A free-boundary model of diffusive valley growth: theory and observation

Valleys that form around a stream head often develop characteristic finger-like elevation contours. We study the processes involved in the formation of these valleys and introduce a theoretical model that indicates how shape may inform the underlying processes. We consider valley growth as the advance of a moving boundary travelling forward purely through linearly diffusive erosion, and we obtain a solution for the valley shape in three dimensions. Our solution compares well to the shape of slowly growing groundwater-fed valleys found in Bristol, Florida. Our results identify a new feature in the formation of groundwater-fed valleys: a spatially variable diffusivity that can be modelled by a fixed-height moving boundary

Methicillin-Resistant Staphylococcus aureus USA400 Clone, Italy

Lette

Land Use and Season Influence Event-Scale Nitrate and Soluble Reactive Phosphorus Exports and Export Stoichiometry from Headwater Catchments

Catchment nutrient export, especially during high flow events, can influence ecological processes in receiving waters by altering nitrogen (N) and phosphorus (P) concentrations and relative amounts (stoichiometry). Event-scale N and P export dynamics may be significantly altered by land use/land cover (LULC) and season. Consequently, to manage water resources, it is important to understand how LULC and season interact to influence event N and P export. In situ, high-frequency spectrophotometers allowed us to continuously and concurrently monitor nitrate (NO3−) and soluble reactive P (SRP) concentrations and therefore examine event-scale NO3− and SRP export dynamics. Here we analyzed event NO3− and SRP concentration-discharge hysteresis patterns and yields for \u3e400 events to evaluate how LULC and seasonality influence event NO3− and SRP export dynamics in three low-order watersheds with different primary LULCs (agricultural, forested, and urban). Differences among event NO3− and SRP hysteresis patterns suggest these nutrients have different source areas and dominant transport pathways that were impacted by both LULC and seasonality. Unexpectedly, we observed similar seasonal patterns in event NO3−:SRP stoichiometry among LULCs, with the most N-enriched events occurring in spring, and event stoichiometry approaching Redfield N:P ratios in the fall. However, seasonal stoichiometry patterns were driven by unique seasonal NO3− and SRP export patterns at each site. Overall these findings suggest LULC and seasonality interact to alter the timing and magnitude of event NO3− and SRP exports, leading to seasonal patterns in event NO3− to SRP stoichiometry that may influence ecological processes, such as productivity, in receiving waters

Human Mas-related G protein-coupled receptors-X1 induce chemokine receptor 2 expression in rat dorsal root ganglia neurons and release of chemokine ligand 2 from the human LAD-2 mast cell line

Primate-specific Mas-related G protein-coupled receptors-X1 (MRGPR-X1) are highly enriched in dorsal root ganglia (DRG) neurons and induce acute pain. Herein, we analyzed effects of MRGPR-X1 on serum response factors (SRF) or nuclear factors of activated T cells (NFAT), which control expression of various markers of chronic pain. Using HEK293, DRG neuron-derived F11 cells and cultured rat DRG neurons recombinantly expressing human MRGPR-X1, we found activation of a SRF reporter gene construct and induction of the early growth response protein-1 via extracellular signal-regulated kinases-1/2 known to play a significant role in the development of inflammatory pain. Furthermore, we observed MRGPR-X1-induced up-regulation of the chemokine receptor 2 (CCR2) via NFAT, which is considered as a key event in the onset of neuropathic pain and, so far, has not yet been described for any endogenous neuropeptide. Up-regulation of CCR2 is often associated with increased release of its endogenous agonist chemokine ligand 2 (CCL2). We also found MRGPR-X1-promoted release of CCL2 in a human connective tissue mast cell line endogenously expressing MRGPR-X1. Thus, we provide first evidence to suggest that MRGPR-X1 induce expression of chronic pain markers in DRG neurons and propose a so far unidentified signaling circuit that enhances chemokine signaling by acting on two distinct yet functionally co-operating cell types. Given the important role of chemokine signaling in pain chronification, we propose that interruption of this signaling circuit might be a promising new strategy to alleviate chemokine-promoted pain

How Low Can You Go?: Widespread Challenges in Measuring Low Stream Discharge and a Path Forward

Low flows pose unique challenges for accurately quantifying streamflow. Current field methods are not optimized to measure these conditions, which in turn, limits research and management. In this essay, we argue that the lack of methods for measuring low streamflow is a fundamental challenge that must be addressed to ensure sustainable water management now and into the future, particularly as climate change shifts more streams to increasingly frequent low flows. We demonstrate the pervasive challenge of measuring low flows, present a decision support tool (DST) for navigating best practices in measuring low flows, and highlight important method developmental needs

Circuit dissection of the role of somatostatin in itch and pain

Stimuli that elicit itch are detected by sensory neurons that innervate the skin. This information is processed by the spinal cord; however, the way in which this occurs is still poorly understood. Here we investigated the neuronal pathways for itch neurotransmission, particularly the contribution of the neuropeptide somatostatin. We find that in the periphery, somatostatin is exclusively expressed in Nppb+ neurons, and we demonstrate that Nppb+somatostatin+ cells function as pruriceptors. Employing chemogenetics, pharmacology and cell-specific ablation methods, we demonstrate that somatostatin potentiates itch by inhibiting inhibitory dynorphin neurons, which results in disinhibition of GRPR+ neurons. Furthermore, elimination of somatostatin from primary afferents and/or from spinal interneurons demonstrates differential involvement of the peptide released from these sources in itch and pain. Our results define the neural circuit underlying somatostatin-induced itch and characterize a contrasting antinociceptive role for the peptide