bioRxiv Science⌕ Search

bioRxiv · 10.1101/177758

Human occipital bone sexual dimorphism in an Archiac period archaeological population

Abstract

PREPRINT NOTESThis paper was submitted for publication the International Journal of Osteoarchaeology in August of 2003. The paper was rejected roughly a year later due to scope and collection issues. I revisited the paper in 2007 with an eye to updating and resubmitting with additional data but the project was triaged from the publication pipeline due to the work involved relative to other projects more relevant to my research interests at the time. The current preprint paper contains updated references on occipital bone sexual dimorphism--all limited to the condylar region rather than the full suite of variation in the region.\n\nI am posting this to the preprint server to contribute the findings to the larger scientific community in the hopes that I might have time to revisit the paper as a student project. A more rigorous study would need to expand the sample either to a study collection that has remains with known sex (either verified via molecular sexing techniques or using a modern study collection) or additional comparative collections from hunter-gatherer populations. If a student is interested in taking up the topic and assuming lead authorship on a co-authored paper, Id be happy to collaborate and see this piece through the publication pipeline.\n\nABSTRACTThis paper presents the results of a comprehensive study of sexual dimorphism in the human occipital region of the skull using the remains of 39 prehistoric adults from the prehistoric Windover (6,000-8,000 BP). The results of a discriminant analysis classified 64% of the individuals correctly (using osteologically identified sex). Sexual dimorphism in this population may not be prevalent due to environmental stress.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Hoover, K. C.. 2017-08-18. Human occipital bone sexual dimorphism in an Archiac period archaeological population. https://doi.org/10.1101/177758

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Burn Wound Excision Drives Acute Hypermetabolism in Mice with Scald Burns

Hypermetabolism (elevated resting energy expenditure) is a hallmark of the pathophysiological response to burns. The contribution of wound excision to acute burn-induced hypermetabolism remains unclear. Importantly, while burn wound excision is a standard component of clinical burn care, it is not typically included in rodent models of burn injury. Here, we tested the hypothesis that burn wound excision drives the acute hypermetabolic response to burn trauma. C57BL/6J mice (n=12-18 per group; ~6-weeks old; 50% male) were acclimated to thermoneutral housing (30C) for 6-weeks. All mice underwent baseline body composition scans and metabolic phenotyping to determine total (TEE) and resting energy expenditure (REE). Mice were then randomized to either sham (control), scald burn (burn), wound excision (excision), or scald burn followed by immediate wound excision (burn+excision) groups. Burns and wound excisions involved ~15% of the body surface area. Mice then recovered for 14 days while individually housed in metabolic phenotyping cages. At day 14 post-injury, mice underwent a second body composition scan prior to euthanasia. There were no fatalities in the control or burn groups, whereas 23% (n=7) and 34% (n=11) of mice in the excision and burn+excision groups died or were euthanized during the 14-day recovery period. Male and female mice exhibited broadly similar responses to injury in terms of REE and TEE. Compared to control, REE was greater in burn (47%), excision (102%), and burn+excision groups (136%) during the first week post-injury (P<0.001 for all). Compared to control mice, wound excision (alone or following burns) resulted in a greater acute loss in body mass than burn injury alone. However, this cachectic response was more sustained in male mice compared to females. Similarly, wound excision (alone or following burns) resulted in greater bone mineral content and density loss compared to sham and burn alone in both sexes. Wound excision is a key contributor to the hypermetabolic and cachectic response to burn trauma in mice. We posit that rodent studies aiming to recapitulate burn-induced hypermetabolism and cachexia should include burn wound excision to better model the clinical sequelae to burns.

physiology↗

Reduced cerebral blood flow and metabolic rate trigger an adaptive mitochondrial remodeling program in a Down syndrome mouse model

Mitochondrial dysfunction is a central feature of Down syndrome (DS), yet how trisomy 21 affects brain bioenergetics across scales--from gene transcription to cellular function to whole-brain metabolism--remains poorly understood. Here, we use the Dp16(1)Yey/+ (abbreviated Dp16) DS mouse model, which carries ~115 triplicated gene orthologs of human chromosome 21, to address this major knowledge gap and to provide direct in vivo evidence of brain-wide metabolic deficit in DS. Using magnetic resonance imaging (MRI) approaches, we show that Dp16 mice have reduced cerebral blood flow and metabolic rate of oxygen, with effects more pronounced in males than in females. Despite the suppression of cerebral metabolic rate, mitochondrial respiratory capacity and ATP synthase activity are largely preserved across brain regions, with sex differences noted. Transcriptomic analyses reveal marked upregulation of mitochondrial OXPHOS genes and the convergence of biological pathways related to proteostasis and mitochondrial function across brain regions, with male cortex and female cerebellum showing the biggest change. Collectively, our data suggest that a brain-wide metabolic deficit in Dp16 mice triggers an adaptive mitochondrial remodeling program across the brain to support bioenergetic demands. This compensatory response, however, is insufficient to normalize the metabolic dysfunction in Dp16 mice. Our findings underscore the value of integrating functional assessments at the organismal and tissue levels with transcriptomic changes to gain a systems view of physiologic perturbations and adaptations in the DS brain which may influence phenotypic outcomes.

physiology↗

Speed judgments during smooth pursuit reflect low gain efference copy

During smooth pursuit eye movements, the visual system must compensate for self-generated retinal motion to achieve stable perception of motion in the environment. This compensation primarily depends on an efferent copy of motor commands. Systematically under- or overweighting the strength of efference copy should lead to correlations between eye movement velocity and perceived object velocity. However, previous examinations of these trial-by-trial perceptual correlations have produced mixed results. It remains unclear how effectively the brain compensates for eye movement induced retinal motion during pursuit, and what this reveals about the way efference copy influences perception. To address this, we developed a speed perturbation paradigm in which 29 participants tracked a moving target that underwent brief speed changes. On each trial, we recorded eye velocity along with perceptual judgments of the sign of the speed change (faster or slower) and confidence ratings for those judgments. Across participants, perceptual and oculomotor sensitivity were correlated (r =0.53), but trial-by-trial perceptual and oculomotor responses appeared independent. A logistic regression model incorporating efference copy gain to predict perceptual reports from stimulus speed and eye speed revealed systematic under-compensation for eye movements; faster eye movements were associated with lower changes in perceived speed. Confidence ratings were well-calibrated to perceptual accuracy and showed a consistent negative relationship with eye movement speed. Collectively, these results are consistent with systematic under compensation for eye movements through the use of efference copy during motion perception.

physiology↗