Subject: [SciPol 615] ScienceWeek June 1, 2007

From: "Dan Agin" <[email-masked]>
Date: Fri, 01 Jun 2007 13:23:39 -0500

SCIENCEWEEK

June 1, 2007

Vol. 11 - Number 21

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Aristotle has said that the sweetest of all things is knowledge.
And he is right. But if you were to suppose that the
_publication_ of a new view were productive of unbounded
sweetness, you would be mightily mistaken. No one who disturbs
his fellow men with a new view remains unpunished.

-- Ernst Mach (1838-1916)

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Contents (full text below):

1. Anthropology: Walking on Trees

2. Physics: Watching Electrons Break Up

3. Ageing: When Less Is More

4. Evolutionary Biology: Animal Personalities

5. Protein Science: Discriminating Taste of Prions

6. Astrophysics: Water Worlds in the Making

7. Parkinson's Disease and Pesticide Exposures

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1.

Science 1 June 2007: Vol. 316. no. 5829, pp. 1292 - 1294 DOI:
10.1126/science.1143571

Anthropology: Walking on Trees

Paul O'Higgins and Sarah Elton

For decades, researchers have viewed standing upright and walking
on the ground on two legs as defining features of the hominins
(humans and our closest extinct relatives). However, we are
beginning to learn that some apes in the Miocene (5 to 23 million
years ago) not only had upright postures (1) but also
incorporated bipedalism into their motion (2, 3). Such movement
may well have occurred in the trees. This raises the possibility
that preadaptations for hominin bipedalism arose in arboreal
settings rather than in terrestrial environments. On page 1328 of
this issue, Thorpe and colleagues present compelling new evidence
in support of this theory (4). Using observational data from
modern orangutans, they argue that hominin bipedal walking is not
novel but rather a development of locomotor behaviors already
established in the ancestor of great apes.

In modern orangutans, hand-assisted bipedalism with extended
lower limbs in the small branches of the forest canopy allows
movement on slender, springy supports. This enables the
orangutans to access resources in the forest canopy that would
otherwise be difficult to procure, or to cross between trees with
minimum energy expenditure. These advantages might well have
provided sufficient selective pressure for bipedal adaptations in
arboreal habitats.

The orangutan model provides three scenarios for the emergence of
modern great ape and human locomotor strategies from hand-
assisted, straight-lower-limbed, arboreal bipedalism (see the
figure). In the first, forest canopy fragmentation during the
Miocene of Africa led to increased vertical climbing, rather than
always crossing from tree to tree at canopy level. Thorpe et al.
suggest that this climbing behavior, which is similar to knuckle
walking, predisposed gorilla and chimpanzee ancestors to the
independent acquisition of forms of knuckle walking. In the
second scenario, orangutan ancestors in Southeast Asia became
even more specialized in traversing, at canopy level, the
shrinking closed-canopy forest. Finally, hominins retained and
further adapted preexisting arboreal bipedalism to exploit
emerging, more open terrain between forested areas. This third
scenario is consistent with the long forelimbs that are found in
association with obviously bipedally adapted hindlimbs in various
early hominins.

It is necessary in a model such as this to simplify the nature
and tempo of environmental change, although Thorpe and colleagues
do point out the probable fluctuations in forest coverage that
occurred during the Miocene. Inevitably, past environments were
complex, and there was no straightforward transition from
forested to more open habitats. Primate adaptations and
radiations were equally complex, and it has been argued (5) that
apes diversified into a variety of environments well before any
substantial Miocene forest shrinkage. Nonetheless, locomotion is
strongly tied to habitat and therefore evolves in response to
external pressures, whether they are caused by environmental
change or by niche differentiation.

The work of Thorpe et al. reopens the debate about the origins of
our own peculiar commitment to bipedal locomotion. To date, there
is no consensus about the adaptive scenario that could have led
to the adoption of terrestrial bipedalism. Many theories have
been proposed, including the postural feeding hypothesis (6); a
model (7) attributing bipedality to the social, sexual, and
reproductive behavior of early hominins, in which bipedalism
allowed better provisioning of offspring and enhanced
reproductive fitness; the thermoregulatory hypothesis (8), where
standing upright on two legs is argued to reduce the amount of
the body directly exposed to sunlight, therefore allowing
foraging during the hottest part of the day; and the appeasement
model (9), which focuses on bipedal displays that allow for the
relatively peaceful resolution of conflicts.

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2.

