Xenogenic Esophagus Scaffolds Fixed with Several Agents: Comparative In Vivo Study of Rejection and Inflammation

Most infants with long-gap esophageal atresia receive an esophageal replacement with tissue from stomach or colon, because the native esophagus is too short for true primary repair. Tissue-engineered esophageal conducts could present an attractive alternative. In this paper, circular decellularized porcine esophageal scaffold tissues were implanted subcutaneously into Sprague-Dawley rats. Depending on scaffold cross-linking with genipin, glutaraldehyde, and carbodiimide (untreated scaffolds : positive control; bovine pericardium : gold standard), the number of infiltrating fibroblasts, lymphocytes, macrophages, giant cells, and capillaries was determined to quantify the host response after 1, 9, and 30 days. Decellularized esophagus scaffolds were shown to maintain native matrix morphology and extracellular matrix composition. Typical inflammatory reactions were observed in all implants; however, the cellular infiltration was reduced in the genipin group. We conclude that genipin is the most efficient and best tolerated cross-linking agent to attenuate inflammation and to improve the integration of esophageal scaffolds into its surrounding tissue after implantation

Soft particles reinforce robotic grippers: robotic grippers based on granular jamming of soft particles

Granular jamming has been identified as a fundamental mechanism for the operation of robotic grippers. In this work, we show, that soft particles like expanded polystyrene beads lead to significantly larger gripping forces in comparison to rigid particles. In contradiction to naive expectation, the combination of jamming and elasticity gives rise to very different properties of the jammed phase, compared to hard-particle systems. This may be of interest also beyond the application in robotic grippers

ERBB2‐amplified lobular breast carcinoma exhibits concomitant CDK12 co‐amplification associated with poor prognostic features

Most invasive lobular breast carcinomas (ILBCs) are luminal‐type carcinomas with an HER2‐negative phenotype (ERBB2 or HER2 un‐amplified) and CDH1 mutations. Rare variants include ERBB2‐amplified subtypes associated with an unfavorable prognosis and less response to anti‐HER2 targeted therapies. We analyzed the clinicopathological and molecular features of ERBB2‐amplified ILBC and compared these characteristics with ERBB2‐unamplified ILBC. A total of 253 patients with ILBC were analyzed. Paraffin‐embedded formalin‐fixed tumor samples from 250 of these patients were added to a tissue microarray. Protein expression of prognostic, stem cell and breast‐specific markers was tested by immunohistochemistry (IHC). Hybrid capture‐based comprehensive genomic profiling (CGP) was performed for 10 ILBCs that were either fluorescent in situ hybridization (FISH) or IHC positive for HER2 amplification/overexpression and 10 ILBCs that were either FISH or IHC negative. Results were compared with a CGP database of 44,293 invasive breast carcinomas. The CGP definition of ERBB2 amplification was five copies or greater. A total of 17 of 255 ILBC (5%) were ERBB2 amplified. ERBB2‐amplified ILBC had higher tumor stage (p < 0.0001), more frequent positive nodal status (p = 0.00022), more distant metastases (p = 0.012), and higher histological grade (p < 0.0001), and were more often hormone receptor negative (p < 0.001) and more often SOX10 positive (p = 0.005). ERBB2 short variant sequence mutations were more often detected in ERBB2‐unamplified tumors (6/10, p = 0.027), whereas CDH1 mutations/copy loss were frequently present in both subgroups (9/10 and 7/10, respectively). Amplification of pathogenic genes were more common in HER2‐positive ILBC (p = 0.0009). CDK12 gene amplification (≥6 copies) was detected in 7 of 10 ERBB2‐amplified ILBC (p = 0.018). There were no CDK12 gene amplifications reported in 44,293 invasive breast carcinomas in the FMI Insights CGP database. ERBB2‐amplified ILBC is a distinct molecular subgroup with frequent coamplification of CDK12, whereas ERBB2 sequence mutations occur only in ERBB2‐unamplified ILBC. CDK12/ERBB2 co‐amplification may explain the poor prognosis and therapy resistance of ERBB2‐amplified ILBC

Association of MICA with rheumatoid arthritis independent of known HLA-DRB1 risk alleles in a family-based and a case control study

