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Yao Huang

Publications and source records attributed to Yao Huang.

35 records · Page 2Linked to original sources

Efficacy and safety of two unfractionated heparin dosing strategies with tenecteplase in acute myocardial infarction (results from Assessment of the Safety and Efficacy of a New Thrombolytic Regimens 2 and 3).

We investigated the effect of smaller dose, weight-adjusted heparin with earlier monitoring of activated partial thromboplastin time on the incidence of ischemic and hemorrhagic complications in patients with ST-elevation myocardial infarction treated with full-dose tenecteplase. We compared the outcomes of patients enrolled in the Second Assessment of the Safety and Efficacy of a New Thrombolytic Regimen (ASSENT-2; n = 8,461) who received heparin stratified by weight (patients weighing >67 kg received a 5,000-U bolus plus infusion at 1,000 U/hour; those weighing < or =67 kg received a 4,000-U bolus plus infusion at 800 U/hour) with patients in ASSENT-3 who received weight-adjusted heparin (60-U/kg bolus, maximum 4,000 U/hour, followed by a 12-U/kg/hour infusion, maximum 1,000 U/hour). Compared with patients in ASSENT-2, those in ASSENT-3 had similar rates of 30-day mortality, recurrent infarction, and intracranial hemorrhage, less major bleeding (2.2% vs 4.7%, p <0.001), and less refractory ischemia (6.5% vs 8.6%, p <0.001). After adjustment for baseline characteristics, patients in ASSENT-3 had similar rates of 30-day mortality (odds ratio [OR] 0.96, 95% confidence interval [CI] 0.77 to 1.19) and intracranial hemorrhage (OR 1.02, 95% CI 0.61 to 1.69) but less major bleeding (OR 0.49, 95% CI 0.35 to 0.67) than did patients in ASSENT-2. These findings support the use of smaller dose, weight-adjusted heparin in patients with ST-elevation myocardial infarction treated with tenecteplase.

Aged↗

Growth hormone alters epidermal growth factor receptor binding affinity via activation of extracellular signal-regulated kinases in 3T3-F442A cells.

Epidermal growth factor receptor (EGFR) is a transmembrane protein that binds EGF in its extracellular domain and initiates signaling via intrinsic tyrosine kinase activity in its cytoplasmic domain. EGFR is important in development, cellular proliferation, and cancer. GH is a critical growthpromoting and metabolic regulatory hormone that binds the GH receptor, thereby engaging various signaling pathways, including ERKs. Prior studies suggest cross-talk between the GH receptor and EGFR signaling systems. Using the GH- and EGF-responsive 3T3-F442A preadipocyte, we previously observed that GH, in addition to causing EGFR tyrosine phosphorylation, also induced EGFR phosphorylation that was detected by PTP101, an antibody reactive with ERK consensus phosphorylation sites. This latter phosphorylation was prevented by pretreatment with MAPK kinase (MEK)1 inhibitors, suggesting ERK pathway dependence. Furthermore, GH cotreatment with EGF markedly slowed EGF-induced EGFR degradation and down-regulation, thereby potentiating EGF-induced EGFR signaling. These effects were also MEK1 dependent and suggested ERK pathway-dependent influence of GH on EGF-induced EGFR postendocytic trafficking and signaling. We now explore the impact of GH on cell surface binding of EGF in 3T3-F442A cells. We found that GH pretreatment caused transient, but substantial, lessening of (125)I-EGF binding. Competitive binding experiments revealed that the decreased binding was primarily due to decreased affinity, rather than a change in the number of EGF binding sites. The effect of GH on EGF binding was concentration dependent and temporally correlated with GH-induced ERK activation and EGFR PTP101-reactive phosphorylation. Blockade of the MEK1/ERK but not the protein kinase C pathway, prevented GH's effects on EGF binding, and our results indicate that the mechanisms of GH- and phorbol-12-myristate-13-acetateinduced inhibition of EGF binding differ substantially. Overall, our findings suggest that GH can modulate both EGF binding kinetics and the EGFR's postbinding signaling itinerary in a MEK1/ERK pathway-dependent fashion.

