AMP-活化蛋白激酶对氧葡萄糖剥夺复氧PC12细胞HMGB1释放及其介导的BY2细胞炎性反应的影响

目的 探讨调节AMP-活化蛋白激酶(AMP-activated protein kinase,AMPK)对PCl2细胞氧葡萄糖剥夺复氧(oxygen glucose deprivation and reoxygenation,OGD/R)后高迁移率族蛋白l(high mobility group box l,HMGB1)释放及其介导的BV2细胞炎性反应的影响.方法 分别培养PCl2和BV2细胞,应用PCl2细胞建立氧葡萄糖剥夺12 h复氧24 h模型,分别给予5-氨基-4-甲酰胺咪唑核糖核苷酸(5-aminoimidazole-4-c arboxamide,AICAR)5、50和100 μmol/L以及Compound C 0.1、l和10 μmol/L激活或抑制AMPK磷酸化后,应用四甲基偶氮唑蓝(methyl thiazolyl tetrazolium,MTT)法检测PC12细胞活性,酶联免疫吸附法检测PC12细胞培养基中HMGB1释放水平.将各组OGD/R后PC12培养基分别作用于BV2细胞正常培养24 h.分别采用免疫印迹法和酶联免疫吸附法检测BV2细胞中NF-κB抑制蛋白(inh~itor of NF-κB,IκB)磷酸化水平和TNF-α释放水平.结果 OGD/R后,PC12细胞活性显著降低[(68.84 ±6.60)％对(100.04±8.82)％;P＜0.01],AMPK磷酸化水平显著增高(1.95±0.39对1.00±0.20;P＜0.05),细胞外HMGB1释放显著增多[(287.66±26.42) pg/μl对(53.05±9.11) pg/μl;P ＜0.01].与OGD/R组比较,AICAR 100 μmol/L能显著增高OGD/R后PC12细胞存活率[(78.60±3.75)％对(68.84±6.60)％;P＜0.05]、促进AMPK磷酸化(3.32±0.66对1.95 ±0.39;P＜ 0.01)和减少细胞外HMGB1的释放[(164.06±12.77) pg/μl对(287.66±26.42) pg/μl;P＜0.01].相比之下,Compound C 10 μmol/L则会显著降低PC12细胞存活率[(40.44±3.79)％对(68.84±6.60)％;P＜0.01]、抑制AMPK磷酸化(1.07±0.21对1.95±0.39;P＜0.05)和增加HMGB1的释放[(337.97±18.90) pg/μl对(287.66±26.42) pg/μl;P＜0.01].AICAR 100 μmol/L组条件培养基能显著抑制BV2细胞的IκB磷酸化(1.68±0.51对3.09±0.10;P＜0.05)和减少TNF-α释放[(669.53±38.58) pg/μl对(841.76±45.82) pg/μ1;P＜0.05];Compound C 10 μmol/L组条件培养基则能显著促进BV2细胞IκB磷酸化(4.98±1.24对3.09 ±0.10;P ＜0.01)和增加TNF-α释放[(1 035.32±128.06) pg/μl对(841.76±45.82) pg/μl;P＜0.05].结论 促进AMPK磷酸化激活能减少PC12细胞OGD/R后HMGB1的释放、抑制其介导的BV2细胞NF-κB炎症通路激活并且减少TNF-α释放,从而减轻神经炎性损伤;相反,抑制AMPK磷酸化则会促进PC12细胞OGD/R后HMGB1释放和加重其介导的BV2细胞炎性反应.     

