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• Digital carbon communication (DCC) exerts positive impacts on market response to carbon disclosure. • The positive effect of DCC is most pronounced when government environmental regulation or media attention is insufficient. • Information asymmetry and corporate environmental performance play mediating roles in the mechanism. • DCC exhibits a stronger impact on the carbon disclosure market responses in firms with low institutional shareholdings, non-state-owned firms, and firms with high emission levels. This study investigates the influence of digital carbon communication quality (DCC) on market response to carbon disclosure within the reality of government environmental regulation and media attention, employing a DCC index constructed by an Autoencoder model. Using Chinese data from 2015 to 2022, we find that DCC mitigates negative market response to carbon disclosure by alleviating information asymmetry and enhancing corporate environmental performance, especially when government environmental regulation or media attention is insufficient. Moreover, DCC exhibits a stronger impact on the carbon disclosure market responses in firms with low institutional shareholdings, non-state-owned firms, and firms with high emission levels. [ABSTRACT FROM AUTHOR]

Copper pollution has become global environmental concern. Widespread Cu pollution results in excessive Cu exposure in human. Epidemiological studies and animal experiments revealed that Cu exposure might have reproductive toxicity. Cuproptosis is a newly reported Cu-dependent and programmed cell death formTsvetkov et al., 2022. However, whether copper exposure at real environmental exposure dose might cause placental cuproptosis and induce miscarriage was completely unexplored. In this study, we found that Cu exposure during pregnancy induced miscarriage or complete pregnancy loss by inducing placenta cuproptosis in CuCl 2 -exposed pregnant mice. Notably, Cu exposure at 1.3 mg/kg/d (a real environmental exposure dose) was enough to cause placenta cuproptosis. CuCl 2 exposure disrupts the TCA cycle, causes proteotoxic stress, increases Cu2+ ion import/decreases Cu2+ export, and results in the loss of Fe–S cluster proteins in mouse placenta, which induces placenta cuproptosis. Moreover, we also identified that Cu exposure down-regulates the expression levels of mmu-miR-3473b, which interacts with Dlst or Rtel1 mRNA and simultaneously positively regulates Dlst or Rtel1 expression, thereby disrupting the TCA cycle and resulting in the loss of Fe–S cluster proteins, and thus epigenetically regulates placental cuproptosis. Treatment with TTM (a cuproptosis inhibitor) suppressed placental cuproptosis and alleviated miscarriage in CuCl 2 -exposed mice. This work provides novel reproductive toxicity of Cu exposure in miscarriage or complete pregnancy loss by causing placental cuproptosis. This study also provides new ways for further studies on other toxicological effects of Cu and proposes a new approach for protection against Cu-induced reproductive diseases. [Display omitted] • Cu exposure during pregnancy induces mice placenta cuproptosis and miscarriage. • Cu down-regulates mmu-miR-3473b. • Mmu-miR-3473b up-regulates Dlst or Rtel1 expression and regulates cuproptosis. • Treatment with TTM suppressed placental cuproptosis and alleviated miscarriage. [ABSTRACT FROM AUTHOR]

Tumor necrosis factor-[alpha] converting enzyme (TACE) is a membrane-anchored, Zn-dependent metalloprotease, which belongs to the ADAM (a disintegrin and metalloprotease) family. TACE functions as a membrane sheddase to release the ectodomain portions of many transmembrane proteins, including the precursors of TNF[alpha] , TGF[alpha], several other cytokines, as well as the receptors for TNF[alpha], and neuregulin (ErbB4). Mice with [TACE.sup.[delta]Zn/[delta]Zn] null mutation die at birth with phenotypic changes, including failure of eyelid fusion, hair and skin defects, and abnormalities of lung development. Abnormal fetal heart development was not previously described. Herein, we report that [TACE.sup.[delta]Zn/[delta]Zn] null mutant mice by late gestation exhibit markedly enlarged fetal hearts with increased myocardial trabeculation and reduced cell compaction, mimicking the pathological changes of noncompaction of ventricular myocardium. In addition, larger cardiomyocyte cell size and increased cell proliferation were observed in ventricles of [TACE.sup.[delta]Zn/[delta]Zn] knockout mouse hearts. At the molecular level, reduced expression of epidermal growth factor receptor, attenuated protein cleavage of ErbB4, and changes in MAPK activation were also detected in [TACE.sup.[delta]Zn/[delta]Zn] knockout heart tissues. The data suggest that TACE-mediated cell surface protein ectodomain shedding plays an essential and a novel regulatory role during cardiac development and modeling. Keywords: TACE; Heart development; Cardiomyocyte

