Reperfusion of the rat brain tissues following acute ischemia: the correlation among diffusion-weighted imaging, histopathology, and aquaporin-4 expression

Background  Although some studies have reported that aquaporin-4 (AQP4) plays a role in the post-ischemic edema formation and diffusion-weighted imaging (DWI), little is known about the AQP4 expression in stage of the reperfusion following acute cerebral ischemia, as well as the correlation between histopathology and DWI. The aim of the study was to investigate the correlation among DWI, histopathology and the AQP4 expression in the reperfused rat brain tissues following acute ischemia.

Methods  Seventy Wistar rats were randomly divided into a control group (group A), and several occluded and reperfusion groups. They had their middle cerebral artery unilaterally occluded (MCAO) for 30 minutes (group B) followed by 30 minutes (group D) or 60 minutes (group E) of reperfusion, or 60 minutes of MCAO (group C) followed by 30 minutes (group F), or 60 minutes (group G) of reperfusion (n=10 for each group). All rats underwent DWI scanning. The relative apparent diffusion coefficient (rADC) value of each rat was calculated. All the rats were sacrificed and the cerebral ischemic tissues were examined for histopathology. Real-time fluro-quantitative polymerase chain reaction (RT-PCR) and Western-blotting were performed. The amount of AQP4 mRNA (Ex^－ΔΔCt) and AQP4 protein (Q) was statistically analyzed. The correlation between rADC values and AQP4 mRNA expression was analyzed with the Pearson correlation test.

Results  In all the reperfusion groups, the areas of hyper-intensity signal in DWI were decreased, and the rADC value increased and the AQP4 expression decreased significantly compared with the occluded group (t=26.89, t=18.26, P <0.01). There was a negative correlation between AQP4 mRNA expression and rADC values (r=-0.72, P <0.01). A mixed edema, composed of cerebral intracelluar edema and vasogenic brain edema, was observed in all the reperfusion groups. It was more prevalent in groups D and F than in the groups E and G. With the reperfusion time postponed, the cerebral intracelluar edema of the rat was significantly mitigated, but the vasogenic brain edema was not significantly changed.

Conclusions  There is a close correlation between AQP4 expression and the cerebral intracellular edema. The change of ADC values may indirectly reflect the level of the AQP4 expression. DWI may become a promising, noninvasive imaging modality to predict early stroke and reperfusion injury.

     

Expression and significance of P53 protein and MDM-2 protein in human gliomas

Background  P53 is one of the most studied tumor suppressors in the cancer research, and over 50% of human tumors carry P53 mutations. MDM-2 is amplified and/or overexpressed in a variety of human tumors of diverse tissue origin. The aim of this study was to examine the expression of P53 protein and MDM-2 protein in gliomas, and to investigate the relationship between the expression of the two proteins and the histopathological grades of glioma. The relationship between MDM-2 protein expression and P53 protein expression was also analyzed.

Methods  The expression of P53 protein and MDM-2 protein was immunohistochemically detected using monoclonal antibodies in 242 paraffin embedded tissues, including 30 normal brain tissues from patients with craniocerebral injury and 212 tissues from patients with primary glioma (grade I–II group: 5 cases of grade I, 119 cases of grade II; and grade III–IV group: 53 cases of grade III, and 35 cases of grade IV).

Results  The P53 positive rate was significantly higher in the glioma groups than in the control group (P <0.0001). The P53 positive rate was significantly higher in glioma tissues of grade III–IV than in glioma tissues of grade I–II group (P=0.001). The MDM-2 positive rate was significantly higher in glioma groups than in the control group (P <0.0001). There was no significant difference in the MDM-2 positive rate between the two glioma groups (P=0.936). The expression of P53 protein was not related to expression of MDM-2 protein (P=0.069)

Conclusions  Overexpression of P53 protein might be related to the occurrence and progression of glioma. Overexpression of MDM-2 protein may play an important role in glioma tumorigenesis, but may not be involved in glioma progression. The overexpression of MDM-2 protein was an early event in malignant transformation of glioma. MDM-2 may be a key player in glioma in its own right.

