Responses of Black Nightshade (Solanum nigrum) to insect herbivory with a special focus on the 18-amino acid polypeptide systemin

To minimize the fitness-imperiling stress caused by phytophageous insects, plants have evolved many defensive adaptations. These plant defenses against herbivory are generally categorized as either tolerance or resistance. Tolerance traits reduce the detrimental effects of herbivore damage on plant fitness without affecting the herbivore. In contrast, resistance traits either directly or indirectly reduce the amount of damage a plant receives by repelling potential herbivores or impairing their performance. While tolerance mechanisms in plants remain nearly uncharacterized on the molecular level, the signal pathways leading to herbivore resistance have been extensively studied. As plants areellknown to show resistance responses to herbivory in not only locally attacked but also distal, undamaged leaves, the signals mediating these so-called systemic responses have received extensive attention. Among the signals proposed to be capable of transmitting information about herbivore attack from the site of wounding to the rest of the plant is the 18-aa polypeptide systemin. Systemin has long been thought to be the mobile wound signal in tomato (Solanum lycopersicum), but according to the revised model, it plays a central role in tomato’s wound response acting at or near the site of wounding by amplifying the jasmonate-derived mobile wound signal. So far, resistance responses to insect herbivory have been studied mainly in crop plants such as tomato. An important question thus arises: do the above-mentioned findings apply to related but undomesticated species. The present thesis aimed to address this question by studying the defense responses of an undomesticated relative of tomato, black nightshade (Solanum nigrum), in general, and the role of systemin, in particular

The influence of glutathione S-transferases M1 and M3 on the development of bladder cancer

Problem: Cigarette smoking is the most important risk factor of transitional cell carcinoma of the urinary bladder. The effect of the glutathione S- transferases M1 (GSTM1) and M3 (GSTM3) on the influence of this risk factor was investigated. Methods: A total of 293 bladder cancer patients from Dortmund and Wittenberg as well as 176 surgical patients without any malignancy from Dortmund were genotyped for GSTM1 und GSTM3 according to standard PCR/RFLP methods. Smoking habits were also qualified by a standardized interview. Results: The percentage of GSTM1 negative cases was 63 % in the entire bladder cancer patient group compared to 50 % in the control group. GSTM3*A/*A genotype was 76 % in the entire group of bladder cancer cases and 74 % in controls. Smokers and ex-smokers were overrepresented in the bladder cancer patient group. A significant association between smoking status and GSTM1 or GSTM3 genotype could not be revealed. Conclusion: The elevated percentage of GSTM1 negative bladder cancer cases shows the important effect of this polymorphic enzyme on the development of bladder cancer. In contrast to some other studies, an influence of GSTM1 on the risk due to cigarette smoking could not be observed. --Bladder cancer,glutathione S-transferase M1,glutathione S-transferase M3,smoking

Methodik der Generierung und Anwendung wertorientierter Performance-Kennzahlen zur Beurteilung der Entwicklung des Unternehmenswertes von Flughafenunternehmen

It is often contended that there is a sharp conflict between the economists and the ecologists approach to the question of sustainability. This paper takes the opposite view. The paper attempts to show that both views can be formulated in a common analytical framework and that carried to its logical consequences the ecologic approach is a special case of the economic approach. --

Diagnostic errors and reflective practice in medicine

Background: Adverse effects of medical errors have received increasing attention. Diagnostic errors account for a substantial fraction of all medical errors, and strategies for their prevention have been explored. A crucial requirement for that is better understanding of origins of medical errors. Research on medical expertise may contribute to that as far as it explains reasoning processes involved in clinical judgements. The literature has indicated the capability of critically reflecting upon one\'s own practice as a key requirement for developing and maintaining medical expertise throughout life. Objectives: This article explores potential relationships between reflective practice and diagnostic errors. Methods: A survey of the medical expertise literature was canducted. Origins of medical errors frequently reported in the literature were explored. The potential relationship between diagnostic errors and the several dimensions of reflective practice in medicine, brought to light by recent research, were theoretically explored. Results and Dissussion: Uncertainty and fallibility inherent to clinical judgements are discussed. Stages in the diagnostic reasoning process where errors could occur and their potential sources are highlighted, including the role of medical heuristics and biases. The authors discuss the nature of reflective practice in medicine, and explore whether and how the several behaviours and reasoning processes that constitute reflective practice could minimize diagnostic errors. Future directions for further research are discussed. They involve empirical research on the role of reflective practice in improving clinical reasoning and the development of educational strategies to enhancing reflective practice

