Arm and leg modelling

No, I’m not looking for people with lithe limbs to be photographed for money. Much more sexily, I’m referring to a recent paper (Pietak et al., 2013) that’s found that the relative length of the segments of human limbs can be modeled with a log-periodic function:

Figure 2 from Pietak et al. 2013. Human within-limb proportions are such that the length of each segment (e.g., H1-6) of a limb, from  fingertip to shoulder (A) and to to hip (B), can be predicted by a logarithmic periodic function (C).

In other words, within a limb, the length of each segment is mathematically fairly predictable on the basis of the segment(s) before and after it. As the authors state, “Being able to describe human limb bone lengths in terms of a log-periodic function means that only one parameter, the wavelength λ, is needed to explain the proportional configuration of the limb.”

The biological significance of this pattern is difficult to discern. The length of a limb segment is determined by a number of factors, including the spacing between the initial limb condensations embryonically, and thereafter the growth rates and duration of growth at proximal and distal epiphyses. As a result, limb proportions aren’t static throughout life, but change from embryo to adult. For instance, here are limb proportion data for the coolest animal ever – gibbons! – from the great anatomist Adolph Schultz.

ResearchBlogging.orgAn important question, and follow-up to Pietak et al’s study, is whether human limb proportions can be described by such log-periodic functions throughout ontogeny, and if so how these change. Plus, it’s also not clear to what extent human proportions might happen to be describable by log periodic functions, simply because each segment is shorter than the one preceding it proximally. In short, this study raises really interesting and pursuable questions about how and why animal limbs grow to the size and proportions that they do.

References
Pietak A, Ma S, Beck CW, & Stringer MD (2013). Fundamental ratios and logarithmic periodicity in human limb bones. Journal of anatomy, 222 (5), 526-37 PMID: 23521756

Schultz, A. (1944). Age changes and variability in gibbons. A Morphological study on a population sample of a man-like ape American Journal of Physical Anthropology, 2 (1), 1-129 DOI: 10.1002/ajpa.1330020102

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Pre-publication: Brain growth in Homo erectus (plus free code!)

The annual meetings of the American Association of Physical Anthropologists were going on all last week, and I gave my first talk before the Association (co-authored with Jeremy DeSilva). The talk focused on using resampling methods and the abysmal human fossil record to assess whether human-like brain size growth rates were present in our >1 mya ancestor Homo erectus. This is something I’ve actually been sitting on for a while, and wanted to wait til after the talk to post for all to see. I haven’t written this up yet for publication, but before then I’d like to briefly share the results here.

Background: Humans’ large brains are critical for giving us our unique capabilities such as language and culture. We achieve these large (both absolutely, and relative to our body size) brains by having really high brain growth rates across several years; most notable are exceptionally high, “fetal-like” rates during the first 1-2 years of life. Thus, rapid brain growth shortly after birth is a key aspect of human uniqueness – but how ancient is this strategy?

Materials: We can plot brain size at birth in humans and chimpanzees (our closest living relatives) to visualize what makes humans stand out (Figure 1).

Figure 1. Brain size (volume) at given ages. Humans=black, chimpanzees=red. Ranges of brain size at birth, and the chronological age of the Mojokerto fossil, in blue.

Human data come from Cogueugniot and Hublin (2012), and chimpanzees from Herndon et al. (1999) and Neubauer et al. (2012). The earliest fossil evidence able to address this question comes from Homo erectus. Because of the tight relationship between newborn and adult brain size (DeSilva and Lesnik 2008), we can use adult Homo erectus brain volumes (n=10, mean = 916.5 cm^3) to predict that of the species’ newborns: mean = 288.9 cm^3, sd = 17.1). An almost-recent analysis of the Mojokerto Homo erectus infant calvaria suggests a size of 663 cm^3 and an age of 0.5-1.25 years (Coqueugniot et al. 2004; this study actually suggests an oldest age of 1.5 years, but the chimpanzee sample here requires us to limit the study to no more than 1.25 years). Because we have a H. erectus fossil less than 2 years of age, and we can estimate brain size at birth, we can indirectly assess early brain growth in this species.

