World Society and the University as Formal Organization

This paper describes and interprets the worldwide transformation of universities with respect to how they account for excellence. It first reflects on the rationalized university as an organizational ideal and the implications of rationalization on standardizing university practices. The paper then focuses on two interrelated phenomena: the assessment of faculty and the assessment of universities, as illustrations of accounting-for-excellence. Examining the annual faculty report and tenure protocol as examples of common organizational practices within American universities, it argues that these practices facilitate American university participation in national and international university rankings. Finally, it is argued that American universities underwent earlier organizational rationalization and differentiation than universities in other countries in part because they were less differentiated from other social institutions. In the absence of the buffering authority of the state and the professoriate, American universities early on became organizational actors dealing with multiple stakeholders in search of resources and legitimacy

Linoleic Acid Improves Piezo2 Dysfunction in a Mouse Model of Angelman Syndrome

Angelman syndrome (AS) is a neurogenetic disorder characterized by intellectual disability and atypical behaviors. AS results from loss of expression of the E3 ubiquitin-protein ligase UBE3A from the maternal allele in neurons. Individuals with AS display impaired coordination, poor balance, and gait ataxia. PIEZO2 is a mechanosensitive ion channel essential for coordination and balance. Here, we report that PIEZO2 activity is reduced in Ube3a deficient male and female mouse sensory neurons, a human Merkel cell carcinoma cell line and female human iPSC-derived sensory neurons with UBE3A knock-down, and de-identified stem cell-derived neurons from individuals with AS. We find that loss of UBE3A decreases actin filaments and reduces PIEZO2 expression and function. A linoleic acid (LA)-enriched diet increases PIEZO2 activity, mechano-excitability, and improves gait in male AS mice. Finally, LA supplementation increases PIEZO2 function in stem cell-derived neurons from individuals with AS. We propose a mechanism whereby loss of UBE3A expression reduces PIEZO2 function and identified a fatty acid that enhances channel activity and ameliorates AS-associated mechano-sensory deficits

Infância, exclusão social e educação como utopia realizável

A infância, como construção social, tem sofrido, no decurso da 2ª modernidade, processos de reinstitucionalização que, em larga medida, põem em causa as representações e imagens das crianças, dominantes nos últimos 200 anos. A análise da (re)construção das identidades sociais e das subjectividades infantis constitui, desse modo, uma tarefa teórica da mais exigente actualidade. O que, entretanto, aqui se assinala é que este processo de reinstitucionalização da infância, apesar da construção de consensos globais sobre os direitos das crianças, tem vindo a aumentar os factores e as condições de exclusão das gerações mais jovens face aos direitos sociais e da cidadania. Neste artigo inventariam-se alguns dos principais indicadores de exclusão, considerando diversos espaços estruturais, e assinalam-se alguns dos pontos de ruptura por onde pode passar a construção de uma educação escolar centrada na afirmação activa dos direitos das crianças.Along the second modernity, childhood, as a social construction, has undergone reinstatement processes that question the representations and images of children that have prevailed over last two hundred years. An analysis of the (re) construction of the social identities and childhood subjectivity thus constitute a theoretical task of the most contemporary exigence. Nevertheless, even though a global consensus about children’s rights has been constructed, the increase of factors and conditions that exclude the youngest generations from social rights and citizenship, induced by this reinstatement process of childhood, is here emphasized. This paper lists some of the main indicators of exclusion, considering different structural spaces, and pinpoints some turning points through which the construction of a school education centered on the active affirmation of the children’s rights could be attained.CIFPEC/CIEC - Centro de Investigação em Estudos da Criança, UM (UI 644 e 317 da FCT

"Outroduction”: A Research Agenda on Collegiality in University Settings

Collegiality is the modus operandi of universities. Collegiality is central to academic freedom and scientific quality. In this way, collegiality also contributes to the good functioning of universities’ contribution to society and democracy. In this concluding paper of the special issue on collegiality, we summarize the main findings and takeaways from our collective studies. We summarize the main challenges and contestations to collegiality and to universities, but also document lines of resistance, activation, and maintenance. We depict varieties of collegiality and conclude by emphasizing that future research needs to be based on an appreciation of this variation. We argue that it is essential to incorporate such a variation-sensitive perspective into discussions on academic freedom and scientific quality and highlight themes surfaced by the different studies that remain under-explored in extant literature: institutional trust, field-level studies of collegiality, and collegiality and communication. Finally, we offer some remarks on methodological and theoretical implications of this research and conclude by summarizing our research agenda in a list of themes

Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015

SummaryBackground The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. Interpretation Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Funding Bill & Melinda Gates Foundation

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin