叶酸治疗萎缩性胃炎并干预胃癌生成的分子生物学机制

目的：研究萎缩性胃炎患者血清叶酸水平与胃粘膜病变及某些基因变化的关系。方法：胃镜及胃粘膜活检确诊为中度以上的萎缩性胃炎患者80例，测定其基础状态及服用叶酸1年后的血清叶酸水平、粘膜病理及p53、p16 、Fas和增殖细胞核抗原（PCNA）基因表达水平。结果：①血清叶酸水平与萎缩及异型增生负相关显著（P＝001，P＝0．053）,与Fas表达负相关趋向显著；②随机叶酸水平上升，萎缩肌肠化呈减轻趋势，高水平时达到显著（P＝0．001，P＝0．052），并伴p53表达下调（P＝0．056）；③服用叶酸 大幅度提高其血清水平者，呈现异型增生明显减轻（P＝066），并伴Fas及PCNA基因表达的明显下调（P＝0．007，P＝0．083）。结论：补充叶酸可以影响胃粘膜基因调节，减轻损伤，抑制增殖，使萎缩、肠化及异型增生明显改善，从而阻断胃癌前病变的进展。因此，叶酸可以治疗萎缩性胃炎并干预胃癌的发生。     

粪便肿瘤型M2丙酮酸激酶在胃肠道肿瘤检测中的意义

肿瘤型M2丙酮酸激酶（M2-PK）是近年发现的一种新型肿瘤标志物。目的：评价粪便肿瘤型M2-PK在胃肠道肿瘤和癌前状态的检测以及肿瘤分期中的意义。方法：以酶联免疫吸附测定（ELISA）检测34例胃癌、31例结直肠癌、19例胃肠道息肉、26例慢性萎缩性胃炎和19例对照者的粪便肿瘤型M2-PK值，胃癌和结直肠癌患者同时行传统外周血肿瘤标志物癌胚抗原（CEA）、糖链抗原（CA）19-9和CA24-2水平检测。结果：胃癌组和结直肠癌组的粪便肿瘤型M2-PK检测值和阳性率均较对照组显著增高（P〈0．01），胃肠道息肉组的检测值亦较对照组显著增高（P〈0．05）。随着肿瘤临床病理分期的进展和转移的发生，粪便肿瘤型M2-PK检测值逐渐增高（胃癌组：P〈0．05；结直肠癌组：P〈0．01）。胃癌组和结直肠癌组粪便肿瘤型M2-PK检测的阳性率均显著高于血清CEA、CA19．9和CA24．2（P〈0．01）。结论：粪便肿瘤型M2-PK对胃肠道肿瘤和癌前状态之一的胃肠道息肉的诊断有一定临床意义。     

胃癌患者血清和组织IL-1β水平变化及临床意义

目的研究IL-1β与胃癌发生的相关性，探讨IL-1β在胃癌发生中的作用，为胃癌的防治提供新的思路。方法收集70例胃癌、45例癌旁和70例胃炎手术切除组织和胃镜下活检标本，采用免疫组化SABC法测定组织IL-1β蛋白表达水平；以双抗体夹心ELISA法测定胃癌、胃炎患者血清中IL-1β含量，并进行比较。结果胃癌患者血清IL-1β水平显著高于胃炎病人（P〈0．05），且与临床分期有关，进展期胃癌高于早期胃癌（P〈0．05）。IL-1β蛋白在胃癌、癌旁和胃炎中的表达率分别为65．95％、44．44％和22．50％；胃癌组IL-1β表达高于癌旁、胃炎组。低、未分化癌组织IL-1β的表达高于高、中分化癌组织（P〈0．05）；进展期胃癌高于早期胃癌（P〈0．05）。结论胃癌患者血清、胃粘膜组织中IL-1β表达高于胃炎组，提示胃粘膜IL-1β表达与胃癌的发生有一定的关系。     

