P-FLUX: A phosphorus budget dataset spanning diverse agricultural production systems in the United States and Canada.

Quantifying spatial and temporal fluxes of phosphorus (P) within and among agricultural production systems is critical for sustaining agricultural production while minimizing environmental impacts. To better understand P fluxes in agricultural landscapes, P-FLUX, a detailed and harmonized dataset of P inputs, outputs, and budgets, as well as estimated uncertainties for each P flux and budget, was developed. Data were collected from 24 research sites and 61 production systems through the Long-term Agroecosystem Research (LTAR) network and partner organizations spanning 22 U.S. states and 2 Canadian provinces. The objectives of this paper are to (a) present and provide a description of the P-FLUX dataset, (b) provide summary analyses of the agricultural production systems included in the dataset and the variability in P inputs and outputs across systems, and (c) provide details for accessing the dataset, dataset limitations, and an example of future use. P-FLUX includes information on select site characteristics (area, soil series), crop rotation, P inputs (P application rate, source, timing, placement, P in irrigation water, atmospheric deposition), P outputs (crop removal, hydrologic losses), P budgets (agronomic budget, overall budget), uncertainties associated with each flux and budget, and data sources. Phosphorus fluxes and budgets vary across agricultural production systems and are useful resources to improve P use efficiency and develop management strategies to mitigate environmental impacts of agricultural systems. P-FLUX is available for download through the USDA Ag Data Commons (https://doi.org/10.15482/USDA.ADC/1523365).

Advancing the Sustainability of US Agriculture through Long-Term Research.

Agriculture in the United States must respond to escalating demands for productivity and efficiency, as well as pressures to improve its stewardship of natural resources. Growing global population and changing diets, combined with a greater societal awareness of agriculture's role in delivering ecosystem services beyond food, feed, fiber, and energy production, require a comprehensive perspective on where and how US agriculture can be sustainably intensified, that is, made more productive without exacerbating local and off-site environmental concerns. The USDA's Long-Term Agroecosystem Research (LTAR) network is composed of 18 locations distributed across the contiguous United States working together to integrate national and local agricultural priorities and advance the sustainable intensification of US agriculture. We explore here the concept of sustainable intensification as a framework for defining strategies to enhance production, environmental, and rural prosperity outcomes from agricultural systems. We also elucidate the diversity of factors that have shaped the past and present conditions of cropland, rangeland, and pastureland agroecosystems represented by the LTAR network and identify priorities for research in the areas of production, resource conservation and environmental quality, and rural prosperity. Ultimately, integrated long-term research on sustainable intensification at the national scale is critical to developing practices and programs that can anticipate and address challenges before they become crises.

Simulated Soil Organic Carbon Changes in Maryland Are Affected by Tillage, Climate Change, and Crop Yield.

The impact of climate change on soil organic C (SOC) stocks in no-till (NT) and conventionally tilled (CT) agricultural systems is poorly understood. The objective of this study was to simulate the impact of projected climate change on SOC to 50-cm soil depth for grain cropping systems in the southern Mid-Atlantic region of the United States. We used SOC and other data from the long-term Farming Systems Project in Beltsville, MD, and CQESTR, a process-based soil C model, to predict the impact of cropping systems and climate (air temperature and precipitation) on SOC for a 40-yr period (2012-2052). Since future crop yields are uncertain, we simulated five scenarios with differing yield levels (crop yields from 1996-2014, and at 10 or 30% greater or lesser than these yields). Without change in climate or crop yields (baseline conditions) CQESTR predicted an increase in SOC of 0.014 and 0.021 Mg ha yr in CT and NT, respectively. Predicted climate change alone resulted in an SOC increase of only 0.002 Mg ha yr in NT and a decrease of 0.017 Mg ha yr in CT. Crop yield declines of 10 and 30% led to SOC decreases between 2 and 8% compared with 2012 levels. Increasing crop yield by 10 and 30% was sufficient to raise SOC 2 and 7%, respectively, above the climate-only scenario under both CT and NT between 2012 and 2052. Results indicate that under these simulated conditions, the negative impact of climate change on SOC levels could be mitigated by crop yield increases.

Metallothionein accretion in human hepatic cells is linked to cellular proliferation.

The basal amounts of metallothionein (MT) and its rates of biosynthesis were compared in resting and proliferating Chang liver (CCl-13) cells. In resting cells the total amounts of the detectable isoforms MT-2 and MT-1e were approx. 1.6x10(6) and 4x10(5) molecules per cell respectively. In exponentially growing cultures the cellular contents of both isoforms increased co-ordinately approx. 4-fold and decreased again to the initial values within 48 h after entering density-mediated growth arrest. As documented for MT-2 its transient accretion was attributable to a 10-fold rise in the rate of biosynthesis of this protein during the growth phase. Measurements of the relative amounts of MT-2 mRNA indicated the occurrence of a more than 50% increase within the first 12 h after subculturing of the cells, followed by a return to basal levels thereafter. These results denote a direct link between the programming of MT synthesis and proliferation and thus attest to a central housekeeping function of the MTs.

