Subject: [SciPol 531] ScienceWeek April 13, 2007

From: "Dan Agin" <[email-masked]>
Date: Fri, 13 Apr 2007 14:00:09 -0500

SCIENCEWEEK

April 13, 2007

Vol. 11 - Number 14

--------------------------------

To receive the complete text of ScienceWeek each week by Email
via the Science and Politics discussion list, send Email to
[email-masked] with subject line "CONTENTS", and we
will subscribe you and add your name to the distribution list.

You can make relevant comments or queries to the entire
distribution list of ScienceWeek and the Science and Politics
discussion list simply by sending Email to
[email-masked] with an appropriate subject line. Please
do not make any posts not relevant to science or the interface
between science and politics. Announcements of conferences,
symposia, new books, etc. are acceptable.

--------------------------------

Science gains reality when it is viewed not as an abstraction,
but as the concrete sum of work of scientists, past and present,
living and dead. Not a statement in science, not an observation,
not a thought exists in itself. Each was ground out of the harsh
effort of some man, and unless you know the man and the world in
which he worked; the assumptions he accepted as truths; the
concepts he considered untenable; you cannot fully understand the
statement or observation or thought.

-- Isaac Azimov (1920-1992)

--------------------------------

Contents (full text below):

1. Medicine: Light Hits the Liver

2. Planetary Science: As Tiny Worlds Turn

3. Climate Change: Global Warming Is Changing the World

4. Cell Biology: Autophagy and Cancer

5. Obituary: Knut Schmidt-Nielsen (1915-2007)

6. Solid-State Chemistry: Crystal tennis rackets

=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

1.

Science 13 April 2007: Vol. 316. no. 5822, pp. 206 - 207 DOI:
10.1126/science.1142238

Medicine: Light Hits the Liver

Göran K. Hansson

Atherosclerosis, the underlying cause of most cases of myocardial
infarction, stroke, and gangrene, is the most common lethal
disease in Western societies and is expected to become the number
one killer globally by 2020 (1). It is an inflammatory disease
triggered by the accumulation of plasma lipoproteins in the
artery wall (2). In this scenario, lipids cause inflammation.
However, a report by Lo et al. on page 285 in this issue (3)
turns the situation upside-down by showing that two factors
produced by immune cells--the cytokines lymphotoxin and LIGHT--
cause the amount of lipids in the blood to increase.

Several studies have implicated the tumor necrosis factor
superfamily of proinflammatory cytokines in lipid metabolism.
Tumor necrosis factor was discovered not only as a soluble
protein that induces the death of tumor cells but also as a
molecule (cachectin) that causes hypertriglyceridemia and wasting
of muscle and fat tissue (4). These effects are due to its
inhibition of the enzyme lipoprotein lipase, thus limiting the
supply of fatty acids for energy production and fat storage.
These remarkable metabolic effects of this cytokine did not
attract as much attention as its proinflammatory actions and its
ability to promote cell death. However, recent findings of tumor
necrosis factor secretion from adipose tissue of individuals with
metabolic syndrome, a condition predisposing to atherosclerosis,
have focused much interest on the metabolic action of this
cytokine and its cousins (5).

Several of the more than 40 members of the tumor necrosis factor
superfamily of proinflammatory molecules are soluble cytokines;
others are membrane proteins that can ligate receptors on
adjacent cells. There is substantial cross-talk between receptors
and ligands. Two members of this family, lymphotoxin and LIGHT,
share many features with tumor necrosis factor (the prototypic
family member), such as promoting inflammation and host defense
against pathogens, and they have been implicated in several
inflammatory diseases, including rheumatoid arthritis and Crohn's
disease (6). Two other superfamily members, CD40 and OX40L, are
involved in atherosclerosis, and seem to propagate plaque
inflammation (7, 8).