Science 1 June 2007: Vol. 316. no. 5829, pp. 1290 - 1291 DOI:
10.1126/science.1143504

Physics: Watching Electrons Break Up

Piers Coleman

Electrons are surprisingly rugged particles that fiercely
maintain their identity in metals. As they move, they conduct
heat and electric charge in all directions in a precisely fixed
ratio, a universal property of electricity called the Wiedemann-
Franz law. On page 1320 of this issue, Tanatar et al. (1) show
that under the right conditions, metals can exhibit a new type of
electrical conductivity for which the Wiedemann-Franz law no
longer holds. Under these conditions, conventional electrons
appear to live alongside a fundamentally different kind of
electricity in which electrons have broken apart and reformed
into a new class of charge- and heat-carrying excitation. Such
failures of accepted laws in science often signal new and
interesting underlying causes, and these results may help us
understand the mechanisms behind high-temperature superconductors
and other unusual materials.

In the 19th century, physicists empirically discovered two
important laws governing the thermal and electrical properties of
dense matter: the Dulong-Petit law and the Wiedemann-Franz law.
At that time, most scientists believed that Dulong and Petit's
law, stating that the specific heat of all materials is a
constant, was a fundamental law of nature. Yet it was the failure
of the Dulong-Petit law at low temperatures in the 20th century
that helped to usher in the era of quantum mechanics (2). Early
on, physicists did not understand the mechanisms behind the
Wiedemann-Franz law, yet it went on to survive, and we know it
now to be a consequence of the discrete, quantum nature of
electrons in electrical current.

In a normal metal, the quantum motion of electrons is very highly
organized (see the left panel of the figure) and might be likened
to the organization of aircraft traffic near a major airport.
Just as airplanes are stacked by altitude, each in its own slot,
electrons are tightly stacked in velocity up to a maximum value
called the Fermi velocity. Electron traffic is controlled by
quantum physics and the "Pauli exclusion principle," which
prevents more than two electrons per velocity slot and helps
electrons protect their identity, even as they jostle one another
inside the electron cloud. As long as this organization holds,
the Wiedemann-Franz law is expected to remain intact.

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3.

Nature 447, 536-537 (31 May 2007) | doi:10.1038/447536a;
Published online 30 May 2007

Ageing: When Less Is More

Adam Antebi

Restricting dietary intake is one way to promote longevity. The
identification of two genes that specifically mediate this effect
in worms provides insight into the molecular mechanisms
underlying ageing.

Dietary restriction -- a reduction of food intake by 40-60%
without malnutrition -- has remarkable benefits for health and
lifespan, extending the survival of species as diverse as yeast,
worms, flies, rodents and perhaps even primates. Yet despite
intensive study, the molecular basis of the effects of dietary
restriction in animals has remained largely elusive. Elsewhere in
this issue, two groups1, 2 report a role for a pair of
evolutionarily conserved proteins -- PHA-4 and SKN-1 -- in
conferring extended survival under dietary restriction in the
small roundworm Caenorhabditis elegans. Both PHA-4 and SKN-1 are
transcription factors, regulating the expression of many genes.
Moreover, evidence suggests that they may also trigger hormones
that coordinate physiological responses to dietary restriction.

Restricting dietary intake in worms can be achieved by diluting
their bacterial food. At optimum conditions for dietary-
restriction-induced longevity, worms typically live 20-50% longer
than fully fed animals. The PHA-4 protein, which was originally
described for its role in specifying the pharynx in worm embryos,
is a member of the forkhead family of transcription factors, and
is very similar to mammalian FOXA proteins3, 4. In mammals, FOXA
proteins have developmental roles, and regulate glucose
metabolism later in life5. In C. elegans, PHA-4 is present from
embryo to adult, but its functions in later life were largely
unknown.

To examine PHA-4 function in adult worms, Panowski and colleagues
(page 550)1 used genetic manipulations to inactivate the pha-4
gene in adult worms, without affecting its embryonic activity.
Intriguingly, they found that pha-4 mutants did not respond to
dietary manipulations, showing a similar median adult lifespan at
all tested food concentrations; however, other processes such as
food ingestion and feeding behaviour appeared normal. By
inference, therefore, PHA-4 function in adult worms is to respond
to dietary changes, and to increase survival under conditions of
dietary restriction.

The authors also found that the requirement for PHA-4 was very
specific. Systematic knockdown of the other 14 forkhead
transcription factors expressed in the worm - including DAF-
16/FOXO - had little effect on longevity induced by restricting
dietary intake. The DAF-16/FOXO transcription factor works in
another well-known longevity pathway - that of insulin/IGF
signalling, which dramatically influences lifespan in worms,
flies and mice6. A modest reduction of insulin/IGF signalling
activates DAF-16/FOXO, which mediates a twofold extension of worm
lifespan. Similarly, inactivation of DAF-16 completely abolishes
insulin/IGF-signalling-mediated longevity6.

