CD4+ T cells play a critical role in the development of allergic inflammation in several target organs. Various adhesion molecules are involved in the local recruitment of T cells and other inflammatory cells. We investigated the differential contribution of adhesion molecules to T helper 1 (Th1) and Th2 cell-mediated allergic lung and bowel inflammation by employing their neutralizing antibodies. BALB/c mice transferred with in vitro-differentiated antigen-specific Th1 and Th2 cells were intratracheally or intrarectally challenged with a relevant antigen. Infiltration of infused T cells occurred, along with the accumulation of neutrophils and eosinophils in the lungs of Th1 and Th2 cell-transferred recipients, respectively. Th1-mediated neutrophil and Th2-mediated eosinophil accumulation in the large intestine, which occurred after intrarectal challenge with the antigen, was indicated by the significant elevation of myeloperoxidase (MPO) and eosinophil peroxidase (EPO) activity. Blocking experiments with neutralizing antibodies indicated that intercellular cell adhesion molecule (ICAM)-1; vascular cell adhesion molecule (VCAM)-1; and αL, β2, and β7 integrins participate in the accumulation of Th2 cells and eosinophils in the lungs. In contrast, the migration of Th1 cells and neutrophils was diminished by blockage of αL/β2-integrin and ICAM-1, respectively. Mucosal addressin cell adhesion molecule (MadCAM)-1, vascular cell adhesion molecule (VCAM)-1, α4, β1, and β7 contributed to Th1-mediated neutrophilic inflammation in the bowel, though only MadCAM-1, α4, αL, and β2 were involved in Th2-mediated eosinophilic inflammation. We conclude that distinct sets of adhesion molecules are involved in Th1- and Th2-mediated allergic lung and bowel inflammation.
The apoptotic effect of adenosine and its analogues was studied in fibroblast‐like synoviocytes derived from rheumatoid arthritis patients (RA‐FLSs). Evoked cell death was quantitatively examined by assessing DNA fragmentation using an enzyme‐liked immunosorbent assay and by measuring phosphatidylserine exposure through flow cytometric analysis of annexin V binding. Exposing cells for 24 h to 2‐chloroadenosine (2‐CADO), a nonspecific, adenosine deaminase (ADA)‐resistant, adenosine receptor (AdoR) agonist, induced DNA fragmentation, and thus apoptosis, in RA‐FLSs at concentrations 50 μ M . By contrast, incubation with adenosine for up to 72 h did not evoke DNA fragmentation, even in the presence of ADA inhibitor coformycin and nucleoside transporter inhibitor nitrobenzylmercaptopurin (NBMPR). Transcription of all four AdoR isoforms was detected in RA‐FLSs; nevertheless selective AdoR agonists similarly failed to induce DNA fragmentation. DNA fragmentation evoked by 2‐CADO was inhibited by NBMPR and by 5′‐iodotubercidin, an adenosine kinase inhibitor, but not by xanthine amine congener, an A 1 and A 2 receptor antagonist, or by selective AdoR antagonists. The nonspecific caspase inhibitor benzyloxycarbonyl‐Val‐Ala‐Asp fluoromethyl ketone abolished the apoptotic effect of 2‐CADO. These results suggest that 2‐CADO induces apoptosis in RA‐FLSs independently of AdoR‐mediated signalling. Instead, 2‐CADO, but not adenosine, is taken up into RA‐FLSs via human equilibrative nucleoside transporter‐1, where it is phosphorylated by adenosine kinase. The resultant phospho‐2‐CADO induces DNA fragmentation by activating a caspase pathway. British Journal of Pharmacology (2002) 135 , 1477–1486; doi: 10.1038/sj.bjp.0704612
Additional file 7. Validation of A2 compared to the WHO gold standard method of determining dengue immune status. WHO immune classification: dengue immune status according to WHO guidelines. Blue: serological agreement. Red: Serological disagreement.
Additional file 8. Validation of A1 compared to the WHO gold standard method of determining dengue immune status. WHO immune classification: dengue immune status according to WHO guidelines. Blue: serological agreement. Red: Serological disagreement.
Although the cause varies widely, we recently experienced a case of constrictive pericarditis of which cause seemed to be traumatic as described below. The patient was a 62-year-old man having a history of epigastric trauma about 20 years ago. Since then, palpitation appeared and he was recently hospitalized in our department for the purpose of receiving an operation under the diagnosis of constrictive pericarditis. At operation, a hematoma was found in the pericardial region, which was considered to have been caused by trauma in the past. Less reports have so far been available concerning trauma-induced constrictive pericarditis and this case thus seemed to be of rarity as well.
The purpose of this study was to retrospectively compare the subclavian and femoral approaches to a fixed-catheter-tip method of implantation of a port-catheter system for hepatic arterial infusion chemotherapy with respect to complications and dysfunctions.Between April 2006 and April 2012, 153 patients (104 men, 49 women; age range, 23-82 years; mean, 65 years) with unresectable malignant liver tumors underwent percutaneous implantation of indwelling port-catheter systems by the fixed-catheter-tip method via the left subclavian or femoral artery. The success of implantation and outcome of complications were investigated and compared between these approach routes.The overall technical success rate of port-catheter system implantation with the fixed-catheter-tip method was 99% (152 of 153 patients). Seventy-five patients underwent implantation with a port-catheter system via the left subclavian artery, and 77 patients via the femoral artery. Catheter dislocation occurred in 3.9% of the patients; hepatic artery obstruction, 2.6%; catheter occlusion, 3.9%; bleeding at the puncture site, 3.9%; cerebral infarction, 1.3%; and infection related to port-catheter implantation, 2.6%. No significant differences in complications and port-catheter system dysfunction between the left subclavian and femoral approaches to port-catheter system implantation with the fixed-catheter-tip method were seen in any of the parameters. In addition, cerebral infarction occurred exclusively with the left subclavian approach, whereas infection occurred exclusively with the femoral approach.Implantation of the port-catheter system with the fixed-catheter-tip method is equally feasible via both the left subclavian and the femoral approaches.
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