In contrast to tumor necrosis factor, LIGHT is mainly expressed
on the surface of T cells and specialized cells of the immune
system called dendritic cells (9). Lo et al. observed that
transgenic mice engineered to overexpress LIGHT on T cells
developed hyperlipidemia, displaying elevated cholesterol and
triglyceride concentrations in the blood. When T cells from such
mice were transferred into normal mice, plasma cholesterol
concentration increased substantially. LIGHT (and lymphotoxin)
bind to the lymphotoxin beta receptor but also to other
receptors. By treating mice with soluble forms of the receptor,
to function as "decoys," the authors establish that the
hyperlipidemic effect of LIGHT depends on the lymphotoxin beta
receptor.

=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

2.

Science 13 April 2007: Vol. 316. no. 5822, pp. 211 - 212 DOI:
10.1126/science.1141930

Planetary Science: As Tiny Worlds Turn

David P. Rubincam and Stephen J. Paddack

Sunlight changes the rotation rate of an asteroid? The idea seems
absurd, but on page 272 Lowry et al. (1) and on page 274 Taylor
et al. (2) report observations that indicate sunlight is doing
just that to the small asteroid 2000 PH5, and Kaasalainen et al.
indicate the same is happening on 1862 Apollo (3). The mechanism
is the Yarkovsky-O'Keefe-Radzievskii-Paddack effect, mercifully
shortened to YORP. With YORP now on a solid foundation, we may be
able to understand a number of strange observations involving
small spinning asteroids and asteroid binary systems.

The saga of sunlight changing into spin began with Ivan
Yarkovsky, a Polish engineer who realized more than a century ago
that the infrared radiation escaping a body warmed by sunlight
carries off momentum as well as heat (4). Point this heat in the
right direction, and it will function like a rocket motor: Each
infrared photon escaping the object carries away momentum, thanks
to the relationship p = E/c, where p is the photon's momentum, E
is its energy, and c is the speed of light. By the principle of
action-reaction, the object emitting the photon gets a kick in
the opposite direction. (Yarkovsky knew nothing of photons and
based his reasoning on the outmoded ether concept, but his idea
survives the translation to modern physics.) Yarkovsky thrust is
tiny, but space is so empty there is no friction to stop it.
Moreover, because the Sun is always shining, the Yarkovsky effect
goes on century after century with an inexhaustible supply of
photonic fuel, profoundly altering the orbits of meter-sized
meteoroids (5).

V. V. Radzievskii applied the photon thrust idea to rotation by
imagining each face of a cubical meteoroid painted white on one
half and black on the other; sunlight reflected by the white part
pushes that area more than the black half, causing a torque,
which changes the rotation rate (6). His mechanism is weak
because the black half, although it reflects little, makes up
much of the difference by emitting infrared photons. Moreover,
most small solar system objects have fairly uniform albedoes
(that is, the fraction of light reflected) across their surfaces.

Building on this work, John A. O'Keefe and one of us (S.J.P.) at
NASA realized that shape was a much more effective means of
altering a body's spin rate than albedo and set about measuring
spin changes in the laboratory. The idea was that light
reflecting off of various angled surfaces on the object could
alter its rotation. Thus YORP was born.

O'Keefe and Paddack imagined a body shaped rather like that shown
in the figure: two wedges glued to a sphere. As the object
rotates, the Sun shines on the vertical face of one wedge and the
slanted face of the other. The momentum imparted in the direction
of rotation by a photon bouncing off the vertical face is greater
than that imparted by bouncing off the slanted face. As a result,
there is a net torque, speeding up the object's rotation (7, 8).
In addition, infrared radiation emitted by the faces also
produces a torque, and infrared YORP probably dominates on small
solar system bodies, which tend to be dark. To test this notion,
Paddack actually used light (which simulated the Sun) to speed up
objects that were magnetically suspended in a vacuum.

=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

3.

