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Highly sensitive qualitative and quantitative automatednucleic acid amplification tests (NATs) that are commercially available for the detection of hepatitis B virus (HBV)infection have been developed only in the last few years.The potential indications for HBV NATs are: follow-up ofchronic hepatitis B, therapy and antiviral resistance monitoring, determination of infectivity and transmission risk,detection of occult (HBsAg-negative and HBV DNA-positive) infection and mutant virus which may escape serologic diagnosis, blood donor screening, and resolution ofunusual or discordant serologic constellations. Although NATs are now widely implemented in the routine diagnosis of clinical laboratories, there are several importantissues which need to be further investigated. Standardisation of NATs used for the monitoring of antiviral therapyand follow-up of chronic infection is still lacking, and theclinical significance of HBV DNA levels needs to be clarified. The influence of genetic variability in terms of genotype variation has been poorly investigated so far.Although there are highly sensitive automated NATs forblood donor screening available, their implementation is still subject to discussion and certain countries rejectedHBV DNA testing for blood donation for reasons of poor cost-effectiveness.
Fleischmann, Maximilian ; Chatzikonstantinou, Georgios ; Fokas, Emmanouil ; Wichmann, Jörn ; Christiansen, Hans ; Strebhardt, Klaus ; Rödel, Claus ; Tselis, Nikolaos ; Rödel, Franz
Uterine cervical cancer is one of the leading causes of cancer-related mortality in women worldwide. Each year, over half a million new cases are estimated, resulting in more than 300,000 deaths. While less-invasive, fertility-preserving surgical procedures can be offered to women in early stages, treatment for locally advanced disease may include radical hysterectomy, primary chemoradiotherapy (CRT) or a combination of these modalities. Concurrent platinum-based chemoradiotherapy regimens remain the first-line treatments for locally advanced cervical cancer. Despite achievements such as the introduction of angiogenesis inhibitors, and more recently immunotherapies, the overall survival of women with persistent, recurrent or metastatic disease has not been extended significantly in the last decades. Furthermore, a broad spectrum of molecular markers to predict therapy response and survival and to identify patients with high- and low-risk constellations is missing. Implementation of these markers, however, may help to further improve treatment and to develop new targeted therapies. This review aims to provide comprehensive insights into the complex mechanisms of cervical cancer pathogenesis within the context of molecular markers for predicting treatment response and prognosis.
Oertli, Annemarie ; Rinné, Susanne ; Moss, Robin ; Kääb, Stefan ; Seemann, Gunnar ; Beckmann, Britt-Maria ; Decher, Niels
KCNQ1 encodes the voltage-gated potassium (Kv) channel KCNQ1, also known as KvLQT1 or Kv7.1. Together with its ß-subunit KCNE1, also denoted as minK, this channel generates the slowly activating cardiac delayed rectifier current IKs, which is a key regulator of the heart rate dependent adaptation of the cardiac action potential duration (APD). Loss-of-function mutations in KCNQ1 cause congenital long QT1 (LQT1) syndrome, characterized by a delayed cardiac repolarization and a prolonged QT interval in the surface electrocardiogram. Autosomal dominant loss-of-function mutations in KCNQ1 result in long QT syndrome, called Romano–Ward Syndrome (RWS), while autosomal recessive mutations lead to Jervell and Lange-Nielsen syndrome (JLNS), associated with deafness. Here, we identified a homozygous KCNQ1 mutation, c.1892_1893insC (p.P631fs*20), in a patient with an isolated LQT syndrome (LQTS) without hearing loss. Nevertheless, the inheritance trait is autosomal recessive, with heterozygous family members being asymptomatic. The results of the electrophysiological characterization of the mutant, using voltage-clamp recordings in Xenopus laevis oocytes, are in agreement with an autosomal recessive disorder, since the IKs reduction was only observed in homomeric mutants, but not in heteromeric IKs channel complexes containing wild-type channel subunits. We found that KCNE1 rescues the KCNQ1 loss-of-function in mutant IKs channel complexes when they contain wild-type KCNQ1 subunits, as found in the heterozygous state. Action potential modellings confirmed that the recessive c.1892_1893insC LQT1 mutation only affects the APD of homozygous mutation carriers. Thus, our study provides the molecular mechanism for an atypical autosomal recessive LQT trait that lacks hearing impairment.
Ri, Keiken ; Weng, Tsai-Hsuan ; Claveras Cabezudo, Ainara ; Jösting, Wiebke ; Zhang, Yu ; Bazzone, Andre ; Leong, Nancy C. P. ; Welsch, Sonja ; Doty, Raymond T. ; Gursu, Gonca ; Lim, Tiffany Jia Ying ; Schmidt, Sarah Luise ; Abkowitz, Janis L. ; Hummer, Gerhard ; Wu, Di ; Nguyen, Long N. ; Safarian, Schara
Human feline leukaemia virus subgroup C receptor-related proteins 1 and 2 (FLVCR1 and FLVCR2) are members of the major facilitator superfamily1. Their dysfunction is linked to several clinical disorders, including PCARP, HSAN and Fowler syndrome2,3,4,5,6,7. Earlier studies concluded that FLVCR1 may function as a haem exporter8,9,10,11,12, whereas FLVCR2 was suggested to act as a haem importer13, yet conclusive biochemical and detailed molecular evidence remained elusive for the function of both transporters14,15,16. Here, we show that FLVCR1 and FLVCR2 facilitate the transport of choline and ethanolamine across the plasma membrane, using a concentration-driven substrate translocation process. Through structural and computational analyses, we have identified distinct conformational states of FLVCRs and unravelled the coordination chemistry underlying their substrate interactions. Fully conserved tryptophan and tyrosine residues form the binding pocket of both transporters and confer selectivity for choline and ethanolamine through cation–π interactions. Our findings clarify the mechanisms of choline and ethanolamine transport by FLVCR1 and FLVCR2, enhance our comprehension of disease-associated mutations that interfere with these vital processes and shed light on the conformational dynamics of these major facilitator superfamily proteins during the transport cycle.
Background: The increasing number of cases and hospital admissions due to COVID-19 created an urgent need for rapid, reliable testing procedures for SARS-CoV-2 in Emergency Departments (ED) in order to effectively manage hospital resources, allocate beds and prevent nosocomial spread of infection. The ID NOW™ COVID-19 assay is a simple, user-friendly, rapid molecular test run on an instrument with a small footprint enabling point-of-care diagnostics.
Methods: In the first wave, outsourced RT-PCR testing regularly required 36-48 hours before results were available. This prospective study was conducted in the second wave (October 2020-April 2021) and evaluated the impact the implementation of the ID NOW™ COVID-19 test in the ED had on clinical care processes and patient pathways. 710 patients were recruited upon arrival at the ED which included those presenting clinical symptoms, asymptomatic individuals or persons fulfilling epidemiological criteria. The first anterior nasal swab was taken by trained nurses in the ambulance or a separate consultation room. The ID NOW™ COVID-19 test was performed in the ED in strict compliance with the manufacturer’s instructions and positive or suspected cases were additionally tested with RT_PCR (cobas SARS-COV-2 RT-PCR, Roche) following collection of a second nasopharyngeal NP specimen.
Results: Swabs directly tested with the ID NOW™ COVID-19 test showed a diagnostic concordance of 98 % (sensitivity 99.59 %, specificity 94.55 %, PPV 97.6 %, NPV 99.05 %) compared to RT-PCR as reference. The 488 patients that tested positive with the ID NOW™ COVID-19 had a Ct range in RT-PCR results between 7.94 to 37.42 (in 23.2 % > 30). Two false negative results (0.28%) were recorded from patients with Ct values > 30. 14 (1.69%) discordant results were reviewed case-by-case and usually associated with either very early or very advanced stages of infection. Furthermore, patients initially negative with the ID NOW™ COVID-19 test and admitted to the hospital were tested again on days 5 and 12: no patient became positive.
Discussion: The ID NOW™ COVID-19 test for detection of SARS-CoV-2 demonstrated excellent diagnostic agreement with RT-PCR under the above-mentioned patients pathways implemented during the second wave. The main advantage of the system was the provision of reliable results within a few minutes. This not only allowed immediate initiative of appropriate therapy and care for COVID-19 (patient benefit) but provided essential information on isolation and thus available beds. This drastically helped the overall finances of the department and additionally allowed more patients to be admitted including those requiring immediate attention; this was not possible during the first wave since beds were blocked waiting for diagnostic confirmation. Our findings also show that when interpreting the results, the clinical condition and epidemiological history of the patient must be taken into account, as with any test procedure. Overall, the ID NOW™ COVID-19 test for SARS-CoV-2 provided a rapid and reliable alternative to laboratory-based RT-PCR in the real clinical setting which became an acceptable part of the daily routine within the ED and demonstrated that early patient management can mitigate the impact of the pandemic on the hospital.
Molecular surveillance of carbapenem-resistant gram-negative bacteria in liver transplant candidates
(2021)
Schultze, Tilman ; Ferstl, Philip ; Villinger, David ; Hogardt, Michael ; Bechstein, Wolf Otto ; Göttig, Stephan ; Wichelhaus, Thomas A. ; Zeuzem, Stefan ; Trebicka, Jonel ; Waidmann, Oliver ; Welker, Martin-Walter ; Kempf, Volkhard A. J.
Background: Carbapenem-resistant Gram-negative bacteria (CRGN) cause life-threatening infections due to limited antimicrobial treatment options. The occurrence of CRGN is often linked to hospitalization and antimicrobial treatment but remains incompletely understood. CRGN are common in patients with severe illness (e.g., liver transplantation patients). Using whole-genome sequencing (WGS), we aimed to elucidate the evolution of CRGN in this vulnerable cohort and to reconstruct potential transmission routes.
Methods: From 351 patients evaluated for liver transplantation, 18 CRGN isolates (from 17 patients) were analyzed. Using WGS and bioinformatic analysis, genotypes and phylogenetic relationships were explored. Potential epidemiological links were assessed by analysis of patient charts.
Results: Carbapenem-resistant (CR) Klebsiella pneumoniae (n=9) and CR Pseudomonas aeruginosa (n=7) were the predominating pathogens. In silico analysis revealed that 14/18 CRGN did not harbor carbapenemase-coding genes, whereas in 4/18 CRGN, carbapenemases (VIM-1, VIM-2, OXA-232, and OXA-72) were detected. Among all isolates, there was no evidence of plasmid transfer-mediated carbapenem resistance. A close phylogenetic relatedness was found for three K. pneumoniae isolates. Although no epidemiological context was comprehensible for the CRGN isolates, evidence was found that the isolates resulted of a transmission of a carbapenem-susceptible ancestor before individual radiation into CRGN.
Conclusion: The integrative epidemiological study reveals a high diversity of CRGN in liver cirrhosis patients. Mutation of carbapenem-susceptible ancestors appears to be the dominant way of CR acquisition rather than in-hospital transmission of CRGN or carbapenemase-encoding genetic elements. This study underlines the need to avoid transmission of carbapenem-susceptible ancestors in vulnerable patient cohorts.
Neuman, Manuela G. ; Seitz, Helmut K. ; Teschke, Rolf ; Malnick, Stephen ; Johnson-Davis, Kamisha L. ; Cohen, Lawrence B. ; German, Anit ; Hohmann, Nicolas ; Moreira, Bernhardo ; Moussa, George ; Opris, Mihai
Hepatic cells are sensitive to internal and external signals. Ethanol is one of the oldest and most widely used drugs in the world. The focus on the mechanistic engine of the alcohol-induced injury has been in the liver, which is responsible for the pathways of alcohol metabolism. Ethanol undergoes a phase I type of reaction, mainly catalyzed by the cytoplasmic enzyme, alcohol dehydrogenase (ADH), and by the microsomal ethanol-oxidizing system (MEOS). Reactive oxygen species (ROS) generated by cytochrome (CYP) 2E1 activity and MEOS contribute to ethanol-induced toxicity. We aimed to: (1) Describe the cellular, pathophysiological and clinical effects of alcohol misuse on the liver; (2) Select the biomarkers and analytical methods utilized by the clinical laboratory to assess alcohol exposure; (3) Provide therapeutic ideas to prevent/reduce alcohol-induced liver injury; (4) Provide up-to-date knowledge regarding the Corona virus and its affect on the liver; (5) Link rare diseases with alcohol consumption. The current review contributes to risk identification of patients with alcoholic, as well as non-alcoholic, liver disease and metabolic syndrome. Additional prevalence of ethnic, genetic, and viral vulnerabilities are presented.
