ScienceWeek/2006/49
SCIENCEWEEK
December 15, 2006
Vol. 10 - Number 49
We
have
entered
the
cell,
the
mansion
of
our
birth,
and
have
started
the
inventory
of
our
acquired
wealth.
--
Albert
Claude
(1899-1983)
Mục lục
NEUROSCIENCE: ON DENDRITE SPINE SIZE AND FUNCTION[sửa]
The following points are made by C. Kopec and R. Malinow (Science 2006 314:1554):
1)
From
the
overall
body
plan
of
an
organism
to
the
intricate
three-dimensional
fold
of
proteins,
structure
is
a
key
determinant
of
function.
Neurons,
the
fundamental
cells
of
the
nervous
system,
are
no
exception.
The
architecture
of
their
dendritic
and
axonal
arbors
--
the
cellular
extensions
that
receive
and
transmit
information
--
determines
which
neurons
they
can
connect
to,
whereas
the
diameter
of
these
extensions
determines
the
speed
and
filtering
of
electrical
signals
that
travel
down
them.
Tiny
femtoliter
[10^(-15)
liter]-sized
protrusions
from
neuronal
dendrites,
called
spines,
receive
a
functional
connection
from
another
neuron's
axon
at
a
specialized
area
of
contact
known
as
a
synapse.
New
work
(1)
marks
a
large
step
forward
in
our
understanding
of
how
spine
size
and
synaptic
strength
are
balanced.
2)
A
neuron
can
have
up
to
100,000
spines,
each
generally
forming
a
single
synapse.
Spines
function
as
chemical
compartments
for
signaling
molecules
that
become
activated
by
specific
patterns
of
synaptic
transmission
(2-4).
This
organization
provides
each
synapse
with
a
miniature
caldron
in
which
to
concoct
a
chemical
brew
to
effect
changes
in
connections
between
neurons
(5).
3)
Large
spines
contain
strong
synapses
(robust
transmission)
and
small
spines
have
weak
synapses.
A
spine
is
at
least
an
order
of
magnitude
larger
than
a
synapse,
and
thus
there
is
no
physical
requirement
for
this
correlation.
The
reason
for
this
correlation
between
structure
and
function
remains
elusive,
but
an
abundance
of
circumstantial
evidence
points
to
its
importance.
Stimuli
that
cause
stable
changes
in
synaptic
strength
lead
to
corresponding
stable
changes
in
spine
volume.
Heritable
forms
of
mental
retardation
can
present
abnormalities
in
spine
morphology
as
well
as
synaptic
function.
Furthermore,
Alzheimer's
disease
may
involve
a
loss
of
spines
that
is
fundamentally
linked
to
a
decrease
in
the
number
of
neurotransmitter
receptors
at
the
synapse.
Therefore,
understanding
how
and
why
this
correlation
between
synapse
strength
and
spine
size
exists
will
not
only
expand
our
understanding
of
how
synapses
work,
but
may
have
clinical
relevance
as
well.
4)
Park
et
al
(1)
combine
serial
section
electron
microscopy
and
live
cell
fluorescence
microscopy
to
afford
a
view
of
the
inner
workings
of
spines.
The
authors
stimulated
cultured
mammalian
neurons
to
generate
a
stable
increase
in
synaptic
strength
known
as
long-term
potentiation
(LTP),
and
confirmed
that
the
rapid
increase
in
synaptic
strength
is
accompanied
by
a
matched
increase
in
spine
volume.
They
then
probed
the
molecular
and
cellular
mechanisms
behind
this
correlation.
They
focused
on
the
role
of
the
recycling
endosome,
an
intracellular
membrane-bound
compartment
that
is
part
of
the
system
that
transports
membrane-
bound
proteins
onto
and
off
the
cell
surface.
Previous
work
by
this
group
showed
that
the
protein
GluR1
is
delivered
to
the
neuronal
surface
from
the
recycling
endosome
through
exocytosis,
the
cell's
secretory
process.
GluR1
is
a
glutamate
receptor
subunit
that
is
inserted
into
synapses
during
LTP
and
plays
an
important
role
in
mediating
the
increase
in
synaptic
strength.
