Prosocial motives underlie scientific censorship by scientists: A perspective and research agenda.

Science is among humanity's greatest achievements, yet scientific censorship is rarely studied empirically. We explore the social, psychological, and institutional causes and consequences of scientific censorship (defined as actions aimed at obstructing particular scientific ideas from reaching an audience for reasons other than low scientific quality). Popular narratives suggest that scientific censorship is driven by authoritarian officials with dark motives, such as dogmatism and intolerance. Our analysis suggests that scientific censorship is often driven by scientists, who are primarily motivated by self-protection, benevolence toward peer scholars, and prosocial concerns for the well-being of human social groups. This perspective helps explain both recent findings on scientific censorship and recent changes to scientific institutions, such as the use of harm-based criteria to evaluate research. We discuss unknowns surrounding the consequences of censorship and provide recommendations for improving transparency and accountability in scientific decision-making to enable the exploration of these unknowns. The benefits of censorship may sometimes outweigh costs. However, until costs and benefits are examined empirically, scholars on opposing sides of ongoing debates are left to quarrel based on competing values, assumptions, and intuitions.

Association Between Health Insurance and Outcomes After Traumatic Brain Injury: A National ACS-TQP-PUF Database Study.

INTRODUCTION: According to the US Census Bureau, roughly 8.6% of the population lacks health care coverage. Increasing evidence suggests that insurance status plays a role in outcomes after trauma. However, its role in the setting of traumatic brain injury (TBI) remains poorly understood. METHODS: The Trauma Quality Programs Participant Use Files were queried from 2017 to 2019. All patients with isolated TBI were identified. Isolated TBI was defined as: 1) Head Abbreviated Injury Scale (AIS) > 3 and 2) AIS <3 in all other anatomical regions. Patients dead on arrival, with Head AIS = 6, or missing key data were excluded. Demographic and clinical information was compared between those with and without insurance. Multivariate regressions were used to assess associations between insurance status and TBI outcomes (inhospital mortality, discharge to facility, total ventilator days, Intensive Care Unit length of stay (ICU LOS), and hospital LOS). RESULTS: In total, 199,556 patients met inclusion criteria; 18,957 (9.5%) were uninsured. Compared to the insured, uninsured TBI patients were younger with a greater proportion of males. Uninsured patients were less severely injured and less comorbid. Uninsured patients had shorter unadjusted LOS in the ICU and hospital. Yet, uninsured patients experienced greater unadjusted inhospital mortality (12.7% versus 8.4%, P < 0.001). When controlling for covariates, lack of insurance was significantly associated with increased likelihood of mortality (OR 1.62; P < 0.001). This effect was most noticeable in patients with Head AIS = 4 (OR 1.55; P < 0.001) and Head AIS = 5 (OR 1.80; P < 0.001). Lack of insurance was also significantly associated with decreased likelihood of discharge to facility (OR 0.38), decreased ICU LOS (Coeff. -0.61), and decreased hospital LOS (Coeff. -0.82; all P < 0.001). CONCLUSIONS: This study demonstrates that insurance status is independently associated with outcome disparities after isolated TBI. Despite the Affordable Care Act (ACA) reform, lack of insurance appears significantly associated with inhospital mortality, decreased likelihood of discharge to facility, and decreased time spent in the ICU and hospital.

Chronic circadian misalignment results in reduced longevity and large-scale changes in gene expression in Drosophila.

BACKGROUND: Circadian clocks are found in nearly all organisms, from bacteria to mammals, and ensure that behavioral and physiological processes occur at optimal times of day and in the correct temporal order. It is becoming increasingly clear that chronic circadian misalignment (CCM), such as occurs in shift workers or as a result of aberrant sleeping and eating schedules common to modern society, has profound metabolic and cognitive consequences, but the proximate mechanisms connecting CCM with reduced organismal health are unknown. Furthermore, it has been difficult to disentangle whether the health effects are directly induced by misalignment or are secondary to the alterations in sleep and activity levels that commonly occur with CCM. Here, we investigated the consequences of CCM in the powerful model system of the fruit fly, Drosophila melanogaster. We subjected flies to daily 4-h phase delays in the light-dark schedule and used the Drosophila Activity Monitoring (DAM) system to continuously track locomotor activity and sleep while simultaneously monitoring fly lifespan. RESULTS: Consistent with previous results, we find that exposing flies to CCM leads to a ~ 15% reduction in median lifespan in both male and female flies. Importantly, we demonstrate that the reduced longevity occurs independent of changes in overall sleep or activity. To uncover potential molecular mechanisms of CCM-induced reduction in lifespan, we conducted whole body RNA-sequencing to assess differences in gene transcription between control and misaligned flies. CCM caused progressive, large-scale changes in gene expression characterized by upregulation of genes involved in response to toxic substances, aging and oxidative stress, and downregulation of genes involved in regulation of development and differentiation, gene expression and biosynthesis. CONCLUSIONS: Many of these gene expression changes mimic those that occur during natural aging, consistent with the idea that CCM results in premature organismal decline, however, we found that genes involved in lipid metabolism are overrepresented among those that are differentially regulated by CCM and aging. This category of genes is also among the earliest to exhibit CCM-induced changes in expression, thus highlighting altered lipid metabolism as a potentially important mediator of the negative health consequences of CCM.