地塞米松对宫颈癌细胞裸鼠移植瘤生长的抑制作用

目的 探讨超生理剂量的地塞米松对官颈癌HeLa细胞裸鼠移植瘤生长的影响.方法 5～6周龄雌性BALB/c裸鼠皮下接种传代培养的HeLa肿瘤细胞,肿瘤长大后(接种后16 d)每天腹腔内注射超生理剂量的地塞米松(62.5 mg·kg-1·d-1),连续10 d,测量肿瘤直径,计算肿瘤体积及抑瘤率;对肿瘤进行透射电镜观察、原位细胞凋亡检测(TUNEL)、血管内皮生长因子(VEGF)及肿瘤坏死因子-α(TNF-α)检测.结果 超生理剂量的地塞米松体内注射能抑制官颈癌HeLa细胞裸鼠移植瘤生长,诱导肿瘤细胞凋亡;与对照组相比,治疗组肿瘤体积变小[(1.472±0.082)cm3vs(0.383±0.038)cm3,P<0.01],抑瘤率为73.99%,凋亡小体数目增多[(413±87)个vs(160±101)个,P<0.01)],VEGF灰度值降低[(172.833±12.978)vs(177.067±6.875),P<0.01],TNF-α灰度值无差异[(172.833±12.978)vs(177.067±6.875),P>0.05].结论 超生理剂量的地塞米松体内用药能显著抑制肿瘤生长,与诱导凋亡及抑制VEGF有关,而与TNF-α无关.     

腺苷对小鼠前额叶皮质锥体细胞超极化激活阳离子电流的影响

目的 应用膜片钳全细胞记录技术,探讨腺苷对小鼠前额叶皮质锥体细胞的超极化激活阳离子电流(hyperpolarization-activated cation current,IH)的影响.方法 制备小鼠前额叶皮质脑片,在膜片钳全细胞记录模式下,观察腺苷对锥体细胞IH的调节作用.结果 记录的43个细胞中有41个观察到IH;腺苷能够使该电流幅度减小,并使Ⅰ-Ⅴ曲线显著下移(P＜0.01,P＜0.05),此效应呈剂量依赖性(P＜0.05).结论 腺苷具有抑制前额叶皮质锥体细胞IH的作用.     

不稳定逼尿肌中ICCs细胞与逼尿肌收缩的关系

目的 研究不稳定逼尿肌中ICCs细胞的数量、分布形式的变化及其功能改变对逼尿肌肌条收缩的影响,初步探讨ICCs细胞与逼尿肌不稳定的关系.方法 近端尿道结扎法建立大鼠不稳定膀胱模型.分别于正常及不稳定膀胱的相同部位剪取3 mm×4 mm逼尿肌组织进行免疫荧光组织化学法检测c-kit阳性细胞的表达及分布情况;再于相同部位剪取2 mm×7 mm肌条进行收缩特性测定实验,并检测c-kit受体阻断剂对收缩的影响.结果 不稳定逼尿肌中c-kit阳性细胞的数量较正常逼尿肌明显增多(P＜0.05);正常逼尿肌中c-kit阳性细胞以散在分布为主,不稳定逼尿肌中以细胞网络形式存在;不稳定逼尿肌肌条的收缩频率和收缩幅度显著高于正常膀胱(P＜0.05);加入Glevic后,不稳定逼尿肌肌条的收缩幅度显著减弱(P＜0.05),频率无显著差异(P＞0.05).结论 不稳定膀胱中ICCs细胞的数量明显增加,主要以细胞网络的形式存在;不稳定逼尿肌肌条收缩幅度和频率明显增高,但其收缩幅度可以被Glevic削弱,提示ICCs与逼尿肌不稳定的发生有密切关系.     

