Ökonomischer Erfolg durch ökologisches Handeln: der FirmenUmweltIndex FUX für nachhaltiges Wirtschaften

Der vorliegende Beitrag ist ein Ergebnis der studentischen Forschungs- und Arbeitsgruppe sO2lutions der Technischen Hochschule Wildau (FH). Er geht der Frage nach, wie umweltfreundliches Verhalten eines Unternehmens beeinflusst und gefördert werden kann. Dazu werden zunächst die Eckpfeiler Ökonomie, Ökologie und Ethik und deren Zusammenwirken in einer realökonomischen an Stelle einer geldökonomischen Unternehmensführung erörtert. Anschließend wird der FirmenUmweltIndex FUX als Beitrag zur Verwirklichung umweltgerechter, realökonomischer Unternehmensführung vorgestellt und diskutiert. Dieser personenbezogene Ansatz kann in jedweder organisatorischen Einheit und damit beispielsweise in Wohnungsunternehmen oder auch in Krankenhäusern zur Realisierung von Nachhaltigkeit eingesetzt werden.This report is a result of the research activities of the working group sO2lutions of the Technical University of Applied Sciences Wildau. The main question is how we can realize a positive impact on environmentally friendly behavior of managers and employees in a company. Therefore the report examines the key elements of sustainability: (1) economy, (2) ecology and (3) ethics. The combination of these three parts should be the challenge for corporations world-wide instead of money economic based management. Furthermore, the report presents the FirmenUmweltIndex FUX (Company Environment Index), established by sO2lutions, as a contribution to the implementation of a sustainable management based on economy, ecology and ethics. This approach can be used to realize economic leadership and management under consideration of environmental needs. It can be implemented in each organizational unit e. g. in housing companies or hospitals

ABC Transporters B1, C1 and G2 Differentially Regulate Neuroregeneration in Mice

Background: ATP-binding cassette (ABC) transporters are essential regulators of organismic homeostasis, and are particularly important in protecting the body from potentially harmful exogenous substances. Recently, an increasing number of in vitro observations have indicated a functional role of ABC transporters in the differentiation and maintenance of stem cells. Therefore, we sought to determine brain-related phenotypic changes in animals lacking the expression of distinct ABC transporters (ABCB1, ABCG2 or ABCC1). Methodology and Principal Findings: Analyzing adult neurogenesis in ABC transporter-deficient animals in vivo and neuronal stem/progenitor cells in vitro resulted in complex findings. In vivo, the differentiation of neuronal progenitors was hindered in ABC transporter-deficient mice (ABCB1 0/0) as evidenced by lowered numbers of doublecortin + (236%) and calretinin + (237%) cells. In vitro, we confirmed that this finding is not connected to the functional loss of single neural stem/ progenitor cells (NSPCs). Furthermore, assessment of activity, exploratory behavior, and anxiety levels revealed behavioral alterations in ABCB1 0/0 and ABCC1 0/0 mice, whereas ABCG2 0/0 mice were mostly unaffected. Conclusion and Significance: Our data show that single ABC transporter-deficiency does not necessarily impair neuronal progenitor homeostasis on the single NSPC level, as suggested by previous studies. However, loss of distinct ABC transporters impacts global brain homeostasis with far ranging consequences, leading to impaired neurogenic functions i

Deficiency of ABCB1 impairs neuronal differentiation in the SGZ of the dentate gyrus.

<p>Shown are the relative quantities of cells positive for Sox2, DCX, calretinin and BrdU in the SGZ of the dentate gyrus in ABC transporter-deficient mice as compared to the FVB controls. A) Sox2⁺ NSPCs increased significantly in ABCC1 transporter-deficient mice (+17%), while ABCB1- or ABCG2-deficient mice were unaffected. B) Early DCX⁺ neurons were significantly decreased in the absence of ABCB1 (−36%) and ABCG2 (−23%), while later, post-mitotic calretinin⁺ cells (C) were only reduced in ABCB1 transporter-deficient mice by 37%. D) The proliferation capacity (BrdU⁺ cells) was not affected in any of the analyzed ABC transporter-deficient mice. Error bar: SEM; * p<0.05; **p<0.01.</p

ABC transporter-deficiency did not lead to impairments of neuronal differentiation <i>in vitro</i>.

