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Habitat fragmentation and eutrophication have strong impacts on biodiversity. Metacommunity research demonstrated that reduction in landscape connectivity may cause biodiversity loss in fragmented landscapes. Food-web research addressed how eutrophication can cause local biodiversity declines. However, there is very limited understanding of their cumulative impacts as they could amplify or cancel each other. Our simulations of meta-food-webs show that dispersal and trophic processes interact through two complementary mechanisms. First, the ‘rescue effect’ maintains local biodiversity by rapid recolonization after a local crash in population densities. Second, the ‘drainage effect’ stabilizes biodiversity by preventing overshooting of population densities on eutrophic patches. In complex food webs on large spatial networks of habitat patches, these effects yield systematically higher biodiversity in heterogeneous than in homogeneous landscapes. Our meta-food-web approach reveals a strong interaction between habitat fragmentation and eutrophication and provides a mechanistic explanation of how landscape heterogeneity promotes biodiversity. Habitat fragmentation and eutrophication have strong impacts on biodiversity but there is limited understanding of their cumulative impacts. This study presents simulations of meta-food-webs and provides a mechanistic explanation of how landscape heterogeneity promotes biodiversity through rescue and drainage effects.

Pancreatic cancer is projected to become the second deadliest cancer by 2030 in the United States, and the overall five-year survival rate stands still at around 9%. The stroma compartment can make up more than 90% of the pancreatic tumor mass, contributing to the hypoxic tumor microenvironment. The dense stroma with extracellular matrix proteins can be a physical and metabolic barrier reducing therapeutic efficacy. Cancer-associated fibroblasts are a source of extracellular matrix proteins. Therefore, targeting these cells, or extracellular matrix proteins, have been considered as therapeutic strategies. However, several studies show that deletion of cancer-associated fibroblasts may have tumor-promoting effects. Cancer-associated fibroblasts are derived from a variety of different cell types, such as pancreatic stellate cells and mesenchymal stem cells, and constitute a diverse cell population consisting of several functionally heterogeneous subtypes. Several subtypes of cancer-associated fibroblasts exhibit a tumor-restraining function. This review article summarizes recent findings regarding origin and functional heterogeneity of tumor-promoting as well as tumor-restraining cancer-associated fibroblasts. A better understanding of cancer-associated fibroblast heterogeneity could provide more specific and personalized therapies for pancreatic cancer patients in the future.

Pancreatic cancer is currently the fourth leading cause of cancer deaths in the United States, and the overall 5 year survival rate is still only around 10%. Pancreatic cancer exhibits a remarkable resistance to established therapeutic options such as chemotherapy and radiotherapy, in part due to the dense stromal tumor microenvironment, where cancer-associated fibroblasts are the major stromal cell type. Cancer-associated fibroblasts further play a key role in cancer progression, invasion, and metastasis. Cancer-associated fibroblasts communicate with tumor cells, not only through paracrine as well as paracrine-reciprocal signaling regulators but also by way of exosomes. In the current manuscript, we discuss intercellular mediators between cancer-associated fibroblasts and pancreatic cancer cells in a paracrine as well as paracrine-reciprocal manner. Further recent findings on exosomes in pancreatic cancer and metastasis are summarized.

