带真皮下血管网超薄皮瓣血运重建的实验研究（三）超薄皮瓣的再血管化与血供变化

以猪作为动物模型，对带真皮下血管网超薄皮瓣的血运重建规律进行了探讨。以超薄皮瓣为实验组，保留真皮下血管网皮片为对照组，按自身配对原则随机分为６个组。通过荧光素显色，透明标本，组织学，明胶墨汁灌注过程中超薄皮瓣的染色情况等观察，发现超薄皮瓣的再血管化发生在术后第５天，至第７天新生血管通过塑形趋于成熟。它既发生在皮瓣与受床之间，又发生在皮瓣与创缘之间，而且由皮瓣成活部分远端渐至近端。     

Management of chronic calcaneal osteomyelitis with pull-through abductor hallucis muscle flap -a report of three cases

Three patients who had chronic osteomyelitis of the calcaneus were treated with radical debridement of all involved soft tissue and bone and obliteration of dead space with a pull-through abductor hallucis brevis muscle flap. Two patients had calcaneal osteomyelitis without soft tissue loss resulting from previous comminuted calcaneal fractures while a third patient had a large soft tissue defect and calcaneal osteomyelitis resulting from a destructive infection. All of the patients had undergone several surgical procedures for treatment of the osteomyelitis with histories ranging 18 months to 30 months. Following treatment with the pull-through muscle flap there has been no recurrence over the longterm (>two years). We believe that radical removal of all contaminated tissue and immediately coverage with a muscle flap provides an effective single stage treatment of chronic calcaneal osteomyelitis.     

活动性结核标志物'H-多肽的实验与临床研究

本题研究是经免疫学途径直接检测人体感染结核菌的情况，为现代结核病的实验诊断、临床监测、流行病调查提供了一个全新的检验指标。作者首先发现了一种仅存在于活动性结核病患者体液中的蛋白成份—活动性结核标志物（ＡｃｔｉｖｅＴｕｂｅｒｃｕｌｏｓｉｓＭａｒｋ—ＡＴＭ）１Ｈ—多肽；并为之创立了独特的检测方法，经四年多临床１９４６０例样本调查中确定了ＡＴＭ的临床价值。将ＡＴＭ检测与ＯＴ皮试、酶联免疫ＥＬＩＳＡ、ＤＮＡ探针、ＰＣＲ基因扩增技术及典型病例组患者行Ｘ线计算机断层摄影（ＣＴ）、磁共振像（ＭＲＩ）等多组对比试验中，实验与临床研究资料分析证明：ＡＴＭ检测的总敏感度为８６．０６％、特异度９６．２４％、准确度９３．４５％、诊断效率为８２．８２％、批内ＣＶ１．２％、批间ＣＶ２．０％、Ｐ＜０．０５。经ＮＭＲ光谱分析结构含有ＣＣＨ２官能团。     

多发性脑梗塞痴呆动物模型评价

多发性脑梗塞痴呆模型大鼠可出现行为学、病理生理学、生化代谢、神经递质、血液流变学、基因表达等多方面改变，且病理形态学表现与临床上多发性脑梗塞痴呆相似，可以用作血管性痴呆的实验研究。但复习以往有关文献研究发现，该模型仍有待于进一步完善，以期更好地应用于基础研究，保证对药物抗血管性痴呆作用评价及作用机制诠释的准确性。     

Granulocyte-macrophage colony stimulating factor inhibits class II major histocompatibility complex expression and antigen presentation by microglia

Granulocyte-macrophage colony stimulating factor (GM-CSF) modulates various functions of monocytes/ macrophages including antigen-presenting capacity. Recently it was found that astrocytes produce GM-CSF in the central nervous system (CNS) and that GM-CSF can induce proliferation and morphological changes of microglia. Here we show that GM-CSF can down regulate the interferon-γ-mediated induction of major histocompatibility complex (MHC) class II antigens in microglia, but not in astrocytes. GM-CSF pretreatment completely prevents myelin basic protein-specific T cell proliferation induced by microglia but not astrocytes. GM-CSF did not affect the cell surface expression on microglia of either MHC class I or cell adhesion molecules. The inhibition of microglial MHC class II expression and antigen-presenting function is specific for GM-CSF, as treatment with a different CSF (interleukin-3) did not modulate microglial phenotype or functional capacity. These data suggest that GM-CSF might be involved in the regulation of immune responses within the central nervous system.     

