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Les contenus ne sont pas tous disponibles dans la langue choisie. Désirez-vous découvrir le monde de la Rhätische Bahn dans son ensemble? anglais

Darauf legen wir den Fokus

In einem ersten Schritt legt die Rhätische Bahn den Fokus auf die zwei Handlungsfelder «Betriebliches Gesundheitsmanagement» und «Energiesparen». Dadurch soll die Gesundheit der Mitarbeitenden gestärkt sowie die Energieeffizienz gesteigert werden. Projekte und Kampagnen in diesen beiden Handlungsfeldern werden gezielt gefördert und begleitet. Die Entwicklung der übrigen Handlungsfelder wird überwacht, um bei Veränderungen rasch reagieren zu können.

Handlungsfelder der Rhätischen Bahn mit den zwei Fokusthemen «Energiesparen» und «Betriebliches Gesundheitsmanagement».

Im Bereich Energie kann die Rhätische Bahn den grössten Effekt erzielen, da der Energiebedarf sehr gross ist und aufgrund der zunehmenden Zugkilometer sowie der Ausstattung der Züge weiter steigt. Die Energieeffizienz zu steigern ist Teil der Strategie 2020. Massnahmen wie die Automatisierung der Weichenheizungen, die Optimierung von Gebäudeheizungen oder Energiesparmassnahmen an Fahrzeugen sollen dazu führen, dass der gesamte Energiebedarf der Rhätischen Bahn trotz zunehmenden Zugskilometern und höheren Komfortausrüstungen in den Zügen unterproportional ansteigt. Nebst der Steigerung der Energieeffizienz steht die Nutzung erneuerbarer Energie im Vordergrund. Dementsprechend bezieht die Rhätische Bahn den gesamten Strom für ihre Immobilien sowie die elektrisch betriebenen Triebfahrzeuge vollständig aus Wasserkraft.

Die Rhätische Bahn will die Gesundheit der Mitarbeitenden erhalten und stärken. Gesundheit ist nicht nur für jeden einzelnen Mitarbeitenden wichtig. Sie bildet zusammen mit anderen Faktoren auch die Grundlage für die Qualität der Arbeit und damit für den Erfolg des Unternehmens. Um alle gesundheitsrelevanten Aktivitäten, Strukturen und Prozesse zu koordinieren, wurden diese im «Betrieblichen Gesundheitsmanagement (BGM)» zusammengefasst. Arbeitssicherheit und der Eingliederungsprozess von verunfallten oder erkrankten Mitarbeitenden sind ebenso Bestandteile des BGM wie die Betriebliche Gesundheitsförderung.

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Volume 19, Issue 13 , p1123–1127, 14 July 2009
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Published Online: June 18, 2009
Published online: June 18, 2009
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DOI: https://doi.org/10.1016/j.cub.2009.05.058
Publication History
Published online: June 18, 2009 Accepted: May 8, 2009 ; Received in revised form: May 5, 2009 ; Received: April 6, 2009 ;
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Figure 1

miR-122 levels are decreased in mice and patients with HH. () qPCR analysis of miR-122 expression in liver total RNA of WT ( = 8) and ( = 11) mice ( = 0.039). mmu-miR-122, miR-122 stem-loop. () Analysis of miR-122 expression in the liver of WT mice injected with dextran (Dxt; = 5) and iron-dextran (Fe; = 6) ( = 0.187) and () WT mice on a regular ( = 4) or iron-supplemented diet (dFe; = 4) ( = 0.471). () miR-122 levels were reduced in liver biopsies of HH patients ( = 6) compared with the control group without iron overload (Ctr; = 4) ( = 0.068). hsa-miR-122, miR-122 stem-loop. Data were normalized to the appropriate reference genes: miR-194 ( and ), mouse RNU6 (), and human RNU6 (). Data are mean ± SD, and values from WT mouse (–) and control patient () groups were set to 100%. * < 0.05, 2-tailed Student’s test.

Efficient and specific antagonism of miR-122 in murine liver. To functionally investigate a possible link between miR-122 and iron metabolism, we inhibited miR-122 by a single i.p. injection of locked nucleic acid–modified (LNA-modified) anti-miR oligonucleotides ( Vionic Walker Black Mens Shoes Outlet Top Quality Buy Cheap Manchester Great Sale Discount With Credit Card hMltt5
) into age- and sex-matched C57BL/6 WT mice. To inhibit miR-122 specifically, we injected an anti-miR compound with perfect complementarity to miR-122 (perfect match; referred to herein as PM_anti–miR-122). As negative controls, mice were injected either with an LNA control compound with 2 mismatches (referred to herein as 2MM_antimiR-122) or saline vehicle control (0.9% NaCl). Mice were sacrificed 3 and 6 weeks after injection. Independent of treatment, mice were viable and exhibited no overt physical or behavioral abnormalities. To assess the efficiency of miR-122 inhibition, hepatic miR-122 levels were measured by qPCR (Figure 2 A). The amount of detectable miR-122 was reduced compared with saline-injected mice by 28- and 11-fold at 3 and 6 weeks, respectively, after injection with PM_anti–miR-122. Injection of the 2MM_anti–miR-122 control did not significantly reduce miR-122 detectability. Expression of the miR-122 primary transcript was not altered under the experimental conditions (Supplemental Figure 1A). To exclude that PM_anti–miR-122 administration disturbs the expression of other miRNAs we analyzed miRNA expression profiles in the livers, hearts and spleens of the same mice (Supplemental Figure 2). Our data show specific and exclusive inhibition of miR-122 in the liver of PM_anti–miR-122 treated mice. In the spleen, expression of 3 miRNAs was increased in PM_anti–miR-122–treated mice, which may be a consequence of increased extramedullary hematopoiesis (see below). Alteration of the miRNA profile was not detected in the heart, where miR-122 is not expressed ( 26 ).

Figure 2

miR-122 depletion is functional. () miR-122 detectability was decreased in the liver of PM_anti–miR-122–injected mice. Mice were injected i.p. with a single dose of 25 μg/g PM_anti–miR-122 (PM), 2MM_anti–miR-122 (2MM), or saline (SAL) and sacrificed 3 or 6 weeks after injection. Hepatic miR-122 expression was analyzed by qPCR, and data were normalized to the expression of small nucleolar RNA Sno135. Detectability of miR-122 was reduced 3 ( = 0.0001) and 6 ( = 0.0001) weeks after PM_anti–miR-122 administration. () was increased in the liver of PM_anti–miR-122–injected mice 3 ( = 0.0001) and 6 ( = 0.0001) weeks after treatment. Values were normalized to mRNA expression of reference gene . Data are mean ± SD ( = 8), and the saline-treated group was set to 100%. ** < 0.01, 1-way ANOVA.

Furthermore, miR-122 inhibition by PM_anti–miR-122 increased hepatic mRNA levels of the miR-122 target gene aldolase A ( Aldoa ; ref. 31 ) at both 3 weeks (2.8-fold vs. saline; 4.0-fold vs. 2MM_anti–miR-122) and 6 weeks after treatment (3.4-fold vs. saline; 2.7-fold vs. 2MM_anti–miR-122; Figure 2 B). Likewise, serum cholesterol levels were decreased ( 30 , 31 ) 3 weeks after injection of PM_anti–miR-122 (Supplemental Figure 1B). Taken together, these data suggest that PM_anti–miR-122 injection specifically and efficiently antagonizes miR-122 and that miR-122 inhibition is functional.

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