老年胃黏膜病变患者血清胃蛋白酶原变化

目的 探讨老年胃疾病患者胃黏膜病理改变过程中,血清胃蛋白酶原(PG)Ⅰ、Ⅱ的变化规律.方法 选择我院消化内镜中心行胃镜检查老年患者276例,按病理诊断标准分为4组,非萎缩性胃炎组(对照组)34例,慢性萎缩性胃炎组(胃炎组)71例,消化性溃疡组(溃疡组)105例,胃癌组66例.用免疫放射法(IRMA)测定患者血清PGⅠ及PGⅡ,并计算PGⅠ/PGⅡ的比值(PGR).结果 对照组PG Ⅰ、PG Ⅱ和PGR分别为(149.26±62.45)/μg/L、(15.66±8.97)μg/L和10.62±3.30,慢性萎缩性胃炎组PG Ⅰ[(119.32±41.87)μg/L]、PGR(7.19±3.02)较对照组降低(P＜0.05),胃癌组PG Ⅰ[(95.39±22.80)μg/L]、PGR(5.86±3.87)较对照组明显降低(P＜0.01);溃疡组PG Ⅰ[(175.29±33.69)μg/L]、PGⅡ[(21.81±8.91)μg/L]较对照组升高(P＜0.05).结论 血清PGⅠ、PGⅡ含量的变化及PGR对癌前状态和早期胃癌的诊断具有重要的临床意义,当血清PGⅠ及PGR严重降低时,应尽早进行胃镜检查,以明确诊断.     

2型糖尿病患者骨折围手术期血浆生长抑素水平及痛阈变化的初步观察

目的探讨T2DM患者骨折围手术期血浆生长抑素(SST)水平及痛阈的变化。方法选取2018年9月至2019年3月于山西医科大学第二医院骨科住院并择期腰麻下行下肢骨折手术的患者70例,其中T2DM患者(T2DM组)及非T2DM患者(Con组)各35例。手术麻醉前(T1)及术后24 h(T2)分别测定血浆SST水平、热痛阈值、热耐痛阈值、缺血痛阈值、缺血耐痛阈值及触痛阈值。结果与Con组比较,T2DM组T1和T2时SST水平降低[(74. 18±22. 62)vs(62. 38±18. 91)pg/ml,(97. 66±21. 40)vs(84. 65±19. 88)pg/ml,P0. 05];Con、T2DM组T2时SST水平高于T1[(97. 66±21. 40)vs(74. 18±22. 62)pg/ml,(84. 65±19. 88)vs(62. 38±18. 91)pg/ml,P0. 01]。与Con组比较,T2DM组T1时热耐痛阈值、缺血痛阈值及触痛阈值升高[(34. 60±16. 85)vs(43. 26±14. 90)s,(180. 67±55. 50)vs(206. 44±39. 51)mmHg,26. 00(13. 75,100. 00)vs 100. 00(26. 00,300. 00)g,P0. 05];T2DM组T2时热耐痛阈值及触痛阈值低于T1[(34. 02±14. 22)vs(43. 26±14. 90)s,20. 50(7. 50,60. 00)vs 100. 00(26. 00,300. 00)g,P0. 01]。结论 T2DM患者骨折围手术期SST水平升高,热耐痛阈与触痛阈降低。     

血清25-(OH) D3、hsCRP及NT-proBNP与慢性心衰患者心衰程度及预后的关系

目的:探究血清25羟维生素D3[25-(OH)D3]、hsCRP及NT-proBNP与慢性心衰(CHF)患者心衰程度及预后的关系。方法:选择我院CHF患者(心衰组,136例),其中NYHAⅡ级44例、Ⅲ级46例、Ⅳ级46例,另选择同期在我院健康体检正常者为健康对照组(120例)。检测各组研究对象血清中的25-(OH)D3、hsCRP及NT-proBNP水平,并进行比较。结果:与健康对照组比较,心衰组治疗前hsCRP和NT-proBNP水平显著升高,25-(OH)D3水平显著降低(P均0.01);与治疗前比较,心衰组治疗后25-(OH)D3[(13.20±4.12)μg/L比(19.10±4.01)μg/L]水平显著升高,hsCRP[(18.32±3.81)mg/L比(11.53±2.52)mg/L]和NT-proBNP[(1605.56±578.91)pg/ml比(981.43±231.46)pg/ml]水平显著降低(P均0.01);心衰组治疗前及治疗后,随着心衰等级的增加,25-(OH)D3水平均显著降低,hsCRP和NT-proBNP水平均显著升高(P均0.01)。与未发生心脏事件组比较,发生心脏事件组患者血清中的25-(OH)D3[(14.52±2.10)μg/L比(10.04±2.19)μg/L]水平显著降低,hsCRP[(16.02±2.78)mg/L比(19.50±2.34)mg/L]和NT-proBNP[(1359.05±252.56)pg/ml比(1699.13±346.67)pg/ml]水平显著升高(P均0.01)。结论:血清25羟维生素D3、hsCRP和NTproBNP水平对心衰患者心衰程度和预后的评价具有十分重要的意义。     

