Kontinuitäten und Transformationen des erotisierten Frauenkörpers

Anhand einer qualitativen Bild-Text-Analyse werden erotisierte Frauenbilder innerhalb der Neuen Kronen Zeitung (frühen 1960er bis späten 1970er) untersucht. Mithilfe des Analyseapparates sollen die (Teil-)Stränge dieses über die Massenpresse vermittelten korporalen Diskurses untersucht und mit soziokulturellen und institutionellen Entwicklungen in Verbindung gesetzt werden. Die an die Bild-Text-Einheiten gerichteten Fragen umschließen die Bereiche der Inszenierungsmodalitäten, ihre Kontexte und Ursachen. Die erste Hälfte der 1960er Jahre zeichnet sich durch eine Heterogenität des Bild-materials bei einer gleichzeitig geringen Zahl an Publikationen aus. Auch sind die Bilder Aufgrund der gesellschaftlichen Situation wenig explizit. Ab Mitte der 1960er beginnt eine quantitative Ausdehnung der publizierten Bilder die von inszenatorischen Neuerungen begleitet wird. Man versucht durch textuelle und inszenatorische Kompensation ein Plus an Erotik und Nacktheit‘ zu erzeugen. Es galt in dieser Zeit einen bildpolitischen Kompromiss zu finden, der den Rezipientenkreis weder degoutieren noch langweilen durfte. Die Publikationspraxis der zweiten Hälfte der 1970er Jahre unterscheidet sich in der Visualisierung des Brustwarzenbereiches. Dass die NKZ-Redaktion nun auch barbusige Frauenfotografien veröffentlichte, ist wohl in erster Linie den geänderten gesellschaftlichen Rahmen¬be¬dingungen und damit der (marktstrategischen) ‚Notwendigkeit‘ geschuldet. Die inszenatorischen ‚Finessen‘ der Bild-Text-Einheiten verlieren jedoch zusehends an Bedeutung. Dieser Wandel kann auf zwei Ursachen zurückgeführt werden: Einerseits ist die topless-nudity genug ‚sexuelle Attraktion‘, weshalb man auf aufwändigere Strategien der Erotisierung verzichten konnte, andererseits kommt es zu einem grundlegenden Wandel in der der Bild-Text-Produktion, die sich durch Standardisierung und Konzentration auszeichnet

Health professionals' views on maternity care for women with physical disabilities: a qualitative study

Background: During pregnancy, childbirth and puerperium, women receive care from a range of health professionals, particularly midwives. To assess the current situation of maternity care for women with physical disabilities in Austria, this study investigated the perceptions and experiences of health professionals who have provided care for women with disabilities during pregnancy, childbirth and postpartum. Methods: The viewpoints of the participating health professionals were evaluated by means of semistructured interviews followed by an inductive qualitative content analysis of the interview transcripts, as proposed by Mayring. Results: Four main categories emerged from the inductive content analysis: (i) structural conditions and accessibility, (ii) interprofessional teamwork and cooperation, (iii) action competence, and (iv) diversity-sensitive attitudes. According to the participating health professionals, the structural conditions were frequently not suitable for providing targeted group-oriented care services. Additionally, a shortage of time and staff resources also limited the necessary flexibility of treatment measures in the care of mothers with physical disabilities. The importance of interprofessional teamwork for providing adequate care was highlighted. The health professionals regarded interprofessionalism as an instrument of quality assurance and team meetings as an elementary component of high-quality care. On the other hand, the interviewees perceived a lack of action competence that was attributed to a low number of cases and a corresponding lack of experience and routine. Regarding diversity-sensitive attitudes, it became apparent that the topic of mothers with physical disabilities in care posed challenges to health professionals that influenced their natural handling of the interactions. Conclusion: The awareness of one’s own attitudes towards diversity, in the perinatal context in particular, influences professional security and sovereignty as well as the quality of care of women with disabilities. There is a need for optimization in the support and care of women with physical disabilities during pregnancy, childbirth and puerperium

PAGE4 Positivity Is Associated with Attenuated AR Signaling and Predicts Patient Survival in Hormone-Naive Prostate Cancer

