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Background
Over the past two decades, there has been a rising trend in malignant melanoma incidence worldwide. In 2008, Germany introduced a nationwide skin cancer screening program starting at age 35. The aims of this study were to analyse the distribution of malignant melanoma tumour stages over time, as well as demographic and regional differences in stage distribution and survival of melanoma patients.
Methods
Pooled data from 61 895 malignant melanoma patients diagnosed between 2002 and 2011 and documented in 28 German population-based and hospital-based clinical cancer registries were analysed using descriptive methods, joinpoint regression, logistic regression and relative survival.
Results
The number of annually documented cases increased by 53.2% between 2002 (N = 4 779) and 2011 (N = 7 320). There was a statistically significant continuous positive trend in the proportion of stage UICC I cases diagnosed between 2002 and 2011, compared to a negative trend for stage UICC II. No trends were found for stages UICC III and IV respectively. Age (OR 0.97, 95% CI 0.97–0.97), sex (OR 1.18, 95% CI 1.11–1.25), date of diagnosis (OR 1.05, 95% CI 1.04–1.06), ‘diagnosis during screening’ (OR 3.24, 95% CI 2.50–4.19) and place of residence (OR 1.23, 95% CI 1.16–1.30) had a statistically significant influence on the tumour stage at diagnosis. The overall 5-year relative survival for invasive cases was 83.4% (95% CI 82.8–83.9%).
Conclusions
No distinct changes in the distribution of malignant melanoma tumour stages among those aged 35 and older were seen that could be directly attributed to the introduction of skin cancer screening in 2008.
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Aims
Treating patients with acute decompensated heart failure (ADHF) presenting with volume overload is a common task. However, optimal guidance of decongesting therapy and treatment targets are not well defined. The inferior vena cava (IVC) diameter and its collapsibility can be used to estimate right atrial pressure, which is a measure of right‐sided haemodynamic congestion. The CAVA‐ADHF‐DZHK10 trial is designed to test the hypothesis that ultrasound assessment of the IVC in addition to clinical assessment improves decongestion as compared with clinical assessment alone.
Methods and results
CAVA‐ADHF‐DZHK10 is a randomized, controlled, patient‐blinded, multicentre, parallel‐group trial randomly assigning 388 patients with ADHF to either decongesting therapy guided by ultrasound assessment of the IVC in addition to clinical assessment or clinical assessment alone. IVC ultrasound will be performed daily between baseline and hospital discharge in all patients. However, ultrasound results will only be reported to treating physicians in the intervention group. Treatment target is relief of congestion‐related signs and symptoms in both groups with the additional goal to reduce the IVC diameter ≤21 mm and increase IVC collapsibility >50% in the intervention group. The primary endpoint is change in N‐terminal pro‐brain natriuretic peptide from baseline to hospital discharge. Secondary endpoints evaluate feasibility, efficacy of decongestion on other scales, and the impact of the intervention on clinical endpoints.
Conclusions
CAVA‐ADHF‐DZHK10 will investigate whether IVC ultrasound supplementing clinical assessment improves decongestion in patients admitted for ADHF.
Molecular-based subclassifications of breast cancer are important for identifying treatment options and stratifying the prognosis in breast cancer. This study aimed to assess the prognosis relative to disease-free survival (DFS) and overall survival (OS) in patients with triple-negative breast cancer (TNBC) and other subtypes, using a biomarker panel including cytokeratin 5 (CK5), cluster of differentiation 117 (CD117), and epidermal growth factor receptor (EGFR). This cohort–case study included histologically confirmed breast carcinomas as cohort arm. From a total of 894 patients, 572 patients with early breast cancer, sufficient clinical data, and archived tumor tissue were included. Using the immunohistochemical markers CK5, CD117, and EGFR, two subgroups were formed: one with all three biomarkers negative (TBN) and one with at least one of those three biomarkers positive (non-TBN). There were significant differences between the two biomarker subgroups (TBN versus non-TBN) in TNBC for DFS (p = 0.04) and OS (p = 0.02), with higher survival rates (DFS and OS) in the non-TBN subgroup. In this study, we found the non-TBN subgroup of TNBC lesions with at least one positive biomarker of CK5, CD117, and/or EGFR, to be associated with longer DFS and OS.
