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- Estrogen
deficiency, T
cells and bone
loss.: Cellular
immunology,
Vol. 252, No.
1-2. (r 2008),
pp.
68-80.Estrogen
plays a
fundamental
role in the
maintenance of
skeletal
homeostasis.
Although
estrogen is
established to
have direct
effects on
bone cells,
animal studies
have
identified
additional
regulatory
effects of
estrogen
centered at
the level of
the adaptive
immune
response.
Furthermore, a
potential role
for reactive
oxygen species
has now been
identified in
both humans
and animals.
One of the
major
challenges has
been to
integrate a
multitude of
redundant
pathways and
cytokines,
that all
appear capable
of playing a
relevant role,
into a global
model of
postmenopausal
osteoporosis.
This review
presents our
current
understanding
of the process
of estrogen
deficiency
mediated bone
destruction
and explores
some of the
most recent
findings and
hypotheses to
explain
estrogen
action in
bone.R
Pacifici
Source: Cellular immunology, Vol. 252, No. 1-2. (r 2008), pp. 68-80. - Estrogen
deficiency
increases
osteoclastogen
esis
up-regulating
T cells
activity: a
key mechanism
in
osteoporosis.: Bone, Vol. 43,
No. 1. (July
2008), pp.
92-100.Compell
ing evidences
suggest that
increased
production of
osteoclastogen
ic cytokines
by activated T
cells plays a
relevant role
in the bone
loss induced
by estrogen
deficiency in
the mouse.
However,
little
information is
available on
the role of T
cells in
post-menopausa
l bone loss in
humans. To
investigate
this issue we
have assessed
the production
of cytokines
involved in
osteoclastogen
esis (RANKL,
TNFalpha and
OPG), in vitro
osteoclast
(OC) formation
in pre and
post-menopausa
l women, the
latter with or
without
osteoporosis.
We evaluated
also OC
precursors in
peripheral
blood and the
ability of
peripheral
blood
mononuclear
cells to
produce
TNFalpha in
both basal and
stimulated
condition by
flow cytometry
in these
subjects. Our
data
demonstrate
that estrogen
deficiency
enhances the
production of
the
pro-osteoclast
ogenetic
cytokines
TNFalpha and
RANKL and
increases the
number of
circulating OC
precursors.
Furthermore,
we show that T
cells and
monocytes from
women with
osteoporosis
exhibit a
higher
production of
TNFalpha than
those from the
other two
groups. Our
findings
suggest that
estrogen
deficiency
stimulates OC
formation both
by increasing
the production
of TNFalpha
and RANKL and
increasing the
number of OC
precursors.
Women with
post-menopausa
l osteoporosis
have a higher
T cell
activity than
healthy
post-menopausa
l subjects; T
cells thus
contribute to
the bone loss
induced by
estrogen
deficiency in
humans as they
do in the
mouse.P
D'Amelio, A
Grimaldi, S Di
Bella, SZ
Brianza, MA
Cristofaro, C
Tamone, G
Giribaldi, D
Ulliers, GP
Pescarmona, G
Isaia
Source: Bone, Vol. 43, No. 1. (July 2008), pp. 92-100. - T cells:
unexpected
players in the
bone loss
induced by
estrogen
deficiency and
in basal bone
homeostasis.: Annals of the
New York
Academy of
Sciences, Vol.
1116 (November
2007), pp.
360-375.The
bone-immune
interface has
become a
subject of
intense
interest in
recent years.
It has long
been
recognized
that
infection,
inflammation,
and autoimmune
disorders are
associated
with systemic
and local bone
loss. Yet, it
is only
recently that
T lymphocytes
and their
products have
been
recognized as
key regulators
of osteoclast
formation,
life span, and
activity.
Similarly, sex
steroids and
aging have
been known to
regulate the
immune system
and T cells
for decades.
In spite of
the abundance
of clinical
and
physiological
clues, it is
only in the
last few years
that
investigators
have linked
immune cells
to the
etiology of
postmenopausal
and senile
osteoporosis,
as well as to
the bone loss
caused by a
variety of
endocrine
conditions. As
surprising is
new evidence
showing that
in contrast to
their bone
destructive
effects under
certain
pathological
conditions, T
cells are
highly
protective of
basal bone
homeostasis,
through
complex
regulatory
effects on
osteoprotegeri
n (OPG)
production by
B cells,
involving CD40
to CD40 Ligand
(CD40L)
costimulation.
This article
examines the
experimental
evidence
suggesting
that estrogen
prevents bone
loss by
regulating T
cell function,
and that T
cell
costimulation
with B cells
is critical
for OPG
production and
maintenance of
basal bone
homeostasis.MN
Weitzmann, R
Pacifici
Source: Annals of the New York Academy of Sciences, Vol. 1116 (November 2007), pp. 360-375. - End-to-end
packet delay
and loss
behavior in
the internet: SIGCOMM
Comput.
Commun. Rev.,
Vol. 23, No.
4. (October
1993), pp.
289-298.Jean-C
hrysotome
Bolot
Source: SIGCOMM Comput. Commun. Rev., Vol. 23, No. 4. (October 1993), pp. 289-298. - A Performance
Study of Loss
Detection/Reco
very in
Real-world TCP
Implementation
s: Network
Protocols,
2007. ICNP
2007. IEEE
International
Conference on
(2007), pp.
256-265.TCP is
the dominant
transport
protocol used
in the
Internet and
its
performance
fundamentally
governs the
performance of
Internet
applications.