幽门螺杆菌感染与胃癌的关系

目的研究幽门螺杆菌（Hp）与胃癌发生的关系。方法病例组62例均为胃腺癌，正常胃粘膜组34例．每个研究对象均在胃窦部取三块活检组织，胃癌患者在癌灶周围再取三块活检组织．然后进行快速尿素酶试验和细菌培养．结果Hp阳性以细菌培养为标准，两项试验均阳性为Hp阳性．结果病变组Hp阳性数38例，对照组为4例，两组比较OR＝11．9，95％CI＝4．2～33．7，X2＝21．89，P＜0．01，两组间有显著性差异，提示Hp感染与胃癌的危险性相关．进一步研究Hp与胃癌的类型及部位的关系发现，Hp在肠型腺癌和弥漫型腺癌的检出率分别为78％（32／41），29％（6／21），OR分别为26．7，3，95％CI分别为8．8～81．7，＜1，P分别为P＜0．01，P＞0．1．提示Hp感染与肠型胃癌有关．Hp在胃窦和幽门部胃癌检出率为83％（24／29），与正常组比较OR＝36，95％CI＝12．6～102．6，P＜0．01；在胃体和胃底部胃癌检出率为79％，OR＝27．5，95％CI＝6．6～114，P＜0．01；在贲门部胃癌检出率为16％，OR＝1．4，95％CI＜1，P＞0．5，提示Hp感染与非贲门部胃腺癌密切相关，与贲门部胃癌无关。结论Hp感染与胃癌的发生有相关性，与非贲门部胃癌密切相关，与肠型胃癌有关，与弥漫型胃癌无关．     

维生素逆转胃癌的癌前病变——初期临床干预试验

为探索逆转胃癌的癌前病变以预防其发病,本文观察叶酸加维生素B_(12)、合成β-胡萝卜素及天然β-胡萝卜素对56例中重度萎缩性胃炎牯膜病理和DNA甲基化水平的作用。结果:①叶酸加维生素B_(12)对胃牯膜萎缩和肠化的逆转率达77.7％,高于文献统计:②天然β-胡萝卜素显著逆转不典型增生(P=0.04),推测与其所含异构体有关;③血浆叶酸、隐黄素、α-胡萝卜素水平与胃癌癌前病变呈显著负相关:④α-胡萝卜素可使胃粘膜DNA甲基化水平显著提高(P<0.01～0.0001)。本文提示某些维生素可能通过提高胃粘膜细胞DNA甲基化水平,调节某些基因的活性,因而具有逆转胃癌癌前病变的作用。     

叶酸受体α在胃癌组织中的表达及其与叶酸、亚甲基四氢叶酸还原酶基因多态性以及胃癌生物学行为的关系

背景：叶酸缺乏与胃癌发生有关。亚甲基四氢叶酸还原酶（MTHFR）是叶酸代谢途径的关键酶之一，叶酸受体α（FRet）可介导细胞外叶酸进入细胞内。目的：探讨人胃癌组织中FRα的表达及其与叶酸、MTHFR基因多态性以及胃癌生物学行为的关系。方法：收集38例胃癌患者的癌组织、癌旁和外周正常组织标本．以自动化学发光系统测定叶酸含量，以聚合酶链反应（PCR）-限制性片段长度多态性（RFLP）技术检测MTHFR基因677（C→T）和1298（A→C）两个常见多态，并以即时逆转录PCR（real—time RT—PCR）检测FRα的表达。结果：FRα在胃癌组织中的表达显著降低（P〈0．01），且表达降低癌组织与表达无变化癌组织相比，叶酸含量呈降低趋势（胜0．06）。FRα的表达与MTHFR基因多态性无明显相关性。年龄〉160岁、有淋巴结转移以及肿瘤直径≥5cm的胃癌组织FRα表达水平更低（P≤0．05）。结论：胃癌组织中FRα低表达影响了细胞外叶酸进入细胞内，从而参与了胃癌的发生，其表达降低与年龄增长和胃癌的进展有关。     

犬胃大部切除术后残胃粘膜癌变的形态学研究

目的探讨残胃粘膜癌前病变的发生发展过程及与残胃癌的关系方法当地雄性杂种犬16只，随机分为两组：手术组9只，施行BillrothⅡ式胃切除术；对照组7只，单纯剖腹术．两组大术后1mo始喂饲致癌剂MNNG加饱和氯化钠溶液，连续10mo.在实验周期的不同时相点，应用纤维内镜对残胃粘膜进行动态观察并活检．结果手术组浅表性炎、萎缩性炎和腺体增生不仅出现于手术后早期，而且出现于整个实验过程中．肠化和异型增生的发生率显著高于对照组（X2＝5．6，P＜0．05；X2＝7．14，P＜0.01），吻合口部显著高于残胃部（X2＝5．6，P＜0．05；X2＝7.14，P＜0．01）.结论Billroth胃切除术与残胃粘膜的病变有着直接的因果关系．残胃粘膜常见的腺体萎缩及增生性病变是发生癌前病变的重要基础，应成为临床防治的主要对象．     

