Xanthine oxidase inhibitor allopurinol improves atrial electrical remodeling in diabetic rats by inhibiting CaMKII/NCX signaling.

AIMS: Atrial fibrillation (AF) is a common arrhythmia which is associated with higher risk of stroke, heart failure and all-cause mortality. Abnormal Ca2+ handling in diabetes mellitus (DM) can cause delayed depolarization involved with increased NCX activity. Complicated mechanisms are involved in atrial remodeling, of which CaMKII may be a key node signal. Therefore, we intend to explore whether CaMKII activation induces atrial electrical remodeling by regulating NCX expression in this study. MAIN METHODS: Adult male SD rats were used to establish a diabetic rat model, divided into three groups: the control group, DM group and allopurinol group. Hemodynamic and ECG indicators were recorded, after which electrophysiological studies were conducted. The protein expression of CaMKII, p-CaMKII, XO, MnSOD and NCX was measured by Western blot and immunohistochemistry. H&E and Masson staining were applied for observing myocardial fibrosis. HL-1 cells were cultured for the measurement of ROS generation. KEY FINDINGS: The arrangement of atrial myocytes was disordered and the collagen volume fraction of the atrium tissue was elevated in the DM group compared with the control group, and improved by allopurinol. Higher incidence of inducible AF, reduced conduction velocity and higher conduction inhomogeneity were observed in diabetic rats. These electrophysiological abnormalities were accompanied by higher oxidative stress and protein expression of p-CaMKII and NCX. Allopurinol prevented the development of these abnormal changes. SIGNIFICANCE: Allopurinol can improve atrial electrical remodeling by inhibiting CaMKII activity and protein expression of NCX. These data indicate xanthine oxidase inhibition can reduce oxidative stress and ameliorate atrial electrical remodeling.

Electromagnetic pulsed thermography for natural cracks inspection.

Emerging integrated sensing and monitoring of material degradation and cracks are increasingly required for characterizing the structural integrity and safety of infrastructure. However, most conventional nondestructive evaluation (NDE) methods are based on single modality sensing which is not adequate to evaluate structural integrity and natural cracks. This paper proposed electromagnetic pulsed thermography for fast and comprehensive defect characterization. It hybrids multiple physical phenomena i.e. magnetic flux leakage, induced eddy current and induction heating linking to physics as well as signal processing algorithms to provide abundant information of material properties and defects. New features are proposed using 1st derivation that reflects multiphysics spatial and temporal behaviors to enhance the detection of cracks with different orientations. Promising results that robust to lift-off changes and invariant features for artificial and natural cracks detection have been demonstrated that the proposed method significantly improves defect detectability. It opens up multiphysics sensing and integrated NDE with potential impact for natural understanding and better quantitative evaluation of natural cracks including stress corrosion crack (SCC) and rolling contact fatigue (RCF).

Eddy Current Pulsed Thermography with Different Excitation Configurations for Metallic Material and Defect Characterization.

This paper reviews recent developments of eddy current pulsed thermography (ECPT) for material characterization and nondestructive evaluation (NDE). Due to the fact that line-coil-based ECPT, with the limitation of non-uniform heating and a restricted view, is not suitable for complex geometry structures evaluation, Helmholtz coils and ferrite-yoke-based excitation configurations of ECPT are proposed and compared. Simulations and experiments of new ECPT configurations considering the multi-physical-phenomenon of hysteresis losses, stray losses, and eddy current heating in conjunction with uniform induction magnetic field have been conducted and implemented for ferromagnetic and non-ferromagnetic materials. These configurations of ECPT for metallic material and defect characterization are discussed and compared with conventional line-coil configuration. The results indicate that the proposed ECPT excitation configurations can be applied for different shapes of samples such as turbine blade edges and rail tracks.

[Changes of open probability of large conductance Ca(2+)-activated K(+) channels in diabetic coronary smooth muscle cells of rats].