Im Rahmen dieser Arbeit wurde die Rolle des Proteins S100B in humanen Neuroblastomzellen und primären hippokampalen Neurone der Ratte beim apoptotischen Zelltod untersucht. Hierfür wurden verschiedene zelltodinduzierende Agentien und Stresskonditionen verwendet. Für den exzitotoxischen, glutamatabhängigen Zelltod wurde eine NMDA-induzierte Zellschädigung sowie eine Hypoxieinduktion in einer Hypoxiekammer benutzt. Hier konnte für beide Apoptosemodelle und in beiden Zellarten eine signifikante Neuroprotektion in Anwesenheit von S100B gezeigt werden. Besonders in Hinblick auf bereits gezeigte aktive Sezernierung von S100B nach metabolomischem Stress in Astrozyten sollten die weiteren Signalwege und Effekte dieses Proteins erforscht werden. Im Zuge der Untersuchung eines möglichen Wirkungsmechanismus von S100B zeigte sich zunächst eine signifikante Aktivierung des Zellrezeptors RAGE. Weiterhin zeigte sich in primären hippokampalen Neuronen eine Aktivierung des RAF/MEK/MAPKERK-Signalwegs zumindest partiell verantwortlich für die Vermittlung der neuoprotektiven Wirkung von S100B bei NMDA-induzierter Apoptose. Durch Experimente unserer Arbeitsgruppe wurde bereits zuvor eine S100B abhängige Aktivierung von NFκB beobachtet. In dieser Arbeit konnte mit VEGF ein evtl. NFκB-abhängig aktiviertes Zielgen für die neuroprotektive Wirkung von S100B bei hypoxieinduzierter Apotpose gefunden werden. Demnach erklärt sich ein möglicher neuroprotektiver Wirkmechanismus von S100B beim exzitotoxischen Zelltod durch Aktivierung des Rezeptors RAGE an der Zelloberfläche, mit anschließender Aktivierung des MEK-Erk Signalwegs. Dieses kann seinerseits zu einer Aktivierung von NFκB in der Zelle mit Hochregulierung des VEGF-Gens führen.
Ein weiteres untersuchtes Apoptosemodell für die Rolle von S100B war die direkte DNA-Schädigung durch UV-Bestrahlung und Etoposid sowie die Schädigung durch den Proteasom-Inhibitor und p53 Aktivator Epoxomicin in humanen SHSY5Y Neuroblastoma-Zellen und primären hippokampalen Neuronen der Ratte. Auch hier zeigte sich in allen drei Modellen eine signifikante Neuroprotektion in Anwesenheit von S100B.
Da es einige Hinweise (unter anderem noch nicht publizierte Daten unserer eigenen Arbeitsgruppe) für eine Aufnahme von S100B in die Zelle gibt, wurde eine evtl. Wechselwirkung von S100B mit dem, nach DNA-Schädigung hochreguliertem, apoptoseinduzierenden Protein p53 untersucht. Hier zeigte sich, dass S100B sowohl nach DNA-Schädigung durch UV-Bestrahlung, als auch nach Etoposid-Behandlung die Hochregulierung von p53 auf Proteinebene signifikant reduziert und eine Translokation zum Zellkern verhindert. In Zusammenschau dieser Daten und den aktuellen Literaturdaten über direkte Wechselwirkungen von S100B und p53 kann man davon ausgehen, dass S100B seine Wirkung nicht nur über den Zelloberflächenrezeptor RAGE ausübt, sondern nach einem noch nicht vollständig erforschten Aufnahmemechanismus in die Zelle durch direkte Proteininteraktionen, z. B. wie hier mit dem Protein p53, in den Zellprozess insbesondere im Apoptoseprozess eingreift. Abgesehen von der in dieser Arbeit beschriebenen Herunterregulierung des p53-Proteinlevels in Anwesenheit von S100B, welche die Folge einer proteasomalen Degradation nach Formationsänderung sein kann, sollten die weiteren p53-abhängigen Apoptoseinduktionswege wie eine Veränderung von dessen Transkriptionsaktiviät, Hemmung proapoptotischer Proteine und ein evtl. Einfluss auf die Translokation von sog. Todesrezeptoren an die Zellmembran in Anwesenheit von S100B als evtl. Ursachen des neuroprotektiven Effekts von S100B weiter erforscht werden.
Im Rahmen dieser Arbeit bereits durchgeführte Untersuchungen auf Veränderungen der Expressionsrate von möglichen p53-Zielgenen haben noch keine endgültigen Ergebnisse geliefert. Zum einen ist evtl. die Auswahl der ausgewählten Zielgene nicht ausreichend gewesen und zum anderen besteht eine evtl. Limitation der semiquantitativen RT-PCR Methode gegenüber neueren Methoden wie die quantitative Real-Time-PCR in der Detektion auch kleinerer Expressionsunterschiede (siehe oben). Der Mechanismus der Neuroprotektion kann in diesem Modell abschließend noch nicht vollständig geklärt werden. Weiterführende Untersuchungen sollten den genauen Aufnahmemechanismus von S100B in die Zelle untersuchen, und die neuroprotektiven Schritte nach einer Blockierung/Herunterregulierung von p53 weiter klären.
Schätzungen der WHO zufolge waren 2015 weltweit rund 71 Millionen Menschen von einer chronischen Hepatitis C-Infektion betroffen. Die chronische Hepatitis C ist mit einem erhöhten Risiko für die Entstehung einer Leberzirrhose und eines hepatozellulären Karzinoms assoziiert. Die NS3/4A-Protease als zentraler Bestandteil der Replikationsmaschinerie des Virus spaltet das HCV-Polyprotein und ist in die Inaktivierung antiviraler Proteine involviert. Durch ihren maßgeblichen Einfluss auf die virale Fitness stellt sie einen entscheidenden Faktor für die chronische Persistenz des Virus im Wirtsorganismus dar. Die Protease ist auch eine wichtige Zielstruktur für spezifische antivirale Medikamente in der Behandlung der chronischen Hepatitis C. Der natürlich vorkommende Polymorphismus Q80K in der NS3/4A-Protease ist bei bis zu 47 % der Patienten schon vor Therapiebeginn feststellbar, insbesondere beim Genotyp 1a. Q80K führt zum Therapieversagen bei makrozyklischen Proteaseinhibitoren, insbesondere Simeprevir. Phylogenetische Analysen konnten zeigen, dass 96 % aller HCV-Gensequenzen mit Q80K von einem gemeinsamen, genetischen Vorfahren abstammen und sich die Mutation seit Mitte des 20. Jahrhunderts scheinbar stabil ausgehend vom nordamerikanischen Kontinent etabliert hat. Daneben wurden mit A91S/T und S174N sogenannte second site-Austausche identifiziert, die assoziiert mit Q80K vorkommen. Ziel dieser Arbeit war es herauszufinden, welchen Einfluss diese second site-Austausche auf die Enzymaktivität und Proteinfaltung der Protease haben und ob sie mögliche Veränderungen durch den Q80K-Polymorphismus kompensieren. Nach Expression und Aufreinigung der NS3/4A-Protease wurden die Effekte von Q80K, A91S/T und S174N auf die Enzymaktivität und Thermostabilität mittels fluoreszenzbasierter Verfahren untersucht und im Zusammenhang mit einer in silico-3D-Strukturanalyse der Protease interpretiert. Es zeigte sich, dass A91S/T und S174N jeweils zu einer Angleichung der Thermostabilität des Proteins an den Wildtyp führen und somit Defizite in der Faltung der Protease durch Q80K kompensiert werden. Aufgrund der experimentellen Daten und der Topografie dieser Austausche innerhalb der NS3-Protease-Helikase-Struktur ist von indirekten Effekten der second site-Austausche auf die replikative Fitness der Virusvarianten auszugehen. Die hier charakterisierten Austausche in der NS3/4A-Protease tragen durch eine Stabilisierung der Proteinfaltung kritisch zur Stabilität des Q80K-Polymorphismus im Proteasegen des HCV Genotyp 1a bei.
Das Verständnis von Tumorerkrankungen wurde durch neue technologische und ökonomische Verbesserungen für die Next-Generation-Sequencing Analyse (NGS) gefördert. Die Komplexität der Interpretation genomischer Daten erschwert jedoch die Anwendung von NGS-Analysen im klinischen Kontext. Die Herausforderung besteht darin bei stetig wachsendem medizinischem Wissen dieses im klinischen Kontext zu interpretieren und eine personalisierte Therapieempfehlung abzugeben. Einen ressourcensparenden Ansatz können KI-unterstützende Software-Programme bieten, welche die genomischen Varianten mit der aktuellen Literatur vergleichen, eine Bewertung der Therapieoptionen geben und klinische Studien empfehlen können. In dieser retrospektiven Arbeit wurden Patient:innen mit metastasiertem Brustkrebs (n=77) mittels gezielter NGS-Analyse anhand von sogenannten Genpanels mit 126 bzw. 540 krebsrelevanten Genen im Zeitraum von 01/2019-02/2022 untersucht. Mit Hilfe von bioinformatischen Methoden wurden patientenspezifische genomische Veränderungen mit Behandlungsoptionen abgeglichen. Diese Methoden stützen sich vollständig auf öffentliche Datenbanken über somatische Varianten mit prädiktiver Evidenz für das Ansprechen auf bestimmte Medikamente. Diese Versorgungsforschung einer repräsentativen Kohorte des Universitätsklinikums Frankfurt in Kooperation mit Regionalverbund OncoNet Rhein-Main wurden systematisch ausgewertet inklusive der Bedeutung genomischer Varianten. Das OncoNet Rhein-Main ist eine Kooperation aus führenden onkologischen Zentren und Praxen im Rhein-Main-Gebiet, welche sich als Netzwerk der Aufgabe angenommen haben Patient:innen optimal therapeutisch zu versorgen. Für 51% (39/77) der Patient:innen konnte mindestens eine gezielte Therapieoption mit einem effektivem Biomarker im gleichen Tumortyp gemäß Zulassung der Europäischen Arzneimittelbehörde (EMA) gefunden werden.
Bei 12/77 (16%) wurde mindestens eine Alteration mit einem effektivem Biomarker und einer OFF-Label Therapieoption gefunden. Bei 30% der Patient:innen wurden Veränderungen in optionalen Biomarkern gefunden, welche Resistenzmechanismen erklären. Die umfassende molekulare Analyse von Patient:innen mit fortgeschrittenem Brustkrebs erlaubt die Behandlungsoption zu verbessern und ermöglicht durch die Analyse von bekannten Resistenzmarkern auch den klinischen Verlauf besser zu verstehen. Die interdisziplinäre Besprechung der Befunde im molekularem Tumorboard ist im Hinblick auf kontinuierliches Lernen aller Beteiligten sowie zur Qualitätssicherung eine entscheidende obligate Maßnahme.
Hydroxyethylstärke (HES) ist ein kolloidales Volumenersatzmittel, das zur Volumenbehandlung bei Trauma und bei Schock und zur Verbesserung der Rheologie bei Durchblutungsstörungen angewendet wird. Amylopektin, die Grundlage von HES, wird zur Veränderung der physikalischen Eigenschaften substituiert, um eine für die Infusion geeignete Lösung herstellen zu können. Ein wichtiger Begleiteffekt dieser Substitution ist, dass durch die dadurch erzeugten Störstellen der enzymatische Abbau der Volumenersatzmittel durch Serumglykosidasen minimiert wird. Die molekularen Eigenschaften der HES können anhand der Molekulargewichtsverteilung, beschrieben durch den Gewichtsmittelwert der Molmassen Mw, den Zahlenmittelwert der Molmassen Mn und die Molmasse im Peakmaximum Mp, sowie nach dem Ausmaß der Substitution beschrieben werden. Im Handel befindliche HES-Lösungen werden anhand des Gewichtsmittelwertes der Molmassen (Mw) und der molaren Substitution (MS) gekennzeichnet. Nach bisherigen Erkenntnissen zur Speicherung der HES in Organen stellten sich die Fragen, ob die Hypothese, dass HES durch lysosomale Enzyme abgebaut wird untermauert werden kann und ob es möglich ist, die Sicherheit der HES für die Anwendung am Patienten durch gezielte Verwendung bestimmter HES-Fraktionen zu verbessern. Ziel dieser Arbeit war daher, erstmals die Molekulargewichtsverteilung der nach Infusion von HES in Milz und Leber gespeicherten HES mittels Ausschluss-Chromatographie gekoppelt mit Mehrwinkel-Laser-Streulicht-Detektion zu bestimmen. Untersucht wurden drei handelsübliche HES-Präparate mit unterschiedlichem Mw und unterschiedlicher Substitution (die Bezeichnung schließt Mw (kDa) und MS ein): HES 130/0,4 und HES 200/0,5 sowie HES 450/0,7. Je acht Wistar-Ratten pro Versuchsgruppe erhielten 18 ml HES infundiert. Die Organe wurden für die Molmassenbestimmung bis zu fünfzig Tagen nach Infusion entnommen. Die Hämoglobinkonzentrationen und Hämatokritwerte bei den Blutabnahmen in den ersten 48 Stunden wurden ermittelt und gaben Aufschluss über die Hämodilution. Als wichtigstes Ergebnis wurde eine unterschiedliche Molmassenverteilung der HES aus Milz und Leber festgestellt. In der Leber werden vorwiegend niedermolekulare Anteile gespeichert. Das Mw der HES in der Leber lag direkt nach Infusion bei 89.606±8.570 (HES 450/0,7), 20.038±1.600 (HES 200/0,5) und 23.769±2.489 (HES 130/0,4). Im Verlauf der Untersuchungen stieg das Mw in der Leber bis maximal Tag 5 (HES 450/0,7) nach Infusion zwar an, fiel dann aber bei den weiteren Bestimmungen nach mehr als 5 Tagen wieder ab. Das Peakmaximum der Molmassenverteilung der HES in der Leber blieb dabei größtenteils konstant (HES 450/0,7: ~60 kDa; HES 200/0,5: ~30 kDa; HES 130/0,4: ~30 kDa). Die Molmassenverteilung der Milz wies hingegen hochmolekulare HES auf, wobei die Molmassen im Verlauf der Zeit noch zunahmen. Das Mw nach Infusion von HES 450/0,7 stieg dabei von 148.220 Da auf 229.617 Da im Mittel an. Möglicherweise erfolgt in der Milz vor allem eine Speicherung schwer zu spaltender HES. In der Leber konnte nach Infusion aller HES-Präparate und bereits unmittelbar nach Infusion HES gefunden werden. In der Milz war nur nach Infusion der hochmolekularen, hochsubstituierten HES 450/0,7 und der mittelmolekularen, mittelsubstituierten HES 200/0,5 gespeicherte HES nachzuweisen. Nach Infusion der HES 200/0,5 war dabei nur vereinzelt und erst ab einem Tag HES in der Milz auszumachen. In der Leber war die Speicherung der HES 450/0,7 ebenfalls am längsten festzustellen, während bei HES 130/0,4 die Speicherung in der Leber nur bis 3 Tage nach Infusion bestand. Der Verlauf der Molmassenverteilung in der Leber deutet auf einen intrazellulären Abbau der HES durch lysosomale Enzyme hin, während in der Milz über einen langen Zeitraum nicht gespaltene hochmolekulare HES angereichert wird. Die niedermolekulare, niedrigsubstituierte HES ist hinsichtlich der vorhersehbaren Dauer der Speicherung als besonders günstig anzusehen. In der Leber werden jedoch bei allen HES-Präparaten niedermolekulare Anteile in Konkurrenz zur renalen Elimination aufgenommen. Daher ist die wiederholte, hochdosierte Anwendung von HES bei dekompensierter Niereninsuffizienz aufgrund der Gefahr einer mechanischen Beeinträchtigung der Leber durch dort kumulierte HES stets kritisch zu betrachten.
