Comparative kinetics of humans and non-human primates during vertical climbing.

Climbing represents a critical behavior in the context of primate evolution. However, anatomically modern human populations are considered ill-suited for climbing. This adaptation can be attributed to the evolution of striding bipedalism, redirecting anatomical traits away from efficient climbing. Although prior studies have speculated on the kinetic consequences of this anatomical reorganization, there is a lack of data on the force profiles of human climbers. This study utilized high-speed videography and force plate analysis to assess single limb forces during climbing from 44 human participants of varying climbing experience and compared these data with climbing data from eight species of non-human primates (anthropoids and strepsirrhines). Contrary to expectations, experience level had no significant effect on the magnitude of single limb forces in humans. Experienced climbers did, however, demonstrate a predictable relationship between center of mass position and peak normal forces, suggesting a better ability to modulate forces during climbing. Humans exhibited significantly higher peak propulsive forces in the hindlimb compared with the forelimb and greater hindlimb dominance overall compared with non-human primates. All species sampled demonstrated exclusively tensile forelimbs and predominantly compressive hindlimbs. Strepsirrhines exhibited a pull-push transition in normal forces, while anthropoid primates, including humans, did not. Climbing force profiles are remarkably stereotyped across humans, reflecting the universal mechanical demands of this form of locomotion. Extreme functional differentiation between forelimbs and hindlimbs in humans may help to explain the evolution of bipedalism in ancestrally climbing hominoids.

How Pendular Is Human Brachiation? When Form Does Not Follow Function.

Brachiation is a form of suspensory locomotion observed only in Primates. The non-human hominoids (e.g., gibbons, orangutans, chimpanzees, and gorillas) are considered specialized brachiators, yet peculiar among the living apes are anatomically modern humans (Homo sapiens), who have forgone this locomotor mode in favor of bipedal striding. Humans can, however, brachiate and seem to have retained the locomotor capabilities of their arboreal ancestors. However, the mechanics of human brachiation have not been quantified. In this study, we evaluate how closely human brachiation conforms to the expectations of simple pendular motion using triaxial accelerometry and high-speed videography. These data are compared to specialized brachiating non-human primates. We found that humans have lower energy recovery than siamangs (Symphalangus syndactylus) during brachiation and have shorter observed pendular periods than expected compared to other primates. We demonstrate that relatively long forelimb length and high grip forces, a proxy for global forelimb force-generating potential, act as the main driving factors to reduce energetic costs through effective pendular recovery. These data are the first to assess the strategies humans adopt to perform a behavior they are not anatomically specialized to execute and places them within a comparative framework amongst other brachiating primates. We show that although humans demonstrate behavioral flexibility during brachiation (e.g., differing mediolateral and vertical center of mass positional movement patterns), anatomical features are the primary driver of variation in brachiation performance.

Disruption of GMNC-MCIDAS multiciliogenesis program is critical in choroid plexus carcinoma development.

Multiciliated cells (MCCs) in the brain reside in the ependyma and the choroid plexus (CP) epithelia. The CP secretes cerebrospinal fluid that circulates within the ventricular system, driven by ependymal cilia movement. Tumors of the CP are rare primary brain neoplasms mostly found in children. CP tumors exist in three forms: CP papilloma (CPP), atypical CPP, and CP carcinoma (CPC). Though CPP and atypical CPP are generally benign and can be resolved by surgery, CPC is a particularly aggressive and little understood cancer with a poor survival rate and a tendency for recurrence and metastasis. In contrast to MCCs in the CP epithelia, CPCs in humans are characterized by solitary cilia, frequent TP53 mutations, and disturbances to multiciliogenesis program directed by the GMNC-MCIDAS transcriptional network. GMNC and MCIDAS are early transcriptional regulators of MCC fate differentiation in diverse tissues. Consistently, components of the GMNC-MCIDAS transcriptional program are expressed during CP development and required for multiciliation in the CP, while CPC driven by deletion of Trp53 and Rb1 in mice exhibits multiciliation defects consequent to deficiencies in the GMNC-MCIDAS program. Previous studies revealed that abnormal NOTCH pathway activation leads to CPP. Here we show that combined defects in NOTCH and Sonic Hedgehog signaling in mice generates tumors that are similar to CPC in humans. NOTCH-driven CP tumors are monociliated, and disruption of the NOTCH complex restores multiciliation and decreases tumor growth. NOTCH suppresses multiciliation in tumor cells by inhibiting the expression of GMNC and MCIDAS, while Gmnc-Mcidas overexpression rescues multiciliation defects and suppresses tumor cell proliferation. Taken together, these findings indicate that reactivation of the GMNC-MCIDAS multiciliogenesis program is critical for inhibiting tumorigenesis in the CP, and it may have therapeutic implications for the treatment of CPC.