Blocking
this
delivery
by
expressing
mutant
proteins
that
specifically
inhibit
this
exocytosis
prevented
the
stable
increase
in
synaptic
strength.
In
the
present
work,
Park
et
al
(1)
provide
evidence
that
the
lipids
delivered
to
the
neuron's
surface
from
the
vesicles
carrying
GluR1
are
the
raw
materials
that
allow
the
spine
to
enlarge.
References
(abridged):
1.
M.
Park
et
al.,
Neuron
52,
817
(2006).
2. K. Svoboda, D. W. Tank, W. Denk, Science 272, [716] (1996).
3. B. L. Bloodgood, B. L. Sabatini, Science 310, [866] (2005).
4. A. Zador, C. Koch, T. H. Brown, Proc. Natl. Acad. Sci. U.S.A. 87, 6718 (1990).
5.
M.
Sheng,
M.
J.
Kim,
Science
298,
[776]
(2002).
Science
http://www.sciencemag.org
ScienceWeek
http://scienceweek.com
EVOLUTION: ON HUMAN SOCIALITY[sửa]
The following points are made by Robert Boyd (Science 2006 314:1555):
1)
The
scale
and
complexity
of
human
societies
present
an
important
evolutionary
puzzle.
In
every
human
society,
people
cooperate
with
many
unrelated
individuals.
Division
of
labor,
trade,
and
large-scale
conflict
are
common.
The
sick,
hungry,
and
disabled
are
cared
for,
and
social
life
is
regulated
by
commonly
held
moral
systems
that
are
enforced,
albeit
imperfectly,
by
third-party
sanctions.
In
contrast,
in
other
primate
species,
cooperation
is
limited
to
relatives
and
small
groups
of
reciprocators.
There
is
little
division
of
labor
or
trade,
and
no
large-scale
conflict.
No
one
cares
for
the
sick,
or
feeds
the
hungry
or
disabled.
The
strong
take
from
the
weak
without
fear
of
sanctions
by
third
parties.
New
work
(1)
offers
one
explanation
for
the
commonness
of
costly,
prosocial
behavior
in
human
societies.
2)
The
behavior
of
other
primates
is
easy
to
understand.
Natural
selection
only
favors
individually
costly,
prosocial
behavior
when
the
beneficiaries
of
the
behavior
are
disproportionately
likely
to
share
the
genes
that
are
associated
with
the
behavior.
Selection
can
favor
altruism
toward
close
relatives
because
recent
common
descent
provides
a
cue
of
genetic
similarity.
The
small
size
of
primate
families
limits
the
size
and
complexity
of
the
groups
that
can
be
formed
through
this
process.
Thus,
standard
evolutionary
theory
provides
a
perfectly
good
explanation
for
the
behavior
of
other
primates,
but
not
humans.
3)
Bowles
proposes
that
competition
between
genetically
differentiated
groups
led
to
the
evolution
of
our
prosocial
psychology.
Limited
migration
between
groups
can
lead
to
the
buildup
of
genetic
relatedness
(which
measures
how
much
the
possession
of
a
particular
gene
in
one
individual
predicts
the
presence
of
the
same
gene
in
a
second
individual)
among
group
members.
This
means
that
group
membership
can
also
be
a
cue
that
allows
assortative
interaction--genes
that
cause
you
to
help
members
of
your
group
can
be
favored
because
other
group
members
are
disproportionately
likely
to
carry
the
same
genes,
even
though
you
do
not
share
a
recent
common
ancestor.
This
is
an
old
idea.
A
version
appears
in
The
Descent
of
Man
(2)
and
has
reappeared
many
times
since
then.
It
has
never
gained
much
traction,
however,
because
there
have
been
good
reasons
to
doubt
its
importance.
First,
theoretical
work
raised
doubts
about
levels
of
genetic
relatedness
being
high
enough
to
favor
prosocial
behavior
toward
group
members
(3).
Second,
limited
migration
generates
more
competition
within
groups
than
between
groups.
This
means
that
helping
others
in
your
own
group
reduces
your
own
relative
fitness
and
the
fitness
of
your
descendants.
In
some
plausible
models
of
the
evolution
of
altruism
when
migration
is
limited,
this
effect
exactly
balances
increases
in
relatedness,
eliminating
selection
for
altruism
toward
group
members
(4).