Kettner, Mattias ; Birngruber, Christoph Gerhard ; Niess, Constanze ; Baz Bartels, Marco ; Bunzel, Lena Maria ; Verhoff, Marcel A. ; Lux, Constantin Peter ; Ramsthaler, Frank
Mongolian spots (MS) are congenital dermal conditions resulting from neural crest-derived melanocytes migration to the skin during embryogenesis. MS incidences are highly variable in different populations. Morphologically, MS present as hyperpigmented maculae of varying size and form, ranging from round spots of 1 cm in diameter to extensive discolorations covering predominantly the lower back and buttocks. Due to their coloring, which is also dependent on the skin type, MS may mimic hematoma thus posing a challenge on the physician conducting examinations of children in cases of suspected child abuse. In the present study, MS incidences and distribution, as well as skin types, were documented in a collective of 253 children examined on the basis of suspected child abuse. From these data, a classification scheme was derived to document MS and to help identify cases with a need for recurrent examination for unambiguous interpretation of initial findings alongside the main decisive factors for re-examination such as general circumstances of the initial examination (e. g., experience of the examiner, lighting conditions) and given dermatological conditions of the patient (e. g., diaper rash).
Peinelt, Andreas ; Bremm, Melanie ; Kreyenberg, Hermann ; Cappel, Claudia ; Banisharif-Dehkordi, Julia ; Erben, Stephanie ; Rettinger, Eva ; Jarisch, Andrea ; Meisel, Roland ; Schlegel, Paul-Gerhardt ; Beck, Olaf ; Bug, Gesine ; Klusmann, Jan-Henning ; Klingebiel, Thomas ; Hünecke, Sabine ; Bader, Peter
Chimeric antigen receptor (CAR) T cell therapy is a potent new treatment option for relapsed or refractory hematologic malignancies. As the monitoring of CAR T cell kinetics can provide insights into the activity of the therapy, appropriate CAR T cell detection methods are essential. Here, we report on the comprehensive validation of a flow cytometric assay for peripheral blood CD19 CAR T cell detection. Further, a retrospective analysis (n = 30) of CAR T cell and B cell levels over time has been performed, and CAR T cell phenotypes have been characterized. Serial dilution experiments demonstrated precise and linear quantification down to 0.05% of T cells or 22 CAR T cell events. The calculated detection limit at 13 events was confirmed with CAR T cell negative control samples. Inter-method comparison with real-time PCR showed appreciable correlation. Stability testing revealed diminished CAR T cell values already one day after sample collection. While we found long-term CAR T cell detectability and B cell aplasia in most patients (12/17), some patients (5/17) experienced B cell recovery. In three of these patients the coexistence of CAR T cells and regenerating B cells was observed. Repeat CAR T cell infusions led to detectable but limited re-expansions. Comparison of CAR T cell subsets with their counterparts among all T cells showed a significantly higher percentage of effector memory T cells and a significantly lower percentage of naïve T cells and T EMRA cells among CAR T cells. In conclusion, flow cytometric CAR T cell detection is a reliable method to monitor CAR T cells if measurements start without delay and sufficient T cell counts are given.
Kienzl, Melanie ; Hasenoehrl, Carina ; Maitz, Kathrin ; Sarsembayeva, Arailym ; Taschler, Ulrike ; Valadez-Cosmes, Paulina ; Kindler, Oliver ; Ristic, Dusica ; Raftopoulou, Sofia ; Santiso, Ana ; Bärnthaler, Thomas ; Brcic, Luka ; Hahnefeld, Lisa Katharina ; Gurke, Robert ; Thomas, Dominique Jeanette ; Geisslinger, Gerd ; Kargl, Julia ; Schicho, Rudolf
Monoacylglycerol lipase (MGL) expressed in cancer cells influences cancer pathogenesis but the role of MGL in the tumor microenvironment (TME) is less known. Using a syngeneic tumor model with KP cells (KrasLSL-G12D/p53fl/fl; from mouse lung adenocarcinoma), we investigated whether TME-expressed MGL plays a role in tumor growth of non-small cell lung cancer (NSCLC).
In sections of human and experimental NSCLC, MGL was found in tumor cells and various cells of the TME including macrophages and stromal cells. Mice treated with the MGL inhibitor JZL184 as well as MGL knock-out (KO) mice exhibited a lower tumor burden than the controls. The reduction in tumor growth was accompanied by an increased number of CD8+ T cells and eosinophils. Naïve CD8+ T cells showed a shift toward more effector cells in MGL KOs and an increased expression of granzyme-B and interferon-γ, indicative of enhanced tumoricidal activity. 2-arachidonoyl glycerol (2-AG) was increased in tumors of MGL KO mice, and dose-dependently induced differentiation and migration of CD8+ T cells as well as migration and activation of eosinophils in vitro.
Our results suggest that next to cancer cell-derived MGL, TME cells expressing MGL are responsible for maintaining a pro-tumorigenic environment in tumors of NSCLC.
Wenzel, Mike ; Hardenberg, Jost von ; Welte, Maria-Noemi ; Doryumu, Samuel ; Höh, Robert Benedikt ; Wittler, Clarissa ; Höfner, Thomas ; Kriegmair, Maximilian ; Michel, Maurice Stephan ; Chun, Felix ; Herrmann, Jonas ; Mandel, Philipp ; Westhoff, Niklas Christian
Background: To compare severe infectious complication rates after transrectal prostate biopsies between cephalosporins and fluoroquinolones for antibiotic monoprophylaxis.
Material and Methods: In the multi-institutional cohort, between November 2014 and July 2020 patients received either cefotaxime (single dose intravenously), cefpodoxime (multiple doses orally) or fluoroquinolones (multiple-doses orally or single dose intravenously) for transrectal prostate biopsy prophylaxis. Data were prospectively acquired and retrospectively analyzed. Severe infectious complications were evaluated within 30 days after biopsy. Logistic regression models predicted biopsy-related infectious complications according to antibiotic prophylaxis, application type and patient- and procedure-related risk factors.
Results: Of 793 patients, 132 (16.6%) received a single dose of intravenous cefotaxime and were compared to 119 (15%) who received multiple doses of oral cefpodoxime and 542 (68.3%) who received fluoroquinolones as monoprophylaxis. The overall incidence of severe infectious complications was 1.0% (n=8). No significant differences were observed between the three compared groups (0.8% vs. 0.8% vs. 1.1%, p=0.9). The overall rate of urosepsis was 0.3% and did not significantly differ between the three compared groups as well.
Conclusion: Monoprophylaxis with third generation cephalosporins was efficient in preventing severe infectious complications after prostate biopsy. Single intravenous dose of cefotaxime and multiday regimen of oral cefpodoxime showed a low incidence of infectious complications <1%. No differences were observed in comparison to fluoroquinolones.
Einleitung: OTSC Proctology ist ein Verfahren in der Analfistelchirurgie dessen Erfolgsaussichten auch 9 Jahre nach der ersten klinischen Anwendung nicht abschließend beurteilt werden können. Die wenigen bisher publizierten Studien zeigen sehr divergente Ergebnisse mit Heilungsraten von 10 bis 90%.
Material und Methoden: Wir führten eine retrospektive Auswertung der Behandlungsergebnisse aller konsekutiven Patienten, die in dem Zeitraum vom 01.03.2014 bis 31.03.2017 in der koloproktologischen Abteilung der DKD Helios Klinik Wiesbaden mittels OTSC-Verfahren wegen Analfisteln operiert wurden, durch. Erfasst wurden Alter, Geschlecht, OP- und Aufenthaltsdauer, Operateur, Fistelart und –lokalisation, Vorhandensein von Stoma und CED, plastischer Fistelverschluss (PFV) in der Anamnese, Clipverbleib nach der OP, Dauer des Follow-ups, Komplikationen sowie postoperative Schmerzsituation. Die Datenauswertung erfolgte mittels deskriptiver Statistik bei Subgruppenanalyse unter Verwendung der Statistiksoftware SPSS 20.
Ergebnisse: Es wurden insgesamt 68 Fälle eingeschlossen, davon 37% weiblich und 63% männlich. Das durchschnittliche Alter betrug 52 Jahre (25 – 81). 19 (28%) Patienten litten an CED, 11 (16%) Patienten hatten ein Stoma. 34 (50%) der Patienten hatten plastischen Fistelverschluss in der Anamnese. Die Verteilung nach Fisteltyp war wie folgt: 58 (85%) transsphinktär, 4 (6%) suprasphinktär, 3 (4%) intersphinktär, 1 (1,5%) rektovaginal, 1 (1,5%) rektourethral und 1 (1,5%) Pouchfistel. Die häufigsten Fistelokalisationen waren bei 6 h (N = 26, 38%), 12 h (N = 14, 21%), 7 h (N = 7, 10%) und 3h (N = 5, 7%) SSL. Die durchschnittlichen OP-Dauer und stationärer Aufenthalt betrugen 25 min (6 – 90) und 7 Tage (1 – 14 Tage) entsprechend. Die durchschnittliche Dauer des Follow-ups betrug 29 Monate (10 – 36).
Die Fistelheilung im Gesamtkollektiv lag bei 48,5%, 1 (1,5%) Patient war lost-tofollow-up. In der weiblichen (N = 25) und männlichen (N = 43) Kohorte fand die Heilung in 40% und 53% der Fälle entsprechend statt. Die Heilungsraten bei intersphinktären (N = 3), transsphinktären (N = 58) und suprasphinktären (N = 4) Fisteln lagen bei 100%, 46,5% und 50% entsprechend, eine rektovaginale und eine rektourethrale Fistel sind nicht geheilt. Eine Pouchfistel ist geheilt.
Die Heilungsraten bei 6h und 12h SSL lagen bei 58% und 14% entsprechend mit deutlichem Vorteil bei posteriorer Fistellage. Dieser Vorteil blieb nach der Aufteilung der Fisteln in anteriore (N = 30) und posteriore (N = 38), mit
Heilungsraten von 33% und 60,5% entsprechend, bestehen. In den Subgruppen ohne CED (N = 49) und mit CED (N = 19) lagen die Heilungsraten bei 53% und 35% entsprechend. In den Subgruppen ohne PFV (N = 34) und mit PFV (N = 34) lagen die Heilungsraten bei 59% und 38% entsprechend. In der Subgruppe ohne Stoma (N = 57) wurde eine Heilung in 47% der Fälle, in der Subgruppe mit Stoma (N = 11) in 55% beobachtet. In der Subgruppe mit den kryploglandulären Fisteln (N = 47) war die Heilung in 55,3% zu sehen und in der Subgruppe mit
kryptoglandulären Fisteln ohne PFV (N = 27) bei 63%.
In 48 (70,6%) Fällen wurde der Clip aktiv entfernt, in 11 (16,2%) Fällen kam es zum Spontanverlust und in 8 (11,8%) Fällen blieb der Clip in situ. Die durchschnittliche Zeit bis zur Klammerentfernung betrug 4 Monate. Die Heilungsraten bei Clipentfernung, Clipverbleib und Clipspontanabgang lagen bei 42%, 100% und 45% entsprechend.