It is
well-known
that packet
losses can
adversely
affect the
connection
duration of
TCP
connections -
however, what
is not fully
understood is
how well does
the TCP design
deal with
losses. In
this paper, we
systematically
evaluate the
impact of
design
parameters
associated
with TCP's
loss
detection/reco
very
mechanisms on
the
performance of
real-world TCP
connections.
For this, we
rely on an
analysis tool
that partially
emulates the
sender-side
TCP
implementation
s of 5
prominent OSes
for passively
analyzing the
traces of TCP
connections.
Our study
conducts
passive
analysis of
more than 2.8
million real
Internet TCP
connections.
We find that
the
recommended as
well as
widely-impleme
nted settings
of TCP
parameters are
not optimal
for a
significant
fraction of
Internet
connections.S
Rewaskar, J
Kaur, FD Smith
Source: Network Protocols, 2007. ICNP 2007. IEEE International Conference on (2007), pp. 256-265. - Loss as a
lifelong
regenerative
learning
process: Psychodynamic
Counselling,
Vol. 7, No. 4.
(1 November
2001), pp.
413-430.Griffi
n, David
Source: Psychodynamic Counselling, Vol. 7, No. 4. (1 November 2001), pp. 413-430. - Attachment,
loss, and
complicated
grief.: Developmental
Psychobiology,
Vol. 47, No.
3. (November
2005), pp.
253-267.Bereav
ement is a
highly
disruptive
experience
that is
usually
followed by a
painful but
time-limited
period of
acute grief.
An unfortunate
minority of
individuals
experience
prolonged and
impairing
complicated
grief, an
identifiable
syndrome that
differs from
usual grief,
major
depression,
and other DSM
IV diagnostic
entities.
Underlying
processes
guiding
symptoms are
not well
understood for
either usual
or complicated
grief. We
propose a
provisional
model of
bereavement,
guided by
Myron Hofer's
question "What
exactly is
lost when a
loved one
dies?" We
integrate
insights about
biobehavioral
regulation
from Hofer's
animal studies
of infant
separation,
research on
adult human
attachment,
and new ideas
from
bereavement
research. In
this model,
death of an
attachment
figure
produces a
state of
traumatic loss
and symptoms
of acute
grief. These
symptoms
usually
resolve
following
revision of
the
internalized
representation
of the
deceased to
incorporate
the reality of
the death.
Failure to
accomplish
this
integration
results in the
syndrome of
complicated
grief.K Shear,
H Shair
Source: Developmental Psychobiology, Vol. 47, No. 3. (November 2005), pp. 253-267. - Adaptive
Evolution of
Eye
Degeneration
in the Mexican
Blind Cavefish: Journal of
Heredity, Vol.
96, No. 3.
(May 2005),
pp. 185-196.WR
Jeffery
Source: Journal of Heredity, Vol. 96, No. 3. (May 2005), pp. 185-196. - Relevance of
sub-surface
chip layers
for the
lifetime of
magnetically
trapped atoms: The European
Physical
Journal D -
Atomic,
Molecular,
Optical and
Plasma
Physics, Vol.
35, No. 1.
(2005), pp.
97-104.We
investigate
the lifetime
of
magnetically
trapped atoms
above a
planar,
layered atom
chip
structure.
Numerical
calculations
of the thermal
magnetic noise
spectrum are
performed,
based on the
exact magnetic
Green function
and multi
layer
reflection
coefficients.
We have
performed
lifetime
measurements
where the
center of a
side guide
trap is
laterally
shifted with
respect to the
current
carrying wire
using
additional
bias fields.
Comparing the
experiment to
theory, we
find a fair
agreement and
demonstrate
that for a
chip whose
topmost layer
is metallic,
the magnetic
noise depends
essentially on
the thickness
of that layer,
as long as the
layers below
have a much
smaller
conductivity;
essentially
the same
magnetic noise
would be
obtained with
a metallic
membrane
suspended in
vacuum. Based
on our theory
we give
general
scaling laws
of how to
reduce the
effect of
surface
magnetic noise
on the trapped
atoms.B Zhang,
C Henkel, E
Haller, S
Wildermuth, S
Hofferberth, P
Krüger, J
Schmiedmayer
Source: The European Physical Journal D - Atomic, Molecular, Optical and Plasma Physics, Vol. 35, No. 1. (2005), pp. 97-104. - Reduction of
magnetic noise
in atom chips
by material
optimization: The European
Physical
Journal D -
Atomic,
Molecular,
Optical and
Plasma
Physics, Vol.
35, No. 1.
(2005), pp.
87-95.We
discuss the
influence of
the material
type in metal
wires to the
electromagneti
c fluctuations
in magnetic
microtraps
close to the
surface of an
atom chip. We
show that
significant
reduction of
the magnetic
noise can be
achieved by
replacing the
pure noble
metal wires
with their
dilute alloys.
The alloy
composition
provides an
additional
degree of
freedom which
enables a
controlled
reduction of
both magnetic
noise and
resistivity if
the atom chip
is cooled. In
addition, we
provide a
careful
re-analysis of
the
magnetically
induced trap
loss observed
by Yu-Ju Lin
et al. [Phys.
Rev. Lett. 92,
050404 (2004)]
and find good
agreement with
an improved
theory.V
Dikovsky, Y
Japha, C
Henkel, R
Folman
Source: The European Physical Journal D - Atomic, Molecular, Optical and Plasma Physics, Vol. 35, No. 1. (2005), pp. 87-95.
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