Riverine macrosystems ecology: sensitivity, resistance, and resilience of whole river basins with human alterations

Riverine macrosystems are described here as watershed-scale networks of connected and interacting riverine and upland habitat patches. Such systems are driven by variable responses of nutrients and organisms to a suite of global and regional factors (eg climate, human social systems) interacting with finer-scale variations in geology, topography, and human modifications. We hypothesize that spatial heterogeneity, connectivity, and asynchrony among these patches regulate ecological dynamics of whole networks, altering system sensitivity, resistance, and resilience. Long-distance connections between patches may be particularly important in riverine macrosystems, shaping fundamental system properties. Furthermore, the type, extent, intensity, and spatial configuration of human activities (eg land-use change, dam construction) influence watershed-wide ecological properties through effects on habitat heterogeneity and connectivity at multiple scales. Thus, riverine macrosystems are coupled social–ecological systems with feedbacks that influence system responses to environmental change and the sustainable delivery of ecosystem services

Indicators of river system hydromorphological character and dynamics: understanding current conditions and guiding sustainable river management

The work leading to this paper received funding from the EU’s FP7 programme under Grant Agreement No. 282656 (REFORM). The Indicators were developed within the context of REFORM deliverable D2.1, therefore all partners involved in this deliverable contributed to some extent to their discussion and development

Key mechanisms governing resolution of lung inflammation

Innate immunity normally provides excellent defence against invading microorganisms. Acute inflammation is a form of innate immune defence and represents one of the primary responses to injury, infection and irritation, largely mediated by granulocyte effector cells such as neutrophils and eosinophils. Failure to remove an inflammatory stimulus (often resulting in failed resolution of inflammation) can lead to chronic inflammation resulting in tissue injury caused by high numbers of infiltrating activated granulocytes. Successful resolution of inflammation is dependent upon the removal of these cells. Under normal physiological conditions, apoptosis (programmed cell death) precedes phagocytic recognition and clearance of these cells by, for example, macrophages, dendritic and epithelial cells (a process known as efferocytosis). Inflammation contributes to immune defence within the respiratory mucosa (responsible for gas exchange) because lung epithelia are continuously exposed to a multiplicity of airborne pathogens, allergens and foreign particles. Failure to resolve inflammation within the respiratory mucosa is a major contributor of numerous lung diseases. This review will summarise the major mechanisms regulating lung inflammation, including key cellular interplays such as apoptotic cell clearance by alveolar macrophages and macrophage/neutrophil/epithelial cell interactions. The different acute and chronic inflammatory disease states caused by dysregulated/impaired resolution of lung inflammation will be discussed. Furthermore, the resolution of lung inflammation during neutrophil/eosinophil-dominant lung injury or enhanced resolution driven via pharmacological manipulation will also be considered

ICAR: endoscopic skull‐base surgery

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Comprehensive molecular characterization of the hippo signaling pathway in cancer

Hippo signaling has been recognized as a key tumor suppressor pathway. Here, we perform a comprehensive molecular characterization of 19 Hippo core genes in 9,125 tumor samples across 33 cancer types using multidimensional “omic” data from The Cancer Genome Atlas. We identify somatic drivers among Hippo genes and the related microRNA (miRNA) regulators, and using functional genomic approaches, we experimentally characterize YAP and TAZ mutation effects and miR-590 and miR-200a regulation for TAZ. Hippo pathway activity is best characterized by a YAP/TAZ transcriptional target signature of 22 genes, which shows robust prognostic power across cancer types. Our elastic-net integrated modeling further reveals cancer-type-specific pathway regulators and associated cancer drivers. Our results highlight the importance of Hippo signaling in squamous cell cancers, characterized by frequent amplification of YAP/TAZ, high expression heterogeneity, and significant prognostic patterns. This study represents a systems-biology approach to characterizing key cancer signaling pathways in the post-genomic era

Trophic ecology of two savanna grazers, blue wildebeest Connochaetes taurinus and black wildebeest Connochaetes gnou

The feeding niches and trophic ecology of two South African grazers, blue wildebeest Connochaetes taurinus and black wildebeest Connochaetes gnou, are compared using stable carbon and nitrogen isotope data from feces and tooth dentine collagen. As sympatric, closely related taxa predicted to occupy similar trophic positions, the blue and black wildebeest provide a good model for studying the mechanisms of coexistence and macroevolution in mammals. Data from feces collected from a single reserve in the Free State Province reveal different trophic behaviors between two herds of blue wildebeest and between both compared with a single herd of black wildebeest. These data suggest that sympatric coexistence of blue and black wildebeest is facilitated by differential niche occupation at family group or herd levels, rather than between species. However, such separation does not occur over longer time scales: results from dentine collagen support the hypothesis that the two species are indistinct in terms of trophic behavior, although blue wildebeest show more feeding flexibility, probably because of their wider habitat tolerance range. Similarities in premaxillary width of males and females of both species also suggest that both species are adapted to similar feeding styles. Thus, it is unlikely that changes in trophic behavior provided the trigger for divergence of the black from the blue wildebeest lineage in the Middle Pleistocene. We argue that the case of these two species represents an example of speciation that was not driven by resource competition, as is often assumed for many turnover events in mammalian evolution. We briefly discuss a previous suggestion that links black wildebeest evolution to their more territorial breeding behavior associated with Middleto-Late Pleistocene landscape changes in southern Africa