ScienceWeek

SCIENCEWEEK

September 29, 2006

Vol. 10 - Number 39

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Our loyalties are to the species and the planet. We speak for Earth. Our obligation to survive is owed not just to ourselves but also to that Cosmos, ancient and vast, from which we spring.

-- Carl Sagan (1934-1996)

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Contents (full reports below):

1. Neuroscience: On the Pathogenesis of Human Epilepsy. Epilepsy, one of the most common neurological disorders, is caused by abnormal electrical activity in the brain. The symptoms range in severity from mild sensory disruption to recurring seizures and unconsciousness. Most forms of epilepsy have been assumed to stem from brain tissue "scars" acquired through trauma, so that molecular approaches...

2. Geophysics: On Earthquake Rupture. Violent shaking and destruction caused by earthquakes are the result of rupture and frictional slip on tectonic faults, and bigger earthquakes break bigger fault segments. But how do brittle ruptures of Earth's crust grow? Seismologic evidence shows that quakes begin in a small nucleation region and propagate at speeds up to...

3. Climate Science: On Greenland's Ice Loss. The volume of the ice sheet that covers most of Greenland is so large that, were it to melt completely, sea levels across the world would rise by about 7 meters. Furthermore, an increase in its delivery of fresh water to the oceans could weaken or disrupt the "thermohaline" circulation of oceanic salt water (1), profoundly altering the climate of the...

4. Palaeoanthropology: A New Hominin Fossil Child. The fragile bones of infants rarely survive long enough to make it into the hominin fossil record. But if they do, they provide precious evidence about the growth and development of the individual and its species. This helps researchers not only to understand how such processes have changed during hominin evolution, but also to interpret the...

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Special Note: A New Book by the Editor of ScienceWeek:

Junk Science. How Politicians, Corporations, and Other Hucksters Betray Us. Dan Agin. Thomas Dunne Books/St. Martin's Press, New York, 2006. Hardback: 336 pp., $24.95. ISBN 0312352417. Publication date: October 3, 2006. More information at: http://www.amazon.com/exec/obidos/ASIN/0312352417/scienceweek

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Also Noted:

Pursuit of Genius. Flexner, Einstein, and the Early Faculty at the Institute for Advanced Study. Steve Batterson. Peters, Natick, MA, 2006. Hardback: 313 pp., illus. $39. ISBN 1568812590. More information at: http://www.amazon.com/exec/obidos/ASIN/1568812590/scienceweek

Relativistic Astrophysics and Cosmology. A Primer. Peter Hoyng. Springer, Berlin, 2006. Hardback: 303 pp., illus. $79.95. ISBN 1402045212. More information at: http://www.amazon.com/exec/obidos/ASIN/1402045212/scienceweek

To Cherish the Life of the World. The Selected Letters of Margaret Mead. Margaret Caffrey and Patricia Francis, Eds. Basic Books (Perseus), New York, 2006. Hardback: 463 pp., illus. $29.95, C$39.95. ISBN 0465008151. More information at: http://www.amazon.com/exec/obidos/ASIN/0465008151/scienceweek

True Visions. The Emergence of Ambient Intelligence. E. H. L. Aarts and J. L. Encarnação, Eds. Springer, Berlin, 2006. Hardback: 465 pp., illus. $159. ISBN 3540289720. More information at: http://www.amazon.com/exec/obidos/ASIN/3540289720/scienceweek

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1. NEUROSCIENCE: ON THE PATHOGENESIS OF HUMAN EPILEPSY

The following points are made by Solomon H. Snyder (Science 2006 313:1744):

1) Epilepsy, one of the most common neurological disorders, is caused by abnormal electrical activity in the brain. The symptoms range in severity from mild sensory disruption to recurring seizures and unconsciousness. Most forms of epilepsy have been assumed to stem from brain tissue "scars" acquired through trauma, so that molecular approaches to understanding and treating the disease would be fruitless. In recent years, mutations in various ion channels have been linked to rare forms of epilepsy. New work (1) identifies a pairing of proteins in neurons that may be relevant to the pathogenesis of human epilepsy. The agonist-receptor pair regulates the activity of the glutamate-AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor, the subtype that mediates the most prominent form of excitatory neurotransmission in the brain.

2) At the cleft, or synapse, between two communicating neurons, lies the postsynaptic density, the region in the postsynaptic neuron where adhesion and signaling molecules are organized to facilitate rapid response to neurotransmitter molecules released by the presynaptic neuron. Key among these constituent molecules is postsynaptic density-95 (PSD-95), a major scaffolding protein localized to the postsynaptic density of brain synapses. Fukata et al (1) sought binding partners for PSD-95 by monitoring proteins that associate with it in rat brain extracts. The authors identified a protein complex comprising stargazin, LGI1, and ADAM22.