美托洛尔联合稳心颗粒对慢性心衰患者血管内皮功能及MCF-6、PGI2水平的影响

目的:观察美托洛尔联合稳心颗粒对于慢性心衰(CHF)患者血管内皮功能及血浆线粒体偶联因子6(MCF-6)、前列环素(PGI2)水平的影响。方法:选择我院收治的164例CHF患者作为研究对象,被随机均分为美托洛尔组和联合治疗组(美托洛尔联合稳心颗粒治疗)。治疗10周,比较两组患者治疗前后的心功能,血管内皮功能,以及MCF-6、PGI2水平变化。结果:经治疗后两组患者心功能、血管内皮功能均较治疗前明显改善,MCF-6水平均明显降低,PGI2水平均明显升高(P均=0.001);且与美托洛尔组比较,联合治疗组心率[(74.6±3.5)次/min比(67.5±3.2)次/min]、左室舒张末期内径[(55.3±5.1)mm比(51.3±4.2)mm]明显减少,抵抗素水平[(29.5±2.7)μg/L比(23.3±1.9)μg/L]、内皮素1[(71.0±6.2)mg/L比(56.7±5.3)mg/L]、MCF-6[(305.0±27.7)pg/ml比(265.8±25.3)pg/ml]水平均明显下降,左室射血分数[(46.6±4.4)%比(50.7±5.1)%]、降钙素基因相关肽[(42.2±3.6)mg/L比(51.4±6.3)mg/L]、一氧化氮[(73.3±6.9)mg/L比(89.4±7.6)mg/L]、PGI2[(20.6±3.5)pg/ml比(24.3±3.6)pg/ml]水平均明显上升(P均=0.001)。结论:美托洛尔联合稳心颗粒治疗慢性心衰患者能够显著改善患者心功能和血管内皮功能,抑制血浆线粒体偶联因子6释放,并提高前列环素水平。     

氯沙坦钾联合比索洛尔对慢性心衰患者心功能及外周血内皮祖细胞的影响

目的:探讨氯沙坦钾联合富马酸比索洛尔对慢性心力衰竭(CHF)患者心功能及外周血内皮祖细胞(EPCs)的影响。方法:我院CHF患者110例被随机分为氯沙坦钾组(55例,常规治疗基础上采用氯沙坦钾)和联合治疗组(55例,在氯沙坦钾组基础上加用富马酸比索洛尔),均治疗3个月。统计两组临床疗效、治疗前后血清心型脂肪酸结合蛋白(H-FABP)、氨基末端脑钠肽前体(NT-proBNP)、基质金属蛋白酶抑制剂-1 (TIMP-1)水平、外周血EPCs数目、心功能指标水平及不良反应发生率。结果:联合治疗组总有效率显著高于氯沙坦钾组(94.55%比78.18%,P=0.012);治疗后,与氯沙坦钾组比较,联合治疗组血清TIMP-1 [(3.78±0.48)μg/L比(4.55±0.50)μg/L]水平显著升高,H-FABP [(1925.13±125.17)pg/ml比(1265.25±118.18)pg/ml]及NT-proBNP[(1763.08±197.41)pg/ml比(1017.59±181.28)pg/ml]水平显著降低,外周血EPCs[(3.07±0.83)个/μl比(3.61±0.79)个/μl]数目显著增加,心脏指数(CI)[(2.33±0.46)L·min-1·m-2比(3.21±0.58)L·min-1·m-2],LVEF [(46.58±9.43)%比(59.18±10.02)%],每搏输出量(SV)[(4.11±0.40)L/min比(5.18±0.53)L/min]水平显著提高(P均<0.01);两组不良反应发生率无显著差异(P=0.340)。结论:氯沙坦钾联合富马酸比索洛尔治疗CHF患者,可安全地显著增加外周血EPCs数目,显著改善心功能。     