<p>ABCG2^0/0 cells showed a significant increase in proliferation capacity (+62%, A) quantified by detection of BrdU uptake using immunofluorescence (B). The differentiation capacity was not impaired by loss of ABC expression (C) as revealed by quantification of neuronal cells positive for Tuj1 (D). Error bar: SEM; Scale bar: 50 µm.</p

Light/dark box experiments verified altered anxiety and exploratory behavior.

<p>Comparing the running distance of the animals in the open field revealed no significant differences (A). However, the distance traveled by ABCB1-deficient mice (+64%) in the dark compartment (B) was significantly increased compared to the controls. Also, the time in the dark compartment (C) was significantly increased in ABCB1^0/0 mice (+78%) compared to controls. The mean number of transitions between the two compartments (D) was impaired in both ABCB1^0/0 (−59%) and ABCC1^0/0 (−49%) mice. Comparing the rearing frequency in both compartments revealed a significant decrease for ABCC1^0/0 (−67%) mice in the open field (E), while the frequency was increased in the dark compartment (F) for ABCB1^0/0 (+71%) mice. Error bar: SEM, *</p

ABC transporter deficiency promotes anxiety.

<p>The diagrams show parameters assessed via the elevated plus maze. Mice deficient for ABCB1 (−44%) and ABCG2 (−32%) showed a significantly decreased presence in the open arms (A). The time of residence in the closed compartments was significantly increased in all ABC transporter-deficient mouse strains (ABCB1^0/0 +43%; ABCG2^0/0 +24%; ABCC1^0/0 +32%) (B). Running speed (celerity) in the open arms was not changed in any of the ABC transporter-deficient mice (C). ABCB1 (−23%) and ABCC1 (−14%) transporter-deficient mice showed significantly lower celerity values in the closed arms (D). Error bar: SEM, *p<0.05; **p<0.01; ***p<0.001.</p

Neurogenesis is induced by controlled cortical impact (CCI) trauma.

<p>The photomicrographs show the SGZ of the DG after CCI (LEFT: Control hemispheres; RIGHT: hemispheres after CCI). Shown are the marker combinations Sox2/BrdU (A), DCX/BrdU (B) and calretinin/BrdU (C). Arrowheads indicate double labeled cells. Scale bar: 20 µm.</p

ABC transporter-deficiency influences cortical architecture of layers I and VI while neuronal density is not altered.

<p>Paraffin-embedded brain sections (A) were labeled with an antibody against NeuN, digitized, and the NeuN+ area was computer-assisted determined relative to the cortical area to quantify the neuronal density of the cortex (B). The thickness of the cortical layers I, II–IV (combined), V and VI were measured (A) and analyzed (C). The loss of ABCB1 expression significantly decreased the thickness of layer I (−12%) while loss of ABCC1 only affected the thickness of layer VI (+15%) Scale bars: 500 µm (A); Error bars: SEM, *p<0.05; **p<0.01.</p

Lack of ABCB1 or ABCC1 expression leads to impaired exploratory activity.

<p>The diagrams show Y-maze-related parameters. Plotting the animals' course in the Y-maze, the running distance reveals a significant decrease in ABCB1- (−13%) and ABCC1- (−17%) deficient animals (A), while this parameter was only slightly, non-significantly decreased in ABCG2-deficient mice. The same behavioral pattern was detected for exploratory activity as assessed by the arm entries (ABCB1^0/0 −16%; ABCC1^0/0 −23%) (B). Error bar: SEM, *p<0.05.</p

ABC transporters are important for neurogenic functions during disease states as revealed by the CCI paradigm.

<p>The proliferation capacity measured by BrdU incorporation (A) was significantly decreased in the induced hemisphere of all ABC transporter-deficient strains (ABCB1^0/0: −47%; ABCG2^0/0: −31%; ABCC1^0/0: −53%) (right). The number of Sox2⁺ cells was not significantly altered in the induced brain hemisphere (B), but shows a trend toward a decreased number in ABCB1- and ABCC1- deficient mice that resembles the decreases in immature DCX⁺ and calretinin⁺ neurons (C, D). The number of DCX⁺ neuronal progenitors (B) was significantly reduced in the induced hemisphere of ABCB1- (−36%) or ABCC1-deficient (−33%) animals as compared to controls (right). Additionally, the number of early granule cells expressing calretinin (D) was decreased in the induced hemisphere of ABCB1- (29%) and ABCC1-deficient mice (−24%) (right), while there was no change in ABCG2-deficient mice. Error bars: SEM, *p<0.05; **p<0.01; ***p<0.001.</p