Methods: Resampling statistics allow inferences about brain growth rates in this extinct species, incorporating the uncertainty in both brain size at birth, and in the chronological age of the Mojokerto fossil. We thus ask of each species, what growth rates are necessary to grow one of the newborn brain sizes to any infant between 0.5-1.25 years? And from there, we compare these resampled growth rates (or rather, ‘pseudo-velocities’) between species – is H. erectus more similar to modern humans or chimpanzees? There are 294 unique newborn-infant comparisons for humans and 240 for the chimpanzee sample. We therefore compare these empirical newborn-infant pairs from extant species to 7500 resampled H. erectus pairs, randomly selecting a newborn H. erectus size based on the parameters above, and randomly selecting an age from 0.5-1.25 years for the Mojokerto specimen. This procedure is used to compare both absolute size change (the difference between an infant and a newborn size, in cm^3/year), and and proportional size change (infant/newborn size).

Results: Humans’ high early brain growth rates after birth are reflected in the ‘pseudovelocity curve’ (Figure 2). Chimps have a similar pattern of faster rates earlier on, but these are ultimately lower than humans’. Using the Mojokerto infant’s brain size (and it’s probable ages) and the likely range of H. erectus neonatal brain sizes (mean = 288, sd = 17), it is fairly clear that H. erectus achieved its infant brain size with high, human-like rates in brain volume increase.

Figure 2. Brain size growth rates (‘pseudo-velocity’) at given ages. Humans=black, chimpanzees=red, and Homo erectus,=blue.

However, if we look at proportional size change, the factor by which brain size increases from birth to a given age, we see a great deal of overlap both between age groups within a species, and between different species. Cross-sectional data create a great deal of overlap in implied proportional size change between ages within a species; it is easier to consider proportional size change between taxa, conflating ages, then  (Figure 3). Humans show a massive amount of variation in potential growth rates from birth to 0.5-1.25 years, and chimpanzees also show a great deal of variation, albeit generally lower than in the human sample. Relative growth rates in Homo erectus are intermediate between the two extant species.

Figure 3. Proportional brain size increase (infant/newborn size). 

Significance: Brain size growth shortly after birth is critical for humans’ adaptative strategy: growing a large brain requires a lot of energy and parental (especially maternal) investment (Leigh 2004). Plus, in humans this rapid increase may correspond with the creation of innumerable white-matter connections between regions of the brain (Sakai et al. 2012), important for cognition or intelligence. The H. erectus fossil record (1 infant and 10 adults) provides a limited view into this developmental period. However, comparative data on extant animals (e.g. brain sizes from birth to adulthood), coupled with resampling statistics, allow inferences to be made about brain growth rates in H. erectus over 1 million years ago.

Assuming the Mojokerto H. erectus infant is accurately aged (Coqueugniot et al. 2004), and that Homo erectus followed the same neonatal-adult scaling relationship as other apes and monkeys (DeSilva and Lesnik 2008), it is likely that H. erectus had human-like rates of absolute brain size growth. Thus, the energetic and parental requirements to raise such brainy babies, seen in modern humans, may have been present in Homo erectus some 1.5 million years ago or so. This may also imply rapid white-matter proliferation (i.e. neural connections) in this species, suggesting an intellectually (i.e. socially or linguistically) stimulating infancy and childhood in this species. At the same time, relative brain size growth appears to scale with overall brain size: larger brains require proportionally higher growth rates. This is in line with studies suggesting that in many ways, the human brain is a scaled-up version of other primates’ (e.g. Herculano-Houzel 2012).

ResearchBlogging.org
This study was made possible with published data, and the free statistical programming language R.

Contact me if you want the R code used for this analysis, I’m glad to share it!!!

