Redefining our Territory: Reaching Pre-Matriculation Students With Case-Based, Online Instruction

Online educational tools have made it possible for our library to claim some educational territory that was previously unavailable to us, the pre-matriculation period. During the summer of 2015 we were able to add a two-part, case-based, online tutorial to our incoming medical students’ pre-matriculation materials. We created the story of Sarah Pilger, a hypothetical, obese, pregnant teenager whose pregnancy is complicated by a fetal toxoplasmosis. The case introduces the incoming students to almost all the resources they might want to use while enrolled at UNMC and also introduces students to the roles of the many healthcare professionals who are essential to the care of Sarah and her daughter Emily. Questions are posted throughout the Guide-on-the-Side tutorials and instant feedback is provided. Student response to the 2016 tutorial was overwhelmingly positive. We revised the tutorial for use during the summer of 2017, added pre- and post-tests, and will be able to present results of the tests at meeting time. Our dream is to one day have tutorials for each of UNMC’s colleges’ entering classes based on Sarah’s case, and to use these tutorials to foster inter-professional conversation and education. We have already worked with faculty in UNMC’s College of Allied Health Professions to create versions of the tutorial for clinical nutrition and ultrasonography students. The new tutorials are now used as the basis of an interprofessional learning experience in these programs’ obstetric units

The Prophage and Us - Shiga Toxin Phages revisited

The authors first met in 1998 at the University of Würzburg, Germany, at the Institute of Hygiene and Microbiology, in Helge Karch's lab, where Herbert Schmidt worked as a PostDoc and Maite Muniesa visited the lab for a postdoctoral research stay to work on phages encoding Shiga toxin 2e (Stx2e) [1]. Since that time, we have been more or less, as much as our university duties allow, connected by Stx-phage research. Initially described in the early 1980s, Shiga toxin-converting bacteriophages (Stx-phages) have been the subject of numerous publications [ 2,3 ]. The ability to produce Stx, the major pathogenicity factor of enterohemorrhagic E. coli (EHEC), seems to be essentially connected to the location of the Shiga toxin genes (stx) in the genome of lysogenic phages, found always in a similar location within the late transcribed region, and upstream of the lysis and capsid genes [4 - 11]. Stx-phages are double-stranded DNA tailed phages showing a lambdoid or a non-lambdoid genome structure. To the best of our knowledge, stx genes have never been found in other mobile genetic elements other than phages, such as plasmids or pathogenicity islands [12 - 16 ]. Although the genetics and function of Stx-phages have been described in many publications, some basic questions remain still open, for example, (1) why are Stx-phages so successful in terms of evolution and spread among E. coli strains? (2) why do Stx-phages occur mainly in enteropathogenic E. coli strains but not, or only accidentally, in others such as extraintestinal pathogenic E. coli (EXPEC), (3) which advantage do EHEC strains have from the lysogenic state carrying single or multiple Stx-phages

Elevating Librarian-Mediated Search Services: When 2nd Best Isn\u27t Good Enough

Objective: To optimize librarian-mediated search services, librarians must consider all aspects of their search service that affect service utilization and efficacy. The library literature provides little information concerning the format in which libraries are providing literature search results and even less on the effect of format on search service utilization.  At our academic health science library, the number of search requests received rose dramatically after we began providing results in RefShare format. RefShare is the collaboration tool available in ProQuest’s RefWorks®.  We wanted to know how other libraries were providing results and whether they had seen format affect search service utilization. Methods: A survey created using Springshare’s LibWizard® was distributed to the MEDLIB-L listserv, the expertsearching listserv, and through direct email to AAHSL reference and education librarians. The survey was sent out on March 31st, 2019 and closed on April 30th, 2019. We asked about the audience that the librarian/library served and requested basic information about the librarian-mediated search services offered -- with a special focus on formats used to send literature search results to the requester. Results and Conclusion: We have analyzed the survey results, and we share our findings here

Analyse der Auswirkung von Coxiella burnetii Effektorproteinen auf die in vivo Infektion der großen Wachsmottenlarven Galleria mellonella

