Biomimetic surface modification of poly(L-lactic acid) with chitosan and its effects on articular chondrocytes in vitro

The objective of this study was to investigate the efficiency of two treatments for poly(L-lactic acid) (PLLA) surface modification with chitosan, via entrapment and coupling by using 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide and N-hydroxysuccinimide. The properties of original PLLA films, chitosan-entrapped and coupled PLLA films were investigated by water contact angle measurement and electron spectroscopy for chemical analysis (ESCA). The contact angle indicated the change in hydrophilicity and the ESCA data suggested that the modified PLLA films became enriched with nitrogen atoms. The cytocompatibility of modified PLLA films might be improved. Therefore, the attachment and proliferation of bovine articular chondrocyte seeded on modified PLLA films and control one were examined. A whole cell enzyme-linked immunosorbent assay (Cell ELISA) that detects the BrdU incorporation during DNA synthesis and collagen type II secretion was applied to evaluate the chondrocytes on different PLLA films and tissue culture plates. Cell viability was estimated by the MTT assay and cell function were assessed by measuring sulfated glycosaminoglycan secreted by chondrocytes. These results implied that chitosan used to modify PLLA surface through entrapment and coupling could enhance the chondrocyte adhesion, proliferation and function.     

The clinical pathology of severe acute respiratory syndrome (SARS): a report from China

In order to investigate the clinical pathology of severe acute respiratory syndrome (SARS), the autopsies of three patients who died from SARS in Nan Fang Hospital Guangdong, China were studied retrospectively. Routine haematoxylin and eosin (H&E) staining was used to study all of the tissues from the three cases. The lung tissue specimens were studied further with Macchiavello staining, viral inclusion body staining, reticulin staining, PAS staining, immunohistochemistry, ultrathin sectioning and staining, light microscopy, and transmission electron microscopy. The first symptom was hyperpyrexia in all three cases, followed by progressive dyspnoea and lung field shadowing. The pulmonary lesions included bilateral extensive consolidation, localized haemorrhage and necrosis, desquamative pulmonary alveolitis and bronchitis, proliferation and desquamation of alveolar epithelial cells, exudation of protein and monocytes, lymphocytes and plasma cells in alveoli, hyaline membrane formation, and viral inclusion bodies in alveolar epithelial cells. There was also massive necrosis of splenic lymphoid tissue and localized necrosis in lymph nodes. Systemic vasculitis included oedema, localized fibrinoid necrosis, and infiltration of monocytes, lymphocytes, and plasma cells into vessel walls in the heart, lung, liver, kidney, adrenal gland, and the stroma of striated muscles. Thrombosis was present in small veins. Systemic toxic changes included degeneration and necrosis of the parenchyma cells in the lung, liver, kidney, heart, and adrenal gland. Electron microscopy demonstrated clusters of viral particles, consistent with coronavirus, in lung tissue. SARS is a systemic disease that injures many organs. The lungs, immune organs, and systemic small vessels are the main targets of virus attack, so that extensive consolidation of the lung, diffuse alveolar damage with hyaline membrane formation, respiratory distress, and decreased immune function are the main causes of death.     

Loss of imprinting of IGF2 and H19 in osteosarcoma is accompanied by reciprocal methylation changes of a CTCF-binding site

The adjacent insulin-like growth factor 2 (IGF2) and H19 genes are imprinted in most normal human tissues, but imprinting is often lost in tumors. The mechanisms involved in maintenance of imprinting (MOI) and loss of imprinting (LOI) are unresolved. We show here that osteosarcoma (OS) tumors with IGF2/H19 MOI exhibit allele-specific differential methylation of a CTCF-binding site upstream of H19. LOI of IGF2 or H19 in OS occurs in a mutually exclusive manner, and occurs with monoallelic expression of the other gene. Bisulfite sequencing reveals IGF2 LOI occurs with biallelic CpG methylation of the CTCF-binding site, while H19 LOI occurs with biallelic hypomethylation of this site. Our data demonstrate that IGF2 LOI and H19 LOI are accompanied by reciprocal methylation changes at a critical CTCF-binding site. We propose a model in which incomplete gain or loss of methylation at this CTCF-binding site during tumorigenesis explains the complex and often conflicting expression patterns of IGF2 and H19 in tumors.     

Role for macrophage migration inhibitory factor in acute respiratory distress syndrome

The critical role of macrophage migration inhibitory factor (MIF) in mediating inflammatory lung injury in acute respiratory distress syndrome (ARDS) has been raised recently. The present study has identified enhanced MIF protein expression in alveolar capillary endothelium and infiltrating macrophages in lung tissues from ARDS patients. The possibility that MIF up-regulates its synthesis in an autocrine fashion in ARDS was tested using cultured endothelial cells stimulated with MIF and a murine model of lipopolysaccharide (LPS)-induced acute lung injury. MIF induced significant MIF and tumour necrosis factor (TNF)-alpha synthesis in cultured endothelial cells and the effect was blocked by neutralizing anti-MIF antibody. A similar blocking effect was observed when MIF-stimulated endothelial cells were pretreated with neutralizing anti-TNF-alpha antibody or glucocorticoid, supporting the notion that MIF induced TNF-alpha production via an amplifying pro-inflammatory loop. Treatment with anti-MIF or glucocorticoid effectively attenuated pulmonary pathology and the synthesis of MIF or TNF-alpha in mice with LPS-induced acute lung injury. Mildly augmented expression of aquaporin 1 (AQP1) was also detected in alveolar capillary endothelium in ARDS. In vitro studies revealed that both MIF and TNF-alpha induced a small increase of AQP1 synthesis in cultured endothelial cells. These findings suggest that MIF plays a crucial pathological role leading to alveolar inflammation in ARDS. Anti-MIF and early glucocorticoid therapy may represent a novel therapeutic approach for reducing alveolar inflammation in ARDS.     

