分级分相厌氧消化工艺的研究现状

厌氧消化是污泥处理的主要途径之一,分级分相厌氧消化工艺因产酸相和产甲烷相的分离而具有一系列的特点和优势。从污泥的停留时间、TOCD的去除率、COD去除率、应用范围等多角度对分级分相厌氧消化工艺进行了系统的分析。对最新的研究成果进行了总结,并对其在未来污泥处理中的应用前景进行了讨论。     

北柴胡药材的HPLC指纹图谱研究

[目的]建立北柴胡药材的HPLC指纹图谱研究方法。[方法]采用Zorbax SB-C18(250 mm×4.6 mm ID,5μm)色谱柱,在柱温25℃、检测波长220 nm、流速为1.0 ml/min的条件下,以乙腈-0.05%磷酸水溶液为流动相对9个不同产地的柴胡样品进行梯度洗脱,分析其指纹图谱。采用国家药典委员会出版的《中药色谱指纹图谱相似度评价》(2004年A版)软件,对9个不同批次的北柴胡药材指纹图谱进行相似度分析。[结果]各批北柴胡药材中均有11个特征峰,各峰分离度良好,各批次药材间共有峰的相对保留时间RSD均<1.0%,药材间相似度均>90%。[结论]该研究采用HPLC法,以柴胡皂苷a为内参比峰,建立了北柴胡药材的HPLC指纹图谱,方法稳定、重现性好,可有效控制北柴胡药材的质量。     

新型农村合作医疗制度对农民就医决策的影响——基于“中国健康与营养调查”数据的双重差分估计

基于"中国健康与营养调查"数据中2000、2004、2006及2009年共4期的县级面板数据,从农民医疗服务利用中就医决策角度,对新型农村合作医疗制度的政策效果进行实证分析。利用新型农村合作医疗制度逐步覆盖的特征,借鉴双重差分模型,分析了新型农村合作医疗制度对农民到正规医疗机构就诊的影响。结果表明,新型农村合作医疗制度提高了农民患者到正规医疗机构就诊的比例,使得农民患者到正规医疗机构就诊占比提高了2.4%左右。时间趋势研究表明,新型农村合作医疗制度对农民就医决策的影响具有持续性的正效应,且对2009年农民就医决策的影响具有显著的统计学意义,达到11.9%。     

采用HPLC-MS/MS方法同时测定花生中的马来酰肼和丁酰肼

马来酰肼和丁酰肼为2种植物生长调节剂,均有抑制植物生长发芽的作用。马来酰肼又称抑芽丹,化学名称为顺丁烯二酰肼(Maleic hydrazide,MH),国内注册用于控制烟草腋芽的生长。国外注册范围较广,包括烟草、马铃薯、洋葱、柑桔、草坪、观赏植物等。丁酰肼,又名B9,化学名称为N-二甲氨基琥珀酰胺酸(Daminozide),国内注册植物仅有观赏菊     

慢性束缚与慢性不可预期温和应激抑郁模型小鼠的行为学比较及其发生机制研究

【目的】通过比较慢性束缚应激(Chronic restraint stress,CRS)与慢性不可预期温和应激(Chronic unpredictable mild stress,CUMS)对C57BL/6小鼠行为学指标及大脑海马区相关功能的影响,探讨抑郁症的发生机制。【方法】分别建立CRS及CUMS小鼠模型,通过旷场试验、强迫游泳试验和悬尾试验测定小鼠的行为学指标;取小鼠脑组织,制备常规石蜡切片,运用苏木素-伊红(HE)与免疫组化染色考察小鼠大脑海马区组织形态及5-羟色胺1A受体(5-HT1AR)的表达情况,并运用荧光分光光度法测定小鼠海马组织单胺氧化酶活性的变化。【结果】与空白对照组相比,CRS组小鼠的水平穿格数、直立次数及体质量均显著减少,悬尾及强迫游泳试验累计不动时间百分比无明显变化(P>0.05);而CUMS组小鼠自发活动无明显改变(P>0.05),但悬尾及强迫游泳试验累计不动时间百分比极显著增加(P<0.01),体质量显著下降。脑组织形态学研究结果显示,CUMS组小鼠海马CA1、CA3区和齿状回均出现萎缩,而CRS组小鼠海马CA1区未受影响,CA3区和齿状回均发生萎缩。与对照组相比,CRS组与CUMS组小鼠大脑海马单胺氧化酶活性升高,5-HT1AR表达均减少,差异均分别达显著和极显著水平。【结论】CRS和CUMS均可不同程度地引起抑郁样症状,CRS对探索性行为的抑制较明显,CUMS则可引发典型的行为绝望状态;CRS与CUMS组小鼠的行为学差异可能与2组抑郁模型动物脑内海马区组织结构及功能变化的差异存在相关性。     

