肾病患儿免疫细胞对肾小球上皮细胞合成基质的影响

目的为了明确免疫细胞对肾小球上皮细胞（ｇｌｏｍｅｒｕｌａｒｅｐｉｔｈｅｌｉａｌｃｅｌＧＥＣ）合成功能的直接作用。方法应用肾小球细胞体外培养，同位素掺入及放射免疫技术，以总胶原，层粘连蛋白，Ⅲ型前胶原及Ⅳ型胶原的合成为观察指标，动态研究了不同病理类型原发性肾病综合征（ＩＮＳ）患儿外周血单个核细胞（ｐｅｒｉｐｈｅｒａｌｂｌｏｏｄｍｏｎｏｎｕｃｌｅａｒｃｅｌＰＢＭＣ）对ＧＥＣ生物功能的影响。结果（１）肾病极期未经激素治疗组（未治组）ＰＢＭＣ上清明显促进了ＧＥＣ合成层粘连蛋白；（２）未治ＰＢＭＣ上清抑制了ＧＥＣ合成总胶原；（３）未治组ＰＢＭＣ上清促进了Ⅲ型前胶原的合成，而对Ⅳ型胶原的合成无明显影响；（４）肾病患儿ＰＢＭＣ的上述作用与是否足量激素治疗有关，而与尿蛋白能否阴转、肾组织病理类型、肾病临床类型等无直线相关关系。结论原发性肾病患儿循环免疫细胞可影响ＧＥＣ合成细胞外基质的功能。免疫细胞的这种活性可被激素治疗改变。     

Kupffer cell activation in the survival discrepancy between liver grafts from enterally and parenterally fed donors

Abstract This study was designed to investigate the effects of differences in the route of nutritional support of the donor on cold ischemia/reperfusion injury. Participation of Kupffer cells in these effects, based on the analysis of hepatic energy metabolism in early phases of reperfusion was also investigated. Orthotopic liver transplantation was performed between Large-White pigs weighing 20–30 kg after a 4-h cold preservation of the graft in Euro-Collins solution at 4°C. One group was fed orally with a standard laboratory diet (FED group, n = 5), a second group was fasted and given 20% glucose intravenously (12 kJ/kg per day) (PEF group, n = 5), and a third group was fed orally with a standard laboratory diet and given GdCI₃ (10 mg/kg) intravenously 24 h before operation (FEDGD group, n = 5). These treatments were given for 7 days prior to harvesting. The survival time was significantly longer in the PEF (34.8 ± 5.5 days) and FEDGD (28.0 ± 11.9 days) groups than in the FED (9.8 ± 2.0 days) group ( P < 0.05). The serum hyaluronic acid elimination rate determined from 1 to 2 h after reperfusion was significantly lower in the FED group than in the other two groups ( P < 0.001). The glycogen content of the livers 1 h after reperfusion in all three groups had been consumed rapidly, but the ATP content of the livers was significantly reduced in the FED group alone ( P < 0.01). Hepatic FFA clearance (C_FFA) was moderately increased in all three groups in the early phase after reperfusion, but it was higher in the FED group than in the other two groups, with significant differences 1 and 2 h after reperfusion ( P < 0.05). In conclusion, parenteral nutrition of the donors reduced cold ischemia/reperfusion injury which is related to Kupffer cell activation and, thus, was better than enteral nutrition for donor management.     

肿瘤坏死因子刺激牛脑微血管内皮细胞释放内皮素-1及粉防己碱的拮抗作用

目的:观察肿瘤坏死因子（TNF）对培养的牛脑微血管内皮细胞释放内皮素-1（ET－1）的刺激作用及粉防己碱（Tet）对ET－1释放的抑制作用。方法：放免测定法。结果：TNF在（l～100μg·L(-1)）之间能剂量依赖性的促进牛脑微血管内皮细胞释放ET-1，Tet（10(－6)～10(－4)mol·L(－1)）能拮抗TNF诱导的ET－1释放并呈量效关系。     

异搏定对5-氟脲嘧啶抗肾癌效应的体外增效作用

在体外培养的肾透明细胞癌系中,观察了异搏定(Verapamil,VP)对5-氟脲嘧啶(Fluorouracil,5-Fu)细胞毒作用的影响。结果表明,异搏定在本身无细胞毒性的浓度下,可以显著增强5-氟脲嘧啶的细胞毒性,且增效作用随5-氟脲嘧啶浓度及异搏定浓度的增加及用药时间的延长而增强。     

组织工程化肌腱研究进展

对组织工程化肌腱领域中目前研究的主要成果进行综述，着重阐述了肌腱细胞外基质替代物、肌腱细胞生物学性质及肌腱细胞与细胞外基质材料复合研究中的主要问题。认为，研制适于肌腱细胞生长、粘附和发挥功能的细胞外基质材料；建立生长、增殖可调控的肌腱细胞系；在模拟体内力学条件下，进行肌腱细胞三维培养，将是研究具有特定修复功能的组织工程化肌腱的重要问题。     

