Dynamic Expression of Tumor Necrosis Factor-α and Vascular Endothelial Growth Factor in Rat Model of Pulmonary Emphysema Induced by Smoke Exposure

In order to explore the roles of tumor necrosis factor-α(TNF-α) and vascular endothelial growth factor(VEGF) in the pathogenesis of pulmonary emphysema,male Wistar rats were randomized into group A1,group A2.5 and group A4,each with smoke exposure for 1 month,2.5 months or 4 months,respectively.Group B1,group B2.5 and group B4 were used as non smoking controls at corresponding time points.TNF-α in bronchoalveolar lavage fluid(BALF) and expression of VEGF in lung tissue was determined by ELISA or by SABC immunohistochemistry assay either.Lung slices were stained with hematoxylin and eosin(HE).Results showed that in animal with smoke exposure the mean linear interceptor(Lm),an index of pulmonary emphysema and the content of TNF-α in BALF increased gradually,on contrary,the expression of VEGF in lung tissue decreased(P<0.05).This phenomenon was not obvious in animals without smoke exposure.Lm was negatively correlated to the VEGF expression(γ=-0.81,P<0.01) and positively correlated to TNF-α concentration(γ = 0.52,P<0.004),which implies that smoke exposure decreased the expression of VEGF and increased the expression of TNF-α.It is plausible to speculate that the imbalance of TNF-α and VEGF may play an important role in the pathogenesis of smoke-induced pulmonary emphysema.     

Blockade of the sonic hedgehog signalling pathway inhibits choroidal neovascularization in a laser-induced rat model

Sonic hedgehog (Shh) signaling has recently been shown to be involved in the pathological angiogenesis in response to tissue hypoxia and ischemic injury.Hypoxia/ischemia is considered to play an important role in the development of choroidal neovascularization (CNV).This study was aimed to examine the effect of blockade of the Shh signaling pathway on CNV and the underlying mechanism.A total of 64 male Brown-Norway (BN) rats were used in this study.One eye of each rat underwent laser photocoagulation.The other eye served as normal control.After the laser treatment, the 64 rats were divided into four groups (n=16 in each group):Blank control group, in which no intravitreal administration was given; cyclopamine group, recombinant Shh N-terminals protein (rShh) group and phosphate-buffered saline (PBS) group, in which cyclopamine (a Shh inhibitor), rShh (a Shh activator) and PBS were intravitreally injected into the laser-treated eyes respectively every other day for a total of four intravitreal injections immediately after the laser treatment.Fourteen days after the intravitreal administration, the changes of CNV-related variables, including positive CNV lesion percentage, CNV membrane area and CNV membrane thickness, were evaluated by fluorescein anqiography, indocyanine green angiography and pathological examinations.The mRNA and protein expression of PTCH1, Gli1, HIF-1α, VEGF and DLL4 in each group on 14 days of CNV model was detected by real-time quantitative PCR and western blot analysis, and the relationship between the Shh cascade and the HIF-1α-VEGF-DLL4 cascade in CNV was analyzed.The results showed that the CNV membrane area and the CNV membrane thickness were decreased by 62.5% and 41.9% in the cyclopamine group and increased by 85.7% and 64.3% in the rShh group in comparison to those in the blank control group (P<0.01 for each).There was no significant difference in the CNV membrane area and thickness between the blank control group and PBS group (P=0.102 and P=0.063, respectively).Real-time quant     

Activated pancreatic stellate cells can impair pancreatic islet function in mice

Background

Pancreatic or islet fibrosis is often associated with activated pancreatic stellate cells (PSCs). PSCs are considered not only to promote fibrosis, but also to be associated with glucose intolerance in some diseases. We therefore evaluated morphological and functional relationships between islets and PSCs in the normal mouse pancreas and transplanted islets.

Methods

Immunohistochemistry was used to map the presence of PSCs in the normal mouse pancreas and islets implanted under the renal capsule. We isolated and cultured mouse PSCs and characterized them morphologically by immunofluorescence staining. Furthermore, we measured their cytokine production and determined their effects on insulin release from simultaneously cultured islets.