3T3 Cells↗

Physical and functional interaction of growth hormone and insulin-like growth factor-I signaling elements.

GH and IGF-I are critical regulators of growth and metabolism. GH interacts with the GH receptor (GHR), a cytokine superfamily receptor, to activate the cytoplasmic tyrosine kinase, Janus kinase 2 (JAK2), and initiate intracellular signaling cascades. IGF-I, produced in part in response to GH, binds to the heterotetrameric IGF-I receptor (IGF-IR), which is an intrinsic tyrosine kinase growth factor receptor that triggers proliferation, antiapoptosis, and other biological actions. Previous in vitro and overexpression studies have suggested that JAKs may interact with IGF-IR and that IGF-I stimulation may activate JAKs. In this study, we explore interactions between GHR-JAK2 and IGF-IR signaling pathway elements utilizing the GH and IGF-I-responsive 3T3-F442A and 3T3-L1 preadipocyte cell lines, which endogenously express both the GHR and IGF-IR. We find that GH induces formation of a complex that includes GHR, JAK2, and IGF-IR in these preadipocytes. The assembly of this complex in intact cells is rapid, GH concentration dependent, and can be prevented by a GH antagonist, G120K. However, it is not inhibited by the kinase inhibitor, staurosporine, which markedly inhibits GHR tyrosine phosphorylation. Moreover, complex formation does not appear dependent on GH-induced activation of the ERK or phosphatidylinositol 3-kinase signaling pathways or on the tyrosine phosphorylation of GHR, JAK2, or IGF-IR. These results suggest that GH-induced formation of the GHR-JAK2-IGF-IR complex is governed instead by GH-dependent conformational change(s) in the GHR and/or JAK2. We further demonstrate that GH and IGF-I can synergize in acute aspects of signaling and that IGF-I enhances GH-induced assembly of conformationally active GHRs. These findings suggest the existence of previously unappreciated relationships between these two hormones.

3T3 Cells↗

Caveolar and lipid raft localization of the growth hormone receptor and its signaling elements: impact on growth hormone signaling.

The growth hormone receptor (GHR) is a cell surface receptor that mediates the somatogenic and metabolic effects of the growth hormone (GH). GHR signaling is transduced via the receptor-associated cytoplasmic tyrosine kinase called Janus protein kinase 2 (JAK2). The major intracellular signaling systems activated by JAK2 in response to GH include the signal transducer and activator of transcription (STAT) 5 and extracellular signal-regulated kinase (ERK)-1 and -2 pathways. In this report, we investigate the role of cholesterol-rich plasma membrane microdomains (caveolae and lipid rafts) in GH signaling. By subcellular fractionation of the GH-responsive 3T3-F442A murine preadipocyte, we found dramatic enrichment (6.7-fold) of plasma membrane GHR in the caveolae membranes (CM). JAK2 was also represented in the CM fraction, but was less enriched (2.5-fold) than GHR. ERK1/2 and the important ERK pathway upstream small adaptor protein, Grb2 (growth factor receptor-bound protein 2), were also enriched in caveolae (2.3- and 8.3-fold, respectively), but STAT5 was barely detected in the same fraction. Correspondingly, GH-induced tyrosine-phosphorylated GHR, JAK2, and ERK1/2 were highly represented in the CM fraction, whereas tyrosine-phosphorylated STAT5 was enriched in the non-membranous fraction of the post-nuclear supernatant. Additionally, GH induced further accumulation of GHR, Grb2, and SHC proteins in the CM fraction. Interestingly, treatment of the cells with the caveolae-disrupting agent, methyl-beta-cyclodextrin (mbetaCD), selectively inhibited GH-induced ERK1/2 activation but not STAT5 phosphorylation; repletion of cholesterol in mbetaCD-treated cells restored GH-induced ERK activation. Comparison of 3T3-F442A cells with the GHR-expressing human IM-9 lymphoblasts revealed similar enrichment of GHR in the lipid raft fraction of IM-9 as in the CM fraction of 3T3-F442A, but there were dramatic differences in the ERKs and Grb2. The IM-9 cell, in which ERKs are not activated by GH, displayed no enrichment of ERKs and Grb2 in the lipid raft fraction. Our results suggest that localization of GHRs in the CM fraction of the plasma membrane plays important roles in signaling.

