Restored floodplains enhance denitrification compared to naturalized floodplains in agricultural streams

Predicted changes in the timing and magnitude of storms have the potential to amplify water quality challenges associated with agricultural runoff. In agricultural streams of the Midwestern US, floodplain restoration has the potential to enhance inorganic nitrogen (N) removal by increasing the bioreactive surface area for microbially-mediated denitrification. The restoration of inset floodplains via construction of the two-stage ditch increases denitrification compared to channelized systems, however, little is known about how denitrification on restored floodplains compares to those formed naturally when stream channel management lapses. We used sacrificial microcosm incubations and membrane-inlet mass spectrometry (MIMS) to compare denitrification rates in floodplain soils collected along transects in both naturalized and restored floodplains; longitudinal transects spanned two zones in the active floodplain (near-stream, NS vs. middle, MID) and a third zone that reflected upland conditions in the riparian buffer strip (UP). Denitrification rates were 35–49% higher in the restored, inset floodplains compared to naturalized floodplains. Variation in denitrification rates were primarily explained by soil organic matter (OM) and OM was > 20% higher in restored floodplains than naturalized, highlighting the contrasts between stable, constructed floodplains with heterogeneous, depositional bars typical of naturalizing channels. Consequently, restored inset floodplains could remove > 70% more N than the naturalized floodplains during similar storm inundation events.     

Differential regulation of single CFTR channels by PP2C, PP2A, and other phosphatases

Cystic fibrosistransmembrane conductance regulator (CFTR)Cl channel activitydeclines rapidly when excised from transfected Chinese hamster ovary(CHO) or human airway cells because of membrane-associated phosphataseactivity. In the present study, we found that CFTR channels usuallyremained active in patches excised from baby hamster kidney (BHK) cellsoverexpressing CFTR. Those patches with stable channel activity wereused to investigate the regulation of CFTR by exogenous proteinphosphatases (PP). Adding PP2A, PP2C, or alkaline phosphatase toexcised patches reduced CFTR channel activity by >90% but did notabolish it completely. PP2B caused weak deactivation, whereas PP1 hadno detectable effect on open probability(P_o).Interestingly, the time course of deactivation by PP2C was identical tothat of the spontaneous rundown observed in some patches afterexcision. PP2C and PP2A had distinct effects on channel gating;P_o declinedduring exposure to exogenous PP2C (and during spontaneous rundown, whenit was observed) without any change in mean burst duration. Bycontrast, deactivation by exogenous PP2A was associated with a dramaticshortening of burst duration similar to that reported previously inpatches from cardiac cells during deactivation of CFTR by endogenousphosphatases. Rundown of CFTR-mediated current across intact T84epithelial cell monolayers was insensitive to toxic levels of the PP2Ainhibitor calyculin A. These results demonstrate that exogenous PP2C is a potent regulator of CFTR activity, that its effects on single-channel gating are distinct from those of PP2A but similar to those of endogenous phosphatases in CHO, BHK, and T84 epithelial cells, and thatmultiple protein phosphatases may be required for complete deactivationof CFTR channels.

     

Glutathione permeability of CFTR

The cystic fibrosis transmembrane conductanceregulator (CFTR) forms an ion channel that is permeable both toCl and to larger organicanions. Here we show, using macroscopic current recording from excisedmembrane patches, that the anionic antioxidant tripeptide glutathioneis permeant in the CFTR channel. This permeability may account for thehigh concentrations of glutathione that have been measured in thesurface fluid that coats airway epithelial cells. Furthermore, loss ofthis pathway for glutathione transport may contribute to the reducedlevels of glutathione observed in airway surface fluid of cysticfibrosis patients, which has been suggested to contribute to theoxidative stress observed in the lung in cystic fibrosis. We suggestthat release of glutathione into airway surface fluid may be a novelfunction of CFTR.

     

Effects of Population Size and Selection Intensity on Correlated Responses to Selection for Postweaning Gain in Mice

Correlated responses to selection for postweaning gain in mice were studied to determine the influence of population size and selection intensity. Correlated traits measured were three-, six- and eight-week body weights, litter size, twelve-day litter weight, proportion infertile matings and two indexes of reproductive performance. In general, the results agreed with observations made on direct response: correlated responses in the body weight traits and litter size increased as (1) selection intensity increased and (2) effective population size increased. Correlated responses in the body weight traits and litter size were positive in the large population size lines (16 pairs), as expected from the positive genetic correlation between these traits and postweaning gain. However, several negative correlated responses were observed at small population sizes (one and two pairs). Within each level of selection intensity, traits generally associated with fitness tended to decline most in the very small populations (one and two pairs) and in the large populations (16 pairs) for apparently different reasons. The fitness decline at the small effective population sizes was attributable to inbreeding depression. In contrast, it was postulated that the fitness decline at the large effective population size was due to selection moving the population mean for body weight and a trait positively correlated genetically with body weight (i.e., percent body fat) away from an optimum.     

