Impacts of Sediment Dredging on Phosphorus Dynamics in a Restored Riparian Wetland

Global reductions in biodiversity and water quality are having major consequences for ecosystem health and societal well-being. The restoration of riverine floodplains and wetlands provides an ideal opportunity to increase biodiversity and water quality because their hydrologic connectivity to adjacent streams and rivers promotes the formation of heterogeneous habitat while also facilitating their functioning as a nutrient sink, in general. However, many historic floodplains and riverine wetlands have been drained for the creation of agricultural land, resulting in an accumulation of nutrients in the soils. Therefore, restoration practices that hydrologically reconnect former agricultural land to an adjacent stream or river can stimulate the release of nutrients into downstream waters, at least in the short-term, which can result in the restoration of wildlife habitat at the expense of downstream water quality. To avoid the high risk of a wetland habitat restoration project in the Muskegon Lake Area of Concern resulting in phosphorus (P) release to downstream waters, the former agricultural land was dredged prior to hydrologic reconnection. I evaluated restoration success by measuring sediment P release in the wetland after dredging and comparing those results to studies that measured P release before dredging. My results showed that maximum P release rates were reduced by 95-99 % after dredging, regardless of temperature or dissolved oxygen treatment. In turn, this avoided between ~25-250 kg of total phosphorus (TP) from entering a eutrophic lake downstream per year (depending on transport scenarios). While internal P loading was drastically reduced, P adsorption isotherm experiments suggested that the deep dredging depth (~1 m on average) exposed sediments with significantly reduced binding capacities, resulting in the wetland acting as a phosphate sink only when water column soluble reactive phosphorus concentrations exceed 40 μg L-1. This study showed that the ability of sediment dredging to reduce sediment P release largely depends on the underlying sediment characteristics. If prerestoration monitoring indicates that deeper sediments have low TP and labile P concentrations, sediment dredging can be a useful technique for balancing the goals of both habitat restoration and water quality improvements in wetlands restored on former agricultural lands

Myelin down-regulates myelin phagocytosis by microglia and macrophages through interactions between CD47 on myelin and SIRPα (signal regulatory protein-α) on phagocytes

<p>Abstract</p> <p>Background</p> <p>Traumatic injury to axons produces breakdown of axons and myelin at the site of the lesion and then further distal to this where Wallerian degeneration develops. The rapid removal of degenerated myelin by phagocytosis is advantageous for repair since molecules in myelin impede regeneration of severed axons. Thus, revealing mechanisms that regulate myelin phagocytosis by macrophages and microglia is important. We hypothesize that myelin regulates its own phagocytosis by simultaneous activation and down-regulation of microglial and macrophage responses. Activation follows myelin binding to receptors that mediate its phagocytosis (e.g. complement receptor-3), which has been previously studied. Down-regulation, which we test here, follows binding of myelin CD47 to the immune inhibitory receptor SIRPα (signal regulatory protein-α) on macrophages and microglia.</p> <p>Methods</p> <p>CD47 and SIRPα expression was studied by confocal immunofluorescence microscopy, and myelin phagocytosis by ELISA.</p> <p>Results</p> <p>We first document that myelin, oligodendrocytes and Schwann cells express CD47 without SIRPα and further confirm that microglia and macrophages express both CD47 and SIRPα. Thus, CD47 on myelin can bind to and subsequently activate SIRPα on phagocytes, a prerequisite for CD47/SIRPα-dependent down-regulation of CD47^+/+myelin phagocytosis by itself. We then demonstrate that phagocytosis of CD47^+/+myelin is augmented when binding between myelin CD47 and SIRPα on phagocytes is blocked by mAbs against CD47 and SIRPα, indicating that down-regulation of phagocytosis indeed depends on CD47-SIRPα binding. Further, phagocytosis in serum-free medium of CD47^+/+myelin is augmented after knocking down SIRPα levels (SIRPα-KD) in phagocytes by lentiviral infection with SIRPα-shRNA, whereas phagocytosis of myelin that lacks CD47 (CD47^-/-) is not. Thus, myelin CD47 produces SIRPα-dependent down-regulation of CD47^+/+myelin phagocytosis in phagocytes. Unexpectedly, phagocytosis of CD47^-/-myelin by SIRPα-KD phagocytes, which is not altered from normal when tested in serum-free medium, is augmented when serum is present. Therefore, both myelin CD47 and serum may each promote SIRPα-dependent down-regulation of myelin phagocytosis irrespective of the other.</p> <p>Conclusions</p> <p>Myelin down-regulates its own phagocytosis through CD47-SIRPα interactions. It may further be argued that CD47 functions normally as a marker of "self" that helps protect intact myelin and myelin-forming oligodendrocytes and Schwann cells from activated microglia and macrophages. However, the very same mechanism that impedes phagocytosis may turn disadvantageous when rapid clearance of degenerated myelin is helpful.</p