HIV/HCV共感染者外周血辅助性T细胞17和IL-17A水平检测

目的探讨HIV/HCV共感染者外周血辅助性T细胞17(Th17)及白细胞介素(IL)-17A的免疫调节作用。方法随机选取HIV/HCV共感染者、HIV感染者、HCV感染者和健康人各30例,使用流式细胞仪检测外周血CD4+T细胞数量和Th17数量,采用ELISA法检测血清IL-17A水平。结果 HIV感染者和HIV/HCV共感染者CD4+T淋巴细胞分别为(310.23±114.35)个/μl和(218.42±112.47)个/μl,均较健康人明显降低[(735.46±121.52)个/μl,P0.05],HIV/HCV共感染者较HIV感染者CD4+T淋巴细胞更低(P0.05),HCV感染者CD4+T淋巴细胞数为(719.47±123.72)个/μl,与健康人比较无显著性差异;HIV感染者Th17百分比和IL-17A水平分别为(2.48±0.90)%,和(25.18±12.63)pg/ml,均较健康人显著降低[(3.95±1.23)%和(39.15±16.30)pg/ml,P0.05],HCV感染者Th17百分比和IL-17A为(5.48±0.90)%和(45.24±15.72)pg/ml,显著高于健康人(P0.05),而HIV/HCV共感染者Th17百分比为(1.76±0.42)%,IL-17A为(16.49±7.54)pg/m L,均显著低于HIV感染者[(2.48±0.90)%和(25.18±12.63)pg/m L,P0.05]。结论合并HCV感染可能通过影响Th17及其细胞因子IL-17A进一步影响HIV患者的免疫功能。     

盐敏感性高血压病患者血浆血栓素B2、6-酮-前列腺素F1α水平的变化及意义

目的探讨盐敏感性高血压病患者血浆血栓素B2(TXB2)、6-酮-前列腺素F1α(6-k-PG-F1α)水平的变化及意义.方法采用改良的Sullivan急性口服盐水负荷试验的方法将60例高血压病患者分为盐敏感性(SS,28例)和非盐敏感性(NSS,32例)两组.30例正常人为对照组.采用放射免疫法测定其血浆TXB2和6-k-PGF1α水平.结果SS高血压病组血浆TXB2水平[(48.76±21.34)pg/ml]显著高于NSS高血压病组[(31.67±5.30)pg/ml]及正常组[(30.01±7.72)pg/ml](P均＜0.01);SS高血压病组血浆6-k-PGF1α水平[(62.67±17.14)pg/ml]明显低于NSS高血压病组[(92.70±33.72)pg/ml]及正常组[(93.40±20.40)pg/ml](P均＜0.01);NSS高血压病组与正常组间血浆TXB2和6-k-PGF1α水平均无显著性差异(P均＞0.05).结论SS高血压病患者存在血管内皮功能受损和血小板活性增强.     