Results

PSCs were scattered throughout the pancreas, with occasional cells within the islets, particularly in the islet capsule. In islet transplants they were found mainly in the graft periphery. Cultured PSCs became functionally activated and produced several cytokines. Throughout the culture period they linearly increased their production of interleukin-6 and mammalian keratinocyte-derived chemokine. PSC cytokine production was not affected by acute hyperglycemia. Syngeneic islets co-cultured with PSCs for 24–48 h increased their insulin release and lowered their insulin content. However, short-term insulin release in batch-type incubations was unaffected after 48 h of co-culture. Increased islet cell caspase-3 activation and a decreased islet cell replication were consistently observed after co-culture for 2 or 7 days.

Conclusion

Activated PSCs may contribute to impaired islet endocrine function seen in exocrine pancreatitis and in islet fibrosis associated with some cases of type 2 diabetes.     

糖尿病性视网膜病变患者血清microRNA-20a-5p、VEGF水平变化及其临床意义

目的 探讨糖尿病性视网膜病变（DR）患者血清microRNA-20a-5p（miR-20a-5p）、血管内皮生长因子（VEGF）水平变化及其临床意义。方法 选取遵义市第一人民医院眼科2018年1月—2020年12月收治的82例DR患者为DR组,根据DR严重程度分为增殖型糖尿病性视网膜病变（PDR）组（n =27）和非增殖型糖尿病性视网膜病变（NPDR）组（n =55）。选取同期单纯T2DM患者为T2DM组,42例体检健康者为对照组。采用实时荧光定量聚合酶链反应（qRT-PCR）检测各组血清miR-20a-5p mRNA相对表达量;采用酶联免疫吸附试验（ELISA）检测血清VEGF水平;采用葡萄糖氧化酶法测定空腹血糖（FBG）、胶乳凝集反应法测定糖化血红蛋白（HbA1c）水平。Pearson相关性分析DR患者血清miR-20a-5p mRNA相对表达量与VEGF、FBG、HbA1c的相关性,多因素Logistic回归分析血清miR-20a-5p、VEGF与DR发生的关系,ROC曲线分析血清miR-20a-5p、VEGF对DR发生的预测价值。结果 与T2DM组比较,DR组FBG、HbA1c、VEGF水平升高,血清miR-20a-5p mRNA相对表达量降低,与对照组比较,T2DM组FBG、HbA1c、VEGF水平升高,血清miR-20a-5p mRNA相对表达量降低（P <0.05）。与NPDR组比较,PDR组FBG、HbA1c、VEGF水平升高,血清miR-20a-5p mRNA相对表达量降低（P <0.05）。DR患者血清miR-20a-5p mRNA相对表达量与FBG、HbA1c、VEGF水平呈负相关（r =-0611、-0.799和-0.545,均P <0.05）。多因素Logistic回归分析显示,血清miR-20a-5p高水平［O^R=0.254（95% CI：0.154,0.596）］为DR发生的独立保护因素,糖尿病病程长［O^R=2.042（95% CI：1.422,2.933）］、血清HbA1c高水平［O^R=2.307（95% CI：1.101,4.833）］、血清VEGF高水平［O^R=2.570（95% CI：1.584,4.144）］为DR发生的独立危险因素（P <0.05）。ROC曲线显示,血清miR-20a-5p预测DR发生敏感性为97.56%（95% CI：0.915,0.997）、特异性为61.54%（95% CI：0.471,0.748）;血清VEGF敏感性为57.32%（95% CI：0.447,0.683）、特异性为96.15%（95% CI：0.868,0.995）;联合预测敏感性为91.46%（95% CI：0.832,0.965）、特异性为76.92%（95% CI：0.632,0.875）。结论 DR患者血清miR-20a-5p mRNA相对表达量降低,与FBG、HbA1c、VEGF水平密切相关,miR-20a-5p可能通过调控糖代谢和VEGF介导DR发生和发展。     

