CC genotype occurred with lower frequency in HCV patients than in controls (26.1% vs 51.4%, p<0.001). P/R treated patients with the IL28B CC genotype achieved higher SVR rate, as compared to patients with CT (58.6% vs 40.8%, p=0.002). The prevalence of IL10R -1087 GG genotype was lower in patients than in controls (31.8 % vs 52.2%, p<0.001). Among patients achieving SVR, the IL10R -1087 GG genotype occurred with higher frequency than the AA (32.0% vs 17.4%, p=0.013). The IL28B T allele plus IL10R A allele combination was found with higher prevalence in patients than in controls (52% vs 20.7%, p<0.001). The IL28B CC plus IL10R A allele combination occurred with higher frequency among patients with SVR than in non-responders (21.3% vs 12.8%, p=0.026). Both the IL28B CC plus IL10R GG and the IL28B CC plus IL10R A allele combinations occurred with lower frequency in patients than in controls. CONCLUSIONS: In our HCV1 patients, both the IL28B CC and IL10R GG genotypes are associated with clearance of HCV. Moreover, distinct IL28B and IL10R allele combinations appear to be protective against chronic HCV1 infection and predictors of response to P/R therapy