338 research outputs found

    Use of a Portable Rapid Analysis System to Measure Nitrate Concentration of Nutrient and Soil Solution, and Plant Sap in Greenhouse Vegetable Production

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    A rapid analysis ion-selective electrode (ISE) system for measurement of [NO3−] in nutrient solution (NS), soil solution (SS) and petiole sap (PS) was evaluated. For each material, there were 797–2010 samples from 5 to 6 different crops, and from 2 to 4 different species. Accuracy was evaluated by linear regression (LR) with laboratory analysis (automated colorimetry, Cd reduction), and by relative error (RE), the average percentage deviation from laboratory analysis. For NS, the LR was y = 0.982x + 0.76, R² = 0.962 (n = 2010), for combined data from 5 crops (3 pepper, 2 cucumber). For SS, the LR was y = 0.975x + 1.13, R² = 0.965 (n = 797), for combined data from 5 crops (3 pepper, 2 cucumber). For undiluted PS, the LR relationship was y = 0.742x + 168.02, R² = 0.892 (n = 1425), for combined data from 6 crops (3 pepper, 2 cucumber, 1 melon). The underestimation was most pronounced at [NO3−] of >1500 mg NO3−–N L−1. For diluted petiole sap (dilution by 10 for pepper and melon, 5 for other species), the LR relationship was y = 1.010x + 99.26, R² = 0.927 (n = 1182), for combined data from 6 crops (2 pepper, 2 cucumber, 1 melon, 1 tomato). RE values for all measurements in composite datasets were 14%, 22%, 24% and 25% for NS, SS, undiluted PS and diluted PS respectively, and they were lower in concentrations most likely to be measured in practical on-farm work. The ISE system measured [NO3−] in NS, SS and diluted PS with sufficient accuracy to effectively guide on-farm decision making

    Soil Monitoring Methods to Assess Immediately Available Soil N for Fertigated Sweet Pepper

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    Excessive N application occurs in greenhouse vegetable production. Monitoring methods of immediately available soil N are required. [NO3−] in soil solution, sampled with ceramic cup samplers, and [NO3−] in the 1:2 soil to water (v/v) extract were evaluated. Five increasing [N], from very N deficient (N1) to very N excessive (N5) were applied throughout three fertigated pepper crops by combined fertigation/drip irrigation. The crops were grown in soil in a greenhouse. Soil solution [NO3−] was measured every 1–2 weeks, and extract [NO3−] every 4 weeks. Generally, for treatments N1 and N2, both soil solution and extract [NO3−] were continually close to zero, and increased with applied [N] for treatments N3–5. The relationships of both methods to the nitrogen nutrition index (NNI), an indicator of crop N status, were assessed. Segmented linear analysis gave R2 values of 0.68–0.70 for combined data from entire crops, for both methods. NNI was strongly related to increasing [NO3−] up to 3.1 and 0.9 mmol L−1 in soil solution and extracts, respectively. Thereafter, NNI was constant at 1.04–1.05, with increasing [NO3−]. Suggested sufficiency ranges were derived. Soil solution [NO3−] is effective to monitor immediately available soil N for sweet pepper crops in SE Spain. The extract method is promising

    cAMP-mediated secretion of brain-derived neurotrophic factor in developing airway smooth muscle

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    AbstractModerate hyperoxic exposure in preterm infants contributes to subsequent airway dysfunction and to risk of developing recurrent wheeze and asthma. The regulatory mechanisms that can contribute to hyperoxia-induced airway dysfunction are still under investigation. Recent studies in mice show that hyperoxia increases brain-derived neurotrophic factor (BDNF), a growth factor that increases airway smooth muscle (ASM) proliferation and contractility. We assessed the mechanisms underlying effects of moderate hyperoxia (50% O2) on BDNF expression and secretion in developing human ASM. Hyperoxia increased BDNF secretion, but did not alter endogenous BDNF mRNA or intracellular protein levels. Exposure to hyperoxia significantly increased [Ca2+]i responses to histamine, an effect blunted by the BDNF chelator TrkB-Fc. Hyperoxia also increased ASM cAMP levels, associated with reduced PDE4 activity, but did not alter protein kinase A (PKA) activity or adenylyl cyclase mRNA levels. However, 50% O2 increased expression of Epac2, which is activated by cAMP and can regulate protein secretion. Silencing RNA studies indicated that Epac2, but not Epac1, is important for hyperoxia-induced BDNF secretion, while PKA inhibition did not influence BDNF secretion. In turn, BDNF had autocrine effects of enhancing ASM cAMP levels, an effect inhibited by TrkB and BDNF siRNAs. Together, these novel studies suggest that hyperoxia can modulate BDNF secretion, via cAMP-mediated Epac2 activation in ASM, resulting in a positive feedback effect of BDNF-mediated elevation in cAMP levels. The potential functional role of this pathway is to sustain BDNF secretion following hyperoxic stimulus, leading to enhanced ASM contractility and proliferation