血管内皮生长因子、单核细胞趋化蛋白1、分化抑制因子1在脑胶质瘤中的表达及与血管生成的相关性分析

目的 分析血管内皮生长因子（VEGF）、单核细胞趋化蛋白1（MCP-1）、分化抑制因子1（Id1）在脑胶质瘤中的表达及与血管生成的相关性。方法 选取2018年4月—2020年5月湖北省中西医结合医院脑胶质瘤患者150例作为病例组。另选取该院因脑外伤后行颅内减压术的50例非肿瘤患者（正常脑组织）作为对照组。对比两组患者血清VEGF、MCP-1、Id1水平，绘制ROC曲线分析血清VEGF、MCP-1、Id1水平预测脑胶质瘤发生的价值；比较不同级别脑胶质瘤患者血清VEGF、MCP-1、Id1水平及肿瘤微血管密度（MVD）值，Pearson法分析血清VEGF、MCP-1、Id1水平与MVD值的相关性。结果 病例组血清VEGF、Id1水平较对照组高，MCP-1水平较对照组低（P <0.05）。ROC曲线结果显示，血清VEGF、MCP-1、Id1水平及3者联合预测胶质瘤发生的AUC分别为0.873（95% CI：0.823，0.923）、0.776（95% CI：0.699，0.853）、0.898（95% CI：0.850，0.946）、0.908（95% CI：0.851，0.978）。高级别组血清VEGF、Id1水平及MVD较低级别组高，MCP-1水平较低级别组低（P <0.05）。Pearson相关性分析显示，脑胶质瘤患者MVD与血清VEGF水平、Id1水平呈正相关（r =0.532和0.697，均P <0.05），与MCP-1水平呈负相关（r =-0.395，P <0.05）。结论 脑胶质瘤患者血清VEGF、Id1水平上调，MCP-1水平下调，三项指标与肿瘤血管生成密切相关，且可有效预测胶质瘤的发生。     

小鼠胰岛α细胞的缺失对移植胰岛功能的影响

目的　探讨胰岛α细胞的丢失对胰岛素分泌功能的影响。方法　在人胰岛分离过程中 ,经胶原酶的过度消化造成胰岛周边α细胞缺失 ,用免疫组化及胰岛素 /胰高糖素含量分析予以证实。在体外 ,检测葡萄糖刺激引起的实验性糖尿病小鼠胰岛素的分泌 ;在体内 ,评价胰岛移植后对糖尿病小鼠血糖的调节 ,并研究胰高糖素对α细胞缺失胰岛功能的影响。结果　胶原酶的过度消化引起胰岛周边的α细胞丢失 ,使分离胰岛内胰岛素 /胰高糖素比值明显升高。与正常胰岛相比 ,α细胞缺失胰岛对葡萄糖刺激产生的胰岛素明显降低 ,胰岛素释放在正常胰岛和α细胞缺失胰岛分别为2 2 2 7uU/ml± 32 1uU/ml和 12 4 6uU/ml± 12 6uU/ml(P <0 0 1)。在体内 ,移植α细胞缺失的胰岛到糖尿病的C5 7/BL小鼠后不能有效地纠正动物的高血糖 ,胰岛移植后的平均血糖浓度在正常胰岛组和α细胞缺失胰岛组分别为 :8 9mmol/L± 1 98mmol/L和 2 1 3mmol/L± 2 2mmol/L(P <0 0 1) ,而给予外源性的胰高糖素可以在体外及体内明显改善α细胞缺失胰岛的胰岛素分泌功能。结论　胰岛α细胞的缺失明显降低胰岛的胰岛素分泌功能 ,用外源性的胰高糖素可以改善α细胞缺失胰岛的胰岛素分泌功能。     

Improvement of the function of islet beta and alpha cells by intervention against glucotoxicity: experiment with rats