Finally,
the
benefits
of
success
in
intergroup
competition
seems
too
small
and
the
costs
too
large
to
allow
cooperation
to
evolve.
After
all,
other
primates
live
in
similar
groups,
but
show
little
evidence
of
group-level
cooperation.
4)
Bowles
meets
these
objections
with
a
combination
of
data
and
theory.
First,
he
has
assembled
data
on
the
amount
of
genetic
differentiation
among
human
hunter-gatherer
groups
(or
put
another
way,
the
level
of
relatedness
within
such
groups).
These
data
show
that
the
level
of
relatedness
within
such
groups
is
substantially
higher
than
previously
supposed,
a
bit
below
that
of
cousins.
This
means
that
the
cooperation
will
be
favored
as
long
as
the
benefits
to
individuals
are
about
10
times
the
cost.
Second,
because
competition
occurs
between
groups
and
successful
groups
are
able
to
colonize
the
territories
of
extinct
groups,
competition
among
relatives
does
not
attenuate
the
benefits
derived
from
cooperation.
Third,
intergroup
competition
is
common
in
small-scale
societies,
so
the
benefits
derived
from
collective
efforts
to
compete
with
other
groups
are
plausibly
substantial.
Finally,
Bowles
notes
that
human
foraging
groups
typically
have
culturally
transmitted
norms
and
practices,
including
food
sharing
and
socially
imposed
monogamy,
which
reduce
fitness
differences
within
groups.
He
makes
the
original
and
interesting
argument
that
such
"leveling
mechanisms"
act
like
redistributive
taxes
to
reduce
the
disadvantage
of
engaging
in
costly
prosocial
behavior.
The
absence
of
these
kinds
of
leveling
mechanisms
in
primate
groups
may
explain
why
human
societies
differ
from
those
of
other
primates.
5)
Make
no
mistake.
This
is
not
a
"group
selection"
hypothesis
that
competes
with
"kin
selection"
hypotheses
[see
the
Review
by
Nowak
(5)
for
a
discussion
of
conditions
that
favor
the
evolution
of
cooperative
behavior].
Both
concepts
are
equivalent
frameworks
for
describing
the
same
evolutionary
process.
The
group
(also
known
as
multilevel)
selection
approach
describes
all
natural
selection
as
going
on
in
a
series
of
nested
levels:
among
genes
within
an
individual,
among
individuals
within
a
group,
and
among
groups.
The
kin
selection
approach
accounts
all
fitness
effects
back
to
the
individual
gene.
Bowles
adopts
the
multilevel
selection
framework,
but
you
can
pose
exactly
the
same
argument
in
a
kin
selection
framework
and
if
you
do
your
sums
properly,
you
will
get
exactly
the
same
answer.
The
real
questions
are:
Are
amounts
of
genetic
variation
observed
among
contemporary
human
foraging
groups
representative
of
the
Pleistocene
hominin
populations
in
which
distinctively
human
behavior
probably
evolved?
Were
the
benefits
of
success
(survival)
from
intergroup
competition
in
ancestral
human
populations
large
enough
to
compensate
for
the
individual
costs
of
participating
in
such
contests?
And,
do
the
kinds
of
leveling
mechanisms
observed
among
contemporary
foragers
exist
and
work
in
the
same
way
in
ancestral
populations?
References
(abridged):
1.
S.
Bowles,
Science
314,
1569
(2006).
2.
C.
Darwin,
The
Descent
of
Man
(1871).
3.
A.
R.
Rogers,
Am.
Nat.
135,
398
(1990).
4.
P.
D.
Taylor,
Evol.
Ecol.
6,
352
(1992).
5.
M.
A.
Nowak,
Science,
314,
1560
(2006).
Science
http://www.sciencemag.org
ScienceWeek
http://scienceweek.com
CANCER: STEM CELLS AND BRAIN TUMORS[sửa]
The following points are made by Peter B. Dirks (Nature 2006 444:687):
1)
Cancers
are
notorious
for
their
ability
to
survive
treatment
and
recur.
