慢性乙型肝炎患者血清XCL1与免疫损伤的相关性分析

Objective To explore the relevance between serum XCL1 levels and liver damage in hepatitis B patients.Methods The serum concentration of XCL1 was detected by enzyme linked immu-nosorbent assay (ELISA).Peripheral blood T-cell subsets were detected by flow cytometry (FCM).Liver function was assayed by automatic biochemistry analyzer, hepatitis B antigen/antibody semi-quantitative index was detected by time-resolved fluorescence analyzer, and HBV-DNA load was detected by automatic fluorescence quantitative PCR.Results Serum concentration of XCL1 in control group ( n = 20), mild chronic hepatitis B (CHB) group ( n =29), moderate CHB group ( n =20) and severe CHB group ( n =26)were (8.24±1.94) pg/ml, (10.99±1.94) pg/ml, (12.83 ±2.59) pg/ml, (13.72 ±3.13) pg/ml,respectively.The concentration of XCL1 in all CHB groups was significantly higher than control group ( P＜ 0.05 ).The concentration of XCL1 in severe CHB group was significantly higher than mild CHB group (P ＜ 0.05).XCL1 was positively correlated with ALT, AST, TBIL and DBIL, and the coefficients were (r =0.463、 0.472、 0.413、 0.440, P ＜0.01 ), respectively.The serum XCL1 levels in hepatitis B virus with low load group was lower than hepatitis B virus with high load group.The percentage of CD4 + T in hepatitis B virus with low load group and high load group were (41.26 ± 11.33)%, (33.01 ± 5.96)%,and the difference was statistically significant.Conclusion Serum concentrations of XCL1 were closely related to the degree of liver inflammation in hepatitis B patients.XCL1 may be involved in the process of chronic hepatitis B.     

急性乙型肝炎临床特征和病毒标志物动态变化分析

Objective To explore the dynamic change of viral marker and clinical features in acute hepatitis B (AHB)and distinguish AHB from chronic hepatitis B(CHB) in acute onset. Methods Viral marker, HBV DNA in serum and clinical features were analyzed in 105 patients with AHB (AHB group) and 102 patients with CHB in acute onset (CHB group) between 2005 and 2009. Results There was no statistical difference in the mean levels of ALT, TBil, HBsAg, HBeAg and HBV DNA between AHB and CHB group on admission. However, the titer of auti-HBc-IgM in AHB group was(26.34 ±3.74)S/CO, which was obviously higher than that in CHB group, which was( 14.46 ± 3.10)S/CO, there was a statistical difference between the two groups( P < 0.05). After 2 weeks treatment, the levels of ALT and TBil in AHB patients decreased (1540.50±225.54)IU/L and (103.60± 46.48) μmol/L respectively, the decreased levels in AHB group were high compared to CHB group; the levels of HBsAg, HBeAg and HBV DNA in AHB group decreased (2558.46 ±644.26) IU/mL, (420.20± 63.20) S/CO and (4.53± 1.42) log10copies/mL respectively, and the levels decreased obviously compared to CHB group (P < 0.05). The decreased level of anti-HBc-IgM in AHB group was no statistical difference to CHB group after 2 weeks treatment (P > 0.05). 19.04% of the AHB patients were HBV DNA negative seroconversion before they were hospitalized. The level of HBsAg and HBeAg in AHB group declined quickly. Separately, 90.47% and 94.24% of the AHB patients had HBsAg and HBeAg seroconversion at the end of follow-up in AHB group. The level of ALT in AHB decreased quickly but its normalization was slower than the clearance of HBV. Conclusions There is no difference in viral marker, HBV DNA and clinical features between AHB and CHB in acute onset patients on admission, but the recovery of liver function in AHB is obviously after treatment. Anti-HBc-IgM (≥20 S/CO), dynamic change and seroconversion viral marker, ALT ≥20×ULN and recovery can be used to differentiate AHB from CHB in acute onset.     

