Zur Relevanz von Geschlecht in einer Universität - der Feldzugang als Hürde und Erkenntnisquelle

Within the framework of ethnography, field access plays an essential role for the progress and success of research projects using such a methodology. Based on a gender studies project in which we analyzed the change of gender arrangements (LENZ & ADLER, 2010) within a German university, we illustrate how field access not only poses a methodological challenge but also serves as an important source of information. Contrasting two faculties we show how the issue of gender is addressed in different organizational units. The two faculties have in common that they understand the gendering of the faculty culture as a question of numbers. At the same time the topic is externalized and thereby not taken as a relevant organizational task. Finally, we link the empirical results to the theoretical discussion about the "gendered organization" (ACKER, 1990; MÜLLER, RIEGRAF & WILZ, 2013) and deduce methodological challenges for gender studies.In der ethnografischen Forschung spielt der Feldzugang eine entscheidende Rolle für den Fortgang und das Gelingen von Forschungsprojekten. In diesem Beitrag soll am Beispiel eines Geschlechterforschungsprojekts, in dem der Wandel von Geschlechterordnungen (LENZ & ADLER 2010) an einer Universität untersucht wurde, aufgezeigt werden, wie der Feldzugang nicht nur eine forschungspraktische Herausforderung darstellt, sondern bereits als eine wichtige Erkenntnisquelle dienen kann. Auf der Basis von Beobachtungsprotokollen werden zwei Fakultäten kontrastiert und es wird dabei herausgearbeitet, wie unterschiedlich sich Struktureinheiten innerhalb einer Hochschule organisational arrangieren und wie das Thema Geschlecht darin jeweils thematisiert wird. Gemeinsam ist wiederum beiden Fakultäten, dass die Frage nach der Vergeschlechtlichung einer Fachkultur auf die Frage nach numerischen Anteilen reduziert, externalisiert und damit nicht als relevante organisationale Gestaltungsaufgabe aufgegriffen wird. Aus den empirischen Ergebnissen werden zum Schluss Anschlüsse an die geschlechter- und organisationstheoretische Debatte um die "Gendered Organization" (ACKER 1990; MÜLLER, RIEGRAF & WILZ 2013) sowie methodische Herausforderungen für die Geschlechterforschung abgeleitet

Facing the orientation framework of a gender-neutral university. Gender equality in higher education management

Der Beitrag fokussiert kollektive Geschlechterwissensbestände an einer deutschen Universität, die fortbestehende Geschlechterungleichheiten legitimieren und sich als ein Nebeneinander von widersprüchlichen Deutungsmustern beschreiben lassen. Daraus leiten sich Distanzierungen und Vorbehalte gegenüber Gleichstellungsarbeit ab, die eine gleichstellungsorientierte Organisationsentwicklung behindern können. Basis des Artikels bilden Gruppendiskussionen mit Hochschulangehörigen verschiedener Statusgruppen, welche nach der Dokumentarischen Methode (Bohnsack, 2000) ausgewertet wurden. (DIPF/Orig.)The article focuses on collective gender knowledge at a German university, which keeps legitimizing persistent gender inequalities and consists of contradictory interpretive patterns. This leads to a distance towards gender equality efforts possibly impeding an equality-focused organizational development. The article is based on group discussions with members of different academic status, which were analyzed through Documentary Method (Bohnsack, 2000). (DIPF/Orig.

Bone Morphogenetic Protein (BMP)-7 expression is decreased in human hypertensive nephrosclerosis

Background: Bone Morphogenetic Protein (BMP)-7 is protective in different animal models of acute and chronic kidney disease. Its role in human kidneys, and in particular hypertensive nephrosclerosis, has thus far not been described. Methods: BMP-7 mRNA was quantified using real-time PCR and localised by immunostaining in tissue samples from normal and nephrosclerotic human kidneys. The impact of angiotensin (AT)-II and the AT-II receptor antagonist telmisartan on BMP-7 mRNA levels and phosphorylated Smad 1/5/8 (pSmad 1/5/8) expression was quantified in proximal tubular cells (HK-2). Functional characteristics of BMP-7 were evaluated by testing its influence on TGF-b induced epithelial-to-mesenchymal transition (EMT), expression of TGF-b receptor type I (TGF-bRI) and phosphorylated Smad 2 (pSmad 2) as well as on TNF-a induced apoptosis of proximal tubular cells. Results: BMP-7 was predominantly found in the epithelia of the distal tubule and the collecting duct and was less abundant in proximal tubular cells. In sclerotic kidneys, BMP-7 was significantly decreased as demonstrated by real-time PCR and immunostaining. AT-II stimulation in HK-2 cells led to a significant decrease of BMP-7 and pSmad 1/5/8, which was partially ameliorated upon co-incubation with telmisartan. Only high concentrations of BMP-7 (100 ng/ml) were able to reverse TNF-a-induced apoptosis and TGF-b-induced EMT in human proximal tubule cells possibly due to a decreased expression of TGF-bRI. In addition, BMP-7 was able to reverse TGF-b-induced phosphorylation of Smad 2. Conclusions: The findings suggest a protective role for BMP-7 by counteracting the TGF-b and TNF-a-induced negative effects. The reduced expression of BMP-7 in patients with hypertensive nephrosclerosis may imply loss of protection and regenerative potential necessary to counter the disease

