Analysis of ergonomics problems contact-centers

The analysis of the ergonomic problems of the contact center. It allocates main factors of influence on man- operator

Possible Reason for the Unusual Regioselectivity in Nucleophilic Ring Opening of Trisubstituted Aziridines under Mildly Basic Conditions

2,2,3-Trisubstituted aziridines are known to undergo ring opening at the more substituted carbon under mildly basic conditions. However, the reason for the formation of the more sterically encumbered product has never been examined. Several trisubstituted aziridines, with different substitution patterns at the C-2 and C-3 carbons, were synthesized to change the electronics of the aziridine ring system. These changes had no effect on the regioselectivity of the ring-opening reaction. Using the B3LYP/6-31G* DFT basis set it was determined that the transition state for opening at the more substituted carbon proceeds at a lower energy than the transition state at the less substituted carbon

Electrophilic Ln(III) Cations Protected by C–F → Ln Interactions and Their Coordination Chemistry with Weak σ- and π‑Donors

A homoleptic cerium­(III) amide complex, Ce­(NPh^F₂)₃ (<b>1-Ce</b>) (Ph^F = pentafluorophenyl), in an unusual pseudo-trigonal planar geometry featuring six C–F → Ce interactions was prepared. The C–F → Ln interactions in solution were evident by comparison of the ¹⁹F NMR shifts for the paramagnetic <b>1-Ce</b> with those of the 4f⁰ lanthanum­(III) analogue. Coordination of weak σ- and π-donors, including ethers and neutral arene molecules, was achieved by the reversible displacement of the weak C–F → Ce interactions. Computational studies on Ce­(NPh^F₂)₃ and Ce­(NPh^F₂)₃(η⁶-C₆H₃Me₃) provide information on the F → Ce interactions and Ce−η⁶-arene bonding

Double in situ hybridization was carried out by using fluorescein/fast red detection for TrkA (A, E), TrkB (B, F), TrkC (C, G), c-ret (D, H) and DIG/NBT-BCIP for Dok4 (A, B, C, D) and Crip2 (E, F, G, H)

<p><b>Copyright information:</b></p><p>Taken from "A SAGE-based screen for genes expressed in sub-populations of neurons in the mouse dorsal root ganglion"</p><p>http://www.biomedcentral.com/1471-2202/8/97</p><p>BMC Neuroscience 2007;8():97-97.</p><p>Published online 19 Nov 2007</p><p>PMCID:PMC2241628.</p><p></p> In situ signals were converted into pseudo colors and images were superimposed to show co-labelling of cells. Dok4 co-localised with all major subtypes of DRG neurons, Crip2 was specifically excluded from TrkC population. Scale bar 50 μm

Gene expression determined by real-time PCR on P0 and P0 TrkA mutant mouse lumbar DRG

<p><b>Copyright information:</b></p><p>Taken from "A SAGE-based screen for genes expressed in sub-populations of neurons in the mouse dorsal root ganglion"</p><p>http://www.biomedcentral.com/1471-2202/8/97</p><p>BMC Neuroscience 2007;8():97-97.</p><p>Published online 19 Nov 2007</p><p>PMCID:PMC2241628.</p><p></p> TrkA and Ube2e3 (ubiquitin-conjugating enzyme E2E 3) were used as controls. Data (means ± SEM) were calculated by the delta-CT method [37] on three independent experimental replicates. The arithmetic means of the expression levels of two genes (Polr2j, Ddx48) whose expression do not change in the course of development and in TrkA-/- DRG were used to normalize the expression levels. Data were analyzed using the Mann Whitney U-test (*P < 0.05). ND: Not detected

GDNF family ligands influence <i>FXYD2</i> expression in adult DRG neurons in vitro and in vivo.

<p>(A) Quantitative analysis of FXYD2-expressing neurons in DRG cultures in the presence or absence of GDNF/NRTN. The picture is representative of a neuronal culture stained with the anti-FXYD2 antibody revealed with DAB as a substrate. On the graph is reported the proportion of FXYD2+ neurons after 3 h in culture, 3 days in culture without added factors, or 3 days in culture with GDNF/NRTN (10 ng/ml each). <i>FXYD2</i> expression was efficiently maintained by addition of factors. (B) QRT-PCR for FXYD2 on L4/5 DRGs dissected from control animals or mice axotomized and injected intrathecally either with saline, GDNF or NRTN solutions. (C–E″) Combined <i>FXYD2</i> in situ hybridization and FluoroGold staining on adult DRG sections from mice axotomized and injected either with saline (C–C″), GDNF (D–D″) or NRTN (E–E″) solutions during 3 days. Double-labeled neurons are virtually absent with saline injection, while they are numerous after GDNF and NRTN treatments. Insets in C″, D″ and E″ show higher magnifications. Insets in C, D and E represent injection quality controls showing IB4 staining on hemisections of the dorsal spinal cord (brackets) ipsilateral to the axotomy, that is normally lost after axotomy and saline injection, but rescued with GDNF or NRTN <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0029852#pone.0029852-Bennett1" target="_blank">[11]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0029852#pone.0029852-Bennett2" target="_blank">[12]</a>. (F) Quantification of FluoroGold+/FXYD2+ neurons in the indicated conditions, showing that GDNF family ligands efficiently maintain <i>FXYD2</i> in injured neurons. (G) Quantification of the proportion of FXYD2+ neurons per DRG section in naïve animals (Ctrl) or in axotomized mice injected either with saline, GDNF or NRTN solutions. <i>FXYD2</i> is normally expressed in 57% of the DRG neurons and in 16% after axotomy and saline injection. In GDNF and NRTN injected mice, this proportion reaches 32% and 44%, respectively. (H) Triple-labeling for FXYD2, IB4 and FluoroGold (FG) on adult DRG sections from axotomized mice treated with NRTN. Presence of triple-labeled cells (white arrows) shows that FluoroGold+/FXYD2+ neurons are IB4+ nociceptors. Inset show higher magnification.</p

Loss of <i>FXYD2</i> expression in L4/L5 DRG neurons after sciatic nerve axotomy.

