Differences in a K current in schwann cells from normal and neurofibromatosis-infected damselfish

Patch clamp techniques were used to study whole cell ionic currents in Schwann cells (SC) from a tropical marine fish, the bicolor damselfish, Pomacentrus partitus. The bicolor damselfish is affected by a disease termed damselfish neurofibromatosis (DNF), being developed as an animal model of neurofibromatosis-type 1 (NF1) in humans. NF1 affects SC, fibroblasts, and perineurial cells. The sole depolarization-activated ionic current present in cultured SC from normal fish peripheral nerve and from neurofibromas of fish with induced or spontaneously occurring DNF was an inactivating K⁺ current (K current), with a strong dependence on the Nernst potential for K⁺. This K current activated at depolarizations to -40 mV and above and inactivated during a maintained test pulse (0.2-1 s), but inactivation was significantly greater in tumored SC. Both currents were inhibited by 4-aminopyridine (K_d ? 1 mM) and by dendrotoxin (15 μM) but were insensitive to extracellular tetraethyammonium (≤ 150 mM), indicating that the whole cell currents were similar pharmacologically. The currents could be distinguished on the basis of their sensitivity to depolarized holding potential, with normal cells less sensitive. Half-inactivation of the current was -32 mV in normal cells and -38 mV in tumored cells. Inactivation curves constructed from the average normalized current for many SC were significantly different in normal and tumored cells. When the depolarized holding potential was maintained between test depolarizations, greater voltage-dependent inactivation in tumored cells was apparent. Normal cells maintained an average of 36% of peak current at a holding voltage of ?40 mV, while in tumored cells this average was 12%, a significant difference. © 1994 Wiley-Liss, Inc.     

胃肠道基质细胞瘤临床诊治和预后

目的:探讨胃肠道基质细胞瘤的临床诊断、治疗和预后。 方法:回顾性分析1995—2005年收治的31例胃肠道基质细胞瘤临床和病理资料。结果:根据Fletcher风险分级，极低风险3例，低风险5例，中风险15例，高风险8例。CD117，CD34，desmin，SMA，S-100蛋白阳性表达率分别为93.5%，87.1%，38.7%，35.5%，25.8%，其阳性表达率与肿瘤危险程度无关(χ2=0.35，0.12，0.03，0.05，0.01，均P>0.05)。肿瘤是否浸润黏膜肌层或浆膜层与肿瘤危险程度相关(χ2=4.87，P<0.05)。结论:用Fletcher分级对胃肠道基质瘤分级评价更为科学合理。中、高危险程度者复发率26.0%，明显高于极低和低风险者（P<0.001）。根治性手术是治疗胃肠道基质瘤最佳选择。肿瘤浸润黏膜肌层或浆膜层是危险的重要指标。核分裂相是判断预后的独立预后因素。     

2型糖尿病肾病患者血清中TNF-α、NO与ET的水平变化及其临床意义

目的：探讨2型糖尿病肾病患者血清肿瘤坏死因子仅（TNF-α）、一氧化氮（NO）和内皮素（ET）的水平变化及其临床意义。方法：用ELISA法检测91例2型糖尿病患者血清TNF-α水平，NO与ET的水平分别用硝酸还原酶法和放射免疫法测定。结果：2型糖尿病肾病各组患者TNF-α和ET水平较对照组明显升高，其中ODN组最高（P〈0．01）。而2型糖尿病肾病各组患者血清NO水平较对照组明显减少（P〈0．01）。显性糖尿病肾病患者血清TNF-α和ET呈正相关；血清TNF-α和NO、ET和NO均成负相关。结论：TNF-α、NO与ET可能参与2型糖尿病肾病的发病及病程变化过程，检测患者TNF-α、NO与ET水平可作为判断预后、指导治疗的指标。     

