Pancreatic duct lavage cytology with the cell block method for discriminating benign and malignant branch-duct type intraductal papillary mucinous neoplasms.

BACKGROUND: Differentiation between benign and malignant branch-duct type intraductal papillary mucinous neoplasms (IPMNs) remains challenging. OBJECTIVE: To examine the usefulness of pancreatic duct lavage cytology with cell block method for discriminating benign and malignant branch-duct type IPMNs. PATIENTS AND METHODS: Between December 2007 and April 2011, patients with branch-duct type IPMNs having mural nodules on EUS were examined by pancreatic duct lavage cytology by using the cell block method. Cell block sections underwent hematoxylin and eosin staining and mucin immunostainings (MUCs 1, 2, 5AC, and 6). DESIGN: Single-center, prospective study. SETTING: Academic medical center. MAIN OUTCOME MEASUREMENTS: The sensitivity and specificity of cytology were assessed. The agreement between cytological and histological results for MUC was also examined. RESULTS: Cytology with this method was investigated in 44 patients. Cell block diagnosis was cancer positive (class V or IV) in 11 patients and negative (classes I, II, III, and noninformative) in 33. The sensitivity, specificity, and positive and negative predictive values of this method were 92%, 100%, 100%, and 97%, respectively. The cytological and histological results of MUCs 1, 2, 5AC, and 6 agreed in 88% (15/17), 94% (16/17), 88% (15/17), and 100% (17/17), respectively. LIMITATIONS: Single center and small number of patients. CONCLUSIONS: Pancreatic duct lavage cytology with the cell block method may be useful to differentiate between benign and malignant IPMNs preoperatively and as well as to determine their mucin type.

Identification of cerebral response to balloon distention of the bile duct.

AIM: To identify the brain loci that process human biliary sensation. METHODS: In 6 patients (age range: 42-74 years; 4 men), who underwent percutaneous transhepatic biliary drainage (PTBD), the distal biliary tract was stimulated by repeatedly inflating the balloon of the PTBD catheter so that it reached volumes that produced a definite painless sensation. The functional magnetic resonance imaging (fMRI) of the cortical response to biliary sensation was examined. RESULTS: Biliary balloon stimulation elicited activation of the insular cortex, prefrontal cortex, and somatosensory cortex (P < 0.001). CONCLUSION: Biliary balloon stimulation evoked a cerebral cortical response detectable by fMRI.

[Effects of peroxisome proliferator-activated receptor gamma ligands on monocrotaline-induced pulmonary hypertension in rats].

Peroxisome proliferator-activated receptor gamma (PPARgamma) is a member of the nuclear hormone receptor superfamily, which regulates transcription of target genes in a ligand-dependent manner. Ligands for PPARgamma have been shown to attenuate proliferation of vascular smooth muscle cells, and to induce apoptosis in several cell lines in vitro. Since monocrotaline (MCT)-induced pulmonary hypertension in rats is characterized by proliferation of pulmonary vascular smooth muscle cells, we hypothesized that PPARgamma ligands may reduce MCT-induced pulmonary hypertension. To test this hypothesis, we treated MCT-injected rats with pioglitazone and troglitazone, synthetic ligands for PPARgamma, for three weeks and measured pulmonary artery pressure and pulmonary vessel wall thickness. TdT-mediated dUTP-biotin nick end labeling (TUNEL) and immunostaining for proliferating cell nuclear antigen (PCNA) were utilized to assess apoptosis and cell proliferation in the pulmonary arterial walls of pioglitazone-treated rats. MCT with pioglitazone or troglitazone treatment significantly reduced pulmonary hypertension and wall thickening of the pulmonary arteries. TUNEL-positive apoptotic cells were not seen in the pulmonary arterial walls of either MCT-injected or control rats with or without pioglitazone. PCNA-positive cells were only seen in the thickened pulmonary arterial walls of MCT rats, but not in the pulmonary arterial walls of controls and of pioglitazone-treated MCT rats. We conclude that PPARgamma ligands reduce MCT-induced pulmonary hypertension and pulmonary vascular wall thickening in rats. Inhibition of MCT-induced cell proliferation in the pulmonary arterial walls may account for this effect