Body weight plays a crucial role in mate choice, as weight is related to both attractiveness and health. People are quite accurate at judging weight in faces, but the cues used to make these judgments have not been defined. This study consisted of two parts. First, we wanted to identify quantifiable facial cues that are related to body weight, as defined by body mass index (BMI). Second, we wanted to test whether people use these cues to judge weight. In study 1, we recruited two groups of Caucasian and two groups of African participants, determined their BMI and measured their 2-D facial images for: width-to-height ratio, perimeter-to-area ratio, and cheek-to-jaw-width ratio. All three measures were significantly related to BMI in males, while the width-to-height and cheek-to-jaw-width ratios were significantly related to BMI in females. In study 2, these images were rated for perceived weight by Caucasian observers. We showed that these observers use all three cues to judge weight in African and Caucasian faces of both sexes. These three facial cues, width-to-height ratio, perimeter-to-area ratio, and cheek-to-jaw-width ratio, are therefore not only related to actual weight but provide a basis for perceptual attributes as well.

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The liver has a high regenerative capacity. Upon two‐thirds partial hepatectomy, the hepatocytes proliferate and contribute to liver regeneration. After severe liver injury, when the proliferation of residual hepatocytes is blocked, the biliary epithelial cells (BECs) lose their morphology and express hepatoblast and endoderm markers, dedifferentiate into bipotential progenitor cells (BP‐PCs), then proliferate and redifferentiate into mature hepatocytes. Little is known about the mechanisms involved in the formation of BP‐PCs after extreme liver injury. Using a zebrafish liver extreme injury model, we found that mammalian target of rapamycin complex 1 (mTORC1) signaling regulated dedifferentiation of BECs and proliferation of BP‐PCs. mTORC1 signaling was up‐regulated in BECs during extreme hepatocyte ablation and continuously expressed in later liver regeneration. Inhibition of mTORC1 by early chemical treatment before hepatocyte ablation blocked the dedifferentiation from BECs into BP‐PCs. Late mTORC1 inhibition after liver injury reduced the proliferation of BP‐PC‐derived hepatocytes and BECs but did not affect BP‐PC redifferentiation. mTOR and raptor mutants exhibited defects in BEC transdifferentiation including dedifferentiation, BP‐PC proliferation, and redifferentiation, similar to the chemical inhibition. Conclusion: mTORC1 signaling governs BEC‐driven liver regeneration by regulating the dedifferentiation of BECs and the proliferation of BP‐PC‐derived hepatocytes and BECs.

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