<p>(A, B) <i>FXYD2</i> in situ hybridization on naïve DRGs (A) and injured DRGs 3 days post-axotomy (dpa) (B). (C) Quantification of the percentage of <i>FXYD2</i>+ neurons in naïve and axotomized DRGs 3 dpa, showing a reduction from 57% to 16% after lesion of the sciatic nerve. (D, E) Time course analysis of <i>FXYD2</i> expression in the DRGs from 6 hpa to 7 dpa (D). Quantification reveals a major decrease between 2 and 3 dpa that remains stable at 7 dpa (E). (F) Scheme illustrating retrograde labeling of axotomized DRG neurons with Fluorogold. (G–G″) Combined <i>FXYD2</i> in situ hybridization and FluoroGold staining on DRG sections 3 dpa. Virtually no double-positive cells are found. Arrows and arrowheads point to FluoroGold-negative/FXYD2+ and FluoroGold+/FXYD2-negative neurons, respectively.</p

Restricted expression of FXYD2 in TrkB+ mechanoceptive and Ret+/IB4+ non-peptidergic noniceptive neurons within the DRGs.

<p>(A–J) Double-labeling for <i>FXYD2</i> and <i>TrkA</i>, <i>TrkB</i>, <i>TrkC</i>, <i>Ret</i> or IB4 on adult DRG sections. No co-localization is observed between FXYD2 and TrkA or TrkC. Double-positive neurons are detected with TrkB+ mechanoceptors (arrows in E,F) and Ret+/IB4+ non-peptidergic nociceptors (arrows in G–J). Arrowheads in G,H point to large Ret+ mechanoceptive neurons that are <i>FXYD2</i>-negative. (K,L) Percentages of TrkB+ (K) or IB4+ (L) neurons expressing FXYD2 showing that virtually all the TrkB+ mechanoceptors and the non-peptidergic nociceptors are FXYD2+. (M) Distribution of FXYD2+ neurons in two main neuronal types: the TrkB+ (representing 13%) and the Ret+/IB4+ (representing 85%) populations.</p

<i>FXYD2</i> expression depends on Runx1 and Ret signaling in non-peptidergic nociceptors.

<p>(A–D) <i>FXYD2</i> in situ hybridization on adult DRG sections from control (<i>Runx1^F/F</i>; A,C) and mutant (<i>Runx1^F/F;Wnt1Cre</i>; B,D) animals at P15 (A,B) and P90 (C,D). Insets show higher magnification. In control (A,C), small and larger (respectively, red and green brackets in insets) diameter neurons are detected, while in <i>Runx1</i> mutants at both stages (B,D) only the large diameter population expresses <i>FXYD2</i> (green brackets in insets). (E) Quantification of the proportions of FXYD2+ neurons at P90 showing a reduction of 69% in <i>Runx1</i> mutants. (F,G) Double-labeling for FXYD2 and IB4 on adult DRG sections from control and Runx1 mutant animals at P90, showing a loss of FXYD2 specifically in the IB4+ population in the mutants. Insets show higher magnifications. (H,I) <i>Ret</i> in situ hybridization on DRG sections from control (H) and <i>Runx1</i> mutant (I) animals at P90. Insets show higher magnification. <i>Ret</i> expression is lost in small diameter nociceptors (red brackets in insets) and persists only in large diameter mechanoceptive neurons (green brackets in insets) in <i>Runx1</i> mutants. (J–M) <i>FXYD2</i> in situ hybridizations (J,K) and immunochemistry (L,M) on DRG sections at P15 from control (<i>Ret^F/F</i>; J,L) and <i>Ret</i> mutants (<i>Ret^F/F;Wnt1-Cre</i>; K,M) showing a reduced number of FXYD2+ neurons and expression intensity in the mutants. (N) Quantification of the relative number of <i>FXYD2+</i> neurons showing a reduction of 30% in <i>Ret</i> mutants. (O) Epistatic relationships between Runx1, Ret and FXYD2 in non-peptidergic nociceptors. Runx1 controls (directly or indirectly) the onset of FXYD2 expression partly through Ret regulation. Ret signaling seems involved in ensuring proper levels of <i>FXYD2</i> and in its maintenance at subsequent stages (dashed arrows; see text).</p

Expression profile of <i>FXYD2</i> mRNA and protein during DRG neuron development.

<p>(A) Quantitative RT-PCR analysis of <i>FXYD2</i> expression in the developing DRGs and after axotomy. SAGE tag frequencies for FXYD2 at equivalent stages or conditions are indicated below. (B) Western blot using a FXYD2 antibody shows the presence of the FXYD2 isoforms gamma-a and gamma-b in the adult DRG. Kidney extract is a positive control. (C–F) <i>FXYD2</i> in situ hybridization on mouse DRG sections at E13, P0, P15 and adult. Arrow and arrowhead in F point to FXYD2-positive and FXYD2-negative neurons, respectively. (G) FXYD2 immunochemistry on adult DRG sections. Arrows and Arrowheads point respectively to positive cell bodies and nerve fibers.</p