Großflächige Abscheidung von Graphen - Ein wichtiger Schritt für neuartige Bauelemente

Das wachsende Interesse an Graphen beruht auf seiner unverwechselbaren Bandstruktur und seinen damit zusammenhängenden herausragenden physikalischen Eigenschaften. Es wird daher weltweit nach einem Verfahren gesucht, Graphen großflächig und mit hoher Qualität abzuscheiden. In einer an der TH Wildau [FH] speziell für diese Aufgabe konzipierten Reaktionskammer wurde die Herstellung mittels chemischer Gasphasenabscheidung auf katalytischen Metalloberflächen für verschiedene Parameter studiert und deren Verträglichkeit mit der CMOS -Technologie untersucht. Die ersten Tests erfolgten auf Nickel, da hier eine im Volumen stattfindende katalytische Reaktion einsetzt. In weiteren Schritten fiel die Wahl auf Kupfer, da hier die Reaktion an der Oberfläche stattfindet und daher ein stabilerer Prozess realisiert werden konnte. Die Qualitätsprüfung der erzeugten Schichten erfolgte mittels Ramanspektrometrie

Angiotensin-converting enzyme gene insertion/deletion polymorphism in migraine patients

<p>Abstract</p> <p>Background</p> <p>The main objective of this study was to investigate the angiotensin converting enzyme (<it>ACE</it>) genotype as a possible risk factor for migraine (both with and without aura) compared to controls. We also wanted to examine whether a clinical response to an ACE inhibitor, lisinopril, or an angiotensin II receptor blocker, candesartan, in migraine prophylaxis was related to <it>ACE </it>genotype.</p> <p>Methods</p> <p>347 migraine patients aged 18–68 (155 migraine without aura (MoA), 187 migraine with aura (MwA) and 5 missing aura subgroup data) and 403 healthy non-migrainous controls > 40 years of age were included in the study. A polymerase chain reaction (PCR) was performed on the genomic DNA samples to obtain the <it>ACE </it>insertion (I)/deletion(D) polymorphisms.</p> <p>Results</p> <p>No significant differences between migraine patients and controls were found with regard to <it>ACE </it>genotype and allele distributions. Furthermore, there was no significant difference between the controls and the MwA or MoA subgroups.</p> <p>Conclusion</p> <p>In our sample there is no association between <it>ACE </it>genotype or allele frequency and migraine. In addition, <it>ACE </it>genotype in our experience did not predict the clinical response to lisinopril or candesartan used as migraine prophylactics.</p

Ki-67 as a prognostic marker in mantle cell lymphoma—consensus guidelines of the pathology panel of the European MCL Network

Mantle cell lymphoma (MCL) has a heterogeneous clinical course and is mainly an aggressive B cell non-Hodgkin lymphoma; however, there are some indolent cases The Ki-67 index, defined by the percentage of Ki-67-positive lymphoma cells on histopathological slides, has been shown to be a very powerful prognostic biomarker. The pathology panel of the European MCL Network evaluated methods to assess the Ki-67 index including stringent counting, digital image analysis, and estimation by eyeballing. Counting of 2 × 500 lymphoma cells is the gold standard to assess the Ki-67 index since this value has been shown to predict survival in prospective randomized trials of the European MCL Network. Estimation by eyeballing and digital image analysis showed a poor concordance with the gold standard (concordance correlation coefficients [CCC] between 0.29 and 0.61 for eyeballing and CCC of 0.24 and 0.37 for two methods of digital image analysis, respectively). Counting a reduced number of lymphoma cells (2 × 100 cells) showed high interobserver agreement (CCC = 0.74). Pitfalls of the Ki-67 index are discussed and guidelines and recommendations for assessing the Ki-67 index in MCL are given

