椎板切除；脊柱；硬膜；粘连；预防

目的观察应用可吸收医用膜预防椎板切除术后硬膜外粘连的效果.方法在14例患者行椎板切除减压后,于硬膜外放置可吸收医用膜,并定期随访观察.结果全部患者的切口均一期愈合,无不良反应,防粘连效果优良.结论可吸收医用膜是一种良好的预防硬膜外粘连的材料.     

Down-regulation of LFA-1-mediated T cell adhesion induced by the HIV envelope glycoprotein gp160 requires phosphatidylinositol-3-kinase activity

Human immunodeficiency virus binds to CD4⁺ T lymphocyte by the interaction, in part, between its gp120 envelope glycoprotein and the CD4 molecule. We and others have reported that the lipid kinase phosphatidylinositol-3-kinase (PI3-kinase) is associated with the CD4-p56^lck complex and can be activated by various CD4 ligands. In a previous report we showed that the gp160 envelope down-regulates lymphocyte function-associated antigen-1 (LFA-1)-dependent adhesion between CD4⁺ T cells and B cells. This down-regulation was shown to be p56^lck-dependent. Here we investigate the role of PI3-kinase in the inhibition of adhesion induced by gp160 binding to CD4. We found that gp160 activates the PI3-kinase of HUT78 CD4⁺ T cell lines in a way dependent on CD4-p56^lck association, since no activation was detected when the interaction between CD4 and p56^lck was disrupted. It was also shown, using different inhibitors of the PI3-kinase (wortmannin, Ly294002 and antisense oligonucleotides), that this lipid kinase was necessary for the down-regulation of LFA-1-mediated adhesion induced by gp160. These results strongly suggest that PI3-kinase activation induced by gp160 leads to down-regulation of LFA-1-mediated T cell adhesion to B cells. Inhibition by gp160 of cytoskeleton rearrangement-dependent, anti-CD3-mediated T cell adhesion to B cells was blocked by neutralization of PI3-kinase activity, while inhibition of cytoskeleton rearrangement-independent, Mg²⁺-induced T cell adhesion was not. These results emphasize the role of PI3-kinase in the regulation of cytoskeleton structure. It is proposed that gp160 activates both p56^lck and PI3-kinase which lead to a cytoskeleton organization unfavorable for LFA-1 function.     

粘连性肠梗阻55例临床分析

目的：提高粘连性肠梗阻的治疗效果。方法：回顾性分析我院收治的粘连性肠梗阻55例,男31例,女24例,年龄12-76岁,平均46.9岁,单纯性粘连性肠梗阻30例,绞窄性肠梗阻25例。经中西医结合治疗及手术治疗。结果：全部病例治愈出院,结论：治疗粘连性肠梗阻重要的是区别单纯性还是绞窄性,对单纯性肠梗阻。首先应考虑非手术治疗,但必须严密观察,并结合X线或B超动态观察,对治疗12-24h无好转或疑有绞窄者及早手术,这样可避免过分依赖非手术治疗而使病情恶化造成不良后果,对绞窄性肠梗阻阳应快速术前准备,尽早进行手术,争取在肠坏死之前解除梗阻,从而降低死亡率。     

Experimental studies of membrane tethers formed from human neutrophils

Membrane tethers (thin, cylindrical pieces of membrane) have been implicated in the rolling of neutrophils along the endothelium. In our studies, these tethers were formed from passive, stimulated (0.1 M fMLP), and osmotically swollen (170–180 mOsm) human neutrophils; as well as neutrophils treated with 0.3 M latrunculin A to disrupt the cytoskeleton. This tether formation was accomplished by micropipette suction of latex beads coated with antibodies to proteins on the neutrophil membrane surface. From plots of force versus velocity for the tether formation process, we calculated adhesion energies per unit area of the lipid membrane to the cytoskeleton and the viscous resistance (effective viscosity) that occurs during the formation of these tethers at finite velocity. Most of the properties of the neutrophil were altered once it had been treated as described above. We were also able to show mechanical reversibility of membrane tethers, as well as an unexpected formation rate at high tether forces. Since membrane tethers have been implicated in the rolling of neutrophils, then the changes in tether formation may ultimately alter how these cells roll. © 2002 Biomedical Engineering Society. PAC2002: 8716Dg     

