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991.
992.
Objective: By the detection of HBV infection, AFP and AST, the targets of biological behavior and the gene expression of multi-drug resistance gene 1 (MDR1) in hepatocellular carcinoma (HCC), we investigate characteristics of the expression of MDR1 in HCC and its relationship with HCC biological behavior. Methods: Using real-time fluorescence quantitative PCR (FQ-PCR) to detect the expressions of MDR1 in 102 samples of HCC tissue and 20 samples of non-cancerous tissue, we analyze the relationship between expressions of MDR1 and biological characteristics of HCC. Results: The expression of MDR1 in HCC is 0.55±0.27, and in normal liver tissues is 0.23±0.10, respectively. The expression in HCC is higher than it in normal liver tissue, the difference is statistically significant (P<0.05) and the difference between the expression and the HCC envelopes is statistically significant, and the expression increases along with the increase of Edmondson classification (P<0.05). HBV infection, AFP positive, the rise of AST, all these factors have positive correlations with the expression (r=0.463, 0.473, 0.299). In MDR1 expressions of HCC patients, the survival curve of the negative is higher than that of the positive, but the difference is not statistically significant. Conclusion: There are drug resistance phenomena in HCC, MDR1 expression may play an important role in primary HCC drug resistance. HBV infection can be detected as a reference indicator of HCC chemotherapy resistance, plasma levels of AFP, AST can be used as a reference index change dynamic monitoring of MDR1 expression.  相似文献   
993.
We conducted a case-control study to evaluate the association of miR-146a rs2910164 (C>G), miR-149 rs2292832 (T>C), miR-196a2 rs11614913 (T>C) and miR-499 rs3746444 (T>C) polymorphisms with the risk of hepatocellular carcinoma. A total of 274 patients with HCC were collected between January 2013 and December 2014. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was taken to determine the polymorphism of miR-146a C>G, miR-149 T>C, miR-196a2 T>C and miR-499 T>C. By comparing with control groups, patients with HCC were more likely to be males (OR=2.01, 95% CI=1.38-2.95), have older age (OR=1.52, 95% CI=1.09-2.13), have a history of alcohol drinking (OR=2.09, 95% CI=1.49-2.93), and be infected with HBV (OR=32.98, 95% CI=19.70-55.46) and HCV (OR=56.26, 95% CI=23.28-152.98) infection. By conditional regression analysis, individuals carrying the TC and CC genotypes of miR-196a2 T>C were found to be associated with an elevated risk of HCC compared to the TT genotype, and the adjusted odds ratio were 1.50 (1.03-2.17) and 2.86 (1.60-5.16), respectively. Moreover, the TC+CC genotype was correlated with an increased risk of HCC (OR=1.69, 95% CI=1.19-2.41) compared to the wide-type genotype. In conclusion, our results suggested that miR-196a2 T>C polymorphism is associated with HCC risk in Chinese population.  相似文献   
994.
Background: Mesenchymal stem cells (MSCs) came out to attract wide attention and had become one of the hotspots of most diseases’ research in decades. But at present, the mechanisms of how MSCs work on chronic asthma remain undefined. Our study aims at verifying whether MSCs play a role in preventing inflammation and airway remodeling via PI3K/AKT signaling pathway in the chronic asthma rats model. Methods: First, an ovalbumin (OVA)-induced asthma model was built. MSCs were administered to ovalbumin-induced asthma rats. The total cells in a bronchial alveolar lavage fluid (BALF) and inflammatory mediators in BALF and serum were measured. Histological examination of lung tissue was performed to estimate the pathological changes. Additionally, the expression of phosphorylated-Akt (p-Akt) in all groups was measured by western blot and immunohistochemistry (IHC). Results: Compared to normal control group, the degree of airway inflammation and airway remodeling was significantly increased in asthma group. On the contrary, they were obviously inhibited in MSCs transplantation group. Moreover, the expression of p-Akt was increased in lung tissues of asthmatic rats, and suppressed by MSCs transplantation. Conclusion: Our results demonstrated that MSCs transplantation could suppress lung inflammation and airway remodeling via PI3K/Akt signaling pathway in rat asthma model.  相似文献   
995.
目的:探讨降钙素基因相关肽(CGRP)对超高分子聚乙烯(UHMWPE)引起的鼠成骨细胞RANKL代谢的影响。方法:将体外培养的鼠颅骨成骨细胞在UHMWPE微粒预处理后,加入外源性不同浓度的CGRP孵育48 h,提取各组细胞m RNA、蛋白,通过实时定量逆转录聚合酶链反应(RT-PCR)和western blot来观察成骨细胞OPG和RANKL m RNA、蛋白表达水平的变化。结果:微粒明显刺激了RANKL的表达,降低了OPG的表达;CGRP显著抑制了鼠成骨细胞RANKL的表达。结论:CGRP抑制微粒介导的骨质溶解作用是可能是通过下调RANKL的表达实现的。  相似文献   
996.

Background

To investigate the clinicopathological features of six cases of soft tissue recurrent ameloblastoma and explore the role of increased aggressive biological behavior in the recurrences and treatment of this type of ameloblastomas.

Material and Methods

In this study, we retrospectively reviewed recurrent ameloblastomas during a 15-year period; six cases were diagnosed as soft tissue recurrent ameloblastoma. The clinical, radiographic, cytological and immunohistochemical records of these six cases were investigated and analyzed.

