JCBFM 0308
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*1. Spared caudal brainstem SERT binding
in early Parkinson’s disease. Albin et al.
Relevance: Very Low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600599a.pdf
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*2. Circulating CD34-positive cells provide a marker of
vascular risk associated with cognitive impairment.
Taguchi et al.
Sullysummary: CD34+ cells are immature marrow-derived cells
that appear to have some importance in maintaining cerebrovascular health,
probably through involvment in endothelial repair. Here, the authors present
data suggesting that the level of these cells in circulating plasma is
correlated with cognitivie impairment in patients with cerebrovascular
disease--but not with Alzheimer's patients who had no evidence of ischemia.
They propose that the level of circulating CD34+ cells provides a marker of
vascular risk associated with cognitive impairment, and that differences in the
pathobiology of Alzheimer’s- and vascular-type cognitive impairment may be
mirrored in levels of circulating CD34+ cells in these patient populations.
Relevance: Low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600541a.pdf
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*3. Lipocalin 2 is a choroid plexus acute-phase protein. Marques et al.
Relevance: Very Low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600557a.pdf
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*4. Oxygen and glucose deprivation-induced
changes in astrocyte membrane potential and their underlying mechanisms in
acute rat hippocampal slices.
Xie et al.
Sullysummary: The role of astrocytes in cerebral ischemia is
unclear. (Actually, the role of astrocytes in _everything_ is unclear--they
probably play an important role in cognition.) We do know that by about 8 min
of ischemia astrocytes undergo a three-phase depolarization, and the relative
contributions of ecf K+, neurotransmitters and energy failure in these
processes is unclear. The authors, using an OGD/hippocampal slice model with
sharp pipette recordings, show that astrocytes respond reversibly to more >
30 mins oxygen and glucose deprivation
(OGD) treatment with multiphasic depolarized membrane
potentials (Vm): an 11 mins small-amplitude depolarization
plateau, followed by a 6-mins
accelerated depolarization, and then a second plateau. Oxygen and
glucose deprivation-induced
astrocyte Vm depolarization was only marginally (10%) inhibited by inhibition
of ionotropic glutamate, c-aminobutyric acid, purinergic receptors, and
glutamate transporters, suggesting increase in extracellular
[K+ ] was primarily responsible for
the astrocytic Vm change. When glycolysis was inhibited the Vm depol was increased
by 500%. The authors conclude that "Altogether, hippocampal astrocytes
appear to be electrophysiologically more resistant to acute ischemia insults as
compared with neurons, and this should allow astrocytes to rescue
endangered neurons in the face of
acute ischemia insults via their various homeostatic functions."
Relevance: Medium
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600545a.pdf
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*5. Protective role of reactive astrocytes in brain ischemia
Li et al.
Sullysummary: This is a beautiful paper with 22 authors from
Relevance: Medium
Link: http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600546a.pdf
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*6. Nitrite does not provide additional protection to
thrombolysis in a rat model of stroke with delayed reperfusion
Schatlo et al.
Sullysummary: The authors, from the surgical neurology
branch of NIH in
1. It is in fact
acceptable to present data in which thrombolysis has been simulated with
filament MCAO + tPA. Based on this report and others I
have read, the clot model of MCAO has no advantages and many disadvantages, and
should go off and die.
2. The use of
older animals for this kind of research may be critical.
3. Some animals
were excluded from analysis. No big deal: state how many, and why, and then
move the fuck on. I guess if you wanted to, you COULD just throw out the whole
goddam data set and cripple your chances for publication. That's another
option. But these guys--from NIH--just don't roll that way. Maybe there's a
lesson in all that. Dunno.
4. It is possible
to publish negative results, provided that the findings are negative and
well-controlled. Of course, it helps if you're actually FROM the NIH...
Relevance: HIGH
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600542a.pdf
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*7. Acute plasmalemma permeability and protracted clearance
of injured cells after controlled cortical impact in mice.
Whalen, et al.
Sullysummary. The authors basically head-bonked mice and used propidium iodide
to asses plasmalemma permeability. They found early permeability as a
persistent feature of cell injury in cortex and hippocampus. The authors
suggest that plasmalemma damage is a fundamental marker of cellular injury
after CCI; some injured cells might have an extended window for potential
rescue by neuroprotective strategies.
Relevance: Low.
Linke (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600544a.pdf
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*8. Plasminogen potentiates thrombin cytotoxicity and
contributes to pathology of intracerebral hemorrhage in rats.
Fujimoto et al.
Sullysummary: The data presented suggests that the
plasminogen/plasmin system enhances the neurotoxicity of thrombin in the
setting of brain hemorrhage. Since t-PA is often administered for stroke, and
since it activates plasminogen, and since its administration often causes
hemorrhage, this should give advocates of stroke thrombolysis considerable
pause. But whatever.
Relevance: Low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600547a.pdf
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*9. Intracerebral hemorrhage models in rat: comparing
collagenase to blood infusion.
MacLellan, et al.