TGF-[Beta]1 is a known inhibitor of branching morphogenesis when added exogenously to mouse embryonic lungs in culture. However, the issue of whether endogenous TGF-[Beta] signaling has a function in the process of lung organogenesis is not completely resolved. We utilized immunoperturbation and antisense oligodeoxynucleotide inhibitory strategies to abrogate TGF-[Beta] type II receptor function in embryonic mouse lungs undergoing branching morphogenesis in serumless explant culture. Antisera directed against a TGF-[Beta] type II receptor N-terminal peptide that perturbs TGF-[Beta] ligand-receptor binding increased branching by 70%. Similarly, antisense TGF-[Beta] type II receptor oligodeoxynucleotides (40/[[micro]molar]) resulted in a 58% increase in branching, compared to scrambled and mismatched sequence controls, while TGF-[Beta] type II receptor mRNA and its protein expression levels were suppressed by 95 and 84%, respectively. Addition of exogenous TGF-[Beta]1 did not overcome the stimulatory effects either of TGF-[Beta] type II receptor immunoperturbation or of antisense oligodeoxynucleotide treatment on lung branching morphogenesis. Using in situ hybridization and immunohistochemistry, both TGF-[Beta] type II receptor mRNA and protein were localized to the epithelium lining the developing airways, and to the surrounding mesenchyme, indicating that TGF-[Beta] type II receptor is an important regulator of epithelial-mesenchymal interaction. Exogenous TGF-[Beta]1 decreased cyclin A mRNA levels in control embryonic lung explants, while TGF-[Beta] type II receptor antisense oligodeoxynucleotides prevented the downregulation of cyclin A mRNA expression by exogenous TGF-[Beta]1. In addition, PCNA immunostaining of the primitive bronchial epithelium was increased in the presence of TGF-[Beta] type II receptor antisense oligodeoxynucleotides either alone or together with exogenous TGF-[Beta]1, whereas TGF-[Beta]1 alone decreased PCNA staining. Thus, abrogation of TGF-[Beta] type II receptor expression prevented TGF-[Beta]1-induced epithelial cell [G.sub.1] arrest. These results demonstrate, for the first time, that abrogation of the TGF-[Beta] type II receptor stimulates embryonic lung organogenesis in culture and reverses the negative influence of endogenous TGF-[Beta] signaling upon epithelial cell cycle progression.

• Beside the main phase of zincblende, a small amount of wurtzite is existed in CVD ZnS. • The mechanical properties of CVD ZnS were characterized with a slight variation of Zn/S ratio. • Zn 46.84 S 53.16 presents a high flexural strength of 133.8 MPa. • XRD, SEM, and Raman spectra of CVD ZnS were conducted. Polycrystalline ZnS samples with a slight composition fluctuation are grown by chemical vapor deposition (CVD) method, and their optical and mechanical properties and microstructure were investigated in detail. The CVD samples present a maximum transmittance of ∼73% in the 7–10 μm region. By changing the sulfur content, a maximum Knoop hardness of 2.375 GPa was found in the Zn 50.06 S 49.94 sample, while Zn 46.84 S 53.16 presents a high flexural strength of 133.8 MPa. The microstructural origin of this abnormal changing of mechanical properties was discussed according to the results of micrographs, XRD patterns and Raman spectra. The results suggest that beside the main phase of zincblende, a small amount of wurtzite is existed. This composited microstructure is responsible for the higher hardness and strength of CVD ZnS. [ABSTRACT FROM AUTHOR]