     

Characteristics of pulmonary inflammation in combined pulmonary fibrosis and emphysema

Background  The condition of concomitant upper lobe emphysema and lower lobe fibrosis as identified by computer tomography is known as combined pulmonary fibrosis and emphysema (CPFE). CPFE has distinct clinical characteristics compared with emphysema alone (EA) and idiopathic pulmonary fibrosis (IPF) without emphysema. However, the pulmonary inflammation characteristics of CPFE are not well known, and the differences between CPFE and the other two diseases with regards to pulmonary inflammation need to be explored. The pulmonary inflammatory characteristics were investigated in CPFE patients and compared with EA and IPF.

Methods  Fraction exhaled nitric oxide (Fe,NO) and differential cell counts, the concentrations of monokine induced by interferon gamma (MIG/CXCL9), interferon-inducible protein 10 (IP-10/CXCL10), and interferon-inducible T cell alpha chemoattractant (I-TAC/CXCL11) were measured in induced sputum obtained from subjects with CPFE (n=22), EA (n=22), IPF (n=14), and healthy volunteers (HV, n=12). In addition, immunohistochemistry was used to quantify the expression of nitric oxide synthases in alveolar macrophages in 23 lung tissues from patients and control subjects.

Results  The CPFE group had higher alveolar NO than subjects in the EA and HV groups (P=0.009, P=0.001, respectively) but not than the IPF group (P >0.05). Numbers of sputum eosinophils were significantly elevated in CPFE and IPF groups compared with the HV group (P=0.001, P=0.008). In contrast, eosinophil counts in EA group did not differ from those in the HV group. Compared with the EA and HV groups, the CPFE group had a lower concentration of I-TAC/CXCL11 in sputum supernatants (P=0.003, P=0.004). Immunoreactivity for inducible nitric oxide synthase (iNOS) was higher in the CPFE group than in the EA group (P=0.018).

Conclusions  The pulmonary inflammation of CPFE group is more similar to IPF group, while the distal airway inflammation is more significant in CPFE and IPF groups than in EA group. Lung eosinophil cell infiltration and high NOS expression in alveolar macrophage might participate in this pathogenesis.

     

Curative effect of radiotherapy at various doses on subcutaneous alveolar echinococcosis in rats

Background  Alveolar echinococcosis (AE) is a disease in human and animals, and the cure rate is unsatisfactory. This study aimed to investigate the curative efficacy of different doses of locally applied radiotherapy on alveolar echinococcosis in rats.

Methods  Rats infected with Echinococcus multilocularis were randomly divided into 4 groups of 15 rats each: low-, middle-, and high-irradiation groups and a control group. Rats in the control group underwent no treatment, while rats in the irradiation groups received 6-MeV radiotherapy at 20 Gy/8 f, 40 Gy/8 f, and 60 Gy/8 f respectively, once every 3 days for a total of 8 times. One month after radiotherapy, wet weight and AE vesicle inhibitory rate were detected in rats of each group. Histopathologic and ultrastructural observations of tissues with AE lesions were performed.

Results  In the treatment groups, an obvious inhibitory effect was found in AE rats; the inhibitory rates were 50%, 72%, and 82%, respectively. There were also statistical differences in pathological changes and average wet weight of the lesions compared with the control group (P <0.05). In the treatment groups, injuries of various degrees were found in the ultrastructure of the laminated and germinal layers in the capsular wall of AE, and injury was most severe in the high-dose group.

Conclusion  Radiotherapy has a dose-dependent inhibitory effect on the growth of AE.

     

Effects of shenmai injection on pulmonary aquaporin 1 in rats following traumatic brain injury

Background  Aquaporin-1 (AQP1) has involved in fluid transport in diverse pulmonary edema diseases. Our study aimed to explore the dynamic changes of AQP1 in pulmonary water metabolism in rats following traumatic brain injury (TBI) and the protective effect provided by shenmai injection.

