Open ring enhancement in atypical brain demyelination

Open ring enhancement is considered highly specific for atypical demyelination. In this report we present a patient with a history of headache, ataxia and sensory disturbances in the lower extremities. A cranial MRI scan showed a large frontal lesion with mass effect, midline shift and with open ring enhancement. These findings are characteristics of tumefactive multiple sclerosis. Such lesions can be confused with neoplasms and abscesses. Open ring enhancement may help in differentiating atypical demyelination from a neoplasm or an abscess.     

A rare case of pediatric pancreatic pseudocyst

We present a case report of a 2‐year‐old boy who presented to a local hospital to evaluate vague abdominal symptoms of one‐month duration. The patient, therefore, had an open cystogastrostomy and drainage of the free abdominal fluid with minimal complications. He was monitored for several days after his surgery.     

Myxedema Coma and Hypoventilation

Carbon dioxide retention may underlie many treatment failures in myxedema. Exactly why myxedematous patients hypoventilate is unclear. Possible causes of the ineffective breathing are many and include obesity and central nervous system dysfunction. Quick action to improve respiratory function can gain valuable time. In the case reported here, respiratory assistance was lifesaving.     

Thrombospondin-1 and transforming growth factor beta-1 upregulate plasminogen activator inhibitor type 1 in pancreatic cancer

Controlled degradation of the extracellular matrix by proteases is crucial in tumor cell invasion. We have shown that thrombospondin-1 (TSP-1), through activation of transforming growth factor beta-1 (TGF-β1), regulates the plasminogen/plasmin protease system in breast cancer. To determine whether this occurred in other epithelial neoplasms, we studied the role of TSP-1 and TGF-β1 in the regulation of the plasminogen/plasmin system in pancreatic cancer. ASPC-1 and COLO-3S7 pancreatic cancer cells were treated with TSP-1 or TGF-β1 at varying concentrations. The TSP-1 and TGF-β1-treated cells were also treated with either anti-TSP-1, anti-TSP-1 receptor, or anti-TGF-β1 antibodies. Urokinase plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) expression was determined by enzyme-linked immunosorbent assay. TSP-1 and TGF-β1 promoted a dose-dependent upregulation of ASPC-1 and COLO-3S7 PAI-1 expression. The TSP-1 effect could be blocked with anti-TSP-1 or anti-TGF-β1 antibodies. The TGF-β1 effect could be blocked only with anti-TGF-β1 antibody. Anti-TSP-1 receptor antibody blocked the TSP-1 effect on PAI-1 expression but had no effect on TGF-β1-mediated PAI-1 expression. Neither TSP-1 nor TGF-β1 had an effect on uPA production. We conclude that TSP-1, in a receptor-mediated process that involves the activation of TGF-β1, upregulates PAI-1 expression in pancreatic cancer without an effect on uPA production. Supported in part by National Institutes of Health grants CA65675 and CA69722 (Dr. Tuszysnki). Dr. Berger is the recipient of an American Cancer Society Clinical Career Development Award 96-09. Presented at the Thirty-Eighth Annual Meeting of The Society for Surgery of the Alimentary Tract, Washington, D.C., May 11–14,1997.