diff --git a/fulltext/istex/tei/2BFC777973A535C282DAF3B611C27A816EA29A3E.training.fulltext.tei.xml b/fulltext/istex/tei/2BFC777973A535C282DAF3B611C27A816EA29A3E.training.fulltext.tei.xml
index 0740c7b..76c0cf1 100644
--- a/fulltext/istex/tei/2BFC777973A535C282DAF3B611C27A816EA29A3E.training.fulltext.tei.xml
+++ b/fulltext/istex/tei/2BFC777973A535C282DAF3B611C27A816EA29A3E.training.fulltext.tei.xml
@@ -103,7 +103,7 @@
Rubisco would be preferred to these non-physiological substrates. For
either random
or ordered reaction mechanisms, an alternate substrate
acts as a competitive
inhibitor with respect to the appearance of prod-
uct for the normal substrate 28 . Therefore, the K i values derived from
the x-intercepts of
+ type="biblio">28 . Therefore, the K i values derived from
the x-intercepts of
these plots are equivalent to the K m for Lys or MeLys
Figure 1 Lys and MeLys are alternative substrates for Rubisco LSMT. (a) Plot
of
diff --git a/fulltext/istex/tei/39B858D1EC346AFC9C2F80908ADC7F5B4D0BC719.training.fulltext.tei.xml b/fulltext/istex/tei/39B858D1EC346AFC9C2F80908ADC7F5B4D0BC719.training.fulltext.tei.xml
index 47c9fc3..9184f9c 100644
--- a/fulltext/istex/tei/39B858D1EC346AFC9C2F80908ADC7F5B4D0BC719.training.fulltext.tei.xml
+++ b/fulltext/istex/tei/39B858D1EC346AFC9C2F80908ADC7F5B4D0BC719.training.fulltext.tei.xml
@@ -14,19 +14,18 @@
There is very little information and research about the way in which
mobilization
affects reservists and their families. Most of the literature
on this subject
focuses on full-time, active-duty service members and
their families. [Steiner and Neuman (1978)], [Nice (1981)],
- and [Wickham]
(1983) report that family adjustment directly
- influences the soldiers'
combat readiness, retention, and overall
- effectiveness. [Hill (1971)] sug-
gests that good marital
- adjustment prior to separation predicts good
adjustment upon reunion. [Baker (1967)] notes that the effect of a separa-
tion upon a
- child is associated with the child's developmental level. [Bell]
(1991) emphasizes that family adaptation to deployment is a
- dynamic
process which is influenced by both internal and external forces. He
- further suggests that families may require different types of support,
information,
- and resources at various stages of their coping process.
Finally, [Breger (1984)] writes that reunions tend to be more successful
- if
all parties involved expect adjustment difficulties and have open
+ type="biblio">Steiner and Neuman (1978), Nice (1981), and Wickham
(1983)
+ report that family adjustment directly influences the soldiers'
combat
+ readiness, retention, and overall effectiveness. [Hill (1971)]
+ sug-
gests that good marital adjustment prior to separation predicts good
+ adjustment upon reunion. [Baker (1967)] notes that the effect of
+ a separa-
tion upon a child is associated with the child's developmental level.
+ [Bell]
(1991) emphasizes that family adaptation to
+ deployment is a dynamic
process which is influenced by both internal and external
+ forces. He
further suggests that families may require different types of
+ support,
information, and resources at various stages of their coping process.