胃癌组织中核因子-kB和环氧合酶-2的表达及其临床意义

背景：有关核因子（NF）一KB和环氧合酶（COX）一2在肿瘤组织中表达的研究虽然较多．但其临床意义和相互关系尚无定论。目的：研究NF-kB和COX-2在胃癌组织中的表达及其关系。方法：采用免疫组化SP法检测142例胃癌组织中NF-kB和COX-2蛋白的表达，以相应的癌旁正常组织（30例）作对照。结果：NF-kB在胃癌组织中的阳性表达率为62．0％，显著高于对照组（P〈0．01）；NF-kB的表达与组织学类型、淋巴结转移和远处转移的临床指标呈显著相关（P〈0．05）。COX-2在胃癌组织中的阳性率为64．1％，在对照组中无表达，两者比较有显著性差异（P〈0．01），且在淋巴结转移组阳性率显著高于无转移组（P〈0．01）。胃癌组织中NF-kB和COX-2的表达呈显著正相关（r=0．380，P〈0．01）。结论：NF-kB和COX-2在胃癌的发生、发展中起重要作用，NF-kB可能促进了COX-2的表达。     

胃癌患者胃粘膜细胞内维生素的变化

饮食及血清维生素的流行病学研究提示维生素与癌症有关，但也有不同的报道。为此，我们设计了细胞维生素的测定方法，并取２０例胃癌手术标本，分离癌区、癌旁区及正常粘膜区的细胞，测定细胞内维生素Ａ、Ｅ、Ｃ、Ｂ１２、叶酸及β－胡萝卜素的含量，以７例非癌胃为对照。结果表明，胃癌区及癌旁区细胞内维生素Ａ、Ｅ、Ｂ１２及β－胡萝卜素均显著低于非癌胃对应区细胞内含量（Ｐ＜００１），但胃癌区与癌旁区之间无差异。本文初步证实胃癌与维生素的关系，并显示这种关系在癌前阶段细胞内即已发生，因而提示纠正癌前病变细胞内维生素代谢有可能干预胃癌的生成，值得研究。     

15-羟基前列腺素脱氢酶与胃癌发生关系的研究

NAD依赖性15-羟基前列腺素脱氢酶（15-PGDH）是前列腺素和相关廿烷类生物降解、灭活的关键酶，其表达缺失或减低可能与一些恶性肿瘤的发生、发展密切相关。目的：探讨15-PGDH在胃癌组织和癌旁组织中的表达及其与临床病理特征的关系，初步评价15-PGDH在胃癌发生、发展中的作用及其意义。方法：随机收集30例胃癌患者的癌组织、癌旁3cm和6cm的对照组织，以及10例胃息肉、萎缩性胃炎和健康志愿者正常胃黏膜组织标本，以免疫组化和Western blot法检测15-PGDH蛋白表达，半定量逆转录聚合酶链反应（RT-PCR）法检测其mRNA表达，并分析其临床病理特征。结果：癌组织中15-PGDH蛋白和mRNA表达显著低于癌旁3cm、癌旁6cm对照组织和正常胃黏膜（P均〈0.01），约1／3癌组织中15-PGDH表达缺失，胃息肉和萎缩性胃炎组织显著低于正常胃黏膜（P均〈0．01）；癌组织中15-PGDH蛋白表达量较癌旁3cm和6cm对照组织分别平均降低5．7倍和8．3倍，胃息肉和萎缩性胃炎组织较正常胃组织分别平均降低2．0倍和2．1倍；黏液腺癌中15-PGDH蛋白量显著低于高分化腺癌（只〈0．05），印戒细胞癌中15-PGDH蛋白和mRNA的表达均缺失：伴有远处转移组15-PGDH蛋白和mRNA表达显著低于无远处转移组（P〈0．05和P〈0．01）；Ⅳ期胃癌组织15-PGDH蛋白表达量显著低于Ⅰ期（P〈0．01），其mRNA表达在Ⅲ、Ⅳ期胃癌组织中显著低于Ⅰ、Ⅱ期胃癌（P均〈0．01）。结论：15-PGDH在胃癌组织中表达减少甚至缺失，在癌旁组织和胃癌前状态中表达减少；15-PGDH表达缺失或减少可能是胃癌发生、发展．以及胃癌浸润转移的重要机制之一。     

Serial M-mode echocardiography in evaluation of the cardiovascular effects of tiapamil and their relationship to plasma levels in patients with coronary heart disease

