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This book explores sex differences in Mobile Instant Messaging through an evolutionary psychological lens, with a particular focus on the use and perception of text and voice messages in same-sex friendships. Not only are these differences examined from an evolutionary standpoint but also smartphones are considered as a product of evolution. By further integrating media psychological theories, Dorothea C. Adler provides an innovative perspective on sex differences in voice and text message use and perception within same-sex friendships. A total of five studies address these aspects both from the sender's as well as receiver's perspective. Altogether, this work not only presents an evolutionary theoretical foundation for understanding sex differences in Mobile Instant Messenger communication among same-sex friends, but also offers an innovative approach for further evolutionary media psychological research.
Die Ausstellung „Fakt – Fake“ der Universitätsbibliothek Würzburg im Herbst 2024 war Anlass, sich mit der wohl bekanntesten Fossilienfälschung des 18. Jahrhunderts, den sogenannten Würzburger Lügensteinen, erneut zu beschäftigen.
Durch die Untersuchung bislang unberücksichtigter zeitgenössischer Quellen – zu den beteiligten Personen und zu den Lebensbedingungen in Eibelstadt, dem „Fundort“ der Steine – gelingt ein differenzierterer Blick auf die Hintergründe der Affäre.
Ein eigenes Kapitel befasst sich mit der Rezeptionsgeschichte. Deren Analyse zeigt, dass zahlreiche Behauptungen, die scheinbar gesichert sind, sich als spätere Zutaten erweisen, die mehr über ihre eigene Entstehungszeit aussagen als über die Vorgänge selbst.
Im Anhang sind die Verhörprotokolle der amtlichen Untersuchung aus dem Jahr 1726, die sich heute im Staatsarchiv Würzburg befinden, abgebildet und transkribiert, womit weitere Forschungen zu diesem Thema erleichtert werden.
Im Rahmen dieser Arbeit wurde der Autor des ersten zahnmedizinischen Lehrbuches in deutscher Sprache, Philipp Pfaff, im Kontext der medizinischen Aufklärung untersucht. Sein Beitrag zum fachlichen Kenntnisstand ist heterogen zu betrachten. Trotzdem entdeckte Pfaff bedeutende zahnmedizinische Behandlungsverfahren, die in leicht abgewandelter Form bis heute von großer Bedeutung sind. Er ließ sich hierbei durch seine Erfahrungen und insbesondere durch misslungene Behandlungen auch aus seinem Umfeld inspirieren und erbrachte hauptsächlich durch die Dokumentation und Veröffentlichung dieses Wissens in deutscher Sprache einen wichtigen Beitrag für die „Aufklärung der Zahnmedizin“. Der Geist der Aufklärung wurde in Pfaffs Werk vor allem durch die Leitbegriffe „Vernunft“, „Erfahrung“ und „Nützlichkeit“ deutlich. Diese zentrale Rolle des Vernunftbegriffs wird allein schon durch die Omnipräsenz der „Vernunft“ in seinem Werk deutlich. Pfaffs Selbstdarstellung entsprach in diesem Punkt dem Leitbild der Aufklärungszeit. Laut seines Werkes sollte die „Erfahrung“ ein wichtiger Leitbegriff für seine medizinische Tätigkeit sein. Vermutlich nutzte er das Argument der „Erfahrung“ standespolitisch, um sich von ungelernten Zahnbehandlern abzugrenzen und um die Bedeutung seiner Berufsgruppe auszudrücken. Um herauszufinden, inwiefern Pfaffs Biografie und sein Werk charakteristisch für die medizinische Aufklärung der nicht akademischen Heilberufe im 18. Jahrhundert war, wurde es mit den ersten deutschsprachigen Lehrbüchern der Geburtshilfe verglichen. Beide Fachbereiche durchliefen bei dem Versuch, die noch jungen Disziplinen zu etablieren, den zunehmenden Prozess der Professionalisierung und benötigten hierbei das Wohlwollen der akademischen Ärzte.
Trypanosoma, a genus of parasitic protists, is responsible for trypanosomiasis, a disease that affects both humans and animals, with a wide impact across 36 countries in sub-Saharan Africa. The transmission of these parasites is intimately linked to their blood-sucking vector, the tsetse fly. Once the tsetse fly takes up trypanosomes during a bloodmeal, the parasites undergo a complex developmental process within the fly's alimentary tract before reaching the fly's salivary glands or mouthparts and differentiating back into a mammalian infective stage. This intricate relationship underscores the importance of understanding the interaction between trypanosomes and tsetse flies in combating the spread of this neglected tropical disease.
