5种稀土粉尘的细胞毒性研究

本研究应用荧光偏振测量技术测定了豚鼠肺泡巨噬细胞膜流动性,用原子吸收分光光度仪测定细胞钾,并通过测定细胞培养液中乳酸脱氢酶的活性、细胞死亡率及扫描电镜观察巨噬细胞形态学变化,研究了CeO_2、包钢混合稀土、硅铁合金、Y_2O_3及富钇5种粉尘对细胞的毒作用。结果表明,5种粉尘对细胞均产生一定毒性,并有明显的剂量-反应关系。经毒性大小比较,CeO_2毒性较轻,接近TiO_2,包钢混合稀土与硅铁合金相近,毒性居中,Y_2O_3和富钇毒性较大,但轻于SiO_2。     

潜艇常见气体对离体细胞化学发光的影响

目的 :用化学发光法检测O2 、CO2 、CO和正庚烷 (CxHy)四种气体对离体家兔肺泡巨噬细胞 (AM )的直接效应。 方法 :将AM悬液暴露于上述气体 ,不同时间检测用PMA激发的细胞发光及其存活率。结果 :培养在 99.5 %N2 (0 .5 %O2 )中的AM受激发光仅能维持 10h ;高浓度O2 、CO2 、CO和CxHy具有刺激或增强AM发光之效应 ;含 16 %O2 、1.9%CO2 、46mg/m3 CO和 176mg/m3 CxHy的模拟潜艇混合气体未见对AM激发光功能和存活率产生不利影响。结论 :空气氧含量对细胞十分重要 ,提高氧浓度有利于细胞存活 ,但氧浓度 >16 %和 <2 0 %的低氧还原性气体环境更有利细胞长时间生存。     

过敏性肺泡炎并双侧胸腔积液1例诊治

目的:通过探讨该病历提高临床医生对该病认识.方法:通过病史询问,体格检查,辅助检查排除其他常见病.结果:过敏性肺泡炎可以并发胸腔积液.结论:早期诊断,及时给予激素治疗,预后良好.     

COMPLETE BREAKAGE OF THREE-DIMENSIONAL MINIPLATES: UNUSUAL COMPLICATION OF OSTEOSYNTHESIS AFTER SAGITTAL SPLIT OSTEOTOMY: Two case reports

We describe two cases in which three-dimensional miniplates broke after bilateral sagittal split osteotomy. The miniplates broke vertically and the cause was suspected to be excessive shear force on the osteotomy line because of unstable occlusion. In patients with unstable postoperative occlusions the osteosynthesis should be bicortical.     

胎盘生长因子在慢性哮喘大鼠肺组织中的表达

 目的 探讨胎盘生长因子(placenta growth factor,PlGF)在慢性哮喘大鼠肺组织中的表达。方法 45只雄性SD大鼠随机分为3组(每组15只):(1)正常大鼠组(A组):未行特殊干预处理;(2)卵清蛋白(ovalbumin,OVA)致敏及生理盐水吸入大鼠组(B组):应用OVA致敏生理盐水激发;(3)慢性哮喘大鼠组(C组):应用OVA致敏和反复激发制备大鼠慢性哮喘模型。各组大鼠于末次激发后24 h处死。ELISA法测定肺泡灌洗液(BALF)中PlGF水平;大鼠肺组织标本行HE染色、PAS染色及Masson三色染色,并行病理图像形态学测定和分析;免疫组化检测大鼠气道上皮细胞PlGF的表达。结果 慢性哮喘大鼠组(C组)气道上皮细胞PlGF的表达(PI为2.28±0.18)与正常大鼠组(A组)及OVA致敏生理盐水吸入大鼠组(B组),(PI分别为0.89±0.08、0.94±0.12)相比明显增多(A组与C组比较P<0.01,B组与C组比较P<0.01)。慢性哮喘大鼠组(C组)BALF中PlGF水平(18.87±4.53)ng/ml与正常大鼠组(A组)及OVA致敏生理盐水吸入大鼠组(B组),分别为(12.35±1.94)ng/ml、(13.14±2.52)ng/ml相比明显增高(P<0.05)。结论 胎盘生长因子(PlGF)在慢性哮喘大鼠肺组织中表达增多。     

