479 research outputs found
An Insufficient Preoperative Diagnosis of Borrmann Type 4 Gastric Cancer in Spite of EMR
Borrmann type 4 gastric cancers are notorious for the difficulty of finding cancer cells in the biopsy samples obtained from gastrofiberscopy. It is important to obtain the biopsy results for making surgical decisions. In cases with Borrmann type 4 gastric cancer, even though the radiological findings (such as an upper gastrointestinal series, abdominal computed tomography and positron emission tomography/computed tomography) or the macroscopic findings of a gastrofiberscopy examination imply a high suspicion of cancer, there can be difficulty in getting the definite pathologic results despite multiple biopsies. In these cases, we have performed endoscopic mucosal resection under gastrofiberscopy as an alternative to simple biopsies. Here we report on a case in which no cancer cells were found even in the endoscopic mucosal resection specimen, but the radiologic evidence and clinical findings were highly suspicious for gastric cancer. The patient finally underwent total gastrectomy with lymph node resection, and she was pathologically diagnosed as having stage IV gastric cancer postoperatively
Resistin enhances the expansion of regulatory T cells through modulation of dendritic cells
<p>Abstract</p> <p>Background</p> <p>Resistin, a member of adipokine family, is known to be involved in the modulation of immune responses including inflammatory activity. Interestingly, resistin is secreted by adipocytes in mice and rats whereas it is secreted by leukocytes in humans. However, the mechanism behind the effect of resistin on the expansion of regulatory T cells (Tregs) remains poorly understood. Therefore, we examined regulatory effect of resistin on the induction and cellular modification of Tregs.</p> <p>Results</p> <p>Both protein and mRNA expression of <it>FoxP3</it>, a representative marker of Tregs, increased in a dose-dependent manner when peripheral blood mononuclear cells were treated with resistin. At the same time, resistin had no direct effect on the induction of <it>FoxP3 </it>in CD4<sup>+ </sup>T cells, suggesting an indirect role through other cells type(s). Since DCs are an important player in the differentiation of T cells, we focused on the role of DCs in the modulation of Tregs by resistin. Resistin suppressed the expression of interferon regulatory factor (IRF)-1 and its target cytokines, IL-6, IL-23p19 and IL-12p40, in DCs. Furthermore, <it>FoxP3 </it>expression is increased in CD4<sup>+ </sup>T cells when co-cultured with DCs and concomitantly treated with resistin.</p> <p>Conclusion</p> <p>Our results suggest that resistin induces expansion of functional Tregs only when co-cultured with DCs.</p
A New Steroidal Saponin from the Tubers of Ophiopogon japonicus and Its Protective Effect Against Cisplatin-Induced Renal Cell Toxicity
A new furostanol saponin, ophiopogonin T, was isolated from the tubers of Ophiopogon japonicus. Its structure was established by extensive spectroscopic techniques including 1D ( 1 H and 13 C) and 2D nuclear magnetic resonance (NMR) experiments (correlation spectroscopy (COSY), heteronuclear single quantum coherence (HSQC), heteronuclear multiple bond correlation (HMBC) and nuclear Overhauser effect spectroscopy (NOESY)), high-resolution electrospray ionization mass spectrometry (ESIMS), and chemical methods. Using cell-based assays, this compound was evaluated for its cytotoxic effect on cancer cell lines and its protective effect against anticancer drug-induced nephrotoxicity. Cisplatin-induced cytotoxicity in porcine kidney (LLC-PK1) cells was significantly reduced upon treatment with ophiopogonin T, without affecting human hepatoma (HepG2) cancer cell proliferation or tube formation in human umbilical vein endothelial cells (HUVECs). These results collectively reflect the beneficial effect of ophiopogonin T on the side effects of cisplatin
Prognostic Factors of Response to Laparoscopic Splenectomy in Patients with Idiopathic Thrombocytopenic Purpura
Laparoscopic splenectomy (LS) has become the treatment of choice for patients with idiopathic thrombocytopenic purpura (ITP) who do not respond to medical treatment. The aim of this study was to identify factors predictive of outcome after LS for ITP. From May 1997 to December 2002, we performed 30 LS on patients with ITP. A positive response was defined as a postoperative platelet count greater than 50,000/µL and no requirement for maintenance therapy. Chi-square testing was performed to determine the predictive effects of the following variables: age, sex, preoperative response to steroids or immunoglobulin, duration of disease, antiplatelet antibody, platelet associated antibody, and antinuclear antibody. LS was successfully performed in all patients. For a mean follow-up interval of 24.3 months, response to LS was 73.3%. Splenectomy for steroid nonresponders resulted in an inferior complete response rate (10 of 18, 55.6%) as compared with those that experienced relapse after steroid treatment (11 of 12, 91.7%) (p=0.042). The other significant predictor of outcome by univariate analysis was the time between diagnosis and surgery (p=0.049). The other variables showed no significant correlation with successful splenectomy. We conclude that LS can be performed safely with a satisfactory remission rate in patients with ITP who do not respond to medical treatment, and that the factors most frequently associated with surgical success are a response to steroid and disease duration
Genetic diagnosis of inborn errors of immunity using clinical exome sequencing
Inborn errors of immunity (IEI) include a variety of heterogeneous genetic disorders in which defects in the immune system lead to an increased susceptibility to infections and other complications. Accurate, prompt diagnosis of IEI is crucial for treatment plan and prognostication. In this study, clinical utility of clinical exome sequencing (CES) for diagnosis of IEI was evaluated. For 37 Korean patients with suspected symptoms, signs, or laboratory abnormalities associated with IEI, CES that covers 4,894 genes including genes related to IEI was performed. Their clinical diagnosis, clinical characteristics, family history of infection, and laboratory results, as well as detected variants, were reviewed. With CES, genetic diagnosis of IEI was made in 15 out of 37 patients (40.5%). Seventeen pathogenic variants were detected from IEI-related genes, BTK, UNC13D, STAT3, IL2RG, IL10RA, NRAS, SH2D1A, GATA2, TET2, PRF1, and UBA1, of which four variants were previously unreported. Among them, somatic causative variants were identified from GATA2, TET2, and UBA1. In addition, we identified two patients incidentally diagnosed IEI by CES, which was performed to diagnose other diseases of patients with unrecognized IEI. Taken together, these results demonstrate the utility of CES for the diagnosis of IEI, which contributes to accurate diagnosis and proper treatments
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