scholarly journals Nitrogen isotopic fractionations during nitric oxide production in an agricultural soil

2020 ◽  
Author(s):  
Zhongjie Yu ◽  
Emily M. Elliott
Keyword(s):  
Nitric Oxide ◽  
Atmospheric Chemistry ◽  
Agricultural Soil ◽  
Agricultural Soils ◽  
Isotope Effects ◽  
Enzyme Level ◽  
Critical Role ◽  
N2o Emissions ◽  
No Production ◽  
Hypoxic Conditions

Abstract. Nitric oxide (NO) emissions from agricultural soils play a critical role in atmospheric chemistry and represent an important pathway for loss of reactive nitrogen (N) to the environment. With recent methodological advances, there is growing interest in the natural abundance N isotopic composition (δ15N) of soil-emitted NO and its utility in providing mechanistic information on soil NO dynamics. However, interpretation of soil δ15N-NO measurements has been impeded by the lack of constraints on the isotopic fractionations associated with NO production and consumption in relevant microbial and chemical reactions. In this study, anoxic (0 % O2), oxic (20 % O2), and hypoxic (0.5 % O2) incubations of an agricultural soil were conducted to quantify the net N isotope effects (15η) for NO production in denitrification, nitrification, and abiotic reactions of nitrite (NO2−) using a newly developed δ15N-NO analysis method. A sodium nitrate (NO3−) containing mass-independent oxygen-17 excess (quantified by a Δ17O notation) and three ammonium (NH4+) fertilizers spanning a δ15N gradient were used in soil incubations to help illuminate the reaction complexity underlying NO yields and δ15N dynamics in a heterogeneous soil environment. We found strong evidence for the prominent role of NO2− oxidation under anoxic conditions in controlling the apparent 15η for NO production from NO3− in denitrification (i.e., 49 to 60 ‰). These results highlight the importance of an under-recognized mechanism for the reversible enzyme NO2− oxidoreductase to control the N isotope distribution between the denitrification products. Through a Δ17O-based modeling of co-occurring denitrification and NO2− re-oxidation, the 15η for NO2− reduction to NO and NO reduction to nitrous oxide (N2O) were constrained to be 15 to 22 ‰ and −8 to 2 ‰, respectively. Production of NO in the oxic and hypoxic incubations was contributed by both NH4+ oxidation and NO3− consumption, with both processes having a significantly higher NO yield under O2 stress. Under both oxic and hypoxic conditions, NO production from NH4+ oxidation proceeded with a large 15η (i.e., 55 to 84 ‰) possibly due to expression of multiple enzyme-level isotopic fractionations during NH4+ oxidation to NO2− that involves NO as either a metabolic byproduct or an obligatory intermediate for NO2− production. Adding NO2− to sterilized soil triggered substantial NO production, with a relatively small 15η (19 ‰). Applying the estimated 15η values to a previous δ15N measurement of in situ soil NOx emission (NOx = NO + NO2) provided promising evidence for the potential of δ15N-NO measurements in revealing NO production pathways. Based on the observational and modeling constraints obtained in this study, we suggest that simultaneous δ15N-NO and δ15N-N2O measurements can lead to unprecedented insights into the sources of and processes controlling NO and N2O emissions from agricultural soils.

scholarly journals Nitrogen isotopic fractionations during nitric oxide production in an agricultural soil

2021 ◽  
Vol 18 (3) ◽  
pp. 805-829
Author(s):  
Zhongjie Yu ◽  
Emily M. Elliott
Keyword(s):  
Nitric Oxide ◽  
Atmospheric Chemistry ◽  
Agricultural Soil ◽  
Agricultural Soils ◽  
Isotope Effects ◽  
Enzyme Level ◽  
Critical Role ◽  
N2o Emissions ◽  
No Production ◽  
Hypoxic Conditions