Methods  Sixty male Sprague Dawley rats weighting 280–300 g were randomly divided into three groups: the normal control group, the model group and the shenmai injection (SMI) group. One piece skull was taken away without injuring cerebral tissue in normal control group, while rats in model group and SMI group were subject to free fall injury in the cerebral hemisphere. Rats in model group received intraperitoneal normal sodium (15 ml/kg) at one hour post-injury and the same dose of shenmai injection instead in SMI group, respectively. The expression of AQP1 was detected by immunohistochemical analysis and semi-quantitative RT-PCR at 0 hour, 10 hours, 72 hours and 120 hours after TBI. Arterial blood gas analysis and lung wet to dry were also measured.

Results  AQP1 was mainly presented in the capillary endothelium and slightly alveolar epithelial cells in three groups, but the expression of AQP1 in the normal control group was positive and tenuous, weakly positive in the model and SMI groups, respectively. Compared with normal control group, AQP1 mRNA levels were down regulated in the model and SMI groups at 10 hours, 72 hours and 120 hours (P <0.05). While AQP1 mRNA levels in the SMI group was up-regulated than that in the model group (P <0.05). Lung wet to dry weight ratio (W/D) in the model and SMI groups at 10 hours were higher than that in normal control group (P <0.05). Compared with normal control group, PaO₂ was markedly lower in the model and SMI groups (P <0.05), but there were no statistically significant differences between model and SMI groups (P >0.05).

Conclusions  The decreased AQP1 expression may be involved in the increased lung water content and dysfunction of pulmonary water metabolism following TBI. The treatment with SMI could improve water metabolism by promoting AQP1 expression.

     

Effect of anterior nucleus of thalamus stimulation on glucose metabolism in hippocampus of epileptic rats

Background  Electrical stimulation of the anterior nucleus of the thalamus (ANT) appears to be effective against seizures. In this study, we investigated changes in glucose metabolism during high-frequency stimulation of ANT in epileptic rats.

Methods  Three groups of rats were used: (1) a stimulation group (n=12), (2) a sham stimulation group (n=12) with seizures induced by stereotactic administration of kainic acid (KA), and (3) a control group (n=12) with sham surgery. Concentric bipolar electrodes were stereotaxically implanted unilaterally in the ANT. High-frequency stimulation was performed in each group except the sham stimulation group. Microdialysis probes were lowered into the CA3 region of the hippocampus unilaterally but bilaterally in the stimulation group. The concentrations of glucose, lactate, and pyruvate in dialysate samples were determined by an ISCUS microdialysis analyzer.

Results  The extracellular concentrations of lactate and lactate/pyruvate ratio (LPR) of epileptic rats were significantly higher than in control rats (P=0.020, P=0.001; respectively). However, no significant difference in the concentration of glucose and pyruvate was found between these groups (P >0.05). Electrical stimulation of ANT induced decreases in lactate and LPR in the ipsilateral hippocampus (KA injected) of the stimulation group (P <0.05), but it did not influence the glucose metabolism in the contralateral hippocampus (P >0.05).

Conclusions  This study demonstrated that the glycolysis was inhibited in the ipsilateral hippocampus of epileptic rats during electrical ANT stimulation. These findings may provide useful information for better understanding the mechanism of ANT-deep brain stimulation.

     

Effect of c-Jun NH2-terminal kinase-mediated p53 expression on neuron autophagy following traumatic brain injury in rats

Background  Activation of c-Jun NH₂-terminal kinase (JNK) has been implicated in neuron apoptosis as well as autophagy in response to various stressors after traumatic brain injury (TBI). However, the underlying molecular pathway remains unclear. Our study assessed whether JNK-mediated p53 phosphorylation might be an important mechanism for enhancing neuron autophagy in response to TBI.

Methods  A total of 186 male Sprague-Dawley (SD) rats (300–350 g) were used in this study. By randomized block method rats were randomly divided into four groups: sham-operated (n=46), TBI (n=60), TBI + dimethyl sulfoxide (DMSO) (n=40), and TBI + SP600125 (n=40). JNK was treated with SP600125, a specific JNK inhibitor. JNK, p-P53, Beclin-1, damage-regulated autophagy modulator (DRAM) and p-bcl-2 were evaluated by Western blotting analysis. The cellular localization and expression of Beclin-1 and DRAM was observed by immunofluorescence and immunohistochemistry, and the expression of Beclin-1-Bcl-2/Bcl-xL complexes was evaluated by immunoprecipitation. Multiple-group comparisons were conducted using analysis of variance (ANOVA). P values of less than 0.05 were considered statistically significant.