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4.

Nature 447, 539-540 (31 May 2007) | doi:10.1038/447539a;
Published online 30 May 2007

Evolutionary Biology: Animal Personalities

Alison M. Bell

That different people differ in their readiness to take risks is
an obvious feature of human personality. Theoretical advances now
help in making sense of observations of analogous behaviour in
animals.

Personality might seem to require a complexity and subtlety that
is unique to humans. But evidence for individual variation in
traits that we would recognize as personality, for example
aggressiveness in fighting or boldness in the face of a predator,
has cropped up in animals ranging from fish to monkeys to squid.
Even an individual spider behaves differently from other spiders,
through time and in different situations1. Wolf et al. (page 581
of this issue2) now show how such variation in behaviour can make
evolutionary sense.

Personality has been difficult to explain from an evolutionary
perspective because, at first glance, it could seem maladaptive3.
An individual that is consistently uninhibited and bold is going
to end up eaten by a predator. The optimal animal should be bold
only when it makes sense to be bold, and adjust its behaviour
when the situation changes. Although animals are legendary for
their remarkable 'behavioural plasticity' (think migration or
camouflage, for example), there is growing evidence that animals
do not always change their behaviour as much as they should. In
other words, behavioural plasticity is limited3.

One possible explanation for this is that individuals should
behave consistently if it's simply too hard to undergo a
personality transformation. If turning off a general tendency to
be aggressive requires time and energy to entirely rewire neural
machinery, or to build a physiology that can support a different
metabolism, then individuals might be better off sticking to an
intermediate strategy4. Similarly, if information about the
immediate environment is uncertain, then it makes sense just to
behave the same way and avoid the risk of making a mistake5.

This line of reasoning can help to explain why a given individual
behaves consistently, but not, for example, why some individuals
are always more aggressive than others. Such variation is
puzzling, because natural selection will favour individuals with
characteristics that perform the best, and less 'fit' individuals
will be removed from the population. If a trait is heritable and
linked to survival or reproductive success, then evolutionary
theory tells us that variation will eventually disappear from the
population. But, empirically, we know that personality traits are
heritable6, are linked to fitness7 and are quite variable.

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5.

Nature 447, 541-542 (31 May 2007) | doi:10.1038/447541b;
Published online 30 May 2007

Protein Science: Discriminating Taste of Prions

Witold K. Surewicz

Prions are infectious proteins that are involved in brain-wasting
disorders such as mad cow disease. In yeast, specific sequences
of amino acids in prions seem to mediate prion propagation and
cross-species transmissibility.

Few diseases have generated as much interest and controversy in
recent years as transmissible spongiform encephalopathies (TSEs)
- a group of fatal neurodegenerative disorders that includes
Creutzfeldt-Jakob disease in humans and 'mad cow' disease1, 2.
The protein-only hypothesis of TSE propagation postulates that
the infectious pathogen, called a prion, is devoid of the nucleic
acids that comprise genes, and is an abnormally shaped version of
the normal prion protein, a naturally occurring molecule of
unknown function. The infectious prion replicates by binding to
its host's normal prion protein and forcing it to take on the
abnormal conformation1. Once heretical, this notion that proteins
alone can be infectious is now rapidly gaining acceptance.
Paradoxically, the most compelling evidence for this idea has
come not from studying TSEs, but from prion-like entities in
yeast and other fungi3, 4, 5, 6. In this issue (page 556),
Tessier and Lindquist7 present intriguing findings that clarify
many of the mechanisms underlying the conversion of yeast prion
proteins to an infectious form.

Whereas mammalian prions cause a dreaded brain-wasting disease,
infectious prions in yeast change the behaviour (or phenotype) of
these simple organisms, with the altered characteristics passing
from one generation to the next3, 4. Thus, yeast prions act as
protein-only 'genes'. The most extensively studied yeast prion
protein is called Sup35, which, when conformationally modified
into an infectious prion, leads to a yeast phenotype that is
defective in terminating protein synthesis. The conversion of
Sup35, and other yeast prions, to the infectious state is
associated with their polymerization into amyloid fibrils -
highly organized, thread-like aggregates that are also linked to
Alzheimer's disease and other 'protein-misfolding' disorders3, 4.