灰树花子实体中水溶性多糖提取工艺优化研究

以水为浸提液,通过单因素试验研究了颗粒度、浸提温度、浸提时间、水料比、醇沉度等因素对灰树花子实体多糖提取率的影响,并采用正交试验对提取工艺进行优化。试验表明,水料比对灰树花子实体多糖提取率的影响最大,其次是浸提时间,浸提温度影响最小。通过对提取条件的优化,结合收益、成本等综合因素选出最佳优化工艺为:浸提温度90℃,浸提时间5 h,水料比25∶1。验证试验显示,在最佳工艺条件下提取的多糖提取率达13.4%。     

Effects of gastrin on expression of cyclooxygenase and growth factors in rat gastric mucosa

AIM: To clarify the effects of gastrin on the expression of cyclooxygenase (COX) and several growth factors in rat gastric mucosa. METHODS: Male Sprague Dawley rats were fasted for 24 hours and subcutaneously injected with saline or gastrin 17 at doses of 1 μg/kg, 10 μg/kg and 100 μg/kg, respectively. The expression of COX-1, COX-2, heparin-binding epidermal growth factor-like growth factor (HB-EGF) and hepatocyte growth factor (HGF) in the gastric mucosa were examined using Western blotting and immunohistochemical staining. Effects of a potent gastrin receptor antagonist YM022 on the expression of COX-1, COX-2, HB-EGF and HGF in gastric mucosa were also evaluated. RESULTS: Gastrin dose-dependently increased the expression of COX-2 and HB-EGF in rat gastric mucosa while the expression of COX-1 and HGF did not change significantly after treatment with gastrin. However, pretreatment with YM022 dose-dependently abolished the up-regulation of COX-2 and HB-EGF expression induced by gastrin. CONCLUSIONS: This study demonstrates that gastrin up-regulates COX-2 and HB-EGF expression in rat gastric mucosa, indicating that COX-2 and HB-EGF are involved in pathogenesis of the gastrin-related gastric mucosal hyperplasia and carcinoma of stomach.     

In vitro growth inhibition effects of rhHGF/cHGF on SMMC-7721 human HCC cell line

AIM:To examine the effects of recombinant human hepatocyte growth factor(rhHGF) and native calf HGF(cHGF) on SMMC-7721 human hepatocellular carcinoma(HCC) cell line. METHODS:Human HCC cell line culture, photometric assay, and flow cytometric assay were used in this study .RESULTS:A similar type of dose-dependent cell growth inhibition effect on SMMC-7721 human HCC cells by rhHGF(5-20 μg/L) as well as by cHGF(25-100 mg/L) had been found, with the maximal effect at the highest concentration used. Approximately over 50% of the cells treated with rhHGF(5 μg/L, 10 μg/L, 20 μg/L) accumulated in the quiescent G₀/G₁ phase of the cell cycle over incubation periods for 3 d. CONCLUSION:The growth of SMMC-7721 human HCC cells was strongly inhibited by both rhHGF and cHGF. This might be because the cells exposed to HGF became arrested in the G₀/G₁ phase.     

Etoposide induces apoptosis via mitochondrial signaling pathway with cytochrome c release in Jurkat leukemia cells

AIM:To investigate the molecular mechanisms of apoptosis and to elucidate the apoptosis signaling pathway triggered by etoposide in Jurkat human leukemia cells. METHODS:Apoptosis was detected using annexin V-FITC and propidium iodide (PI) staining, respectively, and annexin V-FITC positive cells and hypodiploid cells were analyzed by flow cytometry. Mitochondrial membrane potential (△Ψm) was detected using 3, 3-dihexyloxycarbocyanine iodide ［DiOC6(3)］ staining and △Ψm low cells were analyzed by flow cytometry. Preparation of cytosolic extracts and isolation of mitochondria were completed by centrifugation. Western blotting analysis was used to evaluate the level of cytochrome c, caspase-3, and poly (ADP-ribose) polymerase (PARP) expression. RESULTS:Etoposide induced apoptosis showing phosphatidylserine externalization and DNA fragmentation in a time-dependent manner and the apoptosis could be inhibited by a broad caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD.fmk). Collapse of △Ψm induced by etoposide preceded DNA fragmentation and phosphatidylserine externalization. In contrast, it was not blocked by zVAD.fmk. Etoposide caused cytochrome c release from mitochondria into cytosol, subsequent activation of caspase-3 (32 kD) presented with an intermediate (20 kD) and its active product (17 kD), and cleavage of full-length PARP (116 kD) into the so-called apoptotic 85 kD fragment. CONCLUSION:Etoposide-induced Jurkat cell apoptosis is initiated through mitochondria signaling pathway with cytochrome c release into cytoplasm and caspase is the ultimate executioner of cell apoptosis.