Ia-expressing microglial cells in experimental allergic encephalomyelitis in rats

Summary Monoclonal antibodies (MRC OX-6 and OX-17) recognized three types of cells expressing Ia antigen during the course of acute experimental allergic encephalomyelitis (EAE) in rats. In earlier stages of the disease, in animals with or without paralysis, Ia antigens were mostly localized to subarachnoidal and perivascular lymphocytic and histiocytic cell infiltrates, possibly serving as antigen-presenting cells. On the other hand, in convalescent rats, Ia antigens were expressed in a large number of cells with dendritic processes heavily populating the spinal gray matter. The appearance of these Ia-expressing cells in the convalescent stage coincided with the development of degenerating axon terminals in the spinal gray matter. These Ia-expressing cells possessed morphological features characteristic of microglia and were positive for ML-1 lectin but did not express glial fibrillary acidic protein. Immune electron microscopy disclosed the presence of Ia reaction products in the Golgi apparatus, endoplasmic reticulum and plasma membrane of these cells with dendritic processes, indicating active synthesis of Ia molecules in microglia. In addition, Ia antigens were localized to the cells with ultrastructural features of macrophages. Thus, Ia-expressing cells in EAE seems to play dual roles: the induction of immunological reactions during earlier stages and the participation in reparative processes during convalescence.Supported by Grants-in-aid from the Ministry of Health and Welfare for Intractable Neuroimmunological Diseases and from the Ministry of Education, Science and Culture (Project 61570380 to HK)     

Role of mast cells in experimental anti-glomerular basement membrane glomerulonephritis

Recently, divergent reports on the role of mast cells (MC) in different glomerular diseases have brought our attention to their role in an accelerated model of anti-glomerular basement membrane (GBM) glomerulonephritis (GN). Genetically MC-deficient Kit(W)/Kit(W-v) mice, MC-reconstituted Kit(W)/Kit(W-v) mice and Kit+/+ control mice were subjected to anti-GBM GN. Kit(+/+) mice developed moderate proteinuria and glomerular damage following the induction of anti-GBM nephritis. In contrast, proteinuria and glomerular damage were dramatically increased in MC-deficient Kit(W)/Kit(W-v) mice. MC-reconstituted Kit(W)/Kit(W-v) mice showed proteinuria and glomerular damage comparable to Kit+/+ mice. A significant increase in infiltrating T cells and macrophages was detected in MC-deficient Kit(W)/Kit(W-v) mice as compared to Kit+/+ control mice and MC-reconstituted Kit(W)/Kit(W-v) mice. Accordingly, we observed an increase of TGF-beta1 mRNA in kidneys from Kit(W)/Kit(W-v) mice. Interestingly, we did not detect MC in the kidney using either Giemsa staining or RT-real-time PCR, but MC were found in the regional lymph nodes. Finally, mortality of Kit(W)/Kit(W-v) mice was significantly increased after the induction of anti-GBM GN due to uremia. Our report provides the first direct evidence that MC are protective in anti-GBM GN, possibly by modulating the influx of effector T cells and macrophages to inflammatory sites in the kidney.     