Magnetic resonance imaging after most common form of concussion

<p>Abstract</p> <p>Background</p> <p>Until now there is a lack of carefully controlled studies with conventional MR imaging performed exclusively in concussion with short lasting loss of consciousness (LOC).</p> <p>Methods</p> <p>A MR investigation was performed within 24 hours and after 3 months in 20 patients who had suffered a concussion with a verified loss of consciousness of maximally 5 minutes. As a control group, 20 age- and gender matched patients with minor orthopaedic injuries had a MR investigation using the same protocol.</p> <p>Results</p> <p>In a concussion population with an average LOC duration of 1. 4 minutes no case with unequivocal intracranial traumatic pathology was detected.</p> <p>Conclusion</p> <p>An ordinary concussion with short lasting LOC does not or only seldom result in a degree of diffuse axonal injury (DAI) that is visualized by conventional MR with field strength of 1.0 Tesla (T). Analysis of earlier MR studies in concussion using field strength of 1.5 T as well as of studies with diffusion tensor MR imaging (MR DTI) reveal methodological shortcomings, in particular use of inadequate control groups. There is, therefore, a need for carefully controlled studies using MR of higher field strength and/or studies with MR DTI exclusively in common concussion with LOC of maximally 5 minutes.</p

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation

The Incidence of Diagnosis of Munchausen Syndrome, Other Factitious Disorders, and Malingering

Background. Systematic studies on factitious disorders and malingering in large populations are rare. To address this issue, we performed a nationwide epidemiological study in Norway on the incidence of these diagnoses in an unselected patient population. In particular, we tried to confirm the diagnoses and to estimate the contribution of Munchausen syndrome to the spectrum of factitious disorders. Methods. We analyzed data obtained from the Norwegian Patient Registry (NPR), which provided a deidentified list of all patients from 2008 to 2016 who had received the ICD-10 diagnosis of F68.1 or the diagnosis code Z76.5. Results. Altogether, 237 patients (99 females; 138 males) received a diagnosis of F68.1. Code Z76.5 was applied to 52 patients (12 females; 40 males), all diagnosed within health institutions. Three of 1700 specialists (somatic specialist, psychologist, or psychiatrist) in private practice had diagnosed a factitious disorder in altogether 87 patients. After contacting these specialists, we could identify no true case of F68.1. For 24 of 146 patients who were equally distributed by gender within health institutions, we managed to identify the diagnosing healthcare providers. Of these 24 patients, only 11 correctly qualified for code F68.1. Only two female patients qualified for a Munchausen syndrome diagnosis. Conclusions. There is a male predominance for the diagnosis of malingering. An earlier suspicion of a female predominance for Munchausen syndrome is upheld. There is significant underdiagnosing and misdiagnosing for both conditions and for factitious disorders in general. To separate the most serious form of factitious disorders from milder forms and to facilitate more systematic research, we recommend a specific ICD diagnosis for Munchausen syndrome

The incidence of diagnosis of Munchausen syndrome, other factitious disorders, and malingering

Background. Systematic studies on factitious disorders and malingering in large populations are rare. To address this issue, we performed a nationwide epidemiological study in Norway on the incidence of these diagnoses in an unselected patient population. In particular, we tried to confirm the diagnoses and to estimate the contribution of Munchausen syndrome to the spectrum of factitious disorders. Methods. We analyzed data obtained from the Norwegian Patient Registry (NPR), which provided a deidentified list of all patients from 2008 to 2016 who had received the ICD-10 diagnosis of F68.1 or the diagnosis code Z76.5. Results. Altogether, 237 patients (99 females; 138 males) received a diagnosis of F68.1. Code Z76.5 was applied to 52 patients (12 females; 40 males), all diagnosed within health institutions. Three of 1700 specialists (somatic specialist, psychologist, or psychiatrist) in private practice had diagnosed a factitious disorder in altogether 87 patients. After contacting these specialists, we could identify no true case of F68.1. For 24 of 146 patients who were equally distributed by gender within health institutions, we managed to identify the diagnosing healthcare providers. Of these 24 patients, only 11 correctly qualified for code F68.1. Only two female patients qualified for a Munchausen syndrome diagnosis. Conclusions. There is a male predominance for the diagnosis of malingering. An earlier suspicion of a female predominance for Munchausen syndrome is upheld. There is significant underdiagnosing and misdiagnosing for both conditions and for factitious disorders in general. To separate the most serious form of factitious disorders from milder forms and to facilitate more systematic research, we recommend a specific ICD diagnosis for Munchausen syndrome