References
Coqueugniot H, Hublin JJ, Veillon F, Houët F, & Jacob T (2004). Early brain growth in Homo erectus and implications for cognitive ability. Nature, 431 (7006), 299-302 PMID: 15372030

Coqueugniot H, & Hublin JJ (2012). Age-related changes of digital endocranial volume during human ontogeny: results from an osteological reference collection. American journal of physical anthropology, 147 (2), 312-8 PMID: 22190338

DeSilva JM, & Lesnik JJ (2008). Brain size at birth throughout human evolution: a new method for estimating neonatal brain size in hominins. Journal of human evolution, 55 (6), 1064-74 PMID: 18789811

Herculano-Houzel S (2012). The remarkable, yet not extraordinary, human brain as a scaled-up primate brain and its associated cost. Proceedings of the National Academy of Sciences of the United States of America, 109 Suppl 1, 10661-8 PMID: 22723358

Herndon JG, Tigges J, Anderson DC, Klumpp SA, & McClure HM (1999). Brain weight throughout the life span of the chimpanzee. The Journal of comparative neurology, 409 (4), 567-72 PMID: 10376740

Leigh SR (2004). Brain growth, life history, and cognition in primate and human evolution. American journal of primatology, 62 (3), 139-64 PMID: 15027089

Neubauer, S., Gunz, P., Schwarz, U., Hublin, J., & Boesch, C. (2012). Brief communication: Endocranial volumes in an ontogenetic sample of chimpanzees from the taï forest national park, ivory coast American Journal of Physical Anthropology, 147 (2), 319-325 DOI: 10.1002/ajpa.21641

Sakai T, Matsui M, Mikami A, Malkova L, Hamada Y, Tomonaga M, Suzuki J, Tanaka M, Miyabe-Nishiwaki T, Makishima H, Nakatsukasa M, & Matsuzawa T (2012). Developmental patterns of chimpanzee cerebral tissues provide important clues for understanding the remarkable enlargement of the human brain. Proceedings. Biological sciences / The Royal Society, 280 (1753) PMID: 23256194

Come hear me talk about brains on Tuesday

This coming Tuesday I’ll be giving a talk about the evolution and development of the human brain, as part of the seminar series of the School of Humanities and Social Sciences here at Nazarbayev University. My research doesn’t really fall neatly under the realms of ‘humanities and social sciences,’ so  the talk should be a neat change of pace for these SHSS seminars. I’ll be previewing something I’ve been working on with Dr. Jeremy DeSilva, and that I’ll be presenting at the AAPA conference in a few weeks. So if you can’t make it to Astana, maybe you can catch the shorter show in Knoxville!

Here’s info from the flier (sorry about the title, I’m new to this; also, I won’t be talking for 90 minutes):

Building the Most Powerful Computer: Evo-Devo of the Human Brain


4:20-5:50 pm
Tuesday, 26 March 2013

at Nazarbayev University, Block 7, Room 7-507
53 Kabanbay Batyr Ave.
Astana

Synopsis: Your brain is one of the most remarkable things to emerge in all the history of Life, and has been a critical part of humans’ adaptive success. This talk will examine how this machine came into existence. I will first describe how the brain grows and develops across an individual’s lifetime. Next I turn to the possible ways development was modified during the course of our evolution to result in our singularly powerful brains. Special attention is given to teasing out secrets of brain evolution from the dismal fossil record.

Taking back Epigenetics

If I’m good at anything, it’s looking into one topic and then getting distracted by something else during my search. In a recent case, I was scouring the literature on growth and life history. One ribald thing led to another, and next thing I know I’ve stumbled upon Gunter Wagner’s recent review of the book Epigenetics: Linking Genotype and Phenotype in Development and Evolution. WTF is epigenetics, you ask? That’s actually a pretty good question (see here). In the past several years, the term has most often been associated with the causes/effects of structural modifications to chromatin (the DNA-containing stuff that makes up chromosomes). For sure, coincident with Wagner’s review, a paper in last week’s Nature Reviews Genetics defines epigenetics as “the study of mitotically and/or meiotically heritable changes in gene function that cannot be explained by changes in DNA sequence.” (Feil and Fraga 2012).