Der maximale Schmerz nach NRS 0 – 2 bei 61% der Patienten, NRS 3 – 4 bei 28% und NRS 5 – 7 nur bei 11%. Bei 50% der Fälle war kein Opiat erforderlich und bei 39% der Fälle erfolgte die Opiateinnahme nicht länger als 2 Tage.
Die Komplikationen waren sehr selten: eine Nachblutung mit Clipdislokation (1,5%), ein Analabszess (1,5%), 2 Fälle (3%) der neuaufgetretenen Stuhlschmieren und 1 (1,5%) Wundheilungsstörung intraanal, die spontan abheilte. In 4 (6%) Fällen kam es zur Klammerdislokation vom inneren
Fistelostium mit konsekutiver Fistelpersistenz.
Fazit: OTSC ist ein komplikationsarmes und schmerzarmes Verfahren mit kurzer OP-Zeit und könnte einen festen Platz in der Analfistelchirurgie einnehmen. Die bestmöglichen Ergebnisse lassen sich bei dorsal gelegenen Analfisteln in
nichtvoroperierten Patienten ohne CED erzielen.
Background: Mesenchymal stromal cells (MSCs), multipotent progenitors that can be isolated from a variety of different tissues, are becoming increasingly important as cell therapeutics targeting immunopathologies and tissue regeneration. Current protocols for MSC isolation from bone marrow (BM) rely on density gradient centrifugation (DGC), and the production of sufficient MSC doses is a critical factor for conducting clinical MSC trials. Previously, a Good Manufacturing Practice (GMP)–compatible non-woven fabric filter device system to isolate MSCs was developed to increase the MSC yield from the BM. The aim of our study was to compare high-resolution phenotypic and functional characteristics of BM-MSCs isolated with this device and with standard DGC technology.
Methods: Human BM samples from 5 donors were analyzed. Each sample was divided equally, processing by DGC, and with the filter device. Stem cell content was assessed by quantification of colony-forming units fibroblasts (CFU-F). Immunophenotype was analyzed by multicolor flow cytometry. In vitro trilineage differentiation potential, trophic factors, and IDO-1 production were assessed. Functionally, immunomodulatory potential, wound healing, and angiogenesis were assayed in vitro.
Results: The CFU-F yield was 15-fold higher in the MSC preparations isolated with the device compared to those isolated by DGC. Consequently, the MSC yield that could be manufactured at passage 3 per mL collected BM was more than 10 times higher in the device group compared to DGC (1.65 × 109 vs. 1.45 × 108). The immunomodulatory potential and IDO-1 production showed donor-to-donor variabilities without differences between fabric filter-isolated and DGC-isolated MSCs. The results from the wound closure assays, the tube formation assays, and the trilineage differentiation assays were similar between the groups with respect to the isolation method. Sixty-four MSC subpopulations could be quantified with CD140a+CD119+CD146+ as most common phenotype group, and CD140a+CD119+CD146+MSCA-1–CD106–CD271– and CD140a+CD119+CD146–MSCA-1–CD106–CD271– as most frequent MSC subpopulations. As trophic factors hepatocyte growth factor, epidermal growth factor, brain-derived neurotrophic factor, angiopoietin-1, and vascular endothelial growth factor A could be detected in both groups with considerable variability between donors, but independent of the respective MSC isolation technique.
Conclusion: The isolation of MSCs using a GMP-compatible fabric filter system device resulted in higher yield of CFU-F, producing substantially more MSCs with similar subpopulation composition and functional characteristics as MSCs isolated by DGC.
Kann, Gerrit ; Juling, Hermann ; Ilievski, Valentina ; Burger, Gerrit ; Göttig, Stephan ; Stephan, Christoph ; Wetzstein, Nils
A 24-year-old patient from Cameroon presented to our hospital because of a foreign structure in her left eye. To our knowledge, for the first time, fluorescent microscopy revealed motile microfilariae, and the diagnosis of loiasis was established. Despite substantial microfilaremia, eosinophilia only unmasked after the initiation of antiparasitic therapy.
Arsović, Aleksandar ; Halbach, Melanie Vanessa ; Canet Pons, Júlia ; Esen-Sehir, Dilhan ; Döring, Claudia ; Freudenberg, Florian ; Czechowska, Nicoletta ; Seidel, Kay ; Baader, Stephan L. ; Gispert, Suzana ; Şen, Nesli Ece ; Auburger, Georg
Spinocerebellar ataxia type 2 (SCA2) is caused by polyglutamine expansion in Ataxin-2 (ATXN2). This factor binds RNA/proteins to modify metabolism after stress, and to control calcium (Ca2+) homeostasis after stimuli. Cerebellar ataxias and corticospinal motor neuron degeneration are determined by gain/loss in ATXN2 function, so we aimed to identify key molecules in this atrophic process, as potential disease progression markers. Our Atxn2-CAG100-Knock-In mouse faithfully models features observed in patients at pre-onset, early and terminal stages. Here, its cerebellar global RNA profiling revealed downregulation of signaling cascades to precede motor deficits. Validation work at mRNA/protein level defined alterations that were independent of constant physiological ATXN2 functions, but specific for RNA/aggregation toxicity, and progressive across the short lifespan. The earliest changes were detected at three months among Ca2+ channels/transporters (Itpr1, Ryr3, Atp2a2, Atp2a3, Trpc3), IP3 metabolism (Plcg1, Inpp5a, Itpka), and Ca2+-Calmodulin dependent kinases (Camk2a, Camk4). CaMKIV–Sam68 control over alternative splicing of Nrxn1, an adhesion component of glutamatergic synapses between granule and Purkinje neurons, was found to be affected. Systematic screening of pre/post-synapse components, with dendrite morphology assessment, suggested early impairment of CamKIIα abundance together with the weakening of parallel fiber connectivity. These data reveal molecular changes due to ATXN2 pathology, primarily impacting excitability and communication.
Spohner, Anna Katharina ; Jakobi, Katja ; Trautmann, Sandra ; Thomas, Dominique Jeanette ; Schumacher, Fabian ; Kleuser, Burkhard ; Lütjohann, Dieter ; El-Hindi, Khadija ; Grösch, Sabine ; Pfeilschifter, Josef ; Saba, Julie D. ; Meyer zu Heringdorf, Dagmar
Sphingosine 1 phosphate (S1P) lyase (Sgpl1) catalyses the irreversible cleavage of S1P and thereby the last step of sphingolipid degradation. Loss of Sgpl1 in humans and mice leads to accumulation of sphingolipids and multiple organ injuries. Here, we addressed the role of hepatocyte Sgpl1 for regulation of sphingolipid homoeostasis by generating mice with hepatocyte-specific deletion of Sgpl1 (Sgpl1HepKO mice). Sgpl1HepKO mice had normal body weight, liver weight, liver structure and liver enzymes both at the age of 8 weeks and 8 months. S1P, sphingosine and ceramides, but not glucosylceramides or sphingomyelin, were elevated by ~1.5–2-fold in liver, and this phenotype did not progress with age. Several ceramides were elevated in plasma, while plasma S1P was normal. Interestingly, S1P and glucosylceramides, but not ceramides, were elevated in bile of Sgpl1HepKO mice. Furthermore, liver cholesterol was elevated, while LDL cholesterol decreased in 8-month-old mice. In agreement, the LDL receptor was upregulated, suggesting enhanced uptake of LDL cholesterol. Expression of peroxisome proliferator-activated receptor-γ, liver X receptor and fatty acid synthase was unaltered. These data show that mouse hepatocytes largely compensate the loss of Sgpl1 by secretion of accumulating sphingolipids in a specific manner into blood and bile, so that they can be excreted or degraded elsewhere.
Erikson, Elina ; Wratil, Paul Robin ; Frank, Martin ; Ambiel, Ina ; Pahnke, Katharina ; Pino, Maria ; Azadi, Parastoo ; Izquierdo-Useros, Nuria ; Martinez-Picado, Javier ; Meier, Chris ; Schnaar, Ronald L. ; Crocker, Paul R. ; Reutter, Werner ; Keppler, Oliver Till
Siglec-1 (sialoadhesin, CD169) is a surface receptor on human cells that mediates trans-enhancement of HIV-1 infection through recognition of sialic acid moieties in virus membrane gangliosides. Here, we demonstrate that mouse Siglec-1, expressed on the surface of primary macrophages in an interferon-α-responsive manner, captures murine leukemia virus (MLV) particles and mediates their transfer to proliferating lymphocytes. The MLV infection of primary B-cells was markedly more efficient than that of primary T-cells. The major structural protein of MLV particles, Gag, frequently co-localized with Siglec-1, and trans-infection, primarily of surface-bound MLV particles, efficiently occurred. To explore the role of sialic acid for MLV trans-infection at a submolecular level, we analyzed the potential of six sialic acid precursor analogs to modulate the sialylated ganglioside-dependent interaction of MLV particles with Siglec-1. Biosynthetically engineered sialic acids were detected in both the glycolipid and glycoprotein fractions of MLV producer cells. MLV released from cells carrying N-acyl-modified sialic acids displayed strikingly different capacities for Siglec-1-mediated capture and trans-infection; N-butanoyl, N-isobutanoyl, N-glycolyl, or N-pentanoyl side chain modifications resulted in up to 92 and 80% reduction of virus particle capture and trans-infection, respectively, whereas N-propanoyl or N-cyclopropylcarbamyl side chains had no effect. In agreement with these functional analyses, molecular modeling indicated reduced binding affinities for non-functional N-acyl modifications. Thus, Siglec-1 is a key receptor for macrophage/lymphocyte trans-infection of surface-bound virions, and the N-acyl side chain of sialic acid is a critical determinant for the Siglec-1/MLV interaction.
Kohlhase, Konstantin David ; Strzelczyk, Adam ; Porto, Luciana ; Beißel, Achim ; Curry, Daniel J. ; Rosenow, Felix ; Schubert-Bast, Susanne
Einleitung: Die stereotaktische Laserthermoablation (SLTA) stellt eine minimal-invasive Behandlung für therapierefraktäre Epilepsien auf dem Boden eines hypothalamischen Hamartoms (HH) dar. Durch die weitreichenden Folgen einer therapierefraktären Epilepsie können hohe direkte Kosten entstehen, die durch eine zu erzielende Anfallsfreiheit gesenkt werden können.
Methoden: Anhand einer Patientin mit einem HH sollen die Auswirkungen einer solchen Erkrankung beleuchtet und der Krankheitsverlauf nach erfolgter SLTA dargestellt werden. Zur Beurteilung der Kosteneffizienz der SLTA wurden die direkten Kosten, basierend auf den Krankenversicherungsdaten der Patientin, über die Versicherungsjahre 2017 bis 2020 analysiert.
Ergebnisse:
Bei der Patientin bestand eine hochaktive, medikamentenrefraktäre Epilepsie mit erhöhtem Verletzungsrisiko und zunehmender Verschlechterung der schulischen Leistung und der psychischen Verfassung. Begleitend bestand durch das HH eine Pubertas praecox. Nach SLTA entwickelte die Patientin mit einem Follow-up von 26 Monaten eine vollständige Anfallsfreiheit sowie eine endokrinologische Stabilisierung, sodass die antikonvulsive als auch die hormonelle Medikation im Verlauf beendet werden konnten. Relevante persistierende Komplikationen wurden nicht beobachtet. Die direkten jährlichen Kosten (stationär [ausschließlich der SLTA selbst]/ambulant/Medikamente) reduzierten sich von € 6603 in 2017 und € 12.903 in 2018 auf € 3609 in 2019 und zuletzt € 617 in 2020, was einer Reduktion von bis zu 95 % (2018 gegenüber 2020) entsprach. Zusätzlich konnten die Kosten einer geplanten Integrationsassistenz von schätzungsweise € 18.000/Jahr eingespart werden.
Schlussfolgerung: Die SLTA stellt eine effektive und risikoarme Behandlung von HH dar und führt bereits nach 2 Jahren zu einer relevanten Einsparung der direkten Kosten, was bei der Kosten-Nutzen-Abwägung der SLTA einzubeziehen ist.
Rauch, Maximilian ; Tausch, Daniel ; Stera, Susanne ; Blanck, Oliver ; Wolff, Robert Jürgen ; Meissner, Markus ; Urban, Hans ; Hattingen, Elke
Introduction: Combination therapy for melanoma brain metastases (MM) using stereotactic radiosurgery (SRS) and immune checkpoint-inhibition (ICI) or targeted therapy (TT) is currently of high interest. In this collective, time evolution and incidence of imaging findings indicative of pseudoprogression is sparsely researched. We therefore investigated time-course of MRI characteristics in these patients.
Methods: Data were obtained retrospectively from 27 patients (12 female, 15 male; mean 61 years, total of 169 MMs). Single lesion volumes, total MM burden and edema volumes were analyzed at baseline and follow-up MRIs in 2 months intervals after SRS up to 24 months. The occurrence of intralesional hemorrhages was recorded.