Modeling pollination ecosystem services requires a spatially explicit, process‐based approach because they depend on both the behavioral responses of pollinators to the amount and spatial arrangement of habitat and on the within‐ and between‐season dynamics of pollinator populations in response to land use. We describe a novel pollinator model predicting flower visitation rates by wild central‐place foragers (e.g., nesting bees) in spatially explicit landscapes. The model goes beyond existing approaches by: (1) integrating preferential use of more rewarding floral and nesting resources; (2) considering population growth over time; (3) allowing different dispersal distances for workers and reproductives; (4) providing visitation rates for use in crop pollination models. We use the model to estimate the effect of establishing grassy field margins offering nesting resources and a low quantity of flower resources, and/or late‐flowering flower strips offering no nesting resources but abundant flowers, on bumble bee populations and visitation rates to flowers in landscapes that differ in amounts of linear seminatural habitats and early mass‐flowering crops. Flower strips were three times more effective in increasing pollinator populations and visitation rates than field margins, and this effect increased over time. Late‐blooming flower strips increased early‐season visitation rates, but decreased visitation rates in other late‐season flowers. Increases in population size over time in response to flower strips and amounts of linear seminatural habitats reduced this apparent competition for pollinators. Our spatially explicit, process‐based model generates emergent patterns reflecting empirical observations, such that adding flower resources may have contrasting short‐ and long‐term effects due to apparent competition for pollinators and pollinator population size increase. It allows exploring these effects and comparing effect sizes in ways not possible with other existing models. Future applications include species comparisons, analysis of the sensitivity of predictions to life‐history traits, as well as large‐scale management intervention and policy assessment. We describe and demonstrate novel pollinator model that predicts visitation rates by nesting bees to flowers in heterogeneous landscapes, and the response of pollinator populations to land use. Limitations of existing approaches are addressed by (1) integrating resource‐quality‐ and resource‐quantity‐dependent foraging by central‐place foragers; (2) considering population growth over time; and (3) providing flower visitation rates that can be used in crop pollination models.

Pancreatic stellate cells (PSCs) constitute important cells of the pancreatic microenvironment and their close interaction with cancer cells is important in pancreatic cancer. It is currently not known whether PSCs accumulate genetic alterations that contribute to tumor biology. Our aim was to analyze genetic alterations in cancer associated PSCs. PSC DNA was matched to DNA isolated from pancreatic cancer patients’ blood ( n  = 5) and analyzed by Next-Generation Sequencing (NGS). Bioinformatic analysis was performed using the GATK software and pathogenicity prediction scores. Sanger sequencing was carried out to verify specific genetic alterations in a larger panel of PSCs ( n  = 50). NGS and GATK analysis identified on average 26 single nucleotide variants in PSC DNA as compared to the matched blood DNA that could be visualized with the Integrative Genomics Viewer. The absence of PDAC driver mutations ( KRAS , p53 , p16/INK4a , SMAD4 ) confirmed that PSC isolations were not contaminated with cancer cells. After filtering the variants, using different pathogenicity scores, ten genes were identified ( SERPINB2 , CNTNAP4 , DENND4B , DPP4 , FGFBP2 , MIGA2 , POLE , SNRNP40 , TOP2B, and ZDHHC18) in single samples and confirmed by Sanger sequencing. As a proof of concept, functional analysis using control and SERPINB2 knock-out fibroblasts revealed functional effects on growth, migration, and collagen contraction. In conclusion, PSC DNA exhibit a substantial amount of single nucleotide variants that might have functional effects potentially contributing to tumor aggressiveness.

Placenta accreta spectrum (PAS) refers to the abnormal adhesion of the placenta to the myometrium, with varying degrees of severity. Placenta accreta involves adhesion to the myometrium, placenta increta invades the myometrium, and placenta percreta extends through the serosa to adjacent organs. The condition is linked to deficient decidualization in scarred uterine tissue, and the risk increases when placenta previa is present and with each prior cesarean delivery. Other risk factors include advanced maternal age, IVF, short intervals between cesareans, and smoking. PAS incidence has risen due to the increase in cesarean deliveries. Placenta previa combined with PAS significantly raises the risk of severe peripartum bleeding, often necessitating a cesarean section with a total hysterectomy. Recognizing PAS prepartum is essential, with sonographic indicators including intraplacental lacunae and uterovesical hypervascularization. However, PAS can be present without sonographic signs, making clinical risk factors crucial for diagnosis. Effective management requires a multidisciplinary approach and proper infrastructure. This presentation covers PAS cases treated at University Hospital Freiburg, detailing patient conditions, diagnostic methods, treatments and outcomes.