This is an extremely narrow focus for a term that was originally meant to be about basically everything besides genes that contribute to an organism’s phenotype (this idea was developed by the great, rather underrated, 20th century biologist Conrad Waddington). Lotsa epigenetics research by the narrow definition (i.e. modifications to histones and chromatin) focuses on how cells – not organisms – retain their identity/function (or, phenotype). Epigenetics in the narrow sense are important determinants of an organism’s phenotype, but these alone are insufficient to understand how and why organisms’ become the way they are. Yes, the narrow definition leaves room for environmental influences on gene expression (though “environment” could refer to the state of affairs within a cell or an organism, in addition to the outside world). But it nevertheless imparts agency solely to genomes in affecting an organism becomes.

And this is what the aforesaid book and review are about. Wagner asks, “what would be lost if the original perspective of epigentics [as defined by Waddington] was lost to science?” This is important because an organism is not simply a robotic readout of its genes, but people cannot seem to shake this centuries-old biological determinism.

Is that a homunculus
in your [sperm’s]
pocket?

In the early days of ‘modern’ (or let’s say ‘recent’) biology, there was a popular idea of “Preformationism,” that animals grew from these pre-formed miniature versions of themselves (homunculi) in germ cells. It did not take long for this idea to be quashed, but the underlying idea persisted. Wagner recounts, “With the rise of genetics during the 20th century, however, a new form of quasi-preformism arose, basically replacing the old homunculus with the genome, whereas the developmental process creating the phenotype was put in a black box” (emphasis mine). [See Gilbert et al. (1996) for a nice historical overview describing how the rise of population genetics in the early 20th century left embryology and developmental biology by the wayside of the Modern Evolutionary Synthesis]

This latent desire to essentialize biology to some singular determinant (be it an homunculus or a gene) is something people just can’t get away from. Srsly, there’s a persistent sentiment in biology that Real Science is only the high-profile, lab-coated work in genetics. Along these lines, even I adopted the recently popular narrow view of “epigenetics” a while back when I dated a woman who worked at an epigenetics lab, in hindsight probably so I would sound more like a capital-S Scientist (below).

Hipster scientist. H3S10 phosphorylation correlates with 
decreased levels of heterochromatin, possibly regulating
chromosome condensation (Chenet al 2008). Image: bit.ly/zEfPaq

Of course, genes code for how a cell should behave, but we have this tendency to want to extrapolate from the cell to the organism, and this is where developmental biology becomes a critical link. And this is what the new Epigenetics book is about (so far as I can tell, I haven’t yet had a chance to read it all).

It’s abundantly clear that phenotypes arise out of an inextricably complex series of interactions – between genes, proteins, cells, tissues, environments, etc. These interactions do not occur solely at the genetic (or narrow-sense epigenetic) level. Developmental biology helps ‘connect the dots’ between genes and morphology, but cannot do so by focusing solely on genes and chromatin.

ResearchBlogging.org

References
Chen, E., Zhang, K., Nicolas, E., Cam, H., Zofall, M., & Grewal, S. (2008). Cell cycle control of centromeric repeat transcription and heterochromatin assembly. Nature, 451 (7179), 734-737 DOI: 10.1038/nature06561

Feil, R., & Fraga, M. (2012). Epigenetics and the environment: emerging patterns and implications. Nature Reviews Genetics DOI: 10.1038/nrg3142

Gilbert, S. (1996). Resynthesizing Evolutionary and Developmental Biology. Developmental Biology, 173 (2), 357-372 DOI: 10.1006/dbio.1996.0032

Hallgrímsson B and Hall BK, eds. 2011. Epigenetics: Linking Genotype and Phenotype in Development and Evolution. Berkeley: University of California Press.

Wagner, G. (2011). Epigenetics in all its beauty Trends in Ecology & Evolution DOI: 10.1016/j.tree.2011.09.003

Evo-devo of the human shoulder?

It’s a new year, and while my mind should be marred by a hangover, instead all I can think about are fossils and scapulas.


