Regionale Bio-Lebensmittel im Handel - Situation, Perspektiven, Handlungsempfehlungen [Regional organic food in the retail: current situation, perspectives and recommended actions]

Der Markt für Ökoprodukte ist angesichts einer stark steigenden Nachfrage 2001 kräftig in Bewegung gekommen. Mit dem Einstieg weiterer Handelsketten ist zu erwarten, dass Bioprodukte in zunehmendem Maße international eingekauft werden. Auch im Naturkostsektor ist diese Internationalisierung des Marktes zu beobachten. Der Ökolandbau läuft damit Gefahr, seine regionale Verankerung zu verlieren und sich der Weltmarktorientierung des konventionellen Handels anzupassen. Auf der anderen Seite gibt es in Deutschland einige hundert Regionalinitiativen, die erfolgreich am Markt bestehen. Da der Trend zu Qualität, Transparenz und Kontrolle geht, werden in der Regionalvermarktung zunehmend Bioprodukte nachgefragt. Nur wenige Biovermarkter haben bislang jedoch diese „Regionalentwicklung des Marktes“ bewusst aufgegriffen und mitgestaltet. Projekte mit Bio-Regionalmarken zeigen, dass es auch gemeinsam geht und erfolgreich sein kann. Dabei gibt es aber nur wenige Vermarkter, die regionale Bio-Ware an den Lebensmitteleinzelhandel liefern, obwohl dieser Vermarktungsweg für eine Steigerung des Absatzvolumens im ökologischen Landbau längst als unverzichtbar gilt. Wie es zum Erfolg der regionalen Bio-Vermarktung an den Lebensmitteleinzelhandel gekommen ist und welche Faktoren bei der Zusammenarbeit wesentlich sind, ist bis heute noch nicht hinreichend untersucht worden. Vornehmliches Ziel dieser Studie ist es daher, neben der Beschreibung vorbildlicher Beispiele die Erfolgsfaktoren von regional vertriebenen Bioprodukten im Handel darzustellen. Zu diesem Zweck wurden zahlreiche Vertreter des Lebensmitteleinzelhandels und regionaler Vermarktungsinitiativen befragt. Am Ende der Untersuchung steht die Formulierung von Handlungsempfehlungen und Forderungen zur Ausweitung und Unterstützung der regionalen Bio-Vermarktung an den Lebensmitteleinzelhandel

Categorizing diffuse parenchymal lung disease in children

Background Aim of this study was to verify a systematic and practical categorization system that allows dynamic classification of pediatric DPLD irrespective of completeness of patient data. Methods The study was based on 2322 children submitted to the kids-lung-register between 1997 and 2012. Of these children 791 were assigned to 12 DPLD categories, more than 2/3 belonged to categories manifesting primarily in infancy. The work-flow of the pediatric DPLD categorization system included (i) the generation of a final working diagnosis, decision on the presence or absence of (ii) DPLD and (iii) a systemic or lung only condition, and (iv) the allocation to a category and subcategory. The validity and inter-observer dependency of this workflow was re-tested using a systematic sample of 100 cases. Results Two blinded raters allocated more than 80 % of the re-categorized cases identically. Non-identical allocation was due to lack of appreciation of all available details, insufficient knowledge of the classification rules by the raters, incomplete patient data, and shortcomings of the classification system itself. Conclusions This study provides a suitable workflow and hand-on rules for the categorization of pediatric DPLD. Potential pitfalls were identified and a foundation was laid for the development of consensus-based, international categorization guidelines

Diffuse alveolar hemorrhage in children with interstitial lung disease: Determine etiologies!

OBJECTIVE: Diffuse alveolar hemorrhage (DAH) in children is a rare condition resulting from different underlying diseases. This study aimed at describing characteristics and diagnostic measures in children with ILD (children\u27s interstitial lung disease, chILD) and DAH to improve the diagnostic approach by increasing clinician\u27s awareness of diagnostic shortcomings. PATIENTS AND METHODS: A retrospective data analysis of patients with ILD and DAH treated in our own or collaborating centers between 01/07/1997 and 31/12/2020 was performed. Data on clinical courses and diagnostic measures were systematically retrieved as case-vignettes and investigated. To assess suitability of diagnostic software-algorithms, the Human Phenotype Ontology (HPO) was revised and expanded to optimize conditions of its associated tool the Phenomizer. RESULTS: For 97 (74%) of 131 patients, etiology of pulmonary hemorrhage was clarified. For 34 patients (26%), no underlying condition was found (termed as idiopathic pulmonary hemorrhage, IPH). Based on laboratory findings or clinical phenotype/comorbidities, 20 of these patients were assigned to descriptive clusters: IPH associated with autoimmune features (9), eosinophilia (5), renal disease (3) or multiorgan involvement (3). For 14 patients, no further differentiation was possible. CONCLUSION: Complete and sometimes repeated diagnostics are essential for establishing the correct diagnosis in children with DAH. We suggest assignment of patients with IPH to descriptive clusters, which may also guide further research. Digital tools such as the Phenomizer/HPO are promising, but need to be extended to increase diagnostic accuracy

Precise Measurements of Beam Spin Asymmetries in Semi-Inclusive π0\pi^0 production

