Søren Kierkegaard - den nye udgave

I februar 2013 afsluttedes den hidtil største – og eneste – samlede, kommenterede udgave af Søren Kierkegaards (1813-1855) trykte og utrykte skrifter, journaler, notesbøger og løse papirer samt breve og dedikationer efter 18 års arbejde i det til formålet af Danmarks Grundforskningsfond i 1994 oprettede Søren Kierkegaard Forskningscenter (SKC), ledet af direktør og dr.theol. Niels Jørgen Cappelørn, der i 2010 blev kaldet til et professorat i Kierkegaard-studier samtidig med, at Forskningscenteret blev indlejret i Det Teologiske Fakultet under Københavns Universitet. I 1999 oprettedes Fonden for Søren Kierkegaard Forskningscenteret, der har været forestået af en bestyrelse,1 udpeget af  Grundforskningsfonden, hvori dekanen for Københavns Universitets Teologiske Fakultet og direktørerne for Det Kongelige Bibliotek og Det Danske Sprog- og Litteraturselskab har været udpeget. På Søren Kierkegaards 200 års fødselsdag d. 5. maj afsluttedes Fondens virke med en overdragelse af den trykte udgave af Søren Kierkegaards Skrifter (kaldet SKS-B), der i 55 bind udkom på Gads Forlag 1997-2013, og rettighederne til den til Københavns Universitet og af den elektroniske (kaldet SKS-E), se <sks. dk>, til Det Kongelige Bibliotek. Ved overrækkelsen i Universitetets festsal holdt bestyrelsens formand Ida Nicolaisen nedenstående overrækkelsestale, der skildrer arbejdet i historisk og nutidigt perspektiv.I februar 2013 afsluttedes den hidtil største – og eneste – samlede, kommenterede udgave af Søren Kierkegaards (1813-1855) trykte og utrykte skrifter, journaler, notesbøger og løse papirer samt breve og dedikationer efter 18 års arbejde i det til formålet af Danmarks Grundforskningsfond i 1994 oprettede Søren Kierkegaard Forskningscenter (SKC), ledet af direktør og dr.theol. Niels Jørgen Cappelørn, der i 2010 blev kaldet til et professorat i Kierkegaard-studier samtidig med, at Forskningscenteret blev indlejret i Det Teologiske Fakultet under Københavns Universitet. I 1999 oprettedes Fonden for Søren Kierkegaard Forskningscenteret, der har været forestået af en bestyrelse,1 udpeget af  Grundforskningsfonden, hvori dekanen for Københavns Universitets Teologiske Fakultet og direktørerne for Det Kongelige Bibliotek og Det Danske Sprog- og Litteraturselskab har været udpeget. På Søren Kierkegaards 200 års fødselsdag d. 5. maj afsluttedes Fondens virke med en overdragelse af den trykte udgave af Søren Kierkegaards Skrifter (kaldet SKS-B), der i 55 bind udkom på Gads Forlag 1997-2013, og rettighederne til den til Københavns Universitet og af den elektroniske (kaldet SKS-E), se <sks. dk>, til Det Kongelige Bibliotek. Ved overrækkelsen i Universitetets festsal holdt bestyrelsens formand Ida Nicolaisen nedenstående overrækkelsestale, der skildrer arbejdet i historisk og nutidigt perspektiv

Quantum-informed plasmonics for strong coupling: the role of electron spill-out

The effect of nonlocality on the optical response of metals lies at the forefront of research in nanoscale physics and, in particular, quantum plasmonics. In alkali metals, nonlocality manifests predominantly as electron density spill-out at the metal boundary, and as surface-enabled Landau damping. For an accurate description of plasmonic modes, these effects need be taken into account in the theoretical modelling of the material. The resulting modal frequency shifts and broadening become particularly relevant when dealing with the strong interaction between plasmons and excitons, where hybrid modes emerge and the way they are affected can reflect modifications of the coupling strength. Both nonlocal phenomena can be incorporated in the classical local theory by applying a surface-response formalism embodied by the Feibelman parameters. Here, we implement surface-response corrections in Mie theory to study the optical response of spherical plasmonic--excitonic composites in core--shell configurations. We investigate sodium, a jellium metal dominated by spill-out, for which it has been anticipated that nonlocal corrections should lead to an observable change in the coupling strength, appearing as a modification of the width of the mode splitting. We show that, contrary to expectations, the influence of nonlocality on the anticrossing is minimal, thus validating the accuracy of the local response approximation in strong-coupling photonics

Clinical interpretation of cell-based non-invasive prenatal testing for monogenic disorders including repeat expansion disorders:potentials and pitfalls

Introduction: Circulating fetal cells isolated from maternal blood can be used for prenatal testing, representing a safe alternative to invasive testing. The present study investigated the potential of cell-based noninvasive prenatal testing (NIPT) for diagnosing monogenic disorders dependent on the mode of inheritance. Methods: Maternal blood samples were collected from women opting for prenatal diagnostics for specific monogenic disorders (N = 7). Fetal trophoblasts were enriched and stained using magnetic activated cell sorting and isolated by fluorescens activated single-cell sorting. Individual cells were subject to whole genome amplification, and cells of fetal origin were identified by DNA-profiling using short tandem repeat markers. The amplified fetal DNA was input for genetic testing for autosomal dominant-, autosomal recessive-, X-linked and repeat expansion disorders by direct variant analysis and haplotyping. The cell-based NIPT results were compared with those of invasive testing. Results: In two cases at risk of skeletal dysplasia, caused by variants in the FGFR3 gene (autosomal dominant disorders), cell-based NIPT correctly stated an affected fetus, but allelic dropout of the normal alleles were observed in both cases. Cell-based NIPT gave an accurate result in two cases at risk of autosomal recessive disorders, where the parents carried either different diastrophic dysplasia causing variants in the SLC26A2 gene or the same cystic fibrosis disease-causing variant in the CFTR gene. Cell-based NIPT accurately identified an affected male fetus in a pregnancy at risk of Duchenne muscular dystrophy (DMD gene, X-linked recessive disorders). In two cases at risk of the myotonic dystrophy type 1 (DMPK gene, repeat expansion disorder), cell-based NIPT correctly detected an affected and an unaffected fetus, respectively. Discussion: Circulating fetal cells can be used to detect both maternally- and paternally inherited monogenic disorders irrespective of the type of variant, however, the risk of allelic dropout must be considered. We conclude that the clinical interpretation of the cell-based NIPT result thus varies depending on the disorders' mode of inheritance.</p