测定胃癌患者肿瘤组织与外周血中前列腺素E2的临床意义

目的 测定胃癌患者肿瘤组织及外周血中前列腺素E2(prostaglandin E2,PGE2)含量.方法 用PGE2酶联免疫试剂盒分别测定40例胃癌患者肿瘤组织、癌旁切缘组织及术前外周血中PGE2含量.结果 胃癌组织的PGE2含量明显高于癌旁切缘组织,分别为(8.225±2.425)、(1.669±0.287)ng/g,两者差异有统计学意义(P<0.01),低分化和高中分化胃癌组织PGE2含量分别为(9.02±2.28)、(5.38±0.35)ng/g,两者有显著性差异(P<0.05).外周血中PGE2含量与胃癌组织PGE2含量呈正相关(r=0.889,P<0.01).肿瘤直径≥5 cm和<5 cm的胃癌患者外周血中PGE2含量差异有统计学意义(P<0.05).低分化和高中分化胃癌患者外周血中PGE2含量差异也有统计学意义(P<0.05).胃癌组织及外周血中PGE2含量与患者年龄、性别无关,与肿瘤部位、浸润深度、临床病理分期及是否淋巴结转移也无关.结论 胃癌患者肿瘤组织中PGE2含量增高,其外周血PGE2含量也随之增高,表明外周血PGE:水平与胃癌组织释放的PGE2含量成正比.测定外周血中PGE2可以间接评估胃癌患者的肿瘤大小与分化程度.     

异种脱蛋白骨修复长骨大段骨缺损实验研究

目的研究改良法制备的异种脱蛋白骨（deproteinated bone,DPB）作为组织工程支架材料修复大动物长骨大段缺损24周后新生骨的生物力学变化。方法山羊18只,采用完全随机设计法分为正常骨对照组、自体骨组和实验组,每组6只,在自体骨组和实验组每只山羊右侧胫骨中下段造成胫骨总长度20％骨膜和骨缺损,正常骨对照组不截骨,其余2组分别在缺损处植入自体骨、DPB＋自体MSCs＋rhBMP2,采用半环槽外固定,术后24周取手术侧胫骨进行生物力学检测。结果术后24周,正常骨对照组、自体骨组和实验组新骨生物力学相比无统计学差异（P〉0．05）。结论改良法制备的异种DPB复合物作为组织工程支架材料修复大动物长骨大段缺损形成的新骨,其生物力学与正常骨对照组、自体骨组相当,可作为骨移植材料试应用于临床。     

Generation of liquid metal double emulsion droplets using gravity-induced microfluidics

Several microfluidic applications are available for liquid metal droplet generation, but the surface oxidation of liquid metal has placed limitations on its application. Multiphase microfluidics makes it possible to protect the inner droplets by producing the structure of double emulsion droplets. Thus, the generation of liquid metal double emulsion droplets has been developed to prevent the surface oxidation of Galinstan. However, the generation using common methods faces considerable challenges due to the gravity effect introduced from the high density of liquid metal, making it difficult for the shell phase to wrap the inner phase. To overcome this obstacle, we introduce an innovative method – a gravity-induced microfluidic device – to creatively generate controllable liquid metal double emulsion droplets, achieved by altering the measurable inclination angle of the plane. It is found that when the inclination angle ranges from 30° to 45°, the device manages to generate liquid metal double emulsion droplets with perfect double sphere-type configuration. Additionally, the core–shell liquid metal hydrogel capsules present potential applications as multifunctional materials for controlled release systems in drug delivery and biomedical applications. By regulating pH or imposing mechanical force, the hydrogel shell can be dissolved to recover the electrical conductivity of Galinstan for applications in flexible electronics, self-healing conductors, elastomer electronic skin, and tumor therapy.

An innovative method – a gravity-induced microfluidic device – to generate liquid metal double emulsion droplets to prevent the formation of an oxide layer on the liquid metal is introduced.     

New possible silver lining for pancreatic cancer therapy: Hydrogen sulfide and its donors

