Carbon flow through continental-scale ground logistics transportation.

The flourishing logistics in both developed and emerging economies leads to huge greenhouse gas (GHG) emissions; however, the emission fluxes are poorly constrained. Here, we constructed a spatial network of logistic GHG emissions based on multisource big data at continental scale. GHG emissions related to logistics transportation reached 112.14 Mt CO2-equivalents (CO2e), with seven major urban agglomerations contributing 63% of the total emissions. Regions with short transport distances and well-developed road infrastructure had relatively high emission efficiency. Underlying value flow of the commodities is accompanied by logistics carbon flow along the supply chain. The main driving factors affecting GHG emissions are driving speed and gross domestic product. It may mitigate GHG emissions by 27.50-1162.75 Mt CO2e in 15 years if a variety of energy combinations or the appropriate driving speed (65-70 km/h) is adopted. The estimations are of great significance to make integrated management policies for the global logistics sector.

[Estimating Methane Fugitive Emissions from Oil and Natural Gas Systems in China].

To achieve its carbon peaking and carbon neutrality objectives, China is committed to promoting a decarbonized energy transition, which has strengthened the shift from coal to oil and gas resources. As a result, methane (CH4) fugitive emissions from China's oil and gas systems are of increasing concern. Fugitive emissions include equipment leaks, venting, and flaring and involve exploration, production, transportation, storage, and distribution of oil and gas resources. However, there is no uniform accounting method for methane fugitive emissions from oil and gas systems, and fugitive emissions have not been included in the national greenhouse gas inventory statistics. Using the relevant methods, methane fugitive emissions from China's oil and gas systems were estimated for the period from 1980-2020. The results showed that CH4 fugitive emissions from oil and gas systems increased rapidly with the growth of production and consumption of oil and gas resources, from less than 0.6 million tons in 1980 to more than 2.6 million tons in 2020. CH4 fugitive emissions from oil and gas systems reached approximately 0.6 million tons and 2.0 million tons, which were 1.38 and 16.6 times larger than those in 1980, respectively. Fugitive emissions from oil and gas systems originated primarily from gas production, oil production, gas transportation, and storage, accounting for 41%, 20%, 18%, and 13% of total emissions, respectively. Gas pipelines were the main fugitive facilities. The emission intensity of unconventional oil and gas resource exploration was higher compared to conventional resource exploration. This study improved the CH4 fugitive emission inventory, which could provide solid scientific data for CH4 reduction.

The effect of different treatments of lymph after intestinal ischemia-reperfusion in rats on macrophages in vitro.

BACKGROUND: To observe the effects of different treatments of lymph after intestinal I/R in rats on macrophages in vitro. METHODS: Forty-eight healthy SPF SD rats weighing 300 ± 20 g, were randomly divided into two groups: group A, and group B. The rats in group A were drained of lymph fluid for 180 min; the rats in group B were subjected to 60 min ischemia by clamping the SMA, followed by 120 min reperfusion and 180 min of lymph drainage. The lymph fluid collected was divided into 4 sub-groups: 1. no treatment (A1, Ly, and B1, I/R Ly); 2. protein degradation (A2, Ly PD, and B2 I/R PD); 3. endotoxin removal (A3, Ly ER, and B3, I/R ER); 4. protein degradation plus endotoxin removal (A4, Ly PD+ER, and B4, I/R PD+ER), then used to stimulate a monocyte-macrophage cell line. RESULTS: Compared with group A1, the levels of the inflammatory cytokines, chemokines, HMGB1 concentration, protein and mRNA expression of TLR4, HMGB1 and NF-κBp65 were significantly increased in group B1. There was a significant reduction in proinflammatory cytokines and of the expression of TLR4, NF-κBp65, and chemokines in groups A2, B2, A4, and B4. However, there were no significant decrease of these factors in groups A3 and B3. CONCLUSIONS: The lymph fluid drained after intestinal I/R can cause inflammation in vivo and in vitro. Deproteinization of lymph fluid with proteinase K significantly reduced the concentration of proinflammatory cytokines, chemokines, TLR4 and NF-κBp65 in cell culture supernatant, exerting a protective effect on inflammatory reaction caused by the intestinal I/R. Passage of lymph fluid through an endotoxin removal column did not reduce the levels of active proinflammatory factors produced by macrophages in vitro.

