Retroperitoneal foregut cyst

A foregut cyst is formed as a result of abnormal budding and pinching of the tracheobronchial tree when bronchial buds develop to form the primitive respiratory tree. Foregut cysts are clinically classified as bronchogenic, esophageal, enterogastric, or ciliated hepatic. We present a foregut cyst that occurred in the retroperitoneum and was difficult to distinguish from other retroperitoneal cystic mass lesions. Magnetic resonance imaging was useful in revealing the cyst's continuity to adjacent organs. Received: 19 June 1995/Accepted: 23 July 1995     

Microheterogeneity of regional myocardial blood flows in low-perfused rat hearts evaluated by double-tracer digital radiography.

Using (3)H- and (125)I-labeled desmethylimipramine (DMI) for regional flow tracers, we established a two-time measurement method for the spatial pattern of myocardial perfusion in cross-circulated rat hearts. Myocardial extractions and retentions of these tracers were confirmed to be satisfactory; however, the latter were less than 90% after 3 min at a perfusion rate of 2.9 ml/min/g, limiting the present application to a short-time perfusion measurement. Distributions of myocardial depositions were separated by subtraction digital radiography with 400-microm pixel resolution. Its feasibility was examined by regression analysis between local deposition densities of (3)H- and (125)I-DMI injected simultaneously. The slope, y-intercept, and correlation coefficient (r) of the regression line were 0.98+/-0.04, 0.02+/-0.04, and 0.95+/-0.03, respectively, indicating the validity of the present image subtraction technique. The spatial pattern of myocardial perfusion in response to flow reduction was evaluated by the injections of (3)H- and (125)I-DMI, respectively, before and after a nearly 70% flow reduction. A significant correlation between normalized density distributions of these tracers was found in both subepicardium (r=0.77+/-0.12) and subendocardium (r=0.73+/-0.20), indicating the stable pattern of myocardial perfusion. However, the coefficient of variation of tracer densities showed a decrease of subendocardial flow heterogeneity from 35+/-15% to 31+/-16%. Thus, flow differences between originally high- and low-flow regions in subendocardium were reduced on a relative basis during low perfusion.     

Calcitonin inhibits proton extrusion in resorbing rat osteoclasts via protein kinase A

Although calcitonin is well known to be a potent inhibitor of bone resorption, it remains unknown how it regulates osteoclastic H(+) transport. In this study, we examined the effects of calcitonin on H(+) extrusion in cultured rat resorbing osteoclasts using an intracellular pH (pHi) indicator, BCECF [2'7'-bis-(2-carboxyethyl)- 5-carboxyfluorescein]. Resorbing osteoclasts were identified by their formation of resorbing pits on calcium phosphate-coated quartz coverslips. Both basal pHi and H(+) extrusion activity were significantly higher compared to non-resorbing osteoclasts. Two types of H(+)-extruding systems were identified by pharmacological and immunocytochemical means: a bafilomycin-A(1)-sensitive and an amiloride-sensitive system [H(+) extrusion mediated by a vacuolar type proton pump (V-ATPase) and by a Na(+)/H(+) exchanger (NHE), respectively]. Calcitonin inhibited both H(+) extrusion activities in a dose-dependent manner and this action was mimicked by protein kinase A (PKA) activators, but not by protein kinase C (PKC) activators. Pretreatment with PKA inhibitors completely suppressed calcitonin-induced inhibition, whereas neither PKC inhibitors nor calcium chelators suppressed it. These results indicate that calcitonin inhibits H(+) extrusion generated by V-ATPase and NHE via PKA activation. These inhibitory mechanisms of H(+) transport by calcitonin are important for the regulation of bone resorption.     

HASTE MR cholangiopancreatography in the evaluation of intraductal papillary-mucinous tumors of the pancreas

PURPOSE: The aim of this study was to determine the usefulness of MR cholangiopancreatography (MRCP) of intraductal papillary-mucinous tumors. METHOD: Thirteen patients with intraductal papillary-mucinous tumors were examined by breath-hold MRCP using a half-Fourier acquisition single-shot turbo spin echo (HASTE) sequence with a body phased-array coil. RESULTS: Endoscopic retrograde cholangiopancreatography (ERCP) and MRCP completely imaged the entire main pancreatic duct in 12 and in all 13 patients, respectively. ERCP demonstrated the whole opacification of the cystic lesion in only one patient. MRCP depicted the whole of the cystic lesion in all 11 patients who had cystic lesions. ERCP and MRCP source images depicted a communicating duct between the main pancreatic duct and the cystic lesion in 8 and in all 11 patients, respectively. ERCP depicted papillary projections in the main pancreatic ducts in two patients. MRCP source images depicted papillary projections in the main pancreatic ducts or cystic lesions in five patients. CONCLUSION: MRCP may be more useful to reveal the main pancreatic duct, cystic lesion, communicating duct between the main pancreatic duct and cystic lesion, and papillary projections than ERCP in patients with intraductal papillary-mucinous tumors of the pancreas.     

