调强适形放射治疗在临床的应用

目的:介绍调强适形放射治疗(intensitymodulatedradiationtherapyIMRT)在美国Stanford大学医学中心放疗科的临床应用情况。方法:详细描述制作CorvusIMRT治疗计划、质量控制和质量监测的整个过程;利用该IMRT,联合外照射和X刀根治性治疗T4N0M0鼻咽癌1例,及单纯IMRT治疗胸椎体转移癌1例。结果:从靶区各个剖面可见高剂量等剂量曲线按计划设计紧扣靶区,重要器官和敏感组织受到保护,治疗计划统计表显示靶区、重要器官和敏感组织的最高及最低受量和受照射体积,而剂量体积直方图则直观地提示肿瘤组织和周围器官的受量比较。结论:IMRT靶区剂量分布均匀,正常组织及敏感器官受到最大限度的保护,可对某些病种的肿瘤组织施以高剂量放疗。

中国延边和韩国京畿道农村地区乙型肝炎病毒感染危险因素的比较

目的 比较中国延边和韩国京畿道农村地区乙型肝炎病毒 (HBV)感染状况及其危险因素 ,为乙型肝炎病毒感染的防制提供依据。方法 1996年 9月至 1997年 9月 ,以居住在中国延边农村地区朝、汉族人群和居住在韩国京畿道农村地区的韩民族人群作为研究对象 ,检测 HBV的血清学指标 ,并进行其危险因素的调查。结果 延边地区汉族 HBV标准化感染率为 6 0 .7% ;延边地区朝鲜族为 77.0 % ;韩国韩民族为 78.6 %。延边地区朝鲜族和韩国韩民族 HBV感染率均高于汉族 (P <0 .0 5 )。多因素分析表明 ,HBV感染的危险因素 ,延边地区汉族为文化程度、乙肝个人史及家族史、针灸史 ;朝鲜族为文化程度、乙肝个人史及家族史、针灸史、医疗机构就诊史 ;韩国韩民族为吸烟史。结论 不同地区、民族

整合禽流感病毒血凝素糖蛋白的假型鼠白血病病毒

本研究通过一个瞬时转染系统将H5N1亚型鹅源禽流感病毒囊膜表面的血凝素(HA)糖蛋白整合到鼠白血病病毒(MuLV)颗粒表面并进行了感染性测定。将包含HA基因的真核表达质粒pcDNA-HA与MuLV假病毒构建体系的两种质粒pHIT60(包括MuLV的结构蛋白基因,即gag和pol)和pHIT111(为MuLV的基因组,还包括一个报告基因LacZ)瞬时共转染转化了SV40大T抗原的人胚肾细胞293T,48小时后收集假病毒上清进行了一系列鉴定。将假病毒上清超速离心后用抗H5亚型禽流感病毒的多抗通过Western-blot证实HA 蛋白能够在此假病毒颗粒表面表达,表明HA能够整合到此病毒粒子表面。通过感染293T、COS 7和NIH3T3 三种不同的靶细胞,均能检测到LacZ基因的表达,证实所构建的假病毒粒子具有感染性。本研究成功构建了具有感染性的MuLV-HA假病毒,为研究鹅源禽流感病毒侵入细胞的机理及其组织嗜性的变异提供一种新方法。

Ketamine suppresses intestinal NF-kappa B activation and proinflammatory cytokine in endotoxic rats

AIM: To investigate the protective effect of ketamine on the endotoxin-induced proinflammatory cytokines and NFkappa B activation in the intestine. ETHODS: Adult male Wistar rats were randomly divided into 6 groups: (a) normal saline control, (b) challenged with endotoxin (5 mg/kg) and treated by saline, (c) challenged with endotoxin (5 mg/kg) and treated by ketamine (0.5 mg/kg), (d) challenged with endotoxin (5 mg/kg) and treated by ketamine (5 mg/kg ), (e) challenged with endotoxin (5 mg/kg) and treated by ketamine (50 mg/kg), and (f) saline injected and treated by ketamine (50 mg/kg). After 1, 4 or 6 h, TNF-α and IL-6 mRNA were investigated in the tissues of the intestine (jejunum) by RT-PCR. TNF-α and IL-6 were measured by ELISA. We used electrophoretic mobility shift assay (EMSA) to investigate NF-kappa B activity in the intestine. RESULTS: NF-kappa B activity, the expression of TNF-α and IL-6 were enhanced in the intestine by endotoxin. Ketamine at a dose of 0.5 mg/kg could suppress endotoxininduced TNF-α mRNA and protein elevation and inhibit NFkappa B activation in the intestine. However the least dosage of ketamine to inhibit IL-6 was 5 mg/kg in our experiment. CONCLUSION: Ketamine can suppress endotoxin-induced production of proinflammatory cytokines such as TNF-α and IL-6 production in the intestine. This suppressive effect may act through inhibiting NF-kappa B.