Science 13 April 2007: Vol. 316. no. 5822, pp. 188 - 190 DOI:
10.1126/science.316.5822.188

Climate Change: Global Warming Is Changing the World

Richard A. Kerr

An international climate assessment finds for the first time that
humans are altering their world and the life in it by altering
climate; looking ahead, global warming's impacts will only worsen
In early February, the United Nations--sponsored
Intergovernmental Panel on Climate Change (IPCC) declared in no
uncertain terms that the world is warming and that humans are
mostly to blame. Last week, another IPCC working group reported
for the first time that humans--through the greenhouse gases we
spew into the atmosphere and the resulting climate change--are
behind many of the physical and biological changes that media
accounts have already associated with global warming. Receding
glaciers, early-blooming trees, bleached corals, acidifying
oceans, killer heat waves, and butterflies retreating up
mountainsides are likely all ultimately responses to the
atmosphere's growing burden of greenhouse gases. "Climate change
is being felt where people live and by many species," says
geoscientist Michael Oppenheimer of Princeton University, a lead
author of the report. "Some changes are making life harder to
cope with for people and other species."

The latest IPCC report (www.ipcc.ch/SPM6avr07.pdf) sees a bleak
future if we humans persist in our ways. The climate impacts,
mostly negative, would fall hardest on the poor, developing
countries, and flora and fauna--that is, on those least capable
of adapting to change. Even the modest climate changes expected
in the next few decades will begin to decrease crop productivity
at low latitudes, where drying will be concentrated. At the same
time, disease and death from heat waves, floods, and drought
would increase. Toward midcentury, up to 30% of species would be
at increasing risk of extinction.

The working group's report had a difficult coming-out party on 6
April. Like the reports from the two other IPCC working groups
(WGI--see Science, 9 February, p. 754--and WGIII, due out on 4
May), Working Group II's involved a couple of hundred scientist
authors from all six continents analyzing and synthesizing the
literature over several years. Reviews by hundreds of experts and
governments generated thousands of comments. Twenty chapters
totaling 700 printed pages led to a Technical Summary of 80 to
100 pages and a Summary for Policymakers (SPM) of 23 pages. Then
came the hard part: the 4-day plenary session in Brussels, which
brought together scientists and representatives of 120
governments. There, unanimity among governments is required on
every word in the SPM, ostensibly to ensure that the phrasing
clearly and faithfully reflects the reviewed science of the
chapters.

=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

4.

Nature 446, 745-747 (12 April 2007) | doi:10.1038/446745a;
Published online 11 April 2007

Cell Biology: Autophagy and Cancer

Beth Levine

Autophagy is the degradation of redundant or faulty cell
components. It occurs as part of a cell's everyday activities and
as a response to stressful stimuli, such as starvation.
Connections with cellular life-and-death decisions and with
cancer are now emerging.

How is autophagy induced?

Autophagy occurs when cells need to 'self-cannibalize' or degrade
their constituents. Underlying 'housekeeping' levels of autophagy
probably occur in most normal cells to prevent the accumulation
of protein aggregates and defective cellular substructures.
Certain environmental cues (such as starvation, high temperature,
low oxygen, hormonal stimulation) or intracellular stress
(damaged organelles, accumulation of mutant proteins, microbial
invasion) activate signalling pathways that increase autophagy.
Classically, most research on how autophagy is induced has
focused on an enzyme called TOR kinase. This enzyme is a sensor
of nutrient status and a master regulator of cell growth; it
negatively regulates autophagy through its effects on a set of
proteins known as autophagy-execution proteins. However, it is
now clear that numerous signalling pathways, such as those
involved in the control of cell growth, DNA-damage repair, a form
of programmed cell death called apoptosis, and immunity, can also
induce autophagy. It is still a mystery how these specific
signals turn on the autophagic machinery.

What happens once autophagy is induced?