用于杀虫剂评价的水池中无脊椎动物的群落结构及其种群动态

实验水池是评价杀虫剂效应和安全生的重要场所，水池中无脊椎动物群落结构和种群动态是评价杀虫剂的基础资料和考核指标，本文报告１９９２年至１９９３年在美国佛罗里达中部地区对应用于杀虫剂评价的实验水池中昆虫与其它无脊椎动物群落结构及其优势种的种群动态研究结果，用羽化诱捕、勺舀、网拉及挖取底物法，从实验水池中共采到昆虫与其它无脊椎动物５０余类，其中，羽化诱捕到的昆虫中摇蚊占９３．９％，蜉蝣目昆虫占４．６％，     

The influence of uric acid treatments on liver glutathione system prevent oxidative damages in experimental autoimmune encephalomyelitis mice

Recently we reported that antioxidant system in brain and spinal cord in experimental autoimmune encephalomyelitis (EAE) mice is mainly affected at early stages of the disease [M. Zargari, A. Allameh, M.H. Sanati, T. Tiraihi, S.H. Lavasani, O. Emadyan, Relationship between the clinical scoring and demyelination in central nervous system with total antioxidant capacity of plasma during experimental autoimmune encephalomyelitis development in mice, Neurosci. Lett. 412 (2007), 24–28]. The aim of the present study was to investigate the role of uric acid (UA) on antioxidant system in liver and plasma of EAE mice. EAE was induced in C57/BL6 mice (n = 60), followed by i.p. administration of UA (10 mg/kg BW) in 30 mice at three distinct clinical stages (A: prior to onset, B: after onset, C: after development of EAE). Livers were removed and processed for measurement of lipid peroxidation products, reduced glutathione (GSH), and glutathione S-transferase (GST) and total antioxidant capacity of plasma (FRAP). The results showed that lipid peroxidation products in liver of EAE mice was increased significantly (∼85%) as compared to normal. UA administration to EAE mice caused a significant suppression of liver lipid peroxidation products (∼45%) at early stages (A and B). There was an inverse relationship between lipid peroxidation and cellular GSH in liver. GSH was significantly depleted in mice liver during the EAE progression, but it was recovered (∼29%) when UA was injected before the onset of the disease (groups A and B). Plasma total antioxidant capacity was significantly decreased during the development of EAE, however it was subsided in mice treated with UA as compared to the corresponding controls (21%) in groups A and B. Elevated liver GST as a result of EAE induction was reversed in mice treated with UA particularly in groups A and B. These results indicate that hepatic glutathione system, particularly GST plays a major role in modulation of oxidative damages to central nervous system (CNS) during EAE induction. The positive response of antioxidant system to UA administration in EAE mice was corroborated with improvement of clinical manifestation of the animals.     

Architectural remodelling in lungs of rabbits induced by type V collagen immunization: a preliminary morphologic model to study diffuse connective tissue diseases

The pathogenesis of diffuse connective tissue diseases (DCTD) is still unknown and has been extensively studied regarding its autoimmunity aspects related to extracellular matrix (ECM) remodelling, with an emphasis on the collagens at the inflammatory site. The present paper describes the pulmonary architectural and repair/remodelling responses to injury after immunization of rabbits with human type V collagen. The animal model consisted of rabbits immunized with collagen mixed with Freund's adjuvant and sacrificed 7, 15, 30, 75, and 120 days after the first of four doses of antigen. Pulmonary architecture remodelling response was evaluated by histology, morphometry, and the immunofluorescence method, according to compartments of reference (parenchyma and interstitium) and injury: 1 inflammation (polymorphonuclear and mononuclear cells); 2-repair (fibrosis) and 3-ECM remodelling (collagen system). The results showed an intense inflammatory involvement of the pulmonary vascular and bronchiolar parenchyma, characterized by increased wall thickness in small arteries, infiltrations by pseudoeosinophils, and mononuclear cells. Progressive remodelling of the pulmonary ECM was characterized by collagen deposition in the septal and bronchovascular interstitium, especially in rabbits sacrifices at 75 and 120 days. The ECM remodelling process was not reproduced when rabbits were inoculated with collagen types I and III. We conclude that the model reproduces morphologic changes similar to those observed in many DCTD, encouraging realization of other experiments to gain a better understanding of the pathogenesis of these diseases.