The Legacy of Frederick Douglass’s Words

poster abstractMore than a century after his death, Frederick Douglass remains an iconic figure widely referenced by politicians, educators, editorialists, community activists, poets, hip hop artists, comedians, and more, both domestically and abroad as a legitimizing and representative historical figure. This fact raises a number of questions— why have Douglass’s rhetorical contributions remained significant to so many persons in the 21st century? What types of individuals and organizations continue to find the legacy of Douglass’s words relevant and what is the underlying significance therein? How well have Douglass’s 19th century words and ideas been adapted to more modern forms of media and audience expectations that have arisen in the subsequent centuries since his 1895 death?—that this exploration into Douglass’s enduring legacy helps to identify. In order to address these issues, we employed techniques from two disciplines, History and Communication Studies, to identify and analyze the impact of the large body of speeches, editorials, and autobiographical writings left by the runaway Maryland slave who rose to become the most influential African American of the nineteenth century. This research was conducted through careful examination of both print and online sources from the 19th through the 20th centuries as we located and then verified the accuracy of quotations purporting to be from Douglass’s works. Finally we assessed the usage of Douglass’s words by modern commentators through the employment of current scholarly lenses such as rhetorical criticism, cultural studies, and Critical Race Theory in order to judge whether this usage was consistent with the values of Douglass’s long public career as a reformer in areas of social justice and politics. This study further demonstrates the need for continued analysis and dissemination of his thinking considering the modern-day relevancy that is still found in Douglass’s commentary and opinions

The Impact on the Ohio River Watershed by the United States Federal Government

poster abstractThis interactive timeline, which currently covers 1775 through the first quarter of 2014, takes accounts of water-related actions of the federal government and places them alongside water-related environmental events. Research drew together water use information within Acts of Congress, legal cases argued before the Supreme Court, actions undertaken by agencies within the Executive Department, and reports of pollution or flood incidents. This data was then charted using Tiki-Toki software into separate bands along the timeline with descriptions, images, and links to add depth of explanation. This juxtaposition reveals a story tracing human interaction along the Ohio River watershed since the American Revolution. In addition, the Tiki-Toki software makes the information available in multiple views through which different patterns emerge allowing future researchers to manipulate the timeline to more easily see connections with their own projects. Because of the data’s inclusiveness and ease of use, this timeline can provide a platform for comparison with the companion site of the Rivers of the Anthropocene study, the River Tyne. However, since the primary region of study in the United States is the Ohio River and its tributaries, only data applicable to this region specifically or all water in the United States generally was utilized. Because of the exclusiveness of the data, frequent gaps in events may risk being misinterpreted as a period of inactivity on the part of the federal government, though this is likely not the case; even apparent inactivity along the Ohio reveals much about human impact on the waterway systems

Canal Pride: When the Public Sector Drove Downtown Development

poster abstractThe Indianapolis Downtown Canal was originally meant to connect Indiana to flows of commerce and trade as part of an interstate canal system. During construction of the canal in the 1830s, the state of Indiana faced an economic recession and the canal was then turned over to the state’s creditors. Over a hundred and fifty years later, in the late 1980s, new political leaders in Indianapolis stepped up and refused to let this historical feature continue to deteriorate. To mitigate the damage caused by years of neglect, combined with a desire to make Downtown Indianapolis more attractive to residents and tourists, the city made it a priority to revitalize the waterway. This transformation from murky, litter-ridden eyesore into one of Downtown’s greatest assets spanned multiple mayoral administrations, bringing together public sector project leaders with private sector interest groups. This research team focused on residential and commercial redevelopment along the downtown canal to show how one of Indianapolis’s greatest follies turned into one of the top reasons to visit or live downtown

Effects of gestational age at birth on cognitive performance : a function of cognitive workload demands