Abstract. Nitric oxide (NO) emissions from agricultural soils play a critical role in atmospheric chemistry and represent an important pathway for loss of reactive nitrogen (N) to the environment. With recent methodological advances, there is growing interest in the natural-abundance N isotopic composition (δ15N) of soil-emitted NO and its utility in providing mechanistic information on soil NO dynamics. However, interpretation of soil δ15N-NO measurements has been impeded by the lack of constraints on the isotopic fractionations associated with NO production and consumption in relevant microbial and chemical reactions. In this study, anoxic (0 % O2), oxic (20 % O2), and hypoxic (0.5 % O2) incubations of an agricultural soil were conducted to quantify the net N isotope effects (15η) for NO production in denitrification, nitrification, and abiotic reactions of nitrite (NO2-) using a newly developed δ15N-NO analysis method. A sodium nitrate (NO3-) containing mass-independent oxygen-17 excess (quantified by a Δ17O notation) and three ammonium (NH4+) fertilizers spanning a δ15N gradient were used in soil incubations to help illuminate the reaction complexity underlying NO yields and δ15N dynamics in a heterogeneous soil environment. We found strong evidence for the prominent role of NO2- re-oxidation under anoxic conditions in controlling the apparent 15η for NO production from NO3- in denitrification (i.e., 49 ‰ to 60 ‰). These results highlight the importance of an under-recognized mechanism for the reversible enzyme NO2- oxidoreductase to control the N isotope distribution between the denitrification products. Through a Δ17O-based modeling of co-occurring denitrification and NO2- re-oxidation, the 15η for NO2- reduction to NO and NO reduction to nitrous oxide (N2O) were constrained to be 15 ‰ to 22 ‰ and −8 ‰ to 2 ‰, respectively. Production of NO in the oxic and hypoxic incubations was contributed by both NH4+ oxidation and NO3- consumption, with both processes having a significantly higher NO yield under O2 stress. Under both oxic and hypoxic conditions, NO production from NH4+ oxidation proceeded with a large 15η (i.e., 55 ‰ to 84 ‰) possibly due to expression of multiple enzyme-level isotopic fractionations during NH4+ oxidation to NO2- that involves NO as either a metabolic byproduct or an obligatory intermediate for NO2- production. Adding NO2- to sterilized soil triggered substantial NO production, with a relatively small 15η (19 ‰). Applying the estimated 15η values to a previous δ15N measurement of in situ soil NOx emission (NOx=NO+NO2) provided promising evidence for the potential of δ15N-NO measurements in revealing NO production pathways. Based on the observational and modeling constraints obtained in this study, we suggest that simultaneous δ15N-NO and δ15N-N2O measurements can lead to unprecedented insights into the sources of and processes controlling NO and N2O emissions from agricultural soils.

Developmental changes in nitric oxide synthase isoform expression and nitric oxide production in fetal baboon lung

2002 ◽  
Vol 283 (6) ◽  
pp. L1192-L1199 ◽  
Author(s):  
Philip W. Shaul ◽  
Sam Afshar ◽  
Linda L. Gibson ◽  
Todd S. Sherman ◽  
Jay D. Kerecman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Critical Role ◽  
Perinatal Period ◽  
Postnatal Period ◽  
Developmental Changes ◽  
No Production ◽  
Third Trimester ◽  
Isoform Expression ◽  
Oxide Synthase ◽  
Nos Isoforms

Nitric oxide (NO), produced by NO synthase (NOS), plays a critical role in multiple processes in the lung during the perinatal period. To better understand the regulation of pulmonary NO production in the developing primate, we determined the cell specificity and developmental changes in NOS isoform expression and action in the lungs of third-trimester fetal baboons. Immunohistochemistry in lungs obtained at 175 days (d) of gestation (term = 185 d) revealed that all three NOS isoforms, neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS), are primarily expressed in proximal airway epithelium. In proximal lung, there was a marked increase in total NOS enzymatic activity from 125 to 140 d gestation due to elevations in nNOS and eNOS, whereas iNOS expression and activity were minimal. Total NOS activity was constant from 140 to 175 d gestation, and during the latter stage (160–175 d gestation), a dramatic fall in nNOS and eNOS was replaced by a rise in iNOS. Studies done within 1 h of delivery at 125 or 140 d gestation revealed that the principal increase in NOS during the third trimester is associated with an elevation in exhaled NO levels, a decline in expiratory resistance, and greater pulmonary compliance. Thus, there are developmental increases in pulmonary NOS expression and NO production during the early third trimester in the primate that may enhance airway and parenchymal function in the immediate postnatal period.