3T3 Cells↗

[CO2 emission from soil-crop system as influenced by crop growth and tissue N content].

To understand the CO2 emission from soil-crop system as influenced by crop growth and tissue N content, pot and field experiments were carried out during 2001-02 wheat and rice growing seasons. Black chambers were used to take gas samples within a closed soil-crop system. The CO2 emission rate was detected by a gas chromatograph. Seasonal change of the CO2 emission was observed from the soil-crop system. Respiration from the soil-rice system was higher than that from the soil-wheat system. Dark respiration of the crop shoot was positively correlated to the shoot biomass. The respiration coefficient Rd, defined as the amount of CO2-C respired by per unit biomass C within one day under a reference temperature of 25 degrees C, can be well quantitatively expressed by shoot N content for either wheat or rice crop. Relationship between the Rd and the N content can be described as a linear regression of Rd = 0.0124N - 0.0076 (R2=0.9879, p<0.001) for the wheat crop and as a quadratic equation of Rd = 0.0085N2 - 0.0049N (R2=0.9776, p<0.001) for the rice crop, respectively. The crop roots promoted the soil respiration greatly, which increased by 178% for the wheat and 338% for the rice in comparison with the respiration from root-free soil. A further calculation of the root respiration, including root autotrophic respiration and rhizosphere respiration, suggested that the contribution of crop rhizosphere respiration to the total soil respiration was greater in the upland soil than that in the irrigated paddy soil.

Carbon Dioxide↗

Growth hormone-induced phosphorylation of epidermal growth factor (EGF) receptor in 3T3-F442A cells. Modulation of EGF-induced trafficking and signaling.

Growth hormone (GH) promotes signaling by causing activation of the non-receptor tyrosine kinase, JAK2, which associates with the GH receptor. GH causes phosphorylation of epidermal growth factor receptor (EGFR; ErbB-1) and its family member, ErbB-2. For EGFR, JAK2-mediated GH-induced tyrosine phosphorylation may allow EGFR to serve as a scaffold for GH signaling. For ErbB-2, GH induces serine/threonine phosphorylation that dampens basal and EGF-induced ErbB-2 kinase activation. We now further explore GH-induced EGFR phosphorylation in 3T3-F442A, a preadipocytic fibroblast cell line that expresses endogenous GH receptor, EGFR, and ErbB-2. Using a monoclonal antibody that recognizes ERK consensus site phosphorylation (PTP101), we found that GH caused PTP101-reactive phosphorylation of EGFR. This GH-induced EGFR phosphorylation was prevented by MEK1 inhibitors but not by a protein kinase C inhibitor. Although GH did not discernibly affect EGF-induced EGFR tyrosine phosphorylation, we observed by immunoblotting a substantial decrease of EGF-induced EGFR degradation in the presence of GH. Fluorescence microscopy studies indicated that EGF-induced intracellular redistribution of an EGFR-cyan fluorescent protein chimera was markedly reduced by GH cotreatment, in support of the immunoblotting results. Notably, protection from EGF-induced degradation and inhibition of EGF-induced intracellular redistribution afforded by GH were both prevented by a MEK1 inhibitor, suggesting a role for GH-induced ERK activation in regulating the trafficking itinerary of the EGF-stimulated EGFR. Finally, we observed augmentation of early aspects of EGF signaling (EGF-induced ERK2 activation and EGF-induced Cbl tyrosine phosphorylation) by GH cotreatment; the GH effect on EGF-induced Cbl tyrosine phosphorylation was also prevented by MEK1 inhibition. These data indicate that GH, by activating ERKs, can modulate EGF-induced EGFR trafficking and signaling and expand our understanding of mechanisms of cross-talk between the GH and EGF signaling systems.