To investigate the precise mechanisms underlying prion
conversion, Tessier and Lindquist7 synthesized a large library of
overlapping peptides derived from the amino-acid sequences of two
regions of Sup35 - its N-terminal (N) and its middle (M) regions,
jointly denoted ScNM - from the budding yeast Saccharomyces
cerevisiae. They then used an array assay to analyse the ability
of these sequences to bind to and modify the full-length protein
(Fig. 1). They found that only a tiny subset of ScNM peptides
could capture the ScNM protein from solution, and that these
peptides selectively promoted the assembly of amyloid fibrils.
The authors conclude that small elements of the Sup35 amino-acid
sequence can recognize soluble conformations of the protein with
unusual specificity, and that this is sufficient to drive the
conversion of soluble proteins to the abnormal prion state.

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6.

Nature 447, 535-536 (31 May 2007) | doi:10.1038/447535a;
Published online 30 May 2007

Astrophysics: Water Worlds in the Making

Roy van Boekel

Meticulous observations of the disk of gas and dust around one
young star seem to imply icy, comet-like bodies in the disk's
inner regions. Could these be the building-blocks of water-rich
planets like Earth?

The disks of dust and gas around newborn stars provide a natural
laboratory for studying the formation of planetary systems. But
even the nearest young stars are so far away that conventional
telescopes lack the sharpness of vision to see into the very
centre of the disk, where habitable planets such as Earth could
form. Using the Keck Interferometer - a system of two telescopes
on the summit of Mauna Kea, Hawaii - J. A. Eisner has zoomed in
on this 'terrestrial region' around one young star. The results1
can be found on page 562. He measures the disk geometry on scales
of less than one astronomical unit (AU) - the distance from Earth
to the Sun - and directly locates hydrogen gas plunging onto the
star. He finds water, too, in the inner disk, arguably stemming
from evaporating icy bodies that might even now be forming water-
rich, Earth-like planets.

The disks around stars consist mostly of hydrogen gas, but they
also contain molecules such as carbon monoxide (CO) and water
that are much less abundant, but easier to detect by virtue of
their much stronger spectral signatures. About 1% of the disk
mass consists of tiny particles of solid material. Put enough of
this 'dust' together, and you can make a rocky planet like Earth,
or the core of one of the giant gas planets found farther out in
our Solar System.

Of the more than 200 'exoplanets' now known to be orbiting stars
other than the Sun, a preponderance are giant gas planets close
to their parent star. That is partly because these planets are
easiest (or rather, least difficult) to detect. Even so, it seems
that our Solar System's architecture, which is apparently so
favourable for the development of life - rocky planets close to
the star, gas giants farther away, all on approximately circular
orbits - is not common2. But exactly how uncommon is it?

To find out, we need to go back to the planetary cradle. In most
of a circumstellar disk, gas and dust are mixed. In the region of
interest close to the star, however, the temperature is so high
that solid material vaporizes, and hot gas swirls its way towards
the star. Dynamical interactions between this hot gas and forming
planets, which cause planets to migrate through the disk, are
considered crucial in determining the final architecture of a
planetary system3.

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7.

British Medical Bulletin 2006 79-80(1):219-231;
doi:10.1093/bmb/ldl018

Parkinson's Disease and Pesticide Exposures

Finlay D. Dick

Introduction: Idiopathic Parkinson's disease (PD) is a
neurodegenerative disorder in which loss of dopaminergic neurons
in the basal ganglia leads to tremor, bradykinesia, rigidity and
postural instability.

Methods: Literature search using Medline

Results: Many studies have found an association between
pesticides and PD, but no one agent has been consistently
identified. Those implicated include organochlorine insecticides,
maneb and paraquat. One meta-analysis of pesticide exposure and
PD found an almost doubling of risk in those exposed.
Associations with specific agents may be confounded by exposure
to other pesticides, making it difficult to identify the
causative agent.

Conclusions: The available evidence indicates that pesticides are
associated with PD, but further research is needed to identify
long-term biomarkers of exposure, improve methods for estimating
pesticide-exposure and undertake prospective cohort studies of
pesticide-exposed workers.

Parkinson's disease (PD) is a movement disorder, which develops
as a consequence of degeneration of the dopaminergic neurons
within the basal ganglia. The disease becomes clinically apparent
once ~70% of the dopaminergic neurons of the substantia nigra are
lost. Neuropathologically, Lewy bodies are typical of PD,
although these intra-cytoplasmic neuronal inclusions, which
contain {alpha}-synuclein, may be found in other conditions such
as dementia with Lewy bodies. PD is principally a disease of
ageing, with a peak age of onset of 65 years, although both young
onset PD, generally defined as disease onset <40 years, and a
rare juvenile form occur.