Specific COX-2 inhibitor NS398 induces apoptosis in human liver cancer cell line HepG2 through BCL-2

AIM: To evaluate the effects of NS-398, a cyclooxygenase2 (COX-2) inhibitor, on the proliferation and apoptosis of HepG2 cells.METHODS: The effects of NS-398 on the proliferation of HepG2 cells were evaluated by MTT. DNA fragmentation gel analysis was used to analyze the apoptotic cells. DNA ploidy and apoptotic cell percentage were calculated by flow cytometry.The expression of COX-2 and Bcl-2 mRNA was identified by competitive RT-PCR. Furthermore, expression level of Bcl-2 was detected using Western blot in HepG2 after treated with NS-398.RESULTS: NS-398 inhibited cell proliferation and induced apoptosis of HepG2 cells in a concentration-dependent manner. DNA ploidy analysis showed that S phase cells were significantly decreased with increase of NS-398 concentration.The quiescent G0/G1 phase was accumulated with decrease of Bcl-2 mRNA. Whereas NS-398 had no effect on the expression of COX-2 mRNA, and no correlations were found between COX-2 mRNA and HepG2 cell proliferation and apoptosis induced by NS-398 (r = 0.056 and r= 0.119,respectively). Bcl-2 protein level was inhibited after treated with NS-398.CONCLUSION: NS-398 significantly inhibits the proliferation and induces apoptosis of HepG2 cells. Mechanisms involved may be accumulation of quiescent G0/G1 phase and decrease of Bcl-2 expression.

Effect of artificial liver support system on patients with severe vira hepatitis:A study of four hundred cases

AIM: To assess the effect of artificial liver support system(ALSS) on patients with severe viral hepatitis, who were divided into treatment group and control group. METHODS: Four hundred in-hospital patients enrolled during 1995-2003 who received ALSS therapy were studied as the treatment group. Four hundred in-hospital patients enrolled during 1986-1994 who received other medical therapies served as the control group. The methods of ALSS used included plasma exchange, hemoperfusion, hemofiltration, continuous hemodiafiltration (CHDF). The effect of ALSS treatment was studied in patients at different stages of the disease.RESULTS: The cure rate of acute and subacute severe hepatitis in the treatment group was 78.9% (30/38), and was 11.9% (5/42) in the control group. The improved rate of chronic severe hepatitis in the treatment group was 43.4% (157/362), and was 15.4% (55/358) in the control group. We found that patients treated with ALSS in the early or middle stage of the disease had much higher survival rates than patients in the end stage of the disease. CONCLUSION: ALSS is an effective and safe therapy for severe viral hepatitis.

Primary adenocarcinomas of lower esophagus,esophagogastric junction and gastric cardia:in special reference to China