血清BNP和Hcy水平预测冠脉旁路移植术疗效及预后的价值

目的:分析评价冠脉旁路移植术(CABG)患者术前血清脑钠肽(BNP)和同型半胱氨酸(Hcy)水平变化预测CABG疗效与预后的价值。方法:收集115例在本院行CABG患者的临床资料,比较不同病变程度、疗效、预后患者术前血清BNP、Hcy水平差异,分析血清BNP、Hcy水平对手术疗效以及预后的影响。结果:与中度、轻度病变组比较,重度病变组术前血清BNP[(151.86±22.57) pg/L比(82.57±10.26) pg/L比(283.51±32.47) pg/L]和Hcy[(18.37±4.51)μmol/L比(12.74±2.04)μmol/L比(31.56±5.17)μmol/L]水平显著升高,且中度病变组显著高于轻度病变组(P均=0.001);与有效、无效组比较,显效组患者术前血清BNP[(227.49±24.52)pg/L比(308.26±34.12)pg/L比(90.13±10.75)pg/L]、Hcy [(29.12±5.83)μmol/L比(46.15±7.49)μmol/L比(19.03±3.77)μmol/L]水平显著降低,且有效组显著低于无效组(P均=0.001);与桥血管狭窄、桥血管畅通组比较,死亡组患者术前血清BNP[(271.47±25.18)pg/L比(92.41±11.06)pg/L比(312.54±35.06)pg/L]、Hcy[(33.08±6.14)μmol/L比(20.05±3.68)μmol/L比(50.21±7.75)μmol/L]水平显著升高,且桥血管狭窄组显著高于桥血管通畅组(P均=0.001)。Spearman相关性分析显示,BNP、Hcy与冠心病严重程度、CABG术后预后呈显著正相关(r=0.624～0.814,P0.05或0.01)。多元Logistic回归分析显示,BNP、Hcy是冠心病患者CABG术后预后的独立危险因素(OR=5.133、1.803,P均=0.001)。结论:冠脉旁路移植术患者术前BNP和Hcy水平越高,疗效越差,发生血管狭窄及死亡预后的风险也越高。     

高龄慢性心力衰竭患者血清CA125、尿酸水平与心功能的相关性

目的:探讨高龄慢性心力衰竭(CHF)患者血清糖蛋白抗原125(CA125)、尿酸(UA)水平与心功能之间的相关性。方法:纳入110例高龄住院患者,根据NYHA心功能分级标准分为心衰组65例(心功能Ⅱ级30例,心功能Ⅲ～Ⅳ级35例)和心功能正常组45例。分别检测比较两组以及不同心功能等级患者间CA125、CA199、癌胚抗原(CEA)、UA、N末端脑钠肽前体(NT-proBNP)水平、二尖瓣舒张早期峰值血流速度/二尖瓣舒张晚期峰值血流速度(E/A)和左室射血分数(LVEF)。结果:与心功能正常组比较,心衰组CA125[(15.9±6.3)U/ml比(40.1±12.2)U/ml]、UA[(319.2±61.3)μmol/L比(435.7±72.9)μmol/L]、NT-proBNP[(298.5±132.4)pg/ml比(1923.7±868.6)pg/ml]显著升高而E/A[(1.02±0.46)比(0.71±0.25)]、LVEF[(62.1±11.9)%比(48.7±14.7)%]显著降低(P均=0.001)。与心功能Ⅱ级组比较,心功能Ⅲ～Ⅳ级组CA125[(28.4±9.3)U/ml比(50.1±13.9)U/ml]、UA[(383.4±71.8)μmol/L比(478.4±73.9)μmol/L]、NT-proBNP[(853.2±361.5)pg/ml比(2841.3±1303.3)pg/ml]水平显著升高而E/A[(0.78±0.23)比(0.65±0.19)]、LVEF[(52.6±10.1)%比(45.3±13.1)%]显著降低(P0.05或0.01)。Pearson直线相关回归分析示:心衰组CA125、UA、NT-proBNP水平与E/A及LVEF均呈显著负相关(r=-0.679～-0.457,P0.05或0.01)。结论:CA125、UA和NT-proBNP水平与高龄CHF患者LVEF均呈显著负相关,有助于心衰严重程度的判断。     

A prospective comparative study of clinical and pathological characteristics in Icelandic and Danish patients with gastric ulcer, duodenal ulcer, and X-ray negative dyspepsia. II. Histological results