Effects of Population Size and Selection Intensity on Short-Term Response to Selection for Postweaning Gain in Mice

The effects of population size and selection intensity on the mean response was examined after 14 generations of within full-sib family selection for postweaning gain in mice. Population sizes of 1, 2, 4, 8 and 16 pair matings were each evaluated at selection intensities of 100% (control), 50% and 25% in a replicated experiment. Selection response per generation increased as selection intensity increased. Selection response and realized heritability tended to increase with increasing population size. Replicate variability in realized heritability was large at population sizes of 1, 2 and 4 pairs. Genetic drift was implicated as the primary factor causing the reduced response and lowered repeatability at the smaller population sizes. Lines with intended effective population sizes of 62 yielded larger selection responses per unit selection differential than lines with effective population sizes of 30 or less.     

Markers of follicle function in Belclare-cross ewes differing widely in ovulation rate.

High prolificacy due to a gene that has a large effect on ovulation rate has been noted in Booroola and Inverdale ewes. High prolificacy in the Belclare breed (a composite developed from stocks selected for very large litter size or high ovulation rate) may be related to the segregation of two genes. The aims of this study were (i) to compare the morphological and functional features of ovulatory follicles from carriers (which could only be heterozygous for the genes of interest) and non-carriers, and (ii) to identify markers of the Belclare genes among secreted or cellular ovarian proteins. Belclare carrier ewes had more ovulatory follicles (4.9 +/- 0.4) than did non-carrier ewes (2.0 +/- 0.2) (P < 0.001). Ovulatory follicles from carriers were also smaller (4.4 +/- 0.1 mm versus 5.7 +/- 0.2 mm, P < 0.001) and contained a significantly reduced number of granulosa cells (P < 0.001). However, the proportion of proliferating granulosa cells in ovulatory follicles was similar in both groups. The in vitro secretion of steroids per follicle was only marginally lower in follicles from Belclare carriers compared with non-carriers. Furthermore, similar concentrations of steroidogenic enzymes were present in both groups, indicating that steroidogenic potential per granulosa cell is similar between carriers and non-carriers. Possible markers of the Belclare genes were identified among cellular proteins of follicular walls by two-dimensional PAGE and image analysis. Two spots at 78 and 49 kDa were always absent in samples from non-carriers. When secreted proteins in follicles from carriers were compared with those from non-carriers, two spots at 53 and 41 kDa were restricted to samples from carriers and three spots at 97, 91 and 45 kDa were unique to samples from non-carriers. Interestingly, the spot at 91 kDa is also affected by the Booroola gene.     

Investing in early human development: Timing and economic efficiency

Policy discussions to ameliorate socioeconomic (SES) inequalities are increasingly focused on investments in early childhood. Yet such interventions are costly to implement, and clear evidence on the optimal time to intervene to yield a high economic and social return in the future is meagre. The majority of successful early childhood interventions start in the preschool years. However socioeconomic gradients in cognitive skills, socio-emotional functioning and health can be observed by age three, suggesting that preventative programmes starting earlier in childhood may be even more effective. We discuss the optimal timing of early childhood intervention with reference to recent research in developmental neuroscience. We motivate the need for early intervention by providing an overview of the impact of adverse risk factors during the antenatal and early childhood periods on outcomes later in life. We provide a brief review of the economic rationale for investing early in life and propose the “antenatal investment hypothesis”. We conclude by discussing a suite of new European interventions that will inform this optimal timing debate.     

Lack of CFTR in Skeletal Muscle Predisposes to Muscle Wasting and Diaphragm Muscle Pump Failure in Cystic Fibrosis Mice

Cystic fibrosis (CF) patients often have reduced mass and strength of skeletal muscles, including the diaphragm, the primary muscle of respiration. Here we show that lack of the CF transmembrane conductance regulator (CFTR) plays an intrinsic role in skeletal muscle atrophy and dysfunction. In normal murine and human skeletal muscle, CFTR is expressed and co-localized with sarcoplasmic reticulum-associated proteins. CFTR–deficient myotubes exhibit augmented levels of intracellular calcium after KCl-induced depolarization, and exposure to an inflammatory milieu induces excessive NF-kB translocation and cytokine/chemokine gene upregulation. To determine the effects of an inflammatory environment in vivo, sustained pulmonary infection with Pseudomonas aeruginosa was produced, and under these conditions diaphragmatic force-generating capacity is selectively reduced in Cftr^−/− mice. This is associated with exaggerated pro-inflammatory cytokine expression as well as upregulation of the E3 ubiquitin ligases (MuRF1 and atrogin-1) involved in muscle atrophy. We conclude that an intrinsic alteration of function is linked to the absence of CFTR from skeletal muscle, leading to dysregulated calcium homeostasis, augmented inflammatory/atrophic gene expression signatures, and increased diaphragmatic weakness during pulmonary infection. These findings reveal a previously unrecognized role for CFTR in skeletal muscle function that may have major implications for the pathogenesis of cachexia and respiratory muscle pump failure in CF patients.