3T3 Cells↗

[Application of spiral CT and post-image processing technique in the staging of central lung cancer].

OBJECTIVE: To assess image processing techniques including multiplanar reconstruction (MPR), volume rendering technique (VRT) and spiral CT angiography (SCTA) in the staging of central lung cancer (CLC), with transverse image, pathology and findings on the operation table as comparison. METHODS: Forty-six suspected CLC received spiral CT examination, on basis of prospective randomization, by a Picker 6 000 scanner. Contrast medium was injected at a rate of 4 ml/s with a power injector. The study volume done in a single breath-hold was from the aortic arch to the inferior pulmonary veins, using 3-mm collimation, pitch of 1.0 and reconstruction at 1-mm interval. Six patients were excluded after operation. Transverse CT scans, MPR and VR images were studied in a double-blind way by 3 experienced radiologists, with the findings compared with the surgical and pathological results. RESULTS: Post-processing image was more accurate than transverse CT scan in T categories (95.7% vs 82.6%), chi(2) = 4.039, P = 0.044. Four cases of N3 category on transverse CT scans were not proved by surgical or pathological results. The sensitivity, specificity and accuracy rates in N categories were 75.0% (12/16), 26.9% (7/26) and 45.2% (19/42). The accuracy rate of staging was 58.7% (27/46) by transverse CT scans and 67.4% (31/46) by post-processing images (chi(2) = 0.746, P = 0.338). CONCLUSION: Post-processing image is more accurate than transverse image in T categorizing.

Adult↗

[Greenhouse gases emission or uptake in Inner Mongolia natural and free-grazing grasslands].

GC-MS was used to measure the greenhouse emission of Inner Mongolia Grassland. The results showed that four kinds of typical semi-arid grasslands in Inner Mongolia had their own special seasonal patterns as the source of atmospheric N2O and CO2 emission and the sink of atmopsheric CH4, which were controlled by seasonal weather variation. Different soil and vegetation types and precipitation influenced the intensity of emission and upatake of the gases. Compared with natural grassland, free grazing decreased CH4 uptake and N2O emission, but increased CO2 emission.

Animal Feed↗

[Integrated effect of incorporation with different organic manures on CH4 and N2O emissions from rice paddy].

Field experiment was conducted in 2001 rice growing season to understand the effect of organic manure application on CH4 and N2O emissions. Five treatments of fertilizer including urea and NH4HCO3 used as chemical fertilizer (CF), chemical fertilizer + pig manure (CF + PM), chemical fertilizer + cow manure (CF + CM), chemical fertilizer + rapeseed cake (CF + RC) and chemical fertilizer + wheat straw (CF + WS) were dedicated to this experiment. Results from the field observations indicated that application of the organic manure did not change the seasonal pattern of CH4 and N2O emissions but significantly affected the seasonal amounts. Seasonal amount of CH4 emission from the treatments of CF + CM, CF + RC and CF + WS was respectively 45%, 252% and 250% higher than that from the treatment of CF, but the application of pig manure (CF + PM) did not significantly influence the CH4 emission. The N2O emissions, on the other hand, were reduced by 18%, 21% and 18% for the treatments of CF + PM, CF + CM and CF + WS, respectively. Incorporation of rapeseed cake enhanced the N2O emission, yielding an increment of 22%. On a time scale of 20-year period, the integrated global warming potential (GWP) of CH4 + N2O released during the rice growing season for the treatments of CF + RC, CF + WS and CF + CM was respectively 154%, 136% and 17% higher than that for the CF treatment, while a reduction of 10% was obtained for the CF + PM treatment. The calculation of the GWP per unit rice grain yield suggested that the application of pig manure took the slight advantages not only in reducing the GWP but also in improving the grain yield.

