Stelleninhaber geht – Wissen bleibt!

In Deutschland nimmt der Anteil älterer Arbeitnehmerinnen und Arbeitnehmer tendenziell zu. Deshalb muss sich die Bibliotheksleitung verstärkt auf das altersbedingte Ausscheiden älterer Arbeitnehmer einstellen. Eine langjährige Fachkraft verfügt über spezielles Erfahrungswissen im direkten Aufgabenfeld. Die Bibliotheksleitung muss den Transfer allen relevanten Wissens, dazu gehört das Erfahrungswissen, vom Stelleninhaber auf seinen Nachfolger ermöglichen und unterstützen. Am Beispiel der Universitätsbibliothek der Bergakademie Freiberg wird untersucht, wie das Wissensmanagement im Rahmen eines Stellenwechsels derzeit geregelt ist. Das geschieht mit Hilfe von Tiefeninterviews in verschiedenen Abteilungen. Die Auswertung der Interviews bildet die Basis für ein Konzept für das Wissensmanagement beim Stellenwechsel an der UB Freiberg. Das Konzept benennt u. a. Maßnahmen zur Identifikation des stellenbezogenen Wissens, Maßnahmen zur Dokumentation des relevanten Wissens und Instrumente zur Wissensweitergabe beim Stellenwechsel

CSC treatment in U937 cells is associated with increased apoptosis.

<p>a) Representative dot plot shows that, compared to vehicle-treated control cells, a significantly higher proportion of U937 cells were positively stained with annexin dye following CSC treatment. b) Bar graph summarizing the percent apoptotic cells in Q2 from CSC treated U937 cells. c) Effect of CSC treatment on cell viability in U937 cells as measured by MTT assay. Results from MTT assay confirm a loss of cell viability in CSC treated U937 cells compared to vehicle-treated control cells. *p≤0.05; **p≤0.01.</p

CSC-mediated changes in expression of CYP1 enzymes in HIV-infected human primary macrophages.

<p>a) Compared to the vehicle-treated control cells, CSC-treatment (4-day) was associated with an enhanced transcription of CYP1A1 gene in HIV-infected primary macrophages (upper panel). However, the expression of CYP1A1 protein was not upregulated following chronic treatment with CSC (lower panel). b) CSC-treatment (4-day) was associated with an enhanced transcription of CYP1B1 gene in HIV-infected primary macrophages (upper panel). CYP1B1 protein was also found to be significantly upregulated in CSC treated macrophages compared to vehicle treated HIV-infected human primary macrophages (lower panel). **p≤0.01.</p

Effect of acute and chronic CSC treatment in HIV-infected U1 cells.

<p>a) CSC treatment (50 μg/ml) for 6H resulted in significantly enhanced level of ROS in U1 cells, compared to control cells. b) Chronic (4-day) daily treatment with CSC (25 μg/ml) resulted in significantly higher ROS levels in U1 cells. c) PMA stimulation following 4-day CSC treatment was associated with statistically significant increase in HIV replication, as measured by HIV-1 p24 antigen level in cell supernatant, in CSC treated U1 cells compared to vehicle-treated control group. *p≤0.05; **p≤0.01.</p

Caspase-3 activation in CSC treated U937 cells.

<p>a) Treatment with CSC was associated with a time-dependent increase in caspase-3 activity. The increase in caspase-3 activity, compared to vehicle-treated cells, was found to be significant 24H and 48H after CSC treatment. b) The CSC-mediated induction of caspase-3 activity was completely blocked following pretreatment with vitamin C in U937 cells. *p≤0.05; **p≤0.01.</p

Effect of CSC treatment on CYP1A1 gene transcription in monocytic cells.

<p>a) mRNA levels of CYP1A1 were found to be significantly higher in CSC treated monocytic cells compared to control cells. Acute (6H) treatment of U937 and U1 cells with CSC resulted in ~25 and ~15 fold higher CYP1A1 mRNA level respectively, as compared to DMSO-treated cells. Chronic treatment (4-day) of U1 cells with CSC was also associated with statistically significant upregulation in CYP1A1 mRNA level (~40 fold). b) The CSC-mediated upregulation in CYP1A1 gene transcription was found to be mediated via the aromatic hydrocarbon receptor (AHR). Pretreatment of U937 cells with the AHR antagonist, CH223191, significantly blocked the CSC-mediated induction of CYP1A1 mRNA level. *p≤0.05; **p≤0.01.</p

Effects of Cigarette Smoke Condensate on Oxidative Stress, Apoptotic Cell Death, and HIV Replication in Human Monocytic Cells - Fig 1

<p>a) Dose-response of cigarette smoke condensate (CSC) treatment on reactive oxygen species (ROS) production in human U937 monocytic cells. CSC treatment at 3H was found to enhance ROS production in a dose-dependent manner. b) Time-kinetic of ROS induction following CSC treatment in U937 cells. CSC treatment (50 μg/ml) in U937 cells resulted in a time-dependent significant enhancement in ROS production as measured using a flow cytometer. Compared to the respective vehicle-treated cells, CSC-treated U937 cells were marked by significantly higher levels of ROS at 1H, 3H, 6H, 9H and 12H post-treatment. The peak for enhanced ROS production was 6H following CSC treatment. c) Effects of vitamin C pretreatment on induction of ROS production by CSC. Pretreatment with vitamin C significantly inhibited the CSC-mediated induction in ROS levels in U937 cells. *p≤0.05; **p≤0.01.</p

Induction of CYP3A4, MRP1, and MDR1 protein expression was analyzed by In-Cell Western (ICW) assay.

<p>Top section in each panel is a respective representative immunoblot of CYP3A4, MRP-1 or MDR1. Bottom plot in each panel demonstrates respective mean CYP3A4, MRP-1 or MDR1 fluorescence signal intensities of triplicates and error bars represent SEM values. *p< 0.05 compared to control, ^#p<0.05 compared to EVG, and ^p<0.05 compared to EVG+COBI, ^$p<0.05 compared to EtOH. Values were mean ± SEM from 3 individual experiments. EVG, Elvitegravir; COBI, Cobicistat; EtOH, ethanol.</p

Intracellular elvitegravir concentration in the presence of MRP1 or MDR1 inhibitors and cobicistat + ethanol.

<p>EVG quantified from cell lysates using LC MS/MS after 24 hours treatment with indicated drugs. Data are expressed as mean ± SEM from 3 independent experiments. *p< 0.05 compared to EVG+COBI+EtOH (Control). EVG, Elvitegravir; COBI, Cobicistat; EtOH, ethanol.</p

Comparison of cytokine and chemokine levels between HIV-negative and-positive alcohol users.

<p>Comparison of cytokine and chemokine levels between HIV-negative and-positive alcohol users.</p