Habitat fragmentation threatens global biodiversity. To date, there is only limited understanding of how the different aspects of habitat fragmentation (habitat loss, number of fragments and isolation) affect species diversity within complex ecological networks such as food webs. Here, we present a dynamic and spatially explicit food web model which integrates complex food web dynamics at the local scale and species-specific dispersal dynamics at the landscape scale, allowing us to study the interplay of local and spatial processes in metacommunities. We here explore how the number of habitat patches, i.e. the number of fragments, and an increase of habitat isolation affect the species diversity patterns of complex food webs ( α -, β -, γ -diversities). We specifically test whether there is a trophic dependency in the effect of these two factors on species diversity. In our model, habitat isolation is the main driver causing species loss and diversity decline. Our results emphasize that large-bodied consumer species at high trophic positions go extinct faster than smaller species at lower trophic levels, despite being superior dispersers that connect fragmented landscapes better. We attribute the loss of top species to a combined effect of higher biomass loss during dispersal with increasing habitat isolation in general, and the associated energy limitation in highly fragmented landscapes, preventing higher trophic levels to persist. To maintain trophic-complex and species-rich communities calls for effective conservation planning which considers the interdependence of trophic and spatial dynamics as well as the spatial context of a landscape and its energy availability.

Habitat fragmentation threatens global biodiversity. To date, there is only limited understanding of how the different aspects of habitat fragmentation (habitat loss, number of fragments and isolation) affect species diversity within complex ecological networks such as food webs. Here, we present a dynamic and spatially explicit food web model which integrates complex food web dynamics at the local scale and species-specific dispersal dynamics at the landscape scale, allowing us to study the interplay of local and spatial processes in metacommunities. We here explore how the number of habitat patches, i.e. the number of fragments, and an increase of habitat isolation affect the species diversity patterns of complex foodwebs (α-, β-, γ-diversities). We specifically test whether there is a trophic dependency in the effect of these two factors on species diversity. In our model, habitat isolation is the main driver causing species loss and diversity decline. Our results emphasize that large-bodied consumer species at high trophic positions go extinct faster than smaller species at lower trophic levels, despite being superior dispersers that connect fragmented landscapes better. We attribute the loss of top species to a combined effect of higher biomass loss during dispersal with increasing habitat isolation in general, and the associated energy limitation in highly fragmented landscapes, preventing higher trophic levels to persist. To maintain trophic-complex and species-rich communities calls for effective conservation planning which considers the interdependence of trophic and spatial dynamics as well as the spatial context of a landscape and its energy availability.

Die Schmerzen waren konstant vorhanden und konnten auf Palpation nicht ausgelöst bzw. verstärkt werden. See PDF.] MRT (Magnetresonanztomographie) Abdomen: massives retroperitoneales Ödem rechts, insbesondere in der adrenalen Loge bei Nebenniereninfarkt mit neuen T2w-hyperintensen Anteile, suspekt auf eine sekundäre Einblutung Therapie Bei nicht ausreichender Analgesie mit Piritramid wurde eine PDA-Anlage (Naropin [Ropivacain] 0,2 % auf 8–10 ml/h) durchgeführt. Acute nonhemorrhagic adrenal infarction in pregnancy: 10-year MRI incidence and patient outcomes at a single institution. Non-hemorrhagic adrenal infarction during pregnancy: the diagnostic imaging keys.

The impacts of habitat fragmentation and eutrophication on biodiversity have been studied in different scientific realms. Metacommunity research has shown that reduction in landscape connectivity may cause biodiversity loss in fragmentated landscapes. Food-web research addressed how eutrophication increases biomass accumulations at high trophic levels causing the breakdown of local biodiversity. However, there is very limited understanding of their cumulative impacts as they could amplify or cancel each other. Here, we show with simulations of meta-food-webs that landscape heterogeneity provides a buffering capacity against increasing nutrient eutrophication. An interaction between eutrophication and landscape homogenization precipitates the decline of biodiversity. We attribute our results to two complementary mechanisms related to source and sink dynamics. First, the \"rescue effect\" maintains local biodiversity by rapid recolonization after a local crash in population densities. Second, the \"drainage effect\" allows a more uniform spreading of biomass across the landscape, reducing overall interaction strengths and therefore stabilizing dynamics. In complex food webs on large spatial networks of habitat patches, these effects yield systematically higher biodiversity in heterogeneous than in homogeneous landscapes. Our meta-food-web approach reveals a strong interaction between habitat fragmentation and eutrophication and provides a mechanistic explanation of how landscape heterogeneity promotes biodiversity. Competing Interest Statement The authors have declared no competing interest.