Objectives Coxiella burnetii is a Gram-negative bacterium and the causative agent of the zoonotic disease Q fever [1]. After phagocytic uptake, the obligate intracellular bacterium C. burnetii modifies the infected host cell [2, 3]. Among other things, it inhibits host cell apoptosis [4]. For this purpose, a type IVB secretion system (T4SS) could be identified as essential, with the help of which C. burnetii is able to inject effector proteins into the host cytosol [5, 6]. Of the approximately 150 effector proteins, only a few have so far been assigned a function [7] AnkG (ankyrin-repeat protein G), CaeA (C. burnetii anti-apoptotic effector A) and CaeB (C. burnetii anti-apoptotic effector B) were found to be anti-apoptotic in vitro [8-14]. Increasing numbers of Q fever cases require a better understanding of the in vivo infection [15, 16]. Studying in vivo infection is difficult for C. burnetii because of its virulence. The avirulent laboratory strain C. burnetii NMII, on the other hand, allows better handling, but can only be used in immunodeficient SCID (severe combined immunodeficiency) mice [17]. In 2014, a suitable in vivo model for C. burnetii NMII was identified in the form of the large wax moth larva Galleria mellonella [18, 19]. The host cells represent the phagocytic haemocytes [20, 21]. Within my work, I was to establish this model in the laboratory, reproduce its suitability for C. burnetii NMII infections and investigate the effect of effector proteins, especially AnkG on G. mellonella infection. Design & Methods Bacteria were grown in cell-free ACCM-2 (acidified citrate- cysteine medium-2). Wild-type C. burnetii NMII, C. burnetii NMII-ΔdotA, which are not capable of forming a T4SS, and overexpression mutants of the effector proteins AnkGNM, AnkGI11E, AnkGF3, AnkGSOYTA, AnkF and a transposon mutant of AnkF were used. The G. mellonella larvae were infected by injection of the bacteria. Larval survival was monitored daily for 10 days, and incubation of larvae was at 37°C and at 21°C [22]. In addition, replication in VI.V. and VI.VI. was checked by quantitative PCR (polymerase chain reaction) and immunofluorescence staining. Observations & Results First, the G. mellonella infection model was confirmed as suitable for C. burnetii NMII infection. Larval death could be identified as dose- and T4SS-dependent. Furthermore, infection with C. burnetii that either overexpressed AnkG or lacked a functional T4SS (ΔdotA) resulted in enhanced survival of G. mellonella larvae. In contrast, infection with C. burnetii NMII::Flag-AnkGI11E overexpressing an AnkG lacking anti-apoptotic function resulted in larval death. This demonstrated that overexpression does not lead to loss of virulence and that the anti-apoptotic function of AnkG is causative for the observed phenotype [14]. This was confirmed by using AnkGF3 and AnkGSOYTA, which do not have a translocation domain and thus cannot be released via the T4SS [23] (VI.IV.). Furthermore, by means of qPCR and immunofluorescence staining of infected haemocytes, a replication defect of the AnkGNM-overexpressing C. burnetii could be excluded as a causal factor for the survival of the infected larvae. Furthermore, it was shown that overexpression of AnkF does not affect the pathogenicity of C. burnetii in G. mellonella larvae. In contrast, the absence of AnkF results in a loss of virulence. Conclusions G. mellonella is a suitable in vivo infection model for C. burnetii NMII. In this work, it was demonstrated that the survival of G. mellonella larvae infected with AnkG-overexpressing C. burnetii was positively influenced. The reduced pathogenicity of C. burnetii NMII::Flag-AnkG could be attributed to the anti-apoptotic protein effect of AnkG. Which probably leads to an increased resilience of infected haemocytes to infection [24]. Since the modification of the host cell transcript has recently been shown to be causative for the anti-apoptotic effect for AnkG [25], the transcriptome of infected G. mellonella should be investigated. In particular, the AnkG-mediated transcriptome changes should be the focus of this research effort. Furthermore, this work demonstrated for the first time that the T4SS effector protein AnkF could play a role in virulence. Partial results on AnkG and AnkF were part of the publication Schäfer et al. [23], which had already been published in 2020.Hintergrund und Ziele Coxiella burnetii ist als Gram-negatives Bakterium der Erreger der Zooanthroponose Q-Fieber [1]. Nach phagozytischer Aufnahme modifiziert das obligat intrazelluläre Bakterium C. burnetii die infizierte Wirtszelle [2, 3] Unter