Morphological and serum hyaluronic acid, laminin and type Ⅳ collagen changes in dimethylnitrosamine-induced hepatic fibrosis of rats

AIM： To study the morphological and serum hyaluronic acid （HA）, laminin （LN）, and type IV collagen changes in hepatic fibrosis of rats induced by dimethylnitrosamine （DMN）.METHODS： The rat model of liver fibrosis was induced by DMN. Serum HA, type IV collagen, and LN were measured by ELISA. The liver/weight index and morphological changes were examined under electron microscope on d 7, 14, 21, and 28 by immunohistochemical alpha smooth muscle actin α-SMA staining as well as Sirius-red and HE staining.RESULTS： The levels of serum HA, type IV collagen and LN significantly increased from d 7 to d 28 （P = 0.043）. The liver/weight index increased on d 7 and decreased on d 28. In the model group, the rat liver stained with lie and Sirius-red showed evident hemorrhage and necrosis in the central vein of hepatic 10 Iobules on d 7. Thin fibrotic septa were formed joining central areas of the liver on d 14. The number of α-SMA positive cells was markedly increased in the model group. Transitional hepatic stellate cells were observed under electron microscope. All rats in the model group showed micronodular fibrosis in the hepatic parenchyma and a network of α-SMA positive cells. Typical myofibroblasts were embedded in the core of a fibrous septum. Compared to the control group, the area-density percentage of collagen fibrosis and pathologic grading were significantly different in the model group （P〈0.05） on different d （7, 14, and 28）. The area-density percentage of collagen fibrosis in hepatic tissue had a positive correlation with the levels of serum HA, LN, and type IV collagen.CONCLUSION： The morphological and serum HA, type IV collagen, and LN are changed in DMN-induced liver fibrosis in rats.

Iron deposition and fat accumulation in dimethylnitrosamine-induced liver fibrosis in rat

AIM： To investigate if iron deposition and fat accumulation in the liver play a pathogenetic role in dimethylnitrosamine （DMN）-induced liver fibrosis in rat.METHODS： Thirty rats were treated with DMN at does consecutive days of 10 μL/kg daily, i.p., for 3 consecutive day each week for 4 wk. Rats （n = 30） were sacrificed on the first day （model group A） and 21st d （model group B） after cessation of DMN injection. The control group （n = 10） received an equivalent amount of saline. Liver tissues were stained with hematoxylin ＆ eosin （HE） and Masson and Prussian blue assay and oberserved under electron microscopy. Serum alanine aminotransferase （ALT）and liver tissue hydroxyproline （Hyp） content were tested.RESULTS： The liver fibrosis did not automaticallyreverse, which was similar to previous reports, the perilobular deposition of iron accompanied with collagen showed marked characteristics at both the first and 21st d after cessation of DMN injection. However, fat accumulation in hepatocytes occurred only at the 21^st d after cessation of DMN injection.CONCLUSION： Iron deposition and fat accumulation may play important roles in pathological changes in DMN-induced rat liver fibrosis. The detailed mechanisms of these characteristics need further research.

An herbal formula,CGX,exerts hepatotherapeutic effects on dimethylnitrosamine-induced chronic liver injury model in rats

AIM： To evaluate the therapeutic effect of Chunggan extract （CGX）, a modified traditional Chinese hepatotherapeutic herbal, on the dimethylnitrosamine （DMN）-induced chronic liver injury model in rats. METHODS： Liver injuries were induced in Wistar rats by injection of DMN （ip, 10 mg/mL per kg） for 3 consecutive days per week for 4 wk. The rats were administered with CGX Coo, 100 or 200 mg/kg per day） or distilled water as a control daily for 4 wk starting from the 15^th d of the DMN treatment. Biochemical parameters （serum albumin, bilirubin, ALP, AST and ALT）, lipid peroxides, hydroxyproline, as well as histological changes in liver tissues were analyzed. In addition, gene expression of TNF-α, TGF-β, TIMP-1, TIMP-2, PDGF-β, and MMP-2, all of which are known to be associated with liver fibrosis, were analyzed using real-time PCR. RESULTS： CGX administration restored the spleen weight to normal alter having been increased by DMN treatment. Biochemical analysis of the serum demonstrated that CGX significantly decreased the serum level of ALP （P 〈 0.05）, ALT （P 〈 0.02）, and AST （P 〈 0.02） that had been elevated by DMN treatment. CGX administration moderately lowered lipid peroxide production and markedly lowered hydroxyproline generation caused by DMN treatment in accordance with histopathological examination. DMN treatment induced a highly upregulated expression of TNF-α, TGF-β,TIMP-1, TIMP-2, PDGF-β, and MMP-2. Of these, the gene expression encoding PDGF-β and MMP-2 was still further enhanced 2 wk after secession of the 4-wk DMN treatment, and was remarkably ameliorated by CGX administration. CONCLUSION： CGX exhibits hepatotherapeutic properties against chronic hepatocellular destruction and consequential liver fibrosis.