Involvement of aldosterone and mineralocorticoid receptors in rat mesangial cell proliferation and deformability

We demonstrated recently that chronic administration of aldosterone to rats induces glomerular mesangial injury and activates mitogen-activated protein kinases including extracellular signal-regulated kinases 1/2 (ERK1/2). We also observed that the aldosterone-induced mesangial injury and ERK1/2 activation were prevented by treatment with a selective mineralocorticoid receptor (MR) antagonist, eplerenone, suggesting that the glomerular mesangium is a potential target for injuries induced by aldosterone via activation of MR. In the present study, we investigated whether MR is expressed in cultured rat mesangial cells (RMCs) and involved in aldosterone-induced RMC injury. MR expression and localization were evaluated by Western blotting analysis and fluorolabeling methods. Cell proliferation and micromechanical properties were determined by [3H]-thymidine uptake measurements and a nanoindentation technique using an atomic force microscope cantilever, respectively. ERK1/2 activity was measured by Western blotting analysis with an anti-phospho-ERK1/2 antibody. Protein expression and immunostaining revealed that MR was abundant in the cytoplasm of RMCs. Aldosterone (1 to 100 nmol/L) dose-dependently activated ERK1/2 in RMCs with a peak at 10 minutes. Pretreatment with eplerenone (10 micromol/L) significantly attenuated aldosterone-induced ERK1/2 phosphorylation. Aldosterone (100 nmol/L) treatment for 30 hours increased [3H]-thymidine incorporation and decreased the elastic modulus, indicating cellular proliferative and deforming effects of aldosterone, respectively. These aldosterone-induced changes in cellular characteristics were prevented by pretreatment with eplerenone or an ERK (MEK) inhibitor, PD988059 (100 micromol/L). The results indicate that aldosterone directly induces RMC proliferation and deformability through MR and ERK1/2 activation, which may contribute to the pathogenesis of glomerular mesangial injury.     

Suppressive effect of the Gly389 allele of the beta1-adrenergic receptor gene on the occurrence of ventricular tachycardia in dilated cardiomyopathy.

Beta-1-adrenergic receptor (beta1-AR) blockers reduce both the incidence of sudden death and the ventricular volume in heart failure. In vitro, the Gly389 variant of beta1-AR mediates less adenylyl cyclase activities than the Arg389 variant, so Arg389Gly polymorphism was investigated with regard to the genesis, progression, or arrhythmogenesis of dilated cardiomyopathy (DCM). Allele and genotype frequencies of the Arg389Gly polymorphism were determined in 163 DCM patients and 157 age- and sex-matched controls. There were no differences in genotype and allele frequencies between patients and controls. Echocardiograms, left ventriculograms and 24h-Holter electrocardiograms were evaluated in the DCM patients and none of the clinical indices, other than ventricular tachycardia (VT), differed among the 3 genotypes. The Gly389 allele was more frequent in the VT(-) group than in the VT(+) group (0.46 vs 0.24, p=0.001). In univariate analysis, the odds ratio for VT in patients carrying 1 or 2 copies of the Gly389 allele was 0.29 ([95% confidence interval, 0.13-0.64], p=0.002), when compared with the Arg389 homozygotes. The Gly389 variant supressed the occurrence of VT in DCM, suggesting that this allele confers a decreased risk of sudden death.     

High incidence of microbleeds in hemodialysis patients detected by T2*-weighted gradient-echo magnetic resonance imaging

The incidence and characteristics of microbleeds in hemodialysis (HD) patients were investigated to elucidate the clinical significance with T(2)(*)-weighted gradient-echo magnetic resonance (MR) imaging. The 57 patients with chronic renal failure maintained by HD had no previous history of stroke. The control group consisted of 53 patients without previous history of stroke or chronic renal failure. The incidence and the number of microbleeds were assessed in the HD and control groups. The findings of microbleeds with T(2)(*)-weighted gradient-echo MR imaging were compared with those of T(1)- and T(2)-weighted MR imaging in HD patients. The incidence of microbleeds was significantly greater in the HD patients compared with the control patients. T(2)(*)-weighted gradient-echo imaging revealed a total of 44 microbleeds in 11 HD patients. T(2)-weighted imaging demonstrated 13 of 44 microbleeds as hyperintensity, whereas T(1)-weighted imaging demonstrated 12 lesions as hypointensity. T(2)- and T(1)-weighted imagings did not demonstrate any findings in 31 and 32 lesions, respectively. T(2)(*)-weighted gradient-echo MR imaging is effective to detect microbleeds which may be a predictor of intracerebral hemorrhage in HD patients and should be included in the protocol for the study of cerebrovascular disease, because T(2)- and T(1)-weighted MR imaging recognizes microbleeds as lacunar infarction.