A strategy-based framework for assessing the flood resilience of cities – the Hamburg case study

Climate change and continuous urbanization contribute to an increased urban vulnerability towards flooding. Only relying on traditional flood control measures is recognized as inadequate, since the damage can be catastrophic if flood controls fail. The idea of a flood-resilient city – one which can withstand or adapt to a flood event without being harmed in its functionality – seems promising. But what does resilience actually mean when it is applied to urban environments exposed to flood risk, and how can resilience be achieved? This paper presents a heuristic framework for assessing the flood resilience of cities, for scientists and policy-makers alike. It enriches the current literature on flood resilience by clarifying the meaning of its three key characteristics – robustness, adaptability and transformability – and identifying important components to implement resilience strategies. The resilience discussion moves a step forward, from predominantly defining resilience to generating insight into “doing” resilience in practice. The framework is illustrated with two case studies from Hamburg, showing that resilience, and particularly the underlying notions of adaptability and transformability, first and foremost require further capacity-building among public as well as private stakeholders. The case studies suggest that flood resilience is currently not enough motivation to move from traditional to more resilient flood protection schemes in practice; rather, it needs to be integrated into a bigger urban agenda

Role of GATA Transcription Factors in the T Cell Lineage

T lymphocytes play a central role in the mammalian immune response against potentially hazardous pathogens, such as parasites, bacteria, viruses and fungi. These cells have the remarkable capacity to specifically recognize foreign substances, termed antigens, to which they respond by clonal amplification and cellular differentiation, conferring lifelong protective immunity to reinfection with the same pathogen. T lymphocytes express an antigen-specific receptor, called the T cell receptor (TCR), which recognizes peptide fragments derived from foreign proteins or pathogens that have entered into host cells. Defective T cell development and function can result in increased susceptibility to infections or even development of leukemias, allergies and autoimmune diseases. On the other hand, T lymphocytes can be manipulated to eradicate tumor and control graft rejection after organ transplantation. Therefore, in addition to biological interest, knowledge on T cell biology is important for understanding the etiology of a wide variety of diseases and potentially improves current therapies

Update of Parton Distributions at NNLO

We present a new set of parton distributions obtained at NNLO. These differ from the previous sets available at NNLO due to improvements in the theoretical treatment. In particular we include a full treatment of heavy flavours in the region near the quark mass. In this way, an essentially complete set of NNLO partons is presented for the first time. The improved treatment leads to a significant change in the gluon and heavy quark distributions, and a larger value of the QCD coupling at NNLO, alpha_S(M_Z^2) = 0.1191 +/- 0.002(expt.) +/- 0.003(theory). Indirectly this also leads to a change in the light partons at small x and modifications of our predictions for W and Z production at the LHC. As well as the best-fit set of partons, we also provide 30 additional sets representing the uncertainties of the partons obtained using the Hessian approach.Comment: 13 pages, 11 figures. Version published. Slight extension and some modification of reference

Interleukin-23 is critical for full-blown expression of a non-autoimmune destructive arthritis and regulates interleukin-17A and RORγt in γδ T cells

Introduction: Interleukin (IL)-23 is essential for the development of various experimental autoimmune models. However, the role of IL-23 in non-autoimmune experimental arthritis remains unclear. Here, we examined the role of IL-23 in the non-autoimmune antigen-induced arthritis (AIA) model. In addition, the regulatory potential of IL-23 in IL-17A and retinoic acid-related orphan receptor gamma t (RORγt) expression in CD4+and TCRγδ+T cells was evaluated systemically as well as at the site of inflammation.Methods: Antigen-induced arthritis was induced in wild-type, IL-23p19-deficient and IL-17 Receptor A - knockout mice. At differe

Social Effectiveness of Tertiary Education for Adults in Mid-life

No abstract available

CCR6+ Th cell populations distinguish ACPA positive from ACPA negative rheumatoid arthritis

Introduction: Patients with rheumatoid arthritis (RA) can be separated into two major subpopulations based on the absence or presence of serum anti-citrullinated protein antibodies (ACPAs). The more severe disease course in ACPA+ RA and differences in treatment outcome between these subpopulations suggest that ACPA+ and ACPA- RA are different disease subsets. The identification of T-helper (Th) cells specifically recognizing citrullinated peptides, combined with the strong association between HLA-DRB1 and ACPA positivity, point toward a pathogenic role of Th cells in ACPA+ RA. In this context we recently identified a potential pathogenic role for CCR6+ Th cells in RA. Therefore, we examined whether Th cell population distributions differ by ACPA status. Methods: We performed a nested matched case-control study including 27 ACPA+ and 27 ACPA- treatment-naive early RA patients matched for disease activity score in 44 joints, presence of rheumatoid factor, sex, age, duration of complaints and presence of erosions. CD4+CD45RO+ (memory) Th cell distribution profiles from these patients were generated based on differential chemokine receptor expression and related with disease duration. Results: ACPA status was not related to differences in total CD4+ T cell or memory Th cell proportions. However, ACPA+ patients had significantly higher proportions of Th cells expressing the chemokine receptors CCR6 and CXCR3. Similar proportions of CCR4+ and CCR10+ Th cells were found. Within the CCR6+ cell population, four Th subpopulations were distinguished based on differential chemokine receptor expression: Th17 (CCR4+CCR10-), Th17.1 (CXCR3+), Th22 (CCR4+CCR10+) and CCR4/CXCR3 double-positive (DP) cells. In particular, higher proportions of Th22 (p = 0.02), Th17.1 (p = 0.03) and CCR4/CXCR3 DP (p = 0.01) cells were present in ACPA+ patients. In contrast, ACPA status was not associated with differences in Th1 (CCR6-CXCR3+; p = 0.90), Th2 (CCR6-CCR4+; p = 0.27) and T-regulatory (CD25hiFOXP3+; p = 0.06) cell proportions. Interestingly, CCR6+ Th cells were inversely correlated with disease duration in ACPA- patients (R2 = -0.35; p < 0.01) but not in ACPA+ (R2 < 0.01; p = 0.94) patients. Conclusions: These findings demonstrate that increased peripheral blood CCR6+ Th cells proportions distinguish ACPA+ RA from ACPA- RA. This suggests that CCR6+ Th cells are involved in the differences in disease severity and tr

GATA-2 Plays Two Functionally Distinct Roles during the Ontogeny of Hematopoietic Stem Cells

GATA-2 is an essential transcription factor in the hematopoietic system that is expressed in hematopoietic stem cells (HSCs) and progenitors. Complete deficiency of GATA-2 in the mouse leads to severe anemia and embryonic lethality. The role of GATA-2 and dosage effects of this transcription factor in HSC development within the embryo and adult are largely unexplored. Here we examined the effects of GATA-2 gene dosage on the generation and expansion of HSCs in several hematopoietic sites throughout mouse development. We show that a haploid dose of GATA-2 severely reduces production and expansion of HSCs specifically in the aorta-gonad-mesonephros region (which autonomously generates the first HSCs), whereas quantitative reduction of HSCs is minimal or unchanged in yolk sac, fetal liver, and adult bone marrow. However, HSCs in all these ontogenically distinct anatomical sites are qualitatively defective in serial or competitive transplantation assays. Also, cytotoxic drug-induced regeneration studies show a clear GATA-2 dose–related proliferation defect in adult bone marrow. Thus, GATA-2 plays at least two functionally distinct roles during ontogeny of HSCs: the production and expansion of HSCs in the aorta-gonad-mesonephros and the proliferation of HSCs in the adult bone marrow