The occurrence of gastritis in antral and body mucosa is compared in an Icelandic and a Danish group of patients with gastric ulcer, duodenal ulcer, and X-ray negative dyspepsia. In all 93 Icelandic and 88 Danish patients were examined. All signs of antral gastritis were more frequent in Icelandic than in Danish patients, but only the incidence of superficial inflammation and decreased mucus content in surface and crypt epithelium differed significantly. In body mucosa pseudopyloric metaplasia was more frequent in Iceland and occurred equally freqeuntly in all three diseases. A statistically significant correlation was found between macroscopic gastritis and occurrence of antral superficial inflammation and between smoking and superficial inflammation and decreased mucus content in the pyloric biopsy specimen. The presence of histological gastritis was not correlated to the intake of alcohol and salicylic acid, nor to the presence of pain at the time of investigation.     

Chronic effect of intragastric ammonia on gastric mucosal structures in rats

The prevalence ofHelicobacter pylori (HP) in the gastric mucosa of patients with chronic atrophic gastritis has been reported to be significantly higher than in normal mucosa. To clarify the role of HP in the etiology of chronic atrophic gastritis, we assessed the effect of ammonia on the gastric mucosal structure in rats, since HP has a strong urease activity and produces abundant amounts of ammonia. Ammonia administered orally at 0.01% and 0.1% as drinking water for two to four weeks decreased the mucosal thickness and the parietal cell number and oxyntic gland number in a dose- and time-dependent manner. The decrease of mucosal thickness was significantly greater in the antral mucosa than in the body mucosa. The border between the antral and body mucosa shifted toward the cardia, reflecting the decrease in oxyntic gland numbers. Furthermore, intracellular mucin was also decreased in a dose- and time-dependent manner, especially in the antral mucosa. Thus, ammonia chronically administered orally in rats led to changes in gastric mucosal structures and functions. The results suggest that the ammonia produced by HP partly plays an etiologic role in chronic atrophic gastritis.     

幽门螺杆菌及胃粘膜肠上皮化生与CD_(44)V_6表达的关系

目的　探讨幽门螺杆菌 (Hp)感染及慢性萎缩性胃窦炎伴肠上皮化生与CD4 4V6表达程度之间的关系。方法　以单克隆抗体及免疫组化技术等方法对Hp阴性单纯慢性胃炎、Hp阴性萎缩性胃炎伴肠上皮化生、Hp阳性萎缩性胃窦炎伴肠上皮化生、胃窦腺癌的胃镜下活检组织标本进行测定分析。结果　在Hp阴性单纯性胃炎组粘膜上皮未见CD4 4V6表达 ,Hp阴性萎缩性胃窦炎伴肠上皮化生、Hp阳性萎缩性胃窦炎伴肠上皮化生、胃窦腺癌各组CD4 4V6表达程度依次逐渐升高 ,各组之间比较差异有显著性 (P <0 .0 5 )。结论　CD4 4V6的表达可能是上皮细胞癌前病变出现的早期生物学信号 ,肠上皮化生细胞可能诱导CD4 4V6的表达 ,而Hp感染则有促进这种诱导表达的作用。     

The Correlation between Gastric Acid Secretion and Histology of Fundic and Antral Gland Area

Correlative studies were performed in 92 patients with gastric or duodenal ulcer, chronic gastritis, or diabetes mellitus. The basal acid secretion and that stimulated maximally by histamine or pentagastrin infusion decreased significantly with increasing severity of atrophic changes in the fundic gland area. Histological changes of antral mucosa were in 72 per cent of cases of similar degree as in fundic gland area. In the remainder of patients antral mucosa showed inflammatory or atrophic changes more advanced than the fundic gland area.     