Public perception and attitude towards chemical industry park in Dalian, Bohai Rim.

Recent decade has witnessed accelerating expansion of chemical industry and increasing conflicts between the local citizens, governmental authorities and project developers, especially in some coastal and port cities in China. Development and transformation of chemical industrial parks has been adopted as a national initiative recently. However, there is a paucity of research examining public perspectives on chemical industrial parks and their risks. Aiming to understand public perception, attitude, and response and the factors underlying the support/acceptance of chemical industry park, this paper investigated 418 residents neighboring to two chemical industrial parks, Dalian in Bohai Rim through face-to-face questionnaire survey. The results showed the knowledge of the respondents on the chemical industrial parks development was very limited. The respondents had complex perceptions on the environmental impacts, risks control, social-economic benefits, and problem awareness. The current levels of information disclosure and public participation were very low. The central governmental official (44.3%) was the most trustworthy group by the respondents. Only 5.5% and 23.2% of the respondents supported the construction of a new CIP nearby and far away their homes, whilst 13% thought new CIP project as acceptable. The spearman correlation analysis results showed a strong NIMBY effect (Not In My Backyard). Factor analysis results demonstrated five latent factors: knowledge, benefit, information, trust, and participation. Multiple linear regression analysis indicated how socio-demographic differences and five latent factors might impact on the support/acceptance of the chemical industrial parks. Education level, trust, information, and participation were significant predictors of public support/acceptance level. This study contributes to our limited knowledge and understanding of public sentiments to the chemical industry parks in China.

Determination of water environment standards based on water quality criteria in China: Limitations and feasibilities.

There is a need to formulate water environment standards (WESs) from the current water quality criteria (WQC) in China. To this end, we briefly summarize typical mechanisms applied in several countries with longer histories of developing WESs, and three limitations to formulating WESs in China were identified. After analyzing the feasibility factors including economic development, scientific support capability and environmental policies, we realized that China is still not ready for a complete change from its current nation-wide unified WES system to a local-standard-based system. Thus, we proposed a framework for transformation from WQC to WESs in China. The framework consists of three parts, including responsibilities, processes and policies. The responsibilities include research authorization, development of guidelines, and collection of information, at both national and local levels; the processes include four steps and an impact factor system to establish water quality standards; and the policies include seven specific proposals.

Pretreatment with the ALDH2 agonist Alda-1 reduces intestinal injury induced by ischaemia and reperfusion in mice.

Many studies demonstrate that activation of aldehyde dehydrogenase 2 (ALDH2) protects against oxidative stress via detoxification of cytotoxic aldehydes, and could attenuate cardiac, cerebral, lung and renal ischaemia-reperfusion (I/R) injuries. However, the effect of ALDH2 in intestinal I/R is unknown. The present study was set up to determine whether an ALDH2 agonist, Alda-1, could alleviate intestinal injury after gut I/R. In a mouse model of intestinal I/R injury, histological grading, proinflammatory cytokines, oxidative stress, cellular apoptosis, chemokine contents, ALDH2 activity, 4-hydroxy-trans-2-nonenal (4-HNE) and malondialdehyde (MDA) were evaluated. The results indicated that I/R treatment conferred elevation in pathological scores, proinflammatory cytokines, oxidative stress, cellular apoptosis and chemokine levels, accompanied by accumulated 4-HNE and MDA. No significant changes in ALDH2 activity were observed after I/R. However, Alda-1 pretreatment significantly decreased these injurious indicators, concomitant with up-regulated ALDH2 activity, and lessened 4-HNE and MDA accumulation. Taken together, our results implicate activation of ALDH2 by Alda-1 in the significant abatement intestinal I/R injury.

Down-regulation of toll-like receptor 4 alleviates intestinal ischemia reperfusion injury and acute lung injury in mice.