Upregulation of TNF-α mRNA in hepatic fibrosis rats induced by dimethylnitrosamine

Objective:To observe the expression level of TNF-α mRNA in rats with hepatic fibrosis induced by dimethylnitrosamine (DMN) and to explore its relationship with collagen metabolism and its diagnostic value for hepatic fibrosis.Methods: Twenty-five male Wistar rats were randomly divided into normal control group (n=10) and model group (n=15). Model rats were induced by DMN for 4 weeks and at final stage were executed. TNF-α mRNA were detected by RT-PCR and the inflammatory necrosis and collagen deposition in hepatic tissue were observed by HE stain and Sirius red stain. The liver functions were determined by automatic biochemical analytic device. The serum marks of liver fibrosis, such as HA, LN and Ⅳ-C were measured with ELISA and RIA. Results: In this study, the rat model of liver fibrosis induced by DMN was successfully constructed. RT-PCR reveals that TNF-α mRNA expression in control group is lower than that of model group. The liver functions of model group were impaired compared with those of the control group (P<0.01). Semi-quantitive analysis revealed that TNF-α/β-actin of normal rats was 0.39±0.12, while 0.93±0.05 of model rats. The concentration of HA (434.44±98.81 vs 252.9±26.59 ng/ml, P<0.01), LN (70.67±6.32 vs 37.90±5.97 ng/ml, P<0.01) and Ⅳ-C (79.39±10.52 vs 21.40±4.17 ng/ml, P<0.01) were significantly increased in the model group as well. Changes of the indexes were similar to the pathological damage of the liver. Conclusion: The results suggested that activation of TNF-α in liver tissues may be the common pathogenic mechanism of liver fibrosis. TNF-α may be a useful index for the diagnosis of hepatic fibrosis which worthies further investigation.

基于数据影响的业务流程一致性检查方法

近年来,业务流程的精确管理受到越来越多的关注,作为业务流程管理内容之一的一致性检查技术正变得越来越重要。现有的一致性检查技术主要从模型的控制流角度出发,并未考虑业务流程中的数据或数据的变化对业务流程产生的影响,为此提出了一种基于数据影响的业务流程一致性检查方法。首先,通过业务流程建模符号(business process modeling notation,BPMN)模型中数据和行为之间的依赖关系来分析数据对偏差活动预期行为的影响,进而获取偏差活动的预期行为集;其次,通过在BPMN模型中引入决策模型和符号(decision model and notation,DMN)决策表来充分捕获当前实例执行的数据上下文与行为上下文之间的关系,以区分有效数据更改和异常数据更改,找到偏差活动的有效预期行为集。最后,通过设计数据对偏差活动影响的各类成本函数提出了有效一致性检查方法。实验结果表明,相比已有工作,该方法在进行业务流程一致性检查时提高了业务流程的一致性,可以成功捕获偏差活动作出反应的适应行为,使得业务流程在复杂多变的环境下表现得更加准确、合理。

丹参提取物对CCl_4和DMN诱导的大鼠肝纤维化的影响

分别采用四氯化碳 (CCl4 )和二甲基亚硝胺 (DMN)诱导的大鼠肝纤维化模型 ,以秋水仙碱和丹参作对照 ,通过肝组织病理学及Ⅰ、Ⅲ型胶原免疫组化观察 ,肝组织羟脯氨酸 (Hyp)、丙二醛(MDA)及血清肝功能部分指标检测 ,探讨丹参提取物预防和治疗肝纤维化的效果及部分作用机理。结果显示 ,丹参提取物可显著改善肝组织损伤和纤维化程度 ,同时能显著降低肝组织Hyp和MDA含量 ,提示丹参提取物有显著的抗肝纤维化作用 ,为丹参的重要有效成分 ,其作用机理与抗脂质过氧化损伤有关 ,对胶原代谢也有直接的影响。

