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Nach HIRSCH (1883) war die Malariasituation im 19. Jahrhundert in Norddeutschland am schlimmsten in Schleswig-Holstein, an der Küste westlich der Elbe sowie in den Moorgebieten von Hannover und Oldenburg. Erst mit Beginn des 20. Jahrhunderts nahm dort die Zahl der Infektionen ab. Dieser Rückgang wurde vielfach auf die Trockenlegung von Marsch-, Sumpf- und Moorgebieten zurückgeführt (MAIER 2004). Aktuell wird deshalb in Teilen der Bevölkerung ein Wiederaufflackern der Malaria bzw. anderer Mückenassoziierter Krankheiten als indirekte Folge von Wiedervernässungsmaßnahmen befürchtet. Hinzu kommen Klima- und weitere Umweltveränderungen, welche nach MAIER et al. (2003) Ursache für neu auftretende oder wiederkehrende Krankheiten sein können. Mit dem Verschwinden der Malaria wurde in Deutschland kaum weitere Forschung zur Verbreitung und Ökologie der Culiciden betrieben. Das Fehlen von fundierten Daten zur Ökologie und Populationsentwicklung der präimaginalen Culicidenstadien in den heute vorhandenen Lebensräumen (z.B. Gräben, Polder, Wiedervernässungsflächen, Mooren) erschwert Aussagen und Prognosen zur Verbreitung potenzieller Vektoren. Die aktuellen Untersuchungen konzentrierten sich zunächst auf die Untersuchung der aquatischen Entwicklungsstadien von Anopheles-Arten (Diptera: Culicidae) in Entwässerungsgräben. Diese Biotope sind für die heutige Landschaftsstruktur der Marschengebiete im Nordwesten Niedersachsens typisch, stellen dort einen hohen Anteil der Wasserflächen dar und sind grundsätzlich als Brutgewässer geeignet (CRANSTON et al. 1987, MOHRIG 1969). Wesentliches Ziel der Untersuchung war zunächst die Darstellung historischer Fundgebiete, der abgesicherte Nachweis aktueller Brutgebiete verschiedener Anopheles-Arten und die Entwicklung einer standardisierten Methode zur Charakterisierung der betreffenden Biotope. Darauf aufbauend sollen mit GISTechniken, Classification and Regression Trees (CART) und Geostatistik zukünftig Möglichkeiten der Übertragung dieser Resultate auf ähnlich ausgestattete Landschaftsräume geprüft werden.
In higher concentrations, the blood pressure regulating hormone angiotensin II leads to vasoconstriction, hypertension, and oxidative stress by activating NADPH oxidases which are a major enzymatic source of reactive oxygen species (ROS). With the help of knockout animals, the impact of the three predominant NADPH oxidases present in the kidney, i.e., Nox1, Nox2 and Nox4 on angiotensin II-induced oxidative damage was studied. Male wildtype (WT) C57BL/6 mice, Nox1-, Nox2- and Nox4-deficient mice were equipped with osmotic minipumps, delivering either vehicle (PBS) or angiotensin II, for 28 days. Angiotensin II increased blood pressure and urinary albumin levels significantly in all treated mouse strains. In Nox1 knockout mice these increases were significantly lower than in WT, or Nox2 knockout mice. In WT mice, angiotensin II also raised systemic oxidative stress, ROS formation and DNA lesions in the kidney. A local significantly increased ROS production was also found in Nox2 and Nox4 knockout mice but not in Nox1 knockout mice who further had significantly lower systemic oxidative stress and DNA damage than WT animals. Nox2 and Nox4 knockout mice had increased basal DNA damage, concealing possible angiotensin II-induced increases. In conclusion, in the kidney, Nox1 seemed to play a role in angiotensin II-induced DNA damage.
Objectives: There is sparse information on the safety of early primary discharge from the emergency department (ED) after rule-out of myocardial infarction in suspected acute coronary syndrome (ACS). This prospective registry aimed to confirm randomised study results in patients at low-to-intermediate risk, with a broader spectrum of symptoms, across different institutional standards and with a range of local troponin assays including high-sensitivity cTn (hs-cTn), cardiac troponin (cTn) and point-of-care troponin (POC Tn).
