No abstract available.
Airports* ; Disasters*

Neuroenteric cyst derives from endodermal tissue displaced dorsally into the spinal canal ventral to the neural plaque through the interposed mesodermal layer that forms the vertebral bodies, embryologically. It is located along the alimentary canal, or ventral to the spinal cord in the cervical, thoracic area, or at the cervicothoracic junction within the boundaries of C3 above and T7 below and lies in an intramedullary or intradural extramedullary location in most patients. To date, retroperitoneal neuroenteric cyst has been described in only few cases. We report a case of asymptomatic retroperitoneal neuroenteric cyst in a 28-year-old man with a brief review of literatures, which found incidentally on health care center.
Adult ; Delivery of Health Care ; Endoderm ; Humans ; Mesoderm ; Neural Tube Defects* ; Spinal Canal ; Spinal Cord

OBJECTIVES:Nitric Oxide(NO) is a toxic, inorganic, gaseous free radical produced during the metabolism of L-Arginine by NO synthase(NOS). It has been implicated in a rapidly growing number of physiological and pathophysiological processes such as cytotoxic effects against microbes and tumor cells, blood vessel dilation and neurotransmitter. Recently there is growing evidence implicating NO in immune regulation, inflammation, autoimmunity, and arthritis. We performed this study to determine a role for nitric oxide in inflammatory arthritis especially rheumatoid arthritis(RA). METHODS: We measured (1) the concentrations of nitrite, a breakdown product of nitric oxide, in serum and synovial fluid from patients with RA and osteoarthritis(OA) and in the serum of controls (2) the concentrations of nitrite in the supernatant of cultured synovial tissue with RA and OA and (3) determined whether human chondrocytes and synoviocytes can synthesize nitric oxide and if so, how production is regulated by cytokines and antirheumatic drugs. RESULTS: 1) Serum nitrite concentrations in patients with RA and OA were higher than in controls. In both disease groups synovial fluid nitrite was higher than serum nitrite. Serum and synovial fluid nitrite concenrations in RA were higher than those in OA. However, those findings are not statistically significant. 2) Although these findings are not statistically significant, the concentration of nitrite in the supernatant of cultured synavial tissue with RA was higher than that in OA. 3) IL-1beta and TNF-alpah induced the biosynthesis of NO by chondrocytes and synoviocytes. IGF-1 and TGF-beta failed to provoke the production of NO. The biosynthesis of NO required an induction period of approximately 6 hours and was inhibited by L-NMMA and cycloheximide. Dexamethasone, indomethacin, gold sodium thiomalate and methotrexate had no effect on the induction of NO biosynthesis. CONCLUSION: These results suggest a role for nitric oxide as an inflommatory mediator in inflammatory arthritis.
Antirheumatic Agents ; Arginine ; Arthritis* ; Arthritis, Rheumatoid ; Autoimmunity ; Blood Cells ; Chondrocytes ; Cycloheximide ; Cytokines ; Dexamethasone ; Gold Sodium Thiomalate ; Humans ; Indomethacin ; Inflammation ; Insulin-Like Growth Factor I ; Metabolism ; Methotrexate ; Neurotransmitter Agents ; Nitric Oxide ; omega-N-Methylarginine ; Synovial Fluid ; Transforming Growth Factor beta

Lymphangiomatosis is a very rare and slow-growing benign tumor generally accepted to be the result of a congenital malformation of the lymphatic system. It is most commonly found in the neck, axilla and less commonly retroperitoneum, mediastinum, mesentery, omentum, pelvis, bone, skin, scrotum, and spleen. We present a patient who had systemic lymphangiomatosis with splenic involvement. She was presented with the cystic neck mass suspected to be a cystic hygroma during the first decade. She complained of the mass on left upper quadrant of abdomen at the age of 28. Under full investigations, we had diagnosed the lymphangiomatosis involving spleen and right adrenal gland, and splenectomy was done. We present a case of systemic lymphangiomatosis with emphasis on diagnosis, management, and prognosis.
Abdomen ; Adrenal Glands ; Axilla ; Diagnosis ; Humans ; Lymphangioma, Cystic ; Lymphatic System ; Mediastinum ; Mesentery ; Neck ; Omentum ; Pelvis ; Prognosis ; Scrotum ; Skin ; Spleen ; Splenectomy

Neoadjuvant imatinib therapy used to treat locally advanced or metastatic gastrointestinal stromal tumors (GI ST) remains under active investigation. We studied three cases of locally advanced gastric GISTs treated with imatinib on a neoadjuvant basis, followed by a complete surgical resection. Three patients were diagnosed with locally advanced unresectable GIST of the stomach and were started on imatinib 400 mg/day. After the imatinib treatment, partial responses were achieved in all patients and the tumors were considered resectable. Surgical resection was done after 7, 11, and 8 months of imatinib therapy, respectively. In one case, a metastatic liver lesion was detected during the imatinib treatment using computed tomography scans, so the imatinib therapy was maintained for 11 months postoperatively. In the other two patients without distant metastasis, imatinib treatment was not restarted after surgery. Mutational analysis revealed a mutation in exon 11 of the c-kit gene in two patients, and wild-type c-kit and PDGFRA in one patient. During pathology review of all three cases, we noted several features common to imatinib treatment. There was no evidence of tumor recurrence in all three patients at respective follow-up visits of 22, 15, and 7 months. These results suggest that the neoadjuvant imatinib therapy is a potentially curative approach for selected patients with locally advanced GIST.
Exons ; Follow-Up Studies ; Gastrointestinal Stromal Tumors* ; Humans ; Liver ; Neoadjuvant Therapy ; Neoplasm Metastasis ; Pathology ; Recurrence ; Stomach* ; Imatinib Mesylate