Results: 17 patients (80 MM) received ICI, 8 (62 MM) TT and 2 (27 MM) ICI + TT concomitantly to SRS. MM-localization was frontal (n = 89), temporal (n = 23), parietal (n = 20), occipital (n = 10), basal ganglia/thalamus/insula (n = 10) and cerebellar (n = 10). A volumetric progression of MM 2–4 months after SRS was observed in combined treatment with ICI (p = 0.028) and ICI + TT (p = 0.043), whereas MMs treated with TT showed an early volumetric regression (p = 0.004). Edema volumes moderately correlated with total MM volumes (r = 0.57; p < 0.0001). Volumetric behavior did not differ significantly over time regarding lesions’ initial sizes or localizations. No significant differences between groups were observed regarding rates of post-SRS intralesional hemorrhages.
Conclusion: Reversible volumetric increases in terms of pseudoprogression are observed 2–4 months after SRS in patients with MM concomitantly treated with ICI and ICI + TT, rarely after TT. Edema volumes mirror total MM volumes. Medical treatment type does not significantly affect rates of intralesional hemorrhage.
Die randomisierte, dreiarmig kontrollierte Studie zu täglicher, peroraler Zusatzkost (ONS) bei Hämodialysepatienten (CHD) im Endstadium der Niereninsuffizienz (ESRD) über 6 Monate zeigte keine signifikanten Verbesserungen hinsichtlich folgender Nutritions-/Retentions- und Inflammationsparameter: Subjective Global Assessment (SGA); Body Mass Index (BMI); Querschnitt des Muskulus Iliopsoas,Oberarmumfang und Dicke des Unterhautfettgewebes (MRT); örperzellmasse und Phasenwinkel (Bioimpedanzanalyse BIA); Tumornekrosefaktor α (TNFα); Interleukin 1β und 6 (IL-1β und IL-6); C-Reaktives Protein (CRP). Der Querschnitt des Muskulus biceps brachii blieb in der Kontrollgruppe anfangs und zum Ende höher wie in den Interventionsgruppen. Der Serumkreatininwert der Interventionsgruppe mit HIV war anfangs geringer als in den übrigen Gruppen, die glomeruläre Filtrationsrate entsprechend besser, zum Ende waren diese Unterschiede nivelliert. Der Hauptbefund liegt in der hohen Mortalitätsrate der HIV-positiven Hämodialysepatienten (2 von 7 Pat., 28,6%), von denen beide im SGA als schwer mangel-/fehlernährt eingestuft wurden. Die Therapie eines Malnutritions-Infalmmations-Komplexes ist nicht allein durch orale Zusatzkost möglich. Weitere Studien müssen multimodale Konzepte zur Diagnose und zur Therapie erforschen. Hierzu kann perorale Zusatzkost ein einfach durchzuführendes Mittel als Teil der Behandlungsstrategie sein, zur erweiterten Diagnose kann die Bioimpedanzanalyse eine Möglichkeit sein, um den Teilaspekt der Nutritionskontrolle zu erfüllen.
Rosentreter, Jelena Lisa ; Alt, Jürgen ; Fried, Marius ; Chakupurakal, Geothy ; Stratmann, Jan Alexander ; Krämer, Irene
Introduction: Cancer patients tend to prefer oral instead of parenteral chemotherapy. To date, there is little evidence on the medication adherence in cancer patients. We investigated medication adherence to tyrosine kinase inhibitors in patients suffering from non-small cell lung cancer. Methods: Tyrosine kinase inhibitor adherence was measured electronically by MEMS® (medication event monitoring system) over at least six months. Adherence rates were calculated in terms of Dosing Compliance, Timing Compliance, Taking Compliance, and Drug Holidays. Patients were dichotomized as adherent when Dosing Compliance and Timing Compliance were ≥80%, Taking Compliance ranged between 90 and 110%, and <1 Drug Holiday was registered. Quality of life was assessed by two questionnaires (EORTC QLQ-C30 version 3.0, EORTC QLQ-LC13) at three time points. Adverse drug events were reported via patient diaries. Results: Out of 32 patients enrolled, data from 23 patients were evaluable. Median Dosing Compliance, Taking Compliance, and Timing Compliance adherence rates of tyrosine kinase inhibitor intake amounted to 100%, 98%, and 99%, respectively; Drug Holidays were observed in three patients. Four patients were dichotomized as non-adherent. Three of them had a twice-daily tyrosine kinase inhibitor regimen. Median quality of life scores amounted to 67 (max. 100) and remained unchanged over the study period. Fatigue and rash were the most frequently reported adverse drug events. Conclusion: Medication adherence of non-small cell lung cancer patients treated with tyrosine kinase inhibitors was extraordinarily high and is likely to support the effectiveness of tyrosine kinase inhibitor treatment and a good quality of life over a long period of time. Adherence facilitating information and education is especially relevant for patients taking tyrosine kinase inhibitors in a twice-daily regimen.
Willmann, Matthias ; Götting, Stephan ; Bezdan, Daniela ; Maček, Boris ; Velic, Ana ; Marschal, Matthias ; Vogel, Wichard ; Flesch, Ingo ; Markert, Uwe ; Schmidt, Annika Mareike ; Kübler, Pierre David Martin ; Haug, Maria ; Javed, Mumina ; Jentzsch, Benedikt ; Oberhettinger, Philipp ; Schütz, Monika ; Bohn, Erwin ; Sonnabend, Michael ; Klein, Kristina ; Autenrieth, Ingo B. ; Ossowski, Stephan ; Schwarz, Sandra ; Peter, Silke
Pseudomonas aeruginosa is a human pathogen that causes health-care associated blood stream infections (BSI). Although P. aeruginosa BSI are associated with high mortality rates, the clinical relevance of pathogen-derived prognostic biomarker to identify patients at risk for unfavorable outcome remains largely unexplored. We found novel pathogen-derived prognostic biomarker candidates by applying a multi-omics approach on a multicenter sepsis patient cohort. Multi-level Cox regression was used to investigate the relation between patient characteristics and pathogen features (2298 accessory genes, 1078 core protein levels, 107 parsimony-informative variations in reported virulence factors) with 30-day mortality. Our analysis revealed that presence of the helP gene encoding a putative DEAD-box helicase was independently associated with a fatal outcome (hazard ratio 2.01, p = 0.05). helP is located within a region related to the pathogenicity island PAPI-1 in close proximity to a pil gene cluster, which has been associated with horizontal gene transfer. Besides helP, elevated protein levels of the bacterial flagellum protein FliL (hazard ratio 3.44, p < 0.001) and of a bacterioferritin-like protein (hazard ratio 1.74, p = 0.003) increased the risk of death, while high protein levels of a putative aminotransferase were associated with an improved outcome (hazard ratio 0.12, p < 0.001). The prognostic potential of biomarker candidates and clinical factors was confirmed with different machine learning approaches using training and hold-out datasets. The helP genotype appeared the most attractive biomarker for clinical risk stratification due to its relevant predictive power and ease of detection.
The detection of multiple biomolecule classes in one go is highly desirable for a wide variety of areas, and in particular for point-of-care diagnostics. For example, wound infections are a major problem for patient’s health and cause huge efforts in our healthcare system. In this regard, monitoring infected wounds through simultaneous detection of pathogens via nucleic acid analysis and detection of local inflammation biomarkers is key in order to enable a personalized therapy, improve the clinical outcome and thus, leading to a reduction of overall healthcare costs. In this regard, wound exudate offers an attractive sample material which can be collected in a non-invasive manner. Here, we report the development of a Multianalyte-Assay detecting inflammation biomarkers and pathogen DNA simultaneously from one sample within 35 min. Protein-compatible amplification and labeling transforms nucleic acid information into the measurement principle for protein detection. The combination with rapid detection via lateral flow immunoassay enables a fast and straightforward analysis of multiple biomolecule classes using identical assay conditions. To demonstrate the feasibility of the Multianalyte-Assay, the proinflammatory cytokine interleukin-6 (IL-6) and gDNA of the opportunistic pathogen Pseudomonas aeruginosa (P. aeruginosa) are used. The detection limits of 4 ng/mL IL-6 and 70 copies/reaction P. aeruginosa gDNA meet the clinically relevant range and thus, having tremendous potential to improve the wound management at the point-of-care.
Majchrzak, Mario ; Bronner, Korbinian ; Laperche, Syria ; Riester, Elena ; Bakker, Ed ; Bollhagen, Ralf ; Klinkicht, Markus ; Vermeulen, Marion ; Schmidt, Michael
Background: The diagnostic accuracy of the Elecsys® HCV Duo antigen-antibody combination immunoassay (Roche Diagnostics GmbH) was evaluated for the detection of hepatitis C virus (HCV) infection, versus commercially available comparators.
Methods: This multicenter study (August 2020–March 2021) assessed the specificity of the Elecsys HCV Duo immunoassay and comparator assays in blood donor and routine clinical laboratory samples; sensitivity was determined in confirmed HCV-positive samples and seroconversion panels. The Elecsys HCV Duo immunoassay was compared with the Monolisa HCV Ag-Ab ULTRA V2, Murex HCV Ag/Ab Combination and ARCHITECT HCV Ag assays, as well as nucleic acid testing (NAT). The antibody (anti-HCV) module of the Elecsys HCV Duo immunoassay was compared with the Elecsys Anti-HCV II, Alinity s Anti-HCV, ARCHITECT Anti-HCV and RIBA HCV 3.0 SIA assays.
Results: The specificity of the Elecsys HCV Duo immunoassay was 99.94% (95% confidence interval [CI], 99.89–99.97) and 99.92% (95% CI, 99.71–99.99) in blood donor (n = 20,634) and routine clinical laboratory samples (n = 2531), respectively. The specificity of the Elecsys HCV Duo immunoassay was similar or better than comparator assays. The sensitivity of the Elecsys HCV Duo immunoassay in confirmed HCV-positive samples (n = 257) was 99.6%. In seroconversion panels, the Elecsys HCV Duo immunoassay detected infections earlier (2.2–21.9 days) than all but one of the comparator assays and detected HCV 1.8 days later than NAT.
Conclusions: The Elecsys HCV Duo immunoassay shows high diagnostic accuracy, reduces the diagnostic window, and could be used when NAT is not possible.
Willems, Laurent M. ; Hochbaum, Maja ; Frey, Katharina ; Schulz, Juliane ; Menzler, Katja ; Langenbruch, Lisa Marie ; Kovać, Stjepana ; Immisch, Ilka ; Podewils, Felix von ; Hamacher, Mario ; Siebenbrodt, Kai ; Rosenow, Felix ; Reese, Jens-Peter ; Strzelczyk, Adam
Objective: This study was undertaken to quantify epilepsy-related costs of illness (COI) in Germany and identify cost-driving factors.
Methods: COI were calculated among adults with epilepsy of different etiologies and severities. Multiple regression analysis was applied to determine any epilepsy-related and sociodemographic factors that serve as cost-driving factors.
Results: In total, 486 patients were included, with a mean age of 40.5 ± 15.5 years (range = 18–83 years, 58.2% women). Mean 3-month COI were estimated at €4911, €2782, and €2598 for focal, genetic generalized, and unclassified epilepsy, respectively. The mean COI for patients with drug-refractory epilepsy (DRE; €7850) were higher than those for patients with non-DRE (€4720), patients with occasional seizures (€3596), or patients with seizures in remission for >1 year (€2409). Identified cost-driving factors for total COI included relevant disability (unstandardized regression coefficient b = €2218), poorer education (b = €2114), living alone (b = €2612), DRE (b = €1831), and frequent seizures (b = €2385). Younger age groups of 18–24 years (b = −€2945) and 25–34 years (b = −€1418) were found to have lower overall expenditures. A relevant disability (b = €441), DRE (b = €1253), frequent seizures (b = €735), and the need for specialized daycare (b = €749) were associated with higher direct COI, and poorer education (b = €1969), living alone (b = €2612), the presence of a relevant disability (b = €1809), DRE (b = €1831), and frequent seizures (b = €2385) were associated with higher indirect COI.
Significance: This analysis provides up-to-date COI data for use in further health economics analyses, highlighting the high economic impacts associated with disease severity, disability, and disease-related loss of productivity among adult patients with epilepsy. The identified cost drivers could be used as therapeutic and socioeconomic targets for future cost-containment strategies.
Rhim, Ha-Young ; Won, Sae-Yeon ; Kashefiolasl, Sepide ; Brawanski, Nina ; Hattingen, Elke ; Berkefeld, Joachim ; Seifert, Volker ; Konczalla, Jürgen
Patient care in a neurointensive care unit (neuro-ICU) is challenging. Multidrug-resistant organisms (MDROs) are increasingly common in the routine clinical practice. We evaluated the impact of infection with MDROs on outcomes in patients with subarachnoid hemorrhage (SAH). A single-center retrospective analysis of SAH cases involving patients treated in the neuro-ICU was performed. The outcome was assessed 6 months after SAH using the modified Rankin Scale [mRS, favorable (0–2) and unfavorable (3–6)]. Data were compared by matched-pair analysis. Patient characteristics were well matched in the MDRO (n = 61) and control (n = 61) groups. In this center, one nurse was assigned to a two-bed room. If a MDRO was detected, the patient was isolated, and the nurse was assigned to the patient infected with the MDRO. In the MDRO group, 29 patients (48%) had a favorable outcome, while 25 patients (41%) in the control group had a favorable outcome; the difference was not significant (p > 0.05). Independent prognostic factors for unfavorable outcomes were worse status at admission (OR = 3.1), concomitant intracerebral hematoma (ICH) (OR = 3.7), and delayed cerebral ischemia (DCI) (OR = 6.8). Infection with MRDOs did not have a negative impact on the outcome in SAH patients. Slightly better outcomes were observed in SAH patients infected with MDROs, suggesting the benefit of individual care.
