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Objectives: Microscopic polyangiitis (MPA) affects various organs. However, echocardiographic findings of MPA are unclear. We aimed to evaluate the echocardiographic features of acute-phase MPA in Japanese patients. Methods: This single-centre retrospective study included 15 patients with MPA who underwent echocardiography within 2 weeks of commencing steroid therapy for induction or reinduction. The echocardiography parameters of thetients were compared with those of 30 age- and sex-matched controls. Results: No significant differences in left ventricular (LV) diameter, LV ejection fraction, or e' were observed between the two groups. However, the MPA group showed a significantly higher left atrial (LA) diameter and LA volume index, as well as higher early diastolic filling velocity, diastolic pulmonary venous flow velocity, and trans-tricuspid pressure gradient, and a shorter deceleration time (DCT). Serum C-reactive protein levels were positively correlated with E wave, E/A, and DCT. These results may indicate that increased LV stiffness, rather than impairment of LV relaxation, contributed to LV diastolic function, resulting in LA enlargement. Conclusions: Patients with acute-phase MPA had LA dilatation associated with LV diastolic dysfunction. This finding indicates the importance of cardiac assessment in patients with MPA, especially in patients with a strong inflammatory reaction. [ABSTRACT FROM AUTHOR]

Objective: Sudden cardiac death (SCD) is the major cause of death in cardiac sarcoidosis (CS). We aimed to identify the prognostic markers for sustained ventricular tachycardia (sVT) and SCD in patients with CS.Methods: We performed a prospective observational cohort study for patients with CS diagnosed according to the Japanese or Heart Rhythm Society guidelines between June 2008 and March 2020 in our hospital. The primary endpoint was a composite of the first sVT and SCD. The levels of urinary 8-hydroxy-2'-deoxyguanosine (U-8-OHdG), a marker of oxidative DNA damage that reflects the inflammatory activity of CS, other biomarkers, and indices of cardiac function and renal function were measured on admission.Results: Eighty-nine consecutive patients with CS were enrolled; 28 patients with no abnormal 18F-fluorodeoxyglucose (18F-FDG) accumulation in the heart were excluded and 61 patients with abnormal 18F-FDG accumulation were followed up for a median of 46 months (IQR: 20-84). During the follow-up period, 15 of 61 patients showed sVT (n=12) or SCD (n=3). A Cox proportional hazard model showed that U-8-OHdG concentration and presence of ventricular aneurysm (VA) were independent predictors of first sVT/SCD. The cut-off U-8-OHdG concentration for predicting first sVT/SCD was 14.9 ng/mg·Cr. Patients with U-8-OHdG concentration ≥14.9 ng/mg·Cr and VA showed a significantly increased risk of sVT/SCD.Conclusions: U-8-OHdG and presence of VA were powerful predictors of first sVT/SCD in patients with CS, facilitating the stratification of cardiac events and providing relevant information about the substrates of ventricular tachycardia. [ABSTRACT FROM AUTHOR]

In the title molecule, C48H33N, the central N atom shows no pyramidalization, so that the N atom and the three C atoms bound to the N atom lie almost in the same plane. The three para-phenylene rings bonded to the N atom are in a propeller form. All of the naphthalene ring systems are slightly bent. In the crystal, molecules form an inversion dimer, through two pairs of C--H interactions, which further interacts with the adjacent dimer via another two pairs of C--H interactions, forming a column structure along the a axis. There are no significant interactions between these column structures. [ABSTRACT FROM AUTHOR]