Results  It was observed that the expression of JNK, p-P53, Beclin-1, DRAM and p-bcl-2 was increasing after TBI, and the expression of Beclin-1 and DRAM was mainly located in the cytoplasm of neurons. But these were significantly inhibited in SP600125 group compared with sham group and TBI+SP600125 group (P <0.05). The expression of Beclin-1-Bcl-2/Bcl-xL complexes was reduced after TBI.

Conclusion  JNK-mediated p53 phosphorylation might be an important mechanism for enhancing neuron autophagy in response to TBI.

     

Proteome analysis and tissue array for profiling protein markers associated with type B thymoma subclassification

Background  The prognostic relevance of World Health Organization (WHO) subtypes within type B thymomas is still controversial. Understanding of the molecular characteristics of the different histologic types of thymomas will provide meaningful information for diagnosis and therapeutic management in type B thymoma.

Methods  Proteins extracted from twelve type B thymoma tissue specimens (six type B1 and six type B2) were analyzed by two-dimensional electrophoresis (2-DE) coupled with MALDI-TOF-MS. Differentially expressed proteins were then assayed in sixty-nine type B thymoma tissues (including B1, B2 and B3) by tissue array analysis with immunohistochemistry staining. The relationship of their expression with clinicopathological parameters, such as tumor stage or WHO classification, was estimated by Spearman’s Rank Correlation Test.

Results  Sixteen differentially expressed proteins between type B1 and B2 thymoma tissues were identified. The differential levels of ezrin and glutathione S-transferase pi (GSTP1) were validated using immunohistochemistry staining. A statistically significant difference was observed in the positive rate of ezrin expression between type B1 thymoma and type B3 thymoma (Z= –2.963, P <0.01). Ezrin showed a tendency to be expressed in higher classification tumors from type B1 to B3. A statistical analysis demonstrated that type B2 and B3 tumors had significantly higher positive expression of GSTP1 than the B1 group (type B2 vs. B1: Z= –2.582, P ≤0.01; type B3 vs. B1: Z= –4.012, P ≤0.001). The results also showed a strong correlation between GSTP1 and WHO type staging of B1 to B3 tumors (Spearman’s correlation coefficient: 0.633, P ≤0.001). Statistical analysis showed that there was close correlation between GSTP1 and ezrin expression with the clinical stage (Spearman’s correlation coefficients, ezrin: 0.481, P <0.05; GSTP1: 0.484, P <0.01).

Conclusions  Differentially expressed proteins between type B1 and B2 thymoma tissues were analyzed by comparative proteomic analysis. The techniques of proteomic analysis and tissue array provide a potential tool for screening of key molecules in type B thymoma histological sub-classifications. The statistical analysis of ezrin and GSTP1 expression by immunohistochemistry, especially GSTP1, may be a useful approach for type B thymoma classification.

     

祛瘀护膜剂调控NLRP3/Caspase-1信号通路对RE模型大鼠食管黏膜修复的影响

目的 从食管黏膜屏障修复的角度,探讨祛瘀护膜剂对反流性食管炎(RE)模型大鼠核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)/天冬氨酸特异性半胱氨酸蛋白酶-1(Caspase-1)信号通路的影响,揭示祛瘀护膜剂治疗RE的作用机制.方法 将大鼠随机分空白组,模型组,西药组,祛瘀护膜剂低、中、高剂量组,每组10只.除空白组...     