anderen hemmt es die Wirtszell-Apoptose [4]. Hierfür konnte ein TypIVB-Sekretionssystem (T4SS) als essenziell identifiziert werden, mit dessen Hilfe C. burnetii in der Lage ist Effektorproteine ins Wirtszytosol zu injizieren [5, 6]. Von den circa 150 Effektorproteinen konnten bislang nur wenigen eine Funktion zugeordnet werden [7]. Anti-apoptotisch wirksam waren in vitro AnkG (engl.: Ankyrin-repeat protein G), CaeA (C. burnetii anti-apoptotischer Effektor A) und CaeB (C. burnetii anti-apoptotischer Effektor B) [8-14]. Steigende Zahlen von Q-Fieber Fällen erfordern es die in vivo Infektion besser zu verstehen [15, 16]. Die Erforschung der in vivo Infektion ist für C. burnetii aufgrund ihrer Virulenz erschwert. Der avirulente Laborstamm C. burnetii NMII hingegen ermöglicht eine bessere Handhabung, kann allerding nur in immundefizienten SCID (engl.: Severe combined immunodeficiency) Mäusen verwendet werden [17]. 2014 konnte ein geeignetes in vivo Modell für C. burnetii NMII in Form der großen Wachsmottenlarve Galleria mellonella identifiziert werden [18, 19]. Die Wirtszellen stellen die phagozytischen Hämozyten dar [20, 21]. Innerhalb meiner Arbeit sollte ich dieses Modell im Labor etablieren, die Eignung für C. burnetii NMII Infektionen reproduzieren und die Wirkung von Effektorproteinen, insbesondere von AnkG auf die G. mellonella Infektion untersuchen. Methoden Die Bakterienanzucht erfolgte in zellfreiem ACCM-2 (engl.: Acidified Citrate Cysteine Medium-2) Medium. Verwendet wurden wildtypische C. burnetii NMII, C. burnetii NMII-ΔdotA, welche nicht zur Ausbildung eines T4SS fähig sind und Überexpressions- Mutanten der Effektorproteine AnkGNM, AnkGI11E, AnkGF3, AnkGSOYTA, AnkF und einer Transposonmutante von AnkF. Die Infektion der G. mellonella Larven erfolgte über Injektion der Bakterien. Das Überleben der Larven wurde über 10 Tage täglich kontrolliert, die Inkubation der Larven erfolgte bei 37°C und bei 21°C [22]. Zusätzlich wurde die Replikation in VI.V. und VI.VI. mittels quantitativer PCR (Polymerase Kettenreaktion) und Immunfluoreszenzfärbung überprüft. Ergebnisse und Beobachtungen Zunächst konnte das Infektionsmodell G. mellonella als geeignet für die Infektion mit C. burnetii NMII bestätigt werden. Das Larvensterben konnte als dosis- und T4SS-abhängig identifiziert werden. Weiterhin führte die Infektion mit C. burnetii, die entweder AnkG überexprimierte oder der ein funktionsfähiges T4SS fehlte (ΔdotA) zu einem Verbesserten Überleben der G. mellonella Larven. Die Infektion mit C. burnetii NMII:: Flag-AnkGI11E, die ein AnkG überexprimieren, das keine anti-apoptotische Funktion aufweist, führte dagegen zum Larvensterben. Damit konnte gezeigt werden, dass die Überexpression nicht zu einem Virulenzverlust führt und, dass die anti-apoptotische Funktion von AnkG ursächlich für den beobachteten Phänotyp ist [14]. Dies wurde durch Verwendung von AnkGF3 und AnkGSOYTA, welche keine Translokationsdomäne besitzen und somit nicht über das T4SS ausgeschleust werden können, bestätigt [23] (VI.IV.). Weiterhin konnte mittels qPCR und Immunfluoreszenzfärbung infizierter Hämozyten ein Replikationsdefekt der AnkGNM überexprimierenden C. burnetii als ursächlich für das Überleben der infizierten Larven ausgeschlossen werden. Weiterhin konnte gezeigt werden das die Überexpression von AnkF zu keiner Beeinflussung der Pathogenität von C. burnetii in G. mellonella Larven führt. Wohingegen das Fehlen von AnkF einen Virulenzverlust zur Folge hat. Schlussfolgerungen und Diskussion G. mellonella ist ein geeignetes in vivo Infektionsmodell für C. burnetii NMII. Im Rahmen dieser Arbeit konnte nachgewiesen werden, dass das Überleben von G. mellonella Larven, die mit AnkG-überexprimierenden C. burnetii infiziert waren, positiv beeinflusst wurde. Die verringerte Pathogenität von C. burnetii NMII::Flag-AnkG konnte der anti-apoptotischen Proteinwirkung von AnkG zugeschrieben werden. Was wahrscheinlich zu einer gesteigerten Resilienz der infizierten Hämozyten gegenüber der Infektion führt [24]. Da für AnkG kürzlich die Modifikation des Wirtszell-Transkripts als ursächlich für die anti-apoptotische Wirkung nachgewiesen werden konnte [25], sollte das Transkriptom von infizierten G. mellonella untersucht werden. Insbesondere die AnkG-vermittelten Transkriptomsänderung sollten im Fokus dieser Forschungsanstrengungen stehen. Weiterhin konnte in dieser Arbeit erstmal nachgewiesen werden, dass das T4SS Effektorprotein AnkF eine Rolle für die Virulenz spielen könnte. Teilergebnisse zu AnkG und AnkF waren Bestandteil der bereits im Jahr 2020 veröffentlichten Publikation Schäfer et al. [23].

