Whose Side are Ethics Codes On? Power, Responsibility and the Social Good

The moral authority of ethics codes stems from an assumption that they serve a unified society, yet this ignores the political aspects of any shared resource. The sociologist Howard S. Becker challenged researchers to clarify their power and responsibility in the classic essay: Whose Side Are We On. Building on Becker's hierarchy of credibility, we report on a critical discourse analysis of data ethics codes and emerging conceptualizations of beneficence, or the "social good", of data technology. The analysis revealed that ethics codes from corporations and professional associations conflated consumers with society and were largely silent on agency. Interviews with community organizers about social change in the digital era supplement the analysis, surfacing the limits of technical solutions to concerns of marginalized communities. Given evidence that highlights the gulf between the documents and lived experiences, we argue that ethics codes that elevate consumers may simultaneously subordinate the needs of vulnerable populations. Understanding contested digital resources is central to the emerging field of public interest technology. We introduce the concept of digital differential vulnerability to explain disproportionate exposures to harm within data technology and suggest recommendations for future ethics codes.Comment: Conference on Fairness, Accountability, and Transparency (FAT* '20), January 27-30, 2020, Barcelona, Spain. Correcte

QTL Mapping of a High Protein Digestibility Trait in Sorghum bicolor

Compared with other cereal grains, Sorghum bicolor shows lower protein digestibility. The low digestibility is thought to result from disulfide cross linking in the β- and γ-kafirins. In contrast, the single recessive high digestibility/high lysine content (HD) mutation which confers greater grain digestibility exists in sorghum that is thought to result from reduced accumulation of γ-kafirin that allows greater access to the high digestible α-kafarin fraction. In an effort to both clearly define the molecular basis for the HD trait and develop tools to improve the introgression of this difficult-to-screen trait, this study focuses on mapping the QTLs linked to this trait. While the HD trait has been defined as a single recessive gene, our results uncovered that two major QTLs on chromosome 1 are associated with protein digestibility—one QTL (locus 1 from the HD parent) unfavorably affects digestibility and one QTL (locus 2 from the HD parent) only 20 cM away favorably affects digestibility. A contrast analysis between genotypic groups at these two loci shows that a higher level of protein digestibility may be obtained when this linkage in repulsion is broken and favorable alleles are allowed to recombine

The children's brain tumor network (CBTN) - Accelerating research in pediatric central nervous system tumors through collaboration and open science

Pediatric brain tumors are the leading cause of cancer-related death in children in the United States and contribute a disproportionate number of potential years of life lost compared to adult cancers. Moreover, survivors frequently suffer long-term side effects, including secondary cancers. The Children's Brain Tumor Network (CBTN) is a multi-institutional international clinical research consortium created to advance therapeutic development through the collection and rapid distribution of biospecimens and data via open-science research platforms for real-time access and use by the global research community. The CBTN's 32 member institutions utilize a shared regulatory governance architecture at the Children's Hospital of Philadelphia to accelerate and maximize the use of biospecimens and data. As of August 2022, CBTN has enrolled over 4700 subjects, over 1500 parents, and collected over 65,000 biospecimen aliquots for research. Additionally, over 80 preclinical models have been developed from collected tumors. Multi-omic data for over 1000 tumors and germline material are currently available with data generation for > 5000 samples underway. To our knowledge, CBTN provides the largest open-access pediatric brain tumor multi-omic dataset annotated with longitudinal clinical and outcome data, imaging, associated biospecimens, child-parent genomic pedigrees, and in vivo and in vitro preclinical models. Empowered by NIH-supported platforms such as the Kids First Data Resource and the Childhood Cancer Data Initiative, the CBTN continues to expand the resources needed for scientists to accelerate translational impact for improved outcomes and quality of life for children with brain and spinal cord tumors