A pretty cool study was published online in the Journal of Human Evolution last week, and I’ve finally gotten to peruse it. Fabio Di Vincenzo and colleagues analyzed the shape of the outline of the glenoid fossa on the scapula (not to be confused with the glenoid on your skull), from Australopithecus africanus to present day humans. The glenoid fossa is essentially the socket in the ball-and-socket joint of your shoulder. The authors found that there is pretty much a single trend of glenoid shape change from Australopithecus through the evolution of the genus Homo: from the fairly narrow joint in Australopithecus africanus and A. sediba, to the relatively wide joint in recent humans. The overall size and shape of the joint influences/reflects shoulder mobility, so presumably this shape change hints that more front-to-back arm motions became more important through the course of human evolution (authors suggest throwing in humans from the Late Pleistocene onward).



The finding of a single predominant trend in glenoid shape evolution is pretty interesting. On top of that, the authors add an ‘evo-devo’ twist by comparing species’ average “shapes” (first principle component scores, on the y-axis in the figure at right) with their estimated ages at skeletal maturity (which appears scaled to the modern human value, on the x-axis). Though it’s not an ideal dataset for running a linear regression, the figure at right shows that there appears to be a fairly linear relationship across human evolution, such that groups with an older age at skeletal maturity tend to have a more rounded (modern human-like) glenoid fossa (note that the individuals in the analysis were all adults). Overall size does not contribute to shape variation among these glenoids.


This work raises two issues, and ultimately leads to a testable evo-devo hypothesis. The first issue is to what extent we can trust their estimates of age at skeletal maturity. These estimates were allegedly taken from a chapter by Helmut Hemmer (2007) in the prohibitively expensive Handbook of Paleoanthropology. Cursorily glancing at this chapter, I can’t find age at skeletal maturation estimated for any hominids. It is possible that in my skimming I missed the estimates, or alternatively that Di Vincenzo and colleagues misinterpreted another variable as skeletal development. Either way, these estimates would still need to be taken with a grain of salt, given that it is almost impossible to know the true age at death of a fossil (but see Antoine et al. 2008), especially if there are no associated cranio-dental elements.


That said, it is perfectly reasonable to suppose that the age at skeletal maturation has increased over the course of human evolution; life-span increased through human evolution, and so all else being equal (which it almost certainly isn’t) we could expect that maturation would occur later over time, too. So this leads to a second issue: given the “evo-devo change” the authors hypothesize, what is the evo-devo mechanism? That is, how was development modified to effect the evolutionary changes we see in the hominid scapula? Because they found adult glenoid shape correlates with estimated age at skeletal maturity, this leads to the hypothesis that postnatal skeletal growth accounts for the shape difference. Indeed, they state:

“If functional and static allometric influences are unlikely, we…interpret the trend…as reflecting growth and developmental factors. A major, albeit gradual, trend of ontogenetic heterochrony occurred in the evolution of the genus Homo… and thus differences within and between taxa in overall growth rates may have produced the pattern of variation between samples, as well as the overall temporal trend observed. The regression of life history variables [they only looked at 1]… with PCA [principle components analysis] scores supports this ‘ontogenetic’ hypothesis.”

The authors suggest that humans’ slower growth rates but longer growth period “led to longer periods of bone deposition along the inferior-lateral edge of the [glenoid fossa]”  The heterochronic process they suggest is “peramorphosis” – the descendant reaches a shape that is ‘beyond’ that of the ancestor.

The figure above is from a seminal “heterochrony” paper by Pere Alberch and colleagues (1979), portraying how peramorphosis can occur. In each, the y-axis represents shape and the x-axis is age. A the descendant’s peramorphic shape (“Ya”) could result from accelerated growth (left graph) or from an extension of growth to later ages than in the ancestor (right graph).


And so this leads to a testable hypothesis. Di Vincenzo and colleagues cite (dental) evidence that humans’ overall body growth rates are slower than earlier hominids’, undermining the hypothesis that acceleration is responsible for humans’ glenoid peramorphosis. Rather, they hypothesize that humans’ slower growth rates coupled with a longer period of skeletal development, to result in a relatively wider glenoid, due to increased development of the secondary growth centers (e.g. the graph at right, above). This developmental scenario predicts that subadult human glenoids should resemble earlier hominid adults’, that “ontogeny recapitulates phylogeny” as far as glenoid shape is concerned. Analyzing glenoid growth can even be extended to include fossils – the >3 million year old human ancestor Australopithecus afarensis has glenoids preserved for an infant (DIK-VP-1; Alemseged et al. 2006) and 2 adults (AL 288 “Lucy” and KSD-VP-1; Johanson et al. 1982, Haile-Selassie et al. 2010). An alternate hypothesis is that species’ distinct glenoid shapes are established early during life (i.e. in utero), and/or that no simple heterochronic process is involved.