As one of the most lethal diseases, pancreatic cancer shows a dismal overall prognosis and high resistance to most treatment modalities. Furthermore, pancreatic cancer escapes early detection during the curable period because early symptoms rarely emerge and specific markers for this disease have not been found. Although combinations of new drugs, multimodal therapies, and adjuvants prolong survival, most patients still relapse after surgery and eventually die. Consequently, the search for more effective treatments for pancreatic cancer is highly relevant and justified. As a newly re-discovered mediator of gasotransmission, hydrogen sulfide (H₂S) undertakes essential functions, encompassing various signaling complexes that occupy key processes in human biology. Accumulating evidence indicates that H₂S exhibits bimodal modulation of cancer development. Thus, endogenous or low levels of exogenous H₂S are thought to promote cancer, whereas high doses of exogenous H₂S suppress tumor proliferation. Similarly, inhibition of endogenous H₂S production also suppresses tumor proliferation. Accordingly, H₂S biosynthesis inhibitors and H₂S supplementation (H₂S donors) are two distinct strategies for the treatment of cancer. Unfortunately, modulation of endogenous H₂S on pancreatic cancer has not been studied so far. However, H₂S donors and their derivatives have been extensively studied as potential therapeutic agents for pancreatic cancer therapy by inhibiting cell proliferation, inducing apoptosis, arresting cell cycle, and suppressing invasion and migration through exploiting multiple signaling pathways. As far as we know, there is no review of the effects of H₂S donors on pancreatic cancer. Based on these concerns, the therapeutic effects of some H₂S donors and NO–H₂S dual donors on pancreatic cancer were summarized in this paper. Exogenous H₂S donors may be promising compounds for pancreatic cancer treatment.KEY WORDS: Pancreatic cancer, Hydrogen sulfide donor, Sulfur-containing compound, Cell proliferation, Antitumor effect, Signaling pathway     

持续动态压应力对骨折愈合时环氧合酶mRNA表达及愈合骨机械特性的影响

目的 探讨持续动态压应力环境下骨折愈合时环氧合酶转录水平的变化以及愈合过程中机械性能的改变. 方法新西兰兔行单侧肱骨干横断截骨,试验组以天鹅记忆接骨器内固定,在骨折端造成持续动态压应力,对照组以加压钢板内固定.分别于术后第3、7、14、21、28、56天时在骨折间隙内取材,行Real-time PCR研究.术后2、4、8、12周时另取肱骨标本用作骨密度和生物力学测试.结果 环氧合酶-2(cyclooxygenase-2, COX-2) mRNA的表达量较骨折前显著上升,且试验组术~4周时明显高于对照组(P<0.05),生物力学结果则显示愈合4周和8周时试验组的弯曲刚度、扭转刚度、最大扭转和弯距均显著高于对照组(P<0.05),而此时试验组局部骨密度也相对较高(P<0.01).结论 天鹅记忆接骨器产生的持续动态压应力诱导了COX-2的转录,而COX-2 mRNA的高表达则促进了成骨细胞的分化和骨痂矿物质的沉积,加速了骨折的愈合和机械性能的恢复.     

吡咯烷二硫代氨基甲酸盐对大鼠缺血性心肌损伤后心室扩张及心衰的干预效应

目的研究核因子-κB（nuclearfactor—κB,NF—κB）抑制剂——吡咯烷二硫代氨基甲酸盐（pyrrolidine dithiocarbamate,PDTC）对异丙肾上腺素（isoprenaline,ISO）所致大鼠缺血性心肌损伤后心室扩张、心衰的防治作用及其作用机制。方法应用大剂量ISO建立大鼠缺血性心肌损伤模型。70只雄性Wistar大鼠利用随机数字表法分为3组：对照组20只,实验组（ISO组）30只,治疗组（ISO＋PDTC组）20只。检查心肌病理形态学、心肌NF—κB激活情况、心肌单核细胞趋化蛋白-1（MCP-1）mRNA表达情况及血清MCP-1水平,并在实验第14天进行超声心动图检查,观察心室扩张及心功能变化情况。结果ISO所致大鼠缺血性心肌损伤后心肌NF—κB被激活,心肌MCP-1mRNA表达增加（P〈0．01）,血清MCP-1增高（P〈0．01）;PDTC能够抑制NF—κB的激活,下调心肌MCP-1mRNA的表达及血清MCP-1水平（P〈0．01）,减轻心肌炎症反应,减小心肌细胞损伤范围,但同时可导致肉芽组织替代受损心肌延迟;实验第14天,治疗组左心室收缩末期内径（LVESD）较实验组减小（P〈0．05）,射血分数（EF）优于实验组（P〈0．05）。结论应用PDTC能够对心肌缺血性损伤后的心室扩张、心功能损害起到-定的防治作用,该作用可能主要得益于在心肌损伤急性期对心肌细胞的保护作用,其机制可能与抑制NF—κB的激活进而下调MCP-1的表达、减轻心肌炎症损伤有关。