铲状电极经尿道前列腺电汽化切割术120例报告

目的：探讨铲状电极经尿道前列腺电汽化切割术中的手术经验及疗效。方法：总结了120例经尿道前列腺电汽化切割手术的治疗资料。结果：术后随访1月～2年，120倒手术患者118例治愈，2例于术后出现急性肾衰，经保守对症治疗痊愈，2例出现压力性尿失禁，经对症治疗好转。结论：铲状电极行前列腺组织的汽化切割，优于滚轮汽化电极或电极弧，术中术后出血少，术中术野清晰，安全可靠。     

肠易激综合征Manning诊断标准的评价

目的 评价Manning标准诊断肠易激综合征(IBS)的真实性。方法 采用自行设计的调查表对499例对象进行调查。结果 1．随着Manning标准中结合指标数的增多，IBS组与非溃疡性消化不良及溃疡性结肠炎组鉴别的灵敏度及其95％CI明显下降，特异度及其95％CI明显上升，同时阳性预测值、阳性似然比及阴性似然比也明显上升。2．符合Manning标准中二项以上结合指标，IBS组就具有较好与健康对照组鉴别的灵敏度及其95％CI、特异度及其95％CI。结论 Manning标准中需要3项以上结合指标可较好地使IBS与非溃疡性消化不良或溃疡性结肠炎鉴别；2项以上结合指标可较好地使IBS与健康人鉴别。     

钙拮抗药及烧伤血浆对大鼠PBMC内NF-κB活化和炎症介质产生的影响

目的 :探讨外周血单个核细胞 (PBMC)内上游信号分子及核因子 κB(NF κB)在烧伤后炎症级联反应中的作用。　方法 :体外检测在烧伤血浆作用下的PBMC内游离Ca2 及NF κB活化的变化 ,观察钙通道阻断药对NF κB活化及IL 6、NO表达水平的调控作用。　结果 :不同时相点的烧伤血浆可使体外PBMC内Ca2 明显增加 ,培养的PBMC核内NF κB的积聚明显增加 ,培养上清中NO和IL 6高表达。应用尼莫通 (Nimodipine)和丹曲林 (Dantrium)对NF κB的活化有调节作用 ,对IL 6和NO亦有下调作用。　结论 :烧伤血浆可使PBMC内信号分子浓度明显增高 ,NF κB过度活化 ,并易位进入细胞核内 ,NF κB介导的促炎性细胞因子和NO过度表达。两种钙通道阻断药有调控细胞内信号转导的作用 ,对烧伤后全身炎症反应综合征 (SIRS)可能有防治作用     

原发性肝癌患者肝切除术前、后免疫细胞表型分析

目的研究原发性肝癌(PrimaryLiverCarcinoma,PLC)患者肝切除术前、后免疫细胞表型的变化。方法采用直接免疫荧光标记,流量血细胞计数法(FlowCytometry,FCM)检测方法,动态观察120例PLC患者肝切除术前后外周血T淋巴细胞亚群、NK细胞和HLA鄄DR含量变化。结果肝切除术前肝功能Child鄄PughB级、OGTTL型和术前施行肝动脉栓塞化疗患者外周血CD8+T细胞含量明显低于正常人组,CD4+/CD8+比值则较高(P<0郾05)。全部肝癌患者肝切除术前、后CD3+CD4+T细胞和NK细胞(CD3-CD16+CD56+)含量无明显差异。术后第1天、第3天、第7天和第2周外周血淋巴细胞CD3+CD8+含量明显低于肝切除术前和术后第3周(P<0.01);而CD4+/CD8+比值则显著高于肝切除术前和术后第3周(P<0郾01)。结论PLC合并肝硬变肝储备功能不足、术前肝动脉栓塞化疗和肝切除术可导致机体细胞免疫功能低下,PLC患者肝切除术前行肝动脉栓塞化疗的价值有待深入研究。     