年龄对健康人红细胞与内皮细胞粘附的影响

本文用流槽系统，定量地研究年龄对健康人红细胞与培养的人脐静脉内皮细胞粘附的影响。在本研究所选用的两个年龄阶段，其结果显示：①红细胞自身特性的改变对粘附的数目没有明显的影响，但随着年龄的增加粘附的强度增大；②在自体血浆存在时，随着年龄的增加红细胞与内皮细胞的粘附增强。这可能与心脑血管病如心肌梗塞、脑血栓形成等多发生在４０岁以上的中老年人有关。     

The effect of the selectin binding polysaccharide fucoidin on eosinophil recruitment in vivo

1. In order to accumulate at sites of inflammation, leukocytes initially roll on endothelial cells of post-capillary venules before becoming firmly attached. This process of rolling is mediated by selectins which bind to carbohydrate counter-ligands present on the surface of both leukocytes and endothelial cells. The polysaccharide fucoidin has been previously shown to inhibit leukocyte rolling in the mesenteric circulation and to reduce neutrophil accumulation in the skin and meninges in experimental inflammation.
2. In the present study we have assessed the effects of fucoidin on eosinophil function in vitro and eosinophil accumulation at sites of inflammation in guinea-pig skin.
3. At concentrations of up to 1200 μg ml⁻¹, fucoidin inhibited phorbol myristate acetate (PMA)-induced eosinophil homotypic aggregation by up to 60% but had no inhibitory effect on PMA-induced eosinophil adhesion to serum-coated plates.
4. Fucoidin effectively reduced the binding of the anti-L-selectin mAb MEL-14 to guinea-pig eosinophils. Binding of a P-selectin-IgG chimera to eosinophils was also partially inhibited by fucoidin, but binding of an anti-CD18 or an anti-VLA-4 mAb were unaffected.
5. When given systemically to guinea-pigs, fucoidin suppressed ¹¹¹In-labelled eosinophil recruitment to sites of allergic inflammation. ¹¹¹In-labelled eosinophil accumulation induced by platelet-activating factor (PAF) and zymosan-activated plasma (as a source of C5a des Arg) was also inhibited.
6. These results demonstrate a role for fucoidin-sensitive selectins in mediating eosinophil recruitment in vivo.

     

An immunohistochemical study of immunological phenomena in minor salivary glands in patients with Sjögren's syndrome

Using different monoclonal antibodies, we performed an immunofluorescent technique on labial salivary glands in order to investigate the immunological phenomena involved in Sjögren's syndrome (SS). An aberrant expression of HLA-DR molecules was detected on cytoplasm of epithelial labial salivary cells in 9 out of 19 (47%) patients, with SS. No such expression was found in 8 patients without SS or in 3 normal controls. HLA-DQ molecules were demonstrated also in two out of ten SS patients without HLA-DR. A lymphocytic infiltration was not correlated with the expression of class II molecules. T cells bearing receptors were not detected. The intracellular adhesion molecules (ICAM-1) and lymphocyte function associated antigen-1 (LFA-1) were not found on epithelial glandular salivary cells of patients and controls. In conclusion, these data suggested that the absence of ICAM-1 and LFA-1 in salivary cells and the absence of infiltrating T cells bearing receptors exclude their immunopathogenetic role in SS; moreover, these data demonstrated that the aberrant expression of HLA class II molecules on epithelial salivary cells of patients with SS is not a phenomenon correlated with the lymphocytic infiltration.     

An immunohistochemical and immunoelectron microscopic study of adhesion molecules in synovial pannus formation in rheumatoid arthritis