Characterisation of Metalloprotease-mediated EGFR Signal Transactivation after GPCR Stimulation
(2011)
In the context of metalloprotease-mediated transactivation of the epidermal growth factor receptor, different monoclonal antibodies against ADAM17 / TACE were characterized for their ability to block the sheddase. Activity of some of them was observed at doses between 2µg/mL and 10µg/mL. Kinetic analyses showed their activity starting at around 30 minutes. In cellular assays performed with the antibodies, especially upon treatment of cells with sphingosine-1-phosphate a reduction in proliferation was observed with some candidates. Moreover this study provides potential new roles for ß-Arrestins. Their involvement in the triple membrane-passing signal pathway of EGFR transactivation was shown. Furthermore, in overexpressing cellular model systems, an interaction between ADAM17 and ß-Arrestin1 could be observed. Detailed analysis discovered that phosphorylation of ß-Arrestin1 is crucial for this interaction. Additionally, the novel mechanism of UV-induced EGFR transactivation was extended to squamous cell carcinoma. The mechanism happens in a dose dependent manner and requires a metalloprotease to shed the proligand Amphiregulin. The involvement of both ADAM9 and ADAM17, being the metalloproteases responsible for this cleavage, was shown for SCC9 cells.
Electro-optical switching between polariton and cavity lasing in an InGaAs quantum well microcavity
(2014)
We report on the condensation of microcavity exciton polaritons under optical excitation in a microcavity with four embedded InGaAs quantum wells. The polariton laser is characterized by a distinct nonlinearity in the input-output-characteristics, which is accompanied by a drop of the emission linewidth indicating temporal coherence and a characteristic persisting emission blueshift with increased particle density. The temporal coherence of the device at threshold is underlined by a characteristic drop of the second order coherence function to a value close to 1. Furthermore an external electric field is used to switch between polariton regime, polariton condensate and photon lasing.
The possibility of investigating macroscopic coherent quantum states in polariton condensates and of engineering polariton landscapes in semiconductors has triggered interest in using polaritonic systems to simulate complex many-body phenomena. However, advanced experiments require superior trapping techniques that allow for the engineering of periodic and arbitrary potentials with strong on-site localization, clean condensate formation, and nearest-neighbor coupling. Here we establish a technology that meets these demands and enables strong, potentially tunable trapping without affecting the favorable polariton characteristics. The traps are based on a locally elongated microcavity which can be formed by standard lithography. We observe polariton condensation with non-resonant pumping in single traps and photonic crystal square lattice arrays. In the latter structures, we observe pronounced energy bands, complete band gaps, and spontaneous condensation at the M-point of the Brillouin zone.
Eczema often precedes the development of asthma in a disease course called the 'atopic march'. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P = 2.1 x 10(-8)) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P = 5.3 x 10(-9)). Additional susceptibility loci identified at genome-wide significance are FLG (1q21.3), IL4/KIF3A (5q31.1), AP5B1/OVOL1 (11q13.1), C11orf30/LRRC32 (11q13.5) and IKZF3 (17q21). We show that predominantly eczema loci increase the risk for the atopic march. Our findings suggest that eczema may play an important role in the development of asthma after eczema.