Tiapamil (Ro 11–1781) is a new calcium antagonist. Several investigators have reported about its efficacy against cardiac arrhythmias and angina pectoris. However, there was no study that assessed a possible relationship between hemodynamic effects and plasma concentration. Our study was aimed to investigate any possible relationship between cardiovascular effects of tiapamil and its plasma concentration. We selected 8 coronary patients (6 males and 2 females) with a mean age of 61.9 yr and a mean weight of 70.9 kg. Tiapamil was administered per os at the dose of 250 mg t.i.d. for 4 consecutive days. Hemodynamic data were obtained by means of echocardiography, ECG and sphygmomanometry. Plasma concentrations of Ro 11–1781 and its major metabolites were measured by means of high pressure liquid chromatography. With tiapamil, the morning systolic BP fell from 130.6 ± 19.5 (mean ± SD, pretreatment) to 114.4 ± 18.2 mm Hg on day 4, the change being clinically and statistically significant (P < 0.02 by paired t-tests). Diastolic BP and HR remained unchanged. LVEDD and LVESD were not affected to any relevant extent, but VCF was significantly (P < 0.05) and persistently increased. Tiapamil was well absorbed, but large interindividual variations were observed. As a general rule, no direct relationship between plasma concentrations and hemodynamic effects could be demonstrated. However, the number of patients is too small to allow general conclusions. At the above dose, tiapamil did not elicit any clinically detectable negative inotropic or negative chronotropic effect, probably because of its lowering effect on systolic BP.     

大鼠肝癌发生过程中癌基因和抑癌基因的表达

目的 探讨癌基因ｒａｓ和抑制基因Ｐ５３蛋白在实验性肝癌中的表达与内在联系。方法 应用原位杂交和免疫组织化学（ＳＡＢＣ０法,在３８例化学致癌剂二乙基亚硝胺（ＤＥＮＡ）诱发大鼠原发性肝细胞癌及癌前增殖结节中。Ｐ５３蛋白和ｒａｓ家族基因蛋白表达。结果 化学诱癌生成为６８．４２％,癌前增生性病例为３１．５８％,在癌与增生性病变中ｒａｓ基因收搞表达分别为８８．４６％和７５％,两组无显著差异,但与癌的恶笥分化     

The relationship between new cardiac conduction defects and extension of valve infection in native valve endocarditis

New conduction defects in the setting of native valve infective endocarditis (IE) are commonly believed to be associated with direct extension beyond the free valve area. At University Hospital in Newark, among 100 cases of IE, in none of five instances of associated conduction defects (excluding first-degree heart block) was this the case. In neither of two instances of direct extension of valve infection was this accompanied by a new conduction defect. To explore this relationship, autopsy, surgical, and echocardiographic findings from other institutions were combined with these data. Among 47 instances of new conduction defects in IE, only 60% could be related to direct extension of valve infection. The cause was coronary embolization in 4% and unknown in 36%. Among 119 cases of complicated valve lesions, significant conduction defects were documented by ECG in only 15%. In IE the appearance of new conduction abnormalities may often result from causes other than extension of valve infection. Furthermore, complicated valve lesions may often be present without electrocardiographic evidence, indicating interruption of normal conduction pathways.     

Estimation of arterial carbon dioxide by end-tidal and transcutaneous PCO2 measurements in ventilated children.

Simultaneous measurements of arterial, end-tidal, and transcutaneous carbon dioxide (PaCO2, PetCO2, PtcCO2, respectively) were obtained in 134 children receiving mechanical ventilation (ages, 2 days to 16 years; mean, 2.5 years). The mean +/- SD PetCO2 bias (PaCO2 - PetCO2) was 3.4 +/- 6.6 mmHg. When the PetCO2 bias was plotted against the PaO2/PAO2 ratio, a change in the scatter was obvious at about 0.3. The PetCO2 bias for patients with PaO2/PAO2 under 0.3 was 7.8 +/- 7.3 mmHg compared to 0 +/- 3.4 in patients with PaO2/PAO2 above 0.3 (P less than 0.001). PetCO2 differed significantly from PaCO2 (P less than 0.001) only for patients with PaO2/PAO2 under 0.3. The slope (PaCO2 versus PetCO2) for these patients was 1.59, while the slope for patients with PaO2/PAO2 above 0.3 coincided with the line of identity (1.00). The mean +/- SD PtcCO2 bias (PaCO2 - PtcCO2) was -1.3 +/- 7.2 mmHg. Skin perfusion was recorded at the area close to the transcutaneous CO2 monitor electrode and was defined as normal when capillary refill was below 3 seconds. The PtcCO2 bias for patients with normal skin perfusion was -0.2 +/- 5.4 mmHg (P = 0.73) compared to -4.1 +/- 9.9 for patients with decreased skin perfusion (P = 0.01). The slope of PtcCO2 against PaCO2 was closer to identity in patients with normal skin perfusion (1.17) than in patients where it was decreased (slope, 1.40). We suggest that PaCO2 estimation by both PetCO2 and PtcCO2 is sufficiently precise and reliable for clinical use in critically ill children. Certain limitations stem from the nature of the techniques.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hepatic cytochrome P450 is directly inactivated by nitric oxide, not by inflammatory cytokines, in the early phase of endotoxemia