Manure↗

Metalloprotease-mediated GH receptor proteolysis and GHBP shedding. Determination of extracellular domain stem region cleavage site.

Growth hormone-binding protein (GHBP) is complexed to a substantial fraction of circulating GH. In humans, rabbits, and other species, GHBP derives from proteolytic shedding of the GH receptor (GHR) extracellular domain. In cell culture studies, stimuli such as phorbol ester, platelet-derived growth factor, or serum induce GHR proteolysis, which concomitantly yields shed GHBP in cell supernatants and a cell-associated cytoplasmic domain-containing GHR remnant. This process is sensitive to metalloprotease inhibition, and genetic reconstitution studies identify tumor necrosis factor-alpha converting enzyme (TACE/ADAM-17), a transmembrane metalloprotease, as a GHR sheddase. Stimuli that induce GHR proteolysis render cells less responsive to GH, but the mechanism(s) of this desensitization is not yet understood. In this study, we mapped the rabbit (rb) GHR cleavage site. We adenovirally expressed a C-terminal epitope-tagged rbGHR lacking most of its cytoplasmic domain, purified the remnant protein induced by the phorbol ester, PMA, and derived the cleavage site by N-terminal sequencing of the purified remnant. The N-terminal sequence, (239)FTCEEDFR(246), matched perfectly the rbGHR and suggests that cleavage occurs eight residues from the membrane in the proximal extracellular domain stem region. Deletion and alanine substitution mutagenesis indicated that, similar to other TACE substrates, the spacing of residues in this region, more than their identity, influences GHR cleavage susceptibility. Further, we determined that PMA pretreatment desensitized a cleavage-sensitive GHR mutant, but not a cleavage-insensitive mutant, to GH-induced JAK2 activation. These results suggest that inducible GHR proteolysis can regulate GH signaling.

Amino Acid Sequence↗

Randomized COMparison of platelet inhibition with abciximab, tiRofiban and eptifibatide during percutaneous coronary intervention in acute coronary syndromes: the COMPARE trial. Comparison Of Measurements of Platelet aggregation with Aggrastat, Reopro, and Eptifibatide.

BACKGROUND: The relative anti-aggregatory effects of currently prescribed platelet glycoprotein IIb/IIIa receptor antagonists during and after percutaneous coronary intervention for acute coronary syndromes have not been established. METHODS AND RESULTS: We randomized 70 acute coronary syndrome patients undergoing percutaneous coronary intervention to receive abciximab, eptifibatide, or tirofiban at doses used in the Evaluation of Platelet IIb/IIIa Inhibitor for STENTing (EPISTENT), Platelet glycoprotein IIb/IIIa in Unstable angina Receptor Suppression Using Integrilin Therapy (PURSUIT), and Platelet Receptor Inhibition in ischemic Syndrome Management in Patients Limited by Unstable Signs and symptoms (PRISM-PLUS)/Randomized Efficacy Study of Tirofiban for Outcomes and Restenosis (RESTORE) trials, respectively. Platelet aggregation (PA) in response to 20 micro mol/L of adenosine diphosphate was measured with turbidimetric aggregometry in both D-phenylalanyl-L-prolyl-L-arginine chloromethylketone and citrate-anticoagulated blood early (15 and 30 minutes) and late (4, 12, and 18 to 24 hours) after drug initiation. At 15 and 30 minutes, PA was significantly less inhibited by the tirofiban-RESTORE regimen compared with abciximab (P=0.028) and eptifibatide regimens (P=0.0001). The abciximab regimen, however, showed increasingly varied anti-aggregatory effects during continued infusion for > or =4 hours. Citrate exaggerated ex vivo platelet inhibition after eptifibatide and tirofiban, but had the opposite effect on abciximab. Of all regimens evaluated, the eptifibatide regimen inhibited PA most consistently throughout both the early and late periods. CONCLUSIONS: Currently recommended drug regimens to inhibit the platelet glycoprotein IIb/IIIa receptor have distinct pharmacodynamic profiles that might affect their relative efficacy in acute coronary syndromes and percutaneous coronary intervention.