scholarly journals NIR Bioluminescence Probe Enables Discovery of Diet-Induced Modulation of the Tumor Microenvironment via Nitric Oxide

2021 ◽  
Author(s):  
Anuj K Yadav ◽  
Michael C. Lee ◽  
Melissa Lucero ◽  
Christopher J. Reinhardt ◽  
ShengZhang Su ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumor Microenvironment ◽  
Tumor Progression ◽  
Critical Role ◽  
Cellular Systems ◽  
Tissue Imaging ◽  
Molecular Evidence ◽  
No Production ◽  
The Impact

<p>Nitric oxide (NO) plays a critical role in acute and chronic inflammation. NO’s contributions to cancer are of particular interest due to its context-dependent bioactivities. For example, immune cells initially produce cytotoxic quantities of NO in response to the nascent tumor. However, it is believed that this fades over time and reaches a concentration that supports the tumor microenvironment (TME). These complex dynamics are further complicated by other factors, such as diet and oxygenation, making it challenging to establish a complete picture of NO’s impact on tumor progression. Although many activity-based sensing (ABS) probes for NO have been developed, only a small fraction have been employed <i>in vivo </i>and fewer yet are practical in cancer models where the NO concentration is < 200 nM. To overcome this outstanding challenge, we have developed BL<sub>660</sub>-NO, the first ABS probe for NIR bioluminescence imaging of NO in cancer. Owing to the low intrinsic background, high sensitivity, and deep tissue imaging capabilities of our design, BL<sub>660</sub>-NO was successfully employed to visualize endogenous NO in cellular systems, a human liver metastasis model, and a murine breast cancer model. Importantly, its exceptional performance facilitated the design of a dietary study to examine the impact of NO on the TME by varying the intake of fat. BL<sub>660</sub>-NO provides the first direct molecular evidence that intratumoral NO becomes elevated in mice fed a high-fat diet who became obese with larger tumors compared to control animals on a low-fat diet. These results indicate that an inflammatory diet can increase NO production via recruitment of macrophages and overexpression of iNOS which in turn can drive tumor progression.<br></p>

scholarly journals Exogenous Heat Shock Cognate Protein 70 Suppresses LPS-Induced Inflammation by Down-Regulating NF-κB through MAPK and MMP-2/-9 Pathways in Macrophages

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2124 ◽  
Author(s):  
Erna Sulistyowati ◽  
Mei-Yueh Lee ◽  
Lin-Chi Wu ◽  
Jong-Hau Hsu ◽  
Zen-Kong Dai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heat Shock ◽  
Critical Role ◽  
Matrix Metalloproteinase 2 ◽  
No Production ◽  
Raw 264.7 ◽  
Tnf Α ◽  
Heat Shock Cognate Protein ◽  
Anti Inflammatory ◽  
Cognate Protein

Heat shock cognate protein 70 (HSC70), a molecular chaperone, is constitutively expressed by mammalian cells to regulate various cellular functions. It is associated with many diseases and is a potential therapeutic target. Although HSC70 also possesses an anti-inflammatory action, the mechanism of this action remains unclear. This current study aimed to assess the anti-inflammatory effects of HSC70 in murine macrophages RAW 264.7 exposed to lipopolysaccharides (LPS) and to explain its pathways. Mouse macrophages (RAW 264.7) in 0.1 µg/mL LPS incubation were pretreated with recombinant HSC70 (rHSC70) and different assays (Griess assay, enzyme-linked immune assay/ELISA, electrophoretic mobility shift assay/EMSA, gelatin zymography, and Western blotting) were performed to determine whether rHSC70 blocks pro-inflammatory mediators. The findings showed that rHSC70 attenuated the nitric oxide (NO) generation, tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) expressions in LPS-stimulated RAW264.7 cells. In addition, rHSC70 preconditioning suppressed the activities and expressions of matrix metalloproteinase-2 (MMP-2) and MMP-9. Finally, rHSC70 diminished the nuclear translocation of nuclear factor-κB (NF-κB) and reduced the phosphorylation of extracellular-signal regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinases (MAPK), and phosphatidylinositol-3-kinase (PI3K/Akt). We demonstrate that rHSC70 preconditioning exerts its anti-inflammatory effects through NO production constriction; TNF-α, and IL-6 suppression following down-regulation of inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX-2), and MMP-2/MMP-9. Accordingly, it ameliorated the signal transduction of MAPKs, Akt/IκBα, and NF-κB pathways. Therefore, extracellular HSC70 plays a critical role in the innate immunity modulation and mechanisms of endogenous protective stimulation.