Objective: Cognitive deficits have been inconsistently described for late or moderately preterm children but are consistently found in very preterm children. This study investigates the association between cognitive workload demands of tasks and cognitive performance in relation to gestational age at birth. Methods: Data were collected as part of a prospective geographically defined whole-population study of neonatal at-risk children in Southern Bavaria. At 8;5 years, n = 1326 children (gestation range: 23–41 weeks) were assessed with the K-ABC and a Mathematics Test. Results: Cognitive scores of preterm children decreased as cognitive workload demands of tasks increased. The relationship between gestation and task workload was curvilinear and more pronounced the higher the cognitive workload: GA2 (quadratic term) on low cognitive workload: R2 = .02, p<0.001; moderate cognitive workload: R2 = .09, p<0.001; and high cognitive workload tasks: R2 = .14, p<0.001. Specifically, disproportionally lower scores were found for very (<32 weeks gestation) and moderately (32–33 weeks gestation) preterm children the higher the cognitive workload of the tasks. Early biological factors such as gestation and neonatal complications explained more of the variance in high (12.5%) compared with moderate (8.1%) and low cognitive workload tasks (1.7%). Conclusions: The cognitive workload model may help to explain variations of findings on the relationship of gestational age with cognitive performance in the literature. The findings have implications for routine cognitive follow-up, educational intervention, and basic research into neuro-plasticity and brain reorganization after preterm birth

Reduced Neutrophil Count in People of African Descent Is Due To a Regulatory Variant in the Duffy Antigen Receptor for Chemokines Gene

Persistently low white blood cell count (WBC) and neutrophil count is a well-described phenomenon in persons of African ancestry, whose etiology remains unknown. We recently used admixture mapping to identify an approximately 1-megabase region on chromosome 1, where ancestry status (African or European) almost entirely accounted for the difference in WBC between African Americans and European Americans. To identify the specific genetic change responsible for this association, we analyzed genotype and phenotype data from 6,005 African Americans from the Jackson Heart Study (JHS), the Health, Aging and Body Composition (Health ABC) Study, and the Atherosclerosis Risk in Communities (ARIC) Study. We demonstrate that the causal variant must be at least 91% different in frequency between West Africans and European Americans. An excellent candidate is the Duffy Null polymorphism (SNP rs2814778 at chromosome 1q23.2), which is the only polymorphism in the region known to be so differentiated in frequency and is already known to protect against Plasmodium vivax malaria. We confirm that rs2814778 is predictive of WBC and neutrophil count in African Americans above beyond the previously described admixture association (P = 3.8×10^−5), establishing a novel phenotype for this genetic variant

Validity of self-reported weight, height, and body mass index among university students in Thailand: Implications for population studies of obesity in developing countries

<p>Abstract</p> <p>Background</p> <p>Large-scale epidemiological studies commonly use self-reported weights and heights to determine weight status. Validity of such self-reported data has been assessed primarily in Western populations in developed countries, although its use is widespread in developing countries. We examine the validity of obesity based on self-reported data in an Asian developing country, and derive improved obesity prevalence estimates using the "reduced BMI threshold" method.</p> <p>Methods</p> <p>Self-reported and measured heights and weights were obtained from 741 students attending an open university in Thailand (mean age 34 years). Receiver operator characteristic techniques were applied to derive "reduced BMI thresholds."</p> <p>Results</p> <p>Height was over-reported by a mean of 1.54 cm (SD 2.23) in men and 1.33 cm (1.84) in women. Weight was under-reported by 0.93 kg (3.47) in men and 0.62 kg (2.14) in women. Sensitivity and specificity for determining obesity (Thai BMI threshold 25 kg/m²) using self-reported data were 74.2% and 97.3%, respectively, for men and 71.9% and 100% for women. For men, reducing the BMI threshold to 24.5 kg/m²increased the estimated obesity prevalence based on self-reports from 29.1% to 33.8% (true prevalence was 36.9%). For women, using a BMI threshold of 24.4 kg/m², the improvement was from 12.0% to 15.9% (true prevalence 16.7%).</p> <p>Conclusion</p> <p>Young educated Thais under-report weight and over-report height in ways similar to their counterparts in developed countries. Simple adjustments to BMI thresholds will overcome these reporting biases for estimation of obesity prevalence. Our study suggests that self-reported weights and heights can provide economical and valid measures of weight status in high school-educated populations in developing countries.</p

Cross-tissue, single-cell stromal atlas identifies shared pathological fibroblast phenotypes in four chronic inflammatory diseases