Relevance: Very Low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600548a.pdf
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*10. Inducible nitric oxide synthase does not mediate brain
damage after transient focal cerebral ischemia in mice.
Pruss, et al.
Sullysummary: This one is liable to shake a few trees. One
of the shibboleths of current thinking about focal ischemia is that iNOS is a
bad boy, contributing to inflammation (WBCs), oxidative stress (ONOO-), DNA
damage and mitochondrial respiratory inhibition. The authors, in a technical
tour de force that you should read just for the damn methods, basically crush
this idea. No iNOS mRNA. No iNOS protein. No protection in iNOS-/- mice. No
iNOS when dural inflammation is instigated by interleukins. The one concern I
have about this study is the short ischemic interval: 45 mins or 60 mins. I
need to do a second, more careful reading to see if I can pick up any other
flaws, but, overall, I have to believe that JCBFM wouldn't take a paper with
such a provocative conclusion (the title alone is going to make some people go
all pale and trembly) if the data wasn't solid and the reviews weren't strong.
Of course, this does nothing to knock down the idea that nNOS is bad for you
(and, as it happens, directly connected to the glutamate receptor through
PSD95).
Relevance: HIGH.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600550a.pdf
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*11. Autophagy is increased after traumatic brain injury in
mice and is partially inhibited by the antioxidant
c-glutamylcysteinyl ethyl ester. Lai1, et al.
Sullysummary (verbatim): Autophagy is a homeostatic process
for recycling of proteins and organelles, induced by nutrient deprivation and
regulated by oxygen radicals. For a quickie review, see:
http://en.wikipedia.org/wiki/Autophagy. We don't know how much of a role it
plays in brain injury. The authors present data
suggesting that autophagy occurs after experimental TBI, and that oxidative
stress contributes to this process. No clues on correct pronunciation of
"authophagy." Sorry.
Relevance: Lo.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600551a.pdf
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*12. Apolipoprotein D is elevated in oligodendrocytes in the
peri-infarct region after experimental stroke: influence of enriched
environment. Rickhag1, Wieloch, et al.
Sullysummary: Zees eez pehper from Sveden, yes? Ze
investigators are eenterested in ze remodeling of ze injured brain and ze role
of lipid trafficking, yes? Somehow, between trying to keep warm and maintaining
their neutrality, these Swedes investigated the role of the well-characterized
lipid trafficking protein apolipoprotein D. They found increased activity
around the core of the infarct, and associated with oligos. Rats that were in a
stimulating environment did better. I didn't read carefully enough to ascertain
what the "stimulating" environment was. I can only assume this means
the rats were transported outside of
Relevance: Low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600552a.pdf
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*13. DJ-1 protects against neurodegeneration caused by focal
cerebral ischemia and reperfusion in rats.
Yanagisawa, Kitamura1, Hiroshi, et al.
Sullysummary: Obviously an Irish paper. DJ-1 is the gene
implicated in familial Parkinson's, and functions as an antioxidant, chaperone
and transcriptional regulator. In this study, instrastriatal injection
protected against ROS production and reduced infarct volumes in a rat MCAO
model. The paper has relevance to us not only becuase of its findings but also
for its methods.
Relevance: HIGH.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600553a.pdf
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*14. Comparison of plasma input and reference tissue models
for analysing [11C]flumazenil studies. Klumpers, et al.
Relevance: Very low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600554a.pdf
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*15. The mechanisms of acute ischemic
injury in the cell processes of developing white matter astrocytes. Salter et al.
Sullysummary. In an OGD model, the
investigators show that injury results in loss of astrocytic processes and
soma, particularly in white matter. They gave some stuff. In accordance with
Krause's law, it seemed to help. Yawn.
Relevance: Low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600555a.pdf
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*16. Lengthening the G1 phase of neural progenitor cells is
concurrent with an increase of symmetric neuron generating division after
stroke. Zhang et al.
Sullysummary: From our good buddy Mike Chopp over at Ford. I
just LOVE THAT MAN. But not in a gay way. Adult rats
were stroked and the cell cycle interrogated with BDU. Mike et al conclude that
stroke triggers a shortening of the cell-cycle that expands the neuroprogenitor
pool early on. Okay, sure. Then why don't our brains just grow back?
Relevance: Medium.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600556a.pdf
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*17. Neuronal HIF-1a protein and VEGFR-2
immunoreactivity in functionally related motor areas following a focal M1
infarct. Stowe1, et al.
Sullysummary: Not much to say. I was pretty underwhelmed.
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Relevance: Low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600560a.pdf
*18. Acute astrocyte activation in brain detected by MRI:
new insights into T1 hypointensity. Sibson et al.
Relevance: Very Low.
*19. The effect of labeling parameters on
perfusion-based fMRI in nonhuman primates. Zappe, et
al.
Relevance: Very Low.
Link (PDF):
http://www.nature.com/jcbfm/journal/v28/n3/pdf/9600564a.pdf
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END SUMMARY.