Gastric cardia adenocarcinoma (GCA) is an under-studied subject. The pathogenesis, molecular changes in the early stage of carcinogenesis and related risk factors have not been well characterized. There is evidence, however, that GCA differs from cancer of the rest of the stomach in terms of natural history and histopathogenesis. Adenocarcinomas of the lower esophagus, esophagogastric junction (EGJ)and gastric cardia have been given much attention because of their increasing incidences in the past decades, which is in striking contrast with the steady decrease in distal stomach adenocarcinoma. In China, epidemiologically, GCA shares very similar geographic distribution with esophageal squamous cell carcinoma (SCC), especially in Linzhou (formerly Linxian County), Henan Province, North China,the highest incidence area of esophageal SCC in the world.Historically, both GCA and SCC in these areas were referred to as esophageal cancer (EC) by the public because of the common syndrome of dysphagia. In Western countries,Barrett's esophagus is very common and has been considered as an important precancerous lesion of adenocarcinoma at EGJ. Because of the low incidence of Barrett's esophagus in China, it is unlikely to be an important factor in early stage of EGJ adenocarcinoma development.However, Z line up-growth into lower esophagus may be one of the characteristic changes in these areas in early stage of GCA development. Whether intestinal metaplasia (IM) is a premalignant lesion for GCA is still not clear. Higher frequency of IM observed at adjacent GCA tissues in Henan suggests the possibility of IM as a precancerous lesion for GCA in these areas. Molecular information on GCA,especially in early stage, is very limited. The accumulated data about the changes of tumor suppressor gene, such as p53 mutation, and ontogeny, such as C-erbB2, especially the similar alterations in GCA and SCC in the same patient,indicated that there might be some similar risk factors,such as nitrosamine, involved in both GCA and SCC in Henan population. The present observations also suggest that GCA should be considered as a distinct entity.

CYP1A1,GSTs and mEH polymorphisms and susceptibility to esophageal carcinoma:Study of population from a high-incidence area in north China

AIM: To characterize cytochrome P4501A1 (CYPIA1), glutathione S-transferases (GSTs) and microsomal epoxide hydrolase (mEH) polymorphisms in Chinese esophageal cancer patients. METHODS: Multiplex polymerase chain reaction (PCR) and PCR based restriction fragment length polymorphisms (PCRRFLP) were used to detect polymorphism changes of CYP,GSTs and mEH on esophageal cancerous and precancerous lesions as well as in case control group. All the examination samples were obtained from Linzhou (formerly Linxian), Henan Province, the highest incidence area for esophageal. RESULTS: The frequency of CYP1A1 3'' polymorphism in case control group (26/38, 68 %) was significantly higher than in esophageal squamous cell carcinoma^roup (ESCC) (29/62, 47 %) (P<0.05). A significant difference in the incidence of mEH slow allele variant was observed between case control group (15/38, 39 %) and esophageal dysplasiagroup (22/32, 69 %) or ESCC group (39/62, 63 %) (P<0.05). However, no significant difference was observed among different groups in the polymorphisms of CYPIA1 exon 7, GSTM1, GSTT1, GSTP1 and mEH fast allele. CONCLUSION: The present results suggest that CYPIA1 3'' polymorphism may be one of the promising protectivef actors and its wild gene type may be an indicator for higher susceptibility to esophageal cancer, mEH slow allele variant,associated with the progression of esophageal precancerous lesions, may conthbute to the high susceptibility to esophageal carcinoma.

Changes of gut flora and endotoxin in rats with D-galactosamine-induced acute liver failure

AIM: To investigate the changes of gut microflora and endotoxin levels in rats with acute liver failure (ALF) induced by D-galactosamine (GaiN).METHODS: Flora and endotoxin levels in the jejunum, ileum and colon in normal rats (group A) and rats with GaIN-induced ALF were determined at 24 h (group B) or 48 h (group C) after GaIN injection, as well as the endotoxin level in portal venous blood (PVB) and right ventricle blood (RVB) were determined by chromogenic limulus amoebocyte assay.RESULTS: Intestinal(jejunum, ileum, colon) lactobacillus count was statistically reduced in group B compared with those in group A (3.4±0.3 vs 4.9±0.3, 6.1±0.4 vs 8.0±0.3,8.1±0.2 vs 9.3±0.2, P＜0.001, P＜0.001 and P＜0.001 respectively) and recovered partially in the group C compared with those in the group B, whereas the count of Enterobacteriaceae in the jejunum, ileum and colon in group B was increased markedly compared with those in the group A (5.1±20.3 vs 3.6±0.2, 6.9±0.5 vs 5.3±0.3,8.7±0.2 vs 7.6±0.1，P＜0.001, P＜0.05 and P＜0.05 respectively)and restored partially in the group C compared with those in the group B. The endotoxin level in ileum was increased in the group B compared with those in the group A (111.3±22.8 vs 51.5±8.9, P＜0.05). In addition, the endotoxin level in PVB was obviously increased in group B compared with that in the group A (76.8±9.1 vs 40.6±7.3,P＜0.01) and reduced to the baseline at 48 h (group C).CONCLUSION: Severely disturbed gut flora in rats with GaiN-induced acute liver failure plays an important role in the elevation of endotoxin level in PVB.

