高氨氮味精废水的亚硝化/反亚硝化脱氮研究

两段SBR法处理经稀释的味精废水有良好的有机质降解和脱氮效果 .整个生物处理过程可分为碳氧化阶段和三个亚硝化 /反亚硝化阶段 .碳氧化阶段主要是有机质的降解和曝气吹脱除氮 ,随后通过亚硝化 /反亚硝化反应实现生物脱氮和有机物的降解 .SBRⅠ碳氧化阶段废水中有机质浓度较高 ,在降解过程中消耗废水中的溶解氧 ,竞争性抑制了亚硝化反应的发生 .而亚硝化 /反亚硝化反应的形成是由于游离氨 (FA)

Study on the Mechanism of Innovative Montmorillonite for Diarrhea Treatment

[Objective] This study aimed to investigate the mechanism of innovative montmorillonite for diarrhea treatment. [Method] Thirty healthy weanling piglets （Duroc x Landrace x Yorkshire） were randomly divided into five groups and fed with basal diet, basal diet ＋ 1 g/kg innovative montmorillonite, basal diet ＋ 3 g/kg innovative montmorillonite, basal diet ＋ 5 g/kg innovative montmorillonite and basal diet ＋ 3 g/kg Bacillus subtilis microecologic agent, respectively. After four weeks, blood samples were collected via precaval vein, to detect the content of TFF3, NO and SOD in serum by ELISA kits. [Result] Compared with blank control group, the content of TFF3, NO and SOD in high-dose innovative montmorillonite group was extremely significantly increased, extremely significantly reduced and significantly in- creased, respectively; the content of TFF3 and NO in middle-dose innovative mont- morillonite group was significantly increased and significantly reduced, respectively. [Conclusion] Innovative montmorillonite may exert beneficial therapeutic actions on diarrhea by increasing TFF3 and SOD levels and decreasing NO level.

Increased intestinal macromolecular permeability and urine nitrite excretion associated with liver cirrhosis with ascites

AIM： To determine intestinal permeability, the serum tumor necrosis factor （TNF）-α level and urine nitric oxide （NO） metabolites are altered in liver cirrhosis （LC） with or without ascites. METHODS： Fifty-three patients with LC and 26 healthy control subjects were enrolled in the study. The intestinal permeability value is expressed as the percentage of polyethylene glycol （PEG） 400 and 3350 retrieval in 8-h urine samples as determined by high performance liquid chromatography. Serum TNF-α concentrations and urine NO metabolites were determined using an enzyme-linked immunosorbent assay （ELISA） and Greiss reaction method, respectively. RESULTS： The intestinal permeability index wassignificantly higher in patients with LC with ascites than in healthy control subjects or patients with LC without ascites （0.88 ± 0.12 vs 0.52 ± 0.05 or 0.53 ± 0.03, P 〈 0.05） and correlated with urine nitrite excretion （r = 0.98）. Interestingly, the serum TNF-α concentration was significantly higher in LC without ascites than in control subjects or in LC with ascites （198.9 ± 55.8 pg/mL vs 40.9 ± 12.3 pg/mL or 32.1 ± 13.3 pg/mL, P 〈 0.05）. Urine nitrite excretion was significantly higher in LC with ascites than in the control subjects or in LC without ascites（ 1170.9± 28.7 μmol/L vs 903.1 ± 55.1 μmol/L or 956.7 ± 47.7 μmol/L, P 〈 0.05）. COMCLUSIOM： Increased intestinal macromolecular permeability and NO is probably of importance in the pathophysiology and progression of LC with ascites, but the serum TNF-α concentration was not related to LC with ascites.

Effect of lipopolysaccharide on diarrhea and gastrointestinal transit in mice: Roles of nitric oxide and prostaglandin E_2

AIM: To investigate the effect of lipopolysaccharide (LPS)on the diarrheogenic activity, gastrointestinal transit (GIT),and intestinal fluid content and the possible role of nitric oxide (NO) and prostaglandin E2 (PGE2) in gastrointestinal functions of endotoxin-treated mice.METHODS: Diarrheogic activity, GIT, and intestinal fluid content as well as nitric oxide and PGE2 products were measured after intraperitoneal administration of LPS in mice.RESULTS: LPS dose-dependently accumulated abundant fluid into the small intestine, induced diarrhea, but decreased the GIT. Both nitric oxide and PGE2 were found to increase in LPS-treated mice. Western blot analysis indicated that LPS significantly induced the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 in mice intestines. Pretreatment with NG-nitro-L-arginine-methyl ester (L-NAME, a non-selective NOS inhibitor) or indomethacin (an inhibitor of prostaglandin synthesis) significantly attenuated the effects of LPS on the diarrheogenic activity and intestine content, but reversed the GIT.CONCLUSION: The present study suggests that the pathogenesis of LPS treatment may mediate the stimulatory effect of LPS on nitric oxide and PGE2 production and NO/prostaglandin pathway may play an important role on gastrointestinal function.

Nitric oxide production and inducible nitric oxide synthase protein expression in human abdominal aortic aneurysms and cultured aneurismal smooth muscle cells

Objective：To investigate the production of nitric oxide（NO） and the expression of inducible nitric oxide synthase （iNOS）, and their possible role in abdominal aortic aneurysm （AAA）. Methods： A total of 28 patients with AAA, 10 healthy controls, and 8 patients with arterial occlusive disease were enrolled into this study. Standard colorimetric assay was used to examine NO concentration in plasma from patients with AAA and normal controls, and in cultured smooth muscle cells （SMCs）. Expression of iNOS in aortas and cultured SMCs were detected by immunochemistry. The correlation of iNOS expression with age of the patient, size of aneurysm, and degree of inflammation was also investigated by Cochran-Mantel-Haenszel χ^2 test and Kendall correlation. Results ： Expression of iNOS increased significantly in the wall of aneurism in the patients with AAA compared to the healthy controls （P〈0.05） and the patients with occlusive arteries （P〈0.05）. iNOS protein and media NOx （nitrite＋nitrate） also increased in cultured SMCs from human AAA （n=4, P〈0.05）, while plasma NOx decreased in patients with AAA （n= 25） compared to the healthy controls （n=20）. There was a positive correlation between iNOS protein and the degree of inflammation in aneurismal wall （Kendall coefficient = 0. 5032, P= 0. 0029）. Conclusion： SMCs and inflammatory cells are main cellular sources of increased iNOS in AAA, and NO may play a part in pathogenesis in AAA through inflammation, SMCs and oxidative stress.