Bone Morphogenetic Protein (BMP)-7 expression is decreased in human hypertensive nephrosclerosis

Abstract Background Bone Morphogenetic Protein (BMP)-7 is protective in different animal models of acute and chronic kidney disease. Its role in human kidneys, and in particular hypertensive nephrosclerosis, has thus far not been described. Methods BMP-7 mRNA was quantified using real-time PCR and localised by immunostaining in tissue samples from normal and nephrosclerotic human kidneys. The impact of angiotensin (AT)-II and the AT-II receptor antagonist telmisartan on BMP-7 mRNA levels and phosphorylated Smad 1/5/8 (pSmad 1/5/8) expression was quantified in proximal tubular cells (HK-2). Functional characteristics of BMP-7 were evaluated by testing its influence on TGF-β induced epithelial-to-mesenchymal transition (EMT), expression of TGF-β receptor type I (TGF-βRI) and phosphorylated Smad 2 (pSmad 2) as well as on TNF-α induced apoptosis of proximal tubular cells. Results BMP-7 was predominantly found in the epithelia of the distal tubule and the collecting duct and was less abundant in proximal tubular cells. In sclerotic kidneys, BMP-7 was significantly decreased as demonstrated by real-time PCR and immunostaining. AT-II stimulation in HK-2 cells led to a significant decrease of BMP-7 and pSmad 1/5/8, which was partially ameliorated upon co-incubation with telmisartan. Only high concentrations of BMP-7 (100 ng/ml) were able to reverse TNF-α-induced apoptosis and TGF-β-induced EMT in human proximal tubule cells possibly due to a decreased expression of TGF-βRI. In addition, BMP-7 was able to reverse TGF-β-induced phosphorylation of Smad 2. Conclusions The findings suggest a protective role for BMP-7 by counteracting the TGF-β and TNF-α-induced negative effects. The reduced expression of BMP-7 in patients with hypertensive nephrosclerosis may imply loss of protection and regenerative potential necessary to counter the disease.</p

Dynamics of Vascular Protective and Immune Supportive Sphingosine-1-Phosphate During Cardiac Surgery

Introduction Sphingosine-1-phosphate (S1P) is a signaling lipid and crucial in vascular protection and immune response. S1P mediated processes involve regulation of the endothelial barrier, blood pressure and S1P is the only known inducer of lymphocyte migration. Low levels of circulatory S1P correlate with severe systemic inflammatory syndromes such as sepsis and shock states, which are associated with endothelial barrier breakdown and immunosuppression. We investigated whether S1P levels are affected by sterile inflammation induced by cardiac surgery. Materials and Methods In this prospective observational study we included 46 cardiac surgery patients, with cardiopulmonary bypass (CPB, n=31) and without CPB (off-pump, n=15). Serum-S1P, S1P-sources and carriers, von-Willebrand factor (vWF), C-reactive protein (CRP), procalcitonin (PCT) and interleukin-6 (IL-6) were measured at baseline, post-surgery and at day 1 (POD 1) and day 4 (POD 4) after surgical stimulus. Results Median S1P levels at baseline were 0.77 nmol/mL (IQR 0.61-0.99) and dropped significantly post-surgery. S1P was lowest post-surgery with median levels of 0.37 nmol/mL (IQR 0.31-0.47) after CPB and 0.46 nmol/mL (IQR 0.36-0.51) after off-pump procedures (P<0.001). The decrease of S1P was independent of surgical technique and observed in all individuals. In patients, in which S1P levels did not recover to preoperative baseline ICU stay was longer and postoperative inflammation was more severe. S1P levels are associated with its sources and carriers and vWF, as a more specific endothelial injury marker, in different phases of the postoperative course. Determination of S1P levels during surgery suggested that also the anticoagulative effect of heparin might influence systemic S1P. Discussion In summary, serum-S1P levels are disrupted by major cardiac surgery. Low S1P levels post-surgery may play a role as a new marker for severity of cardiac surgery induced inflammation. Due to well-known protective effects of S1P, low S1P levels may further contribute to the observed prolonged ICU stay and worse clinical status. Moreover, we cannot exclude a potential inhibitory effect on circulating S1P levels by heparin anticoagulation during surgery, which would be a new pro-inflammatory pleiotropic effect of high dose heparin in patients undergoing cardiac surgery

Filaggrin deficiency results in a dose-dependent impairment of the epidermal barrier in ichthyosis vulgaris

Oncogene-induced senescence acts as a barrier against tumor formation and has been implicated as the mechanism preventing the transformation of benign melanocytic lesions that frequently harbour oncogenic B-RAF or N-RAS mutations. In the present study we systematically assessed the relative importance of the tumor suppressor proteins p53, p21Waf1, pRb and p16INK4a in mediating oncogene-induced senescence in human melanocytes. We now show that oncogenic N-RAS induced senescence in melanocytes is associated with DNA damage, a potent DNA damage response and the activation of both the p16INK4a/pRb andp53/p21Waf1 tumor suppressor pathways. Surprisingly neither the pharmacological inhibition of the DNA damage response pathway nor silencing of p53 expression had any detectable impact on oncogene-induced senescence in human melanocytes. Our data indicate that the pRb pathway is the dominant effector of senescence in these cells, as its specific inactivation delays the onset of senescence and weakens oncogene-induced proliferative arrest.1 page(s