Once the cell receives the appropriate signal, the autophagy-
execution proteins trigger a cascade of reactions that result in
membrane rearrangements to form a double-membrane-bound vesicle
called an autophagosome (Fig. 1). Initially, an 'isolation
membrane' forms, although its origin is still controversial. The
membrane surrounds the cytoplasmic contents to be degraded, and
its edges fuse to form the autophagosome. This vesicle then fuses
with a lysosome (or a vacuole in yeast), with the release of
lysosomal digestive enzymes into the lumen of the resulting
autolysosome. The sequestered cytoplasmic contents are degraded
inside the autolysosome into free nucleotides, amino acids and
fatty acids, which are reused by the cell to maintain
macromolecular synthesis and to fuel energy production. The
nutrient recycling and housekeeping functions of autophagy
promote cell survival, although in certain contexts autophagy may
also promote cell death (Fig. 2, overleaf).

Does autophagy also stop protein synthesis?

No. On the contrary, one of its evolutionarily conserved
functions, through protein recycling, is to help maintain the
synthesis of essential proteins when external nutrients are
limited. Although certain stress stimuli that induce autophagy,
such as starvation, turn off general protein synthesis, they also
turn on the synthesis of specific stress-response proteins,
including autophagy-execution proteins. So in this setting, the
cell uses a coordinated strategy. To ensure that it has enough
amino acids to synthesize the proteins that are essential for its
survival, general protein translation is shut down and autophagy
is activated.

What are autophagy-specific genes?

These are genes that are required for the execution of the
autophagy pathway. Several of them encode proteins that are
components of kinase complexes, which regulate the activity of
proteins and lipids through the addition of a phosphate group.
Alternatively, they encode components of protein-conjugation
systems, which attach to each other or to membrane lipids to form
the membrane of the autophagosome. Deletion of an autophagy-
specific gene blocks autophagy in a cell or organism. These genes
were first identified through genetic screens in yeast that
included a search for genes that are essential for survival
during starvation. Many of these yeast genes are also present in
higher organisms, as are the underlying molecular mechanisms of
autophagy. Although there seems to be a universal requirement in
autophagy for 'autophagy-specific' genes, this does not mean that
these genes are not involved in other cellular processes.

=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

5.

Nature 446, 744 (12 April 2007) | doi:10.1038/446744a; Published
online 11 April 2007

Obituary: Knut Schmidt-Nielsen (1915-2007)

R. McNeill Alexander

Knut Schmidt-Nielsen, one of the all-time greats of animal
physiology, died on 25 January. His influence on the subject was
profound, not only through his original research but also through
his books and the meetings he organized.

Schmidt-Nielsen was born in Norway but moved to the United States
in 1946. Much of his finest work concerns life in deserts, where
the combination of heat and drought makes survival particularly
difficult. The most effective means of keeping cool depend on
evaporation of precious water, either in the breath or as sweat,
but kangaroo rats survive in the Arizona Desert with nothing at
all to drink. They keep reasonably cool by spending the day in
burrows and emerging only at night. But even at night they would
lose much too much water in their breath if it were not for their
remarkable noses. The air they breathe in is relatively cool and
dry, but it is inevitably warmed in the body and becomes
saturated with water vapour. To minimize water loss, this air
must be cooled before it leaves the body to condense out most of
the vapour.

With his first wife Bodil, Schmidt-Nielsen showed that the
incoming air cools the surfaces of the nasal cavity, which, in
turn, cool the air when it is breathed out again. He showed that
the same principle operates in other mammals and birds, but is
particularly effective in kangaroo rats because their nasal
surfaces are enlarged by elaborate nasal bones known as
turbinals. They also save water by producing exceptionally
concentrated urine.

The countercurrent effect in the nose is vital to desert rodents.
But it is potentially troublesome to dogs overheated by exercise,
as they need to let water evaporate to cool themselves. With
colleagues, Schmidt-Nielsen showed that panting dogs avoid the
effect by breathing in through the nose but out through the
mouth.