The intercellular junctions contain two complexes, adhesion junctions (AJ) and connexin (Cx) gap junctions (GJs). GJs provide the pathway for intercellular current flow. AJs mediate normal mechanical coupling and play an important role in the stability of GJs. We investigated the effects of rapid electrical stimulation (RES) on cardiac intercellular junctions, especially β-catenin and Cx43 alterations. We also studied the effects of ANG II receptor blockade on intercellular junction remodeling. Neonatal rats were euthanized by decapitation, and cardiomyocytes were prepared, cultured, and subjected to RES. We used real-time PCR, western blot analysis, and immunohistochemical methods. Conduction properties were examined by an extracellular potential mapping system. Cx43 protein expression in cardiomyocytes was significantly increased after 60 min. β-Catenin expression in the total cell fraction was significantly increased after 30 min. The expression level of β-catenin in the nucleus, which functions as a T cell factor/ lymphocyte enhancer binding factor transcriptional activator of Cx43 with its degradation regulated by glycogen synthase kinase-3β, was dramatically increased after 10 min. Conduction velocity was increased significantly by RES for 60 min. Olmesartan prevented most these effects of RES. We showed an increase of phosphorylated glycogen synthase kinase-3β, which is phosphorylated by activated MAPKs and inhibits β-catenin degradation, was attenuated by olmesartan. The changes in β-catenin precede Cx43 GJ remodeling and might play an important role in the formation and stability of GJs. Olmesartan might be a new upstream arrhythmia therapy by modulating intercellular junction remodeling through the β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

A synergistic approach to Cl−/HCO3−antiport has been demonstrated in POPC lipid bilayers using an ion selective electrode assay showing that, when using combinations of carriers each optimised for a particular component of the transport process, enhanced rates of transport are observed. [ABSTRACT FROM AUTHOR]

We report a facile synthetic protocol for preparation of dinaphtho- [2,3-b:2',3'-d]furan (DNF-V) derivatives. DNF-V derivatives showed high emissive behaviour in solid. A solution-crystallized transistor based on alkylated DNF-V derivatives showed an excellent carrier mobility of up to 1.3 cm² V-1 s-1, thereby proving to be a new solution-processable active organic semiconductor with high emission and high mobility. [ABSTRACT FROM AUTHOR]

The article describes the case of a 62-year-old male complaining of rotary vertigo and pre-syncope amid having hypertrophic cardio myopathy. The patient was subjected to several tests including ultrasonography of the carotid artery, digital subtraction angiography, and 3-dimensional computed tomography angiography and was placed on conservative therapy. He was diagnosed with Bow Hunter's Syndrome. Images of the vertebral artery are also presented.

Aims A domain peptide (DP) matching the Gly2460–Pro2495 region of the cardiac type-2 ryanodine receptor (RyR2), DPc10, is known to mimic channel dysfunction associated with catecholaminergic polymorphic ventricular tachycardia (CPVT), owing to its interference in a normal interaction of the N-terminal (1–600) and central (2000–2500) domains (viz. domain unzipping). Using DPc10 and two other DPs harboring different mutation sites, we investigated the underlying mechanism of abnormal Ca2+ cycling in failing hearts. Methods and results Sarcoplasmic reticulum (SR) vesicles and cardiomyocytes were isolated from dog left ventricular muscles for Ca2+ leak and spark assays. The RyR2 moiety of the SR was fluorescently labelled with methylcoumarin acetate (MCA) using DPs corresponding to the 163–195 and 4090–4123 regions of RyR2 (DP163–195 and DP4090–4123, respectively) as site-directed carriers. Both DPs mediated a specific MCA fluorescence labelling of RyR2. Addition of either DP to the MCA-labelled SR induced domain unzipping, as evidenced by an increased accessibility of the bound MCA to a large-size fluorescence quencher. Both SR Ca2+ leak and Ca2+ spark frequency (SpF) were markedly increased in failing cardiomyocytes. Upon introduction of DP163–195 or DP4090–4123 into normal SR or cardiomyocytes, both Ca2+ leak and SpF increased to the levels comparable with those of failing myocytes. K201 (JTV519) suppressed all of the effects induced by DP163–195 (domain unzipping and increased Ca2+ leak and SpF) or those in failing cardiomyocytes, but did not suppress the effects induced by DP4090–4123. Conclusion Defective inter-domain interaction between N-terminal and central domains induces diastolic Ca2+ leak, leading to heart failure and lethal arrhythmia. Mutation at the C-terminal region seen in CPVT does not seem to communicate with the aforementioned N-terminal and central inter-domain interaction, although spontaneous Ca2+ leak is similarly induced. [ABSTRACT FROM AUTHOR]