BACKGROUND/AIMS: Although the activity of the liver in metabolizing and eliminating various drugs decreases in endotoxemia, the mechanism remains to be elucidated. The generation of nitric oxide by the inducible type of nitric oxide synthase increases in endotoxemia. Nitric oxide readily reacts with heme proteins such as cytochrome P450 that metabolize various compounds, including steroids and eicosanoids. The purpose of this study was to determine the effect of nitric oxide on the function of hepatic cytochrome P450 in endotoxemic rats. METHODS: To determine the dynamic aspects of nitric oxide metabolism, hepatic levels of the inducible type of nitric oxide synthase and heme-iron nitrosyl complexes, and plasma levels of nitrite and nitrate were determined in rats before and after intravenous administration of lipopolysaccharide. Changes in the levels of P450 isoforms and testosterone hydroxylation activity in hepatic microsomes were also determined. To evaluate in vivo CYP3A2 activity, midazolam sleep time was measured. RESULTS: When lipopolysaccharide increased the hepatic inducible type of nitric oxide synthase and plasma levels of nitric oxide metabolites, the intensity of low-spin signal of electron spin resonance responsible for the ferric form of P450 decreased with a concomitant increase in heme-iron nitrosyl complexes in the liver. Lipopolysaccharide-related nitric oxide generation is followed by an early decrease in the levels of cytochrome P450 and of testosterone hydroxylation activity in liver microsomes. Midazolam sleep time was prolonged by lipopolysaccharide. All these early changes were prevented by the inhibitor of nitric oxide synthase, N(G)-iminoethyl-L-ornithine. Moreover, lipopolysaccharide suppressed the gene expression of CYP2C11 and CYP3A2. Decreases in levels of cytochrome P450 and their mRNAs were more pronounced at 24 h after LPS administration, but apparently they are NO-independent. CONCLUSIONS: These results suggest that lipopolysaccharide-induced modulation of cytochrome P450 may occur via the interplay of two different mechanisms and that, especially in the early phase, nitric oxide-dependent inhibition is more important.     

Hypermethylation of the P15INK4b and P16INK4a in agnogenic myeloid metaplasia (AMM) and AMM in leukaemic transformation

Hypermethylation of p15 and p16 genes was determined in 32 patients with agnogenic myeloid metaplasia(AMM), also known as idiopathic myelofibrosis (MF). These included 10 patients in leukaemic transformation phase. Using polymerase chain reaction-based methylation analysis assay methods, with substantiation using Southern blot analysis, the study showed no hypermethylation of p15 or p16 genes in the chronic phase of AMM, but p15 gene hypermethylation was found in four patients (40%) and p16 gene hypermethylation in two patients (20%) when they were in leukaemic transformation stage. Furthermore, two of the patients in leukaemic transformation were found to have both p15 and p16 gene hypermethylation, demonstrating possible multiple gene hypermethylation in the same patient. Thus, hypomethylation agents for treating patients with AMM in leukaemic transformation may be appropriate for future trials.     

Visual and Auditory Event-Related Potentials in Young Children of Alcoholics from High- and Low-Density Families

Event-related potentials (ERPs), particularly the P3 wave, have been proposed as biological markers of genetic risk for alcoholism. The present study assesses the ERPs from 102 boys and girls (7 to 15 years old) divided into three groups: two groups of sons and daughters of alcoholic fathers, with and without other first- or second-degree relatives affected, and a control group of children of nonal-coholics. Both visual and auditory discrimination tasks with three stimuli (standard, target, and infrequent nontarget) were used. P3 amplitudes did not reach significant reduction for the high-risk males and were complex for females. There were significant differences among females in P3 visual latency elicited by targets; delays in this variable were associated with multigenerational familial alcoholism. Results are discussed in light of the tasks used for eliciting the ERPs and the characteristics of the selected sample.     