Design: Prospective, multicentre European registry.
Setting: 18 emergency departments in nine European countries (Germany, Austria, Switzerland, France, Spain, UK, Turkey, Lithuania and Hungary)
Participants: The final study cohort consisted of 2294 patients (57.2% males, median age 57 years) with suspected ACS.
Interventions: Using the new dual markers strategy, 1477 patients were eligible for direct discharge, which was realised in 974 (42.5%) of patients.
Main outcome measures: The primary endpoint was all-cause mortality at 30 days.
Results: Compared with conventional workup after dual marker measurement, the median length of ED stay was 60 min shorter (228 min, 95% CI: 219 to 239 min vs 288 min, 95% CI: 279 to 300 min) in the primary dual marker strategy (DMS) discharge group. All-cause mortality was 0.1% (95% CI: 0% to 0.6%) in the primary DMS discharge group versus 1.1% (95% CI: 0.6% to 1.8%) in the conventional workup group after dual marker measurement. Conventional workup instead of discharge despite negative DMS biomarkers was observed in 503 patients (21.9%) and associated with higher prevalence of ACS (17.1% vs 0.9%, p<0.001), cardiac diagnoses (55.2% vs 23.5%, p<0.001) and risk factors (p<0.01), but with a similar all-cause mortality of 0.2% (95% CI: 0% to 1.1%) versus primary DMS discharge (p=0.64).
Conclusions: Copeptin on top of cardiac troponin supports safe discharge in patients with chest pain or other symptoms suggestive of ACS under routine conditions with the use of a broad spectrum of local standard POC, conventional and high-sensitivity troponin assays.
Trial registration number NCT02490969.
Acute deterioration of liver cirrhosis (e.g., infections, acute‐on‐chronic liver failure [ACLF]) requires an increase in cardiac contractility. The insufficiency to respond to these situations could be deleterious. Left ventricular global longitudinal strain (LV‐GLS) has been shown to reflect left cardiac contractility in cirrhosis better than other parameters and might bear prognostic value. Therefore, this retrospective study investigated the role of LV‐GLS in the outcome after transjugular intrahepatic portosystemic shunt (TIPS) and the development of ACLF. We included 114 patients (48 female patients) from the Noninvasive Evaluation Program for TIPS and Their Follow‐Up Network (NEPTUN) cohort. This number provided sufficient quality and structured follow‐up with the possibility of calculating major scores (Child, Model for End‐Stage Liver Disease [MELD], Chronic Liver Failure Consortium acute decompensation [CLIF‐C AD] scores) and recording of the events (development of decompensation episode and ACLF). We analyzed the association of LV‐GLS with overall mortality and development of ACLF in patients with TIPS. LV‐GLS was independently associated with overall mortality (hazard ratio [HR], 1.123; 95% confidence interval [CI],1.010‐1.250) together with aspartate aminotransferase (HR, 1.009; 95% CI, 1.004‐1.014) and CLIF‐C AD score (HR, 1.080; 95% CI, 1.018‐1.137). Area under the receiver operating characteristic curve (AUROC) analysis for LV‐GLS for overall survival showed higher area under the curve (AUC) than MELD and CLIF‐C AD scores (AUC, 0.688 versus 0.646 and 0.573, respectively). The best AUROC‐determined LV‐GLS cutoff was −16.6% to identify patients with a significantly worse outcome after TIPS at 3 months, 6 months, and overall. LV‐GLS was independently associated with development of ACLF (HR, 1.613; 95% CI, 1.025‐2.540) together with a MELD score above 15 (HR, 2.222; 95% CI, 1.400‐3.528). Conclusion: LV‐GLS is useful for identifying patients at risk of developing ACLF and a worse outcome after TIPS. Although validation is required, this tool might help to stratify risk in patients receiving TIPS.