BackgroundPro-inflammatory fibroblasts are critical for pathogenesis in rheumatoid arthritis, inflammatory bowel disease, interstitial lung disease, and Sjögren’s syndrome and represent a novel therapeutic target for chronic inflammatory disease. However, the heterogeneity of fibroblast phenotypes, exacerbated by the lack of a common cross-tissue taxonomy, has limited our understanding of which pathways are shared by multiple diseases.MethodsWe profiled fibroblasts derived from inflamed and non-inflamed synovium, intestine, lungs, and salivary glands from affected individuals with single-cell RNA sequencing. We integrated all fibroblasts into a multi-tissue atlas to characterize shared and tissue-specific phenotypes.FindingsTwo shared clusters, CXCL10+CCL19+ immune-interacting and SPARC+COL3A1+ vascular-interacting fibroblasts, were expanded in all inflamed tissues and mapped to dermal analogs in a public atopic dermatitis atlas. We confirmed these human pro-inflammatory fibroblasts in animal models of lung, joint, and intestinal inflammation.ConclusionsThis work represents a thorough investigation into fibroblasts across organ systems, individual donors, and disease states that reveals shared pathogenic activation states across four chronic inflammatory diseases.FundingGrant from F. Hoffmann-La Roche (Roche) AG

Cross-tissue, single-cell stromal atlas identifies shared pathological fibroblast phenotypes in four chronic inflammatory diseases

BackgroundPro-inflammatory fibroblasts are critical for pathogenesis in rheumatoid arthritis, inflammatory bowel disease, interstitial lung disease, and Sjögren’s syndrome and represent a novel therapeutic target for chronic inflammatory disease. However, the heterogeneity of fibroblast phenotypes, exacerbated by the lack of a common cross-tissue taxonomy, has limited our understanding of which pathways are shared by multiple diseases.MethodsWe profiled fibroblasts derived from inflamed and non-inflamed synovium, intestine, lungs, and salivary glands from affected individuals with single-cell RNA sequencing. We integrated all fibroblasts into a multi-tissue atlas to characterize shared and tissue-specific phenotypes.FindingsTwo shared clusters, CXCL10+CCL19+ immune-interacting and SPARC+COL3A1+ vascular-interacting fibroblasts, were expanded in all inflamed tissues and mapped to dermal analogs in a public atopic dermatitis atlas. We confirmed these human pro-inflammatory fibroblasts in animal models of lung, joint, and intestinal inflammation.ConclusionsThis work represents a thorough investigation into fibroblasts across organ systems, individual donors, and disease states that reveals shared pathogenic activation states across four chronic inflammatory diseases.FundingGrant from F. Hoffmann-La Roche (Roche) AG

A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction

The developmental and physiological complexity of the auditory system is likely reflected in the underlying set of genes involved in auditory function. In humans, over 150 non-syndromic loci have been identified, and there are more than 400 human genetic syndromes with a hearing loss component. Over 100 non-syndromic hearing loss genes have been identified in mouse and human, but we remain ignorant of the full extent of the genetic landscape involved in auditory dysfunction. As part of the International Mouse Phenotyping Consortium, we undertook a hearing loss screen in a cohort of 3006 mouse knockout strains. In total, we identify 67 candidate hearing loss genes. We detect known hearing loss genes, but the vast majority, 52, of the candidate genes were novel. Our analysis reveals a large and unexplored genetic landscape involved with auditory function

Reduced Neutrophil Count in People of African Descent Is Due To a Regulatory Variant in the Duffy Antigen Receptor for Chemokines Gene

Persistently low white blood cell count (WBC) and neutrophil count is a well-described phenomenon in persons of African ancestry, whose etiology remains unknown. We recently used admixture mapping to identify an approximately 1-megabase region on chromosome 1, where ancestry status (African or European) almost entirely accounted for the difference in WBC between African Americans and European Americans. To identify the specific genetic change responsible for this association, we analyzed genotype and phenotype data from 6,005 African Americans from the Jackson Heart Study (JHS), the Health, Aging and Body Composition (Health ABC) Study, and the Atherosclerosis Risk in Communities (ARIC) Study. We demonstrate that the causal variant must be at least 91% different in frequency between West Africans and European Americans. An excellent candidate is the Duffy Null polymorphism (SNP rs2814778 at chromosome 1q23.2), which is the only polymorphism in the region known to be so differentiated in frequency and is already known to protect against Plasmodium vivax malaria. We confirm that rs2814778 is predictive of WBC and neutrophil count in African Americans above beyond the previously described admixture association (P = 3.8×10−5), establishing a novel phenotype for this genetic variant