肾素-血管紧张素系统对胰岛β细胞功能的影响及AT1R在其中的作用机制

目的 研究血管紧张素Ⅱ对胰岛β细胞的分泌、增殖、凋亡、氧化应激和纤维化的作用.方法 应用βTC3细胞株、Western印迹检测、实时定量PCR检测、共聚焦显微镜监测Furo3标记的细胞内游离钙离子荧光强度的变化和流式细胞仪检测细胞凋亡及活性氧簇(ROS)产生等方法,研究血管紧张素Ⅱ对β细胞功能的影响,并进一步通过RNA干扰技术减少β细胞中AT1R的表达,研究AT1R在其中的作用机制.结果 βTC3细胞在高浓度葡萄糖刺激下胰岛素分泌增加4倍.高糖作用可引起细胞内Ca2+荧光强度急剧增加.血管紧张素Ⅱ急性刺激并不直接引起胰岛素分泌的改变,其对β细胞促分泌作用可能与其促增殖功能相关.血管紧张素Ⅱ部分是通过AT1R和蛋白激酶C介导的NAD(P)H途径在β细胞中引起氧化应激.RNAi减少AT1R的表达可以改善血管紧张素Ⅱ引起的细胞凋亡和纤维化.结论 血管紧张素Ⅱ通过其1型受体在β细胞的激素分泌、增殖、氧化应激、凋亡和纤维化等过程中发挥着重要作用.     

Visual P3a in male alcoholics and controls

The goal of this study was to assess the P3a component of event-related potentials in a population of abstinent, chronic alcoholics. A three-stimulus visual oddball paradigm was used to elicit robust P3a components in a large group of well-characterized male alcoholics (n = 44) and controls (n = 28). The task required subjects to make a difficult perceptual discrimination between randomly presented, frequently occurring vertical lines (.80) and infrequent target lines that were tilted 2 degrees to the right of vertical (.10) by only responding with a button press to the target stimuli. A nontarget infrequent horizontal line occurred (.10) randomly to which no response was made. The target stimulus elicited robust late P3b components with a parietal maximum amplitude, and the nontarget stimulus elicited reliable P3a components with a fronto-central maximum amplitude distribution. Group differences in P3a were assessed using repeated measures ANCOVA analyses in five scalp regions. Alcoholic subjects produced smaller P3a amplitudes over the central, parietal, temporal, and occipital areas compared with controls. Current source density analyses supported these findings with extension of the differences between the groups to the frontal region. The results suggest that the P3a may be important in the evaluation of alcoholism and its heritability. Theoretical implications are discussed.     

抗弓形虫单克隆抗体的制备鉴定及应用

目的制备抗弓形虫全抗原、天然P30、重组P30的单克隆抗体（McAb），为抗原提纯、弓形虫病诊断及亚单位疫苗的研制奠定基础。方法用弓形虫全抗原、天然P30、重组P30分别免疫BALB／c小鼠，取脾细胞与骨髓瘤细胞融合，筛选稳定分泌高滴度McAb的杂交瘤细胞株。用ELISA法测定McAb亚类和效价；通过SDS—PAGE和Western blot进行特异性鉴定;Giemsa染色观察杂交瘤细胞的染色体数目；利用电镜及IFAT观察McAb对弓形虫的杀伤作用及其作用位点。结果筛选出3株（4810、283、1H6）特异性较好的杂交瘤细胞株。Western blot结果显示，283、1H6产生的MeAb与弓形虫全抗原的阳性反应带均在30kDa处，4810反应带主要在22kDa处；283，1H6，4810MeAb的效价（ELISA）分别为：1：102400、1：51200、1：12800；283、1H6为IgM，4810为IgG2b；3株细胞的染色体数均在100条以上。电镜观察到McAb作用后的弓形虫虫体聚集、肿胀，表面出现缺口和空洞，虫体变形破碎、膜变厚。抗弓形虫全抗原及天然P30的McAb能准确识别重组体pET-30a—ROP2、pET-30a-P30的表达蛋白。结论抗弓形虫全抗原、P30抗原的McAb均对弓形虫具有明显的杀伤作用，能准确识别P30抗原，可应用于弓形虫病诊断、抗原鉴定及亚单位疫苗的研制。