Increased mucosal inflammatory cytokines in children with Helicobacter pylori-associated gastritis

The concentrations of tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and IL-1-β in tissue homogenates of gastric mucosal biopsy specimens, and in gastric juice samples from Helicobacter pylori-positive and -negative children, were determined. The study population comprised 30 children with recurrent abdominal pain attending upper gastrointestinal endoscopy. Of these patients 18 were infected with H. pylori. Cytokine concentrations in gastric biopsy homogenate supernatants and in gastric juice were measured by enzyme-linked immunosorbent assay (ELISA). TNF-α levels in gastric juice and in gastric biopsy homogenate supernatants in patients with H. pylori-positive gastritis were found to be significantly higher than those in children without H. pylori infection. IL-6 levels were also higher in H. pylori -infected subjects, but the difference in IL-6 concentrations measured in gastric juice and biopsy homogenate supernatants did not reach statistical significance. IL-1-β concentrations in both specimens showed no significant difference between the two groups of children. It was suggested that increased levels of inflammatory cytokines, especially TNF-α and IL-6 generated locally within the gastric mucosa might be implicated in the pathogenesis of H. pylori-associated gastritis in childhood.     

人ERRα基因小分子干扰RNA慢病毒载体构建及鉴定

目的构建并鉴定靶向人ERRα基因的小分子干扰RNA的慢病毒载体。方法针对ERRαmRNA设计了4条si RNA,并构建pGCSIL-GFP-siERRα慢病毒质粒,PCR扩增阳性克隆并测序鉴定。用pGCSIL-GFP-siERRα、pHelp-er1.0和pHelper2.0质粒共转染293T细胞包装产生慢病毒,测定病毒滴度。将慢病毒干扰RNA及含有ERRα过表达载体共转染293T细胞,Western-blot检测ERRα表达,观察蛋白表达抑制效果。结果 PCR和测序结果与设计的干扰序列一致,病毒滴度达2×109TU/ml。转染细胞中ERRα蛋白表达显著降低。结论成功构建高表达、高效率的人ERRα基因小分子干扰RNA慢病毒载体,为进一步研究ERRα在细胞核内转导中的作用机制和靶向ERRα治疗奠定基础。     

Cytotoxic T-cell response to ectromelia virus-infected cells. Different H-2 requirements for triggering precursor T-cell induction or lysis by effector T cells defined by the BALB/c-H-2(db) mutation

The T(c)-cell response to ectromelia virus infection was studied in BALB/c-H-2(db) mice which carry a loss mutation in the H-2D region that results in the absence from cell surfaces of a molecule (D’) bearing certain public H-2 specificities. When infected, these mice showed a poor response of T(c) cells that recognize H-2D(d) plus virus-specific determinants on infected macrophage targets, but gave a normal response to H-2K d plus virus-specific antigens. However, their own infected macrophages do display wild-type antigenic patterns involving virus and H-2D(d) since they were killed as efficiently as wild-type (BALB/c,H- 2(d))-infected cells by T(c) cells specific only for H-2D(d) plus viral antigens. When tested in vitro, infected BALB/c-H-2(db) cells stimulated a poor T(c)-cell response to H-2D plus virus-specific antigens, but stimulated a normal response (in comparison with infected BALB/c macrophages) to H-2K(d) plus viral antigens. Uninfected BALB/c-H-2(db) cells stimulated a normal T(c)-cell response to minor H antigens or trinitrophenyl in association with H-2D(d), thus suggesting that the defective response to infection may reside in a failure of the relevant H-2D(d) antigens of mutant cells to physically associate with viral antigens. Close association of viral and H-2D-coded molecules was also suggested by ability of specific anti-H-2K or -H-2D to partially block T(c)-cell-mediated lysis of infected targets. These results were interpreted to mean that H-2Dd-dependent, virus- immune T(c) cells recognized an antigenic pattern consisting of virus- specific and H-2D(d) determinants with the latter borne on an H-2D molecule carrying serologically-defined H-2D(d) private specificities. A second H-2D(d)-coded molecule (D’) was not required for recognition and lysis by activated T(c) cells, but was apparently necessary for efficient stimulation of precursor T(c) cells, perhaps by promoting appropriate physical association of viral and H-2D(d) molecules.     

A portrait of interventional radiologists in the United States

OBJECTIVE: In recognition of the emergence of interventional radiology as an important "new component of...radiology," the objective of our study was to provide an extensive and detailed portrait of interventional radiologists, their professional activities, and the practices in which they work. MATERIALS AND METHODS: We tabulated data from the American College of Radiology's 2003 Survey of Radiologists, a stratified random-sample survey that oversampled interventionalists and achieved a 63% response rate with a total of 1,924 responses. Responses were weighted to make them representative of all radiologists in the United States. We compared information about interventionalists with that for other radiologists. RESULTS: Depending on the definition of who is an interventionalist, 8.5-11.5% of radiologists are interventionalists. By most definitions, only slightly under half of interventionalists spend 70% or more of their clinical work time performing interventional procedures. Interventionalists work, on average, 56-58 hr weekly, a few hours longer than other radiologists. The average interventionalist performs procedures in five of the seven categories of procedures into which we divided interventional radiology, compared with one or two categories for other radiologists. The average interventionalist performs procedures in five of the seven broad categories (such as MRI, CT, and nuclear medicine) into which we divided all of radiology, much the same breadth of practice as other subspecialists and also as nonsubspecialists. CONCLUSION: Interventionalists have become a sizable group within radiology. They are in some ways like other radiologists and in other ways different, but they do not spend as much of their time in their subspecialty as some assume and, overall, are not as different.