33 research outputs found
Moving Knowledge Acquisition From the Lecture Hall to the Student Home: A Prospective Intervention Study.
No full textBACKGROUND: Podcasts are popular with medical students, but the impact of podcast use on learning outcomes in undergraduate medical education has not been studied in detail. OBJECTIVE: Our aim was to assess the impact of podcasts accompanied by quiz questions and lecture attendance on short- and medium-term knowledge retention. METHODS: Students enrolled for a cardio-respiratory teaching module were asked to prepare for 10 specific lectures by watching podcasts and submitting answers to related quiz questions before attending live lectures. Performance on the same questions was assessed in a surprise test and a retention test. RESULTS: Watching podcasts and submitting answers to quiz questions (versus no podcast/quiz use) was associated with significantly better test performance in all items in the surprise test and 7 items in the retention test. Lecture attendance (versus no attendance) was associated with higher test performance in 3 items and 1 item, respectively. In a linear regression analysis adjusted for age, gender, and overall performance levels, both podcast/quiz use and lecture attendance were significant predictors of student performance. However, the variance explained by podcast/quiz use was greater than the variance explained by lecture attendance in the surprise test (38.7% vs. 2.2%) and retention test (19.1% vs. 4.0%). CONCLUSIONS: When used in conjunction with quiz questions, podcasts have the potential to foster knowledge acquisition and retention over and above the effect of live lectures
Incidence of sarcopenia in elderly patients undergoing cardiac rehabilitation (CR) an observational cohort study
No full textKnockout of the delta Isoform of CaMKII does not Negatively Influence Cardiomyocyte Excitation-Contraction Coupling in Mice
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Knockout of the delta Isoform of CaMKII does not Negatively Influence Cardiomyocyte Excitation-Contraction Coupling in Mice
No full textWhile systolic cardiomyocyte function is preserved, diastolic myocyte function and recovery from acidosis are impaired in CaMKII delta-KO mice
No full textObjective: CaMKII contributes to impaired contractility in heart failure by inducing SR Ca2+-leak. CaMKII-inhibition in the heart was suggested to be a novel therapeutic principle. Different CaMKII isoforms exist. Specifically targeting CaMKII delta, the dominant isoform in the heart, could be of therapeutic potential without impairing other CaMKII isoforms. Rationale: We investigated whether cardiomyocyte function is affected by isoform-specific knockout (KO) of CaMKII delta under basal conditions and upon stress, i.e. upon beta-adrenergic stimulation and during acidosis. Results: Systolic cardiac function was largely preserved in the KO in vivo (echocardiography) corresponding to unchanged Ca2+-transient amplitudes and isolated myocyte contractility in vitro. CaMKII activity was dramatically reduced while phosphatase-1 inhibitor-1 was significantly increased. Surprisingly, while diastolic Ca2+-elimination was slower in KO most likely due to decreased phospholamban Thr-17 phosphorylation, frequency-dependent acceleration of relaxation was still present. Despite decreased SR Ca2+-reuptake at lower frequencies, SR Ca2+-content was not diminished, which might be due to reduced diastolic SR Ca2+-loss in the KO as a consequence of lower RyR Ser-2815 phosphorylation. Challenging KO myocytes with isoproterenol showed intact inotropic and lusitropic responses. During acidosis, SR Ca2+-reuptake and SR Ca2+-loading were significantly impaired in KO, resulting in an inability to maintain systolic Ca2+-transients during acidosis and impaired recovery. Conclusions: Inhibition of CaMKII delta appears to be safe under basal physiologic conditions. Specific conditions exist (e.g. during acidosis) under which CaMKII-inhibition might not be helpful or even detrimental. These conditions will have to be more clearly defined before CaMKII inhibition is used therapeutically. (C) 2013 Elsevier Ltd. All rights reserved