ResearchBlogging.orgDi Vincenzo’s and colleagues’ study points to the importance of development in understanding human evolution, and their hypothesized “evo-devo change” in glenoid shape is ripe for testing.


References
Pere Alberch, Stephen Jay Gould, George F. Oster, & David B. Wake (1979). Size and shape in ontogeny and phylogeny Paleobiology, 5 (3), 296-317


Alemseged, Z., Spoor, F., Kimbel, W., Bobe, R., Geraads, D., Reed, D., & Wynn, J. (2006). A juvenile early hominin skeleton from Dikika, Ethiopia Nature, 443 (7109), 296-301 DOI: 10.1038/nature05047


Antoine, D., Hillson, S., & Dean, M. (2009). The developmental clock of dental enamel: a test for the periodicity of prism cross-striations in modern humans and an evaluation of the most likely sources of error in histological studies of this kind Journal of Anatomy, 214 (1), 45-55 DOI: 10.1111/j.1469-7580.2008.01010.x


Di Vincenzo, F., Churchill, S., & Manzi, G. (2011). The Vindija Neanderthal scapular glenoid fossa: Comparative shape analysis suggests evo-devo changes among Neanderthals Journal of Human Evolution DOI: 10.1016/j.jhevol.2011.11.010


Haile-Selassie, Y., Latimer, B., Alene, M., Deino, A., Gibert, L., Melillo, S., Saylor, B., Scott, G., & Lovejoy, C. (2010). An early Australopithecus afarensis postcranium from Woranso-Mille, Ethiopia Proceedings of the National Academy of Sciences, 107 (27), 12121-12126 DOI: 10.1073/pnas.1004527107


Hemmer, Helmut (2007). Estimation of Basic Life History Data of Fossil Hominoids Handbook of Paleoanthropology, 587-619 DOI: 10.1007/978-3-540-33761-4_19


Johanson, D., Lovejoy, C., Kimbel, W., White, T., Ward, S., Bush, M., Latimer, B., & Coppens, Y. (1982). Morphology of the Pliocene partial hominid skeleton (A.L. 288-1) from the Hadar formation, Ethiopia American Journal of Physical Anthropology, 57, 403-451 DOI: 10.1002/ajpa.1330570403

A poor depiction, indeed

As I’ve alluded to in some previous posts, in the Spring semester of 2012, I’ll be teaching “Anthrbio 297: Human Evo-devo” at the University of Michigan. It should be a really fun and interesting class, examining the role of development in human evolution.

Ernst Haeckel’s drawing of embryonic stages in some vertebrates. Taken from Richardson et al. 1997

My department recommends I create a flier that can be posted around campus. One of my first ideas was to adapt a Haeckel’s classic illustration of embryos of different animals passing through similar stages in utero (which we know today isn’t exactly correct; Richardson et al. 1997), but spin it to include primates and fossil humans. I started sketching it out (very crudely), but kept getting distracted with my pitiful attempts at multitasking. When I stopped zoning out, I was aghast to find my adaptation had taken a peculiar turn.

ResearchBlogging.orgI won’t quit my day job.
More about vertebrate embryology
Richardson, M., Hanken, J., Gooneratne, M., Pieau, C., Raynaud, A., Selwood, L., & Wright, G. (1997). There is no highly conserved embryonic stage in the vertebrates: implications for current theories of evolution and development Anatomy and Embryology, 196 (2), 91-106 DOI: 10.1007/s004290050082

Pictures worth thousands of words and dollars

ResearchBlogging.orgLooking into subdural empyema, which is a meningeal infection you don’t want, I stumbled upon a study from the roaring 1970s – the glorious Nixon-Ford-Carter years – using computerized axial tomography (hence, CAT scan) to visualize lesions within the skull (Claveria et al. 1976). Nowadays people refer to various similar scanning techniques simply as “CT” (for computed tomography, though this is not exactly the same as magnetic resonance imaging, MRI).