OBJECTIVE: To investigate the effects of intervention against glucotoxicity on improvement of the function and pathological changes of islet beta and alpha cells. METHODS: Thirty-six male Sprague Dawley rats were randomly divided into four equal groups: normal control (NC) group, fed with standard chow, high-fat (HF) group, fed with extra high-fat chow; diabetes mellitus (DM) control group, fed with high-fat chow for 8 weeks followed by 30 mg/kg streptozotocin injection to establish DM models; and insulin (INS) group, treated with subcutaneous injection of long-acting insulin (glargine, 0.5 U x kg(-1) x d(-1)) for 4 weeks after the establishment of DM models. 48 h, 2 weeks, and 4 weeks after the STZ injection to the 2 DM groups oral glucose tolerance test (OGTT) was performed to all rats. Peripheral blood samples were collected from the caudal vein. Serum insulin level was assayed by radioimmunoassay. Total serum cholesterol (TC) and triglyceride (TG) were measured by enzyme-colorimetric method. By the end of experiment the rats were killed with their pancreases taken out. Immunohistochemistry was used to observe the morphological changes of the islet beta and alpha cells. Beta cell and alpha cell masses were calculated by the proportions of positive area in the islet. Proinsulin mRNA level was detected by RT-PCR. Insulin protein content in islets was detected by Western blotting. RESULTS: Four weeks after the insulin intervention against glucotoxicity, the fasting blood glucose and blood glucose 2 h after sugar-taking of the INS group were both significantly lower than those of the DM group (both P < 0.01). The relative beta cell mass of the INS group was 0.38 +/- 0.08, significantly bigger, 2.45 times, that of the DM group (0.11 +/- 0.05, P < 0.01). The relative alpha cells mass in islets of the INS group was 0.16 +/- 0.04, significantly lower, by 43%, than that of the DM group (0.28 +/- 0.15, P < 0.01). The insulin contents in beta cells of the INS group was 0.58 +/- 0.03, significantly higher, by 70.6%, than that of the DM group (0.34 +/- 0.14, P < 0.01). The proinsulin mRNA level of the INS group was 1.52 +/- 0.14, significantly higher, by 20.6%, than that of the DM group. CONCLUSION: The morphology of islet beta, alpha cells in diabetic rats was improved by four weeks of Intervention against glucotoxicity improves the pathology of islet beta and alpha cells in diabetic and insulin synthesis.     

VEGF反义寡核苷酸与低分子肝素联合应用对小鼠Lewis肺癌生长和肺血栓栓塞症的影响

目的探讨血管内皮细胞生长因子(VEGF)反义寡核苷酸(ASODN)与低分子肝素(LMWH)联合应用对小鼠Lewis肺癌生长、凝血及肺血栓栓塞症(PTE)的影响及其机制。方法复制Lewis肺癌模型小鼠40只,随机分为对照组、VEGF-ASODN组、VEGF错义寡核苷酸(MSODN)组、LMWH组及联合治疗组,每组8只,分别给予生理盐水、VEGF-ASODN、VEGF-MSODN、LMWH(法安明)及VEGF-ASODN+法安明皮下注射,隔日1次,共15次。检测皮下移植瘤的变化。应用免疫组织化学方法检测肿瘤组织微血管密度(MVD)。应用酶联免疫吸附方法检测血浆中VEGF和凝血激活剂组织因子(TF)的质量浓度。应用组织HE染色方法检查肿瘤组织、心、肺、脑、肾、肝等组织脏器的血栓和栓塞情况。应用Western blot方法检查肿瘤组织VEGF和TF蛋白表达。结果ASODN、LMWH和联合治疗组的抑瘤率分别为47.34%、27.31%和59.03%,这3组的抑瘤率和MVD与对照组和MSODN组相比差异均有统计学意义(P<0.05)。ASODN组和联合治疗组的血浆VEGF质量浓度分别为(9.66±1.02)ng/L、(9.39±2.26)ng/L,较对照组[(14.39±3.76)ng/L]显著降低(P<0.05);LMWH组和联合治疗组血浆TF质量浓度分别为(20.00±1.26)ng/L、(23.50±5.62)ng/L,较对照组[(27.08±5.40)ng/L]显著降低(P<0.05)。对照组、ASODN组、MSODN组、LMWH组、联合治疗组PTE的发生率分别为37.5%、50.0%、37.5%、25.0%和25.0%;ASODN组肿瘤组织中VEGF蛋白表达较弱,而TF表达较强。结论VEGF-ASODN和LMWH联合有协同抗肿瘤作用;但VEGF-ASODN有促凝作用,使PTE的风险增加,而LMWH可降低高凝倾向。     

Protective roles of α-lipoic acid in rat model of mitochondrial DNA4834bp deletion in inner ear

The protective roles of α-lipoic acid in the rat model of mitochondrial DNA (mtDNA) 4834bp deletion in inner ear were investigated. Forty female Wistar rats at 4 weeks of age were divided into four groups: group A (D-galactose group, n=10), group B (D-galactose+α-lipoic acid group, n=10), group C (α-lipoic acid group, n=10), and group D (control group, n=10). Auditory brainstem response (ABR) was used to detect the hearing threshold. Colorimetry was used to analyze activity of superoxide dismutase (SOD) and...     

