How to do Qualitative Structural Analysis: The Qualitative Interpretation of Network Maps and Narrative Interviews

Zur Analyse der Einbettung von Akteur/innen in soziale Strukturen werden in der Netzwerkforschung zunehmend offene Forschungszugänge auch in Kombination mit standardisierten methodischen Ansätzen verwendet. Die Entwicklung eines Vorgehens zur qualitativen strukturbezogenen Analyse stellt bislang ein Desiderat dar. Am Beispiel der Analyse einer egozentrierten Netzwerkkarte und eines erzählgenerierenden Interviews entwerfen, explizieren und begründen wir ein methodisches qualitatives Analyseverfahren, das Standards einer strukturalen Analyse – als theoretisch-methodologische Position der sozialen Netzwerkanalyse – Rechnung trägt. Entlang des Beispiels entwerfen wir qualitative Verfahren der Interpretation (Sequenzanalyse, sensibilisierendes Konzept, Memos) für die Auswertung von Netzwerkkarten und des narrativen Materials, für das wir Konzepte der formalen Netzwerkanalyse adaptieren. Unser Vorschlag dieser qualitativen strukturalen Analyse – kurz QSA – stellt damit eine Kombination aus der analytischen Perspektive der strukturalen Analyse mit analytischen Standards der qualitativen Sozialforschung dar.URN: http://nbn-resolving.de/urn:nbn:de:0114-fqs150190Para analizar cómo los actores están involucrados en las estructuras sociales, la investigación de redes está empleando cada vez más métodos cualitativos, a veces en combinación con enfoques estandarizados. Hasta ahora sigue siendo una aspiración desarrollar un método para el análisis estructural cualitativo. Utilizando el ejemplo de análisis de un mapa de red egocéntrico y una entrevista narrativa, conceptualizamos, explicamos y fundamentamos un procedimiento de análisis cualitativo que representa adecuadamente los estándares del análisis estructural en tanto posturas teóricas y metodológicas adoptadas por el análisis de redes sociales. Con base en este ejemplo, diseñamos procedimientos cualitativos (análisis secuencial, conceptos sensibilizadores, memos) para analizar los mapas de red y los datos narrativos. Para ello, adaptamos conceptos del análisis formal de red. Nuestra propuesta para este análisis estructural cualitativo (AEC) es, pues, una combinación de la perspectiva del análisis estructural y de los estándares tomados de la investigación social cualitativa.URN: http://nbn-resolving.de/urn:nbn:de:0114-fqs150190To analyze how actors are embedded in social structures, network research is increasingly using qualitative methods, sometimes in combination with standardized approaches. So far, the development of a method for qualitative structural analysis remains a desideratum. Using the example of the analysis of an ego-centric network map and a narrative interview, we conceptualize, explicate and substantiate a qualitative analysis procedure which does justice to the standards of structural analysis as theoretical and methodological stances taken by social network analysis. Based on this example, we design qualitative procedures (sequential analysis, sensitizing concepts, memos) to analyze network maps and narrative data. To do so, we adapt concepts from formal network analysis. Our proposal for this qualitative structural analysis (QSA) is thus a combination of the analytical perspective of structural analysis and analytical standards taken from qualitative social research.URN: http://nbn-resolving.de/urn:nbn:de:0114-fqs15019

RASSF1A promoter methylation and expression analysis in normal and neoplastic kidney indicates a role in early tumorigenesis

<p>Abstract</p> <p>Background</p> <p>Epigenetic silencing of the RAS association domain family 1A (<it>RASSF1A</it>) tumor suppressor gene promoter has been demonstrated in renal cell carcinoma (RCC) as a result of promoter hypermethylation. Contradictory results have been reported for <it>RASSF1A </it>methylation in normal kidney, thus it is not clear whether a significant difference between <it>RASSF1A </it>methylation in normal and tumor cells of the kidney exists. Moreover, RASSF1A expression has not been characterized in tumors or normal tissue as yet.</p> <p>Results</p> <p>Using combined bisulfite restriction analysis (COBRA) we compared RASSF1A methylation in 90 paired tissue samples obtained from primary kidney tumors and corresponding normal tissue. Bisulfite sequence analysis was carried out using both pooled amplicons from the tumor and normal tissue groups and subclones obtained from a single tissue pair. Expression of RASSF1A was analyzed by the use of tissue arrays and immunohistochemistry. We found significantly increased methylation in tumor samples (mean methylation, 20%) compared to corresponding normal tissues (mean methylation, 11%; <it>P </it>< 0.001). Densely methylated sequences were found both in pooled and individual sequences of normal tissue. Immunohistochemical analysis revealed a significant reduced expression of RASSF1A in most of the tumor samples. Heterogeneous expression patterns of RASSF1A were detected in a subgroup of histologically normal tubular epithelia.</p> <p>Conclusion</p> <p>Our methylation and expression data support the hypothesis that <it>RASSF1A </it>is involved in early tumorigenesis of renal cell carcinoma.</p

MRI Extracellular Volume Fraction in Liver Fibrosis-A Comparison of Different Time Points and Blood Pool Measurements.

