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