3) All three proteins have previously been implicated in epilepsy. LGI1 is a known secreted neuronal protein, which is mutated in patients with a rare genetically determined form of epilepsy but whose physiological role has been obscure (2). ADAM22 is a neuronal membrane protein. Its mutation in mice leads to death from seizures, but its normal function has also not been definitively established (3). Stargazin, discovered as the protein that is mutated in Stargazer mice that suffer from epilepsy, is a subunit of the AMPA receptor and regulates AMPA receptor trafficking to the postsynaptic density (4). Fukata et al (1) establish that LGI1 binds selectively to ADAM22, specifically at synaptic sites on the surface of rat brain neurons. Treatment of rat brain slices with LGI1 augmented AMPA receptor-mediated neurotransmission, reflected by the increased amplitude and frequency of postsynaptic AMPA receptor-meditated electric currents. This action was prevented by first treating the brain slices with a soluble form of ADAM22, indicating that synaptic activation by LGI1 is dependent on its binding to ADAM22. The increased neurotransmission appears to reflect recruitment of new AMPA receptors to the postsynaptic density, because LGI1 expression in cultured hippocampal neurons increases surface expression of AMPA receptors.

4) The generation of epileptic seizures has usually been ascribed to changes in neuronal ion channels. The finding that mutation of various proteins associated with AMPA receptors leads to epilepsy suggests that glutamate neurotransmission plays a more prominent pathogenic role than previously appreciated. The postsynaptic density, a structure comprising several scaffolding proteins linked to AMPA receptors, might be disrupted by the "scarring" that underlies many forms of epilepsy. Conceivably, hitherto undetected mutations in the proteins of postsynaptic densities may be responsible for multiple forms of seizure disorders.(5)

References (abridged):

1. Y. Fukata et al., Science 313, 1792 (2006)

2. O.K. Steinlein, Nat. Rev. Neurosci. 5, 400 (2004)

3. K. Sagane et al., BMC Neurosci. 6, 33 (2005)

4. R. A. Nicoll, S. Tomita, D. S. Bredt, Science 311, [1253] (2006)

5. E. Kim, M. Sheng, Nat. Rev. Neurosci. 5, 771 (2004)

Science http://www.sciencemag.org

ScienceWeek http://scienceweek.com

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2. GEOPHYSICS: ON EARTHQUAKE RUPTURE

The following points are made by C. Marone and E. Richardson (Science 2006 313:1748):

1) Violent shaking and destruction caused by earthquakes are the result of rupture and frictional slip on tectonic faults, and bigger earthquakes break bigger fault segments. But how do brittle ruptures of Earth's crust grow? Seismologic evidence shows that quakes begin in a small nucleation region and propagate at speeds up to 16,000 kilometers per hour. Two competing models of rupture growth describe this expansion. In the crack model, the nucleation region slips throughout the quake and the slipping region expands until the rupture stops, a process akin to stretching a penny into the size of a half-dollar. In the pulse model, only a small portion of the total fault area slips at any one time, so as to cover the fault surface the way an inchworm crawls.

2) Distinguishing between the two models is important for hazard assessment because they predict different degrees of strong shaking and ground acceleration with distance from the nucleation site. Recent seismological observations favor the pulse model, but efforts to connect these data with theoretical models of earthquake physics have been stymied because rupture pulses have never been reliably observed in the laboratory. However, new laboratory experimental evidence (1) on brittle fracture, showing the existence of pulse-like ruptures and the conditions under which they exist, may help resolve the debate.

3) Lykotrafitis et al (1) sheared photoelastic material in frictional contact in a dynamic impact apparatus and monitored rupture propagation with high-speed photography. They show that the rupture propagation mode varies systematically with the strength of initial forcing (as produced by impact speed). Pulse-like ruptures are favored by slower impact speeds relative to those for crack-like ruptures. Also, the frictional slip velocity during rupture is lower for pulse-like ruptures than for crack-like ruptures. Thus, pulse-mode ruptures are the slow cousins of breaks that propagate as classical cracks. The data of Lykotrafitis et al (1) show a clear relationship between stress level and rupture propagation mode, with larger shear stress levels resulting in crack-like propagation.

