Upper-limb RIPC performed while patients were under propofol-induced anesthesia did not show a relevant benefit among patients undergoing elective cardiac surgery. (Funded by the German Research Foundation; RIPHeart ClinicalTrials.gov number, NCT01067703.).
Oxidative stress occurs whenever the release of reactive oxygen species (ROS) exceeds endogenous antioxidant capacity. In this paper, we review the specific role of several cardiovascular risk factors in promoting oxidative stress, namely diabetes, obesity, smoking, and excessive pollution. Specifically, the risk of developing heart failure is higher in patients with diabetes or obesity, even with optimal medical treatment, and the increased release of ROS from cardiac mitochondria and other sources likely contributes to the development of cardiac dysfunction in this setting. Here, we explore the role of different ROS sources arising in obesity and diabetes, and the impact of excessive ROS production on the development of cardiac lipotoxicity. In parallel, contaminants in the air that we breathe pose a significant threat to human health. This paper provides an overview of cigarette smoke and urban air pollution, considering how their composition and biological effects have detrimental effects on cardiovascular health.
These data indicate that obesity results in premature cardiac aging in younger patients, which may contribute to an increased risk for heart failure.
We conclude that LOX-1 is regulated by Ang II in vitro and in vivo, that induction of LOX-1 is mediated by the AT(1) receptor, and that repression of LOX-1 by long-term ACE inhibitor treatment may contribute to the antiatherosclerotic potential of this therapy.
Zusammenfassung Fragestellung Die enterale und parenterale Ernährungstherapie kritisch kranker Patienten kann u. a. durch den Zeitpunkt des Beginns, die Wahl des Applikationswegs, die Menge und Zusammensetzung der Makro- und Mikronährstoffzufuhr sowie der Wahl spezieller, immunmodulierender Nährsubstrate variieren. Die Durchführung der Ernährungstherapie nimmt Einfluss auf den klinischen Ausgang dieser Patienten. Ziel der vorliegenden Leitlinie ist es, aktualisierte konsensbasierte Empfehlungen zur klinischen Ernährung kritisch kranker, erwachsener Patienten, die an mindestens einer akuten, medikamentös und/oder mechanisch unterstützungspflichtigen Organdysfunktion leiden, zu geben. Methodik Die früheren Leitlinien der Deutschen Gesellschaft für Ernährungsmedizin (DGEM) wurden in Einklang mit den aktuellen Richtlinien der Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften e. V. (AWMF) als S2k-Leitlinie aktualisiert. Entsprechend der S2k-Klassifikation dieser Leitlinie enthalten die dargestellten Empfehlungen keine Angabe von Evidenz- und Empfehlungsgraden, da keine systematische Aufbereitung der Evidenz zugrunde gelegt wurde. Als Grundlage für die Empfehlungen wurden insbesondere die seit Erscheinen der letzten DGEM-Leitlinien Intensivmedizin publizierten randomisiert-kontrollierten Studien und Metaanalysen, Beobachtungsstudien mit angemessener Fallzahl und hoher methodologischer Qualität (bis Mai 2018) sowie aktuell gültige Leitlinien anderer Fachgesellschaften herangezogen und kommentiert. Die Empfehlungsstärke ist rein sprachlich beschrieben. Jede Empfehlung wurde mittels Delphi-Verfahren abschließend bewertet und konsentiert. Ergebnisse Die Leitlinie beschreibt einführend die pathophysiologischen Konsequenzen einer kritischen Erkrankung, welche den Metabolismus und die Ernährbarkeit der Patienten beeinflussen können, ferner die Definitionen unterschiedlicher Erkrankungsphasen im Krankheitsverlauf und sie diskutiert methodologische Aspekte zu ernährungsmedizinischen Studien. In der Folge werden 69 konsentierte Empfehlungen zu wesentlichen, praxisrelevanten Elementen der klinischen Ernährung kritisch kranker Patienten gegeben, darunter die Beurteilung des Ernährungszustands, die Indikation für die klinische Ernährungstherapie, der Beginn und Applikationsweg der Nahrungszufuhr, die Menge und Art der zugeführten Substrate (Makro- und Mikronährstoffe) sowie ernährungstherapeutische Besonderheiten bei adipösen kritisch kranken Patienten und Patienten mit mechanischen Unterstützungssystemen. Schlussfolgerung Mit der Leitlinie werden aktuelle Handlungsempfehlungen zur enteralen und parenteralen Ernährung erwachsener Patienten geben, die an mindestens einer akuten, medikamentös und/oder mechanisch unterstützungspflichtigen Organdysfunktion leiden. Die Gültigkeit der Leitlinie beträgt voraussichtlich 5 Jahre (2018 – 2023).