三叶因子2在慢性支气管哮喘大鼠肺组织中的表达

目的：进一步探讨三叶因子2(TFF2)在慢性支气管哮喘(简称哮喘)大鼠肺组织中的表达。方法24只雄性 Wistar 大鼠随机分为3组(每组8只)：①正常大鼠组(A 组)：无特殊处理。②鸡卵白蛋白(ovalbumin,OVA)致敏生理盐水吸入组(B 组)：应用 OVA 致敏大鼠,生理盐水激发；③慢性哮喘组(C 组)：应用 OVA 致敏和反复激发的方法制备大鼠慢性哮喘模型。各组大鼠于末次激发后24 h 处死。ELISA 法测定 BALF 中 TFF2水平；肺组织标本行 HE 染色、PAS 染色及Masson 三色染色,并行病理图像形态学测定和分析；免疫组织化学检测大鼠气道上皮细胞 TFF2的表达。结果 C 组大鼠气道上皮细胞 TFF2的表达与 A 组及 B 组相比明显增多(A 组与 C 组比较 q =74.51,P <0.01,B 组与 C 组比较 q =71.93,P <0.01)。C 组大鼠 BALF 中 TFF2水平与 A 组及 B 组相比明显增高(A 组与 C 组比较 q =7.16,P <0.01,B 组与 C 组比较 q =6.13,P <0.01)。结论TFF2在慢性哮喘大鼠肺组织中表达增多。     

Failures and complications in patients with birth defects restored with fixed dental prostheses and single crowns on teeth and/or implants

Objectives: To assess retrospectively, over at least 5 years, the incidences of technical and biological complications and failures in young adult patients with birth defects affecting the formation of teeth. Material and methods: All insurance cases with a birth defect that had crowns and fixed dental prostheses (FDPs) inserted more than 5 years ago were contacted and asked to participate in a reexamination. Results: The median age of the patients was 19.3 years (range 16.6–24.7 years) when prosthetic treatment was initiated. Over the median observation period of 15.7 years (range 7.4–24.9 years) and considering the treatment needs at the reexamination, 19 out of 33 patients (58%) with reconstructions on teeth remained free from all failures or complications. From the patients with FDPs and single unit crowns (SCs) on implants followed over a median observation period of 8 years (range 4.6–15.3 years), eight out of 17% or 47% needed a retreatment or repair at some point due to a failure or a complication. From the three groups of patients, the cases with amelogenesis/dentinogenesis imperfecta demonstrated the highest failure and complication rates. In the cases with cleft lip, alveolus and palate (CLAP) or hypodontia/oligodontia, 71% of the SCs and 73% of the FDPs on teeth (FDP T) remained complication free over a median observation period of about 16 years. Sixty‐two percent of the SCs and 64% of the FDPs on implants remained complication free over 8 years. Complications occurred earlier with implant‐supported reconstructions. Conclusions: Because healthy, pristine teeth can be left unprepared, implant‐supported SCs and FDPs are the treatment choice in young adults with birth defects resulting in tooth agenesis and in whom the edentulous spaces cannot be closed by means of orthodontic therapy. However, the trend for earlier and more frequent complications with implant‐supported reconstructions in young adults, expecting many years of function with the reconstructions, has to be weighed against the benefits of keeping teeth unprepared. In cases with CLAP in which anatomical conditions render implant placement difficult and in which teeth adjacent to the cleft require esthetic corrections, the conventional FDP T still remains the treatment of choice.     

Epithelio-mesenchymal transformation in the embryonic face: implications for craniofacial malformations

A high percentage of craniofacial malformations is ascribed to abnormalities in cell populations derived from the neural crest and ganglionic placodes. Both cell populations originate from the ectoderm of the head-neck area by means of the mechanism of epithelio-mesenchymal transformation (EMT). Neural crest cells are multipotent and form the majority of the mesenchymal compartment of the head-neck area. EMT of the neural crest will stop shortly after closure of the neural tube. The current opinion about ganglionic placodal cells is that they are derived from the surface ectodermal placodes after closure of the cranial neural tube, and transform into neurons of the sensory ganglia only. However, additional EMT sites of the cranial neural and surface ectoderm have also been found to produce multipotent cells. Because of the fact that most craniofacial malformations develop after closure of the cranial neural tube, in this study we focused on the EMT of the surface ectoderm of the head-neck area during the stages of outgrowth of facial swellings and branchial arches. The surface ectoderm was labeled by injecting various tracker dyes into the amniotic cavity of chick embryos after closure of the anterior neuropore, to exclude labeling of the neural ectoderm and the neural crest. After various incubation periods, ranging from 0–24 h, labeled cells were found in the mesenchymal compartment scattered over the embryonic face and neck, originating from non-placodal as well as placodal surface ectoderm. Thus, besides the neural ectoderm and neural crest, it could be shown that the entire surface ectoderm of the face and neck contributes cells to the underlying mesenchymal tissue, and that this phenomenon occurs in a higher frequency at sites of outgrowing swellings. As a consequence, the pathogenesis of congenital craniofacial malformations should be reconsidered. Received: 15 November 1999 / Accepted: 27 January 2000