Preschool Executive Control, Temperament, and Adolescent Dietary Behaviors

Background Child temperament styles characterized by increased emotionality or pleasure seeking may increase risk for less healthful eating patterns, while strong executive control (EC) may be protective. The interaction of these characteristics with longitudinal outcomes has not yet been examined. Purpose The aim of this study was to examine the association of preschool temperament and EC, as well as their interaction with adolescent eating. Methods Preschoolers (N = 313) were recruited into a longitudinal study, with behavioral measurement of EC at age 5.25 years, temperament assessed multiple times across preschool, and eating outcomes assessed in adolescence (mean age = 15.34 years). Results Separate latent moderated structural equation models demonstrated that weaker EC was associated with eating less healthful foods, including high sugar foods, sugar-sweetened beverages (SSBs), and convenience foods (p \u3c .05). In the moderation models, negative affectivity temperament was correlated with eating less healthful foods, high sugar foods, and SSBs (p \u3c .05). Children lower in surgency/extraversion temperament were more likely to drink SSBs. There was an interaction between temperament and EC, such that children high in negative affectivity with weaker EC were particularly more likely to consume less healthful foods, high sugar foods, and SSBs (p \u3c .05). There was no interaction of surgency with EC and food consumption. Conclusions Child characteristics measured early in development were associated with later adolescent eating behaviors. Adequate EC could be necessary to counteract the drive toward eating associated with temperaments high in negative affectivity. Lay Summary A preschool temperament style called Negative Affectivity, characterized by high levels of reactivity and negative emotion, predicted eating patterns a decade later. These children were more likely to eat less healthful foods and drink sugary drinks as adolescents. Strong executive function skills were important for redirecting toward healthful eating in children with Negative Affectivity

Defining boat wake impacts on shoreline stability toward management and policy solutions

Coastal economies are often supported by activities that rely on commercial or recreational vessels to move people or goods, such as shipping, transportation, cruising, and fishing. Unintentionally, frequent or intense vessel traffic can contribute to erosion of coastlines; this can be particularly evident in sheltered systems where shoreline erosion should be minimal in the absence of boat waves. We reviewed the state of the science of known effects of boat waves on shoreline stability, examined data on erosion, turbidity, and shoreline armoring patterns for evidence of a response to boat waves in Chesapeake Bay, and reviewed existing management and policy actions in Chesapeake Bay and nearby states to make recommendations for actions to minimize boat wake impacts. In the literature, as well as in our analyses, boat wake energy may be linked to elevated turbidity and shoreline erosion, particularly in narrow waterways. In Chesapeake Bay, three lines of evidence suggest boat waves are contributing to shoreline erosion and poor water clarity in some Bay creeks and tributaries: 1) nearshore turbidity was elevated in many waterways during periods of expected high boating activity, 2) armoring was placed along about a quarter of the low energy shorelines of three examined tidal creeks that are exposed to relatively high boating pressure, and 3) 15% of the shorelines we examined throughout the Bay (9000 km) are low energy shorelines that are experiencing high erosion (≥0.3 m/yr) that cannot be attributed to wind wave energy. Still, there remain significant data gaps that preclude the determination of the overall contribution of boat waves to shoreline erosion throughout the Bay, notably, shoreline erosion data in low energy waterways, recreational boating traffic patterns, and nearshore bathymetry. Interim protective measures can be (and have been) applied in high risk waterways, such as small, low energy waterways that have high recreational boating activity, to help reduce shoreline erosion. Policy options used in Bay states and elsewhere include setbacks from the shore, wake restrictions, and speed restrictions; other more restrictive policies may include prohibition on boats of a certain size or limiting the number of passages. Finally, a systems-approach to boat wake impact management using uniform boat wake policies is likely to be the most effective for consistent shoreline protection

Posttraumatic stress disorder and accelerated aging: PTSD and leukocyte telomere length in a sample of civilian women.