急性乙型肝炎临床特征和病毒标志物动态变化分析

Objective To explore the dynamic change of viral marker and clinical features in acute hepatitis B (AHB)and distinguish AHB from chronic hepatitis B(CHB) in acute onset. Methods Viral marker, HBV DNA in serum and clinical features were analyzed in 105 patients with AHB (AHB group) and 102 patients with CHB in acute onset (CHB group) between 2005 and 2009. Results There was no statistical difference in the mean levels of ALT, TBil, HBsAg, HBeAg and HBV DNA between AHB and CHB group on admission. However, the titer of auti-HBc-IgM in AHB group was(26.34 ±3.74)S/CO, which was obviously higher than that in CHB group, which was( 14.46 ± 3.10)S/CO, there was a statistical difference between the two groups( P < 0.05). After 2 weeks treatment, the levels of ALT and TBil in AHB patients decreased (1540.50±225.54)IU/L and (103.60± 46.48) μmol/L respectively, the decreased levels in AHB group were high compared to CHB group; the levels of HBsAg, HBeAg and HBV DNA in AHB group decreased (2558.46 ±644.26) IU/mL, (420.20± 63.20) S/CO and (4.53± 1.42) log10copies/mL respectively, and the levels decreased obviously compared to CHB group (P < 0.05). The decreased level of anti-HBc-IgM in AHB group was no statistical difference to CHB group after 2 weeks treatment (P > 0.05). 19.04% of the AHB patients were HBV DNA negative seroconversion before they were hospitalized. The level of HBsAg and HBeAg in AHB group declined quickly. Separately, 90.47% and 94.24% of the AHB patients had HBsAg and HBeAg seroconversion at the end of follow-up in AHB group. The level of ALT in AHB decreased quickly but its normalization was slower than the clearance of HBV. Conclusions There is no difference in viral marker, HBV DNA and clinical features between AHB and CHB in acute onset patients on admission, but the recovery of liver function in AHB is obviously after treatment. Anti-HBc-IgM (≥20 S/CO), dynamic change and seroconversion viral marker, ALT ≥20×ULN and recovery can be used to differentiate AHB from CHB in acute onset.     

热性惊厥患儿血清褪黑素水平和细胞免疫功能的变化及其临床意义

Objective To investigate the changes of melatonin and cellular immunological function in children with febrile seizures and its clinical significance. Methods 50 children, including 23 cases with complex febrile seizure (CFS) and 27 cases with simple febrile seizure (SFS) , and 25 cases with upper respiratory infections children selected as control group were enrolled in this study. Serum melato- nin was measured by enzyme-linked immunosorbent assay (ELISA) and cellular immunological function was measured by flow eytomcter. Results The levels of serum melatonin in the 3 groups of CFS, SFS, control were(14. 91±2. 61) ng/L, (20. 72±2. 54) ng/L, (23.93± 2. Ol) ng/L, respectively. The melatonin levels in CFS children were significantly decreased than that in control group and SFS children (P <0. O1). CD3 + ,CD4 +, the ratio of CD4 + /CD8 + and CD8 + in CFS group were significantly decreased than that in control group and SFS group (P <0.01). The ratio of CD4 +/CD8 + in SFS group was significantly decreased than that in control group (P <0.05), but CD3 + ,CD4 + and CD8 + had no statistics significance among these groups(P >0. 05). The serum rnelatonin level were positive related withdecreaseddegreeofCD3+,CD4+ andtberatioofCD4+ /CDS+ (r≥0. 472, P <0.05). Conclusion The disorder cfcellular immunological function was possible related with the loss of serum melatonin, and the loss of serum melatonin maybe one of the reasons for febrile seizures relapse and brain injured.     