Aspartic proteinases in gastric mucosa of the rat: absence of pepsinogen I, genetic polymorphism of pepsinogen II, and presence of slow-moving proteinase

We have examined relationships among the aspartic proteinases in rat and human gastric mucosa by electrophoretic analysis in polyacrylamide gel and by immunoblotting and immunohistochemical staining using rabbit antisera to human pepsinogen I (PG I), pepsinogen II (PG II), and slow-moving proteinase. By electrophoretic analysis, the major proteolytic bands in mucosal extracts from each of three strains of rats had rates of anodal migration that were similar to the fastest migrating isozymogens of human PG I. However, immunoblots revealed that these bands and several minor proteolytic bands with slower rates of anodal migration reacted with antiserum to PG II. Two proteolytic bands in rat gastric mucosa that migrated concurrently with human slow-moving proteinase reacted with antihuman slow-moving proteinase reacted with antihuman slow-moving proteinase. None of the proteolytic bands in rat gastric mucosa reacted with anti-PG I. By immunohistochemical staining, anti-PG I failed to stain any cells in rat fundic gland or antral mucosa. By contrast, anti-PG II stained mucus neck and chief cells in fundic gland mucosa and pyloric gland cells in antral mucosa, and anti-slow-moving proteinase stained surface and foveolar epithelial cells throughout the stomach. The results indicate that the gastric mucosa of the rat does not contain PG I.     

A quantitative diagnosis of chronic gastritis

To explore a definite diagnostic criterion of chronic gastritis, we undertook a quantitative study of the gastric biopsy specimens taken from 131 subjects. Seven stages were classified from normal gastric mucosa to mild, moderate and severe superficial and atrophic gastritis. The results shown the number of inflammatory cell was much greater in the mild superficial gastritis (128 +/- 84.37/HP) than in normal gastric mucosa (22 +/- 10.54HP, P less than 0.001). In these stages, the numbers of pyloric and fundic gland progressively decreased, the size of the gastric gland gradually enlarged and the percentage of intestinal metaplasia by degrees increased. According to these, we establish the quantitative diagnostic criterion of chronic gastritis.     

Somatostatin and D cells in patients with gastritis in the course of Helicobacter pylori eradication: a six-month,follow-up study

BACKGROUND/AIMS: As well as causing chronic gastritis, Helicobacter pylori predisposes patients to peptic ulcer disease and gastric cancer, and induces gastric functional disorders. The aim of our study was to investigate the effects of H. pylori eradication therapy on the morphological and functional recovery of gastric antral and corpus D cells in patients with chronic gastritis during 6 months of follow-up. PATIENTS AND METHODS: Forty consecutive, dyspeptic patients referred for endoscopy (31 with H. pylori infection and nine controls; mean age 49 years; 17 men, 23 women) entered the study. All patients had histological signs of gastritis but no signs of peptic ulcer or gastric cancer. Antrum (n=8) and corpus (n=6) biopsy specimens were collected for routine histology, radioimmunoassay tissue somatostatin levels, immunohistochemistry and electron microscopy, prior to and 6 months after therapy. Basal plasma somatostatin levels were determined prior to eradication, plus 6 weeks and 6 months after therapy. Eradication therapy consisted of amoxicillin, metronidazole and omeprazole. RESULTS: Basal somatostatin plasma values in antral and corpus tissue were lower in infected patients than in the H. pylori-negative controls at the beginning of the study. A significant increase occurred after successful eradication therapy, together with an increase in the number of D cells in both regions. Changes in the D-cell ultrastructure in antral and corpus mucosa after eradication therapy suggest an increase in somatostatin synthesis and secretion. CONCLUSIONS: The structural and functional restoration of D cells following eradication therapy indicates possible recovery of the diseased mucosa.     