+ Finally, [Breger (1984)] writes that reunions tend to be more
+ successful if
all parties involved expect adjustment difficulties and have open
com-
munication patterns. Overall, the impact that mobilization has on
reservists and their families appears similar to experiences that full-
time
military families encounter. However, it may be even more diffi-
cult for
diff --git a/fulltext/istex/tei/3A8EACA303160EDE4E66A19A97097F6FAECD5358.training.fulltext.tei.xml b/fulltext/istex/tei/3A8EACA303160EDE4E66A19A97097F6FAECD5358.training.fulltext.tei.xml
index 2f6cad3..a204fdf 100644
--- a/fulltext/istex/tei/3A8EACA303160EDE4E66A19A97097F6FAECD5358.training.fulltext.tei.xml
+++ b/fulltext/istex/tei/3A8EACA303160EDE4E66A19A97097F6FAECD5358.training.fulltext.tei.xml
@@ -44,7 +44,7 @@
to the calculated chloride equilibrium
potential (E Cl ¼ 240 mV; [Fig. 1f inset]) and contained components
mediated by GABA C Rs and GABA A
Rs that were blocked by TPMPA
(50 mM) and SR95531 (10 mM), respectively [4] ([Fig. 1f, h]). Glutamate
puffs in
+ type="biblio">4 [(Fig. 1f, h)]. Glutamate
puffs in
the outer plexiform layer (OPL) elicited no responses in RBCs
(see [Supplementary Fig. 2]), indicating that gIPSCs reflected
GABA
release in the IPL. TTXpartially blocked gIPSCs (P ¼ 0.0008; tion of the group II/III mGluR antagonist
(RS)-a-cyclopropyl-4-
phosphonophenylglycine (CPPG, 600 mM, 100 ms) [21] in the OPL,
were blocked by PhTx (P ¼ 0.009; [Fig. 2e, g]) and showed inward
rectification ([Fig. 2f]), indicating that they were mediated by
+ type="figure">Fig. 2e, g) and showed inward
rectification [(Fig. 2f)], indicating that they were mediated by
calcium-
permeable AMPARs. These results corroborate previous physiologi-
cal
data indicating that AMPARs, not NMDARs, mediate synaptic
inputs to A17 cells in
rat retina [5,6,17] , in contrast to teleost retina, where
diff --git a/fulltext/istex/tei/6CDD1BB7BE4988F7EBB93484C0ED304C17EFB0E5.training.fulltext.tei.xml b/fulltext/istex/tei/6CDD1BB7BE4988F7EBB93484C0ED304C17EFB0E5.training.fulltext.tei.xml
index b14c94a..0cace9f 100644
--- a/fulltext/istex/tei/6CDD1BB7BE4988F7EBB93484C0ED304C17EFB0E5.training.fulltext.tei.xml
+++ b/fulltext/istex/tei/6CDD1BB7BE4988F7EBB93484C0ED304C17EFB0E5.training.fulltext.tei.xml
@@ -156,7 +156,7 @@
centrosome/spindle-pole localization was unaffected ([Fig. 3b–]
d; quantified in figure legend). In addition, the C-terminal truncated
Mud protein that was encoded by the mud 3 allele failed to localize to the
cortex
- or spindle poles in larval neuroblasts ([Fig. 3g)]. We conclude
+ or spindle poles in larval neuroblasts [(Fig. 3g)]. We conclude
that
Pins recruits Mud to the neuroblast apical cortex, probably via
interac-
tion with the Mud C-terminal domain.
@@ -172,7 +172,7 @@
[Fig. 4d–g]). We also observed formation of bent spindles in
29–40% of
all mud mutant neuroblasts (described and quantified in [Supplementary]
Information, Fig. S2), but these are not
- correlated with spindle-orien-
tation defects ([Fig. 4g]) and
+ correlated with spindle-orien-
tation defects [(Fig. 4g)] and
arise after spindle orientation is fixed (see
below). We conclude that Mud is
required for metaphase spindle orienta-
tion. Despite severe defects in metaphase
spindle orientation, we found
that the mitotic spindle and cortical polarity
@@ -300,7 +300,7 @@
larval neuroblasts
triple-labelled with Mud, Pins and α-tubulin (α-tub) and imaged
using
identical settings. (e) Wild-type. Mud localization is bipolar cortical and
on
centrosomes/spindle poles (n > 20). (f) mud 3 mutant. This Mud protein
- lacks
the NLM and putative transmembrane domains ([Fig. 1a])
+ lacks
the NLM and putative transmembrane domains [(Fig. 1a)]
and fails to localize
to the cortex or spindle poles (n > 15). (g) mud 4 null
mutant. Only weak Mud
staining on centrosomes/spindle poles was detectable. Similar
results were
seen with mud 2 mutants. Insets show the same neuroblasts imaged at
diff --git a/fulltext/istex/tei/7B500C33DCC28A2530BB5A6E4083F9AFDE902102.training.fulltext.tei.xml b/fulltext/istex/tei/7B500C33DCC28A2530BB5A6E4083F9AFDE902102.training.fulltext.tei.xml
index b05208a..17cb8eb 100644
--- a/fulltext/istex/tei/7B500C33DCC28A2530BB5A6E4083F9AFDE902102.training.fulltext.tei.xml
+++ b/fulltext/istex/tei/7B500C33DCC28A2530BB5A6E4083F9AFDE902102.training.fulltext.tei.xml
@@ -140,11 +140,11 @@
b IP
C o n t r o l IP
105 -
-105
-75
-50
75 -
50
-
M r (K)
Ubi−Myc
IgG
c-Myc -
1
2
3
4
5
6
7
8
9
1 0
1 1
c-Myc
c-Myc
c-Myc (P-T58)
- c-Myc (P-S62)
Blot: anti-
[Figure 1] Ubiquitinated c-Myc
- protein is phosphorylated on Thr 58, but not
on Ser 62. Quiescent REF 52
- fibroblasts were infected with Ad-c-Myc (MOI
= 50). At 16 h after infection, cells
- maintained in low-serum medium were
treated with 10 µM lactacystin for 6 h, except
- for the samples shown in
lanes 1 and 2, which represent 10 and 40 µg of untreated
+ c-Myc (P-S62)
Blot: anti-
Figure 1 Ubiquitinated c-Myc protein is
+ phosphorylated on Thr 58, but not
on Ser 62. Quiescent REF 52 fibroblasts were
+ infected with Ad-c-Myc (MOI
= 50). At 16 h after infection, cells maintained in
+ low-serum medium were
treated with 10 µM lactacystin for 6 h, except for the
+ samples shown in
lanes 1 and 2, which represent 10 and 40 µg of untreated
Ad-c-Myc-
infected cell lysate, respectively. Lactacystin-treated cells were
harvested
and lysates were divided for immunoprecipitation (IP) with an
anti-ubiquitin
antibody or control protein A + G beads. The input lysates (10%
@@ -309,7 +309,7 @@
and sibling 13.5-day embryos
were used to prepare primary MEFs with either +/+ or
−/− genotypes [23] .
