Quercetin inhibits the invasion and mobility of murine melanoma B16-BL6 cells through inducing apoptosis via decreasing Bcl-2 expression

Quercetin has been known to have anti-tumor and anti-oxidation activities. In the present study, we have investigated its in vitro anti-metastatic activity. Quercetin inhibited the invasion and mobility of murine melanoma B16-BL6 cells in a dose-dependent manner but did not affect their adhesion to either laminin, fibronectin, or type VI collagen. Moreover, quercetin significantly inhibited the proliferation of B16-BL6 cells only in the case of time incubation longer than 48 h. Quercetin dose-dependently decreased the cell rates in S and G2–M phases of cell cycle. The effect of quercetin to cause a remarkable apoptosis of B16-BL6 cells was also demonstrated by flow cytometric assay as well as DNA fragmentation with a typical 180-bp ladder band in agarose electrophoresis and a quantitative analysis. Furthermore, quercetin markedly inhibited the expression of anti-apoptotic protein Bcl-2 but hardly influenced Bcl-X_L. These results suggest that the inhibition of quercetin on invasiveness and migration of B16-BL6 cells are closely associated with the arrest of cell cycle as well as the induction of apoptosis by decreasing the Bcl-2 expression. This revised version was published online in July 2006 with corrections to the Cover Date.     

路氏乳杆菌JCM1081黏附相关蛋白的初步鉴定

目的研究路氏乳杆菌(Lactobacillus reuteri,也称罗伊氏乳杆菌)JCM1081菌体表面蛋白对其黏附HT-29细胞的影响。方法将路氏乳杆菌JCM1081菌体进行胰蛋白酶、蛋白酶K处理;用氯化锂和盐酸胍对乳杆菌表面的蛋白进行抽提,进行SDS-PAGE后与黏蛋白受体进行Western blot,并对杂交阳性蛋白进行质谱分析鉴定。结果路氏乳杆菌JCM1081菌体经胰蛋白酶、蛋白酶K处理后,其对HT-29细胞的黏附力显著下降(P<0．01);用氯化锂去除路氏乳杆菌JCM1081菌体外表面的S层蛋白后,路氏乳杆菌JCM1081对HT-29细胞的黏附力无显著变化;Western blot结果显示相对分子质量(Mr)为29×103和14×103的两种菌体表面蛋白与黏蛋白受体杂交中出现了强阳性;质谱分析结果显示29×103蛋白与路氏乳杆菌ATCC55730的h0793蛋白相似性高达71．1％。结论路氏乳杆菌JCM1081菌体表面的蛋白参与了乳杆菌的黏附,其中29×103和14×103的两种胞壁表面蛋白能够特异地识别黏蛋白受体并与之结合,29×103蛋白属ABC转运蛋白家族。     

损毁单侧黑质-纹状体通路的大鼠SVZ、纹状体和黑质神经前体细胞的变化

研究成年大鼠脑室下区 (SVZ)神经前体细胞 (neural precursors)在黑质 -纹状体通路损伤后的反应 ,本研究用 6-羟多巴胺单侧纹状体注射以损毁黑质 -纹状体通路 ,损毁 10 d后腹腔注射 Brd U ,连续 4d,每日两次 ;在 SVZ、纹状体和黑质部位用免疫组化方法检测 Brd U、nestin以及 GFAP阳性细胞。结果显示 :(1) 6-羟多巴胺损毁黑质 -纹状体通路后 ,伤侧 SVZ的 Brd U阳性细胞数明显增多 ,并成簇分布 ;nestin和 GFAP阳性细胞数也增多 ,但以 GF AP阳性细胞增多明显 ;(2 )伤侧纹状体可见大量 Br-d U、GFAP以及少量 nestin阳性细胞分布 ,而健侧只有少量 GFAP阳性细胞 ;(3 )伤侧可见 Brd U阳性细胞在 SVZ和纹状体之间呈条带样分布 ;(4 )伤侧黑质除酪氨酸羟化酶阳性神经元减少外 ,未见 Brd U、GFAP和 nestin阳性细胞表达。上述结果表明 ,6-羟多巴胺损毁黑质 -纹状体通路后 ,SVZ神经前体细胞活动增强 ,有向纹状体迁移的趋势。     

Impact of Dissection after Drug-Coated Balloon Treatment of De Novo Coronary Lesions: Angiographic and Clinical Outcomes