Subspecies of Trypanosoma brucei are the main cause of human African trypanosomiasis (HAT) while also playing a large role in animal African trypanosomiasis (AAT). In the mammalian host, T. brucei has two bloodstream forms, the long, proliferative slender form and the short-lived, cell cycle-arrested stumpy form. Slender forms dominate early on in infections and differentiate into stumpy forms in a density-dependent manner. The dogma of the past two decades suggested that the transition from slender to stumpy forms was thought to accomplish two functions. The first was to regulate the parasite load in the host, thereby reducing virulence, prolonging infections, and consequently increasing the chances of transmission. The second was that the stumpy form was thought to be the only developmental form able to infect the tsetse fly and spread the disease. This was called into question in 2021 however, when it was shown that slender forms could also infect tsetse flies (Schuster et al., 2021). This finding caused a debate as to whether slender forms can truly infect tsetse flies without using the infection-enhancing methods for fly infections commonly applied in a laboratory setting. The differentiation from stumpy cells to the first fly-resident form, the procyclic form has been studied in depth. While it has been known that slender cells can be differentiated to procyclic forms in vitro, the relevance of this to in vivo fly infections has not been extensively considered. The possibility that both bloodstream form trypanosomes might be able to infect the tsetse fly would have major implications in disease epidemiology.
The main focus of this thesis was to confirm that slender bloodstream forms can infect tsetse flies in a natural infection, as well as to look at the marker proteins involved and how the timing of their expression compares to the stumpy form. To do this, fly infections were carried out using monomorphic trypanosomes, which are unable to become stumpy forms, with and without the addition of infection enhancing chemicals. Fly infections with pleomorphic trypanosomes, able to become slender or stumpy, were also carried out with flies of different ages, as these more fully represent flies in the wild. This showed that slender forms can infect tsetse flies in low numbers without additional chemicals, and in both young and old flies. This study further explored the slender to procyclic differentiation process using molecular markers and RNA sequencing, providing evidence that slender forms can directly differentiate to procyclic forms and complete their life cycle within the fly.
The second part of this thesis focused on T. congolense, a sympatric trypanosome species responsible for AAT. Unlike T. brucei, T. congolense is monomorphic, possessing only one bloodstream form. This bloodstream form appears to rely on attachment to host red blood cells (RBCs) rather than active motility to survive in the mammalian bloodstream. The attachment mechanism has long been speculated to involve an enzyme called trans-sialidase (TS), responsible for transferring host sugars to the parasite surface. While the importance of TS for T. brucei survival in the tsetse fly and the American trypanosome T. cruzi in its mammalian hosts has been established, the role of TS in T. congolense remains incompletely understood. Therefore, the second objective of this thesis was to carry out preliminary experiments to investigate whether TS is responsible for T. congolense attachment to host cells. This was done by generating TS expressing T. brucei cells and checking for RBC attachment.
In summary, this work uncovers greater plasticity in the development of trypanosomes than previously known. The linear life cycle originally ascribed to T. brucei has been challenged, revealing multiple forms that can infect tsetse flies. This change in the life cycle and the investigation of molecular signals involved in this transition have significant implications not only for the basic understanding of the parasite, but also for advancing efforts to eliminate trypanosomiasis. Furthermore, the identification of signals crucial for certain trypanosome species, such as TS, which may operate in different life cycle stages in other trypanosomes, highlights the plasticity of trypanosomes and provides insights into the optimal strategies for combatting the various parasite species contributing to trypanosomiasis.
The discovery of UBA6 in 2007 has challenged the ubiquitin field, as for a long time, the ubiquitin-activating enzyme 1 (UBA1) was thought to be the sole E1 responsible for the activation of ubiquitin. UBA6 shares 40% sequence identity with UBA1 in humans. However, UBA6 is present only in mammals, zebrafish, and sea urchins. UBA6 and UBA1 use a different spectrum of E2 enzymes and direct ubiquitin to different subsets of E3 enzymes and consequently substrates. Since UBA1 initiates 99% of the ubiquitylation events, UBA6 is presumably responsible for a subset of substrates. Moreover, UBA6 is an unusual E1 enzyme as it activates both ubiquitin and FAT10. FAT10 is a ubiquitin-like modifier and consists of two ubiquitin-like domains arranged in tandem. FAT10 is present in vertebrates only, and its expression is synergistically induced by the pro-inflammatory cytokines interferon γ (INFγ) and tumor necrosis factor α (TNFα). Furthermore, FAT10 is the only ubiquitin-like modifier besides ubiquitin, which can directly target proteins for proteasomal degradation.
The involvement of UBA6-mediated ubiquitylation and FATylation in a broad spectrum of cellular pathways and diseases, along with the ongoing preclinical development of E1 inhibitors such as MNL4924 (Pevonedistat) and MLN7243 (TAK-243), has spurred increased research efforts to develop additional E1 inhibitors. UBA6, with its more limited role in catalyzing ubiquitin activation and being the sole E1 for FAT10, is considered to be a possible drug target. However, to reach this goal, the dual specificity of UBA6 needs to be understood first. Inhibition of UBA6-mediated FATylation while not affecting ubiquitylation or vice versa will not only provide a possibility to further investigate the roles that UBA6 plays in downstream pathways, but also open a window for targeting either the ubiquitylation or FATylation of UBA6 with specific inhibitors.