后腹腔镜手术切除肾上腺节细胞神经瘤疗效观察

目的 :探讨后腹腔镜微创手术治疗肾上腺节细胞神经瘤的适应证和可行性。方法 :采用后腹腔镜手术治疗肾上腺节细胞神经瘤患者 5例 ,其中左侧肾上腺节细胞神经瘤 2例 ,右侧 3例。结果 :5例后腹腔镜手术全部获得成功 ,4例肾上腺肿瘤为单发 ,1例为多发 (4个肿瘤 ) ;肿瘤最大直径 2 .5～ 8.0 (4 .2± 1.8)cm ;手术时间35～ 10 5 (5 9± 2 7)min ,估计出血量 10～ 30 (19± 7)ml,术后镇痛剂吗啡用量 0～ 2 0 (8± 8)mg ,2例未用镇痛剂 ;排气、恢复进食时间 1～ 3(1.4± 0 .5 )d ;术后住院时间 4～ 7(5 .4± 1.5 )d。无围手术期并发症发生。结论 :后腹腔镜手术切除肾上腺节细胞神经瘤是安全可行的 ,能充分体现腹腔镜手术创伤小、恢复快的优点。肾上腺节细胞神经瘤是腹腔镜手术很好的适应证。     

门诊抽血室医院感染标本检测结果分析

目的 :了解门诊抽血室医院内感染情况。方法 :通过对空气培养、医护人员的手、物体表面、使用中的消毒液 4项指标 112 0份标本进行监测分析。结果 :112 0份标本检验结果合格 10 30份 ,合格率 92 % ,不合格标本 90份 ,培养出细菌 87份。结论 :通过监测抽血室的医院感染标本 ,了解了院内感染情况 ,有效地减少和防止了医护人员之间、医患之间以及和家属之间的交叉感染 ,提高了医疗护理质量 ,预防了医院交叉感染的发生。     

c-myc mRNA在成釉细胞瘤中的表达

目的:研究成釉细胞瘤(AB)和牙源性角化囊肿(OKC)中c-mycmRNA的表达,探讨c-myc在AB和OKC中的发生、发展及其生物学意义。方法:使用原位杂交法检测54例AB、16例OKC和7例口腔正常黏膜(NOM)组织中c-mycmRNA的表达,并将AB按原发、复发、恶变分组,结果使用χ2检验进行统计分析。结果:AB、OKC及NOM组织中c-mycmRNA的阳性表达率分别为81.5%(44/54)、75.0%(12/16)和14.3%(1/7),3组比较有显著性差异(χ2=15.488,P<0.05)。原发组AB中c-mycmRNA的阳性表达率为71.0%,复发组为94.7%,恶变组为100.0%,伴随原发、复发、恶变,差异有显著性(χ2=16.912,P﹤0.05)。结论:c-myc表达在AB的发生、发展中有重要作用;c-mycmRNA的表达与AB的临床生物学行为有关,伴随其生物学行为变化,c-mycmRNA表达增强;提示c-myc有可能成为评价预后的有效指标。     

兔坐骨神经挤压伤的MRI与SEP对比研究

目的:探讨磁共振成像和体感诱发电位以及两者结合在坐骨神经急性挤压伤中的诊断价值。方法:24只兔按钳夹力的不同随机分为A、B两组,左后肢为损伤侧,右后肢为对照侧,建立坐骨神经急性挤压伤模型,于伤后1、2、4、8周行MR扫描,同时行双侧体感诱发电位检查。结果:损伤侧24条神经,有23条MR显示异常,诊断正确率95.8%,假阴性率4.17%(1/24);24条损伤侧坐骨神经,有22条SEP显示异常,诊断正确率91.6%,假阴性率8.3%(2/24)。MRI与SEP对神经损伤的正确诊断率无统计学差异(P>0.05)。MRI与SEP结合起来,24条损伤神经均显示异常,诊断正确率100%。结论:MR与SEP检查可无创、准确地判断神经损伤,两者结合可明显提高神经损伤的正确诊断率,重复性好,可作为神经损伤的较好诊断手段。     

Hybrid tumours of the salivary glands. A report of two cases involving the palate and a review of the literature

Hybrid tumours are very rare salivary gland lesions composed of two or more different tumoural entities in a single neoplasm that arise within a definite topographical region. In most cases adenoid cystic carcinoma has been the predominant component in these lesions. In this study we describe two patients with hybrid tumours located in the palate, one in a 49-year-old woman and one in a 71-year-old man. The first case involved adenoid cystic carcinoma and mucoepidermoid carcinoma, and the patient in the second case exhibited adenoid cystic carcinoma and epithelial-myoepithelial carcinoma. Both patients were treated with surgery and radiotherapy, and there has been no evidence of recurrence after 13 and 36 months of follow-up, respectively. The recognition of the histologic component with the higher grade of malignancy in every case of hybrid tumour of the salivary glands is a necessary step to determine the biological behaviour and, consequently, to determine the proper therapeutic approach.     

Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.