Unlike kangaroo rats, camels are too big to retire to burrows in
the heat of the day. Working in the Sahara Desert, the Schmidt-
Nielsens showed that camels avoid the water loss that evaporative
cooling would incur by allowing their bodies to heat up by day
and cool by night. A camel may start the morning with a body
temperature of only 34 °C, but warms to 41 °C during the
afternoon. This strategy would be ineffective for small animals
such as kangaroo rats, because they would quickly heat up to
lethal temperatures, but it works well for camels. Later, in
Australia, Schmidt-Nielsen showed that camels' noses conserve
water even more effectively than do those of kangaroo rats;
hygroscopic surfaces dry the outgoing air.

=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

6.

Nature 446, 736-737 (12 April 2007) | doi:10.1038/446736a;
Published online 11 April 2007

Solid-State Chemistry: Crystal tennis rackets

J. Michael McBride

The idea of bendy crystals, especially ones that move rapidly and
reversibly in response to light, seems strange. Such materials
have now been prepared - but how do they change shape so
dramatically without cracking?

Most chemical reactions are accompanied by a change of molecular
shape. Impressively, evolution has harnessed this effect to
generate mechanical power for biological 'devices', for example,
in muscles, where the bending of myosin upon release of adenosine
diphosphate is used to drive one fibre past another1. In stark
contrast, science has produced very few artificial analogues. In
most cases, chemical transformations contribute to man-made
mechanical devices only at the crudest level, by supplying a
source of heat, or electrical energy, or indiscriminant swelling.
Current work on nanodevices is changing this situation at the
molecular level2, but problems in linking such devices together
to achieve larger-scale motion have inhibited progress. On page
778 of this issue, Irie and colleagues3 describe a breakthrough
in this area - a light-induced chemical transformation that bends
crystals without shattering them.

So how does one go about exploiting molecular shape-changing to
generate movement at the bulk level? For practical applications,
the chemical transformation should be reversible - both
chemically and mechanically - and the interconverting molecular
states should generally be stable. Numerous reversible, light-
induced reactions might fit the bill, possibly providing the
basis for actuator devices that convert light into motion. For
example, molecules can be constructed that have rigid double
bonds at their centres. But when these compounds are irradiated
with ultraviolet or visible light, rotation about the double bond
becomes possible, and the molecules can change shape. Similarly,
certain chains of six carbon atoms can form a ring upon
irradiation, so as to flatten a previously bulky molecule. This
process can sometimes be reversed by changing the wavelength of
the irradiating light, and it is this sort of system that is used
by Irie and colleagues3.

But for practical purposes, there is another requirement: the
molecules concerned must be ordered and coupled so that millions
or billions of them cooperate to achieve large-scale mechanical
motion. This constitutes a greater challenge, especially when
reversibility is important. A crystalline sample provides
excellent order, but if the coupling between neighbouring
molecules is too inflexible then the crystal will crack
irreversibly as individual molecules change shape. An amorphous
sample is less prone to cracking, but the reduced order makes it
more difficult to optimize the arrangement of molecules so that
their shape changes are macroscopically cooperative.
Nevertheless, several tricks have been identified that impose
suitable molecular orientation in amorphous films and liquid-
crystalline films to achieve slow macroscopic bending or
contraction upon illumination4.

So, a long-cherished aim of solid-state organic chemistry
remains: to discover new single-crystal to single-crystal
transformations, with a smooth transition between the crystal
lattices of the starting material and the product. For this to
happen, the product molecules must form randomly throughout the
starting material, rather than establishing larger 'islands' of a
separate crystal phase that would greatly disrupt the original
bulk lattice. Such phase separation makes cracking all but
inevitable, because just a 1% change in lattice spacing, caused
by product formation, would force neighbouring lattices within a
distance of 50 molecules to fall completely out of register.

=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=

--~--~---------~--~----~------------~-------~--~----~
You received this message because you are subscribed to the Google Groups "Science and Politics" group.
To post to this group, send email to [email-masked]
To unsubscribe from this group, send email to [email-masked]
For more options, visit this group at http://groups.google.com/group/scipol?hl=en
-~----------~----~----~----~------~----~------~--~---