热性惊厥患儿血清褪黑素水平和细胞免疫功能的变化及其临床意义

Objective To investigate the changes of melatonin and cellular immunological function in children with febrile seizures and its clinical significance. Methods 50 children, including 23 cases with complex febrile seizure (CFS) and 27 cases with simple febrile seizure (SFS) , and 25 cases with upper respiratory infections children selected as control group were enrolled in this study. Serum melato- nin was measured by enzyme-linked immunosorbent assay (ELISA) and cellular immunological function was measured by flow eytomcter. Results The levels of serum melatonin in the 3 groups of CFS, SFS, control were(14. 91±2. 61) ng/L, (20. 72±2. 54) ng/L, (23.93± 2. Ol) ng/L, respectively. The melatonin levels in CFS children were significantly decreased than that in control group and SFS children (P <0. O1). CD3 + ,CD4 +, the ratio of CD4 + /CD8 + and CD8 + in CFS group were significantly decreased than that in control group and SFS group (P <0.01). The ratio of CD4 +/CD8 + in SFS group was significantly decreased than that in control group (P <0.05), but CD3 + ,CD4 + and CD8 + had no statistics significance among these groups(P >0. 05). The serum rnelatonin level were positive related withdecreaseddegreeofCD3+,CD4+ andtberatioofCD4+ /CDS+ (r≥0. 472, P <0.05). Conclusion The disorder cfcellular immunological function was possible related with the loss of serum melatonin, and the loss of serum melatonin maybe one of the reasons for febrile seizures relapse and brain injured.     

热性惊厥患儿血清褪黑素水平和细胞免疫功能的变化及其临床意义

Objective To investigate the changes of melatonin and cellular immunological function in children with febrile seizures and its clinical significance. Methods 50 children, including 23 cases with complex febrile seizure (CFS) and 27 cases with simple febrile seizure (SFS) , and 25 cases with upper respiratory infections children selected as control group were enrolled in this study. Serum melato- nin was measured by enzyme-linked immunosorbent assay (ELISA) and cellular immunological function was measured by flow eytomcter. Results The levels of serum melatonin in the 3 groups of CFS, SFS, control were(14. 91±2. 61) ng/L, (20. 72±2. 54) ng/L, (23.93± 2. Ol) ng/L, respectively. The melatonin levels in CFS children were significantly decreased than that in control group and SFS children (P <0. O1). CD3 + ,CD4 +, the ratio of CD4 + /CD8 + and CD8 + in CFS group were significantly decreased than that in control group and SFS group (P <0.01). The ratio of CD4 +/CD8 + in SFS group was significantly decreased than that in control group (P <0.05), but CD3 + ,CD4 + and CD8 + had no statistics significance among these groups(P >0. 05). The serum rnelatonin level were positive related withdecreaseddegreeofCD3+,CD4+ andtberatioofCD4+ /CDS+ (r≥0. 472, P <0.05). Conclusion The disorder cfcellular immunological function was possible related with the loss of serum melatonin, and the loss of serum melatonin maybe one of the reasons for febrile seizures relapse and brain injured.     

热性惊厥患儿血清褪黑素水平和细胞免疫功能的变化及其临床意义

Objective To investigate the changes of melatonin and cellular immunological function in children with febrile seizures and its clinical significance. Methods 50 children, including 23 cases with complex febrile seizure (CFS) and 27 cases with simple febrile seizure (SFS) , and 25 cases with upper respiratory infections children selected as control group were enrolled in this study. Serum melato- nin was measured by enzyme-linked immunosorbent assay (ELISA) and cellular immunological function was measured by flow eytomcter. Results The levels of serum melatonin in the 3 groups of CFS, SFS, control were(14. 91±2. 61) ng/L, (20. 72±2. 54) ng/L, (23.93± 2. Ol) ng/L, respectively. The melatonin levels in CFS children were significantly decreased than that in control group and SFS children (P <0. O1). CD3 + ,CD4 +, the ratio of CD4 + /CD8 + and CD8 + in CFS group were significantly decreased than that in control group and SFS group (P <0.01). The ratio of CD4 +/CD8 + in SFS group was significantly decreased than that in control group (P <0.05), but CD3 + ,CD4 + and CD8 + had no statistics significance among these groups(P >0. 05). The serum rnelatonin level were positive related withdecreaseddegreeofCD3+,CD4+ andtberatioofCD4+ /CDS+ (r≥0. 472, P <0.05). Conclusion The disorder cfcellular immunological function was possible related with the loss of serum melatonin, and the loss of serum melatonin maybe one of the reasons for febrile seizures relapse and brain injured.     