积雪草总苷抗DMN诱导大鼠肝纤维化的作用

目的研究积雪草总苷抗实验性大鼠肝纤维化的作用。方法采用二甲基亚硝氨 (dimethylni trosamine ,DMN)腹腔注射 6周 ,制备大鼠肝纤维化模型。动物随机分为 6组 (正常组、模型组、秋水仙碱组、积雪草总苷大、中、小剂量组 )。于造模开始时同时给予积雪草总苷灌胃 ,实验结束后分别检测血清总蛋白(TP)、白蛋白 (ALB)、谷丙转氨酶 (ALT)、谷草转氨酶 (AST)、透明质酸 (HA)、层粘连蛋白 (LN)含量 ,并作肝组织病理学观察。结果积雪草总苷能改善肝功能 ,与模型组相比可明显降低血清ALT、AST、HA的含量(P <0 0 5 )。肝组织病理学检查显示具有抗肝纤维化作用。结论积雪草总苷对DMN诱导的大鼠慢性肝纤维化具有良好的治疗作用。

DMN诱导的肝纤维化模型伴肾损害的实验观察

目的:观察二甲基亚硝胺(DMN)诱导大鼠肝纤维化时对肾脏的影响,为"肝肾同源"提供实验依据。方法:实验大鼠随机分为正常组和DMN模型组,测定血清ALT、AST、BUN、Scr、透明质酸(HA)、层黏连蛋白(LN)、Ⅳ型胶原(Ⅳ-C)水平,病理学观察肝肾组织切片,免疫组化方法测定α-平滑肌肌动蛋白(α-SMA)和转化生长因子-β1(TGF-β1)在肝肾组织的表达。结果:模型组较正常组大鼠血清各参数水平显著升高;病理学观察到肝肾组织胶原增生,纤维化形成;免疫组化结果发现肝肾组织中α-SMA,TGF-β1的表达明显上调。结论:DMN在导致肝纤维化的同时,也出现了肾脏纤维化病变,提示肝肾纤维化在一定程度上是有相关性的,从病理角度说明中医学"肝肾同源"具有一定的物质基础。

复方861对DMN损伤性大鼠肝纤维化肝脏中MMP-2表达的影响

目的研究抗肝纤维化中药复方861对DMN诱导的肝纤维化大鼠肝脏中MMP-2表达的影响。方法将大鼠随机分成正常对照组,模型组与861防治组。模型组以DMN腹腔内注射,第1周注射3次,随后每周2次,共注射6周;治疗组同法注射DMN同时每日灌胃861冲剂;正常对照组以生理盐水代替腹腔内注射。实验结束处死大鼠,留取的肝脏组织做HE与Masson染色按0～4期标准判定肝纤维化程度,应用半定量RT-PCR检测肝组织中MMP-2mRNA,用免疫组化检测肝组织中MMP-2的表达。结果模型组大鼠肝纤维化程度处于2～4期,其中大部分达3期以上,861防治组大鼠肝纤维化程度明显减轻,只有少部分达3期。模型组大鼠肝组织中MMP-2mRNA水平显著高于正常对照组(t=4.03,P<0.01),而861防治组大鼠肝组织中MMP-2mRNA水平显著低于模型组(t=3.43,P<0.01)。861防治组与正常组之间,肝组织中MMP-2mRNA水平无明显差别。模型组大鼠肝组织MMP-2的阳性表达显著强于正常对照组(t=4.56,P<0.01),861防治组肝组织中MMP-2的阳性表达虽明显强于正常组(t=2.71,P<0.05),但较模型组显著减弱(t=3.24,P<0.01)。结论中药复方861能有效抑制DMN诱导的肝纤维化大鼠肝脏中MMP-2的表达,可能有利于维持HSC处于静止状态所需要的细胞外基质环境,这对于抑制HSC的活化与肝纤维化的发展具有重要意义。

一贯煎对DMN肝纤维化大鼠肝卵圆细胞增殖分化的影响

[目的]探讨一贯煎有效逆转大鼠肝硬化的作用途径,促进中医药在组织结构重构研究中的发展。[方法]二甲基亚硝胺(DMN)制备大鼠肝硬化模型,于肝硬化造模成型后,给予一贯煎治疗,以Thy1.1为肝脏卵圆细胞(HOC)标记物,通过免疫组织化学、蛋白定量检测以及激光共聚焦检测技术,观察一贯煎对肝脏干细胞增殖及分化及相关因子的影响。[结果]DMN大鼠肝硬化形成过程中存在HOC的动态变化,一贯煎组中羟脯氨酸含量减少,与模型组比较差异无显著意义(P>0.05)。Thy1.1与AFP共定位细胞像素密度值明显增高,与模型组比较,差异有显著性意义(P<0.01),Thy1.1与CK19共定位细胞像素密度值略高于模型组,差异无显著性意义(P>0.05)。[结论]具备养阴功能的一贯煎可诱导HOC向肝细胞分化,促进已经成型的肝硬化的逆转,重构损伤的肝组织,从而改善肝脏功能。

