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The cooperative eye hypothesis posits that human eye morphology evolved to facilitate cooperation. Although it is known that young children prefer stimuli with eyes that contain white sclera, it is unknown whether white sclera influences children’s perception of a partner’s cooperativeness specifically. In the current studies, we used an online methodology to present 5-year-old children with moving three-dimensional face models in which facial morphology was manipulated. Children found “alien” faces with human eyes more cooperative than faces with dark sclera (Study 2) but not faces with enlarged irises (Study 1). For more human-like faces (Study 3), children found human eyes more cooperative than either enlarged irises or dark sclera and found faces with enlarged irises cuter (but not more cooperative) than eyes with dark sclera. Together, these results provide strong support for the cooperative eye hypothesis.

Mutations in Cu/Zn Superoxide Dismutase (SOD1) gene represent one of the most common causes of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder that specifically affects motor neurons (MNs). The dismutase-active SOD1 G93A mutant is responsible for the for-mation of toxic aggregates onto the mitochondrial surface, using the Voltage-Dependent Anion Channel 1 (VDAC1) as an anchor point to the organelle. VDAC1 is the master regulator of cellular bioenergetics and by binding to hexokinases (HKs) it controls apoptosis. In ALS, however, SOD1 G93A impairs VDAC1 activity and displaces HK1 from mitochondria, promoting organelle dys-function, and cell death. Using an ALS cell model, we demonstrate that a small synthetic peptide derived from the HK1 sequence (NHK1) recovers the cell viability in a dose–response manner and the defective mitochondrial respiration profile relative to the ADP phosphorylation. This correlates with an unexpected increase of VDAC1 expression and a reduction of SOD1 mutant accumulation at the mitochondrial level. Overall, our findings provide important new insights into the development of therapeutic molecules to fight ALS and help to better define the link between altered mitochondrial metabolism and MNs death in the disease.

Item does not contain fulltext, Human beings have a unique life course. We have evolved a much longer and more helpless childhood, and longer old age, than our closest primate relatives. Many adults are involved in caring for children, including not only mothers, but fathers, grandmothers and grandfathers, and unrelated "alloparents". Why are human children so helpless? Why do they need so much support? Why do humans, especially women, keep living long after they stop reproducing? The central idea in this issue is that these "life-history" characteristics help produce other well-known human advantages such as learning and exploration, cooperation and culture. Biologists, anthropologists and psychologists, studying a wide range of animals and cultures, suggest how childhood, caregiving, and learning might go together.

Item does not contain fulltext, This special issue focuses on the relationship between life history and learning, especially during human evolution. 'Life history' refers to the developmental programme of an organism, including its period of immaturity, reproductive rate and timing, caregiving investment and longevity. Across many species an extended childhood and high caregiving investment appear to be correlated with particular kinds of plasticity and learning. Human life history is particularly distinctive; humans evolved an exceptionally long childhood and old age, and an unusually high level of caregiving investment, at the same time that they evolved distinctive capacities for cognition and culture. The contributors explore the relations between life history, plasticity and learning across a wide range of methods and populations, including theoretical and empirical work in biology, anthropology and developmental psychology. This article is part of the theme issue 'Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals'.

Background: An increase in the frequency of circulating endothelial colony forming cells (ECFCs), the only subset of endothelial progenitor cells (EPCs) truly belonging to the endothelial phenotype, occurs in patients affected by primary myelofibrosis (PMF). Herein, they might contribute to the enhanced neovascularisation of fibrotic bone marrow and spleen. Store-operated Ca 2+ entry (SOCE) activated by the depletion of the inositol-1,4,5-trisphosphate (InsP3)-sensitive Ca2+ store drives proliferation in ECFCs isolated from both healthy donors (N-ECFCs) and subjects suffering from renal cellular carcinoma (RCC-ECFCs). SOCE is up-regulated in RCC-ECFCs due to the over-expression of its underlying molecular components, namely Stim1, Orai1, and TRPC1. Methodology/Principal Findings: We utilized Ca2+ imaging, real-time polymerase chain reaction, western blot analysis and functional assays to evaluate molecular structure and the functional role of SOCE in ECFCs derived from PMF patients (PMFECFCs). SOCE, induced by either pharmacological (i.e. cyclopiazonic acid or CPA) or physiological (i.e. ATP) stimulation, was significantly higher in PMF-ECFCs. ATP-induced SOCE was inhibited upon blockade of the phospholipase C/InsP3 signalling pathway with U73111 and 2-APB. The higher amplitude of SOCE was associated to the over-expression of the transcripts encoding for Stim2, Orai2-3, and TRPC1. Conversely, immunoblotting revealed that Stim2 levels remained constant as compared to N-ECFCs, while Stim1, Orai1, Orai3, TRPC1 and TRPC4 proteins were over-expressed in PMF-ECFCs. ATP-induced SOCE was inhibited by BTP-2 and low micromolar La3+ and Gd3+, while CPA-elicited SOCE was insensitive to Gd3+. Finally, BTP-2 and La 3+ weakly blocked PMF-ECFC proliferation, while Gd3+ was ineffective. Conclusions: Two distinct signalling pathways mediate SOCE in PMF-ECFCs; one is activated by passive store depletion and is Gd 3+-resistant, while the other one is regulated by the InsP 3-sensitive C