热休克蛋白27在缺血后处理肾组织中的表达及意义

目的 观察热休克蛋白27（HSP27）在缺血后处理（IPO）肾组织中的表达及分布情况,探讨其在肾缺血后处理中的作用.方法 结扎右侧肾蒂,夹闭左侧肾蒂60 min、再灌注24 h制备肾缺血/再灌注损伤模型.雄性SD大鼠24只,随机分为假手术组（S组）、缺血/再灌注组（I/R组）、缺血后处理组（IPO组）,每组8只.再灌注24 h后处死大鼠,腹主动脉取血并切取左肾.测定血清肌酐（Cr）、尿素氮（BUN）浓度;光镜下观察肾组织病理学改变;免疫组织化学方法检测肾组织中HSP27的表达;TUNEL法检测肾小管上皮细胞凋亡指数（AI）.结果 与S组比较,I/R组Cr和BUN浓度显著升高,组织损伤明显,肾组织中HSP27表达增多,肾小管上皮细胞凋亡指数较高（P〈0.05）;与I/R组比较,IPO组Cr和BUN浓度显著降低,组织损伤较轻,HSP27表达进一步增强,肾小管上皮细胞凋亡指数较低（P〈0.05）.结论 肾缺血后处理能上调肾组织中HSP27的表达,抑制肾小管上皮细胞凋亡,继而减轻肾缺血/再灌注损伤.     

健胃冲剂治疗大鼠反流性食管炎的机制研究

目的探究健胃冲剂治疗大鼠反流性食管炎的机制。方法复制反流性食管炎大鼠模型,将术后恢复较好的大鼠随机分为模型组,阳性对照组(雷贝拉唑钠肠溶片),健胃冲剂高、中、低剂量组,另设正常对照组,每组10只大鼠。各组末次给药24h后,立即自胃食管交界上0.5cm处向咽喉部截取长约1.5cm的食管组织,测定其pH值,并观察各组大鼠食管黏膜病理形态变化。结果与正常组比较,模型组大鼠食管下段黏膜pH值显著降低(P<0.01),食管下段大体标本肉眼病理评分显著升高(P<0.01),显微镜下病理评分(反向评分)显著降低(P<0.01)。与模型组比较,阳性对照组,健胃冲剂高、中、低剂量组pH值显著升高(P<0.05),大体标本肉眼病理评分显著降低(P<0.01),显微镜下病理评分显著升高(P<0.05,或P<0.01)。健胃冲剂高剂量组在升高pH值和食管黏膜显微镜下病理评分方面优于阳性对照组(P<0.05)。光镜下正常组大鼠食管黏膜组织结构正常;模型组大鼠黏膜上皮细胞层内出现较多炎性细胞浸润,鳞状上皮增生,严重者出现黏膜糜烂;健胃冲剂高、中、低剂量组较模型组均明显改善;雷贝拉唑组改变与健胃冲剂低剂量组基本相同。结论健胃冲剂能改善反流性食管炎大鼠的组织病理形态,其作用机制与降低模型大鼠食管下段黏膜的酸度有关。     

热休克蛋白32对脑缺血再灌注损伤大鼠脑组织抗氧化能力的影响

目的探讨热休克蛋白32(HSP32)在局灶性脑缺血再灌注损伤中的抗氧化作用。方法将36只清洁级雄性SD大鼠随机分为3组,每组12只:假手术组(S组)、缺血再灌注组(IR组)和锌原卟啉IX(Znpp)+缺血再灌注组(Z组)。采用右侧颈内动脉尼龙线线栓法致大脑中动脉栓塞法制备局灶性脑缺血再灌注模型。Z组在造模前经腹腔注射HSP32特异性抑制剂Znpp(45μmol/kg)。所有大鼠再灌注6 h后处死取脑,光镜下观察各组脑组织病理变化,检测脑组织中SOD活性、MDA含量和HSP32蛋白表达。结果与S组比,IR组和S组SOD显著降低(P<0.05),MDA显著升高(P<0.05);IR组HSP32蛋白的表达显著增多(P<0.05),Z组HSP32的表达与S组差异无统计学意义(P>0.05);与IR组比,Z组MDA显著升高(P<0.05),SOD显著降低(P<0.05)。结论脑缺血再灌注可以诱导热休克蛋白32的表达,使再灌注后的氧化损伤减轻。     

