The Influence of Environmental Constraints in 360° Videos on Decision Making in Soccer.

Decision making is an important prerequisite of soccer expertise. Beyond expertise, considering the effects of environmental constraints on decision-making processes could help specify existing theories. To address this gap, expert and nonexpert soccer players were enrolled to test how environmental constraints affect decision-making processes. Environmental constraints were experimentally manipulated: Opponent pressure was implemented by presenting a close opponent player in soccer scenes, time constraint was implemented by providing short time intervals for making the decision, and first-person perspective was implemented by using 360° videos. The experts outperformed the nonexperts, and the results showed significant main effects of time constraint and opponent pressure, but not perspective. The players' option and decision quality improved under the time constraint but were negatively affected by opponent pressure. The negative effects of opponent pressure were especially true under limited time and in third-person perspective. The results, alternative manipulations, and implications of environmental effects are discussed for decision-making research.

mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress.

Mammalian target of rapamycin complex 1 (mTORC1) is a key regulator of cell metabolism and autophagy. Despite widespread clinical use of mTORC1 inhibitors, the role of mTORC1 in renal tubular function and kidney homeostasis remains elusive. By using constitutive and inducible deletion of conditional Raptor alleles in renal tubular epithelial cells, we discovered that mTORC1 deficiency caused a marked concentrating defect, loss of tubular cells, and slowly progressive renal fibrosis. Transcriptional profiling revealed that mTORC1 maintains renal tubular homeostasis by controlling mitochondrial metabolism and biogenesis as well as transcellular transport processes involved in countercurrent multiplication and urine concentration. Although mTORC2 partially compensated for the loss of mTORC1, exposure to ischemia and reperfusion injury exaggerated the tubular damage in mTORC1-deficient mice and caused pronounced apoptosis, diminished proliferation rates, and delayed recovery. These findings identify mTORC1 as an important regulator of tubular energy metabolism and as a crucial component of ischemic stress responses.