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Gram-negative, aerobic, rod-shaped, non-spore-forming, motile bacteria, designated strains F2 T and PGU16, were isolated from the midgut crypts of the bordered plant bug Physopelta gutta , collected in Okinawa prefecture, Japan. Although these strains were derived from different host individuals collected at different times, their 16S rRNA gene sequences were identical and showed the highest similarity to Paraburkholderia caribensis MWAP64 T (99.3 %). The genome of strain F2 T consisted of two chromosomes and two plasmids, and its size and G+C content were 9.28 Mb and 62.4 mol% respectively; on the other hand, that of strain PGU16 consisted of two chromosomes and three plasmids, and its size and G+C content were 9.47 Mb and 62.4 mol%, respectively. Phylogenetic analyses revealed that these two strains are members of the genus Paraburkholderia . The digital DNA-DNA hybridization value between these two strains was 92.4 %; on the other hand, the values between strain F2 T and P. caribensis MWAP64 T or phylogenetically closely related Paraburkholderia species were 44.3 % or below 49.1 %. The predominant fatty acids of both strains were C 16 : 0 , C 17 : 0 cyclo, summed feature 8 (C 18 : 1  ω 7 c /C 18 : 1  ω 6 c ), and C 19 : 0 cyclo ω 8 c , and their respiratory quinone was ubiquinone 8. Based on the above genotypic and phenotypic characteristics, strains F2 T and PGU16 represent a novel species of the genus Paraburkholderia for which the name Paraburkholderia largidicola sp. nov. is proposed. The type strain is F2 T (=NBRC 115765 T =LMG 32765 T ).

Objective: The discontinuation of dual antiplatelet therapy (DAPT) increases the risk of stent thrombosis after coronary stenting. Some patients must discontinue DAPT due to gastrointestinal (GI) tract disease; however, the type of examination that is most useful for detecting GI tract diseases has not been fully evaluated. The purpose of this study was to clarify whether the immunochemical fecal occult blood test (iFOBT) can be used to predict GI tract disease-related DAPT discontinuation following stent implantation in patients with coronary artery disease., Methods: A total of 181 consecutive DAPT-naïve patients who underwent coronary stenting were divided into two groups according to the results of iFOBTs: a positive iFOBT group (n=32) and a negative iFOBT group (n=149). During the 12-month follow-up period, the DAPT discontinuation rate was lower in the negative iFOBT group than in the positive iFOBT group (3.4 vs. 18.8%, p=0.005). Kaplan-Meier event-free curves showed that the DAPT discontinuation rate in the negative iFOBT group was lower than that observed in the positive iFOBT group (log-rank test: p=0.001). Logistic and Cox regression analyses showed that a positive iFOBT result was the strongest predictor of the risk of DAPT discontinuation after coronary stenting., Conclusion: A positive iFOBT result is associated with DAPT discontinuation following coronary stenting.

Background: Transient receptor potential canonical (TRPCs) channels are up-regulated in the development of cardiac hypertrophy. Sildenafil inhibits TRPC6 activation and expression, leading to the prevention of cardiac hypertrophy. However, the effects of sildenafil on the expression of other TRPCs remain unknown. We hypothesized that in addition to its effects of TRPC6, sildenafil blocks the up-regulation of other TRPC channels to suppress cardiomyocyte hypertrophy., Methods and Results: In cultured neonatal rat cardiomyocytes, a 48 h treatment with 10nM endothelin (ET)-1 induced hypertrophic responses characterized by nuclear factor of activated T cells activation and enhancement of brain natriuretic peptide expression and cell surface area. Co-treatment with sildenafil (1 μM, 48 h) inhibited these ET-1-induced hypertrophic responses. Although ET-1 enhanced the gene expression of TRPCs, sildenafil inhibited the enhanced gene expression of TRPC1, C3 and C6. Moreover, co-treatment with sildenafil abolished the augmentation of SOCE in the hypertrophied cardiomyocytes., Conclusions: These results suggest that sildenafil inhibits cardiomyocyte hypertrophy by suppressing the up-regulation of TRPC expression., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background: Statins are frequently administered to reduce low-density lipoprotein cholesterol (LDL-C) and vascular inflammation, because LDL-C and high sensitive C-reactive protein (hs-CRP) are associated with high risk for cardiovascular events. When statins do not reduce LDL-C to desired levels in high-risk patients with coronary artery disease (CAD), ezetimibe can be added or the statin dose can be increased. However, which strategy is more effective for treating patients with CAD has not been established. The present study compares anti-inflammatory effects and lipid profiles in patients with CAD and similar LDL-C levels who were treated by increasing the statin dose or by adding ezetimibe to the original rosuvastatin dose to determine the optimal treatment for such patients., Methods: 46 patients with high-risk CAD and LDL-C and hs-CRP levels of >70 mg/dL and >1.0 mg/L, respectively, that were not improved by 4 weeks of rosuvastatin (2.5 mg/day) were randomly assigned to receive 10 mg (R10, n = 24) of rosuvastatin or 2.5 mg/day of rosuvastatin combined with 10 mg/day of ezetimibe (R2.5/E10, n = 22) for 12 weeks. The primary endpoint was a change in hs-CRP., Results: Baseline characteristics did not significantly differ between the groups. At 12 weeks, LDL-C and inflammatory markers (hs-CRP, interleukin-6, tumour necrosis factor-alpha and pentraxin 3) also did not significantly differ between the two groups (LDL-C: R10 vs. R2.5/E10: -19.4 ± 14.2 vs. -22.4 ± 14.3 mg/dL). However, high-density lipoprotein cholesterol (HDL-C) was significantly improved in the R10, compared with R2.5/E10 group (4.6 ± 5.9 vs. 0.0 ± 6.7 mg/dL; p < 0.05)., Conclusion: Both enhanced therapies exerted similar anti-inflammatory effects under an equal LDL-C reduction in patients with high-risk CAD despite 2.5 mg/day of rosuvastatin. However, R10 elevated HDL-C more effectively than R2.5/E10., Trial Registration: UMIN000003746.