BACKGROUND Extracellular volume (ECV) correlates with the degree of liver fibrosis. PURPOSE To analyze the performance of liver MRI-based ECV evaluations with different blood pool measurements at different time points. STUDY TYPE Prospective. SAMPLE 73 consecutive patients (n = 31 females, mean age 56 years) with histopathology-proven liver fibrosis. FIELD STRENGTH/SEQUENCE 3T acquisition within 90 days of biopsy, including shortened modified look-locker inversion recovery T1 mapping. ASSESSMENT Polygonal regions of interest were manually drawn in the liver, aorta, vena cava, and in the main, left and right portal vein on four slices before and after Gd-DOTA administration at 5/10/15 minutes. ECV was calculated 1) on one single slice on portal bifurcation level, and 2) averaged over all four slices. STATISTICAL TESTS Parameters were compared between patients with fibrosis grades F0-2 and F3-F4 with the Mann-Whitney U and fishers exact test. ROC analysis was used to assess the performance of the parameters to predict F3-4 fibrosis. A P-value <0.05 was considered statistically significant. RESULTS ECV was significantly higher in F3-4 fibrosis (35.4% [33.1%-37.6%], 36.1% [34.2%-37.5%], and 37.0% [34.8%-39.2%] at 5/10/15 minutes) than in patients with F0-2 fibrosis (33.3% [30.8%-34.8%], 33.7% [31.6%-34.7%] and 34.9% [32.2%-36.0%]; AUC = 0.72-0.75). Blood pool T1 relaxation times in the aorta and vena cava were longer on the upper vs. lower slices at 5 minutes, but not at 10/15 minutes. AUC values were similar when measured on a single slice (AUC = 0.69-0.72) or based on blood pool measurements in the cava or portal vein (AUC = 0.63-0.67 and AUC = 0.65-0.70). DATA CONCLUSION Liver ECV is significantly higher in F3-4 fibrosis compared to F0-2 fibrosis with blood pool measurements performed in the aorta, inferior vena cava, and portal vein at 5, 10, and 15 minutes. However, a smaller variability was observed for blood pool measurements between slices at 15 minutes. LEVEL OF EVIDENCE 1 TECHNICAL EFFICACY: Stage 3

Canine Respiratory Coronavirus, Bovine Coronavirus, and Human Coronavirus OC43: Receptors and Attachment Factors

Despite high similarity of canine respiratory coronavirus (CRCoV), bovine coronavirus, (BCoV) and human coronavirus OC43 (HCoV-OC43), these viruses differ in species specificity. For years it was believed that they share receptor specificity, utilizing sialic acids for cell surface attachment, internalization, and entry. Interestingly, careful literature analysis shows that viruses indeed bind to the cell surface via sialic acids, but there is no solid data that these moieties mediate virus entry. In our study, using a number of techniques, we showed that all three viruses are indeed able to bind to sialic acids to a different extent, but these molecules render the cells permissive only for the clinical strain of HCoV-OC43, while for others they serve only as attachment receptors. CRCoV and BCoV appear to employ human leukocyte antigen class I (HLA-1) as the entry receptor. Furthermore, we identified heparan sulfate as an alternative attachment factor, but this may be related to the cell culture adaptation, as in ex vivo conditions, it does not seem to play a significant role. Summarizing, we delineated early events during CRCoV, BCoV, and HCoV-OC43 entry and systematically studied the attachment and entry receptor utilized by these viruses

Aggregation-resistant alpha-synuclein tetramers are reduced in the blood of Parkinson's patients

Synucleinopathies such as Parkinson's disease (PD) are defined by the accumulation and aggregation of the α-synuclein protein in neurons, glia and other tissues. We have previously shown that destabilization of α-synuclein tetramers is associated with familial PD due to SNCA mutations and demonstrated brain-region specific alterations of α-synuclein multimers in sporadic PD patients following the classical Braak spreading theory. In this study, we assessed relative levels of disordered and higher-ordered multimeric forms of cytosolic α-synuclein in blood from familial PD with G51D mutations and sporadic PD patients. We used an adapted in vitro-cross-linking protocol for human EDTA-whole blood. The relative levels of higher-ordered α-synuclein tetramers were diminished in blood from familial PD and sporadic PD patients compared to controls. Interestingly, the relative amount of α-synuclein tetramers was already decreased in asymptomatic G51D carriers, supporting the hypothesis that α-synuclein multimer destabilization precedes the development of clinical PD. Our data, therefore suggest that measuring α-synuclein tetramers in blood may have potential as a facile biomarker assay for early detection and quantitative tracking of PD progression.</p

Hundreds of variants clustered in genomic loci and biological pathways affect human height

Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

Pressure-induced radial collapse in few-wall carbon nanotubes: A combined theoretical and experimental study

Brazilian authors acknowledge funding from CNPq (grant 307317/2010-2, INCT NanoBioSimes) and Central Analítica-UFC/CT-INFRA-FINEP/Pró-Equipamentos-CAPES/CNPq-SisNano-MCTI (grant 402284/2013-5). R. S. Alencar is also in debt to Coordenação de Aperfeiçoamento de Pessoal de Nível Superior under the grant No. 99999.004227/2014-00 for financial support. Alexander Soldatov (University of Lulea, Sweden) is warmly acknowledged for discussions on the RBM Raman spectra interpretation at the collapse region