    Different Responses of Various Chlorophyll Meters to Increasing Nitrogen Supply in Sweet Pepper

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    Intensive vegetable production is commonly associated with excessive nitrogen (N) fertilization and associated environmental problems. Monitoring of crop N status can enhance crop N management. Chlorophyll meters (CMs) could be used to monitor crop N status because leaf chlorophyll (chl) content is strongly related to crop N status. To monitor crop N status, relationships between CM measurements and leaf chl content require evaluation, particularly when excessive N is supplied. The SPAD-502 meter, atLEAF+ sensor, MC-100 Chlorophyll Concentration Meter, and Multiplex sensor were evaluated in sweet pepper with different N supply, throughout the crop, ranging from very deficient to very excessive. CM measurements of all sensors and indices were strongly and positively related to leaf chlorophyll a + b content with curvilinear relationships over the entire range of chl measured (∼0–80 μg cm-2). Measurements with the SPAD-502, and atLEAF+, and of the Multiplex’s simple fluorescence ratio index (SFR) had asymptotic responses to increasing leaf chl. In contrast, the MC-100’s chlorophyll content index (CCI) had a progressively increasing response. At higher chlorophyll a + b contents (e.g., >40 μg cm-2), SPAD-502, atLEAF+ and SFR measurements tended to saturate, which did not occur with CCI. Leaf chl content was most accurately estimated by CCI (R2 = 0.87), followed by the SPAD-502 meter (R2 = 0.85). The atLEAF+ sensor was the least accurate (R2 = 0.76). For leaf chl estimation, CCI measured with the MC-100 meter was the most effective of the four sensors examined because it: (1) most accurately estimated leaf chl content, and (2) had no saturation response at higher leaf chl content. For non-saturating leaf chl content (∼0–40 μg cm-2), all indices were sensitive indicators. As excessive applications of N are frequent in intensive vegetable crop production, the capacity of measuring high leaf chl contents without a saturation response is an important consideration for the practical use of chlorophyll meters

    A Common Variant at the 14q32 Endometrial Cancer Risk Locus Activates AKT1 through YY1 Binding.

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    A recent meta-analysis of multiple genome-wide association and follow-up endometrial cancer case-control datasets identified a novel genetic risk locus for this disease at chromosome 14q32.33. To prioritize the functional SNP(s) and target gene(s) at this locus, we employed an in silico fine-mapping approach using genotyped and imputed SNP data for 6,608 endometrial cancer cases and 37,925 controls of European ancestry. Association and functional analyses provide evidence that the best candidate causal SNP is rs2494737. Multiple experimental analyses show that SNP rs2494737 maps to a silencer element located within AKT1, a member of the PI3K/AKT/MTOR intracellular signaling pathway activated in endometrial tumors. The rs2494737 risk A allele creates a YY1 transcription factor-binding site and abrogates the silencer activity in luciferase assays, an effect mimicked by transfection of YY1 siRNA. Our findings suggest YY1 is a positive regulator of AKT1, mediating the stimulatory effects of rs2494737 increasing endometrial cancer risk. Identification of an endometrial cancer risk allele within a member of the PI3K/AKT signaling pathway, more commonly activated in tumors by somatic alterations, raises the possibility that well tolerated inhibitors targeting this pathway could be candidates for evaluation as chemopreventive agents in individuals at high risk of developing endometrial cancer.The QIMR Berghofer groups were supported by a Rio Tinto Ride to Conquer Cancer (RTCC)/Weekend to End Women's Cancers (WEWC) Grant and NHMRC project grants 1058415 to SLE and 1031333 to ABS. ABS is supported by an NHMRC Senior Research Fellowship (1061779). DFE is a Principal Research Fellow of CR-UK.This is the author accepted manuscript. It is currently under an indefinite embargo pending publication by Cell Press

    Balancing Selection at the Tomato RCR3 Guardee Gene Family Maintains Variation in Strength of Pathogen Defense