热休克蛋白27、60、70在直肠癌中的表达及意义

目的：探讨热休克蛋白27（HSP27）、60、70及其mRNA在直肠癌、癌旁组织、直肠炎和正常直肠粘膜组织中的表达情况,及与临床、病理资料之间的关系。方法：采用免疫组织化学方法、组织芯片技术检测病理诊断明确的54例直肠癌组织标本及对应的距直肠癌组织边缘1．0cm处的癌旁组织、直肠炎组织及距直肠癌组织边缘5cm以上的正常组织中HSP27、60、70的表达差异,RT—PCR法对12例患者的直肠癌组织及对应的癌旁组织、直肠炎组织和正常组织的HSP27、60、70mRNA的表达情况进行检测,结合临床、病理资料进行统计分析。结果：HSP27、60、70的表达：在54例直肠癌组织中的阳性表达率为75．9％、74．1％、77．8％,明显高于癌旁组织、直肠炎组织和正常组织（P〈0．01）;在mRNA水平,直肠癌组织的HSP27、60、70表达也明显高于其余3组（P〈0．01）。HSP27、60、70的表达与病人性别、年龄、浸润直肠壁深度和肿瘤组织类型无明显相关性（P〉0．05）;与远处转移、肿瘤分化程度和临床病理分期具有相关性（P〈0．05）。结论：直肠癌中HSP27、60、70的表达水平明显高于癌旁组织、直肠炎组织和正常组织,提示与直肠癌发生、发展密切相关;而且与病人性别、年龄、浸润直肠壁深度和肿瘤组织娄型无明显相关性;与远处转夥、肿瘤分化程度和临床病理分期具有相关性;HSP27、60、70之间具有关联性．     

胃食管反流病患者食管黏膜Ki-67及Caspase-3的表达

目的 探讨胃食管反流病(gastroesophageal reflux disease,GERD)患者食管黏膜组织中Ki-67、Caspase-3的表达及意义.方法 收集非糜烂性食管炎(non-erosive esophageal reflux disease,NERD)患者、反流性食管炎(reflux esophagitis,RE)患者、Barrett食管患者食管黏膜各20例,正常食管黏膜组织15例作为对照,分别对食管黏膜组织进行常规病理检查、免疫组化及western-blot分析Ki-67、Caspase-3的表达.结果 GERD的各组中均存在食管黏膜组织的明显增生.NERD组、RE组、BE组的食管黏膜Ki-67阳性表达率明显高于正常对照组(分别是80％、85％、95％及6.7％,P＜0.05);在NERD组、RE组、BE组,食管黏膜Caspase-3阳性表达率分别是95％、90％和75％,仅BE组与正常对照组100％比较,差异有统计学意义(P＜0.05).结论 食管黏膜组织中的ki-67、Caspase-3的表达,在一定程度上反映了食管黏膜鳞状上皮细胞的增殖程度,与食管黏膜的组织抵抗力的改变有关,Ki-67和Caspase-3可能同时共同参与了食管癌的发生.     

平肝潜阳方药对高血压肝阳上亢证大鼠下丘脑组织中Tpx II，HSP27 及ANXA1 表达的影响

目的：观察自发性高血压大鼠(spontaneously hypertensive rats,SHR)肝阳上亢证模型下丘脑组织中硫氧还 蛋白过氧化物酶 II(thioredoxin peroxidase II,Tpx II)、热休克蛋白27(heat shock protein 27,HSP27)、膜联蛋白A1(annexin A1,ANXA1)基因在平肝潜阳方药干预下的表达变化,探讨三者在平肝潜阳方药干预的作用。方法：SHR随机分为： 模型组、对照组和治疗组(n=10)。除正常组SD大鼠(n=10)外,其他组大鼠均灌服附子汤复制高血压肝阳上亢证模型。 其中对照组和治疗组分别于复制模型成功后给予依那普利和平肝潜阳方药干预4周。观察大鼠的行为学和血压变化, 采用RT-PCR和Western印迹检测各组大鼠下丘脑组织中Tpx II,HSP27,ANXA1基因和蛋白质表达的变化。结果：与正 常组比较,高血压肝阳上亢证模型大鼠血压、心率和易激惹程度明显升高,而旋转耐受时间降低(P<0.01);平肝潜 阳方药和依那普利能够逆转这种改变。Tpx II和ANXA1基因和蛋白在模型组中的表达较正常组明显升高(P<0.01),而 HSP27基因和蛋白在模型组中的表达较正常组明显降低(P<0.01);Tpx II和ANXA1在对照组及治疗组中的表达较模型组 有明显降低(P<0.05或P<0.01),而HSP27在对照组及治疗组中的表达较模型组有明显升高(P<0.05或P<0.01);对照组与 治疗组比较,Tpx II和ANXA1 蛋白表达明显差异(P<0.05或P<0.01)。结论：平肝潜阳方药不仅能够明显降低血压,而且 能够改善大鼠的宏观表征,其作用可能与调节下丘脑组织中Tpx II,ANXA1及HSP27基因表达有关。     