Many membrane-bound protein precursors, including cytokines and growth factors, are proteolytically shed to yield soluble intercellular regulatory ligands. The responsible protease, tumor necrosis factor- [Alpha] converting enzyme (TACE/ADAM-17), is a transmembrane metalloprotease-disintegrin that cleaves multiple cell surface proteins, although it was initially identified for the enzymatic release of tumor necrosis factor-[Alpha] (TNF-[Alpha]). Mammalian lung growth and development are tightly controlled by cytokines and peptide growth factors. However, the biological function of the cell shedding mechanism during lung organogenesis is not understood. We therefore evaluated the role of TACE as a 'sheddase' during lung morphogenesis by analyzing the developmental phenotypes of lungs in mice with an inactive TACE gene in both in vivo and ex vivo organ explant culture. Neonatal TACE-deficient mice had visible respiratory distress and their lungs failed to form normal saccular structures. These newborn mutant lungs had fewer peripheral epithelial sacs with deficient septation and thick-walled mesenchyme, resulting in reduced surface for gas exchange. At the canalicular stage of E16.5, the lungs of TACE mutant mice were impaired in branching morphogenesis, inhibited in epithelial cell proliferation and differentiation, and delayed in vasculogenesis. Embryonic TACE knockout mouse lungs (E12) branched poorly compared to wild-type lungs, when placed into serumless organ culture. Gene expression of both surfactant protein-C and aquaporin-5 were inhibited in cultured TACE-mutant embryonic lungs, indicating defects in both branching and peripheral epithelial cytodifferentiation in the absence of TACE protein. Furthermore, both the hypoplastic phenotype and the delayed cytodifferentiation in TACE-deficient lungs were rescued by exogenous addition of soluble stimulatory factors including either TNF-[Alpha] or epidermal growth factor in embryonic lung culture. Thus, the impaired lung branching and maturation without TACE suggest a broad role for TACE in the processing of multiple membrane-anchored proteins, one or more of which is essential for normal lung morphogenesis. Taken together, our data indicate that the TACE-mediated proteolytic mechanism which enzymatically releases membrane-tethered proteins plays an indispensable role in lung morphogenesis, and its inactivation leads to abnormal lung development. [C] 2001 Academic Press Key Words: TACE; TNF-[Alpha]; EGF; ectodomain shedding; lung branching morphogenesis; lung explant culture; SP-C; vasculogenesis.

The Wnt signaling pathway has a crucial role in regulating cell growth and differentiation and is required for tissue homeostasis and repair. Although constitutive activation of the Wnt pathway can lead to abnormal cell growth and cancer, modulation of Wnt signaling might have a therapeutic benefit for tissue regeneration in numerous diseases. Recently, preclinical studies have demonstrated that treatments with antibodies against the Wnt inhibitor Dickkopf1 (DKK1) and with the positive Wnt modulator R-Spondin1 (RSpo1) were sufficient to repair the bone lesions in multiple myeloma and rheumatoid arthritis and to restore the damaged mucosa in experimental colitis, respectively. A remarkable balance is set for Wnt signaling by secreted proteins such as RSpo1 and DKK1, which help to regulate tissue homeostasis. As physiological Wnt response is essential for the regeneration of damaged tissues, modulation of the Wnt pathway might be beneficial for the treatment of multiple human diseases. [Copyright &y& Elsevier]