Hopes
of
understanding
how
they
can
do
so,
however,
have
grown
with
the
prospective
identification
of
rare
populations
of
cancer
stem
cells
in
solid
tumours
(1,2).
New
work
(3,4)
marks
a
step
towards
realizing
these
hopes,
and
provides
further
insight
into
the
stem-cell
nature
of
human
glioblastoma,
an
especially
nasty
type
of
brain
cancer.
Both
studies
build
on
the
identification2
of
a
tumour-initiating
subpopulation
of
cells
that
express
a
cell-surface
marker,
CD133,
that
is
a
hallmark
of
neural
precursor
cells.
2)
Bao
et
al
(3)
show
that
glioblastoma
cells
expressing
CD133
(CD133+
cells)
are
resistant
to
ionizing
radiation
because
they
are
more
efficient
at
inducing
the
repair
of
damaged
DNA
than
is
the
bulk
of
the
tumour
cells.
Radiation
therapy
has
been
the
mainstay
of
glioblastoma
treatment
for
more
than
40
years,
but
although
it
is
transiently
effective,
it
offers
no
lasting
cure.
The
implication
of
these
results
is
that
radiation
treatment
fails
in
the
long
run
because
it
cannot
kill
the
subpopulation
of
CD133+
tumour-initiating
cells.
3)
Piccirillo
et
al
(4)
describe
their
work
with
bone
morphogenetic
proteins
(BMPs),
soluble
factors
that
normally
induce
neural
precursor
cells
to
differentiate
into
mature
astrocytes
--
a
subtype
of
brain
cells
called
glial
cells.
The
authors
show
that
BMPs
can
also
prompt
the
differentiation
of
CD133+
brain
tumour
cells,
critically
weakening
their
tumour-
forming
ability.
The
results
further
imply
that
tumour
populations
at
least
partially
retain
a
developmental
hierarchy
based
on
stem
cells,
and
remain
able
to
respond
to
the
normal
signals
that
induce
them
to
mature.
These
findings
should
lead
to
renewed
interest
in
devising
therapies
that
promote
the
differentiation
of
cancer
cells.
4)
Both
groups
(3,4)
arrived
at
their
findings
by
considering
the
functional
hierarchy
of
the
heterogeneous
population
of
tumour
cells.
In
doing
so,
they
add
weight
to
the
importance
in
this
research
of
dissociating
solid-tumour
samples
into
single-cell
suspensions,
purifying
the
stem-cell
fractions,
and
testing
their
response
to
treatment.
Crucially,
both
groups
verified
their
in
vitro
results
with
in
vivo
studies.
A
true
demonstration
that
human
tumour-initiating
cells
can
act
as
such
requires
use
of
the
"gold
standard"
assay
(5)
of
transplanting
them
into
immunodeficient
mice
to
see
if
they
retain
their
stem-cell
capacity.
References
(abridged):
1.
Al-Hajj,
M.
et
al.
Proc.
Natl
Acad.
Sci.
USA
100,
3983-3988
(2003).
2.
Singh,
S.
K.
et
al.
Nature
432,
396-401
(2004).
3.
Bao,
S.
et
al.
Nature
444,
756-760
(2006).
4.
Piccirillo,
S.
G.
M.
et
al.
Nature
444,
761-765
(2006).
5.
Bonnet,
D.
&
Dick,
J.
E.
Nature
Med.
3,
730-737
(1997).
Nature
http://www.nature.com/nature
ScienceWeek
http://scienceweek.com
OCEANOGRAPHY: PLANKTON AND GLOBAL WARMING[sửa]
The following points are made by Scott C. Doney (Nature 2006 444:695):
1)
Oranges
in
Florida,
wildfires
in
Indonesia,
plankton
in
the
North
Pacific
--
what
links
these
seemingly
disparate
items
is
that
they
are
all
affected
by
year-to-year
fluctuations
in
global-scale
climate.
New
work
(1)
describes
how
such
fluctuations,
especially
in
temperature,
are
connected
to
the
productivity
of
phytoplankton
in
the
world's
oceans.
The
analyses
are
based
on
nearly
a
decade
of
satellite
data,
and
for
much
of
the
oceans
they
find
that
recent
warmer
surface
temperatures
correspond
to
lower
oceanic
biomass
and
productivity.