188Re-Herceptin-磁性纳米微粒的体外抗肿瘤作用

目的探讨^188Re—Herceptin-磁性纳米微粒在外置磁场下对HER-2／neu癌基因高表达的SKBR-3乳腺癌细胞的靶向结合性及抗癌作用。方法采用戊二醛交联法使人源性单克隆抗体Her—ceptin与磁性纳米微粒交联，用直接标记法制备^188Re—Herceptin及^188Re—Herceptin-磁性纳米微粒，用羰基铼标记法制备^188Re-磁性纳米微粒。肿瘤细胞体外抑制实验设4个组：^188Re—Herceptin-磁性纳米微粒组、^188Re—Herceptin组、^188Re-磁性纳米微粒组和^188ReO4^-组，各组均设3．7×10^4、18．5×10^4、37×10^4、55．5×10^4、74×10^4Bq／ml5个放射性剂量级别；另设生理盐水对照组。采用四甲基偶氮唑蓝（MTT）法测定各组的抑瘤效应，计算相对抑制率，采用半数抑制放射性浓度（IC50）对各组抑瘤作用进行比较和评价。结果^188Re—Herceptin-磁性纳米微粒和^188Re—Herceptin组对SKBR-3细胞均有较强杀伤作用，且呈剂量依赖性；而^188Re-磁性纳米微粒和^188Re04组的杀伤作用较弱0188Re—Herceptin-磁性纳米微粒组的IC50（53．1×10^4Bq／L）明显低于^188Re—Herceptin组（76．1×10^4Bq／L）；^188Re一磁性纳米微粒组和^188ReO4组的IC50分别为169×10^4和175×10^4Bq／L，明显高于前2组。结论^188Re—Herceptin-磁性纳米微粒和^188Re—Herceptin均可明显抑制体外培养的SKBR-3乳腺癌细胞增殖，且前者的抑制作用较后者强。     

蟾酥注射液对小鼠S180和人结肠癌HT-29裸鼠移植性肿瘤的影响

目的研究蟾酥注射液对小鼠移植性肿瘤 S180和人结肠癌 HT-29裸鼠移植性肿瘤的抑制作用.方法分别用小鼠 S180和人结肠癌 HT-29裸鼠两种荷瘤小鼠模型,观察药物对上述肿瘤的抑瘤作用,并镜下观察后者细胞凋亡情况.结果与荷瘤阴性对照组比较,蟾酥注射液各剂量组对小鼠 S180抑瘤率( IR)为 19.1%～38.2%(P<0.05),呈量效关系;而对人结肠癌 HT-29裸鼠移植性肿瘤的 IR为 9.5%～15.8%(P>0.05),也呈量效关系,但差异均未见统计学意义;环磷酰胺则能显著抑制小鼠 S180和 HT-29细胞裸鼠移植性肿瘤的生长( IR分别为70.7%和 67.1%, P<0.01),镜检可见其有显著促进肿瘤细胞凋亡作用;未发现实验药物出现明显的毒副作用.结论该实验所用的蟾酥注射液,对小鼠 S180有抑制作用,而对人结肠癌 HT-29裸鼠移植性肿瘤,则作用不明显,表明不同类型的肿瘤对其敏感性不同.     

Anti-inflammatory effect of erythropoietin pretreatment on cardiomyocytes with hypoxia/reoxygenation injury and the possible mechanism