Alternative oxidase is an important player in the regulation of nitric oxide levels under normoxic and hypoxic conditions in plants

2019 ◽  
Vol 70 (17) ◽  
pp. 4345-4354 ◽  
Author(s):  
Aprajita Kumari ◽  
Pradeep Kumar Pathak ◽  
Mallesham Bulle ◽  
Abir U Igamberdiev ◽  
Kapuganti Jagadis Gupta
Keyword(s):  
Nitric Oxide ◽  
Alternative Oxidase ◽  
Plant Mitochondria ◽  
No Production ◽  
Complex Iv ◽  
Increase Energy Efficiency ◽  
Hypoxic Conditions ◽  
Cytochrome Pathway ◽  
Important Player ◽  
Elicitor Treatments

Abstract Plant mitochondria possess two different pathways for electron transport from ubiquinol: the cytochrome pathway and the alternative oxidase (AOX) pathway. The AOX pathway plays an important role in stress tolerance and is induced by various metabolites and signals. Previously, several lines of evidence indicated that the AOX pathway prevents overproduction of superoxide and other reactive oxygen species. More recent evidence suggests that AOX also plays a role in regulation of nitric oxide (NO) production and signalling. The AOX pathway is induced under low phosphate, hypoxia, pathogen infections, and elicitor treatments. The induction of AOX under aerobic conditions in response to various stresses can reduce electron transfer through complexes III and IV and thus prevents the leakage of electrons to nitrite and the subsequent accumulation of NO. Excess NO under various stresses can inhibit complex IV; thus, the AOX pathway minimizes nitrite-dependent NO synthesis that would arise from enhanced electron leakage in the cytochrome pathway. By preventing NO generation, AOX can reduce peroxynitrite formation and tyrosine nitration. In contrast to its function under normoxia, AOX has a specific role under hypoxia, where AOX can facilitate nitrite-dependent NO production. This reaction drives the phytoglobin–NO cycle to increase energy efficiency under hypoxia.

scholarly journals Cytokine-induced arginase activity in pulmonary endothelial cells is dependent on Src family tyrosine kinase activity

2008 ◽  
Vol 295 (4) ◽  
pp. L688-L697 ◽  
Author(s):  
Rossana Chang ◽  
Louis G. Chicoine ◽  
Hongmei Cui ◽  
Nancy L. Kanagy ◽  
Benjimen R. Walker ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Tyrosine Kinases ◽  
Critical Role ◽  
Inos Mrna ◽  
No Production ◽  
Appreciable Effect ◽  
Pulmonary Endothelial Cells ◽  
Inflammatory Stimuli ◽  
Arginase Ii

We hypothesized that the Src family tyrosine kinases (STKs) are involved in the upregulation of arginase and inducible nitric oxide synthase (iNOS) expression in response to inflammatory stimuli in pulmonary endothelial cells. Treatment of bovine pulmonary arterial endothelial cells (bPAEC) with lipopolysaccharide and tumor necrosis factor-α (L/T) resulted in increased urea and nitric oxide (NO) production, and this increase in urea and NO production was inhibited by the STK inhibitor PP1 (10 μM). The STK inhibitors PP2 (10 μM) and herbimycin A (10 μM) also prevented the L/T-induced expression of both arginase II and iNOS mRNA in bPAEC. Together, the data demonstrate a central role of STK in the upregulation of both arginase II and iNOS in bPAEC in response to L/T treatment. To identify the specific kinase(s) required for the induction of urea and NO production, we studied human pulmonary microvascular endothelial cells (hPMVEC) so that short interfering RNA (siRNA) techniques could be employed. We found that hPMVEC express Fyn, Yes, c-Src, Lyn, and Blk and that the protein expression of Fyn, Yes, c-Src, and Lyn could be inhibited with specific siRNA. The siRNA targeting Fyn prevented the cytokine-induced increase in urea and NO production, whereas siRNAs specifically targeting Yes, c-Src, and Lyn had no appreciable effect on cytokine-induced urea and NO production. These findings support our hypothesis that inflammatory stimuli lead to increased urea and NO production through a STK-mediated pathway. Furthermore, these results indicate that the STK Fyn plays a critical role in this process.