Background: The involvement of autophagy in heart disease has been reported. Transgenic mice expressing GFP-LC3 have been a useful tool in detecting autophagosomes systemically. It is difficult to differentiate increased formation of autophagosomes from decreased clearance of autophagosomes in the heart using GFP-LC3 mice., Methods and Results: We generated transgenic mice expressing mCherry-LC3 under alphaMyHC promoter and crossed the mice with transgenic mice expressing GFP-LC3. The deference of resistance to acidic conditions between GFP and mCherry overcame the limitation., Conclusions: This method is an innovative approach to examine the role of autophagy and to analyze autophagosome maturation in cardiomyocytes. (Circ J 2010; 74: 203 - 206).

Unlabelled: We have reported that intermediate conductance Ca(2+)-activated K(+) channels (ImK) showed augmented expression in angiotensin II (AII) type 1 receptor-dependent manner in post-ischemic rat heart. ImK has tyrosine phosphorylation sequence in the C-terminus and motifs for NFkappaB and AP1 in the promoter. While statin inhibits AII-mediated vascular remodeling via anti-inflammatory effect independent of cholesterol lowering. To test the possible effect of statin on expression of ImK, Wistar-Kyoto rats received L-nitro-arginine methyl ester (LNAME: 1 mg/ml in drinking water) for 4 weeks in group L. While in L+P group, rats received both LNAME and pitavastatin (PTV: 1 mg/kg/day in drinking water). Temporal profile of ImK mRNA was examined by RT-PCR using specific primers for ImK., Results: Long-term LNAME administration produced significant hypertension and resulted in marked microvascular remodeling characterized by medial thickening and perivascular fibrosis of coronary arterioles (100-200 microm in diameter). RT-PCR revealed significant up-regulation of ImK mRNA with two distinct peaks in L group in the early phase (days 3-7) and the late phase (4 weeks). PTV partially inhibited a rise in systolic blood pressure, but completely abolished the first peak of ImK upregulation (0.76 +/- 0.04 vs. 3.96 +/- 1.43 folds at day 7, p < 0.001). Co-treatments with PTV also significantly inhibited medial thickening and perivascular fibrosis. These findings indicate that statin inhibits microvascular remodeling induced by chronic inhibition of NO synthesis through the action independent of cholesterol lowering., (Copyright 2003 S. Karger AG, Basel)

A 61-year old asymptomatic woman was admitted to our hospital for the examination of an abnormal shadow in the left lower lung lobe in 1978. Enhanced chest computed tomograms and pulmonary arteriograms revealed a pulmonary arteriovenous malformation (PAVM) composed of feeding artery and draining vein. The patient had suffered brain abscesses 3 times because of paradoxical emboli from PAVMs. A diagnosis of hereditary hemorrhagic telangiectasia (HHT) was made according to the criteria. The patient died of septic shock due to urinary tract infection by Candida albicans. We reviewed cases of PAVMs associated with HHT in the Japanese literature. In Japan, 126 HHT families and 144 HHT patients have been reported to date. PAVMs occur in approximately one-third of HHT patients in Japan. Twenty-four out of 45 patients (44.4%) had multiple PAVMs. We also discussed the diagnosis, complications, and treatment of PAVM-associated HHT.