Constitutively active phosphatase inhibitor-1 improves cardiac contractility in young mice but is deleterious after catecholaminergic stress and with aging
No full textPhosphatase inhibitor-1 (I-1) is a distal amplifier element of beta-adrenergic signaling that functions by preventing dephosphorylation of downstream targets. I-1 is downregulated in human failing hearts, while overexpression of a constitutively active mutant form (I-1c) reverses contractile dysfunction in mouse failing hearts, suggesting that I-1c may be a candidate for gene therapy. We generated mice with conditional cardiomyocyte-restricted expression of I-1c (referred to herein as dTGI-1c mice) on an I-1-deficient background. Young adult dTGI-1c mice exhibited enhanced cardiac contractility but exaggerated contractile dysfunction and ventricular dilation upon catecholamine infusion. Telemetric ECG recordings revealed typical catecholamine-induced ventricular tachycardia and sudden death. Doxycycline feeding switched off expression of cardiomyocyte-restricted I-1c and reversed all abnormalities. Hearts from dTGI-1c mice showed hyperphosphorylation of phospholamban and the ryanodine receptor, and this was associated with an increased number of catecholamine-induced Ca2+ sparks in isolated myocytes. Aged dTGI-1c mice spontaneously developed a cardiomyopathic phenotype. These data were confirmed in a second independent transgenic mouse line, expressing a full-length I-1 mutant that could not be phosphorylated and thereby inactivated by PKC-alpha (I-1S67A). In conclusion, conditional expression of I-1c or I-1S67A enhanced steady-state phosphorylation of 2 key Ca2+-regulating sarcoplasmic reticulum enzymes. This was associated with increased contractile function in young animals but also with arrhythmias and cardiomyopathy after adrenergic stress and with aging. These data should be considered in the development of novel therapies for heart failure
Scientific Railway Signalling Symposium 2021 - Abweichungen vom Regelbetrieb – Bleiben Kapazität, Qualität oder Kunde auf der Strecke?
No full textVerspätungen und andere Abweichungen vom Regelbetrieb sind eines der Hauptärgernisse für die Endkunden der Bahn, erschweren aber auch die Planung der am Bahnbetrieb beteiligten Unternehmen und können teilweise ein Sicherheitsrisiko darstellen. Die Ursachen sind vielfältig und erstrecken sich auf alle Komponenten des Systems Bahn. Im Rahmen des Scientific Railway Signalling Symposiums 2021 warfen am 23. Juni 2021 ca. 85 Fachexpertinnen und Fachexperten gemeinsam unter dem Titel „Abweichungen vom Regelbetrieb – Bleiben Kapazität, Qualität oder Kunde auf der Strecke?“ einen vertieften Blick auf das Potenzial der Leit- und Sicherungstechnik zur Verringerung von Abweichungen vom Regelbetrieb.
Die Beiträge der Konferenz zeigen, dass vielfältige Verbesserungsmöglichkeiten durch innovative technologische Ansätze bestehen. So berichtete Martin Messerli von der SBB AG von aktuellen Entwicklungen aus dem Schweizer Programm smartRail 4.0, das nach einer positiven Bewertung durch das Bundesamt für Verkehr von der Konzeptphase in die Umsetzungsphase tritt. Max Schubert von INCYDE erläuterte, wie durch die strukturierte Kombination von Technik, Prozessen und Architektur die Resilienz im Bahnbetrieb gesteigert werden kann. Die Architektur muss dabei modular aufgebaut sein und die einzelnen Komponenten über Standardschnittstellen kommunizieren, so dass einzelne Komponenten bei neuen technologischen und sicherheitsbezogenen Entwicklungen mit vertretbarem Aufwand ausgetauscht werden können. Hierzu stimmen sich europäische Bahnen in der RCA-Initiative ab, deren aktueller Stand von Michael Leining von NEXTRAIL vorgestellt wurde.