SAMHD1 is discussed as a tumour suppressor protein, but its potential role in cancer has only been investigated in very few cancer types. Here, we performed a systematic analysis of the TCGA (adult cancer) and TARGET (paediatric cancer) databases, the results of which did not suggest that SAMHD1 should be regarded as a bona fide tumour suppressor. SAMHD1 mutations that interfere with SAMHD1 function were not associated with poor outcome, which would be expected for a tumour suppressor. High SAMHD1 tumour levels were associated with increased survival in some cancer entities and reduced survival in others. Moreover, the data suggested differences in the role of SAMHD1 between males and females and between different races. Often, there was no significant relationship between SAMHD1 levels and cancer outcome. Taken together, our results indicate that SAMHD1 may exert pro- or anti-tumourigenic effects and that SAMHD1 is involved in the oncogenic process in a minority of cancer cases. These findings seem to be in disaccord with a perception and narrative forming in the field suggesting that SAMHD1 is a tumour suppressor. A systematic literature review confirmed that most of the available scientific articles focus on a potential role of SAMHD1 as a tumour suppressor. The reasons for this remain unclear but may include confirmation bias and publication bias. Our findings emphasise that hypotheses, perceptions, and assumptions need to be continuously challenged by using all available data and evidence.
SAMHD1 is discussed as a tumour suppressor protein, but its potential role in cancer has only been investigated in very few cancer types. Here, we performed a systematic analysis of the TCGA (adult cancer) and TARGET (paediatric cancer) databases, the results of which did not suggest that SAMHD1 should be regarded as a bona fide tumour suppressor. SAMHD1 mutations that interfere with SAMHD1 function were not associated with poor outcome, which would be expected for a tumour suppressor. High SAMHD1 tumour levels were associated with increased survival in some cancer entities and reduced survival in others. Moreover, the data suggested differences in the role of SAMHD1 between males and females and between different races. Often, there was no significant relationship between SAMHD1 levels and cancer outcome. Taken together, our results indicate that SAMHD1 may exert pro-or anti-tumourigenic effects and that SAMHD1 is involved in the oncogenic process in a minority of cancer cases. These findings seem to be in disaccord with a perception and narrative forming in the field suggesting that SAMHD1 is a tumour suppressor. A systematic literature review confirmed that most of the available scientific articles focus on a potential role of SAMHD1 as a tumour suppressor. The reasons for this remain unclear but may include confirmation bias and publication bias. Our findings emphasise that hypotheses, perceptions, and assumptions need to be continuously challenged by using all available data and evidence.
Colorectal cancer (CRC) is one of the most frequently diagnosed tumor in humans and one of the most common causes of cancer-related death worldwide. The pathogenesis of CRC follows a multistage process which together with somatic gene mutations is mainly attributed to the dysregulation of signaling pathways critically involved in the maintenance of homeostasis of epithelial integrity in the intestine. A growing number of studies has highlighted the critical impact of members of the tripartite motif (TRIM) protein family on most types of human malignancies including CRC. In accordance, abundant expression of many TRIM proteins has been observed in CRC tissues and is frequently correlating with poor survival of patients. Notably, some TRIM members can act as tumor suppressors depending on the context and the type of cancer which has been assessed. Mechanistically, most cancer-related TRIMs have a critical impact on cell cycle control, apoptosis, epithelial–mesenchymal transition (EMT), metastasis, and inflammation mainly through directly interfering with diverse oncogenic signaling pathways. In addition, some recent publications have emphasized the emerging role of some TRIM members to act as transcription factors and RNA-stabilizing factors thus adding a further level of complexity to the pleiotropic biological activities of TRIM proteins. The current review focuses on oncogenic signaling processes targeted by different TRIMs and their particular role in the development of CRC. A better understanding of the crosstalk of TRIMs with these signaling pathways relevant for CRC development is an important prerequisite for the validation of TRIM proteins as novel biomarkers and as potential targets of future therapies for CRC.
Multilevel-Untersuchung des nitrinergen Systems bei affektiven Störungen und schizophrenen Psychosen
(2023)
Das nitrinerge System und damit auch NOx als Neurotransmitter werden mit der Entstehung verschiedener psychischer Erkrankungen in Verbindung gebracht. Die genaue Rolle des Botenstoffs ist jedoch nicht ausreichend geklärt und auch die Frage, ob dieser als diagnostischer oder prädiktiver Biomarker nützlich sein könnte, ist unbeantwortet. In der vorliegenden Arbeit wurde folglich untersucht, ob es Unterschiede zwischen den Diagnosegruppen MDD, BIP, SCZ und der Kontrollgruppe bezüglich peripherer NOx- Konzentrationen gibt. Darüber hinaus wurden Unterschiede innerhalb der Diagnosegruppen im Krankheitsverlauf im Sinne von Phasenunterschieden mittels zweier Messzeitpunkte untersucht und analysiert, ob es Korrelationen mit genetischen Variationen in NOS-Genabschnitten gibt. Insgesamt wurden 185 Probanden in die Studie mitaufgenommen: 52 gesunde CTRL, 43 Patienten mit MDD, 41 Patienten mit BIP und 49 Patienten mit SCZ. Biochemische, genetische und klinische Daten wurden bei Aufnahme und Entlassung in der psychiatrischen Abteilung des Universitätsklinikums Frankfurt erhoben. Klinische Daten, die den Symptomverlauf 90 und die Erkrankungsschwere beurteilten, nutzten dazu standardisierte teilstrukturierte klinische Interviews. Biochemische Daten wurden mittels im Serum gemessener NOx- Spiegel quantifiziert. Bezüglich der Untersuchung der Risikogenvarianten wurden Probanden anhand des NOS1 ex1f-VNTR-Polymorphismus sowie SNPs in den Genen NOS1, NOS3 und NOS1AP genotypisiert. Bei Aufnahme wiesen SCZ-Patienten im Vergleich zu CTRL-, MDD- und BIP-Gruppen signifikant höhere NOx- Konzentrationen auf. Während NOx- Spiegel im Behandlungsverlauf bei MDD- und BIP-Patienten signifikant zunahmen, konnte dies bei SCZ-Patienten nicht beobachtet werden. Weiterhin konnte gezeigt werden, dass Patienten, deren depressive Beschwerden nicht relevant zurückgingen, bei Entlassung signifikant höhere NOx- Konzentrationen aufwiesen, was durch die Beobachtung einer signifikant positiven Korrelation zwischen NOx- Serumspiegeln und depressiven Symptomen bei Entlassung unterstützt wurde. Bei der genetischen Untersuchung der Daten fiel auf, dass homozygote Träger des kurzen VNTR-Allels signifikant erhöhte NOx- Konzentrationen besaßen. Diese Ergebnisse blieben bei jenen Trägern auch nach Entlassung signifikant. Insgesamt gibt es Hinweise darauf, dass erhöhte periphere NOx- Metabolitkonzentrationen mit einer Zunahme der Psychopathologie bzw. der Erkrankungsschwere einhergehen könnten, was möglicherweise auf den NOS1 ex1f-VNRT-Polymorphismus zurückzuführen ist. Außerdem zeigten zwei SNPs, welche beide im NOS1AP-Gen lokalisiert sind, bei BIP Patienten signifikant gesteigerte NOx- Werte. Die vorliegenden Ergebnisse deuten darauf hin, dass NO-Signalübertragung und NOS-Genotypen in der Pathogenese psychischer Erkrankungen eine Rolle spielen könnten. Ob diese Veränderungen allerdings kausal mit Krankheitsprozessen zu tun haben oder ob es eher Epiphänomene der Erkrankungen sind, kann mit dieser Studie nicht geklärt werden. Die Genvarianten könnten wiederum bei der Regulierung von peripheren NOx- Konzentrationen von Bedeutung sein. Die Arbeit liefert zudem Hinweise, die Verwendung von NOx als möglichen peripheren Biomarker weiter zu verfeinern und zu untersuchen. Zukünftige Studien, die die Wirksamkeit von NOx- modulierenden Pharmaka untersuchen, könnten davon profitieren, Diagnosegruppen nach Subgruppen einzuteilen, die sowohl NOS Risikogenvarianten als auch periphere NOx- Spiegel im Sinne eines Biomarker beachten.
For medicine to fulfill its promise of personalized treatments based on a better understanding of disease biology, computational and statistical tools must exist to analyze the increasing amount of patient data that becomes available. A particular challenge is that several types of data are being measured to cope with the complexity of the underlying systems, enhance predictive modeling and enrich molecular understanding.
Here we review a number of recent approaches that specialize in the analysis of multimodal data in the context of predictive biomedicine. We focus on methods that combine different OMIC measurements with image or genome variation data. Our overview shows the diversity of methods that address analysis challenges and reveals new avenues for novel developments.
Spontaneous brain activity builds the foundation for human cognitive processing during external demands. Neuroimaging studies based on functional magnetic resonance imaging (fMRI) identified specific characteristics of spontaneous (intrinsic) brain dynamics to be associated with individual differences in general cognitive ability, i.e., intelligence. However, fMRI research is inherently limited by low temporal resolution, thus, preventing conclusions about neural fluctuations within the range of milliseconds. Here, we used resting-state electroencephalographical (EEG) recordings from 144 healthy adults to test whether individual differences in intelligence (Raven’s Advanced Progressive Matrices scores) can be predicted from the complexity of temporally highly resolved intrinsic brain signals. We compared different operationalizations of brain signal complexity (multiscale entropy, Shannon entropy, Fuzzy entropy, and specific characteristics of microstates) regarding their relation to intelligence. The results indicate that associations between brain signal complexity measures and intelligence are of small effect sizes (r ∼ 0.20) and vary across different spatial and temporal scales. Specifically, higher intelligence scores were associated with lower complexity in local aspects of neural processing, and less activity in task-negative brain regions belonging to the default-mode network. Finally, we combined multiple measures of brain signal complexity to show that individual intelligence scores can be significantly predicted with a multimodal model within the sample (10-fold cross-validation) as well as in an independent sample (external replication, N = 57). In sum, our results highlight the temporal and spatial dependency of associations between intelligence and intrinsic brain dynamics, proposing multimodal approaches as promising means for future neuroscientific research on complex human traits.
Ana I., González-González ; Dinh, Truc Sophia ; Brünn, Robin ; Brückle, Janina Maria-Sophie ; Schwarz, Christine ; Dieckelmann, Mirjam ; Müller, Beate ; Akker, Marjan van den
Middle-aged persons with multimorbidity have to take their illnesses into account in their daily work, family and leisure activities. The MuMiA project aims to identify early preventive measures that make it easier for those between 30 and 60 years of age with multiple chronic diseases to manage their illnesses in their everyday lives. An interdisciplinary workshop and interviews with multimorbid middle-aged adults and their principal healthcare providers will be used to collect information on the management of care in the contexts of patients’ daily work, family and leisure activities. Data obtained in the interviews will be coded inductively and analysed using content analysis. Workshop outputs will be transcribed and evaluated by the authors. This study has received ethical approval from the Faculty of Medicine Ethics Committee of Goethe University (2021-47). The project will generate prevention recommendations that reflect the experiences of middle-aged persons living with multimorbidity and the views of their principal healthcare providers. The findings will be disseminated via conferences and peer-reviewed publications.
Cinatl, Jindrich ; Michaelis, Martin ; Hernáiz Drievert, Pablo ; Cinatl, Jaroslav ; Hrabeta, Jan ; Suhan, Tatyana ; Doerr, Hans Wilhelm ; Vogel, Jens-Uwe
The mode of the antitumoral activity of multimutated oncolytic herpes simplex virus type 1 G207 has not been fully elucidated yet. Because the antitumoral activity of many drugs involves the inhibition of tumor blood vessel formation, we determined if G207 had an influence on angiogenesis. Monolayers of human umbilical vein endothelial cells and human dermal microvascular endothelial cells, but not human dermal fibroblasts, bronchial epithelial cells, and retinal glial cells, were highly sensitive to the replicative and cytotoxic effects of G207. Moreover, G207 infection caused the destruction of endothelial cell tubes in vitro. In the in vivo Matrigel plug assay in mice, G207 suppressed the formation of perfused vessels. Intratumoral treatment of established human rhabdomyosarcoma xenografts with G207 led to the destruction of tumor vessels and tumor regression. Ultrastructural investigations revealed the presence of viral particles in both tumor and endothelial cells of G207-treated xenografts, but not in adjacent normal tissues. These findings show that G207 may suppress tumor growth, in part, due to inhibition of angiogenesis.