Abciximab↗

Sustained ventricular arrhythmias among patients with acute coronary syndromes with no ST-segment elevation: incidence, predictors, and outcomes.

BACKGROUND: The prognosis of ventricular arrhythmias among patients with non-ST-elevation acute coronary syndromes is unknown. We studied the incidence, predictors, and outcomes of sustained ventricular arrhythmias in 4 large randomized trials of such patients. METHODS AND RESULTS: We pooled the datasets of the Global Use of Streptokinase and tPA for Occluded Arteries (GUSTO)-IIb, Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT), Platelet IIb/IIIa Antagonism for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network (PARAGON)-A, and PARAGON-B trials (n=26 416). We identified independent predictors of ventricular fibrillation (VF) and ventricular tachycardia (VT) and compared the 30-day and 6-month mortality rates of patients who did (n=552) and did not (n=25 864) develop these arrhythmias during the index hospitalization. Independent predictors of in-hospital VF included prior hypertension, chronic obstructive pulmonary disease, prior myocardial infarction, and ST-segment changes at presentation. Except for hypertension, these variables also independently predicted in-hospital VT. In Cox proportional-hazards modeling, in-hospital VF and VT were independently associated with 30-day mortality (hazard ratio [HR], 23.2 [95% CI, 18.1 to 29.8] for VF and HR, 7.6 [95% CI, 5.5 to 10.4] for VT) and 6-month mortality (HR, 14.8 [95% CI, 12.1 to 18.3] for VF and HR, 5.0 [95% CI, 3.8 to 6.5] for VT). These differences remained significant after excluding patients with heart failure or cardiogenic shock and those who died <24 hours after enrollment. CONCLUSIONS: Despite the use of effective therapies for non-ST-elevation acute coronary syndromes, ventricular arrhythmias in this setting are associated with increased 30-day and 6-month mortality. More effective therapies are needed to improve the survival of patients with these arrhythmias.

Acute Disease↗

The Asian nitrogen cycle case study.

We analyzed nitrogen budgets at national and regional levels on a timeline from 1961-2030 using a model, IAP-N 1.0. The model was designed based upon the Inter-governmental Panel on Climate Change (IPCC) methods using Asia-specific parameters and a Food and Agriculture Organization of the United Nations (FAO) database. In this paper we discuss new reactive-nitrogen and its various fates, and environmental nitrogen enrichment and its driving forces. The anthropogenic reactive nitrogen of Asia dramatically increased from approximately 14.4 Tg N yr-1 in 1961 to approximately 67.7 Tg N yr-1 in 2000 and is likely to be 105.3 Tg N yr-1 by 2030. Most of the anthropogenic reactive-nitrogen has accumulated in the environment. We found that an increasing demand for food and energy supplies and the lack of effective measures to improve the efficiency of fertilizer nitrogen use, as well as effective measures for the prevention of NOx emissions from fossil-fuel combustion, are the principal drivers behind the environmental nitrogen-enrichment problem. This problem may be finally solved by substituting synthetic nitrogen fertilizers with new high-efficiency nitrogen sources, but solutions are dependent on advances in biological technology.

Asia↗

[Influence of environmental factors on the decomposition of organic carbon in agricultural soils].