To investigate the mechanism of synovial pannus formation in rheumatoid arthritis, immunohistochemical and immunoelectron microscopic studies with monoclonal antibodies against the adhesion molecules, CD54 (ICAM-1), CD 11a (LFA-1), CDw49a (VLA-1), CDw49b (VLA-2), CDw49c (VLA-3), Cdw49d (VLA-4) and CDw49e (VLA-5), were carried out to determine the pattern of distribution of these molecules at the rheumatoid synovial cartilage junction. Treatment with anti-ICAM-1 resulted in membrane staining of most of the macrophages and fibroblasts infiltrating the synovial tissue and bordering the pannus-cartilage junction, suggesting the possibility that ICAM-1 may function to facilitate the adhesion of synovial type A cells bearing ICAM-1 to type B cells of the pannus. ICAM-1-positive macrophages and fibroblasts were often found to be in contact with lymphoid cells, suggesting also that a cellular immune reaction occurs in the formation of the pannus. In addition, VLA-3, VLA-4 and, particularly, VLA-5 were the predominant1 integrins expressed by rheumatoid synovial pannus. Since these three integrins all function as fibronectin receptors, it is possible that the fibronectin-rich environment of the rheumatoid cartilage surface effectively traps pannus cells expressing high levels of these molecules. The VLA-5 molecule was found in a pericellular and interterritorial matrix distribution in the present study, strongly suggesting that a recepfor-ligand interaction between VLA-5 and cartilage matrix may occur at the early stage of pannus formation. Furthermore, an increase in1 integrin may be necessary for the growth of the pannus and also for the upregulation of the VLA molecules, leading secondarily to increased attachment.     

Tubular and interstitial factors in the progression of glomerulonephritis

All recent studies of the outcome of different forms of progressive glomerulonephritis concur that a major factor, apparently determining outcome, is the presence and severity of tubulointerstitial changes, and not the degree of glomerular alteration. Moreover, at the time of biopsy, tubulointerstitial changes correlate much better with the glomerular filtration rate. These at first surprising findings are not only useful clinically, but should make us think about our models of how progression takes place in so-called glomerular nephritides. In fact, a major tubulointerstitial infiltrate of immune-competent cells is present in all forms of progressive glomerulonephritis, and again correlates with outcome. In addition, it is now clear the tubular epithelium is capable of synthesising and secreting a number of factors important in fibrogenesis, and of displaying major histocompatibility complex class II antigens and leucocyte-adhesion molecules. Tubular cells could thus present peptides to T helper cells and amplify, or maybe even initiate, immune reactions. Finally, fibrogenesis within the kidney is at last being studied, long after studies have been performed on liver and lung. In the past, too much attention has been paid to reversible inflammation and not enough to irreversible cirrhosis of the kidney.Abbreviations used Ig immunoglobulin, e. g. IgA, IgG, IgM etc. - TBM tubular basement membrane - GBM glomerular basement membrane - WHO World Health Organization - MHC major histocompatibility complex - CD cluster determinant - NK natural killer - IL-1 interleukin-1 - IL-2 interleukin-2 - TNF- tumour necrosis factor alpha - ADCC antibody-dependent complement mediated cytolysis - ACE angiotensin-converting enzyme - m macrophage - ICAM-1 intercellular adhesion molecule-1 - ELAM-1 endothelial leucocyte adhesion molecule-1 - VCAM-1 vascular cell adhesion molecule-1 - LFA leucocyte function associated molecule, e. g. LFA-1, LFA-3 - C complement e. g. C3=third component of complement, etc. - TGF- transforming growth factor beta - TGF- transforming growth factor alpha - PDGF platelet derived growth factor - PAS periodic acid Schiff - TCR T cell receptor - PTEC proximal tubular epithelial cell - GM-CSF granulocyte colony stimulating factor - M-CSF monocyte colony stimulating factor - FGF fibroblast growth factor     

Evaluation of recombinant tissue-type plasminogen activator in adhesion prevention and neoangiogenesis in a rat experimental adhesion model

This study was designed to test the effect of recombinant tissue-type plasminogen activator (rt-PA) in reducing adhesion formation and to observe its influence on peritoneal neoangiogenesis. In 20 Wistar rats, a 4-cm midline incision was made, and a square piece of Silastic, 0.5×0.5 cm and 0.2 mm thick, was fixed on the right side of the peritoneum with two separate angular stitches of nylon 9/O. The rats were randomized into two groups of 10 animals each. In the first group we injected 0.2 mg of rt-PA intraperitoneally three times a day. The second group of 10 rats was used as a control group. Each rat was reoperated on day 12. Intraperitoneal injection of rt-PA seemed not to affect adhesion formation, as a 100% adhesion rate was reported in the treated group compared with 90% of the control group. The results showed that rt-PA acts on the neoangiogenesis involved in postsurgical adhesion formation by reducing the size and length of the vessels. This action seems to slow down peritoneal healing with a negative effect on postsurgical adhesion prevention.