PD presents with resting tremor, slow movements (bradykinesia)
and rigidity and, later, postural instability occurs. Almost half
of PD sufferers show asymmetry with signs and symptoms being more
marked on one side of the body. The condition was first described
by Parkinson,1 an English surgeon, in 1817 in his classic
monograph `an essay on the shaking palsy´. He described the main
features of what is now known as PD and gave case histories of
six sufferers, one of whom was a gardener (case I).

The reported incidence of PD varies across the world,2 although
whether this reflects genuine differences in disease incidence or
better case ascertainment in North American and Western European
populations is less clear. There is some evidence to suggest that
PD is commoner in Caucasians than Chinese, although this may
reflect differing environmental exposures rather than greater
genetic susceptibility to the disease.

The diagnosis of PD is essentially a clinical one, but diagnosis
can be difficult and other causes of parkinsonism should be
considered. Vascular parkinsonism, due to cerebral infarcts, may
be confused with PD, but the stepwise progression typical of
vascular parkinsonism together with a failure to respond to L-
dopa should alert the treating clinician to the correct
diagnosis. Patients treated with major tranquilizers or anti-
emetics may develop drug-induced parkinsonism but this should be
distinguished from PD. Post-mortem studies in the early 1990s
found that 24% of patients clinically thought to have had PD
actually had another condition (e.g. progressive supra-nuclear
palsy or multi-system atrophy). More recently, the diagnostic
accuracy of PD, at least among movement disorder specialists, has
improved to 90%.3 Diagnostic imprecision has implications for
research into the causes of PD, especially when considering
studies carried out before the early 1990s, as studies that
included a significant proportion of people with parkinsonism
rather than PD would have had reduced statistical power to detect
associations.

A number of different clinical diagnostic criteria for PD have
been published, including the Ward and Gibb criteria, the Gelb
criteria and the UK Parkinson's Disease Society (PDS) Brain Bank
clinical diagnostic criteria.4 Of these, the most widely used
have been the three-step UK PDS Brain Bank criteria: step 1
requires the presence of bradykinesia and at least one of
muscular rigidity, 4-6 Hz rest tremor and postural instability;
step 2 lists 16 exclusion criteria including a history of
definite encephalitis and step 3 lists eight supportive criteria,
at least three of which are required for a diagnosis of definite
PD.

Genetic research has identified a number of rare familial forms
of PD because of single gene mutations.5 These breakthroughs have
given researchers valuable new insights into some of the
mechanisms that may underlie PD, but nonetheless most cases of PD
remain unexplained. Two large twin studies6,7 failed to find
evidence of a significant genetic contribution to the burden of
typical PD, although in one study,6 genetic factors did seem to
make a contribution in younger onset PD (defined in that study as
onset <50 years of age).

The generally held view is that PD is due to both environmental
and genetic factors and that it is not one disease but rather a
number of phenotypically similar conditions.

Studies of environmental risk factors for PD received a fillip
following reports of parkinsonism in a small number of drug
abusers who had consumed a synthetic opiate, 1-methy-4-phenyl-
1,2,3,6-tetrahydropyridine (MPTP).8 MPTP is metabolized to the
neurotoxin 1-methyl-4-phenylpyridinium (MPP+), which was
originally developed as the herbicide, cyperquat. The chemical
structure of MPP+ is similar to the widely used bipyridinium
herbicide paraquat. This finding prompted a number of
epidemiological studies of the association between pesticide
exposure and PD.

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From: Thomas Chacko <[email-masked]>
Date: Wed, 6 Jun 2007 11:10:06 +0100 (BST)

Under these conditions, conventional electrons
appear to live alongside a fundamentally different kind of
electricity in which electrons have broken apart and reformed
into a new class of charge- and heat-carrying excitation.

  In the interest of scientific exactitude, " reformed" should be written as " re-formed", shouldn' it? Otherwise, the more frequent and familiar word "reformed", which is homophonous with the intended word, will interfere with the processing of the sentence.
  Thomas Chacko
Dan Agin <[email-masked]> wrote:
  
SCIENCEWEEK

June 1, 2007

Vol. 11 - Number 21

1.

2.

Piers Coleman

3.

Adam Antebi

4.

Alison M. Bell

5.

Witold K. Surewicz

6.

Roy van Boekel

7.

Finlay D. Dick

=== message truncated ===

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Ph. 00-31-50- 3134226
Cell: 0031621983720
E-mail: [email-masked]
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