University of Vienna

About: University of Vienna is a education organization based out in Vienna, Austria. It is known for research contribution in the topics: Population & Stars. The organization has 44686 authors who have published 95840 publications receiving 2907492 citations.

Risk factors for chronic thromboembolic pulmonary hypertension

Abstract: Traditional concepts of the pathogenesis of chronic thromboembolic pulmonary hypertension (CTEPH) invoke a thromboembolic origin. However, neither classic plasmatic risk factors for venous thromboembolism nor defects in fibrinolysis are associated with CTEPH. These observations have lent support to the concept of alternative nonthromboembolic pathogenetic grounds for CTEPH. Compared with the general population, no increased prevalence of the factor V Leiden mutation was found. Other hereditary thrombotic risk factors, such as deficiencies in antithrombin, protein C, protein S, and the prothrombin gene mutation, lack an association with CTEPH. Efforts to identify functional defects or genetic polymorphisms in the pulmonary vascular fibrinolytic system of affected individuals have failed. Alterations in plasma levels of neither type 1 plasminogen activator inhibitor nor tissue-type plasminogen activator could be linked with CTEPH development. However, conditions that account for both venous and arterial thrombosis, such as antiphospholipid antibodies, malignancies, infection, elevated plasma lipoprotein levels, and hormone treatment providing a pathophysiological link between arterial and venous thrombosis, have recently appeared as risk factors for CTEPH. Growing knowledge of these conditions has a significant impact on clinical routine. The identification of conditions predisposing to CTEPH development may provide important clues to disease pathology. In this chapter, risk factors are categorized by odds ratios (ORs) as they appear in case-control or cohort studies, and are discussed in the order of the strength of the statistical relationship to a control cohort. According to our own data the ORs did not change significantly irrespective of whether patients with pulmonary hypertension, normal age-matched controls, or patients with pulmonary emboli who did not develop CTEPH were considered as the controls.

E-cadherin regulates cell growth by modulating proliferation-dependent β-catenin transcriptional activity

Abstract: β-Catenin is essential for E-cadherin–mediated cell adhesion in epithelial cells, but it also forms nuclear complexes with high mobility group transcription factors. Using a mouse mammary epithelial cell system, we have shown previously that conversion of epithelial cells to a fibroblastoid phenotype (epithelial-mesenchymal transition) involves downregulation of E-cadherin and upregulation of β-catenin transcriptional activity. Here, we demonstrate that transient expression of exogenous E-cadherin in both epithelial and fibroblastoid cells arrested cell growth or caused apoptosis, depending on the cellular E-cadherin levels. By expressing E-cadherin subdomains, we show that the growth-suppressive effect of E-cadherin required the presence of its cytoplasmic β-catenin interaction domain and/or correlated strictly with the ability to negatively interfere with β-catenin transcriptional activity. Furthermore, coexpression of β-catenin or lymphoid enhancer binding factor-1 or T cell factor 3 with E-cadherin rescued β-catenin transcriptional activity and counteracted E-cadherin–mediated cell cycle arrest. Stable expression of E-cadherin in fibroblastoid cells decreased β-catenin activity and reduced cell growth. Since proliferating cells had a higher β-catenin activity than G1 phase–arrested or contact-inhibited cells, we conclude that β-catenin transcriptional activity is essential for cell proliferation and can be controlled by E-cadherin in a cell adhesion-independent manner.

Progress and Challenges in the Calculation of Electronic Excited States

Abstract: A detailed understanding of the properties of electronic excited states and the reaction mechanisms that molecules undergo after light irradiation is a fundamental ingredient for following light-driven natural processes and for designing novel photonic materials. The aim of this review is to present an overview of the ab initio quantum chemical and time-dependent density functional theory methods that can be used to model spectroscopy and photochemistry in molecular systems. The applicability and limitations of the different methods as well as the main frontiers are discussed. To illustrate the progress achieved by excited-state chemistry in the recent years as well as the main challenges facing computational chemistry, three main applications that reflect the authors' experience are addressed: the UV/Vis spectroscopy of organic molecules, the assignment of absorption and emission bands of organometallic complexes, and finally, the obtainment of non-adiabatic photoinduced pathways mediated by conical intersections. In the latter case, special emphasis is put on the photochemistry of DNA. These applications show that the description of electronically excited states is a rewarding but challenging area of research.

High-Glucose–Triggered Apoptosis in Cultured Endothelial Cells

Abstract: High ambient glucose concentration, linked to vascular complications in diabetes in vivo, modulates mRNA expression of fibronectin, collagen, tissue-type plasminogen activator, and plasminogen activator inhibitor and induces delayed replication and excess cell death in cultured vascular endothelial cells. To determine the role of high ambient glucose (30 mmol/l) in apoptosis, paired cultures of individual isolates of human umbilical vein endothelial cells (HUVECs) were exposed to both high (30 mmol/l) and low (5 mmol/l) concentrations of glucose for short-term (24, 48, and 72 h) and long-term (13 +/- 1 days) experiments. Incubation of HUVECs with high glucose for > 48 h increased DNA fragmentation (13.7 +/- 6.5% of total DNA, mean +/- SD) versus cultures kept in 5 mmol/l glucose (10.9 +/- 5.6%, P < 0.005), as measured by [3H]thymidine assays. Data were confirmed by apoptosis-specific fluorescence-activated cell sorter analysis of confluent HUVEC cultures, which displayed after long-term exposure to 30 mmol/l glucose a 1.5-fold higher prevalence of apoptosis than control cultures exposed to 5 mmol/l glucose (P < 0.005). In contrast, no increase in DNA fragmentation in response to 30 mmol/l glucose was seen for standardized cell lines (K 562, P 815, YT) and fibroblasts. Expression of clusterin mRNA, originally reported to be a molecular marker of apoptosis, was only slightly affected by short-term (24-h) high-glucose exposure but was significantly reduced after long-term incubation in 30 mmol/l glucose (82.2 +/- 13.8% of control) versus 5 mmol/l glucose, which questions the role of clusterin gene expression as a marker of apoptosis.(ABSTRACT TRUNCATED AT 250 WORDS)