scholarly journals Mechanisms of Medicinal Plant Activity on Nitric Oxide (NO) Bioavailability as Prospective Treatments for Atherosclerosis

2020 ◽  
Vol 26 (22) ◽  
pp. 2591-2601 ◽  
Author(s):  
Khojasteh Malekmohammad ◽  
Robert D.E. Sewell ◽  
Mahmoud Rafieian-Kopaei
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Medicinal Plants ◽  
Bioactive Compounds ◽  
Protein Tyrosine Kinase ◽  
Critical Role ◽  
Nitrite Reduction ◽  
No Production ◽  
Vascular Effects ◽  
No Bioavailability

Background and objective: Atherosclerosis is one of the leading causes of human morbidity globally and reduced bioavailability of vascular nitric oxide (NO) has a critical role in the progression and development of the atherosclerotic disease. Loss of NO bioavailability, for example via a deficiency of the substrate (L-arginine) or cofactors for endothelial nitric oxide synthase (eNOS), invariably leads to detrimental vascular effects such as impaired endothelial function and increased smooth muscle cell proliferation, deficiency of the substrate (Larginine) or cofactors for eNOS. Various medicinal plants and their bioactive compounds or secondary metabolites with fewer side effects are potentially implicated in preventing cardiovascular disease by increasing NO bioavailability, thereby ameliorating endothelial dysfunction. In this review, we describe the most notable medicinal plants and their bioactive compounds that may be appropriate for enhancing NO bioavailability, and treatment of atherosclerosis. Methods: The material in this article was obtained from noteworthy scientific databases, including Web of Science, PubMed, Science Direct, Scopus and Google Scholar. Results: Medicinal plants and their bioactive compounds influence NO production through diverse mechanisms including the activation of the nuclear factor kappa B (NF-κB) signaling pathway, activating protein kinase C (PKC)-α, stimulating protein tyrosine kinase (PTK), reducing the conversion of nitrite to NO via nitrate-nitrite reduction pathways, induction of eNOS, activating the phosphatidylinositol 3-kinase (PI3K)/serine threonine protein kinase B (AKT) (PI3K/AKT/eNOS/NO) pathway and decreasing oxidative stress. Conclusion: Medicinal plants and/or their constituent bioactive compounds may be considered as safe therapeutic options for enhancing NO bioavailability and prospective preventative therapy for atherosclerosis.

scholarly journals Amphiphysin IIm Is Required for Survival of Chlamydia pneumoniae in Macrophages

2004 ◽  
Vol 200 (5) ◽  
pp. 581-586 ◽  
Author(s):  
Elizabeth S. Gold ◽  
Randi M. Simmons ◽  
Timothy W. Petersen ◽  
Lee Ann Campbell ◽  
Cho-Chou Kuo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Chlamydia Pneumoniae ◽  
Bacterial Pathogens ◽  
Critical Role ◽  
Adaptor Protein ◽  
Acquired Immunity ◽  
No Production ◽  
Phagosome Maturation ◽  
Wild Type ◽  
Unique Ability

Macrophages play a critical role in both innate and acquired immunity because of their unique ability to internalize, kill, and degrade bacterial pathogens through the process of phagocytosis. The adaptor protein, amphiphysin IIm, participates in phagocytosis and is transiently associated with early phagosomes. Certain pathogens, including Chlamydia pneumoniae, have evolved mechanisms to subvert macrophage phagosome maturation and, thus, are able to survive within these cells. We report here that, although amphiphysin IIm is usually only transiently associated with the phagosome, it is indefinitely retained on vacuoles containing C. pneumoniae. Under these wild-type conditions, C. pneumoniae do not elicit significant nitric oxide (NO) production and are not killed. Abrogation of amphiphysin IIm function results in C. pneumoniae–induced NO production and in the sterilization of the vacuole. The data suggest that C. pneumoniae retains amphiphysin IIm on the vacuole to survive within the macrophage.

