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Distinct cellular roles for PDCD10 define a gut-brain axis in cerebral cavernous malformation
(2019)
Cerebral cavernous malformation (CCM) is a genetic, cerebrovascular disease. Familial CCM is caused by genetic mutations in KRIT1, CCM2, or PDCD10. Disease onset is earlier and more severe in individuals with PDCD10 mutations. Recent studies have shown that lesions arise from excess mitogen-activated protein kinase kinase kinase 3 (MEKK3) signaling downstream of Toll-like receptor 4 (TLR4) stimulation by lipopolysaccharide derived from the gut microbiome. These findings suggest a gut-brain CCM disease axis but fail to define it or explain the poor prognosis of patients with PDCD10 mutations. Here, we demonstrate that the gut barrier is a primary determinant of CCM disease course, independent of microbiome configuration, that explains the increased severity of CCM disease associated with PDCD10 deficiency. Chemical disruption of the gut barrier with dextran sulfate sodium augments CCM formation in a mouse model, as does genetic loss of Pdcd10, but not Krit1, in gut epithelial cells. Loss of gut epithelial Pdcd10 results in disruption of the colonic mucosal barrier. Accordingly, loss of Mucin-2 or exposure to dietary emulsifiers that reduce the mucus barrier increases CCM burden analogous to loss of Pdcd10 in the gut epithelium. Last, we show that treatment with dexamethasone potently inhibits CCM formation in mice because of the combined effect of action at both brain endothelial cells and gut epithelial cells. These studies define a gut-brain disease axis in an experimental model of CCM in which a single gene is required for two critical components: gut epithelial function and brain endothelial signaling.
When this journal was founded in 1992 by Tudor Rickards and Susan Moger, there was no academic outlet available that addressed issues at the intersection of creativity and innovation. From zero to 1,163 records, from the new kid on the block to one of the leading journals in creativity and innovation management has been quite a journey, and we would like to reflect on the past 28 years and the intellectual and conceptual structure of Creativity and Innovation Management (CIM). Specifically, we highlight milestones and influential articles, identify how key journal characteristics evolved, outline the (co-)authorship structure, and finally, map the thematic landscape of CIM by means of a text-mining analysis. This study represents the first systematic and comprehensive assessment of the journal's published body of knowledge and helps to understand the journal's influence on the creativity and innovation management community. We conclude by discussing future topics and paths of the journal as well as limitations of our approach.
Implementing innovation laboratories to leverage intrapreneurship are an increasingly popular organizational practice. A typical feature in these creative environments are semi-autonomous teams in which multiple members collectively exert leadership influence, thereby challenging traditional command-and-control conceptions of leadership. An extensive body of research on the team-centric concept of shared leadership has recognized the potential for pluralized leadership structures in enhancing team effectiveness; however, little empirical work has been conducted in organizational contexts in which creativity is key. This study set out to explore antecedents of shared leadership and its influence on team creativity in an innovation lab. Building on extant shared leadership and innovation research, we propose antecedents customary to creative teamwork, that is, experimental culture, task reflexivity, and voice. Multisource data were collected from 104 team members and 49 evaluations of 29 coaches nested in 21 teams working in a prototypical innovation lab. We identify factors specific to creative teamwork that facilitate the emergence of shared leadership by providing room for experimentation, encouraging team members to speak up in the creative process, and cultivating a reflective application of entrepreneurial thinking. We provide specific exemplary activities for innovation lab teams to increase levels of shared leadership.
The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia
(2019)
The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.