Spreading remote lab usage: A system — A community — A Federation

Experiments have been at the heart of scientific development and education for centuries. From the outburst of Information and Communication Technologies, virtual and remote labs have added to hands-on labs a new conception of practical experience, especially in Science, Technology, Engineering and Mathematics education. This paper aims at describing the features of a remote lab named Virtual Instruments System in Reality, embedded in a community of practice and forming the spearhead of a federation of remote labs. More particularly, it discusses the advantages and disadvantages of remote labs over virtual labs as regards to scalability constraints and development and maintenance costs. Finally, it describes an actual implementation in an international community of practice of engineering schools forming the embryo of a first world wide federation of Virtual Instruments System in Reality nodes, under the framework of a project funded by the Erasmus+ Program.info:eu-repo/semantics/publishedVersio

Chapter 1

Experimenting is fundamental to the training process of all scientists and engineers. While experiments have been traditionally done inside laboratories, the emergence of Information and Communication Technologies added two alter-natives accessible anytime, anywhere. These two alternatives are known as virtual and remote labs, and are sometimes indistinguishably referred as online labs. Sim-ilarly to other instructional technologies, virtual and remote labs require some ef-fort from teachers in integrating them into curricula, taking into consideration sev-eral factors that affect their adoption (i.e. cost) and their educational effectiveness (i.e. benefit). This chapter analyses these two dimensions and sustains the case where only through international cooperation it is possible to serve the large num-ber of teachers and students involved in engineering education. It presents an ex-ample in the area of Electrical and Electronics Engineering, based on a remote lab named Virtual Instruments System in Reality, and it then describes how a number of European and Latin-American institutions have been cooperating under the scope of an Erasmus+ project2, for spreading its use in Brazil and Argentina.info:eu-repo/semantics/publishedVersio

Preterm infants' early developmental status is associated with later developmental outcome

Aim: To assess the development of preterm infants from 40 weeks gestational age to 18 months corrected age in order to identify early predictors of later development. Methods: Fifty-one infants were involved. Infant development was assessed at 40 and 44 weeks gestational age with the Brazelton Neonatal Behavioral Assessment Scale and a Self-Regulation Scale and at 3, 6, 10, 18 months corrected age with the Bayley Scales of Infant Development. The quality of general movements was assessed at 1 and 3 months corrected age and maternal attachment style at infant's age of 6 months corrected age with the Relation Scale Questionnaire. Results: At term age and 1 month corrected age, preterm infants were less mature and had lower levels of self-regulation than full-term infants. At 3 months corrected age, a higher proportion of preterm infants (43%) had mildly abnormal motor quality compared to the general population (25%). At all follow-ups, preterm infants had delayed mental, motor, and behavioral development, which was associated with the level of self-regulation, motor quality, and maternal attachment style. Maternal education level was the most predominant background factor related to infant development. Conclusion: Preterm infants show early-in-life deviations in self-regulation, motor quality, and development. These deviations are risk factors for later optimal functioning

Loss of polycomb repressive complex 1 activity and chromosomal instability drive uveal melanoma progression.

Chromosomal instability (CIN) and epigenetic alterations have been implicated in tumor progression and metastasis; yet how these two hallmarks of cancer are related remains poorly understood. By integrating genetic, epigenetic, and functional analyses at the single cell level, we show that progression of uveal melanoma (UM), the most common intraocular primary cancer in adults, is driven by loss of Polycomb Repressive Complex 1 (PRC1) in a subpopulation of tumor cells. This leads to transcriptional de-repression of PRC1-target genes and mitotic chromosome segregation errors. Ensuing CIN leads to the formation of rupture-prone micronuclei, exposing genomic double-stranded DNA (dsDNA) to the cytosol. This provokes tumor cell-intrinsic inflammatory signaling, mediated by aberrant activation of the cGAS-STING pathway. PRC1 inhibition promotes nuclear enlargement, induces a transcriptional response that is associated with significantly worse patient survival and clinical outcomes, and enhances migration that is rescued upon pharmacologic inhibition of CIN or STING. Thus, deregulation of PRC1 can promote tumor progression by inducing CIN and represents an opportunity for early therapeutic intervention

Loss of polycomb repressive complex 1 activity and chromosomal instability drive uveal melanoma progression.

Chromosomal instability (CIN) and epigenetic alterations have been implicated in tumor progression and metastasis; yet how these two hallmarks of cancer are related remains poorly understood. By integrating genetic, epigenetic, and functional analyses at the single cell level, we show that progression of uveal melanoma (UM), the most common intraocular primary cancer in adults, is driven by loss of Polycomb Repressive Complex 1 (PRC1) in a subpopulation of tumor cells. This leads to transcriptional de-repression of PRC1-target genes and mitotic chromosome segregation errors. Ensuing CIN leads to the formation of rupture-prone micronuclei, exposing genomic double-stranded DNA (dsDNA) to the cytosol. This provokes tumor cell-intrinsic inflammatory signaling, mediated by aberrant activation of the cGAS-STING pathway. PRC1 inhibition promotes nuclear enlargement, induces a transcriptional response that is associated with significantly worse patient survival and clinical outcomes, and enhances migration that is rescued upon pharmacologic inhibition of CIN or STING. Thus, deregulation of PRC1 can promote tumor progression by inducing CIN and represents an opportunity for early therapeutic intervention