Climate Change Demands Adaptive Management of Urban Lakes: Model-Based Assessment of Management Scenarios for Lake Tegel (Berlin, Germany)

Lakes are known to be strongly affected by climate change as a result of their sensitivity to atmospheric forcing. The combined response of urban lakes to climatic changes and to urbanization of the catchment may be further altered by water quality management measures. We studied Lake Tegel in Berlin, Germany as a representative urban lake profoundly influenced by intense water management measures and a resulting complex hydrodynamic situation: Lake Tegel is fed by nutrient-rich river discharges and effluents from a phosphorus elimination plant (PEP). We estimated changes in water temperatures, the Wedderburn number, and the buoyancy frequency, as well as concentrations of dissolved oxygen and phosphate under climate change using a one-dimensional vertical hydrodynamic model coupled to a water quality model. Further, we investigated how four management scenarios with varying discharges of the PEP could affect the lake system. In all simulations, water temperatures increased and summer stratification extended. The modeling results demonstrated that the water management system buffers the high nutrient supply from the river inflow and can effectively mitigate negative effects of climate change on Lake Tegel, thus highlighting its importance for the lake ecosystem.DFG, 248198858, GRK 2032: Grenzzonen in urbanen Wassersysteme

Sulfatbelastung der Spree

SULFATBELASTUNG DER SPREE Sulfatbelastung der Spree / Gelbrecht, Jörg (Rights reserved) ( -

LpL^p-approximation of the integrated density of states for Schr\"odinger operators with finite local complexity

We study spectral properties of Schr\"odinger operators on \RR^d. The electromagnetic potential is assumed to be determined locally by a colouring of the lattice points in \ZZ^d, with the property that frequencies of finite patterns are well defined. We prove that the integrated density of states (spectral distribution function) is approximated by its finite volume analogues, i.e.the normalised eigenvalue counting functions. The convergence holds in the space $L^p(I)$ where $I$ is any finite energy interval and $1\leq p< \infty$ is arbitrary.Comment: 15 pages; v2 has minor fixe

Arad'ın resimleri

Taha Toros Arşivi, Dosya No: 43-Agop AradUnutma İstanbul projesi İstanbul Kalkınma Ajansı'nın 2016 yılı "Yenilikçi ve Yaratıcı İstanbul Mali Destek Programı" kapsamında desteklenmiştir. Proje No: TR10/16/YNY/010

Autoimmunity and immunodeficiency associated with monoallelic LIG4 mutations via haploinsufficiency

BACKGROUND: Biallelic mutations in LIG4 encoding DNA-ligase 4 cause a rare immunodeficiency syndrome manifesting as infant-onset life-threatening and/or opportunistic infections, skeletal malformations, radiosensitivity and neoplasia. LIG4 is pivotal during DNA repair and during V(D)J recombination as it performs the final DNA-break sealing step. OBJECTIVE: We explored whether monoallelic LIG4 missense mutations may underlie immunodeficiency and autoimmunity with autosomal dominant inheritance. METHODS: Extensive flow-cytometric immune-phenotyping was performed. Rare variants of immune system genes were analyzed by whole exome sequencing. DNA repair functionality and T cell-intrinsic DNA damage tolerance was tested with an ensemble of in vitro and in silico tools. Antigen-receptor diversity and autoimmune features were characterized by high-throughput sequencing and autoantibody arrays. Reconstitution of wild-type vs. mutant LIG4 were performed in LIG4 knock-out Jurkat T cells and DNA damage tolerance was subsequently assessed. RESULTS: A novel heterozygous LIG4 loss-of-function mutation (p.R580Q), associated with a dominantly inherited familial immune-dysregulation consisting of autoimmune cytopenias, and in the index patient with lymphoproliferation, agammaglobulinemia and adaptive immune cell infiltration into nonlymphoid organs. Immunophenotyping revealed reduced naïve CD4$^{+}$ T cells and low TCR-Vα7.2$^{+}$ T cells, while T/B-cell receptor repertoires showed only mild alterations. Cohort screening identified two other non-related patients with the monoallelic LIG4 mutation p.A842D recapitulating clinical and immune-phenotypic dysregulations observed in the index family and displaying T cell-intrinsic DNA damage intolerance. Reconstitution experiments and molecular dynamics simulations categorize both missense mutations as loss-of-function and haploinsufficient. CONCLUSION: We provide evidence that certain monoallelic LIG4 mutations may cause human immune dysregulation via haploinsufficiency