Objective： To investigate the anti-inflammatory effect of erythropoietin （EPO） pretreatment on cardiomyocytes exposed to hypoxialreoxygenation injury （H/R） and explore the possible mechanism.
Methods： The cultured neonatal rats＇ ventricular cardiomyocytes were divided randomly into 4 groups, control group （C group）, EPO pretreatment group （E group）, EPO and pyrrolidine dithiocarbamate （PDTC） pretreatment group （EP group） and PDTC pretreatment group （P group）. After 24 hours＇ pretreatment, the cardiomyocytes were exposed to H/R. After pretreatment and H/R, the expression of tumor necrosis factor- α （TNF- α ） gene in all the groups was detected by RT-PCR and Western blot. The nuclear factor- κ B （NF- κB） activity was detected by electrophoretic mobility shift assay （EMSA） and the inhibitor- κB α （Ⅰ- κB α） protein level was detected by Western blot.
Results： The decrement of Ⅰ- κB a protein and the increasing NF- KB activity were found in cardiomyocytes pretreated with EPO before H/R compared to other groups （t=3.321, 4.183, P〈0.01）. However, after H/R, NF- κB activity and expression of TNF- α gene were significantly reduced, Ⅰ- κB a protein expression was increased in cardiomyocytes of E group compared to other groups （t=-3.425, 3.687, 3.454, P〈0.01）. All theses changes caused by EPO pretreatment were eliminated by the intervention of PDTC （an antagonist to NF- κB） during pretreatment.
Conclusions： EPO pretreatment can inhibit the activation of NF- κB and upregulation of TNF- α gene in cardiomyocytes exposed to H/R through a negative feedback of NF- κB signaling pathway, and thus produces the anti-inflammatory effect. This might be one of the ways EPO produces the anti-inflammatory effect.     

腮腺间隙良性肿瘤的MRI诊断

目的探讨腮腺间隙常见良性肿瘤的影像特征及其诊断与鉴别诊断。方法良性肿瘤20例，包括多形性腺瘤13例、乳头状淋巴囊腺瘤3例、淋巴管瘤2例、血管瘤1例、脂肪瘤1例。经手术病理证实15例，穿刺活检证实4例，典型MR特征结合病史确诊1例。结果13例多形性腺瘤中有11例位于腮腺浅叶，2例位于深叶；9例表现为均匀等T1长T2信号．4例在T2WI上信号明显不均匀；静脉注射Gd—UIPA后3例瘤实质均匀强化，4例增强后明显不均匀强化。3例Warthin瘤中2例发生于一侧，1例累及双侧腮腺，在T1WI上呈低信号，T2WI上信号等于或低于正常腺实质，增强后无明显强化。2例淋巴管瘤呈明显长T1长T2信号，并有多房现象。1例血管瘤信号不均质，呈明显长T1长T2信号，静1脉注射Gd—DTPA后病变往往显著异常强化。1例脂肪瘤在T1WI及T2WI上均表现为明显高信号强度。结论运用MR成像研究腮腺间隙的良性肿瘤，有利于疾病的定位，有助于病变的诊断与鉴别诊断。     

失血性大鼠休克后肠、肝、肺组织中细胞因子表达、释放时相及其伴随的病理变化

目的：探讨休克后促炎细胞因子的表达、释放时相及伴随的肠、肝、肺组织病理变化。方法：80只SD大鼠随机均分为失血性休克组和对照组。采用RT-PCR、ELISA方法检测失血性休克后30、60、90min及复苏后30、90min肠、肝、肺组织内TNF-α、IL-6 mRNA表达及血清中TNF-α、IL-6含量；HE和IHC染色检测伴随的组织病理变化。结果：①休克30min时，肠、肝、肺内的促炎细胞因子表达未见升高；60min时肠道先出现TNF-αmRNA表达升高（P〈0．05）：而肝脏在90min开始表达升高（P〈0．05），肺脏则在复苏后30min开始表达升高（P〈0．05）。复苏后90min肠、肝、肺的细胞因子表达都继续显著升高（P〈0．01）。②TNF-α 在肠、肝、肺的表达升高最早，其后为IL-6 mRNA。③30min时门静脉和外周血中TNF-α、IM的含量与对照组相比无显著差异，而60min时门静脉血中含量显著升高（P〈0．01）。④休克后肠黏膜坏死脱落；肝组织结构紊乱、肝窦增宽、肝细胞变性坏死；肺脏间质水肿、炎症细胞浸润。结论：失血性休克时细胞因子的释放顺序是肠道、肝脏和肺脏，推测存在“肠-肝-肺”细胞因子释放轴的可能，有待进一步确定。