BACKGROUND: Studies in male combat veterans have suggested posttraumatic stress disorder (PTSD) is associated with shorter telomere length (TL). We examined the cross-sectional association of PTSD with TL in women exposed to traumas common in civilian life. METHODS: Data are from a substudy of the Nurses' Health Study II (N = 116). PTSD and subclinical PTSD were assessed in trauma-exposed women using diagnostic interviews. An array of health behaviors and conditions were assessed. DNA was extracted from peripheral blood leukocytes (collected 1996-1999). Telomere repeat copy number to single gene copy number (T/S) was determined by quantitative real-time PCR telomere assay. We used linear regression models to assess associations and examine whether a range of important health behaviors (e.g., cigarette smoking) and medical conditions (e.g., hypertension) previously associated with TL might explain a PTSD-TL association. We further examined whether type of trauma exposure (e.g., interpersonal violence) was associated with TL and whether trauma type might explain a PTSD-TL association. RESULTS: Relative to not having PTSD, women with a PTSD diagnosis had shorter log-transformed TL (β = -.112, 95% confidence interval (CI) = -0.196, -0.028). Adjustment for health behaviors and medical conditions did not attenuate this association. Trauma type was not associated with TL and did not account for the association of PTSD with TL. CONCLUSIONS: Our results add to growing evidence that PTSD may be associated with more rapid cellular aging as measured by telomere erosion. Moreover, the association could not be explained by health behaviors and medical conditions assessed in this study, nor by type of trauma exposure

Executive Control in Early Childhood as an Antecedent of Adolescent Problem Behaviors: A Longitudinal Study with Performance-based Measures of Early Childhood Cognitive Processes

Identifying childhood cognitive processes that predict adolescent problem behaviors can help guide understanding and prevention of these behaviors. In a community sample of 313 youth recruited in a small Midwestern city between 2006 and 2012 (49% male, 64% European American), executive control and foundational cognitive abilities were assessed at age 5 in a lab setting with performance-based measures. In adolescence, youth provided self-report of problem behaviors in surveys administered annually between ages 14 and 16. Executive control was negatively associated with externalizing behavior problems and adolescents getting in trouble at school, accounting for foundational cognitive abilities and family background covariates. Executive control had negative but nonsignificant associations with internalizing problems and substance use initiation. The findings point to deficits in executive control as a childhood risk factor for later problems and a potential target for preventive interventions

A 3-D PYRAMID/PRISM APPROACH TO VIEW KNOWLEDGE REQUIREMENTS FOR THE BATCH MEANS METHOD WHEN TAUGHT IN A LANGUAGE-FOCUSED, UNDERGRADUATE SIMULATION COURSE

We develop a 3-D knowledge pyramid/prism model to structure the relationships of (i) lower-level learning, (ii) ‘optional ’ knowledge bases, (iii) concurrent knowledge, and (ii) new knowledge; so one may view the learning needs of a higher-level learning objective. Our paradigm stems from Bloom’s taxonomy of learning, but has the advantage of supporting ‘just-in-time ’ and ‘learn-by-doing’ delivery, teaching and learning styles. We illustrate the paradigm through the BMMKP (the 3-D knowledge pyramid/prism model of the highest-level, batch-means-method learning objective for our language-focused, undergraduate course). The BMMKP reveals how highly dependent and fully integrated this learning is to calculus, probability, statistics, and queuing theory—regardless of the simulation modeling language chosen to teach in the course. The BMMKP is then used to develop a set of lower-level learning objectives for the undergraduate course. The 3-D pyramid/prism approach should lend itself well as a communication tool for visualizing other simulation learning objectives.

Mitotic stress is an integral part of the oncogene-induced senescence program that promotes multinucleation and cell cycle arrest

Oncogene-induced senescence (OIS) is a tumor suppression mechanism that blocks cell proliferation in response to oncogenic signaling. OIS is frequently accompanied by multinucleation; however, the origin of this is unknown. Here, we show that multinucleate OIS cells originate mostly from failed mitosis. Prior to senescence, mutant H-RasV12 activation in primary human fibroblasts compromised mitosis, concordant with abnormal expression of mitotic genes functionally linked to the observed mitotic spindle and chromatin defects. Simultaneously, H-RasV12 activation enhanced survival of cells with damaged mitoses, culminating in extended mitotic arrest and aberrant exit from mitosis via mitotic slippage. ERK-dependent transcriptional upregulation of Mcl1 was, at least in part, responsible for enhanced survival and slippage of cells with mitotic defects. Importantly, mitotic slippage and oncogene signaling cooperatively induced senescence and key senescence effectors p21 and p16. In summary, activated Ras coordinately triggers mitotic disruption and enhanced cell survival to promote formation of multinucleate senescent cells