大剂量抗氧化剂对高脂饲养大鼠胰岛β细胞分泌功能的影响及机制

目的:探讨大剂量抗氧化剂-N-乙酰半胱氨酸(N-acetyl-l-cysteine,NAC)对高脂饲养大鼠胰岛β细胞分泌功能的影响及可能机制。方法:将59只8周龄SD大鼠随机分为正常饲料组(NC组)、高脂饲料组(HF组)和高脂 NAC组(NAC组)。饲养20周,(1)测血浆及胰腺组织丙二醛(MDA)和还原型谷胱甘肽(GSH)水平;(2)正常血糖高胰岛素钳夹实验,评价外周组织胰岛素抵抗程度;(3)胰岛细胞表面灌注实验,评价离体胰岛β细胞动态分泌功能;(4)实时荧光定量PCR方法比较各组大鼠胰岛素受体底物-1(IRS-1)、胰岛素受体底物-2(IRS-2)和葡萄糖转运子-2(Glut-2)mRNA表达的变化。结果:(1)HF组血浆及胰腺MDA水平明显高于NC组,GSH水平低于NC组,NAC可以改善以上变化;(2)HF组葡萄糖输注率(GIR)比NC组降低(P<0.01),用NAC后GIR明显改善(P<0.01);HF组葡萄糖刺激的胰岛素分泌(GSIS)功能下降,用NAC后可逆转上述变化;(3)HF组胰岛细胞IRS-1、IRS-2、Glut-2mRNA表达降低42.3%、28.1%、22.9%(P均<0.05);NAC组胰岛细胞IRS-1、IRS-2、Glut-2 mRNA表达与HF组相比增加40.2%、30.2%,19.1%(P均<0.05)。结论:大剂量抗氧化干预治疗能改善胰岛细胞胰岛素信号传导,逆转高脂饲养导致的大鼠胰岛细胞分泌功能紊乱,其机制可能与NAC纠正机体氧化及抗氧化失衡有关。     

妇痛宁对子宫内膜异位症COX2-PGE2作用途径的影响

[目的] 通过研究化瘀散结中药妇痛宁对子宫内膜异位症（EMs）病灶中环氧化酶2（COX2）-前列腺素E2（PGE2）作用途径中相关分子基因和蛋白的表达,探讨妇痛宁对EMs中血管生成、侵袭和转移方面的影响。[方法] 收集EMs患者的异位病灶组织,原代消化培养子宫内膜细胞,将25×10⁶/mL浓度混合培养的异位子宫内膜细胞注射到裸鼠腹部皮下,成功建立模型后,将成模裸鼠分为空白对照组、低剂量组、中剂量组、高剂量组和阳性对照组,分别予无菌生理盐水、低剂量中药、中剂量中药、高剂量中药和孕三烯酮灌胃,3周后处死裸鼠,取病灶,测量病灶体积,免疫组化法检测各组病灶中血管内皮生长因子（VEGF）的表达和微血管密度（MVD）,逆转录-聚合酶链反应（RT-PCR）法检测病灶中COX2、PGE2、VEGF、Snail和E-cadherin mRNA的表达,Western-blot法检测病灶中Snail和E-cadherin蛋白的表达。[结果] 中剂量及高剂量妇痛宁治疗组裸鼠异位病灶体积减小、VEGF表达及MVD均降低,与空白对照组比较差异有统计学意义（P<0.05）。各剂量治疗组裸鼠异位病灶中COX2、PGE2、VEGF、Snail mRNA表达降低,E-cadherin mRNA表达升高,且Snail蛋白表达降低,E-cadherin蛋白表达升高,与空白对照组比较差异有统计学意义（P<0.05）。[结论] 妇痛宁可影响COX2-PGE2作用途径中与血管生成、侵袭和转移相关分子的表达,通过抑制异位病灶的血管生成、侵袭和转移能力而抑制病灶的生长。     

