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In peer assessment, students assess a task done by their peers, provide feedback and usually a grade. The extent to which these peer grades can be used to formally grade the task is unclear, with doubts often arising regarding their validity. The instructor could supervise the peer assessments, but would not then benefit from workload reduction, one of the most appealing features of peer assessment for instructors. Our proposal uses a probabilistic model to estimate a grade for each test, accounting for the degree of precision and bias of grading peers. The grade that the instructor would assign to a test can help enhance the model. Our main hypothesis is that guiding the instructor through supervision of a peer-assessed task by pointing out to them which test to evaluate next can lead to improvement in the validity of the model-estimated grades at an early stage. Moreover, the instructor can decide how many tests to grade based on their own criteria of tolerable uncertainty, as measured by the model. We validate the method using both synthetically generated data and real data collected in an actual class. Models that link the roles of the student as grading peer and as test-taker appear to better exploit available information, although simpler models are more appropriate in specific conditions. The best performing technique for guiding the instructor is that which selects the test with the highest expected entropy reduction. In general, empirical results are in line with the hypothesis of this study.

The mechanisms that restrict regeneration and maintain cell identity following injury are poorly characterized in higher vertebrates. Following β-cell loss, 1-2% of the glucagon-producing α-cells spontaneously engage in insulin production in mice. Here we explore the mechanisms inhibiting α-cell plasticity. We show that adaptive α-cell identity changes are constrained by intra-islet insulin- and Smoothened-mediated signalling, among others. The combination of β-cell loss or insulin-signalling inhibition, with Smoothened inactivation in α- or δ-cells, stimulates insulin production in more α-cells. These findings suggest that the removal of constitutive 'brake signals' is crucial to neutralize the refractoriness to adaptive cell-fate changes. It appears that the maintenance of cell identity is an active process mediated by repressive signals, which are released by neighbouring cells and curb an intrinsic trend of differentiated cells to change.

After centuries as a flagship economic activity, pastoralism in Spain is today in danger of collapse due to the simultaneous processes of abandonment and industrialisation. With a consensus on the need to revert this decline, a characterisation of pastoralism is needed in the design of an efficient framework for action. Through a participatory process with experts, we carried out this characterisation of Spanish pastoralism, identifying the most representative systems and communities. We studied the causes and consequences of pastoral evolution over the last 250 years, explained by biophysical, technological, governance and social parameters. We achieved a harmonised classification of eleven pastoral systems, classified into four groups with mobility parameters (large migratory systems, short-distance transterminance, daily mobile grazing and semi-wilderness). Large mobility systems were subdivided into ten pastoral communities, characterised by strong sociocultural ties beneath farm management. The consideration of pastoral systems and communities in policy can orient effective rural development, while optimising the allocation of resources for environmental conservation and climate neutrality. [ABSTRACT FROM AUTHOR]

The dogma that life without insulin is incompatible has recently been challenged by results showing the viability of insulin-deficient rodents undergoing leptin monotherapy. Yet, the mechanisms underlying these actions of leptin are unknown. Here, the metabolic outcomes of intracerebroventricular (i.c.v.) administration of leptin in mice devoid of insulin and lacking or re-expressing leptin receptors (LEPRs) only in selected neuronal groups were assessed. Our results demonstrate that concomitant re-expression of LEPRs only in hypothalamic γ-aminobutyric acid (GABA) and pro-opiomelanocortin (POMC) neurons is sufficient to fully mediate the lifesaving and antidiabetic actions of leptin in insulin deficiency. Our analyses indicate that enhanced glucose uptake by brown adipose tissue and soleus muscle, as well as improved hepatic metabolism, underlies these effects of leptin. Collectively, our data elucidate a hypothalamic-dependent pathway enabling life without insulin and hence pave the way for developing better treatments for diseases of insulin deficiency.