Biotic interactions, ecological knowledge and agriculture

This paper discusses biotic interactions in agroecosystems and how they may be manipulated to support crop productivity and environmental health by provision of ecosystem services such as weed, pest and disease management, nutrient cycling and biodiversity conservation. Important elements for understanding biotic interactions include consideration of the effects of diversity, species composition and food web structure on ecosystem processes; the impacts of timing, frequency and intensity of disturbance; and the importance of multitrophic interactions. All of these elements need to be considered at multiple scales that depend in part on the range of the movement of the organisms involved. These issues are first discussed in general, followed by an examination of the application of these concepts in agricultural management. The potential for a greater use of ecological management approaches is high; however, owing to the nature of complex interactions in ecosystems, there is some inherent unpredictability about responses to management interventions under different conditions. Such uncertainty needs to be accommodated in the development of recommendations for farm management. This requires an increased emphasis on the effective synthesis of complex and often apparently contradictory information and on field-based adaptive research, monitoring and social learning by farmer/researcher collaborations.     

Hyposmotically-Activated Efflux of L-Carnitine from a Human Mammary Cancer Cell Line

Cell-swelling, induced by a hyposmotic challenge, stimulated the efflux of L-carnitine from a human mammary cancer cell line, MDA-MB-231. The response was dependent upon the extent of the osmotic shock. Hyposmotically-activated L-carnitine efflux was inhibited by the anion transport blocker diiodosalicylate. The efflux of taurine from MDA-MB-231 cells was also stimulated by a hyposmotic shock via a pathway sensitive to diiodosalicylate. L-carnitine efflux from MDA-MB-231 cells was stimulated by isosmotic swelling in a manner which was inhibited by diiodosalicylate. The results suggest that L-carnitine may exit cells via a volume-sensitive pathway: it is possible that L-carnitine efflux may utilize the same pathway as amino acids. The efflux of L-carnitine via this route could have a major effect on the intracellular concentration of L-carnitine and could facilitate transepithelial L-carnitine transport.     

Volume-activated K(+)(Rb(+)) efflux in lactating rat mammary tissue

The effect of cell swelling, induced by a hyposmotic shock, on K(+)(Rb(+)) efflux from lactating rat mammary tissue explants has been studied. A hyposmotic challenge increased the fractional release of K(+)(Rb(+)) from mammary tissue in the absence and presence of the loop-diuretic bumetanide (100 microM). However, the volume-sensitive moiety of K(+)(Rb(+)) efflux was proportionately larger when bumetanide was present in the incubation medium. On the other hand, a hyposmotic shock appeared to reduce the bumetanide-sensitive component of K(+)(Rb(+)) efflux. The increase in K(+)(Rb(+)) efflux, induced by cell swelling, was dependent upon the extent of the hyposmotic challenge. In the presence of bumetanide, substituting Cl(-) with NO(3)(-) reduced the initial increase in volume-sensitive K(+)(Rb(+)) efflux. However, volume-sensitive K(+)(Rb(+)) release was prolonged in the presence of NO(3)(-). Volume-activated K(+)(Rb(+)) efflux from rat mammary tissue explants was inhibited by quinine. Cell swelling increased the intracellular concentration of Ca(2+) in a fashion which depended on the presence of extracellular Ca(2+). However, removing extracellular Ca(2+) did not inhibit volume-activated K(+)(Rb(+)) efflux from rat mammary tissue explants. The results are consistent with the presence of volume-activated K(+) channels in lactating rat mammary tissue. Volume-activated K(+) efflux may play a central role in mammary cell volume regulation.     

The regulation of Na(+)-dependent anionic amino acid transport by the rat mammary gland.