PurposeDissection after plain balloon angioplasty is required to achieve adequate luminal area; however, it is associated with a high risk of vascular events. This study aimed to examine the relationship between non-flow limiting coronary dissections and subsequent lumen loss and long-term clinical outcomes following successful drug-coated balloon (DCB) treatment of de novo coronary lesions.Materials and MethodsA total of 227 patients with good distal flow (Thrombolysis in Myocardial Infarction flow grade 3) following DCB treatment were retrospectively enrolled and stratified according to the presence or absence of a non-flow limiting dissection. The primary endpoint was late lumen loss (LLL) at 6-month angiography, and the secondary endpoint was target vessel failure (TVF, a composite of cardiac death, target vessel myocardial infarction, target vessel revascularization, and target vessel thrombosis).ResultsThe cohort consisted of 95 patients with and 132 patients without a dissection. There were no between-group differences in LLL (90.8%) returning for angiography at 6 months (0.05±0.19 mm in non-dissection and 0.05±0.30 mm in dissection group, p=0.886) or in TVF (6.8% in non-dissection and 8.4% in dissection group, p=0.799) at a median follow-up of 3.4 years. In a multivariate analysis, the presence of dissection and its severity were not associated with LLL or TVF. Almost dissections (93.9%) were completely healed, and there was no newly developed dissection at 6-month angiography.ConclusionThe presence of a dissection following successful DCB treatment of a de novo coronary lesion may not be associated with an increased risk of LLL or TVF (Impact of Drug-coated Balloon Treatment in de Novo Coronary Lesion; {"type":"clinical-trial","attrs":{"text":"NCT04619277","term_id":"NCT04619277"}}NCT04619277).     

非开胸食管内翻剥脱术

目的　研讨非开胸食管内翻剥脱的手术方法、优缺点及适应症。方法 :分析我院 1 992年至 2 0 0 0年 6月非开胸食管内翻剥脱胃重建食管术的 1 8例病历 ,其中下咽癌 5例、甲状腺鳞癌 1例、喉癌侵犯下咽者 4例、食管颈段癌 8例。结果 :本组病人食管床出血量均在 1 0 0ml以下 ,无吻合口漏等严重并发症 ,无手术死亡。结论 :本手术安全具有简便创伤小的优点 ,适用于颈段食管癌、下咽癌及甲状腺癌和喉癌侵及下咽者、部分早期食管癌和贲门癌。     

神经生长因子对脊髓损伤后脊髓组织一氧化氮生成的影响

目的 :探讨神经生长因子 ( NGF)对脊髓损伤保护作用的机制 ,为临床应用提供理论依据。方法 :采用 Allen法以 2 5 g/cm3力致伤大鼠 T8脊髓 ,插蛛网膜下隙导管于术后即刻、2、4、8、12、2 4 h各注入神经生长因子 ( NGF)溶液 ,并与生理盐水组和正常对照组作对照。采用免疫组化法 ( ABC法 )和原位杂交法检测神经元型固有型一氧化氮合成酶 ( nc NOS)在脊髓中的表达。结果 :大鼠伤后脊髓前角运动神经元出现 nc NOS蛋白和 nc NOS m RNA异常表达 ,NGF组与生理盐水组相比较 ,nc NOS蛋白和nc NOS m RNA异常表达明显减少 ( P<0 .0 1或 P<0 .0 5 )。结论 :NGF能通过抑制脊髓损伤 nc NOS的异常表达 ,抑制一氧化氮( NO)过多释放所致的神经毒性作用 ,从而保护了损伤的神经组织。     

肾衰透析患者拔牙的临床研究

目的 :探讨肾衰透析患者拔牙的安全性。　方法 :对 42例肾衰血透患者行 98次拔牙手术 ,共拔除患牙 12 2颗 ,术前采取全口洁治、服用抗生素、控制血压等措施 ,术后加强局部止血处理 ,预防出血、感染及心血管系统等并发症的发生。　结果 :透析组术后出血 44次 ,拔牙创口血块充盈不良或脱落 2 7次 ;对照组分别为 4和 5次 (94次手术 ,P<0 .0 5 )。拔牙创口定期观察 1个月 ,均愈合良好。　结论 :慢性肾衰患者通过透析 ,尿毒症得到控制和改善时 ,在作好围拔牙期处理的情况下 ,行拔牙手术是安全可行的     

玉米浆用量、渗透压和耗糖速率对甘油发酵的影响

Candida krusei发酵生产甘油过程中,菌体生长由玉米浆限制,菌体对玉米浆的得率为1．63g/g,培养其中玉米浆浓度相同时,增加渗透压或通过流加补料限制生长阶段的菌体生长,可使甘油生产阶段的比耗糖速率减慢,比耗糖速率保持在不很高的水平,可以因消耗的葡萄糖用于生长,维持,甘油和副产物形成所占比例的变化而提高甘油得率。     

蠕变局部损伤开裂的有限元模型

建立了蠕变局部损伤法模型,并给出单元进入损伤态的判据和失效的临界拉伸应变条件,局部蠕变损伤理论的实质就是试样是多种不同蠕变性能材料的统一,并由蠕变应力再分布得到证实,应用有限元对双缺口圆试样作了蠕变局部损伤分析,启裂时间和断裂蠕变应变值均与实验结果相吻合。