Telmisartan protects against insulin resistance by attenuating inflammatory response in rats

This study investigated the effects of telmisartan on insulin resistance in high-fat diet-treated rats and the possible mechanism.A total of 40 male Sprague-Dawley rats enrolled in the study were divided into 4 groups at random:ND group(n=10) and HD group(n=10),in which the rats were given a normal chow diet or a high-fat diet for 20 weeks following a one-week adaptation;ND+telmisartan(n=10) group and HD+telmisartan group(n=10),in which the rats were initially administered in the same way as the ND or HD group,and then they were orally gavaged with telmisartan(5 mg/kg daily) additionally for 5 weeks.Related inflammatory factors were measured by ELISA.Monocyte chemotactic protein 1(MCP-1),phosphorylated JNK and IκB-α expressions in both adipose and liver were detected by Western blotting.CRP and angiotensin Ⅱ receptor 1(AT1) mRNA expressions in both adipose and liver were determined by RT-PCR.The results showed that telmisartan administration in vivo reversed insulin resistance as evidenced by a decrease in plasma fasting glucose levels,plasma fasting insulin levels and homeostasis model of assessment-insulin resistance(HOMA-IR).Furthermore,telmisartan administration significantly reduced serum CRP,TNF-α and IL-1β levels,and elevated serum IL-10 levels.It was also found to hamper the high-fat diet-induced increase in CRP mRNA,AT1 mRNA and MCP-1,and decrease in IκB-α in both adipose and liver.It was concluded that telmisartan administration in vivo may improve insulin resistance through attenuated inflammatory response pathways.     

Protection of human islets from induction of apoptosis and improved islet function with HO-1 gene transduction

Background Islet transplantation represents an ideal therapeutic approach for treatment of type 1 diabetes but islet function and regeneration may be influenced by necrosis or apoptosis induced by oxidative stress and other insults. Heme oxygenase-1 (HO-1) is the rate-limiting enzyme in the catabolism of heme into biliverdin, releasing free iron and carbon monoxide. It has also been reported to be an antioxidant enzyme which can improve the function of grafted islets by cytoprotection via free radical scavenging and apoptosis prevention. In the present study, we investigated whether transduction of HO-1 genes into human islets with an adenovirus vector has cytoprotective action on islets cultured in vitro and discuss this method of gene therapy for clinical islet transplantation.Methods Cadaveric pancreatic islets were isolated and purified in vitro. Transduction efficiency of islets was determined by infecting islets with adenovirus vector containing the enhanced green fluorescent protein gene (Ad-EGFP) at multiplicities of infection (MOI) of 2, 5, 10, or 20. Newly isolated islets were divided into three groups: EGFP group, islets transduced with Ad-EGFP using MOI＝20; HO-1 group, transduced with adenovirus vectors containing the human HO-1 gene using MOI＝20; and control group, mock transduced islets. Insulin release after glucose stimulation of the cell lines was determined by a radioimmunoassay kit and the stimulation index was calculated. Flow cytometry was used to detect apoptotic cells in the HO-1 group and in the control group after induction by recombinant human tumor necrosis factor-α (rTNFα) and cycloheximide (CHX) for 48 hours.Results Adenovirus vectors have a high efficiency of gene transduction into adult islet cells. Transduction of islets with the Ad-EGFP was most successful at MOI 20, at which MOI fluorescence was very intense on day 7 after transduction and EGFP was expressed in cultured islet cells for more than four weeks in vitro. The insulin release in the control group was (182.36±58.96) mIU/L after stimulation by high glucose media (16.7 mmol/L), while insulin release from the HO-1 group and the EGFP group were (270.09±89.37) mIU/L and (175.95±75.05) mIU/L respectively. Compared to the control group and the EGFP group, insulin release in the HO-1 group increased significantly (P＜0.05). After treatment with rTNFα and CHX the apoptotic ratio of islet cells was (63.09±10.86)% in the HO-1 group, significantly lower than (90.86±11.25)% in the control group (P&lt;0.05).Conclusions Transduction of human islets with Ad-HO-1 can protect against TNF-α and CHX mediated cytotoxicity. The HO-1 gene also appears to facilitate insulin release from human islets. Transduction of donor islets with the adenovirus vector containing an HO-1 gene might have potential value in clinical islet transplantation.     