The regulation of anionic amino acid transport, using radiolabelled D-aspartate as a tracer, by rat mammary tissue explants has been examined. Na(+)-dependent D-aspartate uptake by mammary tissue increased between late pregnancy and early lactation and again at peak lactation but thereafter declined during late lactation. In contrast, the Na(+)-independent component of D-aspartate uptake by mammary explants did not change significantly with the physiological state of the donor animals. Premature weaning of rats during peak lactation markedly decreased Na(+)-dependent D-aspartate uptake by mammary tissue. In addition, premature weaning also reduced the effect of reversing the trans-membrane Na(+)-gradient on the fractional loss of D-aspartate from mammary tissue explants. Unilateral weaning of rats during peak lactation revealed that milk accumulation per se reduced the Na(+)-dependent moiety of D-aspartate uptake by mammary tissue suggesting that the transport of anionic amino acids is regulated to match supply with demand. Treating lactating rats with bromocryptine reduced D-aspartate uptake by mammary tissue explants suggesting that the transport of anionic amino acids by the rat mammary gland is regulated by prolactin.     

Crystal structures and kinetic properties of enoyl‐acyl carrier protein reductase I from Candidatus Liberibacter asiaticus

Huanglongbing (HLB) is a destructive citrus disease. The leading cause of HLB is Candidatus Liberibacter asiaticus. Fatty acid biosynthesis is essential for bacterial viability and has been validated as a target for the discovery of novel antibacterial agents. Enoyl−acyl carrier protein reductase (also called ENR or FabI and a product of the fabI gene) is an enzyme required in a critical step of bacterial fatty acid biosynthesis and has attracted attention as a target of novel antimicrobial agents. We determined the crystal structures of FabI from Ca. L. asiaticus in its apoform as well as in complex with b-nicotinamide adenine dinucleotide (NAD) at 1.7 and 2.7 Å resolution, respectively, to facilitate the design and screening of small molecule inhibitors of FabI. The monomeric ClFabI is highly similar to other known FabI structures as expected; however, unlike the typical tetramer, ClFabI exists as a hexamer in crystal, whereas as dimer in solution, on the other hand, the substrate binding loop which always disordered in apoform FabI structures is ordered in apo-ClFabI. Interestingly, the structure of ClFabI undergoes remarkable conformational change in the substrate-binding loop in the presence of NAD. We conclude that the signature sequence motif of FabI can be considered as Gly-(Xaa)₅-Ser-(Xaa)_n-Val-Tyr-(Xaa)₆-Lys-(Xaa)_n-Thr instead of Tyr-(Xaa)₆-Lys. We have further identified isoniazid as a competitive inhibitor with NADH.     

Identification of a high affinity taurine transporter which is not dependent on chloride

Taurine transport by lactating gerbil mammary tissue has been examined. Taurine uptake is, mediated by a high-affinity system which is specific for -amino acids. The uptake of taurine is Na⁺-dependent but appears not to be obligatorly dependent upon Cl^–. Thus, replacing Na⁺ with choline almost abolished taurine uptake. Substituting Cl^– with NO ₃ ^– had no effect whereas SCN^– induced a small but significant increase in taurine influx. Taurine uptake was Na⁺-dependent under conditions where Cl^– had been replaced with NO ₃ ^– . However, it is apparent that the Na⁺-dependent taurine transport system requires the presence of a permeable anion because replacing Cl^– with gluconate markedly reduced taurine uptake. Cell-swelling, induced by a hyposmotic challenge, increased the efflux of taurine from gerbil mammary tissue via a pathway sensitive to niflumic acid.Abbreviations Tris (Tris(hydroxymethyl)aminomethane - BES (N,N-bis[2-hydroxyethyl]-2-aminoethane sulphonic acid)     

Development and validation of a risk prediction model of preterm birth for women with preterm labour symptoms (the QUIDS study): A prospective cohort study and individual participant data meta-analysis