热性惊厥患儿血清褪黑素水平和细胞免疫功能的变化及其临床意义

Objective To investigate the changes of melatonin and cellular immunological function in children with febrile seizures and its clinical significance. Methods 50 children, including 23 cases with complex febrile seizure (CFS) and 27 cases with simple febrile seizure (SFS) , and 25 cases with upper respiratory infections children selected as control group were enrolled in this study. Serum melato- nin was measured by enzyme-linked immunosorbent assay (ELISA) and cellular immunological function was measured by flow eytomcter. Results The levels of serum melatonin in the 3 groups of CFS, SFS, control were(14. 91±2. 61) ng/L, (20. 72±2. 54) ng/L, (23.93± 2. Ol) ng/L, respectively. The melatonin levels in CFS children were significantly decreased than that in control group and SFS children (P <0. O1). CD3 + ,CD4 +, the ratio of CD4 + /CD8 + and CD8 + in CFS group were significantly decreased than that in control group and SFS group (P <0.01). The ratio of CD4 +/CD8 + in SFS group was significantly decreased than that in control group (P <0.05), but CD3 + ,CD4 + and CD8 + had no statistics significance among these groups(P >0. 05). The serum rnelatonin level were positive related withdecreaseddegreeofCD3+,CD4+ andtberatioofCD4+ /CDS+ (r≥0. 472, P <0.05). Conclusion The disorder cfcellular immunological function was possible related with the loss of serum melatonin, and the loss of serum melatonin maybe one of the reasons for febrile seizures relapse and brain injured.     

慢性乙型肝炎患者血清XCL1与免疫损伤的相关性分析

目的 探讨慢性乙型肝炎患者血清XCL1含量与肝损程度及HBV DNA含量的相关性,探讨XCL1表达变化的可能原因.方法 采用酶联免疫吸附法（ELISA）检测血清XCL1浓度;流式细胞仪检测T淋巴细胞亚群;时间分辨荧光分析仪检测乙型肝炎抗原/抗体半定量指标;全自动荧光定量PCR仪检测HBV-DNA载量;全自动生化仪检测肝功能.结果 （1）正常对照组、慢性乙肝（轻度）组、慢性乙肝（中度）组、慢性乙肝（重度）组血清XCL1浓度分别为（8.24±1.94）pg/ml、（10.99±1.94）pg/ml、（12.83±2.59）pg/ml、（13.72±3.13）pg/ml,慢性乙肝（轻、中、重度）组血清XCL1浓度显著高于对照组（P＜0.05）;慢性乙肝（重度）组血清XCL1浓度明显高于慢性乙肝（轻度）组（P＜0.05）;慢性乙肝（中度）组与慢性乙肝（轻、重）度组血清XCL1浓度比较,差异无统计学意义（P＞0.05）;XCL1浓度与ALT、AST、TBIL、DBIL水平呈正相关（r=0.463、0.472、0.413、0.440,P＜0.01）.（2）乙肝病毒低载量组血清XCL1浓度为（11.43±2.01）pg/ml,与高载量组相比差异有统计学意义（P＜0.05）,乙肝病毒低载量组及高载量组血清CD4＋T细胞百分比分别为（41.26±11.33）%、（33.01±5.96）%,两者比较差异有统计学意义（P＜0.05）.结论 XCL1水平与肝脏炎症程度密切相关,可反映HBV感染后机体的免疫状态.     