Proteomic analysis of blood level of proteins before and after operation in patients with esophageal squamous cell carcinoma at high-incidence area in Henan Province

AIM: To characterize the protein files in blood from same patients with esophageal squamous cell carcinoma (ESCC) before and after operation at Me high-incidence area for ESCC in Henan Province, China. METHODS: Two-dimensional electrophoresis, silver staining and ImageMaster 2-DE analysis software were applied to the determination of protein files in the blood obtained from normal controls and ESCC patients before and after operation. RESULTS: A total of 655, 662 and 677 protein spots were identified, respectively, from the normal controls and ESCC patients before and after operation. No significant difference in the number of protein spots was observed between Me normal group and ESCC patients. A total of seven protein spots were identified wi~ a dramatic difference among the samples before and after operation. Six protein spots were up-regulated and one protein spot was down-regulated in the group after operation compared with those in normal and before operation. Three protein spots were further characterized by matrix-assisted laser desorption/ionization time of flying mass spectrometry (MALDI-TOF-MS). The proteins from these three spots were identified as serum amyloid A (SAA), amyloid related serum protein and haptoglobin. CONCLUSION: Serum amyloid A, amyloid related serum protein and haptoglobin may be related with ESCC and/or surgery. The significance of ~ese proteins needs to be further characterized. The present study provides informative data for Me establishment of serum protein profiles related with ESCC.

Alterations of p53 and PCNA in cancer and adjacent tissues from concurrent carcinomas of the esophagus and gastric cardia in the same patient in Linzhou,a high incidence area for esophageal cancer in northern China

AIM: To characterize the alteration and significance of p53and PCNA in cancer and adjacent tissues of concurrent cancersfrom the esophagus and gastric cardia in the same patient.METHODS: P53 and PCNA protein accumulation in 25patients with concurrent cancers from the esophagus andgastric cardia (CC, concurrent carcinomas of esophagealsquamous cell carcinoma and gastric cardia adenocarcinoma)were detected by immunohistochemical method (ABC).RESULTS: In CC patients, both esophageal squamous cellcarcinoma (SCC) and gastric cardia adenocarcinoma (GCA)tissues showed different positive immunostaining extent ofp53 and PCNA protein (P＞0.05). The positive immunostainingrates for p53 and PCNA were 60 % (15/25) and 92 % (23/25), respectively in SCC; and 40 % (10/25) and 88 % (22/25), respectively in GCA. 'Diffuse' immunostaining patternwas frequently observed in both p53 and PCNA. Highcoincidence rates for p53 and PCNA positive staining wereobserved in SCC and GCA from the same patients, andaccounted for 56 % and 96 %. In SCC patients, with thelesions progressed from normal esophageal epithelium (NOR)to basal cell hyperplasia (BCH) to dysplasia (DYS) tocarcinomain situ (CIS) to SCC, the positive rates for p53were 27 %, 50 %, 50 %, 29 % and 72 %, and 55 %, 70 %,75 %, 71% and 93 % for PCNA, respectively. In GCA, withthe lesions progressed from normal gastric cardia epitheliumto DYS to CIS to GCA, the positive rates of p53 expressionwere 44 %, 27 %, 22 % and 36 % respectively, the differencewas not significant; the positive rates of PCNA proteinexpression were 67 %, 64 %, 67 % and 86 %, respectively.The x2 test, Fisher's Exact Test, Mantel-Haenszel x2 Testand Kappa Test were used for the statistics.CONCLUSION: The high coincident alterations for P53 andPCNA in SCC and GCA from the same patient indicate thepossibility of similar molecular basis, which providesimportant molecular basis and etiological clue for similargeographic distribution and risk factors in SCC and GCA.