Intestinal ischemia reperfusion (IR) injury is a critical problem, which can cause intestinal injury locally and acute lung injury (ALI) distally by inflammatory responses and oxidative stress. Toll-like receptor 4 (TLR4) is involved in innate immune and inflammatory responses. This study was to determine whether TLR4 mutant can attenuate intestinal and lung injuries after intestinal IR. Wild type (WT) and TLR4 mutant mice were submitted to intestinal IR by occluding the superior mesenteric artery. Histological assessment of the intestine and the lung were conducted by HE staining. The levels of proinflammatory cytokines, oxidative stress markers, apoptotic index and other mediators were measured. In addition, a 24-hour survival study was performed. Histological assessment showed that intestinal IR caused serious injuries in the intestine and the lung, corroborated by increased proinflammatory cytokines in the circulation. TLR4 mutant suppressed the histological injuries as demonstrated by significantly decreased pathological scores. Consistent with the morphological results, the TLR4 mutant mice exhibited remarkably lowered cytokine expressions in the intestine (TNF-α, IL-6, IL-1ß, and NF-κB) and the lung (NO, iNOS, MCP-1, MIP-2, NF-κB, and Caspase-3). ALT and creatinine were also significantly dampened in the liver and kidney, respectively. Furthermore, the survival rate over the course of 24 hours was significantly improved. Collectively, the findings reveal that TLR4 mutant significantly abated the intestinal IR injury and ALI at least in part by alleviating the inflammatory response and oxidative stress.

Protective effects of fenofibrate against acute lung injury induced by intestinal ischemia/reperfusion in mice.

This experiment was conducted to evaluate whether pretreatment with fenofibrate could mitigate acute lung injury (ALI) in a mice model of intestinal ischemia/reperfusion (I/R). Male C57BL/6 mice were randomly assigned into three groups (n = 6): sham, intestinal I/R + vehicle, and intestinal I/R + fenofibrate. Intestinal I/R was achieved by clamping the superior mesenteric artery. Fenofibrate (100 mg/kg) or equal volume of vehicle was injected intraperitoneally 60 minutes before the ischemia. At the end of experiment, measurement of pathohistological score, inflammatory mediators and other markers were performed. In addition, a 24-hour survival experiment was conducted in intestinal I/R mice treated with fenofibrate or vehicle. The chief results were as anticipated. Pathohistological evaluation indicated that fenofibrate ameliorated the local intestine damage and distant lung injury. Pretreatment with fenofibrate significantly decreased inflammatory factors in both the intestine and the lung. Consistently, renal creatine levels and hepatic ALT levels were significantly decreased in the fenofibrate group. Moreover, serum systemic inflammatory response indicators were significantly alleviated in the fenofibrate group. In addition, fenofibrate administration significantly improved the survival rate. Collectively, our data indicated that pretreatment with fenofibrate prior to ischemia attenuated intestinal I/R injury and ALI.

[Effect of Intestinal Ischemia-reperfusion Injury on the Expression of Chemerin in Mice].

OBJECTIVE: To investigate the effect of intestinal ischemia-reperfusion on the protein expression of chemerin in C57BL/6J mice. METHODS: A total of 16 mice (C57BL/6J, specific pathogen free level) were randomly assigned into two groups (n=8 each): the intestinal ischemia-reperfusion group and the sham group. The intestinal ischemia-reperfusion state was achieved by blocking the super-mesenteric artery. After 60 minutes of ischemia followed by 60 minutes of reperfusion,we determined the protein level of chemerin in various organs and tissues by enzyme-linked immunosorbent assay and Western blot. The sham group underwent the same operation process except for the blocking of the super-mesenteric artery. RESULT: The protein level of chemerin was significantly elevated in distinctive organs and tissues in the state of intestinal ischemia-reperfusion (P<0.05). CONCLUSION: The intestinal ischemia-reperfusion can remarkably increase the protein expression of chemerin in some organs and tissues.

[The role of high mobility group box 1 in the signaling pathways of mouse intestinal ischemia-reperfusion injury].