To quantitatively investigate the effects of environmental factors on organic carbon decomposition, CO2-C was measured from the incubation of wheat and rice straw as well as their roots mixed with a paddy soil over a 90-day period. Results showed that decomposition of the straw carbon was faster than that of the roots. Amount of CO2-C released from the organic matter decomposition was quantitatively related to its properties of C/N ratio. Increase of temperature within a lower temperature range enhanced greatly the decomposition while such an enhancement weakened within a higher temperature range. Under the moist condition, the temperature coefficient of organic carbon decomposition declined exponentially with the incubation time. The temperature coefficient did not significantly decrease with the time for the submerged condition after one-week incubation. The effect of water status showed that the decomposition at the water contents of 300 g.kg-1 and 500 g.kg-1 was faster than that under the treatments of 200 g.kg-1 and the submerged. Within the first month period of incubation, carbon amount released from the incubation of wheat straw was negatively related to the clay fraction of the soils.

Agriculture↗

[Methane emission from rice paddy soils as influenced by soil physicochemical properties].

To identify the key soil parameters influencing methane emission from rice paddies, and to quantitatively describe the relationship of methane emission with the soil properties, an outdoor pot experiment with a total of 18 paddy soils sampled from different regions in Jiangsu province was conducted in Nanjing Agricultural University during 2000 rice growing season. Seasonal average rate of CH4 emission for all the 18 soils was 6.42 +/- 2.70 mg.(m2.h)-1, ranging from 1.96 to 11.06 mg.(m2.h)-1, approximately a 5.6-fold difference between the maximum and the minimum. Correlation analysis indicated that the seasonal average of CH4 emission was positively dependent on soil sand content (r = 0.528, p = 0.024) and negatively on soil clay content (r = -0.484, p = 0.042). Negative correlation of CH4 emission against soil total nitrogen (r = -0.449, p = 0.062), available nitrogen (r = -0.611, p = 0.007) and NH4(+)-N(r = -0.649, p = 0.004) was also observed. Copper content of soils has a significant negative impact on CH4 emission. The correlation coefficient (r) of CH4 emission against soil available copper and with total copper was -0.594 (p = 0.009) and -0.547 (p = 0.019), respectively. No clear relationship existed between CH4 emission and soil carbon content. A further investigation suggests that the seasonal average rate of CH4 emission can be quantitatively determined by a linear combination of soil available copper, total manganese, and a ratio of available to total iron (R2 = 0.755, p = 0.0001).

Methane↗

[Determination of net exchange of CO2 between paddy fields and atmosphere with static poaque-chamber-based measurements].

We firstly introduced the method for determining the net ecosystem exchange fluxes of CO2 (NEE) between croplands and atmosphere, based on field measurements using static opaquechamber/gas chromatography methods was introduced, and the application of this method in the FACE (free-air CO2 enrichment) study to examine the effects of elevated CO2 on the NEE over a typical paddy ecosystem was carried out, because of lacking in observation data for some necessary parameters, e.g., dark maintenance respiration coefficient, only the minimum value of NEE (NEEmin) was calculated based on opaque-chamber measurements. The NEEmin data indicate that CO2 elevated by 200 +/- 40 mumol.mol-1 significantly increased the ecosystem uptake of atmospheric CO2 by a factor ca. 3. To accurately determine the NEE based on opaquechamber measurements, dark maintenance respiration coefficient, above-ground biomass and root: shoot, i.e. R:S, ratio of root to shoot should be observed over the whole growing season.

Air↗

[Effects of elevated atmospheric CO2 on CH4 and N2O emissions from paddy fields].

Effects of elevated atmospheric CO2 on CH4 and N2O emissions during the paddy rice-growing season were examined in a FACE (free-air carbon dioxide enrichment) study. The emission fluxes of CH4 and N2O from paddy rice fields were measured using methods based on static opaque-chamber and gas chromatography techniques. Synthetic fertilizer N was amended for the rice-growing season at two rates, 150 and 250 kgN.hm-2 and the atmospheric CO2 was enriched by 200 mumol.mol-1. At both N levels, the preliminary results indicate that no significant effect of CO2 enrichment on CH4 and N2O emissions from the rice paddy fields was detected. The result on CH4 emissions is inconsistent with the most literatures, and the result on N2O emissions is consistent with the most literatures.

Air↗