应用内置钛镍记忆合金牵张器在下颌骨牵张成骨的初步研究

目的　探索利用钛镍记忆合金牵张成骨增高下颌牙槽嵴和修复下颌骨节段性缺损的可行性。方法　 2 0只成年杂种犬分为 5组 ,Ⅰ组和Ⅱ组进行牵引成骨增高下颌骨牙槽嵴 ,Ⅲ组和Ⅳ组进行牵引成骨修复下颌骨缺损 ,Ⅴ组作为对照。牵引成骨用自行设计制作的内置型钛镍合金牵张器 ,在牵张手术前及术后 1、5、13周拍X线片 ,分别在牵张完成后 1、3个月处死动物 ,进行组织学研究。结果　钛镍牵张器显示了良好的组织相容性 ,自动完成牵引骨形成 ,牵张器安置完成后骨块即开始移动 ,X线片可见牵张完成后 1个月牵张区骨密度增高 ,有新骨生成 ;3个月时新生骨密度与周围骨接近 ,有效地增加了牙槽嵴的高度和初步修复了下颌骨的节段性缺损。组织学观察可见牵张区新骨形成良好。结论　内置自加载钛镍记忆合金牵张器自动牵引成骨是一种具有良好应用前景的简便实用的牵引成骨技术。     

预防肺泡胸膜漏临床分析（附110例恶性肺肿瘤肺叶切除）

目的 探讨恶性肺肿瘤行肺叶切除后影响住院时间的因素。方法 研究分析1995年11月至2002年10月我科收治的110例恶性肺肿瘤行肺叶切除患者的临床病理资料，相关因素数值化后，以Logistic回归分析得到对住院时间影响较大的因素。结果 术后并发症气胸和术前肺功能指标第一秒用力呼气量(FEVl)是较大的影响住院时间因素。结论 提高术前肺功能储备及预防术后气胸的发生是缩短住院时间的关键。     

肺泡巨噬细胞对肺气虚证局部神经—内分泌—免疫系统功能影响

检测４０例慢性支气管炎肺气虚证、３９例慢支隐性肺证患者及３６例正常人外周血、支气管肺灌洗液（ＢＡＬＦ）Ｔ淋巴细胞亚群（ＯＫＴ８）、皮质醇及去甲肾上腺素以及肺泡巨噬细胞（ＡＭ）分泌ＴＸＢ２／ＰＧＦ１ａ。结果表明：肺气虚证局部ＮＥＩＳ紊乱较明显，它与ＡＭ分泌的ＴＸＢ２和ＰＧＦ１ａ有关。隐性肺证局部病理生理变化较轻，局部与整体ＮＥＩＳ功能相互作用，尤其是整体对局部的调节稳定作有更加明显，而ＡＭ产生炎症介质对局部ＮＥＩＳ破坏的作用相对减弱     

人工牙种植中牙槽骨骨量不足和颌骨缺损的处理

目的 探讨人工牙种植中牙槽骨骨量不足和颌骨缺损的处理。方法 总结32例多种原因、多种类型牙槽骨骨量不足和颌骨缺损，应用植骨、植入Bio-Oss、骨引导膜等方法，创造条件进行人工牙种植。结果 32例病例、48个牙位，除1例植骨行即刻种植2枚种植体失败外，其余均取得满意的种植效果。结论 传统意义上认为不适合种植的牙槽骨骨量不足和颌骨缺损病例，通过创造条件能够取得良好的种植效果。     

Spray-dried fucoidan microparticles for pulmonary delivery of antitubercular drugs

Pulmonary tuberculosis accounts for 80% of cases and the delivery of antitubercular drugs into the lungs allows targeting the infected organ and, possibly, reducing systemic drug toxicity. This work aimed at using fucoidan as matrix of inhalable microparticles that associate two first-line antitubercular drugs, for an application in pulmonary tuberculosis therapy. Fucoidan is composed of fucose and sulphated sugar residues, moieties described as being recognised by surface receptors of alveolar macrophages, which host mycobacteria. Inhalable fucoidan microparticles loaded with antitubercular drugs were successfully produced with high association efficiencies of either isoniazid (95%) or rifabutin (81%). The microparticles evidenced no cytotoxicity on lung epithelial cells (A549). However, rifabutin-loaded microparticles showed a certain degree of toxicity on macrophage-like cells (THP-1) at the highest tested concentration (1?mg/mL). Furthermore, microparticles showed favourable aerodynamic properties for deep lung delivery (MMAD 2.0–3.8?µm) and, thus, show potential for an application as inhalable tuberculosis therapy.     