慢性乙肝患者乙肝病毒载量与PBMC凋亡及Caspase-8的相关性研究

目的 探讨慢性乙肝（CHB）患者血清HBVDNA载量与外周血单个核细胞（PBMC）凋亡及Caspase-8活性的关系.方法 选取30例CHB患者为实验组,并按单位血清中HBVDNA载量高低分为A（高病毒载量）、B（中病毒载量）、C（低病毒载量）三小组,选取10例正常成年人为对照组,用淋巴细胞分离液分离两组的PBMC,体外与植物血凝素（PHA）共同培养72 h,用PI对PBMC进行染色并以流式细胞仪检测PBMC的凋亡百分率,同时以比色法检测PBMC细胞内Caspase-8的活性.结果 实验组PBMC的凋亡率（26.88±7.37）%高于健康对照组（14.95±2.53）%（P〈0.01）;实验组中A、B、C三个小组PBMC的凋亡率依次递减,分别为（34.75±4.59）%,（25.63±3.55）%,（18.91±3.81）%;实验组Caspase-8的活性2.99±0.82高于健康对照组1.43±0.91（P〈0.01）,且A、B、C三个小组的Caspase-8活性亦依次递减,分别为3.87±0.35,2.95±0.36,1.95±0.29.实验组PBMC凋亡率与Caspase-8活性呈正相关（r=0.825,P〈0.01）.结论 CHB患者PBMC存在活化诱导细胞死亡（AICD）现象,凋亡酶蛋白Caspase-8在此过程中活性升高,可能参与了凋亡信号的转导过程;HBVDNA载量与PBMC凋亡率及Caspase-8的活性相关,可能是诱发PBMC凋亡的原因之一.     

NF-κB p65在早产和足月产胎盘组织中的不同表达

目的 比较NF-κB p65蛋白在足月和早产孕妇绒毛、脐带、胎膜等胎盘组织中的表达情况,探索NF-κB p65蛋白在早产发生中的意义.方法 收集本院早产分娩产妇50例,足月分娩产妇30例为对照组,按分娩方式不同分为阴道分娩组和剖宫产组.采用免疫组织化学法对其绒毛、脐带、胎膜和蜕膜等胎盘组织进行NF-κB p65蛋白检测,比较不同组间NF-κB p65蛋白的表达强度.结果 （1）足月产孕妇在不同胎盘组织中NF-κB P65蛋白表达强度均以阴性和弱阳性为主,部分阳性主要表达部位为细胞浆.足月孕妇临产前后绒毛、脐带和胎膜等不同胎盘组织中NF-κB P65蛋白的表达强度差异均无统计学意义（P＞0.05）.（2）早产孕妇胎盘组织中NF-κB p65蛋白表达以阳性和强阳性为主,阳性表达部位为胞浆和胞核均有.早产组孕妇绒毛和胎膜中NF-κB p65蛋白表达水平（18%,56%）高于足月组（6.7%,13.3%,P＜0.01）,早产剖宫产组胎膜、蜕膜NF-κB p65蛋白表达（52.9%,58.8%）高于足月剖宫产组（13.3%,6.7%,P＜0.01）,早产阴道产绒毛、胎膜（24.2%,57.6%）高于足月阴道产（6.7%,13.3%,P＜0.01）.结论 足月分娩孕妇临产前后不同胎盘组织中NF-κB p65蛋白表达强度变化不明显;且与分娩方式无关.NF-κB p65蛋白在早产胎盘组织中表达强度高于足月组,其参与了早产的发生和发展机制.     