It’s pretty amazing how medical imaging has advanced in the 35 years since this study. For example, to the right is a CAT scan from Claveria et al. (1976, Fig. 4). These are transverse images (“slices”) through the brain case, the top of the images corresponding to the front of the face. You can discern the low-density (darker) brain from the higher density (lighter) bone – the sphenoid lesser wings and dorsum sellae, and petrous pyramids of the temporal bones are especially prominent in the top left image. In the bottom two images you can see a large, round abscess in the middle cranial fossa. Whoa.

What makes this medical imaging technique so great is that it allows a view inside of things without having to dissect into them. Of course, the downside is that it relies on radiation, so ethically you can’t be so cavalier as to CT scan just any living thing. If I’d been alive in 1976, CAT scanning would’ve blown my mind. Still, the image quality isn’t super great here, there’s not good resolution between materials of different densities, hence the grainy images.

But since then, some really smart people have been hard at work to come up with new ways to get better resolution from computerized tomography scans, and the results are pretty amazing. To the left is a slice from a synchrotron CT scan of the MH1 Australopithecus sediba skull (Carlson et al. 2011, Supporting on line material, Fig. S10). You’re basically seeing the fossil face-to-face … if someone had cut of the first few centimeters of the fossil’s face. Just like the movie Face Off.

Quite a difference from the image above. Here, we can distinguish fossilized bone from the rocky matrix filling in the orbit, brain case and sinuses. Synchrotron even distinguishes molar tooth enamel from the underlying dentin (see the square). The post-mortem distortion to the (camera right) orbit is clear. It also looks as though the hard palate is thick and filled with trabecular bone, as is characteristic of robust Australopithecus (McCollum 1999). Interesting…

Even more remarkable, the actual histological structure of bone can be imaged with synchrotron imaging. Mature cortical bone is comprised of these small osteons (or Haversian systems), that house bone cells and transmit blood vessels to help keep bone alive and healthy. Osteons are very tiny, submillimetric. To the right is a 3D reconstruction of an osteon and blood vessels, from synchrotron images (Cooper et al. 2011). The scale bar in the bottom right is 250 micrometers. MICROmeters! Note the scan can distinguish the Haversian canal (red part in B-C) from vessels (white part in B). Insane!

Not only has image quality improved over the past few decades, but CT scanning is being applied outside the field of medicine for which it was developed; it’s becoming quite popular in anthropology. What I’d like to do, personally, with such imaging is see if it can be used to study bone morphogenesis – if it can be used to distinguish bone deposition vs. resorption, and to see how these growth fields are distributed across a bone during ontogeny. This could allow the study the proximate, cellular causes of skeletal form, how this form arises through growth and development. If it could be applied to fossils, then we could potentially even see how these growth fields are altered over the course of evolution: how form evolves.

References
Carlson KJ, Stout D, Jashashvili T, de Ruiter DJ, Tafforeau P, Carlson K, & Berger LR (2011). The endocast of MH1, Australopithecus sediba. Science (New York, N.Y.), 333 (6048), 1402-7 PMID: 21903804

Claveria, L., Boulay, G., & Moseley, I. (1976). Intracranial infections: Investigation by computerized axial tomography Neuroradiology, 12 (2), 59-71 DOI: 10.1007/BF00333121

Cooper, D., Erickson, B., Peele, A., Hannah, K., Thomas, C., & Clement, J. (2011). Visualization of 3D osteon morphology by synchrotron radiation micro-CT Journal of Anatomy, 219 (4), 481-489 DOI: 10.1111/j.1469-7580.2011.01398.x

McCollum, M. (1999). The Robust Australopithecine Face: A Morphogenetic Perspective Science, 284 (5412), 301-305 DOI: 10.1126/science.284.5412.301