4) These experiments address perhaps the most important question in earthquake physics: What controls seismic slip at a point on a fault? Virtually every quantifiable aspect of earthquakes depends on slip, but local fault slip cannot be measured directly from seismograms. If the initial tectonic shear stress determines slip, it would imply that dynamic frictional strength is zero and that stress on the fault drops to zero during an earthquake. In this scenario, seismic slip ceases because the local energy budget is depleted, but this runs counter to laboratory data on frictional stick-slip and seismic estimates of radiated energy, which indicate that seismic stress drop is a mere 10% of the tectonic stress level. Or, if the boundary conditions of fault strength determine seismic slip, then earthquake rupture stops when it encounters a strong barrier. Alternatively, frictional behavior during rupture -- possibly abetted by dynamic variations in normal stress -- could determine slip. The self-healing pulse model belongs to this last class of models. In order for rupture to propagate as a slip pulse, the fault must strengthen rapidly after slip so that local slippage ceases.(2)

References:

1. G. Lykotrafitis, A. J. Rosakis, G. Ravichandran, Science 313, 1765 (2006)

2. K. Aki, J. Geophys. Res. 72, 1217 (1967)

Science http://www.sciencemag.org

ScienceWeek http://scienceweek.com

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3. CLIMATE SCIENCE: ON GREENLAND'S ICE LOSS

The following points are made by Tavi Murray (Nature 2006 443:277)

1) The volume of the ice sheet that covers most of Greenland is so large that, were it to melt completely, sea levels across the world would rise by about 7 meters. Furthermore, an increase in its delivery of fresh water to the oceans could weaken or disrupt the "thermohaline" circulation of oceanic salt water (1), profoundly altering the climate of the Northern Hemisphere. Such doomsday scenarios are well rehearsed, but -- expressed in this way -- not necessarily accurate. If cold areas such as the centre of Greenland warm up, it might actually snow more. That would, in turn, thicken the ice sheet and remove water from the global oceans. The very different densities of snow, ice and water mean that measuring the volume of the Greenland ice sheet does not provide the complete answer as to whether it is growing or shrinking. The ideal method is to measure how the mass of the ice sheet is changing with time.

2) In two complementary studies, Velicogna and Wahr (2) and Chen et al (3) do just that. They show that the Greenland ice sheet lost between 192 million and 258 million tonnes of ice each year between April 2002 and April 2006 (equivalent to a volume of 212-284 km^3). This rate of ice loss is equivalent to a rise in sea level of 0.5 +- 0.1 mm/yr, which is higher than many previous estimates. Both studies also show that the rate at which ice was being lost increased dramatically in the course of the study: the loss rate in the period 2004-06 was 2.5 times higher than that between 2002 and 2004 (2). Both studies used data from the Gravity Recovery and Climate Experiment (GRACE), funded by NASA and the German Aerospace Center (DLR), which measures Earth's gravity field from space. GRACE consists of two satellites orbiting Earth. These satellites are separated by a distance of around 220 km that varies slightly as the satellites pass over anomalies in the gravity field. Since their launch in March 2002, the GRACE satellites have mapped the global gravity field every 30 days. Over time, that field should show evidence of changes in the ice-sheet mass.

3) But calculated ice-mass changes are only as accurate as the models used to remove other mass-change signals -- those caused by tidal and non-tidal changes in the oceans, and by changes in the atmosphere and in Earth's mantle as it rebounds after the last ice age. At high latitudes, these models are not without error. The GRACE studies (2,3) attempt to account for these other variations and their uncertainties, leaving a residual signal that results from the net loss of glacier ice into the oceans alone. In particular, the high density of mantle rocks means that the gravity signal is very sensitive to even small errors in the model of rebound. But Velicogna and Wahr's estimate of uncertainty in the rebound rate (2) would have to be increased by a factor of ten to change their conclusion of an overall loss of ice-sheet mass to an overall gain. And as this error would be constant over the timescale of the GRACE measurements, the change in the rate of mass loss is a highly stable result.

4) The GRACE data can also be used to indicate where the ice is being lost. Most of the loss is from south or southeast Greenland (2,3), with Chen et al. reporting an additional area of loss in the northeast (3). Airborne and satellite altimetry over the ice sheet shows further detail of the spatial pattern, albeit over different periods. The central portions of the ice sheet, with elevations above 1500 m, are indeed thickening, fed by increased snowfall (4). The margins, in contrast, are thinning (5). The outlet glaciers that feed ice from the centre of Greenland to the ocean are also depleting rapidly. This is occurring particularly in the southeast, where thinning rates can be more than 10 m/yr. This depletion coincides with mass loss identified in the southeast using GRACE (2,3). The mass loss in the northeast (2) is possibly caused by thinning of the northeast Greenland ice stream (4). Chen et al postulate that changes in glaciers in the Svalbard archipelago, which lies northeast of Greenland between Norway and the North Pole, might be part of the explanation (3).