Tanneberger, Anna Maria ; Maawi, Sarah al- ; Herrera-Vizcaíno, Carlos ; Orlowska, Anna ; Kubesch, Alica ; Sader, Robert Alexander ; Kirkpatrick, Charles James ; Ghanaati, Shahram Michael
Objectives: The aim of the present study was to characterize the cellular reaction to a xenogeneic resorbable collagen membrane of porcine origin using a subcutaneous implantation model in Wistar rats over 30 days.
Materials and methods: Ex vivo, liquid platelet-rich fibrin (PRF), a leukocyte and platelet-rich cell suspension, was used to evaluate the blood cell membrane interaction. The material was implanted subcutaneously in rats. Sham-operated rats without biomaterial displayed physiological wound healing (control group). Histological, immunohistological, and histomorphometric analyses were focused on the inflammatory pattern, vascularization rate, and degradation pattern.
Results: The membrane induced a large number of mononuclear cells over the observation period, including lymphocytes, macrophages, and fibroblasts. After 15 days, multinucleated giant cells (MNGCs) were observed on the biomaterial surface. Their number increased significantly, and they proceeded to the center of the biomaterial on day 30. These cells highly expressed CD-68, calcitonin receptor, and MMP-9, but not TRAP or integrin-ß3. Thus, the membrane lost its integrity and underwent disintegration as a consequence of the induction of MNGCs. The significant increase in MNGC number correlated with a high rate of vascularization, which was significantly higher than the control group. Physiological wound healing in the control group did not induce any MNGCs at any time point. Ex vivo blood cells from liquid-PRF did not penetrate the membrane.
Conclusion: The present study suggests a potential role for MNGCs in biomaterial degradation and questions whether it is beneficial to accept them in clinically approved biomaterials or focus on biomaterials that induce only mononuclear cells. Thus, further studies are necessary to identify the function of biomaterial-induced MNGCs.
Clinical relevance: Understanding the cellular reaction to biomaterials is essential to assess their suitability for specific clinical indications and outline the potential benefit of specific group of biomaterials in the respective clinical indications.
Wenzel, Mike ; Welte, Maria-Noemi ; Grossmann, Lina ; Preißer, Felix Martin ; Theißen, Lena Hermine ; Humke, Clara Julia ; Deuker, Marina ; Bernatz, Simon ; Gild, Philipp ; Ahyai, Sascha ; Karakiewicz, Pierre I. ; Bodelle, Boris ; Kluth, Luis A. ; Chun, Felix ; Mandel, Philipp ; Becker, Andreas
Objective: To investigate the value of standard [digital rectal examination (DRE), PSA] and advanced (mpMRI, prostate biopsy) clinical evaluation for prostate cancer (PCa) detection in contemporary patients with clinical bladder outlet obstruction (BOO) scheduled for Holmium laser enucleation of the prostate (HoLEP).
Material and Methods: We retrospectively analyzed 397 patients, who were referred to our tertiary care laser center for HoLEP due to BOO between 11/2017 and 07/2020. Of those, 83 (20.7%) underwent further advanced clinical PCa evaluation with mpMRI and/or prostate biopsy due to elevated PSA and/or lowered PSA ratio and/or suspicious DRE. Logistic regression and binary regression tree models were applied to identify PCa in BOO patients.
Results: An mpMRI was conducted in 56 (66%) of 83 patients and revealed PIRADS 4/5 lesions in 14 (25%) patients. Subsequently, a combined systematic randomized and MRI-fusion biopsy was performed in 19 (23%) patients and revealed in PCa detection in four patients (5%). A randomized prostate biopsy was performed in 31 (37%) patients and revealed in PCa detection in three patients (4%). All seven patients (9%) with PCa detection underwent radical prostatectomy with 29% exhibiting non-organ confined disease. Incidental PCa after HoLEP (n = 76) was found in nine patients (12%) with advanced clinical PCa evaluation preoperatively. In univariable logistic regression analyses, PSA, fPSA ratio, and PSA density failed to identify patients with PCa detection. Conversely, patients with a lower International Prostate Symptom Score (IPSS) and PIRADs 4/5 lesion in mpMRI were at higher risk for PCa detection. In multivariable adjusted analyses, PIRADS 4/5 lesions were confirmed as an independent risk factor (OR 9.91, p = 0.04), while IPSS did not reach significance (p = 0.052).
Conclusion: In advanced clinical PCa evaluation mpMRI should be considered in patients with elevated total PSA or low fPSA ratio scheduled for BOO treatment with HoLEP. Patients with low IPSS or PIRADS 4/5 lesions in mpMRI are at highest risk for PCa detection. In patients with a history of two or more sets of negative prostate biopsies, advanced clinical PCa evaluation might be omitted.
Seiler, Alexander ; Nöth, Ulrike ; Hok, Pavel ; Reiländer, Annemarie ; Maiworm, Michelle ; Baudrexel, Simon ; Meuth, Sven ; Rosenow, Felix ; Steinmetz, Helmuth ; Wagner, Marlies ; Hattingen, Elke ; Deichmann, Ralf ; Gracien, René-Maxime
Magnetic resonance imaging (MRI) is the gold standard imaging technique for diagnosis and monitoring of many neurological diseases. However, the application of conventional MRI in clinical routine is mainly limited to the visual detection of macroscopic tissue pathology since mixed tissue contrasts depending on hardware and protocol parameters hamper its application for the assessment of subtle or diffuse impairment of the structural tissue integrity. Multiparametric quantitative (q)MRI determines tissue parameters quantitatively, enabling the detection of microstructural processes related to tissue remodeling in aging and neurological diseases. In contrast to measuring tissue atrophy via structural imaging, multiparametric qMRI allows for investigating biologically distinct microstructural processes, which precede changes of the tissue volume. This facilitates a more comprehensive characterization of tissue alterations by revealing early impairment of the microstructural integrity and specific disease-related patterns. So far, qMRI techniques have been employed in a wide range of neurological diseases, including in particular conditions with inflammatory, cerebrovascular and neurodegenerative pathology. Numerous studies suggest that qMRI might add valuable information, including the detection of microstructural tissue damage in areas appearing normal on conventional MRI and unveiling the microstructural correlates of clinical manifestations. This review will give an overview of current qMRI techniques, the most relevant tissue parameters and potential applications in neurological diseases, such as early (differential) diagnosis, monitoring of disease progression, and evaluating effects of therapeutic interventions.
Kognitive Beeinträchtigungen (KB) sind ein häufiges Symptom bei Patienten mit Multipler Sklerose (MS). Diese führen im Alltags- und Berufsleben oft zu Einschränkungen. In der Standarddiagnostik der Multiplen Sklerose fehlt es aktuell an validierten, zeitsparenden, kostengünstigen sowie sprach- und bildungsunabhängigen Screening-Verfahren von KB. Ziel des Screenings ist es zu diskriminieren, welche Patienten einer ausführlichen neuropsychologischen Diagnostik unterzogen werden sollten. Als mögliche neue Screening-Verfahren wurden erstens die Sound-induced Flash Illusion (SiFI) als Paradigma multisensorischer Integration und zweitens das visuelle Suchverhalten anhand von Bildern natürlicher Umgebungen mit Hilfe der Technik des Eyetrackings (ET) verwendet.
Mittels SiFI wurden 39 Patienten mit schubförmiger (relapsing-remitting) MS (RRMS) und 16 primär- bzw. sekundär-progrediente (progressive) MS-Patienten (PMS) versus 40 gesunde Kontrollen (healthy controls, HC) auf eine verlängerte Perzeption der Illusion getestet. Im ET Versuch wurden 36 RRMS- und 12 PMS-Patienten versus 39 HC auf abweichende Fixationszeiten und Genauigkeiten untersucht. Um Zusammenhänge zwischen den Testleistungen der SiFI bzw. des ET und kognitiven Beeinträchtigungen herstellen zu können, wurde eine ausführliche neuropsychologische Testung durchgeführt.
Insgesamt nahmen MS-Patienten die Illusion der SiFI häufiger wahr als HC. Insbesondere PMS-Patienten erfuhren die Illusion bei großen Interstimulus-Intervallen signifikant öfter als HC. Zusätzlich ist bei MS-Patienten eine erhöhte Prädisposition, die Illusion der SiFI wahrzunehmen mit einem unterdurchschnittlichen Abschneiden in der neuropsychologischen Testung assoziiert. Des Weiteren ist die SiFI sprach- und bildungsunabhängig, kostengünstig und unterliegt bei Mehrfachtestung keiner Lerneffekte.
Beim ET zeigten MS-Patienten im Vergleich zu HC signifikant veränderte Fixationszeiten und reduzierte Genauigkeiten bei der Betrachtung von Bildern natürlicher Umgebungen. Beeinträchtigtes visuelles Suchverhalten war ein Prädiktor für eine verlangsamte Informationsverarbeitungsgeschwindigkeit in der neuropsychologischen Testung. Zudem konnte anhand der ET-Daten zwischen RRMS- und PMS-Patienten diskriminiert werden.
Zusammenfassend bestätigte die Studie, dass durch die SiFI erfasste multisensorische Integration und durch ET analysiertes visuelles Suchverhalten geeignet sind, um KB bei MS-Patienten zu screenen. Insbesondere lieferte die Testleistung der SiFI einen robusten Bezug zum Abschneiden in der neuropsychologischen Testung. Gleichzeitig war durch die Analyse von visuellem Suchverhalten eine Vorhersage über den Krankheitsprogress möglich. Diese Forschungsergebnisse liefern Evidenz, um beide Methoden nach ergänzender Forschungsarbeit potentiell in den klinischen Alltag integrieren zu können. Eine frühe Detektion von KB bei MS-Patienten ist von hoher Relevanz, um lange eine hohe Lebensqualität zu gewährleisten. Daher können Erkenntnisse dieser Studie genutzt werden, um den Krankheitsverlauf langfristig positiv zu beeinflussen.
Hintergrund: Amblyopie ist nach Fehlsichtigkeit die häufigste Sehstörung bei Kindern. Sie ist eine wesentliche Ursache für eine lebenslange Minderung der bestkorrigierten Sehschärfe und ist meist unilateral. Eine Asymmetrie in der Qualität des visuellen Eindrucks während der sensiblen Phase führt in der Regel zu einer unzureichenden Entwicklung des binokularen Sehsystems. Die Standardtherapie der Amblyopie besteht aus optimaler optischer Korrektur vorhandener Brechungsfehler und der direkten Okklusion, wobei das funktionsbessere Auge zeitweise mit einem Augenpflaster abgedeckt wird. Bisherige Studien haben gezeigt, dass besonders bei Patienten mit tiefer Amblyopie, die Therapietreue oft mäßig ist. In einigen Fällen kann das amblyope Auge nicht mit der Foveola fixieren. Diese exzentrische Fixation beeinflusst den Therapieerfolg negativ. Unser Ziel war, bei dieser speziellen Patientengruppe die Okklusionsdauer objektiv zu registrieren und deren Auswirkung auf die Visusentwicklung und die Fixationsänderung in Abhängigkeit vom Alter über einen langen Zeitraum zu untersuchen.
Methoden: In unserer prospektiven multizentrischen Pilotstudie untersuchten wir amblyope Kinder mit exzentrischer Fixation im Alter von 3-16 Jahren während 12-monatiger Okklusionsbehandlung. Der Nahvisus wurde mittels Landoltringen und Lea-Symbolen (jeweils Reihenoptotypen) bestimmt. Die Okklusionsdauer wurde kontinuierlich mit einem TheraMon®-Mikrosensor aufgezeichnet, der am Augenpflaster angebracht wurde. Der Fixationsort am Augenhintergrund wurde mit einem direkten Ophthalmoskop bestimmt. Unsere Ziele waren: Evaluierung der Sehfunktion, Therapieadhärenz und Beurteilung des Fixationsortes des amblyopen Auges. Der Anteil des korrigierten Visusdefizits, die Dosis-Wirkungs-Beziehung und die Therapieeffizienz wurden berechnet.
Ergebnisse: In unserer Studie wurden 12 Patienten mit Schiel- und kombinierter Schiel- und Anisometropieamblyopie im Alter von 2,9-12,4 Jahren (im Mittel 6,5 ± 3,4 Jahre) untersucht. Der Anfangsvisus der amblyopen Augen nach 3 Monaten refraktiver Adaptationsphase lag im Mittel bei 1,4 ± 0,4 logMAR (Spannweite 0,9-2,0), und der 5 Führungsaugen bei 0,3 ± 0,3 logMAR (Spannweite -0,1-0,8). Die mittlere interokuläre Visusdifferenz (IOVAD, Visusunterschied zwischen dem amblyopen Auge und dem Führungsauge) zu Beginn betrug im Mittel 1,1 ± 0,4 log Einheiten (Spannweite 0,5-1,8). Die verschriebene Okklusionsdauer lag im Median bei 7,7 Stunden/Tag (Spannweite 6,6-9,9), die tatsächlich erreichte bei 5,2 Stunden/Tag (Spannweite 0,7-9,7). Nach 12 Monaten betrug die mediane Visusbesserung der amblyopen Augen 0,6 log Einheiten (Spannweite 0-1,6), die mediane IOVAD 0,3 log Einheiten (Spannweite 0-1,8). Multiple Regressionsanalyse mit Rückwärtselimination zeigte, dass sowohl das Alter (p=0,0002) als auch die Okklusionsdosis (p=0,046) signifikante Einflussfaktoren für den Visusanstieg waren. Kinder unter 4 Jahren zeigten das beste Ansprechen mit der niedrigsten Rest-IOVAD (Median 0,1 log Einheiten, Spannweite 0-0,3). Die Effizienzberechnung ergab eine Visusbesserung von etwa einer log Visusstufe pro 100 Stunden Okklusion in den ersten zwei Monaten und einer halben log Visusstufe nach 6 Monaten. Die Therapieeffizienz nahm mit zunehmendem Alter ab (p = 0,01). Trotz einer gewissen Visusbesserung auch bei Patienten im Alter von ≥8 Jahren (Median 0,4 log Einheiten), zeigten diese eine geringere Therapieadhärenz sowie -effizienz (mediane Rest-IOVAD 0,8 log Einheiten). Zentrale Fixation wurde von 9 Patienten nach im Median 3 Monaten erreicht (Spannweite 1-4 Monate). Drei Patienten (>6 Jahre) erreichten keine zentrale Fixation.