PURPOSE: Fluoropyrimidine (F) and platinum (P) combination chemotherapy has been widely used for the first line treatment of advanced gastric cancer (AGC). Docetaxel (D) has shown promising activity in this disease. The present study retrospectively investigated the efficacy of D monotherapy as salvage chemotherapy for AGC that is failing F and P combination chemotherapy. MATERIALS AND METHODS: A total of 34 patients, fitting the eligibility criteria, were included in this study. D was administered at a dose of 75 mg/m2 IV every 3 weeks, with dexamethasone prophylaxis. Twenty-nine patients had measurable lesions. The median treatment-free interval was 38.5 days, and 91.2% of patients had progressed within 4 months of withdrawal of the first line chemotherapy. RESULTS: A total of 133 cycles of D were administered, with a median of 3.5 (1~8) cycles. From an intention-to-treat analysis, 6 patients achieved partial responses (PR), with a response rate of 20.7% (95% CI, 6.0~35.4). The duration of objective PRs in these six were 2.3+, 2.5+, 2.9, 3.0+, 6.2 and 6.8 months, respectively. Six patients showed a stable disease, but 15 showed progression. The median time to progression was 4.2 months (95% CI, 2.8~5.5), with a median overall survival since the start of D monotherapy of 8.4 months (95% CI, 5.5~11.3). Grade 3/4 neutropenia and febrile neutropenia occurred in 12.9% of patients and 3.1% of cycles. The incidence of grade 3 or worse non-hematological toxicities were as follows; peripheral sensory neuropathy 9.7%, asthenia 3.2% and allergic reaction 2.7%. CONCLUSION: Docetaxel, 75 mg/m2, is active in AGC as second-line chemotherapy after failure of prior exposure to the F and P combination chemotherapy, with a favorable toxicity profile.
Asthenia ; Dexamethasone ; Drug Therapy* ; Drug Therapy, Combination* ; Febrile Neutropenia ; Humans ; Hypersensitivity ; Incidence ; Neutropenia ; Platinum* ; Retrospective Studies ; Salvage Therapy ; Stomach Neoplasms*

OBJECTIVES: Polymerase chain reaction (PCR) technology was eamine synovial fluid and peripheral T cells in patients with rheumatoid arthritis(RA) to determine the preferential usage of the T cell receptor(TCR) variable region(V) gene. METHODS: Oligonucleotide primers specific for individual TCR Vfi gene families were used to amplify the TCR gene products in a semiquantitative assay of their relative utilization in unselected T cell populations. RESULTS: The result of Vfi utilization was generally heterogenous, similar with previous reports. However, the mean expression of Vfi16 and Vfi18 in RA was more preferentially utilized compared to normal donors. The usage of Vfi in peripheral blood from 3 patients with RA demonstrated restrictions in Vfi16, Vfi 20 and Vfi18 genes, respectively. Analyses of synovial fluid resulted in restriction in Vfi12, Vfi20 and Vfi20, respectively. Although there was no significant pattern of skewed Vfi gene mean usage when comparing the synovial fluids with the peripheral blood T cells from RA patients, there were significant biased Vfi genes, Vfi12, V~I and Vfi20, each 3 patients. As the HLA type is a determining factor in shaping TCR repertoire of peripheral T cells, we compared the Vfi utilization in HLA-DR4 expressing groups that have susceptibility and gene dosage effect in disease progression. It was a little different that comparing the pattern of Vfi usage in peripheral blood and synovial fluid from RA patients between HLA-DR4 positive and negative group. CONCLUSION: The results were consistent with the conclusion that the increased Vfi family T cells infiltrate synovium and are dependent on each patient and may be involved in inducing and maintaining the synovitis that characterizes RA. The different outcome of each patient may be due to the difference in disease duration, genetic background and geographic region. A more important factor may be the stage of disease, because epitope 'induced immune reaction may change over time. Therefore, selecting patients early in the course of disease may be important and may facilitate the need for more in-depth TCR analysis in the future.
Arthritis, Rheumatoid* ; Bias (Epidemiology) ; Disease Progression ; DNA Primers ; Gene Dosage ; Genes, T-Cell Receptor ; HLA-DR4 Antigen ; Humans ; Polymerase Chain Reaction ; Synovial Fluid ; Synovial Membrane ; Synovitis ; T-Lymphocytes ; Tissue Donors