The tumor promoter arsenite stimulates AP-1 activity by inhibiting a JNK phosphatase.

Trivalent arsenic (As3+) is highly carcinogenic, but devoid of known mutagenic activity. Therefore, it is likely to act as a tumor promoter. To understand the molecular basis for the tumor-promoting activity of As3+, we examined its effect on transcription factor AP-1, whose activity is stimulated by several other tumor promoters. We found that As3+, but not As5+, which is toxic but not carcinogenic, is a potent stimulator of AP-1 transcriptional activity and an efficient inducer of c-fos and c-jun gene expression. Induction of c-jun and c-fos transcription by As3+ correlates with activation of Jun kinases (JNKs) and p38/Mpk2, which phosphorylate transcription factors that activate these immediate early genes. No effect on ERK activity was observed. As5+, on the other hand, had a negligible effect on JNK or p38/Mpk2 activity. Biochemical analysis and co-transfection experiments strongly suggest that the primary mechanism by which As3+ stimulates JNK activity involves the inhibition of a constitutive dual-specificity JNK phosphatase. This phosphatase activity appears to be responsible for maintaining low basal JNK activity in non-stimulated cells and its inhibition may lead to tumor promotion through induction of proto-oncogenes such as c-jun and c-fos, and stimulation of AP-1 activity. The same phosphatase may also regulate p38/Mpk2 activity.

Induction of c-fos expression through JNK-mediated TCF/Elk-1 phosphorylation.

Growth factors induce c-fos transcription by stimulating phosphorylation of transcription factor TCF/Elk-1, which binds to the serum response element (SRE). Under such conditions Elk-1 could be phosphorylated by the mitogen-activated protein kinases (MAPKs) ERK1 and ERK2. However, c-fos transcription and SRE activity are also induced by stimuli, such as UV irradiation and activation of the protein kinase MEKK1, that cause only an insignificant increase in ERK1/2 activity. However, both of these stimuli strongly activate two other MAPKs, JNK1 and JNK2, and stimulate Elk-1 transcriptional activity and phosphorylation. We find that the JNKs are the predominant Elk-1 activation domain kinases in extracts of UV-irradiated cells and that immunopurified JNK1/2 phosphorylate Elk-1 on the same major sites recognized by ERK1/2, that potentiate its transcriptional activity. Finally, we show that UV irradiation, but not serum or phorbol esters, stimulate translocation of JNK1 to the nucleus. As Elk-1 is most likely phosphorylated while bound to the c-fos promoter, these results suggest that UV irradiation and MEKK1 activation stimulate TCF/Elk-1 activity through JNK activation, while growth factors induce c-fos through ERK activation.

Antitumor promotion by phenolic antioxidants: inhibition of AP-1 activity through induction of Fra expression.

Induction of phase 2 detoxification enzymes by phenolic antioxidants can account for prevention of tumor initiation but cannot explain why these compounds inhibit tumor promotion. Phase 2 genes are induced through an antioxidant response element (ARE). Although the ARE resembles an AP-1 binding site, we show that the major ARE binding and activating protein is not AP-1. Interestingly, AP-1 DNA binding activity was induced by the phenolic antioxidant tert-butylhydroquinone (BHQ), but the induction of AP-1 transcriptional activity by the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) was inhibited by this compound. BHQ induced expression of c-jun, junB, fra-1, and fra-2, which encode AP-1 components, but was a poor inducer of c-fos and had no effect on fosB. Like c-Fos and FosB, the Fra proteins heterodimerize with Jun proteins to form stable AP-1 complexes. However, Fra-containing AP-1 complexes have low transactivation potential. Furthermore, Fra-1 repressed AP-1 activity induced by either TPA or expression of c-Jun and c-Fos. We therefore conclude that inhibitory AP-1 complexes composed of Jun-Fra heterodimers, induced by BHQ, antagonize the transcriptional effects of the tumor promoter TPA, which are mediated by Jun-Fos heterodimers. Since AP-1 is an important mediator of tumor promoter action, these findings may explain the anti-tumor-promoting activity of phenolic antioxidants.

Cell- and inducer-specific accretion of human isometallothioneins.

The synthesis of metallothionein (MT) was investigated in three different human epithelial cell lines, each derived from one of the embryonic germ layers. The accretion of different isoforms of the protein was monitored using a sensitive neutral-pH h.p.l.c. method. Induction of MT synthesis by zinc ions and dexamethasone revealed differences between the three cell lines, both with respect to the number and the amounts of the different isoMTs formed. Dose-response experiments showed that an increase in dexamethasone concentration enhances MT accretion asymptotically to a limit, whereas within the concentration range explored zinc produces an exponential augmentation.

Augmentation of parasympathetic contraction in tracheal and bronchial airways by PGF2 alpha in situ.