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    Coevolution between hosts and pathogens is thought to occur between interacting molecules of both species. This results in the maintenance of genetic diversity at pathogen antigens (or so-called effectors) and host resistance genes such as the major histocompatibility complex (MHC) in mammals or resistance (R) genes in plants. In plant-pathogen interactions, the current paradigm posits that a specific defense response is activated upon recognition of pathogen effectors via interaction with their corresponding R proteins. According to the''Guard-Hypothesis,'' R proteins (the ``guards'') can sense modification of target molecules in the host (the ``guardees'') by pathogen effectors and subsequently trigger the defense response. Multiple studies have reported high genetic diversity at R genes maintained by balancing selection. In contrast, little is known about the evolutionary mechanisms shaping the guardee, which may be subject to contrasting evolutionary forces. Here we show that the evolution of the guardee RCR3 is characterized by gene duplication, frequent gene conversion, and balancing selection in the wild tomato species Solanum peruvianum. Investigating the functional characteristics of 54 natural variants through in vitro and in planta assays, we detected differences in recognition of the pathogen effector through interaction with the guardee, as well as substantial variation in the strength of the defense response. This variation is maintained by balancing selection at each copy of the RCR3 gene. Our analyses pinpoint three amino acid polymorphisms with key functional consequences for the coevolution between the guardee (RCR3) and its guard (Cf-2). We conclude that, in addition to coevolution at the ``guardee-effector'' interface for pathogen recognition, natural selection acts on the ``guard-guardee'' interface. Guardee evolution may be governed by a counterbalance between improved activation in the presence and prevention of auto-immune responses in the absence of the corresponding pathogen

    Evidence of a Causal Association Between Insulinemia and Endometrial Cancer: A Mendelian Randomization Analysis.

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    BACKGROUND: Insulinemia and type 2 diabetes (T2D) have been associated with endometrial cancer risk in numerous observational studies. However, the causality of these associations is uncertain. Here we use a Mendelian randomization (MR) approach to assess whether insulinemia and T2D are causally associated with endometrial cancer. METHODS: We used single nucleotide polymorphisms (SNPs) associated with T2D (49 variants), fasting glucose (36 variants), fasting insulin (18 variants), early insulin secretion (17 variants), and body mass index (BMI) (32 variants) as instrumental variables in MR analyses. We calculated MR estimates for each risk factor with endometrial cancer using an inverse-variance weighted method with SNP-endometrial cancer associations from 1287 case patients and 8273 control participants. RESULTS: Genetically predicted higher fasting insulin levels were associated with greater risk of endometrial cancer (odds ratio [OR] per standard deviation = 2.34, 95% confidence internal [CI] = 1.06 to 5.14, P = .03). Consistently, genetically predicted higher 30-minute postchallenge insulin levels were also associated with endometrial cancer risk (OR = 1.40, 95% CI = 1.12 to 1.76, P = .003). We observed no associations between genetic risk of type 2 diabetes (OR = 0.91, 95% CI = 0.79 to 1.04, P = .16) or higher fasting glucose (OR = 1.00, 95% CI = 0.67 to 1.50, P = .99) and endometrial cancer. In contrast, endometrial cancer risk was higher in individuals with genetically predicted higher BMI (OR = 3.86, 95% CI = 2.24 to 6.64, P = 1.2x10(-6)). CONCLUSION: This study provides evidence to support a causal association of higher insulin levels, independently of BMI, with endometrial cancer risk.This study was supported by MRC grant MC_UU_12015/1 and by the Innovative Medicines Initiative Joint Undertaking under EMIF grant agreement n° 115372 (contributions from the European Union's Seventh Framework Programme (FP7/2007-2013) and EFPIA companies). ANECS recruitment was supported by project grants from the National Health and Medical Research Council of Australia (ID#339435), The Cancer Council Queensland (ID#4196615) and Cancer Council Tasmania (ID#403031 and ID#457636). SEARCH recruitment was funded by a programme grant from Cancer Research UK [C490/A10124]. Case genotyping was supported by the National Health and Medical Research Council (ID#552402). Control data was generated by the Wellcome Trust Case Control Consortium (WTCCC), and a full list of the investigators who contributed to the generation of the data is available from the WTCCC website. We acknowledge use of DNA from the British 1958 Birth Cohort collection, funded by the Medical Research Council grant G0000934 and the Wellcome Trust grant 068545/Z/02. Funding for this project was provided by the Wellcome Trust under award 085475. Recruitment of the QIMR controls was supported by the National Health and Medical Research Council of Australia (NHMRC). The University of Newcastle, the Gladys M Brawn Senior Research Fellowship scheme, The Vincent Fairfax Family Foundation, the Hunter Medical Research Institute and the Hunter Area Pathology Service all contributed towards the costs of establishing the Hunter Community Study. K.T.N. was supported by the Gates Cambridge Trust. R.K.S. is supported by the Wellcome Trust (grant number WT098498). A.B.S. is supported by the National Health and Medical Research Council (NHMRC) Fellowship Scheme. D.F.E. is a Principal Research Fellow of Cancer Research UK. A.M.D is supported by the Joseph Mitchell Trust.This is the final version of the article. It first appeared from Oxford University Press via http://dx.doi.org/10.1093/jnci/djv17
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