Helicobacter pyloripromote gastric cancer cells invasion through a NF-κB and COX-2-mediated pathway

AIM: To examine the effects of Helicobacter pylori ( Hpylort)infection on the invasiveness of gastric cancer cells, and to elucidate its mechanism.METHODS: Gastric carcinoma cells, MKN-45, were incubatedwith CagA-positive H pylori, and cell invasion was determined by Matrigel analysis. The expression of matrix metalloproteinase-9 (MMP-9), vascular endothelial growth factor (VEGF), and cyclooxygenase-2 (COX-2) were assessed by Western-blot analysis, and transcriptional activation of the COX-2 promoter was examined by measuring luciferase and β-galactosidase activities. Lastly, the proteinDNA interaction was confirmed by an electrophoretic mobility shift assay.RESULTS: The current studies showed that: (1) incubation of CagA-positive H pylori with MKN-45 cells significantly promotes gastric cancer cells invasion, and this effect is attenuated by pre-treatment with NS-398, a COX-2 inhibitor, or PDTC, a nuclear factor κB (NF-κB) inhibitor; (2) the induction of MKN-45 cells invasion by H pyloriis associated with increases in COX-2, MMP-9, and VEGF protein expression, and co-incubation of NS-398 or PDTC significantly reduces these effects; (3) H pylori infectiontransactivates COX-2 promoter activity and increases the binding of NF-κB to this promoter.CONCLUSION: Our data demonstrate that H pylori infectionpromotes gastric epithelial cells invasion by activating MMP-9 and VEGF expression. These effects appear to be mediated through a NF-κB and COX-2 mediated pathway,as COX-2 or NF-κB inhibitor significantly attenuate the invasiveness of gastric cancer cells and the expressions of MMP-9 and VEGF protein.

Attenuation of graft ischemia-reperfusion injury by urinary trypsin inhibitor in mouse intestinal transplantation

AIM: Ischemia/reperfusion (I/R) injury is one of the major obstacles for intestinal transplantation (ITx). Urinary trypsin inhibitor (Ulinastatin, UTI) suppresses proteases and stabilizes lysosomal membranes. We supposed that Ulinastatin would diminish I/R injury of intestinal graft.METHODS: UTI- treated group and untreated control group were investigated by histological assessment at 1.5, 4, 24, and 72 h after ITx. Myeloperoxidase (MPO)activity was used as the activity of neutrophils, and malondialdehyde (MDA) was used as an index of lipid peroxidation. TNFα and i-NOS mRNA expression in graft tissue were measured by semi-quantitative RT-PCR.CD11b+ Gr1+ cells in graft lamina propria were analyzed by flow cytometry.RESULTS: Histological scores of the graft showed that the tissue injury was markedly attenuated by UTI treatment at different time points after ITx, with reduced MPO and MDA value in the grafts. The expression of TNFα and i-NOS mRNA was profoundly inhibited, while the infiltration of CD11b+ Gr1+ cells into the intestinal graft was decreased in UTI group.CONCLUSION: Urinary trypsin inhibitor attenuates I/R injury in mouse intestinal transplantation by reducing monocytes infiltration and down-regulation of TNFα and i-NOS mRNA expression.

Tumor suppressor gene p16 and Rb expression in gastric cardia precancerouslesions from subjects at a high incidence area in northern China

AIM: To further understand the molecular basis for gastriccardia carcinogenesis and to provide etiological clues.METHODS: Endoscopic mucosa biopsy and histopathologicalexaminations were made on 37 subjects from a high incidencearea for both esophageal and gastric cardia carcinomas innorthem China. All the biopsy samples were fixed in 850 mi. -1 Lalcohol and embedded in paraffin. Each block contained onepiece of tissue and was serially section at 5 μm.Immunohistochemistry (ABC) was carried out on these gastriccardia samples to determine the alterations of p16 and Rb.RESULTS: Based on the histopathlogical examinationtherewere 11 cases of chronic superficial gastritis, 12 cases ofchronic atrophic gastritis and 14 cases of dysplasia. Theimmunostaining demonstrated different levels of unclearimmunostaining of p16 and Rb in normal gastric cardiatissue and the tissues with different severity of lesions. Withthe lesions progressing, the positive immunostaining ratesfor pi6 protein had a decreasing tendency. In contrast, thepositive immunostaining rate for Rb protein had anincreasing tendency. There was a significant negativerelationship between the two parameters. Changes of p16wasCSG 11(100 % ), CAG 7(58 % ), DYS 4(29 % ) andchanges of Rb was CSG 2(18 %), CAG 8(67 %) and DYS 12(86 %), (p＜0.05).CONCLUSION: The alterations of p16 and Rb protein may playa role in the early stages of gastric cardia carcinogenesis.