血管内皮生长因子和微血管密度在结直肠癌中的意义

目的　探讨血管内皮生长因子 (VEGF)和微血管密度 (MVD)在结直肠癌中的表达以及它们之间的关系。方法　应用免疫组织化学S P法检测 87例结直肠癌组织中血管内皮生长因子的表达以及微血管密度。结果　 87例结直肠癌组织中VEGF的表达阳性率为 6 6 .7% ,MVD为 32 .80± 12 .11。VEGF和MVD在侵及浆膜层的结直肠癌中明显高于侵及肌层者 ,在淋巴结转移阳性组高于淋巴结转移阴性组 ,在DukesC、D期明显高于A、B期 ,差异均有显著性 (P <0 .0 5 ) ,且随着肿瘤分化程度的降低而增高 (P <0 .0 5 ) ;VEGF阳性组中的MVD值显著高于VEGF阴性组 (P <0 .0 1)。结论　VEGF与结直肠癌血管生成密切相关 ,VEGF的表达和MVD可作为判断结直肠癌恶性程度的生物学指标     

胃浆膜下层与门静脉胰岛移植治疗糖尿病大鼠的实验研究

目的 通过比较胃浆膜下层与门静脉胰岛移植治疗糖尿病大鼠的功效,探讨胰岛移植的最适宜部 位。方法 链脲佐菌素诱导糖尿病大鼠,将其分为胃浆膜组、门静脉组、对照组,每组6 只;经胆总管灌注 胶原酶Ⅺ消化胰腺组织,分离、纯化胰岛,采用双硫腙（DTZ）特性染色并计数胰岛当量（IEQ）及纯度,台 盼蓝染色判断胰岛活性;同期分别将500 IEQ 大鼠胰岛移植入胃浆膜下层和门静脉,对照组输注等量RPMI 1640 液体,移植后分别检测大鼠的血糖浓度,腹腔葡萄糖耐量实验,评判胰岛功能。结果 每只大鼠可获取 胰岛（310±42）个,DTZ 染色显示胰岛纯度为（89.00±4.52）% ;台盼蓝染色显示胰岛活性良好[（89.08± 3.76）%] ;胰岛移植后胃浆膜组、门静脉组大鼠血糖较之前下降（P <0.05）,与对照组血糖浓度比较,差异有 统计学意义（P <0.05）;胃浆膜组与门静脉组胰岛移植后大鼠血糖浓度比较,差异有统计学意义（P <0.05）; 胃浆膜组与门静脉组大鼠有效控制血糖时间分别为（18.0±1.9）和（11.6±2.5）d,差异有统计学意义（P <0.05）。 胃浆膜组与门静脉组大鼠腹腔葡萄糖耐量实验提示糖耐受功能良好。结论 短期内,胃浆膜下层胰岛移植治 疗糖尿病大鼠的疗效优于门静脉移植;与门静脉相比,胃浆膜下层胰岛移植操作简单,安全性高,是胰岛移植 的最适宜部位之一。     

血管内皮生长因子与骨巨细胞瘤预后的关系

目的:研究血管内皮生长因子(VEGF)及微血管密度(MVD)对估计人骨巨细胞瘤预后的价值。方法:通过对69例骨巨细胞瘤患者的随访,将他们分为无复发和无转移组及复发或转移组。采用免疫组织化学SABC法检测骨巨细胞瘤中VEGF、CD34的表达,用MVD值衡量CD34的表达。结果:无复发组42例的中位阳性细胞率为28%,复发转移组27例的中位阳性细胞率为48%,两组间差别有极显著性意义(P<0.001)。无复发组MVD值为33.55±10.82,复发转移组MVD值为56.78±16.17,两组间MVD值的差别有极显著性意义(P<0.001)。VEGF阳性细胞率与MVD值的关系经Spearman等级相关检验,两者呈显著正相关(r=0.845,P<0.01)。结论:VEGF和MVD是估计骨巨细胞瘤预后的新指标,VEGF是重要的促血管生成因子。