The role of DNA modifications in pluripotency and differentiation

DNA methylation plays a crucial role in the epigenetic control of gene expression during mammalian development and differentiation. Whereas the de novo DNA methyltransferases (Dnmts), Dnmt3a and Dnmt3b, establish DNA methylation patterns during development; Dnmt1 stably maintains DNA methylation patterns during replication. DNA methylation patterns change dynamically during development and lineage specification, yet very little is known about how DNA methylation affects gene expression profiles upon differentiation. Therefore, we determined genome-wide expression profiles during differentiation of severely hypomethylated embryonic stem cells (ESCs) lacking either the maintenance enzyme Dnmt1 (dnmt1-/- ESCs) or all three major Dnmts (dnmt1-/-; dnmt3a-/-, dnmt3b-/- or TKO ESCs), resulting in complete loss of DNA methylation, and assayed their potential to transit in and out of the ESC state. Our results clearly demonstrate that upon initial differentiation to embryoid bodies (EBs), wild type, dnmt1-/- and TKO cells are able to activate differentiation processes. However, transcription profiles of dnmt1-/- and TKO EBs progressively diverge with prolonged EB culture, with dnmt1-/- EBs being more similar to wild type EBs, indicating a higher differentiation potential of dnmt1-/- EBs compared to TKO EBs. Remarkably though, after dissociation of late EBs and further cultivation under pluripotency promoting conditions, both dnmt1-/- and TKO but not wild type cells rapidly revert to expression profiles typical of undifferentiated ESCs. Thus, while DNA methylation is dispensable for the initial activation of differentiation programs, it seems to be crucial for permanently restricting the developmental fate during differentiation. Based on the essential role of Uhrf1 in maintenance DNA methylation, we investigated the structurally highly similar second member of the Uhrf protein family, Uhrf2, whose function in maintenance methylation or other biological processes is completely unknown. Expression analysis of uhrf1 and uhrf2 in various cell lines and tissues revealed a time- and developmental switch in transcript levels of both genes with uhrf1 being highly expressed in undifferentiated, proliferating cells and uhrf2 being predominately expressed in differentiated, non-dividing cells. These opposite expression patterns together with no detectable effect on DNA methylation levels upon knock down of uhrf2 suggests that Uhrf2 is rather involved in maintaining DNA methylation patterns in differentiated cells and points to non-redundant functions of both proteins. The discovery of the “6th base” of the genome, 5-hydroxymethylcytosine (5hmC), resulting from the oxidation of 5mC by the family of Tet dioxygenases (Tet1-3), once again ignited the debate about how DNA methylation marks can be modified and removed. To gain insights into the biological function of this newly identified modification, we developed a sensitive enzymatic assay for quantification of global 5hmC levels in genomic DNA. Similar to 5mC levels, we found that also 5hmC levels dynamically change during differentiation of ESCs to EBs, which correlates with the differential expression of tet1-3. Furthermore, we characterized a novel endonuclease, PvuRts1I that selectively cleaves 5hmC containing DNA and show first data on its application as a tool to map and analyze 5hmC patterns in mammalian genomes. Finally, we investigated designer transcription activator-like effector (dTALEs) proteins targeting the oct4 locus. Our results show that the epigenetic state of the target locus interferes with the ability of dTALEs to activate transcriptionally silent genes, which however can be overcome using dTALEs in combination with low doses of epigenetic inhibitors. In conclusion, this work gives further insights into the biological roles of methylation mark writers (Dnmts), readers (Uhrfs) and modifiers (Tets) and advances our understanding on the function of DNA methylation in the epigenetic control of gene expression during development and cellular differentiation