Effects of atorvastatin on vascular remodeling in spontaneously hypertensive rats

Objective: To investigate the structural changes of aorta, and evaluate the effects of atorvastatinon the remodeling of thoracic aorta in spontaneously hypertensive rats(SHR) . Methods : Twelve eight-week-old SHR were randomized into atorvastatin treated group( ATV group, n = 6) and distilled water group( DW group, n = 6) ; Wistar-Kyoto rats(WKY) were used as normal controls. Atorvastatin was administered to ATV group for 10 weeks by gavage in mixture with distilled water( 1ml) ; the latter two groups were given the same amount of distilled water by gavage for 10 weeks. Systolic blood pressure of caudal artery was examined before and after treatment, and serum concentrations of total cholesterol, triglycerides and HDL-C were measured.Wall thickness, media thickness, medial cross-sectional area and lumen diameter of thoracic aorta were assessed with computed video processing. Results: Systolic blood pressure in ATV group was markedly lower than that in DW group( P < 0.01). Compared with DW group and WKY group, serum concentrations of total cholesterol, triglycerides and HDL-C in ATV group were significantly lower( P < 0.01, P < 0.05). Wall thickness, media thickness, and medial cross-sectional area to lumen ratio in DW group were significantly higher than those in WKY group and ATV group( P < 0.01, P < 0.05), but no such difference was found between WKY group and ATV group( P > 0.05 ). Conclusion : Vascular structural changes of aorta are due to the alteration of the vessel wall in early stage of SHR. Atorvastatin can markedly improve vascular remodeling.

Study on the effect of doxorubicin on expressions of genes encoding myocardial sarcoplasmic reticulum Ca^2＋ transport proteins and the effect of taurine on myocardial protection in rabbits

To investigate the effect of doxorubicin(DOX) on gene expression of the myocardial sarcoplasmic reticulum (SR)Ca^2+ transport proteins and the mechanism of taurine(Tau) protecting cardiac muscle cells, 9 rabbits were injected with DOX , 8 rabbits with DOX and Tau, and 9 rabbits with normal saline. Cardiac function , concentration of calcium in cardiomyocytes ( Myo [ Ca^2+ ]i ), activity of SR Ca^2+ -ATPase (SERCA2a) , level of SERCA2a mRNA and Ca^2+ released channels(RYR2) mRNA were detected. The left ventricle tissues were observed by electron microscopy. The results showed that cardiac index, left ventricular systolic pressure, activity of SR Ca^2+ -ATPase and level of SERCA2a mRNA decreased , while Myo[ Ca^2+ ]i increased in DOX-treated rabbits. DOX could not affect the level of RYR2 mRNA. Tau intervention could alleviate the increase of left ventricular diastolic pressure, Myo[ Ca^2+ ] i and the decrease of SERCA2a mRNA induced by doxorubicin. Tile results suggested that downregulation of SERCA2a gene expression was an important mechanism of DOX-induced cardiomyopathy and that Tau could partially improve the heart function by reducing calcium overload and alleviating downregulation of SERCA2a mRNA.

Changes of Expressions of VEGF, bFGF, and Angiogenesis, and Effect of Benazepril, bFGF on Angiogenesis in Acute Myocardial Infarction Model of the Rabbits

