178,550 research outputs found
Consent of the injured party to harm
No full textNačelo volenti non fit injuria poznamo že iz časa rimskega prava, v slovenskem pravnem redu pa je kodificirano v 140. členu OZ oziroma v institutu privolitve oškodovanca v škodo. Oškodovančeva privolitev izključuje protipravnost ravnanja in povzročene škode, posledično pa tudi odškodninsko odgovornost povzročitelja škode. Kljub temu da gre za institut, ki ima razmeroma dolgo pravno zgodovino, v slovenskem pravnem prostoru še ni zadostno raziskan. Magistrsko delo se osredotoča na prikaz geneze izvora načela volenti non fit injuria oziroma instituta privolitve oškodovanca v škodo in na njegovo umestitev v slovenski pravni sistem. Avtor analizira pravno naravo instituta privolitev oškodovanca v škodo in na tej podlagi prikaže, na kakšen način privolitev oškodovanca izključi protipravnost ravnanja in povzročene škode. Nadalje avtor analizira predpostavke, ki morajo biti izpolnjene, da privolitvi oškodovanca pripišemo pravno veljavnost in predstavi relevantna stališča obstoječe slovenske pravne teorije. Predstavljeni so tudi razlikovalni kriteriji, ki institut privolitve oškodovanca v škodo ločujejo od instituta ravnanja na lastno odgovornost, končno pa avtor poskuša začrtati tudi vsebinske meje pravno priznane privolitve oškodovanca v škodo.The principle of volenti non fit injuria has been known since the time of Roman law, and in the Slovenian legal system, it is codified in Article 140 of the Obligations Code, which deals with the institute of the injured party\u27s consent to harm. The injured party\u27s consent excludes the illegality of the act and the resulting damage, and consequently, the liability for damages of the perpetrator. Although this principle has a relatively long legal history, it has not been sufficiently researched in the Slovenian legal space.
This master\u27s thesis focuses on presenting the genesis of the principle of volenti non fit injuria or the institute of the injured party\u27s consent to harm and its placement with-in the Slovenian legal system. The author analyses the legal nature of the institute of the injured party\u27s consent to harm and on this basis, demonstrates how the injured party\u27s consent excludes the illegality of the act and the resulting damage. Further-more, the author analyses the prerequisites that must be met for the injured party\u27s consent to be legally valid and presents relevant viewpoints of existing Slovenian le-gal theory. The distinguishing criteria that separate the institute of the injured party\u27s consent to harm from the institute of acting at one\u27s own risk are also presented. Finally, the author attempts to delineate the substantive boundaries of legally recognized consent to harm
Rokitansky-Kuster-Hauser syndrome with ectrodactyly
No full textThis paper describes an 18-year-old patient with Rokitansky-Kuster-Hauser (R-K-H) syndrome. In this case, apart from the usual alterations associated with the R-K-H syndrome, such as aplasia of the Mullerian ducts, renal agenesis, ectopic kidney and anomalies of vertebral column, ribs and hips, rare skeletal, unilateral abnormalities of the left hand and foot were present, such as ectrodactyly. This malformation, seen in prepubertal age, had led to an incorrect diagnosis of acrorenal syndrome
Beratung nutzen zur Schulentwicklung
No full textFaix A-C, Kuster R, Anderegg N, eds. Beratung nutzen zur Schulentwicklung. Lernende Schule. Vol 104. Hannover: Friedrich Verlag; 2023
Training in coordinate metrology - experiences with a blended learning approach
No full textW1.1. - ID13
NADPH oxidase (NOX) in the heart : the interplay of NOX-derived ROS in β1-integrin-induced survival signalling
No full textModerate levels of reactive oxygen species (ROS) act as mediators in cellular signalling processes. An important source of cardiac ROS is the highly expressed NADPH oxidase (NOX) family isoform NOX2. However, little is known about whether NOX-derived ROS are protective in the heart.
In this study we show that CD29 (β1-integrin), a cell adhesion receptor highly expressed on cardiac muscle cells, induces NOX-dependent ROS. CD29 is known to be mandatory in cell growth and survival, and non-functional CD29 causes severe heart disease. We demonstrate that NOX2-derived ROS are essential for CD29-induced survival signalling, including the PI3K/PKB and MEK/ERK pathways. Furthermore, CD29-induced NOX-derived ROS are indispensible in the inhibition of the pro-apoptotic kinase GSK-3β, which we uncovered as a downstream target of both the ERK and PKB survival pathways in cardiac muscle cells. These findings clearly add to the growing body of evidence suggesting that moderate ROS levels are beneficial to the cell and highlight the crucial role of NOX2-derived ROS for cell survival in the heart
Appropriate Similarity Measures for Author Cocitation Analysis
No full textWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
SHOX duplications found in some cases with type I Mayer-Rokitansky-Kuster-Hauser syndrome
No full textPurpose: The Mayer-Rokitansky-Kuster-Hauser syndrome is defined as congenital aplasia of mullerian ducts derived structures in females with a normal female chromosomal and gonadal sex. Most cases with Mayer-Rokitansky-Kuster-Hauser syndrome are sporadic, although familial cases have been reported. The genetic basis of Mayer-Rokitansky-Kuster-Hauser syndrome is largely unknown and seems heterogeneous, and a small number of cases were found to have mutations in the WNT4 gene. The aim of this study was to identify possible recurrent submicroscopic imbalances in a cohort of familial and sporadic cases with Mayer-Rokitansky-Kuster-Hauser syndrome. Methods: Multiplex ligation-dependent probe amplification was used to screen the subtelomeric sequences of all chromosomes in 30 patients with Mayer-Rokitansky-Kuster-Hauser syndrome (sporadic, n = 27 and familial, n = 3). Segregation analysis and pyrosequencing were applied to validate the MLPA results in the informative family. Results: Partial duplication of the Xpter pseudoautosomal region 1 containing the short stature homeobox (SHOX) gene was detected in five patients with Mayer-Rokitansky-Kuster-Hauser syndrome (familial, n = 3 and sporadic, n = 2) and not in 53 healthy controls. The duplications were not overlapping, and SHOX was never entirely duplicated. Haplotyping in the informative family revealed that SHOX gene duplication was inherited from the unaffected father and was absent in two healthy sisters. Conclusions: Partial duplication of SHOX gene is found in some cases with both familial and sporadic Mayer-Rokitansky-Kuster-Hauser type I syndrome
"Closing the R&D Gap, Evaluating the Sources of R&D Spending"
No full textBoth spending and tax policies have been implemented in the United States with the goal of stimulating private sector research and development (R&D). Karier questions whether current R&D policy, especially the research and experimentation tax credit, can contribute to closing the gap between nondefense expenditures on R&D in the United States and such expenditures in other countries, such as Japan and Germany. He also explores possible changes to our current R&D policy to make it more effective.
Mayer-Rokitansky-Kuster-Hauser syndrome associated with pulmonary stenosis
No full textTwo siblings with Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome associated with pulmonary valvular stenosis are reported. Although the syndrome is well documented, the genetic background and familial occurrence is not known and the association with cardiac anomalies has not previously been reported. This report is the first report which describes the combination of cardiac anomaly with MRKH syndrome
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