Background & Aims: R-spondin 1 (Rspo1) is a novel epithelial mitogen that stimulates the growth of mucosa in both the small and large intestine. Methods: We investigated the therapeutic potential of Rspo1 in ameliorating experimental colitis induced by dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) as well as nonsteroidal anti-inflammatory drug–induced colitis in interleukin (IL)-10–decifient mice. Results: Therapeutic administration of recombinant Rspo1 protein reduced the loss of body weight, diarrhea, and rectal bleeding in a mouse model of acute or chronic DSS-induced colitis. Histologic evaluation revealed that Rspo1 improved mucosal integrity in both villus and/or crypt compartments in the small intestine and colon by stimulating crypt cell growth and mucosal regeneration in DSS-treated mice. Moreover, Rspo1 significantly reduced DSS-induced myeloperoxidase activity and inhibited the overproduction of proinflammatory cytokines, including tumor necrosis factor-α, IL-1α, IL-6, interferon-γ, and granulocyte-macrophage colony–stimulating factor, in mouse intestinal tissue, indicating that Rspo1 may reduce DSS-induced inflammation by preserving the mucosal barrier function. Likewise, Rspo1 therapy also alleviated TNBS–induced interstitial inflammation and mucosal erosion in the mouse colon. Furthermore, Rspo1 substantially decreased the histopathologic severity of chronic enterocolitis by repairing crypt epithelium and simultaneously suppressing inflammatory infiltration in piroxicam-exposed IL-10−/− mice. Endogenous Rspo1 protein was localized to villus epithelium and crypt Paneth cells in mouse small intestine. Conclusions: Our results show that Rspo1 may be clinically useful in the therapeutic treatment of inflammatory bowel disease by stimulating crypt cell growth, accelerating mucosal regeneration, and restoring intestinal architecture. [Copyright &y& Elsevier]

Effective communication of cancer-related genetic and genomic testing (CGT) with patients and the public is paramount to transforming and managing cancer prevention, detection, and care. Behavioral and social science theories could improve communication effectiveness and, in turn, health outcomes. In this study, we characterized the use of theory in recent research on communication about CGT from 2010 to 2017. Of 513 empirical papers focusing on communication about CGT, only 119 (23%) utilized any theory in the study design. Behavior change and health psychology/cognitive representation theories (24.2% and 21.9%, respectively) were the most commonly used with minimal use of communication theories (3%). Theories were primarily used to guide hypotheses or research question development (73.9%), and for selecting measures or codes (68.9%). Approximately half of the papers (48.3%) related their study findings to the referenced theory. Fewer papers (14.3%) discussed implications of the findings for the theory. While theories are being utilized to inform study design, few discuss their results in the context of theoretical implications and thus decrease potential generalizability. Greater use of theory could help scholars to identify and develop theories suited to this clinical context and inform our understanding of related communication processes more broadly. • Atheoretical approaches are more prominent in communication of CGT scholarship. • These approaches limit evidence-based policy, research foci, standards of care. • Theory-driven studies use theory for RQ development and measure selection. • Majority of studies did not discuss their results to cited theory nor implications. • More theory-driven studies are needed to enhance generalizability of findings. [ABSTRACT FROM AUTHOR]

Earthworms may influence soil N 2 O emissions by stimulating free-living denitrifiers due to the restructuring of the soil environment, and by inoculating gut-stimulated denitrifying bacteria during the excretion process. However, the relative importance of each effect on soil N 2 O emissions is still not clear. To determine the differences in earthworm ( Eisenia fetida )-induced N 2 O emissions, sterilized (from which the impacts of indigenous soil microbes are limited) and unsterilized soils were used in the 30-days microcosm experiment. Earthworm inoculation improved soil ammonium ( N H 4 + –N ) , nitrate ( N O 3 − –N ) and dissolved organic carbon (DOC) concentrations in both soils. Soil N 2 O emission also increased with the addition of earthworms, but the significant difference on cumulative N 2 O emissions were only detected in the sterilized soil (362.22 and 645.86 μg N 2 O–N kg −1 dry soil with and without earthworm inoculation, respectively). Redundancy analysis indicated that the earthworm inoculation changed the soil microbial community structure in both soils. The relative density of nirS genes was significantly increased due to earthworm inoculation in sterilized soil, but no obvious difference was detected in the unsterilized soil. In conclusion, by changing the soil bacterial community via gut-stimulated denitrifiers, earthworms may increase N 2 O emissions in the sterilized soil, while this effect may be diminished by competition with indigenous soil microorganisms in unsterilized soil. [ABSTRACT FROM AUTHOR]