脂多糖经MyD88／NF-KB信号途径抑制Bewo细胞中乙型肝炎病毒复制

目的探讨Toll样受体4（TLR4）配体脂多糖（LPS）抑制人滋养层细胞Bewo中乙型肝炎病毒（rtBv）复制的作用机制,为防治HBV宫内感染提供依据。方法首先将2txg1．3倍HBV全基因重组质粒pcDNA3．1（＋）-HBV1．3转染Bewo细胞12h后,以TLR4配体LPS处理3d。尔后用LPS处理Bewo细胞,观察IFN—β、TNF-a表达的动力学、NF—KB拮抗剂二硫代氨基甲酸吡咯烷（PDTC）对LPS诱导Bewo细胞产生细胞因子的作用。采用微粒子酶免疫分析法（MEIA）和荧光定量PCR法分别检测HBsAg、HBeAg和HBVDNA水平,并以ELISA和RT—PCR分别检测IFN-β、TNF—a水平及TIR结构域的转接蛋白（TRIF）、髓样分化蛋白（MyD88）表达。结果与对照组比较,LPS可显著抑制Bewo细胞中HBV复制（P〈0．01）,且LPS可显著诱导Bewo细胞产生TNF-a（P〈0．05）,呈时间和剂量依赖性。PDTC可抑制LPS诱导细胞产生TNF-a,显著低于对照组（P〈0．01）,但对IFN—β无显著作用（P〉0．05）。与对照组比较,LPS可诱导HBV重组质粒转染的Bewo细胞表达MyD88（P〈0．01）。结论通过MyD88／NF—KB信号途径诱导Bewo细胞产生TNF—a,TLR4配体LPS可显著抑制HBV复制。     

CD147、NF-κB在食管鳞状细胞癌组织中的表达及意义

目的 研究基质金属蛋白酶刺激因子（CD147）、核转录因子-κB[NF-κB（p65）]在食管鳞状细胞癌组织中的表达及其在食管鳞癌侵袭转移的作用及可能机制.方法 应用免疫组织化学方法检测40例食管鳞癌患者癌组织及其癌旁正常对照组织CD147、NF-κB的表达.结果 CD147、NF-κB在食管鳞癌表达阳性率为77.5%、87.5%,在癌旁正常对照组为25%、42.5%,2组差异有统计学意义（P＜0.05）;CD147在早期和中晚期食管癌表达阳性率为33.3%、90.3%,在NF-κB为55.6%、96.8%,2组差异均有统计学意义（P＜0.05）;CD147在食管鳞癌无转移和转移组表达阳性率为28.6%、87.9%,在NF-κB为42.9%、97%,2组差异均有统计学意义（P＜0.05）.结论 CD147、NF-κB在食管鳞癌组织表达增高,与肿瘤的浸润、转移相关,它们可能是通过共同的作用途径来实现的.     

喉鳞癌组织NF—kB的表达和淋巴管计数的临床意义及相关性研究

目的研究喉鳞癌组织中核因子-kB（NF—kB）表达水平和淋巴管计数,探讨两者在喉鳞癌中的临床病理意义及相互关系。方法收集50例喉鳞癌手术切除组织标本,另取10例声带息肉组织作对照,常规制作石蜡包埋切片,NF-kB表达的检测和淋巴管计数均采用SP免疫组化法。结果喉鳞癌NF-KB表达阳性率和淋巴管计数为明显高于声带息肉组[60％vs10％,P〈0．05,（13．3±3．4）个／HP vs（6．1±3．8）个／HP,P〈0．01];高分化喉鳞癌和未转移病例NF—KB表达阳性率和淋巴管计数明显低于低分化喉鳞癌和转移病例[33．3％vs84．2％,（9．6±2．7）个／HP vs（16．9±3．4）个／HP,P〈0．05或P〈0．01];NF—KB表达阳性的喉鳞癌淋巴管计数明显高于阴性表达者[（14．9±4．1）个／HP vs（9．8±3．1）个／HP,P〈0．01]。结论NF—kB表达和淋巴管计数均为反映喉鳞癌进展、转移等生物学特性及预后的重要标记物,喉鳞癌细胞分泌的NF—kB可能促进淋巴管生成。     