大鼠胃黏膜萎缩过程中的组织学变化和p16、Bcl-2、增殖细胞核抗原表达

慢性萎缩性胃炎尤其是胃窦萎缩性胃炎与胃癌关系密切。胃黏膜恶变过程中，细胞增殖与凋亡异常发挥重要作用。目的：研究大鼠胃黏膜萎缩过程中的组织学变化，以及p16、Bcl-2、增殖细胞核抗原（PCNA）表达情况．探讨这些调控因子的改变对萎缩性胃炎形成的影响。方法：以氨水、脱氧胆酸钠和乙醇三种损伤因素联合作用诱导慢性萎缩性胃炎。大鼠分为正常对照组和模型组，分别于2、4、6个月后处死。取胃黏膜行大体观察和组织学检查，以免疫组化方法检测胃窦黏膜p16、Bcl-2、PCNA表达。结果：模型组胃黏膜炎症细胞浸润明显；胃窦小凹增生．腺体层厚度和腺体数目明显减少；胃体病变较轻，仅于后期出现壁细胞数目减少。在胃窦黏膜萎缩过程中，p16表达逐渐降低，Bcl-2和PCNA表达逐渐升高。萎缩组p16表达较非萎缩组显著降低，Bcl-2、PCNA表达较非萎缩组显著升高。结论：多因素长期慢性刺激可致大鼠胃黏膜萎缩。模型大鼠胃黏膜细胞处于高增殖状态．抑癌基因p16蛋白表达低下．凋亡抑制基因Bcl-2蛋白高表达，萎缩性胃炎的发病与细胞增殖与凋亡失衡相关。     

Antral gastrin cells and serum gastrin in achlorhydria.

Forty-five patients with achlorhydria due to severe atrophic corpus gastritis or gastric atrophy were studied by determination of serum gastrin, histological examination of multiple biopsy from the antrum, and quantitation of gastrin cells revealed by an indirect immunofluorescence technique. In a reference group of 12 persons with normal gastric secretion and without atrophic antral gastritis the mean number of gastrin cells per field of vision was 52 +/- 6.5 (S.E.M.). In a group of achlorhydric patients having normal antral mucosa (n = 24), the serum gastrin levels was 324 +/- 56 pmol/l and the number of gastrin cells was 79.6 +/- 7.5 cells/field of vision. The corresponding values for a group of achlorhydric patients with chronic superficial antral gastritis (n = 11) were 361 +/- 186 pmol/l and 88.0 +/- 14.4 cells/field of vision. In a group of achlorhydric patients with atrophic antral gastritis (n = 10) serum gastrin was 15.0 +/- 3.3 pmol/l, and the number of gastrin cells was 6.2 +/- 3.3 cells/field of vision. Compared to the subjects in the reference group, the number of gastrin cells was significantly higher in the groups of achlorhydric patients with normal or superficially inflamed antral mucosa and significantly lower in achlorhydric patients with atrophic antral gastritis. It is concluded that serum gastrin in general is a good indicator for the presence or absence of antral atrophic gastritis in achlorhydria.     

Antral Gastrin Cells and Serum Gastrin in Achlorhydria

Forty-five patients with achlorhydria due to severe atrophic corpus gastritis or gastric atrophy were studied by determination of serum gastrin, histological examination of multiple biopsy specimens from the antrum, and quantitation of gastrin cells revealed by an indirect immunofluorescence technique. In a reference group of 12 persons with normal gastric secretion and without atrophic antral gastritis, the mean number of gastrin cells per field of vision was 52±6.5 (S.E.M.). In a group of achlorhydric patients having normal antral mucosa (n = 24), the serum gastrin level was 324±56 pmol/1 and the number of gastrin cells was 79.6±7.5 cells/field of vision. The corresponding values for a group of achlorhydric patients with chronic superficial antral gastritis (n = 11) were 361±186 pmol/1 and 88.0±14.4 cells/field of vision. In a group of achlorhydric patients with atrophic antral gastritis (n = 10) serum gastrin was 15.0±3.3 pmol/1, and the number of gastrin cells was 6.2±3.3 cells/field of vision. Compared to the subjects in the reference group, the number of gastrin cells was significantly higher in the groups of achlorhydric patients with normal or superficially inflamed antral mucosa and significantly lower in achlorhydric patients with atrophic antral gastritis. It is concluded that serum gastrin in general is a good indicator for the presence or absence of antral atrophic gastritis in achlorhydria.