A case of extrapleural empyema

A 49-year-old man with diabetes mellitus and alcoholic liver cirrhosis presented with dyspnoea and fever. A chest computed tomography scan revealed three areas of loculated pleural effusion. Initially, the patient was thought to have an intrapleural empyema and was treated with intravenous antibiotics and closed drainage. However, as he did not improve, he was then treated with open drainage. During open drainage, the patient was diagnosed to have an extrapleural empyema and improved following open drainage treatment.     

Microsatellite instability in gallbladder carcinoma: two independent genetic pathways of gallbladder carcinogenesis

Although the genetic basis for gallbladder carcinogenesis has not been clarified, considerable evidence has shown that genetic alterations play an important role in the development and progression of human cancers. In this study, we analyzed 30 gallbladder carcinomas to investigate the role of genetic alterations in their tumorigenesis, and to study correlations with their clinicopathological features. Tissue samples were obtained from 30 patients with gallbladder carcinoma (11 men and 19 women; mean age, 62 years; age range, 38–80 years). Genomic DNAs were extracted from fresh tumor tissue. We examined loss of heterozygosity (LOH) in the p53, APC, DCC, RB, and NM23-H1 gene regions by polymerase chain reaction (PCR)-LOH assay using an automated fluorescent DNA sequencer employing four microsatellite markers (p53, APC, DCC, NM23-H1). Five additional microsatellite markers were used for the determination of microsatellite instability (MSI). LOH was found at p53 in 9 of 15 informative cases (60%), at DCC in 10 of 22 (45%), at APC in 5 of 15 (33%), at RB in 1 of 8 (13%), and at NM23-H1 in 1 of 15 (7%). MSI was observed in 5 of 30 cases (17%) in at least one chromosomal loci of these nine microsatellite markers. None of the patients with MSI-positive tumors showed lymph node metastasis, and there was an inverse correlation between MSI and the presence of LOH in gallbladder carcinoma. These results suggest that there are two independent genetic pathways in gallbladder carcinogenesis; that is, an MSI pathway and an LOH pathway. Received: December 24, 1999 / Accepted: May 26, 2000     

A patient undergoing pancreaticoduodenectomy in whom involved common hepatic artery anomalously arising from the superior mesenteric artery was removed and reconstructed

Identifying anatomical variations of the celio-mesenteric arterial branches is important when performing pancreaticoduodenectomy. A relatively rare variation is the common hepatic artery entirely originated as a branch of the superior mesenteric artery. This type of variation is termed hepatomesenteric trunk type common hepatic artery, in which an accessory left hepatic artery arising from the celiac trunk is absent. Preservation of hepatomesenteric trunk type common hepatic artery is indispensable during pancreaticoduodenectomy because fatal hepatic injury or leak of hepaticojejunostomy can occur. The present case report shows a patient with pancreatic head tumor in whom hepatomesenteric trunk type common hepatic artery was involved by the tumor. The patient underwent pancreaticoduodenectomy during which the involved hepatomesenteric type common hepatic artery was removed and reconstructed using saphenous venous grafts. Histopathological examination showed double cancers which were composed of an advanced ductal adenocarcinoma of the pancreas and early bile duct adenocarcinoma. The patient is alive 18 months after the surgery without recurrence.     

Helicobacter pylori induces antiapoptosis through buclear factor-kappaB activation

Although Helicobacter pylori is classified as a definite carcinogen, the mechanism underlying gastric carcinogenesis is not yet clear. We previously have shown that H. pylori activates an antiapoptotic gene, the cellular inhibitor of apoptosis protein 2 (c-IAP2), the underlying mechanism of which was investigated in the present study. cDNA array and real-time PCR analyses indicated that H. pylori showed a stimulatory effect on the expression of c-IAP2. Isogenic mutant strains with impaired cag pathogenicity island (cagPAI) expression showed weaker induction. Analyses that used the in situ terminal deoxynucleotide transferase-mediated dUTP nick end-labeling method indicated suppression of antiapoptosis by the antisense c-IAP2 oligonucleotide. Reporter assays with deletion and mutation constructs for the c-IAP2 promoter showed that nuclear factor-kappaB (NF-kappaB) binding sites are indispensable for transactivation. Super-repressor IkappaBalpha or NF-kappaB inhibitor reduced c-IAP2 transactivation by H. pylori, and exogenous expression of c-IAP2 inhibited apoptosis seen with H. pylori. In conclusion, H. pylori induces antiapoptosis through c-IAP2 transactivation following cagPAI-dependent NF-kappaB activation. The interaction of these stimuli may play a role in gastric carcinogenesis.     

Redox modification of cell signaling in the cardiovascular system

Oxidative stress is presumed to be involved in the pathogenesis of many diseases, including cardiovascular disease. However, oxidants are also generated in healthy cells, and increasing evidence suggests that they can act as signaling molecules. The intracellular reduction-oxidation (redox) status is tightly regulated by oxidant and antioxidant systems. Imbalance between them causes oxidative or reductive stress which triggers cellular damage or aberrant signaling, leading to dysregulation. In this review, we will briefly summarize the aspects of ROS generation and neutralization mechanisms in the cardiovascular system. ROS can regulate cell signaling through oxidation and reduction of specific amino acids within proteins. Structural changes during post-translational modification allow modification of protein activity which can result in altered cellular function. We will focus on the molecular basis of redox protein modification and how this regulatory mechanism affects signal transduction in the cardiovascular system. Finally, we will discuss some techniques applied to monitoring redox status and identifying redox-sensitive proteins in the heart. This article is part of a Special Section entitled "Post-translational Modification."     

Focal Lesion in Upper Part of Brachial Plexus can be Detected by Magnetic Cervical Motor Root Stimulation

BackgroundThe utilities of magnetic cervical motor root stimulation are well known for lesions in the lower part of the brachial plexus, but not for lesions in the other parts.ObjectiveThe aim of paper is to show the utilities of magnetic cervical motor root stimulation for lesions in the upper part of the brachial plexus.MethodsWe analyzed the brachial plexus using both electrical stimulation at Erb's point and magnetic cervical motor root stimulation in a patient with brachial plexopathy caused by tumor invasion.ResultsOn the fourth day after onset, magnetic cervical motor root stimulation revealed abnormal findings in the upper part of the brachial plexus. Two weeks after onset, needle electromyography supported the existence of the focal lesion.ConclusionMagnetic cervical motor root stimulation is useful in detecting abnormal findings in the upper part of the brachial plexus, even at the acute phase.