ABSTRACT
Recurrent peritonitis is the major complication of continuous ambulatory peritoneal dialysis (CAPD) and a common reason for discontinuation of this form of therapy. Polymicrobial peritonitis by gram- negative organisms suggests intraabdominal pathology not directly associated with CAPD, necessitating early removal of catheter and/or abdominal exploration. The source of infection may still be gastrointestinal, especially in light of the polymicrobial gram-negative peritonitis and rarely be gastrointestinal malignancy. We recently experienced a case of 64-year-old woman with recurrent CAPD peritonitis by polymicrobial gram-negative organisms, originated from colon cancer. Colon cancer was confirmed by barium enema, abdominal CT and colonoscopic biopsy. She underwent right hemicolectomy and removal of catheter simultaneously. The biopsy revealed a moderately to poorly differentiated adenocarcinoma with abundant mucin production.
Subject(s)
Female , Humans , Middle Aged , Adenocarcinoma , Barium , Biopsy , Catheters , Colon , Colonic Neoplasms , Enema , Mucins , Pathology , Peritoneal Dialysis, Continuous Ambulatory , Peritonitis , Tomography, X-Ray ComputedABSTRACT
Toxic effects of ozone, 4-(N-methyl-N-nitrosamino)-1-(3- pyridyl)-1-butanone (NNK), and/or dibutyl phthalate (DBP) were examined through NF-kappaB, AP-1, Nrf2, and osteopontin (OPN) in lungs and livers of B6C3F1 mice. Electrophoretic mobility shift assay (EMSA) indicated that mice treated with combination of toxicants induced high NF-kappaB activities. Expression levels of p105, p65, and p50 proteins increased in all treated mice, whereas IkB activity was inhibited in NNK-, DBP-, and combination-treated ones. All treated mice except ozone-treated one showed high AP-1 binding activities. Expression levels of c-fos, c-jun, junB, jun D, Nrf2, and OPN proteins increased in all treated mice. Additive interactions were frequently noted from two-toxicant combination mice compared to ozone-treated one. These results indicate treatment of mixture of toxicants increased toxicity through NF-kappaB, AP-1, Nrf2, and OPN. Our data could be applied to the elucidation of mechanism as well as the risk assessment of mixture-induced toxicity.
Subject(s)
Animals , Mice , Blotting, Western , DNA-Binding Proteins/metabolism , Dibutyl Phthalate/toxicity , Electrophoretic Mobility Shift Assay , Kidney/drug effects , Liver/drug effects , Mice, Inbred Strains , NF-E2-Related Factor 2 , NF-kappa B/metabolism , Nitrosamines/toxicity , Osteopontin , Ozone/toxicity , Proto-Oncogene Proteins/metabolism , Risk Assessment , Sialoglycoproteins/metabolism , Trans-Activators/metabolism , Transcription Factor AP-1/metabolismABSTRACT
Although myocardial bridge is not thought to have any hemodynamic significance in most cases, some have suggested that when it produces severe systolic narrowing, ischemia or infarction may result. Myocardial bridge in adults with hypertrophic cardiomyopathy may be associated with a higher incidence of sudden death, myocardial wall-motion abnormalities, and perfusion defects on thallium-201 scintigraphy. When myocardial bridge is associated with left ventricular hypertrophy, it is known to affect longer segment and cause more severe compression during systole. We report a case of hypertrophic cardiomyopathy with myocardial bridge at the middle part of the left anterior descending coronary artery, who also showed reversible perfusion defect on the thallium scan at the same coronary territory.