OBJECTIVETranscriptional peroxisome proliferator–activated receptor-γ coactivator-1α (PGC-1α) plays a key role in mitochondrial biogenesis and energy metabolism and is suggested to be involved in the exercise-induced increase in mitochondrial content. PGC-1α activity is regulated by posttranslational modifications, among them acetylation or phosphorylation. Accordingly, the deacetylase SIRT1 and the kinase AMPK increase PGC-1α activity.RESEARCH DESIGN AND METHODSWe tested whether chronic treadmill exercise or a single exercise session modifies PGC-1α activation and mitochondrial biogenesis differentially in obese ob/ob mice with dysregulated adiponectin/leptin-mediated AMPK activation compared with C57BL/6J wild-type mice.RESULTSExercise training (12 weeks) induced adiponectin and lowered plasma insulin and glucose, suggesting improved insulin sensitivity in wild-type mice. It enhanced mitochondrial biogenesis in red gastrocnemius muscle, as indicated by increased mRNA expression of transcriptional regulators and primary mitochondrial transcripts, increased mtDNA content, and citrate synthase activity. Parallel to this, we observed AMPK activation, PGC-1α deacetylation, and SIRT1 induction in trained wild-type mice. Although none of these exercise-induced changes were detected in ob/ob mice, comparable effects on mitochondrial respiration were observed. A single exercise session resulted in comparable changes in wild-type mice. These changes remained detectable 6 h after the exercise session but had disappeared after 24 h. Treatment of C2C12 myoblasts with leptin or adiponectin resulted in increased AMPK phosphorylation and PGC-1α deacetylation.CONCLUSIONSChronic exercise induces mitochondrial biogenesis in wild-type mice, which may require intact AMPK activation by adipocytokines and involve SIRT1-dependent PGC-1α deacetylation. Trained ob/ob mice appear to have partially adapted to reduced mitochondrial biogenesis by AMPK/SIRT1/PGC-1α–independent mechanisms without mtDNA replication.
In patients with haemophilia A, factor VIII (FVIII) prophylaxis reduces bleeding frequency and joint damage compared with on-demand therapy. To assess the effect of prophylaxis initiation age, magnetic resonance imaging (MRI) was used to evaluate bone and cartilage damage in patients with severe haemophilia A. In this cross-sectional, multinational investigation, patients aged 12–35 years were assigned to 1 of 5 groups: primary prophylaxis started at age <2 years (group 1); secondary prophylaxis started at age 2 to <6 years (group 2), 6 to <12 years (group 3), or 12−18 years (group 4); or on-demand treatment (group 5). Joint status at ankles and knees was assessed using Compatible Additive MRI scoring (maximum and mean ankle; maximum and mean of all 4 joints) and Gilbert scores in the per-protocol population (n = 118). All prophylaxis groups had better MRI joint scores than the on-demand group. MRI scores generally increased with current patient age and later start of prophylaxis. Ankles were the most affected joints. In group 1 patients currently aged 27−35 years, the median of maximum ankle scores was 0.0; corresponding values in groups 4 and 5 were 17.0 and 18.0, respectively [medians of mean index joint scores: 0.0 (group 1), 8.1 (group 2) and 13.8 (group 4)]. Gilbert scores revealed outcomes less pronounced than MRI scores. MRI scores identified pathologic joint status with high sensitivity. Prophylaxis groups had lower annualized joint bleeds and MRI scores vs. the on-demand group. Primary prophylaxis demonstrated protective effects against joint deterioration compared with secondary prophylaxis.
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