Increased expression of MHC class II antigens in rejecting canine lung allografts

Expression of major histocompatibility complex class II antigens was investigated in the normal lungs and in lung allografts of mongrel dogs after single-lung transplantation. Cryostat sections were stained with an indirect immunoperoxidase technique that used B1F6 and 7.5.10.1 as anti-MHC class II monoclonal antibodies. In the normal lungs and native lungs of the recipient dogs after single-lung transplantation, only some cells of lymphoid tissue and macrophages/dendritic cells were MHC class II-positive. During acute rejection, increased infiltration with MHC class II-positive cells in perivascular, peribronchial, and interstitial areas and intraalveolar spaces was found in lung allografts. In addition, expression of MHC class II antigens was induced on the bronchial epithelium and vascular endothelium. Induced expression of MHC class II antigens on the bronchial epithelium and vascular endothelium in rejecting lung allografts was found as early as two days after single-lung transplantation. The intensity of MHC class II antigen expression on bronchial epithelium and vascular endothelium in graft lungs increased with the progression of rejection response and directly correlated with the bronchoalveolar lavage fluid (BALF) levels of biochemical markers, as tumor necrosis factor alpha, gamma-interferon (IFN-gamma), interleukin 2 (IL-2) and soluble interleukin 2 receptor (SIL-2R). Abnormal expression of MHC class II antigens on bronchial epithelium and vascular endothelium and abnormal elevation of BALF levels of the cytokines in lung allografts could be prevented by cyclosporine (CsA) treatment. Our results suggested that MHC class II antigen expression could be induced on the bronchial epithelium and vascular endothelium of canine lung allografts during acute rejection. This abnormal expression of MHC class II antigens on bronchial epithelium and vascular endothelium of graft lungs may serve as a specific index for diagnosis of lung allograft rejection when infection as an inducing factor can be excluded. Furthermore, bronchial epithelium and vascular endothelium of lung allografts have become MHC class II-positive, and are likely to be the targets for low-grade rejection, resulting in the development of bronchiolitis obliterans and occlusive vascular disease in lung allografts.     

真皮下血管网岛状皮瓣抗菌力的实验研究

为研究真皮下血管网薄皮瓣用于感染创面的可行性，在家猪臀部两侧分别形成以旋髂深血管主干分支为蒂的传统岛状皮瓣和远侧５０％修薄的真皮下血管网岛状皮瓣。用细菌计数、吖啶橙荧光染色测定白细胞吞噬指数和白细胞内杀菌率，应用激光多普勒、墨汁灌注、透明标本等方法，对两种皮瓣的抗菌力作自身对照研究。结果表明，真皮下血管网岛状皮瓣的抗菌力明显降低，可能与皮瓣修薄后血供减少，白细胞功能相应降低有关。     

Effect of Yag-laser anterior capsulotomy on the biochemical content of aqueous humor

Elevation of prostaglandins and protein in the aqueous humor is an immediate response to Yag-laser anterior capsulotomy. There was a significant correlation between prostaglandins and thromboxane to the elevation of intraocular pressure. The elevation of protein concentration was proportional to the elevation of prostaglandin F1, but not to thromboxane. The biochemical changes in the aqueous humor were more severe as laser power was increased above 3 mj. While the role of prostaglandins in the elevation of intraocular pressure is uncertain, the present data recommend the selection of laser power below 3 mj to avoid pressure rise instead of inhibition of all prostaglandin synthesis by medication.     

纸质病案保存期限的思考

本文作者比较了不同时期的纸质病案的使用率,讨论了旧病案的缺点,如难于保存,占用空间及实用价值不大.作者提出了改进保存病案的办法.     

SOME ANATOMICAL DATA RELATED TO THE TRANSNASO- SPHENOIDAL RESECTION OF PITUITARY FOSSA TUMORS

Since the beginning of this century, trans- naso-sphenoidal resection of the pituitary fossa tumors has been widely used clinically. It has more merits than other operative approaches used before. In China it has been adopted by both ENT doctors and neurosurgeons since 1959.1 In order to afford some relevant anatomical data, we measured 137 adult sagittal plane skulls with distinct landmarks.     

An intracellular self protein synthesized in macrophages is presented but fails to induce tolerance

Mice deficient for the fifth component of murine complement (C5), unlike normal mice, do not possess the secreted form of C5 in their body fluids and can be readily immunized to serum-derived normal C5. Although macrophages from C5-deficient mice do not secrete C5, they synthesize the precursor form (pro-C5). Therefore contact of T cells with autologous pro-C5 presented by macrophages is theoretically possible. We show that macrophages from C5-deficient mice can indeed stimulate a class II restricted C5-specific T cell clone without addition of exogenous C5. Immunization of C5-deficient mice with autologous pro-C5 induces vigorous C5-specific T cell proliferation and pro-C5 is recognized by C5-specific T cells in vitro, demonstrating that this protein fails to induce tolerance under physiological conditions. Thus, intracellular pro-C5 is processed and presented by C5-deficient macrophages and can activate T cell clones in vitro, yet is neither immunogenic nor tolerogenic for T cells in vivo.