Computerunterstützte Auswertung in der automatisierten zweidimensionalen Dünnschichtchromatographie
(2002)
Die vorliegende Arbeit beschäftigt sich mit der zweidimensionalen Dünnschichtchromatographie (DC) und deren quantitativer Auswertung. Es wird auf die Grundlagen der DC eingegangen. Darüberhinaus werden die Vorgehensweisen der quantitativen Auswertung gegenübergestellt und bewertet. Besonders behandelt werden die nichtlinearen Regressionsmethoden. Die in dieser Arbeit verwendete Entwicklungstechnik wird erklärt und die Vorteile beschrieben. Der im Rahmen dieser Arbeit entwickelte Scanner und die dazugehörige Software werden vorgestellt. Als Lichtquelle dient eine 30 W Deuteriumlampe, die ohne Sperrfilter betrieben wird. Dies ermöglicht die Verwendung von Licht auch im Bereich von 198-210 nm. Auf einen Betrieb der Lichtquelle im Vakuum wurde verzichtet. Die Einblendtechnik der Lichtstrahlen in den Lichtwellenleiter wurde nicht verändert. Der bewegliche Teil des Scanners besteht aus einem Kreuztisch, dessen Vorschubeinheiten um 90° versetzt angebracht wurden, um die Platte in x- und in y-Richtung bewegen zu können. Die Wahl der Spindelsteigung ermöglicht eine Schrittweite von 0.1 mm im Bedarfsfall. Jede Vorschubeinheit wird durch eine eigene Steuerkarte angesprochen. Damit kann in beide Richtungen unabhängig voneinander verfahren werden. Die Vorschubgeschwindigkeit ist in zwei Stufen wählbar. Um den Intensitätsverlust bei der Lichtübertragung gering zu halten und einen modularen Aufbau realisieren zu können, wurde als Übertragungsmedium zwischen Lampe und Platte ein Lichtleiter gewählt. Dieser ist in der Lage, sowohl eine als auch mehrere Wellenlängen zu übertragen. Durch den Einsatz eines optimierten Faserbündels, das mit Wasserstoff begast wurde, um die Bildung von Farbzentren zu verhindern, kann die Alterung stark verlangsamt werden. Die Dämpfung der Lichtintensität innerhalb der Faser spielt durch die Verwendung kurzer Fasern nur eine untergeordnete Rolle. Als Detektionseinheit werden Photodiodenarrays verwendet, die 256 bzw. 512 Dioden besitzen. Eingebaut wird jeweils nur das vorjustierte Array, das auf eine Platine aufgebracht ist, die die Elektronik zum Auslesen sowie die Möglichkeit zur Ansteuerung des Auslesevorganges bereits enthält. Die Minimalkonfiguration erlaubt das Verwenden eigener, für den Einsatzzweck optimierter Bauteile. Die erstellte Software verarbeitet die registrierten Daten und ordnet die Signale den entsprechenden Wellenlängen zu. Die Rohdaten werden nach der bekannten Gleichung von Kubelka und Munk in Remissionswerte umgerechnet. Ein neues Verfahren zur Glättung von zweidimensional verrauschten Daten wird eingeführt, mit Hilfe dessen die Signale in eine verwertbare Form übergeführt werden. Hierzu wird eine Regressionsrechnung in zwei Dimensionen mittels eines Polynoms durchgeführt. Die Glättungsbreite kann variabel für beide Dimensionen bestimmt werden. Die Faltungsoperation kann im Gegensatz zu bisher bekannten Verfahren auch während der Auswertung durchgeführt werden. Statische Faltungsoperatoren werden nicht mehr benötigt. Peaks werden gesucht und ihre Lage mit Hilfe einer Basisfläche korrigiert. Diese Fläche berücksichtigt Matrixeinflüsse der Platte, Schwankungen im Lichtstrom der Lampe und Änderungen der mobilen Phase während der Entwicklung. Die transformierten und geglätteten Daten werden in zwei Dateien geschrieben, die sich nur in der Art der Speicherung unterscheiden, um sie mit Fremdprogrammen weiterverarbeiten zu können. Es wird die Möglichkeit untersucht, Remissionsspektren unterschiedlicher Herkunft und UV-Spektren miteinander zu vergleichen. Um auf umfangreiche existierende UV- Spektrenkataloge zurückgreifen zu können, wird eine Möglichkeit gesucht, mit deren Hilfe die Remissionsspektren