基于DMN的高光谱图像分割方法研究

简述高光谱遥感光谱特征体系(包括光谱曲线特征、光谱变换特征和光谱度量特征3个层面)。研究马尔科夫网的概念和方法,生成基于光谱角(SA)特征度量的DMN,并以DMN为证据对高光谱图像进行分割;研究和实验表明基于SA信息的马尔科夫网可以很好地综合高光谱数据空间特征与光谱特征间的关系,为进一步数据处理提供优化控制(其实质是概率神经网络)。最后提出未来应用和研究方向。

沙苑子黄酮对DMN诱导的大鼠肝纤维化形成的影响

目的 观察沙苑子黄酮对二甲基亚硝胺 (DMN)诱导的大鼠肝纤维化形成的影响。方法 采用DMN诱导大鼠肝纤维化 ,期间给予灌服沙苑子黄酮 (30 ,6 0 ,12 0mg·kg-1) ,设秋水仙碱组作对照 ,给药 4wk后 ,测定血清谷丙氨转氨酶(ALT)、谷草转氨酶 (AST)活性、总蛋白 (TP)和白蛋白 (Alb)含量 ,放射免疫分析法测定血清透明质酸 (HA)、层粘连蛋白(LN)含量。光镜和电镜观察肝细胞结构和肝纤维化程度。结果 沙苑子黄酮预防给药 ,明显降低DMN诱导肝纤维化大鼠血清ALT、AST活性 (P <0 0 1,P <0 0 1) ,提高血清TP和Alb含量 (P <0 0 5 ,P <0 0 1) ,降低血清HA和LN含量 (P <0 0 1)。病理学观察结果 ,沙苑子黄酮预防组大鼠胶原纤维沉积明显减轻 ,假小叶结构明显减少 ,电镜观察显示 ,沙苑子黄酮组肝细胞结构接近正常 ,disse间隙、肝细胞内胶原纤维明显减少。结论 沙苑子黄酮预防给药 。

Effects of Aqueous Extract of Plumbago zeylanica L. in the Reversal of DMN-induced Hepatic Fibrosis in Rat

[ Objectives ] This study was conducted to evaluate the action of the aqueous extract of a medicinal plant Plumbago zeylanica L. in the reversal of dime- thylnitrosamine （DMN） -induced hepatic fibrosis in rats, and to provide a scientific basis for the utilization of P. zeylanica in treatment of hepatic fibrosis. [Meth- ods ] Hepatic fibrosis in rats was induced by intraperitoneal injection of DMN. The rats were then given the aqueous extract of P. zeylanica at high, medium or low concentration by garage for five weeks. Serum level of alanine aminotransferase （ALT） was determined by lactate dehydrogenase （LDH）-release assay, and serum level of aspartate transaminase （AST） was measured by UV-malate dehydrogenase （MDH） assay. Serum levels of total bilirubin （TBIL）, direct bilirubin （DBIL） and indirect bilirubin （1BIL） were measured by vanadate oxidation assay. Four indices of hepatic fibrosis （hyaluronic acid, laminin, procollagen type III and colla- gen type IV） were determined by radioimmunoassay （RIA） assay. Morphological damage of liver tissue was observed by hematoxylin-eosin staining （H＆E stai- ning）. Immunohistochemical staining was performed to determine the location and area of deposited collagen type I, collagen type III and ct-smeoth muscle actin （a-SMA） in liver tissue. [ Results] Compared with the negative control （rats with diseased fiver and untreated with P. zeylanica aqueous extract）, the serum lev- els of ALT, AST, TBIL, DBIL and IBIL were significantly decreased by P. zeylanica aqueous extract; the levels of the four serum indices of hepatic fibrosis were also obviously reduced. H＆E staining showed that hepatic fibrosis in rats was obviously inhibited or even reversed by P. zeylanica aqueous extract. Immunohisto- chemical staining proved that the aqueous extract of P. zeylanica significantly reduced the area and coloration of collagen type I, collagen type III and ct-SMA in rat liver. [ Conclusions] The aqueous extract of P. zeylanica has a definite effect in reversal of DMN-indueed hepatic fibrosis in rat by promoting the recovery of liver function, reversal of histopathological changes and reducing fibrotic collagen.

