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

Cocaine and HIV synergistically down-regulate miR-155 and 20a.

<p>MDDCs (1×10⁶ cells/ml) from normal donors were cultured with 3 different concentrations (0.1, 1 and 10 µM) of cocaine for 15 and 24 hrs.Total cellular microRNA was extracted and amplified by specific RT-PCR for miR-155 and 20a gene expression. Cocaine down regulates <b>(A)</b> miR-155 <b>(B)</b> and 20a gene expression. (<b>C)</b> Cocaine treatment does not induce cytotoxicity. Cell suspension (200 µl) was subjected to XTT-PMS (100 µl) followed by a 4 hr incubation period. Cytotoxicity was measured by ELISA reader and cell suppression was calculated by: suppression index (%)  =  ((Abs cocaine – Abs blank)/(Abs control - Abs blank))×100%. (<b>D</b>) MDDCs (1×10 cells/ml) from normal donors were infected with HIV-1_BAL at a concentration of 20 ng for 2 hr, followed by treatment ± cocaine (1 µM) for 7 days. Total cellular microRNA was extracted and amplified by specific RT-PCR for miR-155 and 20a gene expression. Results shown are representative of mean ± SEM of three experiments. Graphs are represented as % of TAI compared to the non-treated control. p-value≤0.05 were considered to be significant.</p

HIV replication increased in MDDCs treated with cocaine.

<p><b>(A)</b> MDDCs (1×10⁶ cells/ml) from normal donors were infected with HIV-1_BAL at a concentration of 20 ng for 2 hr, followed by treatment ± cocaine (1 µM) for 7 days. The culture supernatants were quantitated for p24 Ag. Significance is calculated with respect to HIV-1 treated control cells. (<b>B</b>) Effect of cocaine on HIV-1 transcription was determined using an LTR-CAT reporter data normalized to total protein concentration. (<b>C</b>) HIV-1 transcription was determined in MDDCs from normal donors infected with HIV-luciferase viruses competent for a single round of infection (∼20 ng per (1×10⁶ cells) in the presence/absence of cocaine (1 µM) for 72 hours. Cultures were harvested 72 hours post infection and luciferase assayed. Results shown are representative of mean ± SEM of three experiments. p-value≤0.05 were considered to be significant.</p

Overview of Cocaine-enhancement of HIV infectivity in MDC via the down-regulation of miR-155.

<p>(<b>A</b>) In absence of cocaine or HIV miR155 targets DC-SIGN and PU.1, reducing the expression post-transcriptionally. Lowered PU.1 and DC-SIGN expression is observed in mature DCs. (<b>B</b>) In the presence of Cocaine or HIV alone miR-155 levels are reduced resulting in elevated PU.1 and DC-SIGN expression. This phenotype is evident in immature DCs (iDCs). Together HIV and cocaine, synergize to dramatically lower miR-155 resulting in elevated levels of the transcription factor Pu.1. In turn, Pu.1 binds sites within the DC-SIGN promoter as well as the HIV LTR and promotes transcription. The resulting elevated DC-SIGN expression in DCs lead to maintenance an immature DC phenotype and thus increased HIV infectivity. By binding NF-κB sites within the LTR, PU.1 increases viral transcription and pathogenesis.</p

Alcohol Induces Protein Levels of HDACs <i>ex vivo</i> in MDDCs from Alcohol Users.

<p><b>A)</b> Representative blot is shown for MDDC from alcohol users and non-users. Whole cell lysates (20 μg) were used for western blot analysis. <b>B)</b> Optical densities (OD) were analyzed using Image J software. Protein quantification is expressed as percentage of control ± SEM of ten OD readings per HDAC. p≤0.05 is considered significant.</p

Effects of Alcohol and/or HDACi on Oxidative Stress and Antioxidant Defense Genes.

<p>Effects of Alcohol and/or HDACi on Oxidative Stress and Antioxidant Defense Genes.</p

miR-155 modulates PU.1 levels.

<p>MDDCs (1×10⁶ cells/ml) from normal donors were transfected with anti-miR-155, at a final concentration of 75 nM, followed by infection with HIV-1 (20 ng) and treatment ± cocaine (1 µM). Total RNA was extracted and amplified by RT-PCR for PU.1 gene expression. Values were normalized against GAPDH and significance is calculated with respect to control. Graphs are represented as % difference from control. Results shown are representative of mean ± SEM of three experiments. p-value≤0.05 were considered to be significant.</p

<i>in silico</i> Oxidative Stress and Antioxidant Defense Gene Network Interactions with Class I HDACs.

<p>Non-specific interactions between <b>A)</b> antioxidant, <b>B)</b> ROS metabolism genes, <b>C)</b> all class I HDACs. Tissue-specific interactions between <b>D)</b> HDAC1, HDAC2 and HDAC3 with PCR array gene targets (CSDE1, CYBA, SGK2, TXNDC2) and individual HDACs interactions including <b>E)</b> HDAC1, <b>F)</b> HDAC2, and <b>G)</b> HDAC3. Interactions are color-coded by down-regulation, up-regulation, regulation, co-expression, chemical modification, physical interaction, predicted protein interaction, and predicted TFactor regulation.</p

Effects of Alcohol or HDACi (TSA and MGCD0103) on MDDCs Viability.

<p>MDDCs were treated for 24 and 48 hours with <b>A and B</b>) different percentages of alcohol (EtOH 0.05–0.4%) and <b>C and D</b>) different concentrations of HDACi: TSA (50-100nM) and MGCD0103 (1–6μM). Viability was assessed by dye exclusion method using trypan blue. Data are expressed as averages of percent viable cells normalized to control ± SE, (n = 7).</p

Effect of intracellular 5-LOX expression in cocaine users and HIV infected patients.

<p>IDC (5×10⁵ cells/ml) were isolated from normal, cocaine users, HIV positives and HIV positive cocaine users intracellular expression of 5-LOX (A) and % 5-LOX positive cells (B) was analyzed by flow cytometry. Data are expressed and represented as mean± SD of six independent experiments.</p