Behrenfeld
et
al
(1)
argue
that
these
patterns
arise
because
climate-induced
changes
in
ocean
circulation
reduce
the
supply
of
nutrients
needed
for
photosynthesis.
2)
Small
photosynthetic
phytoplankton
grow
in
the
well-
illuminated
upper
ocean,
forming
the
base
of
the
marine
food
web
and
supporting
the
fish
stocks
we
harvest.
They
also
form
the
basis
of
the
biogeochemical
cycling
of
carbon
and
many
other
elements
in
the
sea.
Phytoplankton
growth
depends
on
temperature
and
the
availability
of
light
and
nutrients,
including
nitrogen,
phosphorus,
silicon
and
iron.
Most
of
this
nutrient
supply
to
the
surface
ocean
comes
from
the
mixing
and
upwelling
of
cold,
nutrient-rich
water
from
below,
with
an
additional
source
of
iron
from
mineral
dust
swept
off
the
continental
deserts.
Phytoplankton
biomass
can
vary
by
a
factor
of
100
in
surface
waters;
its
geographical
distribution
is
determined
largely
by
ocean
circulation
and
upwelling,
with
the
highest
levels
being
found
along
the
Equator,
in
temperate
and
polar
latitudes,
and
along
the
western
boundaries
of
continents.
3)
Although
the
broad
spatial
patterns
of
phytoplankton
biomass
and
productivity
are
well
documented
(2),
large-scale
temporal
variations
have
only
recently
become
quantifiable
with
the
advent
of
satellite
ocean-colour
sensors
(3).
The
ocean
is
vast,
and
the
limited
number
of
research
ships
move
at
about
the
speed
of
a
bicycle,
too
slow
to
map
the
ocean
routinely
on
ocean-basin
to
global
scales.
By
contrast,
a
satellite
can
observe
the
entire
globe,
at
least
the
cloud-free
areas,
in
a
few
days.
Phytoplankton
biomass
and
growth
rates
can
be
estimated
remotely
from
space
because
chlorophyll,
the
main
photosynthetic
pigment
in
phytoplankton,
absorbs
blue
and
red
sunlight
more
readily
than
green
sunlight.
Ocean-colour
sensors
measure,
by
wavelength
band,
the
small
fraction
of
sunlight
scattered
back
to
space
from
below
the
surface.
The
resulting
surface-chlorophyll
data
can
be
combined
with
empirical
relationships
to
estimate
phytoplankton
growth
rates
or
net
primary
production
(4).
4)
Not
that
this
procedure
is
straightforward:
other
constituents
of
sea
water
absorb
light;
many
photons
reaching
the
satellite
sensor
come
from
atmospheric
aerosols
or
reflection
at
the
water
surface;
and
optical
detectors
on
satellites
degrade
with
time.
But
with
careful
calibration,
high-quality,
long-term
records
of
ocean-colour
data
can
be
constructed
for
detecting
climate-driven
trends.
The
best
such
record
at
present
is
from
GeoEye
and
from
NASA's
Sea-viewing
Wide
Field-of-view
Sensor
(SeaWiFS)
(3),
launched
in
1997.
In
the
SeaWiFS
time
series,
global
chlorophyll
and
productivity
increase
sharply
during
1997-98
and
then
decline
gradually
to
2005.
Behrenfeld
et
al
(1)
show
that
these
trends
closely
follow
changes
in
climate.
References
(abridged):
1.
Behrenfeld,
M.
J.
et
al.
Nature
444,
752-755
(2006).
2.
Longhurst,
A.
Ecological
Geography
of
the
Sea
2nd
edn
(Academic,
New
York,
2006).
3.
McClain,
C.
R.,
Feldman,
G.
C.
&
Hooker,
S.
B.
Deep-Sea
Res.
II
51,
5-42
(2004).
4.
Carr,
M.-E.
et
al.
Deep-Sea
Res.
II
53,
741-770
(2006).
5.
Polovina,
J.
J.,
Mitchum,
G.
T.
&
Evans,
G.
T.
Deep-Sea
Res.
I
42,
1701-1716
(1995).
Nature
http://www.nature.com/nature
ScienceWeek
http://scienceweek.com
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