OBJECTIVE: To investigate the role of high mobility group box 1 (HMGB1) in the signaling pathway of mouse intestinal ischemia-reperfusion injury. METHODS: Twenty-four Specific Pathogen free male C57BL / 6 mice were randomly divided into three groups (n = 8) : the sham operation group (sham), the control group(control) and the HMGB1 antibody group (anti-HMGB1). The vehicle alone or anti-HMGB1 antibody(1 mg/kg, 0. 025%) was injected respectively via the caudal vein 30 min prior to ischemia in the control group or the anti-HMGB1 group. All mice were anesthetized,opened abdominal wall and exposed arteria mesenterica superior. The control group and the anti-HMGBl group underwent 60 min of mesenteric ischemia and 60 min of reperfusion and the sham group were merely opened abdominal wall for 120 min without ischemia-reperfusion. The levels of NF-κB p65, IL-6 and TNF-α in plasma and the activity of MPO in lung and liver and the morphological changes of lung and intestinal tissue were measured. The mRNA levels of HMGB1 and NF-κB were evaluated using real-time quantitative PCR and the protein levels of HMGB1 and NF-KB were evaluated using Western blot. The experimental data was analyzed using one-way analysis of variance. RESULTS: The levels of IL-6, TNF-α and NF-κB p65 in plasma was significantly higher in the control group and the anti-HMGB1 group compared with the sham group (the sham group vs. the control group vs. the anti-HMGB1 group, NF-κB p65, 104. 64 ± 11. 89: 228. 53 ± 24. 85: 145. 00 ± 33. 63, F = 38. 036, P <0. 05; IL-6,50. 02 ± 6. 33:104. 91 ± 31. 18:62. 28 ± 6. 73, F = 49. 763, P < 0. 05; TNF-α, 43. 79 ± 4. 18: 70. 81 ± 6. 97: 52. 76 ± 5. 71, F = 34. 571, P < 0. 05). The increasing degree in the anti- HMGB1 group was significantly reduced compared with the control group (P <0. 05). The activity of MPO of liver and lung in the control group and the anti-HMGB1 group was significantly higher than those in the sham group (P <0. 05). Compared with the sham group, the degree of tissue injury in jejunum, ileum and lung was serious in the control group, and that in the anti-HMGB1 group was significantly lower than the control group. The expression of HMGB1 mRNA and NF-κB mRNA in the lung and the ileum in the sham group and the control group were all higher than the sham group (HMGB1 mRNA in lung: sham group 1. 04 ± 0. 19 vs. control group 2. 25 ± 0. 18 vs. anti-HMGB1 group 1. 89 0. 18, F = 66. 203, P < 0. 05; in ileum: 1. 14 ± 0. 54 vs. 6. 26 ± 0. 60 vs. 4. 93 0. 55, F = 133. 427, P < 0. 05; NF-κB mRNA in lung: 1. 03 ± 0. 21 vs. 2. 04 ± 0. 29 vs. 1. 42 ± 0. 23, F =26. 229, P < 0. 05; ileum: 1. 03 ± 0. 23 vs. 3. 71 ± 0. 53 vs. 2. 23 ± 0. 55, F = 50. 477, P <0. 05). Subjected to intestinal ischemia-reperfusion injury, the protein expression of HMGB1 and NF-κB in the lung, jejunum and ileum in the control group and the anti-HMGB1 group increased compared with the sham group(P <0. 05), but that was significantly lower in the anti-HMGB1 group than the control group (P <0. 05). CONCLUSION: The administration of anti-HMGB1 antibodies may reduce the damage caused by ischemia-reperfusion effectively.

TLR4-HMGB1-, MyD88- and TRIF-dependent signaling in mouse intestinal ischemia/reperfusion injury.