Transformer-based end-to-end classification of variable-length volumetric data

The automatic classification of 3D medical data is memory-intensive. Also, variations in the number of slices between samples is common. Naive solutions such as subsampling can solve these problems, but at the cost of potentially eliminating relevant diagnosis information. Transformers have shown promising performance for sequential data analysis. However, their application for long-sequences is data, computationally, and memory demanding. In this paper, we propose an end-to-end Transformer-based framework that allows to classify volumetric data of variable length in an efficient fashion. Particularly, by randomizing the input slice-wise resolution during training, we enhance the capacity of the learnable positional embedding assigned to each volume slice. Consequently, the accumulated positional information in each positional embedding can be generalized to the neighbouring slices, even for high resolution volumes at the test time. By doing so, the model will be more robust to variable volume length and amenable to different computational budgets. We evaluated the proposed approach in retinal OCT volume classification and achieved 21.96% average improvement in balanced accuracy on a 9-class diagnostic task, compared to state-of-the-art video transformers. Our findings show that varying the slice-wise resolution of the input during training results in more informative volume representation as compared to training with fixed number of slices per volume. Our code is available at: https://github.com/marziehoghbaie/VLFAT

Gaps in affiliation indexing in Scopus and PubMed.

OBJECTIVE: The authors sought to determine whether unexpected gaps existed in Scopus\u27s author affiliation indexing of publications written by the University of Nebraska Medical Center or Nebraska Medicine (UNMC/NM) authors during 2014. METHODS: First, we compared Scopus affiliation identifier search results to PubMed affiliation keyword search results. Then, we searched Scopus using affiliation keywords (UNMC, etc.) and compared the results to PubMed affiliation keyword and Scopus affiliation identifier searches. RESULTS: We found that Scopus\u27s records for approximately 7% of UNMC/NM authors\u27 publications lacked appropriate UNMC/NM author affiliation identifiers, and many journals\u27 publishers were supplying incomplete author affiliation information to PubMed. CONCLUSIONS: Institutions relying on Scopus to track their impact should determine whether Scopus\u27s affiliation identifiers will, in fact, identify all articles published by their authors and investigators

Alpha Band Signatures of Social Synchrony

Previous research has reported changes in mu rhythm, the central rhythm of the alpha frequency band, in both intentional and spontaneous interpersonal coordination. The current study was designed to extend existing findings on social synchrony to the pendulum swinging task and simultaneously measured time unfolding behavioral synchrony and EEG estimation of mu activity during spontaneous, intentional in-phase and intentional anti-phase interpersonal coordination. As expected, the behavioral measures of synchrony demonstrated the expected pattern of weak synchronization for spontaneous coordination, moderate synchronization for intentional anti-phase coordination, and strong synchronization for in-phase coordination. With respect to the EEG measures, we found evidence for mu enhancement for spontaneous coordination in contrast to mu suppression for intentional coordination (both in phase and anti-phase), with higher levels of synchronization associated with higher levels of mu suppression in the right hemisphere. The implications of the research findings and methodology for understanding the underlying mechanisms contributing to social problems in psychological disorders, leader-follower relationships, and inter-brain dynamics are discussed

Spinal Cord Pathology in Alpha-Synuclein Transgenic Mice

Accumulation of α-synuclein is observed in neurodegenerative diseases like Parkinson's disease and Multiple System Atrophy. In previous studies with transgenic C57BL/6 mice overexpressing α-synuclein carrying the mutations A53T and A30P found in Parkinson's disease or with a parkin-null background, we reported severe mitochondrial impairments in neurons and to a larger extent in glial cells of the mesencephalon. Neuron death was not observed in the brain. Here we show that the mice show severe motor impairments in behavioral tests. In addition, these mice exhibit astrocytic cell death in the spinal cord, accompanied by extensive gliosis and microglial activation. This is shown by cell death staining and immunohistochemistry. Ultrastructural analyses revealed severe mitochondrial impairments not only in astrocytes, but also in oligodendrocytes and, to a small extent, in neurons. Thus, the transgenic mice show a profound pathology in glial cells of the spinal cord

Bacteriophages of Shiga toxin-producing Escherichia coli and their contribution to pathogenicity

Shiga toxins (Stx) of Shiga toxin-producing Escherichia coli (STEC) are generally encoded in the genome of lambdoid bacteriophages, which spend the most time of their life cycle integrated as prophages in specific sites of the bacterial chromosome. Upon spontaneous induction or induction by chemical or physical stimuli, the stx genes are co-transcribed together with the late phase genes of the prophages. After being assembled in the cytoplasm, and after host cell lysis, mature bacteriophage particles are released into the environment, together with Stx. As members of the group of lambdoid phages, Stx phages share many genetic features with the archetypical temperate phage Lambda, but are heterogeneous in their DNA sequences due to frequent recombination events. In addition to Stx phages, the genome of pathogenic STEC bacteria may contain numerous prophages, which are either cryptic or functional. These prophages may carry foreign genes, some of them related to virulence, besides those necessary for the phage life cycle. Since the production of one or more Stx is considered the major pathogenicity factor of STEC, we aim to highlight the new insights on the contribution of Stx phages and other STEC phages to pathogenicity