BackgroundTimely interventions in women presenting with preterm labour can substantially improve health outcomes for preterm babies. However, establishing such a diagnosis is very challenging, as signs and symptoms of preterm labour are common and can be nonspecific. We aimed to develop and externally validate a risk prediction model using concentration of vaginal fluid fetal fibronectin (quantitative fFN), in combination with clinical risk factors, for the prediction of spontaneous preterm birth and assessed its cost-effectiveness.Methods and findingsPregnant women included in the analyses were 22⁺⁰ to 34⁺⁶ weeks gestation with signs and symptoms of preterm labour. The primary outcome was spontaneous preterm birth within 7 days of quantitative fFN test. The risk prediction model was developed and internally validated in an individual participant data (IPD) meta-analysis of 5 European prospective cohort studies (2009 to 2016; 1,783 women; mean age 29.7 years; median BMI 24.8 kg/m²; 67.6% White; 11.7% smokers; 51.8% nulliparous; 10.4% with multiple pregnancy; 139 [7.8%] with spontaneous preterm birth within 7 days). The model was then externally validated in a prospective cohort study in 26 United Kingdom centres (2016 to 2018; 2,924 women; mean age 28.2 years; median BMI 25.4 kg/m²; 88.2% White; 21% smokers; 35.2% nulliparous; 3.5% with multiple pregnancy; 85 [2.9%] with spontaneous preterm birth within 7 days). The developed risk prediction model for spontaneous preterm birth within 7 days included quantitative fFN, current smoking, not White ethnicity, nulliparity, and multiple pregnancy. After internal validation, the optimism adjusted area under the curve was 0.89 (95% CI 0.86 to 0.92), and the optimism adjusted Nagelkerke R² was 35% (95% CI 33% to 37%). On external validation in the prospective UK cohort population, the area under the curve was 0.89 (95% CI 0.84 to 0.94), and Nagelkerke R² of 36% (95% CI: 34% to 38%). Recalibration of the model’s intercept was required to ensure overall calibration-in-the-large. A calibration curve suggested close agreement between predicted and observed risks in the range of predictions 0% to 10%, but some miscalibration (underprediction) at higher risks (slope 1.24 (95% CI 1.23 to 1.26)). Despite any miscalibration, the net benefit of the model was higher than “treat all” or “treat none” strategies for thresholds up to about 15% risk. The economic analysis found the prognostic model was cost effective, compared to using qualitative fFN, at a threshold for hospital admission and treatment of ≥2% risk of preterm birth within 7 days. Study limitations include the limited number of participants who are not White and levels of missing data for certain variables in the development dataset.ConclusionsIn this study, we found that a risk prediction model including vaginal fFN concentration and clinical risk factors showed promising performance in the prediction of spontaneous preterm birth within 7 days of test and has potential to inform management decisions for women with threatened preterm labour. Further evaluation of the risk prediction model in clinical practice is required to determine whether the risk prediction model improves clinical outcomes if used in practice.Trial registrationThe study was approved by the West of Scotland Research Ethics Committee (16/WS/0068). The study was registered with ISRCTN Registry (ISRCTN 41598423) and NIHR Portfolio (CPMS: 31277).

Sarah J Stock and colleagues develop and validate a risk prediction model of spontaneous preterm birth for women with preterm labour symptoms, based on vaginal fluid fetal fibronectin and clinical risk factors.     

Detection of glycosaminoglycans on the surface of human umbilical vein endothelial cells using gold-conjugated poly-l -lysine with silver enhancement

Summary Endothelial glycosaminoglycans are important in a diverse range of vascular functions. In the course of a biochemical and histological study exploring the role of glycosaminoglycans in inflammation, we have investigated the use of gold-conjugated poly-l-lysine with silver enhancement to establish the nature and physical location of glycosaminoglycans on the surface of cultured human umbilical vein endothelial cells. Cationic gold was effective in locating anionic sites in both cultured endothelial cells and in paraffin-embedded renal tissue. By manipulating pH, and by using enzymes specific for degrading glycosaminoglycans, it was found that, at pH 1.2, staining was directed primarily at glycosaminoglycans. The surface of human umbilical vein endothelial cells was found to be extensively covered in heparan sulphate, the histological appearance of which was dependent upon the fixation procedure employed. Heparan sulphate was also seen to co-distribute with the extracellular matrix protein, fibronectin, when endothelial cultures were simultaneously stained with cationic gold and an antibody to cellular fibronectin.