BPDE up-regulates lnc-HZ11, which down-regulates EGR1/NF-κB/CXCL12 pathway and suppresses trophoblast cell migration/invasion at intracellular levels. BPDE promotes donor trophoblast cells to secrete more EV-HZ11, which suppresses migration/invasion of the recipient trophoblast cells at intercellular levels, and is associated with unexplained miscarriage. Knockdown of murine lnc-Hz11 by EV-AS-Hz11 could efficiently alleviate miscarriage in BaP-exposed mice. The levels of EV-HZ11 in serum could predict the risk of miscarriage. [Display omitted] • BPDE up-regulates lnc-HZ11, which suppresses EGR1/NF-κB/CXCL12 and migration/invasion of trophoblast cells. • BPDE or lnc-HZ11 promotes trophoblast cells to secrete more EV-HZ11. • EV-HZ11 is transferred from donor cells to recipient cells and suppresses their migration/invasion. • Lnc-HZ11 and EV-HZ11 are closely associated with miscarriage. • Knockdown of murine lnc-Hz11 recovers migration/invasion and alleviates mouse miscarriage. • EV-HZ11 in serum predicts miscarriage risk. Extracellular vesicles (EVs) mediate the intercellular crosstalk by transferring functional cargoes. Recently, we have discovered that BaP/BPDE exposure suppresses trophoblast cell migration/invasion and induces miscarriage, which are also regulate by lncRNAs at intracelluar levels. However, the EVs-mediated intercellular regulatory mechanisms are completely unexplored. Specifically, whether EVs might transfer BPDE-induced toxic lncRNA to fresh recipient trophoblast cells and suppress their migration/invasion to further induce miscarriage is completely unknown. In this study, we find that BPDE exposure up-regulates a novel lnc-HZ11, which suppresses EGR1/NF-κB/CXCL12 pathway and migration/invasion of trophoblast cells. Intercellular studies show that EV-HZ11 (lnc-HZ11 in EVs), which is highly expressed in BPDE-exposed donor cells, suppresses EGR1/NF-κB/CXCL12 pathway and migration/invasion in recipient cells by transferring lnc-HZ11 through EVs. Analysis of villous tissues collected from UM (unexplained miscarriage) patients and HC (healthy control) group shows that the levels of BPDE-DNA adducts, lnc-HZ11 or EV-lnc-HZ11, and EGR1/NF-κB/CXCL12 pathway are all associated with miscarriage. Mouse assays show that BaP exposure up-regulates the levels of lnc-Hz11 or EV-Hz11, suppresses Egr1/Nf-κb/Cxcl12 pathway, and eventually induces miscarriage. Knockdown of lnc-Hz11 by injecting EV-AS-Hz11 could effectively alleviate miscarriage in BaP-exposed mice. Furthermore, EV-HZ11 in serum samples could well predict the risk of miscarriage. Collectively, this study not only discovers EVs-HZ11-mediated intercellular mechanisms that BaP/BPDE suppresses trophoblast cell migration/invasion and induces miscarriage but also provides new approach for treatment against unexplained miscarriage through EV-HZ11. [ABSTRACT FROM AUTHOR]