AIM: To characterize high-mobility group protein 1-toll-like receptor 4 (HMGB1-TLR4) and downstream signaling pathways in intestinal ischemia/reperfusion (I/R) injury. METHODS: Forty specific-pathogen-free male C57BL/6 mice were randomly divided into five groups (n = 8 per group): sham, control, anti-HMGB1, anti-myeloid differentiation gene 88 (MyD88), and anti-translocating-chain-associating membrane protein (TRIF) antibody groups. Vehicle with the control IgG antibody, anti-HMGB1, anti-MyD88, or anti-TRIF antibodies (all 1 mg/kg, 0.025%) were injected via the caudal vein 30 min prior to ischemia. After anesthetization, the abdominal wall was opened and the superior mesenteric artery was exposed, followed by 60 min mesenteric ischemia and then 60 min reperfusion. For the sham group, the abdominal wall was opened for 120 min without I/R. Levels of serum nuclear factor (NF)-κB p65, interleukin (IL)-6, and tumor necrosis factor (TNF)-α were measured, along with myeloperoxidase activity in the lung and liver. In addition,morphologic changes that occurred in the lung and intestinal tissues were evaluated. Levels of mRNA transcripts encoding HMGB1 and NF-κB were measured by real-time quantitative PCR, and levels of HMGB1 and NF-κB protein were measured by Western blot. Results were analyzed using one-way analysis of variance. RESULTS: Blocking HMGB1, MyD88, and TRIF expression by injecting anti-HMGB1, anti-MyD88, or anti-TRIF antibodies prior to ischemia reduced the levels of inflammatory cytokines in serum; NF-κB p65: 104.64 ± 11.89, 228.53 ± 24.85, 145.00 ± 33.63, 191.12 ± 13.22, and 183.73 ± 10.81 (P < 0.05); IL-6: 50.02 ± 6.33, 104.91 ± 31.18, 62.28 ± 6.73, 85.90 ± 17.37, and 78.14 ± 7.38 (P < 0.05); TNF-α, 43.79 ± 4.18, 70.81 ± 6.97, 52.76 ± 5.71, 63.19 ± 5.47, and 59.70 ± 4.63 (P < 0.05) for the sham, control, anti-HMGB1, anti-MyD88, and anti-TRIF groups, respectively (all in pg/mL).Antibodies also alleviated tissue injury in the lung and small intestine compared with the control group in the mouse intestinal I/R model. The administration of anti-HMGB1, anti-MyD88, and anti-TRIF antibodies markedly reduced damage caused by I/R, for which anti-HMGB1 antibody had the most obvious effect. CONCLUSION: HMGB1 and its downstream signaling pathway play important roles in the mouse intestinal I/R injury, and the effect of the TRIF-dependent pathway is slightly greater.

Omega-3 polyunsaturated fatty acids inhibit the increase in cytokines and chemotactic factors induced in vitro by lymph fluid from an intestinal ischemia-reperfusion injury model.

OBJECTIVE: To investigate the active factors and the intervention effect of ω-3 polyunsaturated fatty acids (PUFAs) during intestinal ischemia-reperfusion (I/R) injury, which causes the inflammation of monocytes-macrophages cultured in lymph fluid and stimulated with ω-3 PUFAs. METHODS: Forty-eight Sprague-Dawley male rats were randomly divided into the following two groups: A. (N + D) group and B. (I/R + D) group. The rats in the (N + D) group were drained of lymph for 180 min; the rats in the (I/R + D) group were subjected to 60 min ischemia by clamping the superior mesenteric artery followed by 120 min reperfusion and 180 min of lymph draining. Lymph fluid from each group was further divided into 4 subgroups, respectively: lymph group (A1, B1); eicosopentaenoic acid (EPA)-treated group (A2, B2); EPA + docosahexaeonic acid (DHA)-treated group (A3, B3); and DHA-treated group (A4, B4), then cultured monocyte-macrophage cell line. RESULTS: The levels of tumor necrosis factor-α, interleukin (IL)-1 ß, IL-6, soluble cell adhesion molecule-1, chemotactic factors macrophage chemoattractant protein-1, macrophage inflammatory protein-2, and high mobility group box protein 1 in the B1 group were significantly higher than in the A1 group. Importantly, addition of EPA, EPA + DHA, and DHA to the culture media significantly reduced the levels of the above-mentioned factors. Cell stimulation with EPA, EPA + DHA, and DHA also significantly decreased the expression of Toll-like receptor 4, nuclear factor-κB p65, macrophage chemoattractant protein-1, and macrophage inflammatory protein-2 with the combined treatment of EPA and DHA showing the strongest effect. CONCLUSIONS: The factors induced in lymph during intestinal I/R injury can cause inflammation in vitro. These data provide in vitro evidence that ω-3 PUFAs provide a protective effect by reducing the inflammatory response caused by intestinal I/R lymph. Moreover, the synergism of EPA and DHA had the greatest effect, which is possibly mediated through Toll-like receptor 4 and nuclear factor-κB p65.