亚低温对大鼠局灶性脑缺血后HSP70 mRNA表达影响

①目的观察亚低温对大鼠局灶性脑缺血后热休克蛋白70(HSP70)mRNA表达的影响。②方法取成年健康Wistar大鼠145只,应用线栓法建立大脑中动脉闭塞(MCAO)再灌注模型,随机分为健康对照组、假手术组、缺血再灌注对照组(H0)、缺血后即刻亚低温组(H1)、缺血再灌注后亚低温组(H2)。采用原位杂交方法检测各组脑组织HSP70mRNA表达。③结果H0组HSP70mRNA表达于缺血再灌注2h出现,24h明显,48h减少,72h降到最低。H1和H2组HSP70mRNA阳性表达6~48h明显,72h、7d额叶皮质仍有HSP70mRNA表达,较H0组表达增多,差异有显著性(F=96.72~716.59,q=11.95~124.73,P<0.001)。H1组与H2组比较,前者HSP70mRNA表达更为明显,差异有显著性(q=7.56~60.49,P<0.001)。④结论亚低温治疗后脑组织HSP70mRNA表达增多,缺血后即刻亚低温的作用优于缺血再灌注后。     

细胞增殖调控基因在反流性食管炎及其并发症中的表达变化

胃镜检查或手术中取得正常对照组(25例)、反流性食管炎(RE,35例)、Barrett食管(BE,20例)及食管腺癌(EA,9例)患者的食管组织标本,采用免疫组化法检测cyclin D_1、CDK_1和CDK_4基因表达。结果发现EA组的cyclin D_1和CDK_4表达较正常对照组显著增强(P<0.01,P<0.05),SE组的cyclin D_1表达亦较对照组增强(P<0.05),EA组的cyclin D_1表达较RE组增强(P<0.05),而其他组间的cyclin D_1或CDK_4表达以及各组间CDK_1表达均无显著性差异。提示BE、EA患者食管组织中cyclin D_1、CDK_4基因的表达明显改变,反流可能为导致此系列疾病的机制之一,而CDK_1的作用不显著。检测cyclin D_1和CDK_4的表达可能对RE和BE患者的预后监测具有较大意义。     

食管鳞癌患者肿瘤组织及血清中E-钙黏蛋白表达的临床意义

目的:检测食管鳞癌患者肿瘤组织及血清中E-钙 黏蛋白(E-cadherin,E-cad) 的表达并探讨其临床意义。方法:采用免疫组织化学法对48 例食管鳞癌、23 例糜烂性食管炎、24 例正常食管黏膜组织中E-cad 的表达进行检测;同时采用酶联免疫吸附法(ELISA) 对上述研究对象血清中可溶性E-cad (sE-cad) 的表达进行检测,并且收集完整的临床病理资料。结果:E-cad 表达水平在食管鳞癌组织中明显降低,与正常食管黏膜上皮组织及糜烂性食管炎黏膜上皮组织相比,差异有统计学意义(P<0.05)。不同浸润深度、有无淋巴结转移及不同分化程度的食管鳞癌,其癌组织中E-cad 的表达水平差异有统计学意义(P<0.05)。血清sE-cad 在食管鳞癌组表达水平明显高于正常食管组及糜烂性食管炎组(P<0.05)。血清sE-cad 水平与食管鳞癌的临床病理特征无关。食管鳞癌患者肿瘤组织中E-cad 高表达者与低表达者相比,血清sE-cad 水平差异无统计学意义(P=0.134)。结论:E-cad 可作为食管鳞癌诊断及预后判断的辅助指标。血清sE-cad 可作为食管鳞癌诊断筛查的血清学辅助指标。