We studied the effect of exogenous prostaglandin F2 alpha (PGF2 alpha) on airway smooth muscle contraction caused by parasympathetic stimulation in 22 mongrel dogs in situ. Voltage (0-30 V, constant 20 Hz) and frequency-response (0-25 Hz, 25 V) curves were generated by stimulating the cut ends of both cervical vagus nerves. Airway response was measured isometrically as active tension (AT) in a segment of cervical trachea and as change in airway resistance (RL) and dynamic compliance (Cdyn) in bronchial airways. One hour after 5 mg/kg iv indomethacin, a cumulative frequency-response curve was generated in nine animals by electrical stimulation of the vagus nerves at 15-s intervals. Reproducibility was demonstrated by generating a second curve 7 min later. A third frequency-response curve was generated during active contraction of the airway caused by continuous intravenous infusion of 10 micrograms X kg-1 X min-1PPGF2 alpha. Additional frequency-response studies were generated 15 and 30 min after PGF2 alpha, when airway contractile response (delta RL = +2.8 +/- 0.65 cmH2O X 1(-1) X s; delta Cdyn = -0.0259 +/- 0.007 1/cmH2O) returned to base line. Substantial augmentation of AT, RL, and Cdyn responses was demonstrated in every animal studied (P less than 0.01 for all points greater than 8 Hz) 15 min after PGF2 alpha. At 30 min, response did not differ from initial base-line control. In four animals receiving sham infusion, all frequency-response curves were identical. We demonstrate that PGF2 alpha augments the response to vagus nerve stimulation in tracheal and bronchial airways. Augmentation does not depend on PGF2 alpha-induced active tone.

Autonomic response characteristics of porcine airway smooth muscle in vivo.

We studied the autonomic response characteristics of airways in 65 swine in vivo. Tracheal smooth muscle response was measured isometrically in situ; bronchial response was measured simultaneously as change in airway resistance and dynamic compliance. To determine the optimal resting length at which maximal tracheal contraction was obtained, length-tension studies were generated in four animals using maximal electrical stimulation of the vagus nerves determined from stimulus-response characteristics in eight other swine. Pharmacological studies were performed in 25 animals to determine the relative potency and intrinsic activity of agonists (acetylcholine greater than histamine much greater than norepinephrine) causing contraction of trachea and bronchial airways. In 13 swine, the effects of autonomic stimulation were studied by intravenous administration of dimethylphenylpiperazinium (DMPP) after muscarinic blockade with 1.5 mg/kg iv atropine. Tracheal contraction caused by topical application of 3.4 X 10(-4) mol histamine (13.4 +/- 1.54 g/cm) was 96 +/- 7.2% blocked by 25 micrograms/kg iv DMPP in adrenal-intact animals; minimal relaxation was demonstrated in adrenalectomized animals, indicating absence of substantial sympathetic innervation to porcine trachea. Nonadrenergic innervation was not demonstrated. After beta-adrenergic blockade, sympathetic stimulation caused alpha-adrenergic contraction in bronchial airways but not in trachea. These data define the unique response characteristics of the airways of swine and demonstrate their utility for acute experimental study of airway responses in vivo.

Selectivity of the intrinsic sympathomimetic activity of the beta-adrenergic blocking drug bucindolol.

We studied the comparative effects of beta-adrenergic blockade with propranolol (PROP) and bucindolol (BUC), a beta-adrenergic agonist having both alpha-adrenergic blocking properties and intrinsic sympathomimetic activity (ISA) on airway and cardiovascular responses, in 38 mongrel dogs in situ. Intravenous infusion of 0.6 mg/kg + 6 micrograms/kg/min BUC and 2.0 mg/kg + 20 micrograms/kg/min PROP caused identical shifts in the isoproterenol (ISO) EC50 for chronotropic and hypotensive arterial blood pressure responses. After PROP administration, resting heart rate (HR) decreased from 188 +/- 15 to 142 +/- 12 beats/min (p less than 0.02); BUC caused no decrease in HR. In contrast, the effects of BUC and PROP on mean arterial blood pressure response to ISO were similar. No change in bronchomotor tone was observed after bolus injection of either BUC or PROP. Beta-Adrenergic relaxation to ISO and alpha-adrenergic contraction to norepinephrine (NE) were studied simultaneously in tracheal and bronchial airways using chronotropically equivalent beta-adrenoceptor blocking doses of PROP and BUC. Comparable inhibition of ISO-induced airway relaxation after contraction with 120 micrograms/kg/min i.v. serotonin was demonstrated in both PROP (n = 5) and BUC (n = 5) groups (p less than 0.01 for doses greater than 5 X 10(-11) mol/kg). Similarly, both BUC (n = 5) and PROP (n = 5) blocked beta-adrenergic relaxation and caused identical alpha-adrenergic airway contraction to intravenous NE. We conclude that the ISA of the beta-adrenergic blocking drug BUC can be demonstrated on the spontaneous rate of the heart but not on the activity of bronchial smooth muscle. BUC neither augments ISO-induced relaxation nor inhibits NE-induced contraction of airways after effective chronotropic blockade.