采用中试规模的好氧膜生物反应器（MBR）工艺处理城市污水,考查了在浓缩过程下膜生物反应器的生物特性对膜渗透性及渗透性恢复的的影响.在试验中通过投加蔗糖溶液使系统维持恒定污泥负荷（food to microorganisms,F/M）在0.13,测定了活...采用中试规模的好氧膜生物反应器（MBR）工艺处理城市污水,考查了在浓缩过程下膜生物反应器的生物特性对膜渗透性及渗透性恢复的的影响.在试验中通过投加蔗糖溶液使系统维持恒定污泥负荷（food to microorganisms,F/M）在0.13,测定了活性污泥的一系列的生化与理化参数,并通过SPSS软件对污泥性质与动态变化的膜渗透性及渗透性恢复水平的相关性做了进一步的评估.结果表明,混合液悬浮固体（MLSS）浓度对膜渗透性的影响最大（rp=-0.958,P=0.000）;溶解性微生物产物（SMP）浓度、溶解性化学需氧量（s COD）浓度、污泥粒径（PSD）及毛细吸水时间（CST）对膜渗透性的影响属于同一个水平（｜rp｜=0.82～0.85,P=0.000）;而污泥沉降性能与丝状菌指数对膜渗透性的影响不大.并且发现随着MLSS浓度的增大,膜丝廊道内积累的堵塞固体（ACS）的质量以及膜渗透性的绝对恢复量（ΔL）也有增加的趋势,表明MLSS浓度直接影响着膜生物反应器的堵塞性能,也进一步证明了膜堵塞是除膜污染之外影响膜渗透性的另一个重要因素.在低通量[5～6L/（m2·h）]的操作条件下离线清堵联合强化化学反洗（CEB）的方式可以保证膜生物反应器工艺在高MLSS浓度运行下实现膜渗透性的可持续恢复。展开更多
AIM: To study the mechanisms by which Campylobacter jejuni (C. jejuni) causes inflammation and diarrhea. In particular, direct interactions with intestinal epithelial cells and effects on barrier function are poorly u...AIM: To study the mechanisms by which Campylobacter jejuni (C. jejuni) causes inflammation and diarrhea. In particular, direct interactions with intestinal epithelial cells and effects on barrier function are poorly under- stood. METHODS: To model the initial pathogenic effects of C. jejuni on intestinal epithelium, polarized human colonic HCA-7 monolayers were grown on permeabilized filters and infected apically with clinical isolates of C. jejuni. Integrity of the monolayer was monitored by changes in monolayer resistance, release of lactate dehydrogenase, mannitol fluxes and electron microscopy. Invasion of HCA-7 cells was assessed by a modified gentamicin protection assay, translocation by counting colony forming units in the basal chamber, stimulation of mediator release by immunoassays and secretory responses in monolayers stimulated by bradykinin in an Ussing chamber. RESULTS: All strains translocated across monolayers but only a minority invaded HCA-7 cells. Strains that invaded HCA-7 cells destroyed monolayer resistance over 6 h, accompanied by increased release of lactate dehydrogenase, a four-fold increase in permeability to [3H] mannitol, and ultrastructural disruption of tight junctions, with rounding and lifting of cells off the filter membrane. Synthesis of interleukin (IL)-8 and prostaglandin E2 was increased with strains that invaded the monolayer but not with those that did not. CONCLUSION: These data demonstrate two distinct effects of C. jejuni on colonic epithelial cells and provide an informative model for further investigation of initial host cell responses to C. jejuni.展开更多
文摘采用中试规模的好氧膜生物反应器（MBR）工艺处理城市污水,考查了在浓缩过程下膜生物反应器的生物特性对膜渗透性及渗透性恢复的的影响.在试验中通过投加蔗糖溶液使系统维持恒定污泥负荷（food to microorganisms,F/M）在0.13,测定了活性污泥的一系列的生化与理化参数,并通过SPSS软件对污泥性质与动态变化的膜渗透性及渗透性恢复水平的相关性做了进一步的评估.结果表明,混合液悬浮固体（MLSS）浓度对膜渗透性的影响最大（rp=-0.958,P=0.000）;溶解性微生物产物（SMP）浓度、溶解性化学需氧量（s COD）浓度、污泥粒径（PSD）及毛细吸水时间（CST）对膜渗透性的影响属于同一个水平（｜rp｜=0.82～0.85,P=0.000）;而污泥沉降性能与丝状菌指数对膜渗透性的影响不大.并且发现随着MLSS浓度的增大,膜丝廊道内积累的堵塞固体（ACS）的质量以及膜渗透性的绝对恢复量（ΔL）也有增加的趋势,表明MLSS浓度直接影响着膜生物反应器的堵塞性能,也进一步证明了膜堵塞是除膜污染之外影响膜渗透性的另一个重要因素.在低通量[5～6L/（m2·h）]的操作条件下离线清堵联合强化化学反洗（CEB）的方式可以保证膜生物反应器工艺在高MLSS浓度运行下实现膜渗透性的可持续恢复。
基金Supported by The Medical Research Council (UK), No. G9716348
文摘AIM: To study the mechanisms by which Campylobacter jejuni (C. jejuni) causes inflammation and diarrhea. In particular, direct interactions with intestinal epithelial cells and effects on barrier function are poorly under- stood. METHODS: To model the initial pathogenic effects of C. jejuni on intestinal epithelium, polarized human colonic HCA-7 monolayers were grown on permeabilized filters and infected apically with clinical isolates of C. jejuni. Integrity of the monolayer was monitored by changes in monolayer resistance, release of lactate dehydrogenase, mannitol fluxes and electron microscopy. Invasion of HCA-7 cells was assessed by a modified gentamicin protection assay, translocation by counting colony forming units in the basal chamber, stimulation of mediator release by immunoassays and secretory responses in monolayers stimulated by bradykinin in an Ussing chamber. RESULTS: All strains translocated across monolayers but only a minority invaded HCA-7 cells. Strains that invaded HCA-7 cells destroyed monolayer resistance over 6 h, accompanied by increased release of lactate dehydrogenase, a four-fold increase in permeability to [3H] mannitol, and ultrastructural disruption of tight junctions, with rounding and lifting of cells off the filter membrane. Synthesis of interleukin (IL)-8 and prostaglandin E2 was increased with strains that invaded the monolayer but not with those that did not. CONCLUSION: These data demonstrate two distinct effects of C. jejuni on colonic epithelial cells and provide an informative model for further investigation of initial host cell responses to C. jejuni.