Factors influencing polychlorinated dibenzo-p-dioxin and polychlorinated dibenzofuran (PCDD/F) emissions and control in major industrial sectors: case evidence from Shandong Province, China.

Analyzing determinants that influence polychlorinated dibenzo-p-dioxin and polychlorinated dibenzofuran (PCDD/F) emissions is helpful for decision-makers to find effective and efficient ways to mitigate PCDD/F emissions. The PCDD/F emissions and the contributions of the scale effect, structure effect and technology effect to emissions from eight main industrial sectors in 2006, 2008 and 2010 in Shandong Province, were calculated in this article. Total PCDD/F emissions in Shandong increased by 52.8% in 2008 (614.1g I-TEQ) and 49.7% in 2010 (601.8 g I-TEQ) based on 2006 (401.9 g I-TEQ). According to the decomposition method, the largest influencing factor on PCDD/F emission changes was the composition effect (contributed 43.4% in 2008 and 120.6% in 2010 based on 2006), which was also an emission-increasing factor. In this case, the present industrial restructuring policy should be adjusted to control the proportion of production capacities with high emission factors, such as iron ore sintering and steel making and the secondary non-ferrous metal sector. The scale effect increased the emissions in 2008 (contributed 21.9%) and decreased the emissions in 2010 (contributed -28.0%). However, as a source control measure, the excess capacity control policy indeed had a significant role in emission reduction. The main reason for the technology effect (contributed 34.7% in 2008 and 7.4% in 2010 based on 2006) having an emission-increasing role was the weakness in implementing policies for restricting industries with outdated facilities. Some specific suggestions were proposed on PCDD/F reduction for local administrators at the end.

[Construction of index system for early warning of persistent organic pollutants (POPs) pollution incidents in China].

Early warning of pollution incidents caused by persistent organic pollutants (POPs) is urgently needed for China in the circumstances of serious POPs pollution and in increasing demand for improvement in chemical risk management. Given different categories of POPs and pollution incidents, the index system for early warning of POPs pollution accidents was built based on lifecycle theory and POPs formation mechanisms. It will be helpful for decision makers to enhance the early warning management of POPs pollution incidents in China. The index system for early warning includes two parts, early warning and mechanism for system operation. The indices include risk source indicators, warning indicators and warning level indicators. To ensure the effective implementation of this system, the mechanisms for response and policy guarantee were also formulated. These mechanisms contain dynamic inventory management and periodical assessment of risk sources, timely and effective report of warning conditions, as well as coordination and cooperation among the relevant departments.

Why small and medium chemical companies continue to pose severe environmental risks in rural China.

In China, rural chemical SMEs are often believed to still largely operate below the sustainability radar. This paper investigates to what extent and how chemical SMEs are already experiencing pressure to improve their environmental performance, using an in-depth case study in Jasmine County, Hebei province. The results show that local residents had rather low trust in the environmental improvement promises made by the enterprises and the local government, and disagreed with the proposed improvement plans. Although the power of local residents to influence decision making remained limited, the chemical SMEs started to feel increasing pressures to clean up their business, from governments, local communities and civil society, and international value chain stakeholders. Notwithstanding these mounting pressures chemical SME's environmental behavior and performance has not changed radically for the better. The strong economic ties between local county governments and chemical SMEs continue to be a major barrier for stringent environmental regulation.

Environmental pollution liability insurance in China: in need of strong government backing.

Environmental pollution liability insurance was officially introduced in China only in 2006, as part of new market-based approaches for managing environmental risks. By 2012, trial applications of pollution insurance had been launched in 14 provinces and cities. More than ten insurance companies have entered the pollution insurance market with their own products and contracts. Companies in environmentally sensitive sectors and high-risk industries bought pollution insurance, and a few successful compensation cases have been reported. Still, pollution insurance faces a number of challenges in China. The absence of a national law weakens the legal basis of pollution insurance, and poor technical support stagnates further implementation. Moreover, current pollution insurance products have limited risk coverage, high premium rates, and low loss ratios, which make them fairly unattractive to polluters. Meanwhile, low awareness of environmental and social liabilities leads to limited demand for pollution insurance products by industrial companies. Hence, the pollution insurance market is not yet flourishing in China. To improve this situation, this economic instrument needs stronger backing by the Chinese state.