In this thesis, the crystal structure of UBA6 in complex with FAT10 will be described. In the UBA6-FAT10 complex, the C-terminal domain of FAT10 interacts with UBA6 in a similar manner as ubiquitin with UBA1, while its N-terminal domain binds to the 3-helix bundle inserted into the inactive adenylation domain of UBA6. The structure was corroborated by functional studies, which, surprisingly, identified UBA6 residues specifically abrogating the activation of either ubiquitin or FAT10. These results provide the foundation to study the individual roles that UBA6 is playing in the activation of either ubiquitin or FAT10 in downstream cellular pathways.
In addition, a high-throughput screening (HTS) assay for the identification of compounds inhibiting UBA6 was established, which provides the starting point to identify small molecules exclusively inhibiting the UBA6-activated ubiquitylation or FATylation.
Lastly, FATylation shares a common UBA6-USE1 cascade with UBA6-activated ubiquitylation, and several studies demonstrated that the cooperation between UBA6 and USE1 is functionally crucial in different pathways. Given that USE1 is currently one of the main dedicated E2 enzymes for UBA6, the underlying mechanism regarding the transfer is unclear yet. To visualize the transthioesterification between UBA6 and USE1, a cross-linking strategy was applied to form the binary UBA6-USE1 complex. Besides, to improve the yield and homogeneity of the complex samples, a non-catalytical cysteine variant of USE1 (3M_USE1) was generated, thus representing promising starting point samples that can be used for cryo-EM screening and x-ray crystallography. Ultimately, visualizing the catalytic transfer of ubiquitin/FAT10 from UBA6 to USE1 would provide insights into the molecular basis of UBA6-USE1 pathway mediated ubiquitylation and FATylation.
Periodic shadowing, a concept used in spectroscopy for stray light reduction, has been implemented to improve the temporal contrast of streak camera imaging. The capabilities of this technique are first proven by imaging elastically scattered picosecond laser pulses and are further applied to fluorescence lifetime imaging, where more accurate descriptions of fluorescence decay curves were observed. This all-optical approach can be adapted to various streak camera imaging systems, resulting in a robust technique to minimize space-charge induced temporal dispersion in streak cameras while maintaining temporal coverage and spatial information.
Bubble needs strings
(2021)
In this paper, we want to emphasize the pivotal role played by strings in the model realizing de Sitter using an expanding bubble, proposed and subsequently developed in [1–3]. Contrary to the Randall-Sundrum model of brane-localized gravity, we use the end points of radially stretched strings to obtain matter sourcing gravity induced on the bubble wall. This allows us to reinterpret the possible volume divergence coming from naive dimensional reduction as mass renormalization in four dimensional particle physics. Furthermore, we argue that the residual time dependence in the bulk, pointed out by some recent work as a possible shortcoming of such models, is automatically cured in presence of these stringy sources.
Dark bubbles and black holes
(2021)
In this paper we study shells of matter and black holes on the expanding bubbles realizing de Sitter space, that were proposed in [4]. We construct explicit solutions for a rigid shell of matter as well as black hole like solutions. The latter of these can also be used to construct Randall-Sundrum braneworld black holes in four dimensions.
Background
Degenerative aortic valve disease accounts for 10–20% of all cardiac surgical procedures. The impact of pre-existing comorbidities on the outcome of patients undergoing surgical aortic valve replacement (SAVR) needs further research.
Methods
The IMPACT registry is a non-interventional, prospective, open-label, multicenter, international registry with a follow-up of 5 years to assess the impact of pre-existing comorbidities of patients undergoing SAVR with the INSPIRIS RESILIA aortic valve on outcomes. IMPACT will be conducted across 25 sites in Austria, Germany, The Netherlands and Switzerland and intends to enroll approximately 500 patients. Patients will be included if they are at least 18 years of age and are scheduled to undergo SAVR with the INSPIRIS RESILIA Aortic Valve with or without concomitant ascending aortic root replacement and/or coronary bypass surgery. The primary objective is to determine all-cause mortality at 1, 3, and 5 years post SAVR. Secondary objectives include cardiac-related and valve-related mortality and structural valve deterioration including hemodynamics and durability, valve performance and further clinical outcomes in the overall study population and in specific patient subgroups characterized by the presence of chronic kidney disease, hypertension, metabolic syndrome and/or chronic inflammation.
Discussion
IMPACT is a prospective, multicenter European registry, which will provide much-needed data on the impact of pre-existing comorbidities on patient outcomes and prosthetic valve performance, and in particular the performance of the INSPIRIS RESILIA, in a real-world setting. The findings of this study may help to support and expand appropriate patient selection for treatment with bioprostheses.
Trial registration
ClinicalTrials.gov identifier: NCT04053088.
We propose a BGK model of the quantum Boltzmann equation for gas mixtures. We also provide a sufficient condition that guarantees the existence of equilibrium coefficients so that the model shares the same conservation laws and
-theorem with the quantum Boltzmann equation. Unlike the classical BGK for gas mixtures, the equilibrium coefficients of the local equilibriums for quantum multi-species gases are defined through highly nonlinear relations that are not explicitly solvable. We verify in a unified way that such nonlinear relations uniquely determine the equilibrium coefficients under the condition, leading to the well-definedness of our model.