Aberrant activation of the androgen receptor (AR) plays a key role during prostate cancer (PCa) development and progression to castration-resistant prostate cancer (CR-PCa) after androgen deprivation therapy, the mainstay systemic treatment for PCa. New strategies to abrogate AR activity and biomarkers that predict aggressive tumor behavior are essential for improved therapeutic intervention. PCa tissue microarrays herein reveal that prostate-associated gene 4 (PAGE4), an X-linked cancer/testis antigen, is highly up-regulated in the epithelium of preneoplastic lesions compared with benign epithelium, but subsequently decreases with tumor progression. We show that AR signaling is attenuated in PAGE4-expressing cells both in vitro and in vivo, most likely via impaired androgen-induced AR nuclear translocation and subsequently reduced AR protein stabilization and phosphorylation at serines 81 and 213. Consistently, epithelial PAGE4 protein levels inversely correlated with AR activation status in hormone-naive and CR-PCa clinical specimens. Moreover, PAGE4 impaired the development of CR-PCa xenografts, and strong PAGE4 immunoreactivity independently predicted favorable patient survival in hormone-naive PCa. Collectively, these data suggest that dysregulation of epithelial PAGE4 modulates AR signaling, thereby promoting progression to advanced lethal PCa and highlight the potential value of PAGE4 as a prognostic and therapeutic target

Elevated levels of Dickkopf-related protein 3 in seminal plasma of prostate cancer patients

<p>Abstract</p> <p>Background</p> <p>Expression of Dkk-3, a secreted putative tumor suppressor, is altered in age-related proliferative disorders of the human prostate. We now investigated the suitability of Dkk-3 as a diagnostic biomarker for prostate cancer (PCa) in seminal plasma (SP).</p> <p>Methods</p> <p>SP samples were obtained from 81 patients prior to TRUS-guided prostate biopsies on the basis of elevated serum prostate-specific antigen (PSA; > 4 ng/mL) levels and/or abnormal digital rectal examination. A sensitive indirect immunoenzymometric assay for Dkk-3 was developed and characterized in detail. SP Dkk-3 and PSA levels were determined and normalized to total SP protein. The diagnostic accuracies of single markers including serum PSA and multivariate models to discriminate patients with positive (N = 40) and negative (N = 41) biopsy findings were investigated.</p> <p>Results</p> <p>Biopsy-confirmed PCa showed significantly higher SP Dkk-3 levels (100.9 ± 12.3 vs. 69.2 ± 9.4 fmol/mg; <it>p </it>= 0.026). Diagnostic accuracy (AUC) of SP Dkk-3 levels (0.633) was enhanced in multivariate models by including serum PSA (model A; AUC 0.658) or both, serum and SP PSA levels (model B; AUC 0.710). In a subpopulation with clinical follow-up > 3 years post-biopsy to ensure veracity of negative biopsy status (positive biopsy N = 21; negative biopsy N = 25) AUCs for SP Dkk-3, model A and B increased to 0.667, 0.724 and 0.777, respectively.</p> <p>Conclusions</p> <p>In multivariate models to detect PCa, inclusion of SP Dkk-3 levels, which were significantly elevated in biopsy-confirmed PCa patients, improved the diagnostic performance compared with serum PSA only.</p

Toxicity of oxidized phospholipids in cultured macrophages

Background: The interactions of oxidized low-density lipoprotein (LDL) and macrophages are hallmarks in the development of atherosclerosis. The biological activities of the modified particle in these cells are due to the content of lipid oxidation products and apolipoprotein modification by oxidized phospholipids. Results: It was the aim of this study to determine the role of short-chain oxidized phospholipids as components of modified LDL in cultured macrophages. For this purpose we investigated the effects of the following oxidized phospholipids on cell viability and apoptosis: 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine (PGPC), 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) and oxidized alkylacyl phospholipids including 1-O-hexadecyl-2-glutaroyl-sn-glycero-3-phosphocholine (E-PGPC) and 1-O-hexadecyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (E-POVPC). We found that these compounds induced apoptosis in RAW264.7 and bone marrow-derived macrophages. The sn-2 carboxyacyl lipid PGPC was more toxic than POVPC which carries a reactive aldehyde function in position sn-2 of glycerol. The alkylacyl phospholipids (E-PGPC and E-POVPC) and the respective diacyl analogs show similar activities. Apoptosis induced by POVPC and its alkylether derivative could be causally linked to the fast activation of an acid sphingomyelinase, generating the apoptotic second messenger ceramide. In contrast, PGPC and its ether analog only negligibly affected this enzyme pointing to an entirely different mechanism of lipid toxicity. The higher toxicity of PGPC is underscored by more efficient membrane blebbing from apoptotic cells. In addition, the protein pattern of PGPC-induced microparticles is different from the vesicles generated by POPVC. Conclusions: In summary, our data reveal that oxidized phospholipids induce apoptosis in cultured macrophages. The mechanism of lipid toxicity, however, largely depends on the structural features of the oxidized sn-2 chain

Protective effect of stromal Dickkopf-3 in prostate cancer: opposing roles for TGFBI and ECM-1