Objective To explore the changes of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and angiogenesis, and the effects of bFGF, angiotensin converting enzyme inhibiter(ACEI) benazepril on the angiogenesis in acute myocardial infarction (AMI) model of rabbits, and to provide a probable evidence for the treatment of AMI. Methods AMI model was established by ligating anterior descending branch of coronary artery of Japan-Sino hybridization white rabbits. The postoperative rabbits were randomly divided into 6 groups and each group was treated with different drugs. Groups 1 and 2 were treated with normal saline (NS) for 28 and 14 days (d), group 3 and 4 with bFGF for 28 and 14 d, groups 5 with benazepril for 14 d, and group 6 with benazepril and bFGF for 14 d respectively. The rabbits were killed on the 14th or 28th d and their hearts were excised, sectioned and stained with HE, Masson trichrome to observe VEGF, bFGF and CD34 under a microscope, which were quantified with a computer-assisted morphometry. Results Compared with group 1, the granulation tissue of infarction zone (IZ) in group 2 freshened up, and the capillary density (CD) in IZ was increased (P=0.002). The CD in the IZ as well as VEGF and bFGF in groups 3 and 4 were increased respectively (P=0.011-0.037). In group 5 the changes of VEGF and bFGF were not found in the IZ and the border zone (BZ) while CD was significantly increased (35.4% and 25.6%, P=0.036 and 0.037). Compared with group 2, the CD in the IZ and BZ of group 6 was significantly increased (63.4% and 44.3% P=0.007 and 0.007), meanwhile VEGF and bFGF were increased. Compared with group 5, only VEGF was increased. Conclusion Intravenous bFGF may increase VEGF and bFGF significantly, thus promoting the angiogenesis in the IZ and BZ in cardiac infarction as VEGF and bFGF are the potent angiogenic growth factors. Benazepril may promote angiogenesis in the IZ and BZ in cardiac infarction, but its mechanism is irrelative to the expression of VEGF and bFGF. The combination of benazepril and bFGF may promote, to some extent, the expression of VEGF and bFGF, but their effect on angiogenesis has not been found.

Ozone Emitted During Copying Process-A Potential Cause of Pathological Oxidative Stress and Potential Oxidative Damage in the Bodies of Operators

To estimate the impact of copying on the indoor air quality, and to investigate whether ozone emitted during such a process induces pathological oxidative stress and potential oxidative damage in the bodies of operators. Methods 67 copying operators (CO) and 67 healthy volunteers (HV) were enrolled in a random control study, in which levels of lipoperoxide (LPO) in plasma and erythrocytes, and levels of vitamin C (VC), vitamin E (VE) and b-carotene (b-CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined by spectrophotometric methods. Results Compared with the HV group, the average values of LPO in plasma and erythrocytes in the CO group were significantly increased (P<0.0001), while those of VC, VE and b-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CO group were significantly decreased (P<0.0001). Pearson product-moment correlation analysis showed that with increase of ozone level in copying sites and duration of exposure to ozone, the values of LPO in plasma and erythrocytes in the bodies of operators were gradually increased,while those of VC, VE, b-CAR, SOD, CAT and GPX were decreased in the same manner. Odds ratio (OR) of risk of biochemical parameters reflecting potential oxidative damage of the copying operators ranged from 4.440 to 13.516, and 95 % CI of OR was from 2.113 to 34.061. Reliability coefficient () of the biochemical parameters used to reflect the potential oxidative damage of the operators was 0.8156, standardized item =0.9929, P<0.0001. Conclusion Findings in the present study suggest that there exist a series of free radical chain reactions and pathological oxidative stress induced by high dose ozone in the operators, thereby causing potential oxidative and lipoperoxidative damages in their bodies.

Trial of a novel endoscopic tattooing biopsy forceps on animal model

AIM: To tattoo gastric mucosa with a novel medical device which could be used to monitor and follow-up gastric mucosal lesions.METHODS: Combining endoscopic biopsy with sclerotherapy injection, we designed a new device that could perform biopsy and injection simultaneously. We performed endoscopies on a pig by using a novel endoscope tattoo biopsy forceps for 15 mo. At the same time, we used two-step method combining sclerotherapy injection needle with endoscopic biopsy. The acuity, inflammation and duration of endoscopy were compared between two methods.RESULTS:Compared with the old two-step method,although the inflammation induced by our new device was similar, the duration of procedure was markedly decreased and the acuity of tattooing was better than the old two-step method. All characteristics of the novel device complied with national safety guidelines. Follow-up gastroscopy after 15 mo showed the stained site with injection of 1:100 0.5 mL of India ink was still markedly visible with little inflammatory reaction.CONCLUSION: Endoscopic tattooing biopsy forceps can be widely used in monitoring precancerous lesions.Its safety and effectiveness has been established in animals.