Context: This systematic review aims to (1) characterize strategies used to identify individuals at increased risk for hereditary breast and ovarian cancer syndrome and Lynch syndrome outside of oncology and clinical genetic settings, (2) describe the extent to which these strategies have extended the reach of genetic services to underserved target populations, and (3) summarize indicators of the potential scalability of these strategies.Evidence Acquisition: Investigators searched PubMed, EMBASE, and PsycINFO for manuscripts published from October 2005 to August 2019. Eligible manuscripts were those published in English, those that described strategies to identify those at risk for hereditary breast and ovarian cancer syndrome or Lynch syndrome, those implemented outside of an oncology or genetic specialty clinic, and those that included measures of cancer genetic services uptake. This study assessed strategies used to increase the reach of genetic risk screening and counseling services. Each study was evaluated using the 16-item quality assessment tool, and results were reported according to the PRISMA guidelines.Evidence Synthesis: Of the 16 eligible studies, 11 were conducted in clinical settings and 5 in public health settings. Regardless of setting, most (63%, 10/16) used brief screening tools to identify people with a family history suggestive of hereditary breast and ovarian cancer syndrome or Lynch syndrome. When reported, genetic risk screening reach (range =11%-100%) and genetic counseling reach (range =11%-100%) varied widely across studies. Strategies implemented in public health settings appeared to be more successful (median counseling reach=65%) than those implemented in clinical settings (median counseling reach=26%). Most studies did not describe fundamental components relevant for broad scalability.Conclusions: Efforts to expand cancer genomic services are limited outside of traditional oncology and genetic clinics. This is a missed opportunity because evidence thus far suggests that these efforts can be successful in expanding the reach of genetic services with the potential to reduce health inequities in access. This review highlights the need for accelerating research that applies evidence-based implementation strategies and frameworks along with process evaluation to understand barriers and facilitators to scalability of strategies with high reach. [ABSTRACT FROM AUTHOR]

BaP/BPDE exposure up-regulated free Fe2+ level and accelerated lipid peroxidation. Meanwhile, BaP/BPDE exposure also up-regulated MARCHF1 protein level, promoted its mediated ubiquitination degradation of GPX4, and hence decreased GPX4 protein level. Both pathways led to ferroptosis and further suppressed angiogenesis, which possibly induced miscarriage. Supplement with Gpx4 could efficiently suppress ferroptosis and recover angiogenesis in BPDE-exposed HUVECs and also alleviate miscarriage in BaP-exposed mouse miscarriage model. This study discovered novel toxicological effects and their underlying mechanisms that BaP/BPDE exposure induced ferroptosis, suppressed angiogenesis, and eventually induced miscarriage, as well as provided a promising approach to predict and treat against miscarriage. [Display omitted] • BPDE promoted HUVEC ferroptosis and suppressed angiogenesis by down-regulating GPX4 level. • BPDE promoted MARCHF1-mediated ubiquitination degradation of GPX4. • High level of BPDE-DNA adduct, ferroptosis, and defective angiogenesis in decidual tissues were associated with miscarriage. • Supplement with GPX4 suppressed ferroptosis, recovered angiogenesis, and alleviated miscarriage in BaP-exposed mouse model. • The levels of free Fe2+ and VEGFA in serum might reflect the risk of miscarriage. Environmental benzo(a)pyrene (BaP) and its ultimate metabolite BPDE (benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide) are universal and inevitable persistent organic pollutants and endocrine disrupting chemicals. Angiogenesis in placental decidua plays a pivotal role in healthy pregnancy. Ferroptosis is a newly identified and iron-dependent cell death mode. However, till now, BaP/BPDE exposure, ferroptosis, defective angiogenesis, and miscarriage have never been correlated; and their regulatory mechanisms have been rarely explored. In this study, we used assays with BPDE-exposed HUVECs (human umbilical vein endothelial cells), decidual tissues and serum samples collected from unexplained recurrent miscarriage and their matched healthy control groups, and placental tissues of BaP-exposed mouse miscarriage model. We found that BaP/BPDE exposure caused ferroptosis and then directly suppressed angiogenesis and eventually induced miscarriage. In mechanism, BaP/BPDE exposure up-regulated free Fe2+ level and promoted lipid peroxidation and also up-regulated MARCHF1 (a novel E3 ligase of GPX4) level to promote the ubiquitination degradation of GPX4, both of which resulted in HUVEC ferroptosis. Furthermore, we also found that GPX4 protein down-regulated the protein levels of VEGFA and ANG-1, two key proteins function for angiogenesis, and thus suppressed HUVEC angiogenesis. In turn, supplement with GPX4 could suppress ferroptosis, recover angiogenesis, and alleviate miscarriage. Moreover, the levels of free Fe2+ and VEGFA in serum might predict the risk of miscarriage. Overall, this study uncovered the crosstalk among BaP/BPDE exposure, ferroptosis, angiogenesis, and miscarriage, discovering novel toxicological effects of BaP/BPDE on human reproductive health. This study also warned the public to avoid exposure to polycyclic aromatic hydrocarbons during pregnancy to effectively prevent adverse pregnancy outcomes. [ABSTRACT FROM AUTHOR]