TIBIA AS DONOR SITE FOR ALVEOLAR BONE GRAFTING IN PATIENTS WITH CLEFT LIP AND PALATE: LONG TERM EXPERIENCE

Tibial bone grafts were studied in 137 patients with clefts of the lip and palate. Twenty-one had clefts of the lip and primary palate and 116 had complete unilateral clefts of the lip and palate. Bone grafting was performed secondarily or late secondarily. Bone was harvested from the proximal part of the tibia distal to the tuberosity through an incision about 15 mm long. The mean follow-up time after bone grafting was 5.5 years (range 2-11). There were no operative, or early or late postoperative complications reported (such as haematoma, fracture, or shortening of the limb). Harvesting time was about 15 minutes. The possibility of operating with two teams makes the total operating time shorter. Bleeding was negligible (less than 15 ml) and the amount of bone obtained was always sufficient. Patients were mobilised the next day and were back to full physical activity by one month. Indications for tibial bone grafting included facilitation of tooth eruption into the graft, giving bony support to the neighbouring teeth, making it possible to insert a titanium fixture, raising the alar base of the nose, and closing an oronasal fistula. Compared with iliac, cranial, mandibular, and costal donor sites, using the tibia took less time, gave less bleeding, made it possible for two teams to operate simultaneously, gave a smaller scar, and there were minimal complications and satisfactory quantity and quality of bone in all cases. The results suggested that the tibia is an excellent choice of graft for residual alveolar clefts in patients with cleft lip and palate.     

Harmful at non-cytotoxic concentrations: SiO2-SPIONs affect surfactant metabolism and lamellar body biogenesis in A549 human alveolar epithelial cells

The pulmonary delivery of nanoparticles (NPs) is a promising approach in nanomedicine. For the efficient and safe use of inhalable NPs, understanding of NP interference with lung surfactant metabolism is needed. Lung surfactant is predominantly a phospholipid substance, synthesized in alveolar type II cells (ATII), where it is packed in special organelles, lamellar bodies (LBs). In vitro and in vivo studies have reported NPs impact on surfactant homeostasis, but this phenomenon has not yet been sufficiently examined. We showed that in ATII-like A549 human lung cancer cells, silica-coated superparamagnetic iron oxide NPs (SiO₂-SPIONs), which have a high potential in medicine, caused an increased cellular amount of acid organelles and phospholipids. In SiO₂-SPION treated cells, we observed elevated cellular quantity of multivesicular bodies (MVBs), organelles involved in LB biogenesis. In spite of the results indicating increased surfactant production, the cellular quantity of LBs was surprisingly diminished and the majority of the remaining LBs were filled with SiO₂-SPIONs. Additionally, LBs were detected inside abundant autophagic vacuoles (AVs) and obviously destined for degradation. We also observed time- and dose-dependent changes in mRNA expression for proteins involved in lipid metabolism. Our results demonstrate that non-cytotoxic concentrations of SiO₂-SPIONs interfere with surfactant metabolism and LB biogenesis, leading to disturbed ability to reduce hypophase surface tension. To ensure the safe use of NPs for pulmonary delivery, we propose that potential NP interference with LB biogenesis is obligatorily taken into account.     

Interstitial lung diseases in children

Interstitial lung disease (ILD) in children (chILD) is a heterogeneous group of rare respiratory disorders that are mostly chronic and associated with high morbidity and mortality. The pathogenesis of the various chILD is complex and the diseases share common features of inflammatory and fibrotic changes of the lung parenchyma that impair gas exchanges. The etiologies of chILD are numerous. In this review, we chose to classify them as ILD related to exposure/environment insults, ILD related to systemic and immunological diseases, ILD related to primary lung parenchyma dysfunctions and ILD specific to infancy. A growing part of the etiologic spectrum of chILD is being attributed to molecular defects. Currently, the main genetic mutations associated with chILD are identified in the surfactant genes SFTPA1, SFTPA2, SFTPB, SFTPC, ABCA3 and NKX2-1. Other genetic contributors include mutations in MARS, CSF2RA and CSF2RB in pulmonary alveolar proteinosis, and mutations in TMEM173 and COPA in specific auto-inflammatory forms of chILD. However, only few genotype-phenotype correlations could be identified so far. Herein, information is provided about the clinical presentation and the diagnosis approach of chILD. Despite improvements in patient management, the therapeutic strategies are still relying mostly on corticosteroids although specific therapies are emerging. Larger longitudinal cohorts of patients are being gathered through ongoing international collaborations to improve disease knowledge and targeted therapies. Thus, it is expected that children with ILD will be able to reach the adulthood transition in a better condition.