Performance evaluation of reverse osmosis (RO) pre-treatment technologies for in-land brackish water treatment

Integration of renewable energy with desalination technologies has emerged as an attractive solution to augment fresh water supply sustainably. Fouling and scaling are still considered as limiting factors in membrane desalination processes. For brackish water treatment, pre-treatment of reverse osmosis (RO) feed water is a key step in designing RO plants avoiding membrane fouling. This study aims to compare at pilot scale the rejection efficiency of RO membranes with multiple pre-treatment options at different water recoveries (30, 35, 40, 45 and 50%) and TDS concentrations (3500, 4000, and 4500mg/L). Synthetic brackish water was prepared and performance evaluation were carried out using brackish water reverse osmosis (BWRO) membranes (Filmtec LC-LE-4040 and Hydranautics CPA5-LD-4040) preceded by 5 and 1μm cartridge filters, 0.02μm ultra-filtration (UF) membrane, and forward osmosis (FO) membrane using 0.25M NaCl and MgCl2 as draw solutions (DS). It was revealed that FO membrane with 0.25M MgCl2 used as a draw solution (DS) and Ultra-filtration (UF) membrane followed by Filmtec membrane gave overall 98% rejection but UF facing high fouling potential due to high applied pressure. Use of 5 and 1μm cartridge filter prior to Filmtec membrane also showed effective results with 95% salt rejection

Cell-based non-invasive prenatal testing for monogenic disorders:confirmation of unaffected fetuses following preimplantation genetic testing

PURPOSE: Proof of concept of the use of cell-based non-invasive prenatal testing (cbNIPT) as an alternative to chorionic villus sampling (CVS) following preimplantation genetic testing for monogenic disorders (PGT-M). METHOD: PGT-M was performed by combined testing of short tandem repeat (STR) markers and direct mutation detection, followed by transfer of an unaffected embryo. Patients who opted for follow-up of PGT-M by CVS had blood sampled, from which potential fetal extravillous throphoblast cells were isolated. The cell origin and mutational status were determined by combined testing of STR markers and direct mutation detection using the same setup as during PGT. The cbNIPT results with respect to the mutational status were compared to those of genetic testing of the CVS. RESULTS: Eight patients had blood collected between gestational weeks 10 and 13, from which 33 potential fetal cell samples were isolated. Twenty-seven out of 33 isolated cell samples were successfully tested (82%), of which 24 were of fetal origin (89%). This corresponds to a median of 2.5 successfully tested fetal cell samples per case (range 1–6). All fetal cell samples had a genetic profile identical to that of the transferred embryo confirming a pregnancy with an unaffected fetus, in accordance with the CVS results. CONCLUSION: These findings show that although measures are needed to enhance the test success rate and the number of cells identified, cbNIPT is a promising alternative to CVS. TRIAL REGISTRATION NUMBER: N-20180001 SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10815-021-02104-5

Clinical interpretation of cell-based non-invasive prenatal testing for monogenic disorders including repeat expansion disorders: potentials and pitfalls

Introduction: Circulating fetal cells isolated from maternal blood can be used for prenatal testing, representing a safe alternative to invasive testing. The present study investigated the potential of cell-based noninvasive prenatal testing (NIPT) for diagnosing monogenic disorders dependent on the mode of inheritance.Methods: Maternal blood samples were collected from women opting for prenatal diagnostics for specific monogenic disorders (N = 7). Fetal trophoblasts were enriched and stained using magnetic activated cell sorting and isolated by fluorescens activated single-cell sorting. Individual cells were subject to whole genome amplification, and cells of fetal origin were identified by DNA-profiling using short tandem repeat markers. The amplified fetal DNA was input for genetic testing for autosomal dominant-, autosomal recessive-, X-linked and repeat expansion disorders by direct variant analysis and haplotyping. The cell-based NIPT results were compared with those of invasive testing.Results: In two cases at risk of skeletal dysplasia, caused by variants in the FGFR3 gene (autosomal dominant disorders), cell-based NIPT correctly stated an affected fetus, but allelic dropout of the normal alleles were observed in both cases. Cell-based NIPT gave an accurate result in two cases at risk of autosomal recessive disorders, where the parents carried either different diastrophic dysplasia causing variants in the SLC26A2 gene or the same cystic fibrosis disease-causing variant in the CFTR gene. Cell-based NIPT accurately identified an affected male fetus in a pregnancy at risk of Duchenne muscular dystrophy (DMD gene, X-linked recessive disorders). In two cases at risk of the myotonic dystrophy type 1 (DMPK gene, repeat expansion disorder), cell-based NIPT correctly detected an affected and an unaffected fetus, respectively.Discussion: Circulating fetal cells can be used to detect both maternally- and paternally inherited monogenic disorders irrespective of the type of variant, however, the risk of allelic dropout must be considered. We conclude that the clinical interpretation of the cell-based NIPT result thus varies depending on the disorders’ mode of inheritance