喉鳞癌组织NF-κB的表达和淋巴管计数的临床意义及相关性研究

目的 研究喉鳞癌组织中核因子-κB(NF-κB)表达水平和淋巴管计数,探讨两者在喉鳞癌中的临床病理意义及相互关系.方法 收集50例喉鳞癌手术切除组织标本,另取10例声带息肉组织作对照,常规制作石蜡包埋切片,NF-κB表达的检测和淋巴管计数均采用SP免疫组化法.结果 喉鳞癌NF-κB表达阳性率和淋巴管计数为明显高于声带息肉组[60%vs10%,P<0.05,(13.3±3.4)个/HP vs(6.1±3.8)个/HP,P<0.01] ;高分化喉鳞癌和未转移病例NF-κB表达阳性率和淋巴管计数明显低于低分化喉鳞癌和转移病例[33.3%vs 84.2%,(9.6±2.7)个/HP vs(16.9±3.4)个/HP,P<0.05或P<0.01] ;NF-κB表达阳性的喉鳞癌淋巴管计数明显高于阴性表达者[(14.9±4.1)个/HP vs(9.8±3.1)个/HP,P<0.01] .结论 NF-κB表达和淋巴管计数均为反映喉鳞癌进展、转移等生物学特性及预后的重要标记物,喉鳞癌细胞分泌的NF-κB可能促进淋巴管生成.     

血清高迁移率族蛋白-1在不同慢性乙肝相关性肝病患者的含量变化及临床意义

目的 研究晚期炎症介质高迁移率族蛋白-1（HMGB1）在慢性乙型肝炎、慢性重型乙型肝炎及乙肝肝硬化病程中的临床意义.方法 选择慢性乙型肝炎患者40例,慢性重型乙型肝炎患者18例,乙肝肝硬化患者18例,健康对照者20例,应用ELISA法检测血清HMGB1含量;同时检测各组患者肝功能生化指标、凝血酶原活动度（PTA）及肝纤维化指标.结果 HMGB1检出含量在乙型肝炎患者慢性重型肝炎组高于慢性肝炎组（P＜0.01）,慢性肝炎组高于正常对照组（P＜0.01）,肝硬化组与慢性重型肝炎组、慢性肝炎组之间差异有统计学意义（P＜0.01）.HMGB1检出含量与外周血TBIL、AST/ALT、HA及PⅢNP均呈正相关（r=0.865,0.646,0.783,0.662,P＜0.01）,与PTA及白蛋白水平呈负相关（r=-0.915,-0.852,P＜0.01）.结论 乙肝相关性肝病患者血清HMGB1含量与其疾病严重程度密切相关,同时HMGB1也是辅助诊断肝纤维化的指标.     

大鼠实验性胃炎中PGP9．5、C—kit及胃泌素、生长抑素表达的观察研究

目的通过观察胃炎大鼠组织PGP9．5及c—kit与胃泌素（GAS）、生长抑素（SS）表达变化，探讨胃cajal间质细胞（ICC）、肠神经及胃肠激素在胃炎发病中的作用。方法45只大鼠分胃炎A组、胃炎B组、对照组3组，分别灌喂幽门螺杆菌（Hp）SS1菌株、2％阿司匹林和0．6N盐酸1：1混合液、生理盐水，处死后取胃窦及胃体组织PGP9．5染色及检测胃体黏膜C-kit及胃窦黏膜GAS、SS表达，测量胃壁神经元胞体、c—kit阳性表达的ICC最长直径（Dmax，μm）、平均面积（μm^2）及光密度（nm）以及GAS、SS表达的积分光密度，并进行比较。结果（1）胃炎A组、B组胃壁神经元表达PGP9．5细胞平均面积、光密度均低于对照组（P〈0．01），胃炎A组与B组比较差异无统计学意义（P〉0．05）；（2）胃炎A组GAS表达明显高于对照组，而SS表达则低于对照组（P〈0．05）。胃炎B组与对照组比较两项表达结果差异均无统计学意义（P〉0．05）。直线相关分析显示SS与GAS呈负相关（r=-0．333，P〈0．01）；（3）胃炎A组、B组C-kit表达细胞分布面积和直径均明显小于对照组（P〈0．05），胃炎A组与B组比较差异无统计学意义（P〉0．05），三组c—kit表达细胞的积分光密度比较差异无统计学意义（P〉0．05）。结论Hp感染和NSAID可能改变胃壁神经元及ICC的形态结构。Hp感染可明显抑制胃窦SS分泌，而增加GAS分泌；NSAID诱导的胃炎对GAS与SS的影响不显著。