UV-Spektren zugeordnet werden können. Ein automatisiertes Vorgehen alleine reicht nicht aus, der Eingriff des Benutzers ist unerläßlich. Bei Remissionsdaten findet eine nicht reproduzierbare Verschiebung der Wellenlängen statt, die ein direktes Inbezugsetzen verhindert. Es wird ein Auftrageschema vorgestellt, das auch für quantitative Analysen 2D- entwickelter Platten anwendbar ist. Zusätzlich zu dem zu untersuchenden Gemisch werden 3 Standardgemische bekannter Konzentration und Zusammensetzung aufgetragen. Die erste Entwicklung erfolgt von gegenüberliegenden Seiten bis zur Mitte der Platte, nach Trocknen und Drehen um 90° wird die zweite Entwicklung ebenfalls beidseitig durchgeführt. So wird die Plattenoberfläche optimal ausgenutzt und die Kriterien zur quantitativen Auswertung werden erfüllt. Die Leistungsfähigkeit des neu eingeführten Glättungsalgorithmus wird gezeigt. Auf die Besonderheiten einer Auswertung anhand des Peakvolumen und nicht wie bisher anhand der Peakfläche wird eingegangen. Ein Datensatz von aufgenommenen Spektren wird nach der Verarbeitung gezeigt. Das entwickelte System aus Hard- und Software ist in der Lage, jeden Punkt auf der Platte anzusteuern und Daten zur weiteren Auswertung in genügend hoher Genauigkeit zu liefern.
Aims
Various studies have reported that young European women are more likely to develop early‐onset periodontitis compared to men. A potential explanation for the observed variations in sex and age of disease onset is the natural genetic variation within the autosomal genomes. We hypothesized that genotype‐by‐sex (G × S) interactions contribute to the increased prevalence and severity.
Materials and methods
Using the case‐only design, we tested for differences in genetic effects between men and women in 896 North‐West European early‐onset cases, using imputed genotypes from the OmniExpress genotyping array. Population‐representative 6823 controls were used to verify that the interacting variables G and S were uncorrelated in the general population.
Results
In total, 20 loci indicated G × S associations (P < 0.0005), 3 of which were previously suggested as risk genes for periodontitis (ABLIM2, CDH13, and NELL1). We also found independent G × S interactions of the related gene paralogs MACROD1/FLRT1 (chr11) and MACROD2/FLRT3 (chr20). G × S‐associated SNPs at CPEB4, CDH13, MACROD1, and MECOM were genome‐wide‐associated with heel bone mineral density (CPEB4, MECOM), waist‐to‐hip ratio (CPEB4, MACROD1), and blood pressure (CPEB4, CDH13).
Conclusions
Our results indicate that natural genetic variation affects the different heritability of periodontitis among sexes and suggest genes that contribute to inter‐sex phenotypic variation in early‐onset periodontitis.
Introduction
The term primary progressive aphasia (PPA) sums up the non‐fluent (nfv), the semantic (sv), and the logopenic (lv) variant. Up to now, there is only limited data available concerning magnetic resonance imaging volumetry to monitor disease progression.
Methods
Structural brain imaging and an extensive assessment were applied at baseline and up to 4‐year(s) follow‐up in 269 participants. With automated atlas‐based volumetry 56 brain regions were assessed. Atrophy progression served to calculate sample sizes for therapeutic trials.
Results
At baseline highest atrophy appeared in parts of the left frontal lobe for nfvPPA (–17%) and of the left temporal lobe for svPPA (–34%) and lvPPA (–24%). Severest progression within 1‐year follow‐up occurred in the basal ganglia in nfvPPA (–7%), in the hippocampus/amygdala in svPPA (–9%), and in (medial) temporal regions in lvPPA (–6%).
Conclusion
PPA presents as a left‐dominant, mostly gray matter sensitive disease with considerable atrophy at baseline that proceeds variant‐specific.