Winter-flooded paddy is a typical rice-based cropping system to conserve water for the next rice growing season. Conversion of winter-flooded paddy to rice-wheat rotation has been widely adopted with the development of the water conservation infrastructure and the government's encouragement of winter agriculture in China in recent decades. However, the effects of this conversion on N 2 O emission are still not clear. Three winter-flooded paddy fields were studied in a split-plot design. One-half of each field was converted to rice-wheat rotation (RW), and the other half remained winter-flooded as rice-fallow (RF). Each plot of RW and RF was further divided into four subplots: three subplots for conventional N fertilizer application (RW-N C and RF-N C ) and one for unfertilized treatment (RW-N 0 and RF-N 0 ). Conversion of RF-N C to RW-N C increased the N 2 O emission up to 6.6-fold in the first year and 4.4-fold in the second year. Moreover, N 2 O emissions for the entire wheat season were 1.74–3.74 kg N ha −1 and 0.24–0.31 kg N ha −1 from RW-N C and RW-N 0 , respectively, and accounted for 78%–94% and 78%–97% of the total annual amount. N 2 O emitted during the first 11–21 days of the wheat season from RW-N C was 1.48–3.28 kg N ha −1 and that from RW-N 0 was 0.14–0.17 kg N ha −1 , which contributed to 66%–82% and 45%–71% of the total annual amount, respectively. High N 2 O fluxes occurred when the soil water-filled pore space (WFPS) was in the range of 68%–72% and the ratio of available carbon to nitrogen in the soil was <1.42. The contribution of WFPS and dissolved organic carbon (DOC) explained most of the variation of the N 2 O fluxes compared with the other measured environmental and soil factors. These findings suggest that the conversion of winter-flooded paddy to rice-wheat rotation increased N 2 O emissions that could be mitigated by controlling the soil moisture and ratio of available soil carbon to nitrogen. [ABSTRACT FROM AUTHOR]

The conversion from rice to vegetable production widely occurs in China. However, the effects of this conversion on N 2 O emission and the underlying mechanisms are not well understood. In the present study, 12 rice paddies (R) were selected and half of them converted to vegetable fields (V) with the following treatments: rice paddies without N-fertilizer (R-CK), rice paddies with conventional N-fertilizer (R-CN), converted vegetable fields without N-fertilizer (V-CK), and converted vegetable fields with conventional N-fertilizer (V-CN) in a randomized block design with 3 replicates. N 2 O emissions were measured with static chambers from December 2012 to December 2015. Within each V-CN plot, a root exclusion subplot was established to measure soil heterotrophic respiration (CO 2 effluxes), a proxy for soil organic matter mineralization. Conversion of rice paddies to vegetable production dramatically increased N 2 O emissions. The three-year cumulative N 2 O emissions were 0.59, 1.90, 55.50 and 160.14 kg N ha − 1 for R-CK, R-CN, V-CK and V-CN, respectively. The annual N 2 O emissions from vegetable fields ranged between 5.99 and 113.45 kg N ha − 1 yr − 1 , with substantially higher emissions in the first year. N 2 O fluxes from V-CN were significantly and positively related to CO 2 fluxes and inorganic N concentrations. The linear relationship between natural logarithms of N 2 O and CO 2 fluxes was stronger and the regression coefficient higher in the first year, showing the dependence of N 2 O on soil organic matter mineralization. These results suggest that soil organic matter and N mineralization contributes significantly to N 2 O emission following conversion of rice paddies to vegetable production. [ABSTRACT FROM AUTHOR]