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OBJECTiVE.Inflammatory pseudotumor of the liver is a localized mass consisting of a fibrous stroma and chronic inflammatory infiltrate without anaplasia. Diagnosis of this rare disease Is important to avoid surgery. The purpose of this study was to determine if CT is useful in the diagnosis of this lesion.SUBJECTS AND METHODS. CT scans of nine patients with a proved diagnosis of inflammatory pseudotumor of the liver were reviewed. Diagnosis was made by the surgical resection In three patients and by percutaneous biopsy In six patients. Six patients had symptoms and laboratory data suggesting active inflammation caused by the pseudotumor. The remaining three patients were asymptomatic.CT scans were performed with IV administration of the contrast material; scans were obtained in the portal venous and delayed phases In six patients and In the delayed phase In three patients. CT scans were analyzed for the number and size of the hepatic masses, and the degree and pattern of contrast enhancement on portal venous phase and delayedphase images.RESULTS. Eight patients had a solitary hepatic mass, and one patient had two masses on the CT scan. The average size of the masses in the symptomatic patients (8.3 cm) was larger than that in the asymptomatic group (3.6 cm). CT scans In the portal venous phase showed a variable degree of contrast enhancement (seven masses). At least a part of seven masses, six of which were in symptomatic patients, showed greater contrast enhancement on delayed-phase CT scans than on the normal liver parenchyma.No constant pattern of enhancement was observed on delayed-phase CT scans In asymptomatic patients. CONCLUSION.Inflammatory pseudotumor of the liver should be included in a differential diagnosis in patients with a hepatic mass on a CT scan, especially when patients are symptomatic and the mass is fairly large and solitary showing contrast enhancement greater than that of liver parenchyma on delayed-phase CT scans. Percutaneous biopsy should be performed to obtain a histologic confirmation.

Background: Recent studies have shown that heat shock protein (HSP) 70 may serve as a ''damage signal'' to the immune system and could be the endogenous ligand for Toll-like receptor (TLR) 4 mediating synthesis of inflammatory cytokines. Aims: To explore the relationship between circulating HSP70 levels and activation of monocyte TLR4 and myocardial damage after AMI. Methods and results: This study examined circulating HSP70 and monocyte TLR4 levels in 52 patients with AMI and 20 controls, and analyzed ex vivo inflammatory cytokine productions using HSP70-stimulated monocytes. Circulating HSP70 levels were higher in AMI patients on day 1 after onset than in controls and remained elevated in AMI patients 14 days after onset. HSP70 levels were positively correlated with monocyte TLR4, plasma interleukin-6 and tumor necrosis factor-a levels in AMI patients. HSP70 levels 14 days after onset were higher in AMI patients with heart failure (n = 15) than in those without heart failure. In our in vitro study, HSP70-stimulated monocytes resulted in dose-dependent TLR4 expression and release of inflammatory cytokines. TLR4 antibody inhibited inflammatory cytokines release. Conclusions: Elevated circulating levels of HSP70 may be involved in TLR4 signal-mediated immune response and the progression of heart failure after AMI.

Supramolecular photocatalysts comprising [Ru(diimine)3]2+ photosensitiser and fac-[Re(diimine)(CO)3{OC(O)OC2H4NR2}] catalyst units can be used to reduce CO2 to CO with high selectivity, durability and efficiency. In the presence of triethanolamine, the Re...

Background: Osteopontin (OPN), an extracellular matrix (ECM) protein, plays an important role in myocardial remodeling by promoting collagen synthesis and accumulation in experimental animal models. Aims: We hypothesized that OPN could be expressed in myocardial tissues and contribute to collagen accumulation and myocardial dysfunction in human dilated cardiomyopathy (DCM). Methods and results: Endomyocardial biopsy tissues were obtained from 51 patients with DCM and 15 controls by right ventricular endomyocardial biopsy. OPN, collagen types I (Col I) and III (Col III) mRNA levels were measured by real-time reverse transcriptase polymerase chain reaction (RT-PCR). The cellular source of OPN was analyzed using immunohistochemistry and in situ hybridization. Myocardial collagen volume fraction (CVF) was determined by digital planimetry. OPN, Col I and Col III mRNA levels were higher in DCM patients than in controls ( Pb0.01). OPN mRNA levels were positively correlated with Col I levels and CVF in DCM patients (OPN vs. Col I: r=0.60, Pb0.01; OPN vs. CVF: r=0.52, Pb0.001). Immunostaining of OPN was present in cardiomyocytes from DCM patients. In situ hybridization identified cardiomyocytes as the major source of OPN mRNA transcription in DCM patients. OPN and Col I mRNA levels were highly expressed in the DCM subgroup with large left ventricular (LV) end-systolic diameter (LVESDz54.5 mm) or low LV ejection fraction (LVEFb29.5%). There was a weak positive correlation between OPN mRNA levels and LV end-systolic diameter (r=0.39, Pb0.01). Levels of OPN mRNA were also negatively correlated with LV ejection fraction (r=À0.43, Pb0.01). Conclusions: These results suggest that OPN may play a pivotal role in the development of Col-I-induced cardiac fibrosis and dysfunction in human DCM.