scholarly journals Nitric oxide and superoxide transport in a cross section of the rat outer medulla. II. Reciprocal interactions and tubulovascular cross talk

2010 ◽  
Vol 299 (3) ◽  
pp. F634-F647 ◽  
Author(s):  
Aurélie Edwards ◽  
Anita T. Layton
Keyword(s):  
Nitric Oxide ◽  
Cross Sections ◽  
Cross Talk ◽  
Three Dimensional ◽  
No Production ◽  
Outer Medulla ◽  
Nacl Transport ◽  
Hypoxic Conditions ◽  
Outer Stripe ◽  
Main Determinants

In a companion study (Edwards A and Layton AT. Am J Physiol Renal Physiol. doi:10.1152/ajprenal.00680.2009), we developed a mathematical model of nitric oxide (NO), superoxide (O2−), and total peroxynitrite (ONOO) transport in mid-outer stripe and mid-inner stripe cross sections of the rat outer medulla (OM). We examined how the three-dimensional architecture of the rat OM, together with low medullary oxygen tension (Po2), affects the distribution of NO, O2−, and ONOO in the rat OM. In the current study, we sought to determine generation rate and permeability values that are compatible with measurements of medullary NO concentrations and to assess the importance of tubulovascular cross talk and NO-O2− interactions under physiological conditions. Our results suggest that the main determinants of NO concentrations in the rat OM are the rate of vascular and tubular NO synthesis under hypoxic conditions, and the red blood cell (RBC) permeability to NO ( PNORBC). The lower the PNORBC, the lower the amount of NO that is scavenged by hemoglobin species, and the higher the extra-erythrocyte NO concentrations. In addition, our results indicate that basal endothelial NO production acts to significantly limit NaCl reabsorption across medullary thick ascending limbs and to sustain medullary perfusion, whereas basal epithelial NO production has a smaller impact on NaCl transport and a negligible effect on vascular tone. Our model also predicts that O2− consumption by NO significantly reduces medullary O2− concentrations, but that O2− , when present at subnanomolar concentrations, has a small impact on medullary NO bioavailability.

scholarly journals Identification of Potential Calorie Restriction-Mimicking Yeast Mutants with Increased Mitochondrial Respiratory Chain and Nitric Oxide Levels

2011 ◽  
Vol 2011 ◽  
pp. 1-16 ◽  
Author(s):  
Bin Li ◽  
Craig Skinner ◽  
Pablo R. Castello ◽  
Michiko Kato ◽  
Erin Easlon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Calorie Restriction ◽  
Mitochondrial Respiration ◽  
Molecular Mechanisms ◽  
Mitochondrial Respiratory Chain ◽  
Yeast Cells ◽  
Mitochondrial Activity ◽  
No Production ◽  
Hypoxic Conditions ◽  
Yeast Mutants

Calorie restriction (CR) induces a metabolic shift towards mitochondrial respiration; however, molecular mechanisms underlying CR remain unclear. Recent studies suggest that CR-induced mitochondrial activity is associated with nitric oxide (NO) production. To understand the role of mitochondria in CR, we identify and studySaccharomyces cerevisiaemutants with increased NO levels as potential CR mimics. Analysis of the top 17 mutants demonstrates a correlation between increased NO, mitochondrial respiration, and longevity. Interestingly, treating yeast with NO donors such as GSNO (S-nitrosoglutathione) is sufficient to partially mimic CR to extend lifespan. CR-increased NO is largely dependent on mitochondrial electron transport and cytochrome c oxidase (COX). Although COX normally produces NO under hypoxic conditions, CR-treated yeast cells are able to produce NO under normoxic conditions. Our results suggest that CR may derepress some hypoxic genes for mitochondrial proteins that function to promote the production of NO and the extension of lifespan.

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