肝达康对DMN致大鼠肝损伤血清ALT、AST、TBIL、TP及ALB的影响

目的:研究肝达康对二甲基亚硝胺(DMN)致大鼠肝损伤模型的保护作用。方法:雄性Wistar大鼠55只,随机分为正常对照组(n=10)、模型组(n=15)、肝达康预防组(n=15)及秋水仙碱组(n=15)。模型组、肝达康预防组和秋水仙碱组以10mg/kg DMN腹腔注射,每日1次,每周连续3天,共4周。以上3组在造模同时给予药物或生理盐水灌胃。于第4周末处死全部大鼠,留取血清。采用全自动生化分析仪检测ALT、AST、TBIL、TP、ALB。结果:与正常对照组比较,模型组大鼠血清ALT和AST活性显著增高,TBIL水平明显升高,ALB和TP含量降低。肝达康颗粒治疗后使ALT和AST活性降低,TBIL水平降低,TP和Alb含量升高。秋水仙碱组可降低ALT和AST活性,使ALB含量升高,但对TP含量和TBIL水平均无调节作用。结论:肝达康对实验性大鼠肝损伤模型具有明显改善肝功能的作用。

虫草多糖逆转DMN诱导大鼠肝纤维化的作用及机制研究

目的:研究虫草多糖抗肝纤维化作用的机制。方法:将SD大鼠随机分为正常组、模型组、虫草多糖组。采用二甲基亚硝胺诱导的大鼠肝纤维化模型。经过虫草多糖治疗4周后,大鼠肝脏用丽春红胶原染色观察大鼠胶原纤维沉积的变化,观察大鼠血清肝功能的变化,盐酸水解法检测肝组织羟脯氨酸含量,Envision两步法测定肝组织Ⅳ型胶原含量和金属蛋白酶组织抑制因子2(TIMP-2)含量;酶图法检测肝组织金属蛋白酶2(MMP-2)活性,同时检测肝组织超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量的改变。结果:镜下检查可见模型组大鼠肝脏胶原纤维间隔形成;血清肝功能指标异常,MMP-2含量降低;组织Hyp含量,Ⅳ型胶原含量,I型胶原蛋白表达,TIMP-2,MDA含量,均较正常组均显著增加,SOD活性下降,而虫草多糖组的上述指标较模型组均有不同程度的显著下降,使SOD活性升高,MMP-2含量升高。结论:虫草多糖有显著的抗肝纤维化作用,其机制与促进胶原降解和抗脂质过氧化作用有关。

DMN肝纤维化模型肝组织I、Ⅲ型胶原和TIMP-1 mRNA表达及复方861的干预作用

目的 研究二甲基亚硝胺 (DMN)肝纤维化模型I型胶原 (CoL -1)、Ⅲ型胶原 (CoL -Ⅲ )和基质金属蛋白酶组织抑制因子 (TIMP -1)mRNA表达以及复方 86 1的干预作用。材料和方法 采用 1%DMN 1ml /kg腹腔注射模型组大鼠 ,复制DMN诱导的大鼠肝纤维化模型 ,同时复方 86 1灌胃 3g/kg ,共 8周 ,以RT -PCR法观察肝纤维化模型肝组织CoL -Ⅰ、CoL -Ⅲ及TIMP -1mRNA表达水平。结果 DMN大鼠肝纤维化模型组CoL -I、CoL -Ⅲ及TIMP-1mRNA分别为 0 82 7± 0 0 94、 0 95 3± 0 0 33及 0 92 4± 0 110 ,明显高于正常对照组 (P <0 0 1) ;复方 86 1治疗组CoL -I、CoL -Ⅲ及TIMP -1mRNA为 0 4 97± 0 0 5 7、 0 85 1± 0 0 6 5和 0 6 48± 0 10 7,明显低于模型对照组 (P <0 0 1或P <0 0 5 )。结论 DMN肝纤维化模型肝组织CoL -Ⅰ、CoL -Ⅲ及TIMP -1mRNA表达水平增高 ,复方 86 1能够抑制肝组织CoL -Ⅰ、CoL -Ⅲ及TIMP -1mRNA的表达 ,从而发挥其抗肝纤维化的作用。