Fast and slow: Recording neuromodulator dynamics across both transient and chronic time scales

Neuromodulators transform animal behaviors. Recent research has demonstrated the importance of both sustained and transient change in neuromodulators, likely due to tonic and phasic neuromodulator release. However, no method could simultaneously record both types of dynamics. Fluorescence lifetime of optical reporters could offer a solution because it allows high temporal resolution and is impervious to sensor expression differences across chronic periods. Nevertheless, no fluorescence lifetime change across the entire classes of neuromodulator sensors was previously known. Unexpectedly, we find that several intensity-based neuromodulator sensors also exhibit fluorescence lifetime responses. Furthermore, we show that lifetime measures in vivo neuromodulator dynamics both with high temporal resolution and with consistency across animals and time. Thus, we report a method that can simultaneously measure neuromodulator change over transient and chronic time scales, promising to reveal the roles of multi-time scale neuromodulator dynamics in diseases, in response to therapies, and across development and aging

Gas-phase oxidation of atomic boron and boron monoxide

Rate constants for the reactions of B + O/sub 2/ and BO + O/sub 2/ have been measured over the temperature range 298 to 1180 K using the laser photolysis/laser-induced fluorescence technique. The rate of the B + O/sub 2/ reaction increases slightly with increasing temperature. In contrast, the BO + O/sub 2/ reaction has a negative temperature dependence and is believed to proceed via a stable intermediate complex

Photofragment fluorescence as an analytical technique: application to gas-phase alkali compounds

Photodissociation of gas-phase compounds using a laser at suitably short ultraviolet wavelengths can produce electronically excited photofragments. Detection of fluorescence from these excited fragments, particularly atomic fragments, allows sensitive and quantitative density measurements while signal strength as a function of dissociation laser wavelength allows differentiation between compounds that yield the same photofragment. Application of the technique to the detection of gas-phase alkali compounds is discussed and the results of experiments to detect sodium and potassium chlorides are presented

Enhancement of the electric dipole moment of the electron in PbO

The a(1) state of PbO can be used to measure the electric dipole moment of the electron d_e. We discuss a semiempirical model for this state, which yields an estimate of the effective electric field on the valence electrons in PbO. Our final result is an upper limit on the measurable energy shift, which is significantly larger than was anticipated earlier: $2|W_d|d_e \ge 2.4\times 10^{25} \textrm{Hz} [ \frac{d_e}{e \textrm{cm}} ]$.Comment: 4 pages, revtex4, no figures, submitted to PR

Targeted ASO-mediated Atp1a2 knockdown in astrocytes reduces SOD1 aggregation and accelerates disease onset in mutant SOD1 mice

Astrocyte-specific ion pump α2-Na+/K+-ATPase plays a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS). Here, we test the effect of Atp1a2 mRNA-specific antisense oligonucleotides (ASOs) to induce α2-Na+/K+-ATPase knockdown in the widely used ALS animal model, SOD1*G93A mice. Two ASOs led to efficient Atp1a2 knockdown and significantly reduced SOD1 aggregation in vivo. Although Atp1a2 ASO-treated mice displayed no off-target or systemic toxicity, the ASO-treated mice exhibited an accelerated disease onset and shorter lifespan than control mice. Transcriptomics studies reveal downregulation of genes involved in oxidative response, metabolic pathways, trans-synaptic signaling, and upregulation of genes involved in glutamate receptor signaling and complement activation, suggesting a potential role for these molecular pathways in de-coupling SOD1 aggregation from survival in Atp1a2 ASO-treated mice. Together, these results reveal a role for α2-Na+/K+-ATPase in SOD1 aggregation and highlight the critical effect of temporal modulation of genetically validated therapeutic targets in neurodegenerative diseases