Clinical Outcomes of Myocardial Bridging versus No Myocardial Bridging in Patients with Apical Hypertrophic Cardiomyopathy.

OBJECTIVE: To determine the prevalence and clinical effects of myocardial bridging (MB) in patients with apical hypertrophic cardiomyopathy (AHCM). METHODS: Angiograms from 212 AHCM patients were reviewed to identify MB. The patients were classified into 2 groups: AHCM with and AHCM without MB. We reviewed patient records on cardiovascular (CV) risk factors, symptoms, CV events, and CV mortality. RESULTS: In all, 60 patients with MB and 100 without MB were included. Rates of angina (61.7 vs. 40%; p = 0.008), mimicking non-ST-segment elevation myocardial infarction (15 vs. 3%, p = 0.013), and Canadian Cardiovascular Society class III/IV angina (18.3 vs. 4%; p = 0.003) were higher in patients with MB than in those without. Mean follow-up periods (65.5 ± 50.5 vs. 64.4 ± 43.6 months, p = 0.378) and CV mortality (3.3 vs. 1%; p = 0.652) were similar in the 2 groups. Kaplan-Meier estimates demonstrated that CV event-free survival rates were lower in patients with MB than in those without (71.7 vs. 88%; p = 0.022). MB, late gadolinium enhancement, and female sex were independent risk factors for CV events in a multivariate Cox regression analysis adjusted for other risk factors. CONCLUSION: More serious symptoms and a higher risk of CV events were observed in AHCM patients with MB than in those without MB. CV mortality was similar in these 2 groups.

Gene Regulation and Signal Transduction in the ICE-CBF-COR Signaling Pathway during Cold Stress in Plants.

Low temperature is an abiotic stress that adversely affects the growth and production of plants. Resistance and adaptation of plants to cold stress is dependent upon the activation of molecular networks and pathways involved in signal transduction and the regulation of cold-stress related genes. Because it has numerous and complex genes, regulation factors, and pathways, research on the ICE-CBF-COR signaling pathway is the most studied and detailed, which is thought to be rather important for cold resistance of plants. In this review, we focus on the function of each member, interrelation among members, and the influence of manipulators and repressors in the ICE-CBF-COR pathway. In addition, regulation and signal transduction concerning plant hormones, circadian clock, and light are discussed. The studies presented provide a detailed picture of the ICE-CBF-COR pathway.

[Model design and stray light suppression technology of stray-light testing equipment for plane grating].

Grating scatter is an important performance index for plane grating, and its measurement is a difficult problem for grating research field. In order to achieve stray-light of the instrument itself to be less than 10(-8) so that the grating scatter can be accurately measured, stray light in diffraction grating monochromators has been studied and an opto-mechanical model of measure instrument for plane grating is designed, which works in parallel light environment and based on the scalar diffraction theory and classical Fresnel-Kirchhoff diffraction theory. Main pathway of the instrumentation's stray light is calculated and analyzed by the simulation of stray-light testing equipment with ASAP software. Accordingly, four stray-light suppression structures including blocking rings, vanes, aperture stops and light traps are proposed to reduce instrument's scattered light and grating's multiple diffraction. Finally, contrast analysis of the instrumentation's stray light is made before and after adding stray-light suppression structures. Simulation and analysis results show that the max of instrument's stray light reduces from more than 10(-6) to less than 10(-8) after adding stray-light suppression structures and has met the stray-light testing equipment's design requirements whose goal is to realize accurate measurement greater than or equal to 10(-7) for grating scatter with grating's groove density changing from 300 to 3 600 gr x mm(-1). The research methods and results above will provide a theoretical basis for the research and development of the stray-light testing equipment for plane grating.

Dapk1 improves inflammation, oxidative stress and autophagy in LPS-induced acute lung injury via p38MAPK/NF-κB signaling pathway.

OBJECTIVE: To investigate the impact of death-associated protein kinase 1 (Dapk1) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) via p38MAPK/NF-κB pathway. METHODS: Dapk1+/+ and Dapk1-/- mice were randomized into Control, LPS, SB203580 (a p38MAPK pathway inhibitor) + LPS, and PDTC (a NF-κB pathway inhibitor) + LPS groups. Cell counts, lung wet to dry weight ratio (W/D weight ratio), as well as indicators of oxidative stress were determined followed by the detection with HE staining, ELISA, qRT-PCR, Western blotting and Immunofluorescence. Besides, to explore whether the effect of Dapk1 on ALI directly mediated via p38MAPK/NF-κB pathway, mice were injected with TC-DAPK 6 (a Dapk1 inhibitor) with or without SB203580/PDTC before LPS administration. RESULTS: LPS induced lung injury with increased lung W/D weight ratio, which could be partly reversed by SB203580 and PDTC in LPS-induced mice with activated p38MAPK/NF-κB pathway in lung tissues, especially in Dapk1-/- mice. SB203580 and PDTC reduced total cells and neutrophils in BALF in LPS-induced mice, accompanying with decreased levels of TNF-α, IL-6, MPO, LPO and MDA and the expressions of beclin-1, Atg5 and LC3II, but with the up-regulated activities of SOD and GSH-Px, as well as p62 protein expression. Besides, TC-DAPK 6 aggravated the pathologic injury in LPS-induced ALI with more serious inflammatory response, oxidative stress and autophagy as well as the activated p38MAPK/NF-κB pathway, which were reversed by SB203580 or PDTC. CONCLUSION: Dapk1 improved oxidative stress, inhibited autophagy, and reduce inflammatory response of LPS-induced ALI mice by inhibiting p38MAPK/NF-κB pathway.

Long-term survival after acute myocardial infarction in patients with hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is associated with poor prognosis. It has been reported that there is no difference in in-hospital mortality after acute myocardial infarction (AMI) between patients with and without HCM. However, whether there is a difference in long-term survival after AMI between patients with and without HCM remains unclear. HYPOTHESIS: Long-term survival after AMI is worse in patients with vs without HCM. METHODS: The clinical profiles of 91 consecutive patients with HCM and AMI (HCM group) and 91 sex- and age-matched patients with AMI without HCM (non-HCM group) were analyzed. The study endpoint was all-cause mortality. RESULTS: During a follow-up period of 4.9 ± 3.6 years, all-cause mortality occurred in 25 patients (27.5%) in the HCM group and 13 patients (14.3%) in the non-HCM group. The survival of the HCM group was inferior to that of the non-HCM group (log-rank P = 0.039). During the first year of follow-up, 3 deaths (3.3%) occurred in the HCM group and 7 deaths (7.7%) occurred in the non-HCM group (log-rank P = 0.177). Among patients who survived beyond the first year of follow-up (172 patients), the annual mortality rates were 6.3% (95% confidence interval: 4.0%-9.3%) in the HCM group and 1.6% (95% confidence interval: 0.6%-3.5%) in the non-HCM group (log-rank P = 0.001). CONCLUSIONS: AMI patients with HCM exhibited worse long-term survival than did AMI patients without HCM.