Aberrant transforming growth factor–β (TGF-β) signaling is a hallmark of the stromal microenvironment in cancer. Dickkopf-3 (Dkk-3), shown to inhibit TGF-β signaling, is downregulated in prostate cancer and upregulated in the stroma in benign prostatic hyperplasia, but the function of stromal Dkk-3 is unclear. Here we show that DKK3 silencing in WPMY-1 prostate stromal cells increases TGF-β signaling activity and that stromal cellconditioned media inhibit prostate cancer cell invasion in a Dkk-3-dependent manner. DKK3 silencing increased the level of the cell-adhesion regulator TGF-β–induced protein (TGFBI) in stromal and epithelial cell-conditioned media, and recombinant TGFBI increased prostate cancer cell invasion. Reduced expression of Dkk-3 in patient tumors was associated with increased expression of TGFBI. DKK3 silencing reduced the level of extracellular matrix protein-1 (ECM-1) in prostate stromal cell-conditioned media but increased it in epithelial cell-conditioned media, and recombinant ECM-1 inhibited TGFBI-induced prostate cancer cell invasion. Increased ECM1 and DKK3 mRNA expression in prostate tumors was associated with increased relapse-free survival. These observations are consistent with a model in which the loss of Dkk-3 in prostate cancer leads to increased secretion of TGFBI and ECM-1, which have tumor-promoting and tumor-protective roles, respectively. Determining how the balance between the opposing roles of extracellular factors influences prostate carcinogenesis will be key to developing therapies that target the tumor microenvironment

Sildenafil, a Phosphodiesterase Type 5 Inhibitor, augments sphincter bursting and bladder afferent activity to enhance storage function and voiding efficiency in mice

OBJECTIVES: To investigate the influence of low dose phosphodiesterase type 5 inhibitors (PDE5-I) on the function of the mouse lower urinary tract (LUT).MATERIALS AND METHODS: Adult male mice were decerebrated and arterially-perfused with a carbogenated Ringer’s solution to establish the decerebrate arterially-perfused mouse (DAPM). To allow distinction between central neural and peripheral actions of sildenafil, experiments were conducted in both the DAPM and in a ’pithed’ DAPM which has no functional brainstem or spinal cord. The action of systemic and intrathecal sildenafil on micturition was assessed in urethane-anaesthetised mice.RESULTS: In the DAPM, systemic perfusion of sildenafil (30pM) decreased the voiding threshold pressure (to 84.7 ± 3.8% of control) and increased bladder compliance (to 140.2 ± 8.3% of control, an effect replicated in the pithed DAPM). Sildenafil was without effect on most voiding parameters but significantly increased the number of bursts of external urethral sphincter per void in DAPM (to 130.1 ± 6.9% of control at 30pM) and in urethane-anaesthetised mice (to 117.5 ± 5.8% of control at 14ng/kg). Sildenafil (10 and 30 pM) increased pelvic afferent activity during both bladder filling and the isovolumetric phase (to 205.4 ± 30.2% of control at 30pM). Intrathecal application of sildenafil (5μl of either 150pM or 1.5nM) did not alter cystometry and EUS-EMG parameters in urethane-anaesthetised mice.CONCLUSIONS: Low dose sildenafil increases bladder compliance, increases pelvic nerve afferent activity and augments the bursting activity of the external urethral sphincter. We propose that the novel actions on afferent traffic and sphincter control may contribute to its beneficial actions to restore storage and voiding efficiency in LUT dysfunction. This article is protected by copyright. All rights reserved

Proteomic identification of prognostic tumour biomarkers, using chemotherapy-induced cancer-associated fibroblasts

Cancer cells grow in highly complex stromal microenvironments, which through metabolic remodelling, catabolism, autophagy and inflammation nurture them and are able to facilitate metastasis and resistance to therapy. However, these changes in the metabolic profile of stromal cancer-associated fibroblasts and their impact on cancer initiation, progression and metastasis are not well-known. This is the first study to provide a comprehensive proteomic portrait of the azathioprine and taxol-induced catabolic state on human stromal fibroblasts, which comprises changes in the expression of metabolic enzymes, myofibroblastic differentiation markers, antioxidants, proteins involved in autophagy, senescence, vesicle trafficking and protein degradation, and inducers of inflammation. Interestingly, many of these features are major contributors to the aging process. A catabolic stroma signature, generated with proteins found differentially up-regulated in taxol-treated fibroblasts, strikingly correlates with recurrence, metastasis and poor patient survival in several solid malignancies. We therefore suggest the inhibition of the catabolic state in healthy cells as a novel approach to improve current chemotherapy efficacies and possibly avoid future carcinogenic processes