Results

All the six soft tissue recurrent ameloblastomas occurred after radical bone resection, and were located in the adjacent soft tissues around the osteotomy regions. In Case 4, the patient developed pulmonary metastasis, extensive skull-base infiltration and cytological malignancy after multiple recurrences and malignant transformation was diagnosed. In the other five cases, although there were no cytological signs are sufficient to justify an ameloblastoma as malignant, some malignant features were observed. In Case 1, the tumor showed moderate atypical hyperplasia and the Ki-67 staining percentage was 40% positive, which are strongly suggestive of potential malignance. In Case 5, the patient developed a second soft tissue recurrence in the parapharyngeal region and later died of tumor-related complications. All the remaining three patients showed cytology atypia of varying degrees and high expression of PCNA or Ki-67, which confirmed active cell proliferation.

Conclusions

Increased aggressiveness is an important factor of soft tissue recurrence. An intraoperative rapid pathological examination and more radical treatment are suggested for these cases. Key words: Ameloblastoma, soft tissue recurrence, aggressive biological behaviour.  相似文献   
997.
目的探讨高脂血症性急性胰腺炎(HAP)和非高脂血症性急性胰腺炎的特点及临床救治效果。方法回顾分析我院在2013年1月至2013年12月收治的99例急性胰腺炎的临床资料,根据患者有无高脂血症将其分为HAP组(高脂血症患者)和对照组(无高脂血症的AP患者);患者均接受标准化临床治疗,比较2组患者病情、血浆生化指标、治疗转归、住院时间与费用、复发等情况。结果 HAP组重度胰腺炎比例(13.6%)明显高于对照组(7.8%),HAP组血糖和尿酸均显著高于对照组,其中HAP组血糖平均值达到对照组的171%,而HAP组的血淀粉酶却仅为对照组的44.5%;HAP组1年内的复发率(13.6%)显著高对于照组(2.6%),P0.01差异有统计学意义。结论高血脂对急性胰腺炎的病情、表现和治疗结果均有明显影响,应引起高度重视。  相似文献   
998.
目的分析2008—2012年成人浮膝损伤患者的临床特点,探讨青年患者与中老年患者性别、合并骨折及骨折类型构成的差异,为此类骨折的诊治、预防等临床研究提供参考。方法回顾性分析河北医科大学第三医院2008年1月—2012年12月间诊治的成人(≥16岁)浮膝损伤患者资料,排除陈旧骨折、病理骨折及假体周围骨折等。所有影像资料由经过培训的4名本院骨科住院医师进行整理分型,并由本院2名骨科主任医师及1名放射科主任医师进行监督检验,统计年龄、性别、骨折类型及合并骨折等数据。≤45岁患者为青年组,>45岁患者为中老年组。结果5年间共诊治成人浮膝损伤204例208侧,占成人全身骨折的0.40%(204/52225),占成人股骨骨折的3.93%(204/5196),占成人胫腓骨骨折2.49%(204/8199)。其中男173例,女31例;年龄16~85岁;青年组153例,中老年组51例。青年患者和中老年患者中均以男性为主,分别占90.20%(138/153)和68.63%(35/51),差异有统计学意义(字2=13.808,P<0.01)。浮膝损伤患者中131例合并其他部位骨折,占浮膝损伤患者的64.22%(131/204),主要为合并足部骨折37例,尺桡骨骨折33例,骨盆-髋臼骨折31例,股骨近端骨折25例,对侧股骨骨折25例等;其中青年组合并其他部位骨折95例,中老年组36例,差异无统计学意义(字2=1.202,P>0.05)。 FraserⅠ型骨折87侧,Ⅱ型骨折121侧,青年组与中老年组患者FraserⅠ型、Ⅱa型、Ⅱb型、Ⅱc型分别是70、40、16、30侧和17、12、5、18侧,两组各型骨折构成比差异并无统计学意义(字2=5.502,P>0.05);Ⅱ型骨折中Ⅱb型骨折最少(21侧),Ⅱa、Ⅱc型骨折所占比例相近,但青年患者Ⅱa型(46.51%,40/86)骨折多于Ⅱc型(34.88%,30/86)骨折,中老年患者中Ⅱc型(51.43%,18/35)骨折较Ⅱa型(34.29%,12/35)骨折更多。结论青年男性为浮膝损伤的高危人群,常合并其他部位骨折。胫骨平台较股骨髁发生骨折的风险高,且骨折风险均随着年龄的增长而增高。  相似文献   
999.
1000.
The Fas/FasL system transmits intracellular apoptotic signaling, inducing cell apoptosis. However, Fas signaling also exerts non-apoptotic functions in addition to inducing tumor cell apoptosis. For example, Fas signaling induces lung cancer tumor cells to produce prostaglandin E2 (PGE2) and recruit myeloid-derived suppressor cells (MDSCs). Activated cytotoxic T lymphocytes (CTLs) induce and express high levels of FasL, but the effects of Fas activation initiated by FasL in CTLs on apoptosis-resistant tumor cells remain largely unclear. We purified activated CD8+ T cells from OT-1 mice, evaluated the regulatory effects of Fas activation on tumor cell escape and investigated the relevant mechanisms. We found that CTLs induced tumor cells to secrete PGE2 and increase tumor cell-mediated chemoattraction of MDSCs via Fas signaling, which was favorable to tumor growth. Our results indicate that CTLs may participate in the tumor immune evasion process. To the best of our knowledge, this is a novel mechanism by which CTLs play a role in tumor escape. Our findings implicate a strategy to enhance the antitumor immune response via reduction of negative immune responses to tumors promoted by CTLs through Fas signaling.  相似文献   
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