Schlussfolgerung: Amblyopie mit exzentrischer Fixation stellt auch bei guter Adhärenz eine Herausforderung für den Therapieerfolg dar. Unsere Studie zeigte erstmals prospektive quantitative Daten basierend auf elektronischer Erfassung der Okklusion bei dieser seltenen Patientengruppe. Es konnte die deutliche Abnahme der Therapieeffizienz mit zunehmendem Alter gezeigt werden. Die Visusbesserung wurde viel stärker vom Alter als von der Okklusionsdosis beeinflusst. Nur Kinder, die zum Okklusionsbeginn jünger als 4 Jahre waren, konnten im Studienzeitraum in ihren amblyopen Augen eine für ihr Alter annähernd normale Sehschärfe und eine IOVAD <0,2 log Einheiten erreichen. Demzufolge sind, trotz möglicher geringer Visusbesserung auch bei älteren Patienten, eine frühzeitige Diagnose und Therapie dieser Patientengruppe unerlässlich für den Therapieerfolg.
Förderung: bereitgestellt durch den Forschungspreis des Vereins „Augenstern e.V.“
Introduction: Studies of vocational ballet students are sparce. In particular, there is a lack of gender comparisons. The aim of the present study, therefore, was to give a musculoskeletal and sociodemographic description of the typical vocational ballet student in gender comparison. Methods: In this study, n = 414 female and n = 192 male students of the John Cranko School (JCS), aged between 5 and 22 years (Mean ± SD: 13.9 ± 3.5), were examined by an experienced orthopedist and dance physician. Results: Males started ballet (5.8/8.2 years, p < 0.001) and training at later age than females (13.5/14.6 years, p < 0.05). There was a high prevalence of low body weight among both sexes; however, particularly among female participants (58.4/16.2%, p < 0.001). Both sexes showed a large external rotation of the hip (f/m: 59/62°, p < 0.001), a large turnout (f/m: 82/86°, p < 0.01), high values for plantarflexion of the ankle joint (f/m: 72/68°, p < 0.001) and dorsiflexion of the metatarsophalangeal joint of the big toe (f/m: 90/87°, p < 0.001). Discussion: Differences in ballet-specific characteristics between genders (f/m) are converging and are smaller than described in the past. The particularly high prevalence of low body weight among students in the vocational training sector, particularly among females, highlights the need for deeper diagnostic investigation.
The yeast Rcf1 protein is a member of the conserved family of proteins termed the hypoxia-induced gene (domain) 1 (Hig1 or HIGD1) family. Rcf1 interacts with components of the mitochondrial oxidative phosphorylation system, in particular the cytochrome bc1 (complex III)-cytochrome c oxidase (complex IV) supercomplex (termed III-IV) and the ADP/ATP carrier proteins. Rcf1 plays a role in the assembly and modulation of the activity of complex IV; however, the molecular basis for how Rcf1 influences the activity of complex IV is currently unknown. Hig1 type 2 isoforms, which include the Rcf1 protein, are characterized in part by the presence of a conserved motif, (Q/I)X3(R/H)XRX3Q, termed here the QRRQ motif. We show that mutation of conserved residues within the Rcf1 QRRQ motif alters the interactions between Rcf1 and partner proteins and results in the destabilization of complex IV and alteration of its enzymatic properties. Our findings indicate that Rcf1 does not serve as a stoichiometric component, i.e. as a subunit of complex IV, to support its activity. Rather, we propose that Rcf1 serves to dynamically interact with complex IV during its assembly process and, in doing so, regulates a late maturation step of complex IV. We speculate that the Rcf1/Hig1 proteins play a role in the incorporation and/or remodeling of lipids, in particular cardiolipin, into complex IV and. possibly, other mitochondrial proteins such as ADP/ATP carrier proteins.
In den letzten Jahren haben sich die Therapiemöglichkeiten des Mammakarzinoms deutlich verbessert. Durch die Analyse von genetischen Veränderungen in den Tumorzellen oder in der Keimbahn ist eine zielgerichtete Tumortherapie bei einigen Subgruppen möglich; z.B. mit PARP- und PIK3CA-Inhibitoren.
In einer retrospektiven Analyse wurde in dieser Arbeit untersucht, wie genetische Mutationsanalysen in einer onkologischen Schwerpunktpraxis eingesetzt werden. Es sollte untersucht werden, wie häufig PatientInnen in einer onkologischen Praxis mit metastasiertem Mammakarzinom eine Mutationsanalyse brustkrebsassoziierter Gene erhalten haben, und welche Konsequenzen daraus gezogen wurden. Dabei wurde der Zeitraum von 2019 – 2022 betrachtet. Mithilfe der Software Albis wurden Daten von 49 PatientInnen identifiziert. 40 PatientInnen haben eine Keimbahndiagnostik der Gene BRCA1/2 erhalten. Von den PatientInnen, die die BRCA1/2-Analyse bekommen haben, konnten in 20% der PatientInnen eine Mutation in BRCA1 oder 2 detektiert werden. Bei den meisten dieser PatientInnen wurde der PARP Inhibitor Olaparib therapeutisch eingesetzt. 10 PatientInnen erhielten eine PIK3CA-Analyse, 9 von ihnen mittels PCR und eine mittels NGS. In dieser Gruppe wurde bei einer Patientin eine Mutation im PIK3CA-Gen ermittelt. 15 PatientInnen haben eine Multigenpanel-Diagnostik erhalten. Dabei ist eine Reihe weiterer genetischer Veränderungen nachgewiesen worden. Für einige dieser Veränderungen stehen therapeutische Möglichkeiten zur Verfügung, die zwar nicht für das Mammakarzinom, aber für andere Tumorentitäten bereits zugelassen sind.
Myocardial fibrosis and inflammation by CMR predict cardiovascular outcome in people living with HIV
(2021)
Leuw, Philipp de ; Arendt, Christophe ; Haberl, Annette E. ; Froadinadl, Daniel ; Kann, Gerrit ; Wolf, Timo ; Stephan, Christoph ; Schüttfort, Gundolf ; Vasquez, Moises ; Arcari, Luca ; Zhou, Hui ; Zainal, Hafisyatul ; Gawor, Monika ; Vidalakis, Eleftherios ; Kolentinis, Michael ; Albrecht, Moritz Hans Ernst ; Escher, Felicitas ; Vogl, Thomas J. ; Zeiher, Andreas M. ; Nagel, Eike ; Puntmann, Valentina O.
Objectives_: The goal of this study was to examine prognostic relationships between cardiac imaging measures and cardiovascular outcome in people living with human immunodeficiency virus (HIV) (PLWH) on highly active antiretroviral therapy (HAART).
Background: PLWH have a higher prevalence of cardiovascular disease and heart failure (HF) compared with the noninfected population. The pathophysiological drivers of myocardial dysfunction and worse cardiovascular outcome in HIV remain poorly understood.
Methods: This prospective observational longitudinal study included consecutive PLWH on long-term HAART undergoing cardiac magnetic resonance (CMR) examination for assessment of myocardial volumes and function, T1 and T2 mapping, perfusion, and scar. Time-to-event analysis was performed from the index CMR examination to the first single event per patient. The primary endpoint was an adjudicated adverse cardiovascular event (cardiovascular mortality, nonfatal acute coronary syndrome, an appropriate device discharge, or a documented HF hospitalization).
Results: A total of 156 participants (62% male; age [median, interquartile range]: 50 years [42 to 57 years]) were included. During a median follow-up of 13 months (9 to 19 months), 24 events were observed (4 HF deaths, 1 sudden cardiac death, 2 nonfatal acute myocardial infarction, 1 appropriate device discharge, and 16 HF hospitalizations). Patients with events had higher native T1 (median [interquartile range]: 1,149 ms [1,115 to 1,163 ms] vs. 1,110 ms [1,075 to 1,138 ms]); native T2 (40 ms [38 to 41 ms] vs. 37 ms [36 to 39 ms]); left ventricular (LV) mass index (65 g/m2 [49 to 77 g/m2] vs. 57 g/m2 [49 to 64 g/m2]), and N-terminal pro–B-type natriuretic peptide (109 pg/l [25 to 337 pg/l] vs. 48 pg/l [23 to 82 pg/l]) (all p < 0.05). In multivariable analyses, native T1 was independently predictive of adverse events (chi-square test, 15.9; p < 0.001; native T1 [10 ms] hazard ratio [95% confidence interval]: 1.20 [1.08 to 1.33]; p = 0.001), followed by a model that also included LV mass (chi-square test, 17.1; p < 0.001). Traditional cardiovascular risk scores were not predictive of the adverse events.
Conclusions: Our findings reveal important prognostic associations of diffuse myocardial fibrosis and LV remodeling in PLWH. These results may support development of personalized approaches to screening and early intervention to reduce the burden of HF in PLWH (International T1 Multicenter Outcome Study; NCT03749343).
A recent in-vivo experiment has shown that force can be transmitted between the gastrocnemius and the hamstring muscles due to a direct tissue continuity. However, it remains unclear if this mechanical interaction is affected by the stiffness of the structural connection. This study therefore aimed to investigate the impact of the knee angle on myofascial force transmission across the dorsal knee. A randomized, cross-over study was performed, including n = 56 healthy participants (25.36 ± 3.9 years, 25 females). On two separate days, they adopted a prone position on an isokinetic dynamometer (knee extended or 60° flexed). In each condition, the device moved the ankle three times from maximal plantarflexion to maximal dorsal extension. Muscle inactivity was ensured using EMG. High-resolution ultrasound videos of the semimembranosus (SM) and the gastrocnemius medialis (GM) soft tissue were recorded. Maximal horizontal tissue displacement, obtained using cross-correlation, was examined as a surrogate of force transmission. SM tissue displacement was higher at extended (4.83 ± 2.04 mm) than at flexed knees (3.81 ± 2.36 mm). Linear regression demonstrated significant associations between (1) SM and GM soft tissue displacement (extended: R2 = 0.18, p = 0.001; flexed: R2 = 0.17, p = 0.002) as well as (2) SM soft tissue displacement and ankle range of motion (extended: R2 = 0.103, p = 0.017; flexed: R2 = 0.095, p = 0.022). Our results further strengthen the evidence that local stretching induces a force transmission to neighboring muscles. Resulting remote exercise effects such as increased range of motion, seem to depend on the stiffness of the continuity.
Trial registration: DRKS (Deutsches Register Klinischer Studien), registration number DRKS00024420, first registered 08/02/2021, https://drks.de/search/de/trial/DRKS00024420.
Myofacial Pain is the most common form of temporomandibular disorders (TMD), affecting principally women in reproductive age. The etiology of TMD is still controversial. Currently a multifactorial theory has received a great support among the scientific community. This theory draws attention to the interaction of psychological, neuromuscular and oral pathogenic factors. Objectives: to describe the possible etiological factors of the Myofacial Pain; and to evaluate the effectiveness of the current treatments for Myofacial Pain. Materials and methods: a narrative review of the etiological factors and epidemiological data of Myofacial Pain introduces this work. Thereafter the author presents five systematic reviews of RCTs which have been published during the last thirteen years (1999-2012) for the use of acupuncture, low level laser therapy, drugs, physiotherapeutical interventions, splint therapy, and psychosocial interventions in the treatment of Myofacial Pain. Moreover, the author reports a systematic review and meta-analysis of all the available literature of two modern approaches for the treatment of Myofacial Pain. A comparison between the “usual treatment” based on splint therapy and psychosocial interventions was conducted. Results: the author did not find sufficient evidence to support therapies based on one single intervention. However, the condition of the patients with myofacial pain could be treated more effectively with combined treatments. After comparing “usual treatment” with psychosocial interventions, the author observed a tendency of the latter to improve psychological outcomes, whereas the first one was slightly more effective to enhance clinical functional outcomes. In general, a high level of heterogeneity was observed among the included studies of the different systematic reviews. The quality of the studies is susceptible to be improved. Clinical implications: the author proposes core outcomes to be implemented within the research on myofacial pain in particular and temporomandibular disorders in general, in order to enable scientifical comparisons between different therapies.