We present studies of single-spin asymmetries for neutral pion electroproduction in semi-inclusive deep-inelastic scattering of 5.776 GeV polarized electrons from an unpolarized hydrogen target, using the CEBAF Large Acceptance Spectrometer (CLAS) at the Thomas Jefferson National Accelerator Facility. A substantial $\sin \phi_h$ amplitude has been measured in the distribution of the cross section asymmetry as a function of the azimuthal angle $\phi_h$ of the produced neutral pion. The dependence of this amplitude on Bjorken $x$ and on the pion transverse momentum is extracted with significantly higher precision than previous data and is compared to model calculations.Comment: to be submitted PL

Single-cell multi-omics analysis of the immune response in COVID-19

Peer reviewedPublisher PD

Single-cell multi-omics analysis of the immune response in COVID-19

Funder: Lister Institute of Preventive Medicine; doi: https://doi.org/10.13039/501100001255Funder: University College London, Birkbeck MRC Doctoral Training ProgrammeFunder: The Jikei University School of MedicineFunder: Action Medical Research (GN2779)Funder: NIHR Clinical Lectureship (CL-2017-01-004)Funder: NIHR (ACF-2018-01-004) and the BMA FoundationFunder: Chan Zuckerberg Initiative (grant 2017-174169) and from Wellcome (WT211276/Z/18/Z and Sanger core grant WT206194)Funder: UKRI Innovation/Rutherford Fund Fellowship allocated by the MRC and the UK Regenerative Medicine Platform (MR/5005579/1 to M.Z.N.). M.Z.N. and K.B.M. have been funded by the Rosetrees Trust (M944)Funder: Barbour FoundationFunder: ERC Consolidator and EU MRG-Grammar awardsFunder: Versus Arthritis Cure Challenge Research Grant (21777), and an NIHR Research Professorship (RP-2017-08-ST2-002)Funder: European Molecular Biology Laboratory (EMBL)Abstract: Analysis of human blood immune cells provides insights into the coordinated response to viral infections such as severe acute respiratory syndrome coronavirus 2, which causes coronavirus disease 2019 (COVID-19). We performed single-cell transcriptome, surface proteome and T and B lymphocyte antigen receptor analyses of over 780,000 peripheral blood mononuclear cells from a cross-sectional cohort of 130 patients with varying severities of COVID-19. We identified expansion of nonclassical monocytes expressing complement transcripts (CD16+C1QA/B/C+) that sequester platelets and were predicted to replenish the alveolar macrophage pool in COVID-19. Early, uncommitted CD34+ hematopoietic stem/progenitor cells were primed toward megakaryopoiesis, accompanied by expanded megakaryocyte-committed progenitors and increased platelet activation. Clonally expanded CD8+ T cells and an increased ratio of CD8+ effector T cells to effector memory T cells characterized severe disease, while circulating follicular helper T cells accompanied mild disease. We observed a relative loss of IgA2 in symptomatic disease despite an overall expansion of plasmablasts and plasma cells. Our study highlights the coordinated immune response that contributes to COVID-19 pathogenesis and reveals discrete cellular components that can be targeted for therapy

Immune dysregulation as a consequence of genetic variants within the JAK-STAT signalling pathway

Research in immunology has been a rapidly evolving field in recent years, largely facilitated by the advent of next-generation sequencing techniques. The opportunity to study the entire coding sequence of the genome has resulted in the discovery of more than 400 well-characterized, monogenic inborn errors of immunity. Research on these rare patients, who mostly present early in life to pediatric hospitals, has informed our understanding of human immunity since it allows to study the function of a mutated gene product in the context of human disease. Whilst the power of the immune system has evolved to fight infection, fine-tuned regulatory mechanisms gained importance. Keeping the balance between tolerance and protection involves close communication between immune cells and their environment. Such interactions are often mediated by soluble factors, i.e. cytokines. The work presented in this thesis is centered around two important signalling pathways: Interleukin-2 signalling has long been recognized pivotal for T cell immunity. The discovery of homozygous loss-of-function variants in IL2RB underscores its non-redundant role in preventing autoimmunity by promoting regulatory T cell survival and function. Additionally, a terminal differentiation defect of cytotoxic lymphocytes renders affected patients specifically susceptible to Cytomegalo-virus disease. Additional work on patients with loss- and gain-of-functions in the downstream signalling molecule STAT5B expands the phenotypic spectrum and explores potential treatment op-tions using Janus tyrosine kinase inhibitors. The second pathway under study is type I interferon signalling. Functional validation of a new biallelic IFNAR1 variant abrogating responses to type I interferon was undertaken in an individual presenting with haemophagocytic lymphohistiocytosis following receipt of live-viral vaccine. Lethal autoinflammation was also seen in patients where homozygous STAT2 variants were found to hamper negative feedback regulation and thus causing unrestrained type I interferon activity. Mechanistic studies on the inflammatory consequences of dysregulated type I interferon responses in STAT2- and IRF9-deficient primary cells and induced pluripotent stem cell derived macrophages offer a molecular explanation for the clinically observed inflammation in these individuals. By dissecting the molecular mechanisms underlying immune dysregulation in these rare patients with monogenic errors of immunity I am hoping to contribute to improved diagnostic rates and to help pave the way for personalized treatment options in these ‘orphan’ diseases