OBJECTIVE: To investigate the changes of open probability (Po) of large conductance Ca(2+)-activated K(+) channel (BK channel) in diabetic coronary smooth muscle cells and elucidate the underlying cellular electrophysiology mechanisms of coronary dysfunction. METHODS: Rat coronary smooth muscle cells were isolated from control group and diabetic group. BK single channel currents were recorded by patch clamp technique in inside-out configuration. Open probabilities were calculated and compared between two groups. After exposure to DHS-1, a specific BK channel activator, Po at 0.2 and 1 µmol/L free Ca(2+) were compared between control and diabetic groups. RESULTS: In the presence of 0.2 µmol/L free Ca(2+), the Po at baseline was significantly lower in diabetic rats than in control rats (0.0032 ± 0.0012 vs. 0.095 ± 0.036, P < 0.05). Cytoplasmic application of DSH-1 significantly increased the Po to 0.335 ± 0.096 (P < 0.05 vs. baseline) in control rats, whereas DSH-1 had no effect in diabetic rats (Po = 0.022 ± 0.018, P > 0.05 vs. baseline). In the presence of 1 µmol/L free Ca(2+), the Po at baseline was also significantly lower in diabetic rats than in control rats (0.210 ± 0.055 vs. 0.458 ± 0.077, P < 0.05). Cytoplasmic application of DHS-1 further robustly enhanced Po to 0.823 ± 0.019 (P < 0.05 vs. baseline) in control rats and to 0.446 ± 0.098 in diabetic rats (P < 0.05 vs. baseline of diabetic rats; P < 0.05 vs. control rats with DHS-1). CONCLUSION: The decrease of Po of BK single channel in coronary smooth muscle cells may be a potential cause for coronary dysfunction in diabetic rats.

[Evaluation of left ventricular function and twist in patients with diabetic cardiovascular autonomic neuropathy by speckle tracking imaging].

OBJECTIVE: To evaluate left ventricular (LV) function and twist in patients with diabetic cardiovascular autonomic neuropathy (CAN) by two-dimensional speckle tracking imaging (STI). METHODS: STI was performed in 56 subjects with type 2 diabetes mellitus (DM) (35 with DM only: group A, 21 with CAN: group B) and 34 normal subjects (Control) from LV short-axis view. LV peak systolic, peak early (E') and peak late (A') diastolic circumferential strain in 18 myocardial segments were measured at the levels of mitral annulus, papillary muscle and apex and the rotation at mitral annulus and apex levels were also measured. LV peak systolic and the ratio of E' and A' of global and three levels, twist, untwisting rate and untwisting half-time were calculated. RESULTS: In group A, compared with control group, LV peak systolic radial circumferential strain has no significant difference (P > 0.05), E'/A' was reduced (P < 0.05), twist at aortic valve closure and twist at mitral valve opening were significantly increased (P < 0.05), untwisting rate reduced, and untwisting half time delayed. In group B, compared with control group and group A, circumferential strain parameters [(-12.64 ± 6.49)% vs. (-19.11 ± 9.98)% and (-21.14 ± 10.13)%, P < 0.05] and E'/A' [(0.90 ± 0.35) vs. (1.24 ± 0.47) and (1.98 ± 0.63), P < 0.05] were significantly decreased, twist at aortic valve closure [(19.08 ± 5.62)° vs. (16.57 ± 2.84)° and (14.36 ± 4.06)°, P < 0.05] and twist at mitral valve opening [(13.99 ± 2.31)° vs. (11.36 ± 2.63)° and (9.04 ± 5.63)°, P < 0.05] were significantly increased, untwisting rate [(0.40 ± 0.28)%/ms vs. (0.46 ± 0.14)%/ms and (0.53 ± 0.21)%/ms, P < 0.05] reduced, and untwisting half time [(489.61 ± 97.14) ms vs. (445.21 ± 54.53) ms and (410.60 ± 50.23) ms, P < 0.05] delayed. CONCLUSION: Speckle tracking imaging could be used to evaluate early changes on LV twist deformation and LV systolic function in patients with type 2 diabetes mellitus.