Enhancement of mucosal immune responses by chimeric influenza HA/SHIV virus-like particles

To enhance mucosal immune responses using simian/human immunodeficiency virus-like particles (SHIV VLPs), we have produced novel phenotypically mixed chimeric influenza HA/SHIV VLPs and used them to immunize C57BL/6J mice intranasally. Antibody and cytotoxic T-cell (CTL) responses as well as cytokine production in both systemic and mucosal sites were compared after immunization with SHIV VLPs or chimeric HA/SHIV VLPs. By using enzyme-linked immunosorbent assay (ELISA), the levels of serum IgG and mucosal IgA to the HIV envelope protein (Env) were found to be highest in the group immunized with chimeric HA/SHIV VLPs. Furthermore, the highest titer of serum neutralizing antibody against HIV Env was found with the group immunized with chimeric HA/SHIV VLPs. Analysis of the IgG1/IgG2a ratio indicated that a T(H)1-oriented immune response resulted from these VLP immunizations. HA/SHIV VLP-immunized mice also showed significantly higher CTL responses than those observed in SHIV VLP-immunized mice. Moreover, a MHC class I restricted T-cell activation ELISPOT assay showed a mixed type of T(H)1/T(H)2 cytokines in the HA/SHIV VLP-immunized mice, indicating that the chimeric VLPs can enhance both humoral and cellular immune responses to the HIV Env protein at multiple mucosal and systemic sites. The results indicate that incorporation of influenza HA into heterotypic VLPs may be highly effective for targeting vaccines to mucosal surfaces.     

悬雍垂腭咽成形术62例临床分析

目的 探讨对阻塞性睡眠呼吸暂停综合征（OSAS）患者行悬雍垂腭咽成形术（UPPP）的疗效、适应症的选择以及并发症的防治。方法 利用悬雍垂腭成形术对62例OSAS进行手术治疗。结果 本组62例UPPP经术后的观察症状明显改善者达50%，总有效率90%以上。结果 悬雍垂腭咽成形术对于OSAS的治疗有一定的效果，但要注意适应证的选择，术前术后的治疗。     

Is the genus<Emphasis Type="Italic"> Digramma</Emphasis> synonymous to the genus<Emphasis Type="Italic"> Ligula</Emphasis> (Cestoda: Pseudophyllidea)?

The genus Digramma (Cestoda: Pseudophyllidea) described by Cholodkovsky in 1915 differs from the genus Ligula only by the number of the reproductive organs per proglottis. However, the occurrence of transitional forms in Digramma raises much confusion concerning its generic validity. In the present study, cestodes previously designated as Digramma and Ligula were collected from lakes in the lower and middle reaches of the Yangtze River, and also from Qinghai Lake on Qingzang plateau, China. The entire internal transcribed spacer of the ribosomal DNA (ITS rDNA) and 5' end of 28S rDNA were compared between the Digramma and Ligula specimens. The low level of nucleotide variation between the two genera may imply that cestodes in the genus Digramma are paraphyletic to the Ligula genus, and Digramma is a synonym of Ligula. However, whether previously identified Digramma cestodes represent different species in the genus Ligula requires further investigation.     

在中国发现普马拉型汉坦病毒

目的：确定我国是否存在普马拉（Puumala)病毒。方法：从我国东北地区棕背Bing肺标本中用RT－PCR扩增汉坦病毒S片段基因序列，对所扩增序列进行核苷酸序列测定和分析。结果：从我国东北地区棕背Bing肺标本中扩增出长度为926碱基对的cDNA片段，核苷酸序列测定证实为普马拉病毒S片段序列。与不同型别汉坦病毒代表株进行比较表明，此次发现为新的普马拉病毒株，系统发生分析结果表明，此次发现的病毒与普马拉病毒P360、K27、CG－820、CG－17株种系相近，同源性达到99％以上。结论：我国存在普马拉病毒，我国新发现的普马拉病毒核苷酸序列和俄罗斯远东地区普马拉病毒接近。     

先天性髋脱位与HOXB9基因或COL1A1基因传递不平衡研究

目的 探讨先天性髋脱位(congenital dislocation of the hip，CDH)与HOXB9基因或COL1Al基因是否存在相关性。方法 在胚胎肢体发育调控相关的HOXB9基因和COL1A1基因共同所在的染色体区域17q21内选择微卫星DNA标记D17S1820，应用聚合醇链反应及变性聚丙烯酰胺凝胶电泳技术，对101个CDH核心家系的303名成员进行基因型分析，并进行传递不平衡检验(transmission disequilibrium test,TDT)。结果 在D17S1820多态性标记位点上共检测到12个等位基因。TDT分析显示，CDH与D17S1820遗传标记位点的第4个等位基因存在传递不平衡(x^2＝6．025，P＝0．014)。结论 CDH与HOXB9基因和COLlAl基因共同所在的染色体区域17q21有关联，HOXB9基因和(或)COLlAl基因可能是CDH的易感基因。