芪参益气滴丸对DMN大鼠肝纤维化及肝组织TIMP-1表达的影响

目的：应用二甲基亚硝胺(DMN)建立肝纤维化大鼠模型,研究芪参益气滴丸对纤维化肝组织中TIMP-1表达的影响。方法：60只大鼠随机分为正常对照组、6 wk模型组、芪参益气滴丸干预组(干预组)、10 wk模型组及芪参益气滴丸治疗组(治疗组)。采用DMN腹腔内注射的方法建立肝纤维化大鼠模型。按6期分类法评价各组肝纤维化程度。应用RT-PCR检测各组肝组织中TIMP-1 mRNA水平；应用免疫组织化学技术检测各组动物肝组织TIMP-1的表达。结果：芪参益气滴丸干预组与治疗组的大鼠肝纤维化程度分别较6 wk模型组与10 wk模型组显著减轻(P<0．01)。干预组与治疗组肝组织中TIMP-1 mRNA水平分别较6 wk模型组与10 wk模型组显著下降(P<0．01),TIMP-1的阳性表达均分别较6 wk模型组与10 wk模型组显著减弱(P<0．05,P<0．01)。结论：芪参益气滴丸能明显改善纤维化肝组织病理改变和减轻肝纤维化程度,抑制TIMP-1的表达是其抗肝纤维化的机制之一。

DMN所致小鼠肝损伤模型中血清IL-18和肝脏TNF-α mRNA的表达

目的 观察二甲基亚硝胺 (DMN )诱导实验性肝损伤模型过程中 ,小鼠血清IL - 18及肝脏TNF -αmRNA表达的动态变化。方法 0 .1%DMN腹腔注射 ,制备小鼠实验性肝损伤模型。用ELASA法测定血清IL -18水平 ,半定量逆转录聚酶链反应 (RT -PCR)检测肝组织TNF -αmRNA的表达。结果 随着肝脏炎症坏死程度的加重 ,血清IL - 18水平及肝脏TNF -αmRNA的表达逐渐增加 ,均于第 5次注射DMN后达到最高峰 (P <0 .0 1) ,损伤后自行恢复期内明显回落。两者呈正相关趋势。结论 IL - 18、TNF -α均参与了DMN诱导的肝脏毒性反应 ,具有协同的促炎性。两者皆在肝损伤的自行恢复中发挥了一定作用。

磁导向^(131)I-Sc-7269-DMN治疗荷人肝癌裸鼠的实验研究

目的 研究磁导向1 31 I标记抗血管内皮生长因子单克隆抗体Sc 72 6 9和葡聚糖磁性纳米颗粒复合物 (Sc 72 6 9 DMN)在荷人肝癌裸鼠模型体内的生物学分布、抑瘤效能及安全性。方法 于 18只荷人肝癌裸鼠肿瘤部位体表持续设置磁场 ,分别自瘤体内均匀注射 (n =9)或尾静脉注射 (n =9) 1 31 I Sc 72 6 9 DMN约 0 74MBq ,进行生物学分布研究。另 2 5只平均分为 5组 ,其中 4组瘤内分别注射1 31 I Sc 72 6 9 DMN、1 31 I Sc 72 6 9、1 31 I DMN及1 31 I(放射性浓度均为 74MBq ml) ,其中1 31 I Sc 72 6 9 DMN组和1 31 I DMN组裸鼠肿瘤部位体表持续设置磁场 ;余 1组作为对照组注射生理盐水。治疗后观察肿瘤生长延迟时间 (TGD)及体重变化 ,并计算抑制率和检测外周血白细胞计数。结果 给药后 4、2 4和 4 8h局部瘤内给药组肿瘤组织百分注射剂量率 (%ID g)分别为 10 4 0 6、10 1 5 8和 10 0 96 ;静脉给药组分别为85 33、89 6 7和 90 0 0 ,两组间差异有显著性 (P <0 0 5 )。1 31 I Sc 72 6 9 DMN组TGD为 (13 3± 3 3)d ,肿瘤抑制率为 89 0 % ,与其他组相比差异有显著性 (P <0 0 5 ) ;该组治疗后外周血白细胞虽有下降[(390 0± 30 9) μl],但与对照组相比差异无显著性。 结论 1 31 I Sc 72 6 9

图像分割中MRF与DMN方法评述与比较

综述马尔科夫随机场(Markov Random Field,MRF)的研究和应用历史,着重讨论了图像分割中MRF的原理和应用。分析了可分解马尔科夫网(Decomposable Markov Networks,DMN)的一般方法以及DMN在图像分割问题中的应用。比较研究了MRF和DMN的区别和联系。