Previous studies have demonstrated that inflammatory cytokine expression associated with enteroviral (EV) infection may play an important role in human myocarditis. However, the mechanism of the host immune response against viral pathogens has not been fully understood. The aim of the present study was to determine whether Toll-like receptor 4 (TLR4) and EV RNA are present in human myocarditis. Endomyocardial biopsy samples were obtained from 44 patients with myocarditis and five controls. Levels of plus- and minus-strand EV RNAs and TLR4 mRNA were measured by real-time reverse transcriptase-PCR. Immunohistochemical analysis was performed to identify the cellular source of TLR4 and the EV capsid protein VP1. EV RNA was present in 21 patients with myocarditis and these patients were defined as having either active viral replication ( n =15) or latent viral persistence ( n =6). Neither strand of EV RNA was detected in controls. TLR4 mRNA expression levels were higher in myocarditis patients than in controls (TLR4/glyceraldehyde-3-phosphate dehydrogenase ratio 1.48+/-0.17 compared with 0.08+/-0.06, P <0.001). A positive correlation was found between EV RNA and TLR4 levels (plus-strand vs TLR4: r =0.66, P <0.001; minus-strand vs TLR4: r =0.48, P <0.001). TLR4 immunostaining was observed in infiltrating cells and myocytes in patients with myocarditis. The EV capsid protein VP1 was also found in myocytes. The myocarditis group with EV replication and high levels of TLR4 showed significantly lower systolic function. The present study has shown that increased expression of TLR4 is associated with EV replication and that these RNA levels are related to cardiac dysfunction in human myocarditis.

Expressions of innate immune response proteins, most notably proinflammatory cytokines, against enteroviral (EV) infection have been documented in the heart of human dilated cardiomyopathy (DCM). Toll-like receptor 4 (TLR4) activates signaling pathways leading to the expression of proinflammatory cytokines implicated the etiology of DCM. We sought to determine whether EV replication activates TLR4-dependent immune response in myocardium obtained from patients with DCM. Endomyocardial biopsy tissues were obtained from 56 patients with DCM and 10 controls. Levels of plus-and minus-strand EV RNA and TLR4 mRNA were measured by real-time RT-PCR. Immunohistochemical analysis was performed to identify the cellular source of EV capsid protein VP1 and TLR4. Both plus-and minus-strand EV RNA were detected in 19 DCM patients (34%). Neither strand of EV RNA was detected in controls. TLR4 mRNA levels were higher in DCM patients than in controls (Po0.001). A positive correlation was found between TLR4 levels and each strand type of EV RNA in EV RNApositive patients (plus-strand vs TLR4: r ¼ 0.69, Po0.001; minus-strand vs TLR4: r ¼ 0.65, P ¼ 0.002). VP1/TLR4 double staining showed extensive colocalization of VP1 and TLR4 proteins in cytoplasm of cardiac myocytes in myocardium obtained from DCM patients. EV RNA-positive patients showed lower systolic function and larger ventricular volume compared with EV RNA-negative patients left ventricular ejection fraction (LVEF): P ¼ 0.002; left ventricular end-systolic diameter (LVESD): P ¼ 0.004). The DCM subgroup with high TLR4 levels showed lower LVEF and larger LVESD than the subgroup with TLR4 levels (both Po0.001). This study suggests that myocardial expression of TLR4 associates with EV replication in human DCM. EV RNA and TLR4 mRNA levels may correlate with LV dysfunction in DCM. The expression of TLR4 against EV replication may be involved in the pathogenesis of DCM.