[Risk communication in construction of new nuclear power plant].

Accompanied by construction of new nuclear power plants in the coming decades in China, risk management has become increasingly politicized and contentious. Nuclear risk communication is a critical component in helping individuals prepare for, respond to, and recover from nuclear power emergencies. It was discussed that awareness of trust and public attitudes are important determinants in nuclear power risk communication and management. However, there is limited knowledge about how to best communicate with at-risk populations around nuclear power plant in China. To bridge this gap, this study presented the attitudinal data from a field survey in under-building Haiyang nuclear power plant, Shandong Province to measure public support for and opposition to the local construction of nuclear power plant. The paper discussed the structure of the communication process from a descriptive point of view, recognizing the importance of trust and understanding the information openness. The results showed that decision-making on nuclear power was dominated by a closed "iron nuclear triangle" of national governmental agencies, state-owned nuclear enterprises and scientific experts. Public participation and public access to information on nuclear constructions and assessments have been marginal and media was a key information source. As information on nuclear power and related risks is very restricted in China, Chinese citizens (51%) tend to choose the government as the most trustworthy source. More respondents took the negative attitudes toward nuclear power plant construction around home. It drew on studies about risk communication to develop some guidelines for successful risk communication. The conclusions have vast implications for how we approach risk management in the future. The findings should be of interest to state and local emergency managers, community-based organizations, public health researchers, and policy makers.

[Impact of glutamine and ω-3 polyunsaturated fatty acids on intestinal permeability and lung cell apoptosis during intestinal ischemia-reperfusion injury in a rat model].

OBJECTIVE: To investigate the impact of intestinal lymphatic vessels ligation and different enteral nutrition support during ischemia/reperfusion on intestinal permeability, systemic inflammatory response and pulmonary dysfunction in a rat model. METHODS: Seventy-two Sprague-Dawley male rats were randomized into normal diet group, regular enteral nutrition group, glutamine-enriched group, 0-3 polyunsaturated fatty acids (wo-3PUFA) group, and sham control after gastrostomy. All the enteral nutrition group were isocaloric (1046 kJ kg-' d-1) and isonitrogenous (1.8 g N kg-' d-'). After enteral nutrition for 7 days, the rats were subjected to intestinal ischemia for 60 min, or ischemia plus mesenteric lymph duct ligation except for the sham group followed by 3 days of nutrition (72 h). Intestinal permeability (lactose/mannitol ratio in the urine, L/M) was determined on the 5th, 7th and 9th day after gastrostomy. The levels of serum diamine oxidase, endotoxin, cytokines, ALT and AST were detected at the 11th day after gastrostomy. Mucosal thickness was measured using small intestine and villusheight. Myeloperoxidase (MPO), nitric oxide (NO), NO synthase, and apoptotic index were detected in lung tissue. RESULTS: Ischemia for 60 min could cause intestinal injury. Intestinal permeability(L/M)was increased significantly in every group on the first day after ischemia (P<0.05). However, L/M decreased significantly 3 days after ischemia (P<0.05). The groups with Glu and o-3PUFA-enriched nutrition almost restored to normal level (P>0.05). The level of L/M in lymphatic ligation group was significantly lower than non-ligation group (P<0.05). The levels of endotoxin and cytokine were reduced, mucosal thickness and villous height were significantly higher (P<0.05) in the groups of Glu and o-3PUFA-enriched nutrition compared with enteral nutrition and normal diet groups during intestinal ischemia-reperfusion injury. MPO, NO, NOS and the apoptosis index of lung tissue decreased in the groups of Glu and o-3PUFA-enriched as well as after lymph duct ligation (P<0.05). CONCLUSIONS: The distant tissue-lung damage and systemic inflammation caused by intestinal ischemia-reperfusion injury may be related to some factors in the intestinal lymph. Blocking the gut-lymph pathway and/or adding Glu and o-3PUFA in enteral nutrition may reduce intestinal permeability and endotoxin, increase mucosal thickness, attenuate the systemic inflammatory reaction, and prevent lung injury