Aus der Praxis berichtete Jens Deutschmann von der DB Netz AG über die erfolgreiche Umsetzung der FPGA-Technologie im badischen Gengenbach, mit der Relaisstellwerke über einen sicheren Compiler effizient in elektronische Logik überführt werden können, wodurch sie u. a. robuster gegenüber Störungen und Ausfällen gemacht werden. Für einen robusten Bahnbetrieb ist auch eine hochverfügbare Ortung entscheidend. Bernd Drapp von AP Sensing gab hierzu einen Einblick in die Potenziale faseroptischer Sensortechnologie (FOS) und Alexandra Grefe von SIGNON stellte das Mobile Mapping System „SATengine“ zur kontinuierlichen Erfassung von Infrastrukturdaten vor, das auf der Auswertung georeferenzierter Videodaten während Messfahrten auf regulär verkehrenden Fahrzeugen basiert.
Bevor innovative Technologien in der Praxis erprobt werden können, muss allerdings die Wissenschaft zunächst Grundlagenarbeit leisten. In diesem Tagungsband möchten wir daher neben den Business Papers von Frau Grefe und Herren Leining und Drapp ebenfalls die wissenschaftliche Arbeit der Tagung veröffentlichen, die an der TU Darmstadt entstanden ist. Bilal Üyümez beschäftigt sich mit dem Vergleich verschiedener Umsetzungsmöglichkeiten von ETCS Level 3, um die Streckenkapazität zu erhöhen und somit die Auswirkungen von Abweichungen vom Regelbetrieb zu verringern
Impact Of High Sarcopenic Risk In Patients Undergoing Inpatient Cardiac Rehabilitation After Cardiac Procedure
No full textCalcium/Calmodulin-Dependent Protein Kinase II Contributes to Cardiac Arrhythmogenesis in Heart Failure
No full textBackground-Transgenic (TG) Ca/calmodulin-dependent protein kinase II (CaMKII)delta(C) mice have heart failure and isoproterenol (ISO)-inducible arrhythmias. We hypothesized that CaMKII contributes to arrhythmias and underlying cellular events and that inhibition of CaMKII reduces cardiac arrhythmogenesis in vitro and in vivo. Methods and Results-Under baseline conditions, isolated cardiac myocytes from TG mice showed an increased incidence of early afterdepolarizations compared with wild-type myocytes (P < 0.05). CaMKII inhibition (AIP) completely abolished these afterdepolarizations in TG cells (P < 0.05). Increasing intracellular Ca stores using ISO (10(-8) M) induced a larger amount of delayed afterdepolarizations and spontaneous action potentials in TG compared with wild-type cells (P < 0.05). This seems to be due to an increased sarcoplasmic reticulum (SR) Ca leak because diastolic [Ca](i) rose clearly on ISO in TG but not in wild-type cells (+20 +/- 5% versus +3 +/- 4% at 10(-6) M ISO, P < 0.05). In parallel, SR Ca leak assessed by spontaneous SR Ca release events showed an increased Ca spark frequency (3.9 +/- 0.5 versus 2.0 +/- 0.4 sparks per 100 mu m(-1).s(-1), P < 0.05). However, CaMKII inhibition (either pharmacologically using KN-93 or genetically using an isoform-specific CaMKII delta-knockout mouse model) significantly reduced SR Ca spark frequency, although this rather increased SR Ca content. In parallel, ISO increased the incidence of early (54% versus 4%, P < 0.05) and late (86% versus 43%, P < 0.05) nonstimulated events in TG versus wild-type myocytes, but CaMKII inhibition (KN-93 and KO) reduced these proarrhythmogenic events (P < 0.05). In addition, CaMKII inhibition in TG mice (KN-93) clearly reduced ISO-induced arrhythmias in vivo (P < 0.05). Conclusions-We conclude that CaMKII contributes to cardiac arrhythmogenesis in TG CaMKII delta(C) mice having heart failure and suggest the increased SR Ca leak as an important mechanism. Moreover, CaMKII inhibition reduces cardiac arrhythmias in vitro and in vivo and may therefore indicate a potential role for future antiarrhythmic therapies warranting further studies. (Circ Heart Fail. 2009; 2: 664-675.