乙型肝炎患者可溶性白细胞介素2受体水平变化

本研究应用酶联免疫吸附试验(ELISA)检测了103例乙型肝炎各型患者及26倒乙肝病毒(HBV)携带者血清中可溶性白细胞介素2受体(sIL-2R)水平,并结合临床资料进行分析。结果发现:各型患者及HBV 携带者sIL-2R 水平均明显高于正常对照(P<0.01～0.001),其升高程度与病情轻重呈正比,在去除危重患者酶—胆分离时谷丙转氨酶(ALT)过低的影响后,sIL-2R 水平与ALT 有良好的正相关关系(r=0.38.p<0.05);作者认为sIL-2R 能够较好地反映疾病的活动状况,动态观察血清sIL-2R 水平的变化,对判断和评价HBV 感染后的病情演变及免疫失衡状态具有重要意义。     

胃癌c-erbB-2过度表达与预后的关系

探讨c－erbB－2过度表达与胃癌预后的关系。方法：用免疫组化ABC法对103例胃癌手术标本及151个转移淋巴结进行c－erbB－2表达检测。结果：21．4％胃癌手术标本出现阳性表达．其中进展期胃癌、乳头状腺癌、高中分化胃癌及伴淋巴与肝转移的胃癌阳性率显著增高（P＜0．05与＜0．01）；转移淋巴结表达阳性率高于胃癌原发灶（X2＝3．7．P＞0．05）。高中分化胃癌伴c－erbB－2过度表达者5年生存率显著低于阴性者（P＜0．01）。结论：c－erbB－2过度表达可作为胃癌预后估计指标之一。     

育龄期妇女输卵管结扎后上皮细胞超微结构的改变

应用扫描电镜观察9位育龄期妇女正常和结扎后的输卵管上皮。结果表明:在输卵管结扎疤痕两侧各0.5cm处,粘膜上皮细胞的纤毛大量扭曲和粘连,局部上皮纤毛和微绒毛脱落,细胞形态不规则,而在距输卵管结扎疤痕两侧各1.0cm处,上皮细胞的纤毛和微绒毛形态和结构均正常。表明输卵管结扎后上皮的超微结构变化,使卵细胞输送功能丧失,可能是输卵管复通术后不孕的重要原因。因此,施行输卵管复通术时,输卵管疤痕切除的范围应不少于疤痕两侧各0.5cm,以提高输卵管复通率。此外,发现输卵管小孔仅位于输卵管积水处粘膜的分泌细胞间,可能与输卵管浆膜下毛细淋巴管相沟通,与引流输卵管积水有关。在输卵管积水处粘膜的表面纤毛细胞的纤毛大量脱落,微绒毛增生,许多纤毛细胞转变为分泌细胞。提出了形成输卵管积水新的发病机理。     

NGF Augmentation rescues trigeminal ganglion and principalis neurons,but not brainstem or cortical whisker patterns,after infraorbital nerve injury at birth

Prior studies indicate that neonatal nerve injury kills many trigeminal (V) first- and second-order cells, and interrupts pattern formation in the brainstem and cerebral cortex. Yet it is not known whether effects upon cell survival and pattern formation are causally related. To determine whether axotomized V ganglion cells can be rescued by an exogenous trophic agent, rats received 5 mg/kg of nerve growth factor (NGF) prior to, and every day after, infraorbital nerve section on the day of birth until sacrifice on postnatal day (PND) 1, 3, 5, 7, or 14. Other animals received identical lesions without NGF. Ganglion cell numbers were significantly reduced by PNDl in pups not given NGF, while NGF-treated rats displayed no significant cell loss through PND7. However, NGF did not permanently rescue V neurons because ganglion cell numbers were reliably reduced by PND14. Cell numbers in V nucleus principalis were reduced by PNDl in pups not given NGF, while NGF-treated animals displayed no cell loss through PND14. NGF's rescue of second-order cells is probably an indirect effect of NGF actions upon V ganglion cells because, in other newborns, NGF failed to maintain principalis cells after direct lesion of the left V ganglion. To determine whether preventing cell death permits whisker-related pattern formation, other rats also received NGF prior to and after infraorbital nerve section at birth. After 3–14 days, patterns were assessed in the brainstem and cortex with cytochrome oxidase histochemistry and serotonin immunocytochemistry. Whisker-related patterns failed to develop as in cases not given NGF. These data indicate that communication with the periphery is necessary for the maintenance of central whisker-related patterns. They also suggest that V ganglion cells can be rescued, albeit temporarily, from rapid injury-induced death by NGF, thereby delaying injury-induced cell death in nucleus principalis. However, the mechanism(s) responsible for injury-induced pattern alterations in the developing V system remains to be elucidated. © 1993 Wiley-Liss, Inc.     

内皮超极化因子的研究进展

内皮超极化因子（EDHF）是由内皮释放的NO和PGI_2以外的另一种舒张因子,它通过使平滑肌细胞膜超极化而舒张血管,是内皮依赖性血管松驰的第3种重要机制。EDHF可能是花生四烯酸的细胞色素P450代谢产物EET-s,乙酰胆碱、缓激肽等激动剂作用于内皮细胞,使细胞内游离钙浓度升高,合成和（或）释放EDHF,作用于平滑肌细胞膜,激活钙依赖性钾通道,使细胞膜超极化,抑制电压依赖性钙通道的开放,引起血管松弛。在大血管中NO-cGMP松弛机制可能占主导地位,并且抑制EDHF生成;而在阻力小血管,EDHF则可能是引起血管松弛的主要因素。