Introduction The gene MICA encodes the protein major histocompatibility complex class I polypeptide-related sequence A. It is expressed in synovium of patients with rheumatoid arthritis (RA) and its implication in autoimmunity is discussed. We analyzed the association of genetic variants of MICA with susceptibility to RA. Methods Initially, 300 French Caucasian individuals belonging to 100 RA trio families were studied. An additional 100 independent RA trio families and a German Caucasian case-control cohort (90/182 individuals) were available for replication. As MICA is situated in proximity to known risk alleles of the HLA-DRB1 locus, our analysis accounted for linkage disequilibrium either by analyzing the subgroup consisting of parents not carrying HLA-DRB1 risk alleles with transmission disequilibrium test (TDT) or by implementing a regression model including all available data. Analysis included a microsatellite polymorphism (GCT)n and single-nucleotide polymorphisms (SNPs) rs3763288 and rs1051794. Results In contrast to the other investigated polymorphisms, the non-synonymously coding SNP MICA-250 (rs1051794, Lys196Glu) was strongly associated in the first family cohort (TDT: P = 0.014; regression model: odds ratio [OR] 0.46, 95% confidence interval [CI] 0.25 to 0.82, P = 0.007). Although the replication family sample showed only a trend, combined family data remained consistent with the hypothesis of MICA-250 association independent from shared epitope (SE) alleles (TDT: P = 0.027; regression model: OR 0.56, 95% CI 0.38 to 0.83, P = 0.003). We also replicated the protective association of MICA-250A within a German Caucasian cohort (OR 0.31, 95% CI 0.1 to 0.7, P = 0.005; regression model: OR 0.6, 95% CI 0.37 to 0.96, P = 0.032). We showed complete linkage disequilibrium of MICA-250 (D' = 1, r2= 1) with the functional MICA variant rs1051792 (D' = 1, r2= 1). As rs1051792 confers differential allelic affinity of MICA to the receptor NKG2D, this provides a possible functional explanation for the observed association. Conclusions We present evidence for linkage and association of MICA-250 (rs1051794) with RA independent of known HLA-DRB1 risk alleles, suggesting MICA as an RA susceptibility gene. However, more studies within other populations are necessary to prove the general relevance of this polymorphism for RA

NFDI4Culture - Consortium for research data on material and immaterial cultural heritage

Digital data on tangible and intangible cultural assets is an essential part of daily life, communication and experience. It has a lasting influence on the perception of cultural identity as well as on the interactions between research, the cultural economy and society. Throughout the last three decades, many cultural heritage institutions have contributed a wealth of digital representations of cultural assets (2D digital reproductions of paintings, sheet music, 3D digital models of sculptures, monuments, rooms, buildings), audio-visual data (music, film, stage performances), and procedural research data such as encoding and annotation formats. The long-term preservation and FAIR availability of research data from the cultural heritage domain is fundamentally important, not only for future academic success in the humanities but also for the cultural identity of individuals and society as a whole. Up to now, no coordinated effort for professional research data management on a national level exists in Germany. NFDI4Culture aims to fill this gap and create a usercentered, research-driven infrastructure that will cover a broad range of research domains from musicology, art history and architecture to performance, theatre, film, and media studies. The research landscape addressed by the consortium is characterized by strong institutional differentiation. Research units in the consortium's community of interest comprise university institutes, art colleges, academies, galleries, libraries, archives and museums. This diverse landscape is also characterized by an abundance of research objects, methodologies and a great potential for data-driven research. In a unique effort carried out by the applicant and co-applicants of this proposal and ten academic societies, this community is interconnected for the first time through a federated approach that is ideally suited to the needs of the participating researchers. To promote collaboration within the NFDI, to share knowledge and technology and to provide extensive support for its users have been the guiding principles of the consortium from the beginning and will be at the heart of all workflows and decision-making processes. Thanks to these principles, NFDI4Culture has gathered strong support ranging from individual researchers to highlevel cultural heritage organizations such as the UNESCO, the International Council of Museums, the Open Knowledge Foundation and Wikimedia. On this basis, NFDI4Culture will take innovative measures that promote a cultural change towards a more reflective and sustainable handling of research data and at the same time boost qualification and professionalization in data-driven research in the domain of cultural heritage. This will create a long-lasting impact on science, cultural economy and society as a whole

TRY plant trait database – enhanced coverage and open access

Plant traits - the morphological, anatomical, physiological, biochemical and phenological characteristics of plants - determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait‐based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits - almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

Schlussfolgerungen

Sack D, Straßheim H, Zimmermann K. Schlussfolgerungen. In: Sack D, Straßheim H, Zimmermann K, eds. Renaissance der Verkehrspolitik. Politik- und mobilitätswissenschaftliche Perspektiven. Wiesbaden: Springer; In Press

Einleitung.

Sack D, Straßheim H, Zimmermann K. Einleitung. In: Sack D, Straßheim H, Zimmermann K, eds. Renaissance der Verkehrspolitik. Wiesbaden: Springer; In Press

Renaissance der Verkehrspolitik. Politik- und mobilitätswissenschaftliche Perspektiven

Sack D, Straßheim H, Zimmermann K, eds. Renaissance der Verkehrspolitik. Politik- und mobilitätswissenschaftliche Perspektiven. Wiesbaden: Springer; In Press