Substantially more c-Myc protein
accumulated in Pin1 −/− cells, com-
pared with wild-type MEFs after Ad-Myc infection
- [(Fig. 5a], compare
)lanes 1 and 2. This increase in
+ [(Fig. 5a, compare]
)lanes 1 and 2. This increase in
c-Myc levels was caused by the absence
of Pin1, as re-introduction of Pin1 (using
Ad-Pin1) into the Pin1 −/−
MEFs reduced c-Myc levels to those detected in wild-type
MEFs [(Fig.]
5a, compare lanes 1 and 3). Furthermore, a
@@ -379,7 +379,7 @@
was induced at 3 h
after serum stimulation in Pin1 −/− cells [(Fig. 6, lane 6)]. In contrast to
wild-type MEFs, however, c-Myc levels
increased continuously with
time, reaching maximal levels at 24 h after serum
- stimulation [(Fig. 6,]
lane 8). This result is very similar
+ stimulation [(Fig. 6,]
lane 8). This result is very similar
to that resulting from inhibition of
GSK-3β activity [11]
and is consistent with stabilization of c-Myc in the
Pin1 −/− cells. In addition,
the increased levels of c-Myc in the Pin1 −/−
cells correlated with enhanced Ser 62
diff --git a/fulltext/istex/tei/9F00CE81E0A84A812B5407E2F4E02BFEAD7E8CD8.training.fulltext.tei.xml b/fulltext/istex/tei/9F00CE81E0A84A812B5407E2F4E02BFEAD7E8CD8.training.fulltext.tei.xml
index 74a89fe..a1a769c 100644
--- a/fulltext/istex/tei/9F00CE81E0A84A812B5407E2F4E02BFEAD7E8CD8.training.fulltext.tei.xml
+++ b/fulltext/istex/tei/9F00CE81E0A84A812B5407E2F4E02BFEAD7E8CD8.training.fulltext.tei.xml
@@ -306,7 +306,7 @@
pigments is accompanied
by the emergence of a carotenoid peak at 18.9
minutes
retention time [(Fig. 7)]. The net result is a
gradual
carotenoid enrichment due to grazing, as
observed in the field by [LEAVITT and BROWN (1988)].
Whether or not this pigment was
+ type="biblio">LEAVITT and BROWN (1988).
Whether or not this pigment was
associated with the
faecal pellets remains to be investigated. Size
fractio-
nation of the suspended matter in the bottles and
subsequent HPLC
analysis of the different fractions
(diatom cells, pellets, and copepods) did not
@@ -371,10 +371,10 @@
the results of our experiments
either. Between 17 and 45% of the total amount
of
phaeopigments (expressed in chl.a equivalents) con-
sisted of the
phaeophytins-a' and ,~'. Observations in
the field by [NELSON (1989)], [VERNET and LORENZEN]
(1987), [ROY (1989)] and by [GIESKES and KRAAY
- (1986)]
support our conclusion that a variety of phaeopig-
ments can
- be the result when copepods graze
phytoplankton.
+ >NELSON (1989), VERNET and LORENZEN
(1987), ROY (1989) and by [GIESKES and KRAAY (1986)]
support our conclusion that a
+ variety of phaeopig-
ments can be the result when copepods graze
+ phytoplankton.
The question why the recovery (ratio of phaeo-
pigments appearing: chlorophyll
disappearing) was
so different between experiments (recently also
described by