References (abridged):

1. Fichefet, T. et al. Geophys. Res. Lett. 30, 1911 (2003)

2. Velicogna, I. & Wahr, J. Nature 443, 329-331 (2006)

3. Chen, J. L. , Wilson, C. R. & Tapley, B. D. Science doi:10.1126/science.1129007 (2006)

4. Johannessen, O. M. , Khvorostovsky, K. , Miles, M. W. & Bobylev, L. P. Science 310, 1013-1016 (2005)

5. Thomas, R. , Frederick, E. , Krabill, W. , Manizade, S. & Martin, C. Geophys. Res. Lett. 33, L10503 (2006)

Nature http://www.nature.com/nature

ScienceWeek http://scienceweek.com

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4. PALAEOANTHROPOLOGY: A NEW HOMININ FOSSIL CHILD

The following points are made by Bernard Wood (Nature 2006 443:278):

1) The fragile bones of infants rarely survive long enough to make it into the hominin fossil record. But if they do, they provide precious evidence about the growth and development of the individual and its species. This helps researchers not only to understand how such processes have changed during hominin evolution, but also to interpret the function and the taxonomic significance of the better-sampled adult specimens. In this respect, the remarkably complete 3.3-million-year-old skeleton of a three-year-old Australopithecus afarensis female, found in Dikika, Ethiopia, is a veritable mine of information about a crucial stage in human evolutionary history. The fossil is described by Alemseged et al (1), and its geological and palaeontological context is reported by Wynn et al (2).

2) Thanks to efforts in Ethiopia and elsewhere, we already know a good deal about A. afarensis. It has been called an "archaic" hominin for at least two reasons. First, it is old: its fossils date from between 4 million and 3 million years ago. Second, its morphology is archaic, in the sense that its brain case, jaws and limb bones are much more ape-like than those of later taxa that are rightly included in our own genus, Homo. When adjusted for its body size, the brain of A. afarensis is not much larger than that of a chimpanzee, and although it has lost the large canines that distinguish apes from hominins, other aspects of its dentition, such as its relatively large chewing teeth, are still primitive.

3) There remains a great deal of controversy regarding the posture and locomotion of A. afarensis. Most researchers accept that it could stand upright and walk on two feet, but whether it could climb up and move through trees is still disputed. Some suggest that its adaptations to walking on two feet preclude any significant arboreal locomotion, and interpret any limb features that support such locomotion as evolutionary baggage without any useful function (3). Others suggest that a primitive limb morphology would not have persisted unless it served a purpose (4).

4) The Dikika infant is not the first early hominin infant to be found. That distinction belongs to the Taung child, whose discovery was reported just over 80 years ago (5). What makes the Dikika infant remarkable is its unprecedented completeness for such a geologically ancient specimen. The infant was found in sediments that formed the bottom of a small channel close to where a river discharged into a lake (2). This was not a turbulent stream or river. The flow was sluggish, typical of the type of braided streams that make up a river delta. The corpse of the infant was buried more or less intact, and the sediment in flood waters must have swiftly covered it. Some parts of the specimen -- the pelvis, the lowest part of the back and parts of the limbs -- are still missing, but what is preserved is remarkably complete. The face, the brain case and the base of the cranium, the lower jaw, all but two of the teeth (including unerupted adult teeth still in the jaw), both collar bones, the vertebrae down to the lower back, many ribs, both knee caps and the delicate bone that holds open the throat, the hyoid, are all there. Even the medial epicondyle of the humerus has survived. This is the bony projection on the inside of your elbow against which your left thumb rubs if you hold your right elbow with your left hand. In a three-year-old infant, this tiny piece of bone is still separate from the main shaft of the humerus. One must travel forward in time more than three million years, to a Neanderthal infant from Dederiyeh, Syria, to find a comparably complete hominin infant skeleton.

References (abridged):

1. Alemseged, Z. et al. Nature 443, 296-301 (2006)

2. Wynn, J. G. et al. Nature 443, 332-336 (2006)

3. Latimer, B. , Ohman, J. C. & Lovejoy, C. O. Am. J. Phys. Anthropol. 74, 155-175 (1987)

4. Stern, J. T. Evol. Anthropol. 9, 113-133 (2000)

5. Dart, R. A. Nature 115, 195-199 (1925)

Nature http://www.nature.com/nature

ScienceWeek http://scienceweek.com

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