Abstract-Hypertrophied cardiac myocytes exhibit prolonged action potentials and decreased transient outward potassium current (I to

BackgroundLeukocyte telomere length (LTL) is regarded as a potential marker of biological aging. Oxidative stress plays a major role in the rate of telomeric DNA loss. The aim of this study was to explore whether the LTL was shorter in Chinese patients with premature coronary artery disease (PCAD) than in non-CAD controls and to determine the relationship between oxidative stress and LTL shortening in this population.Material/MethodsPatients for coronary angiography were recruited. In total, 128 patients with PCAD and 128 non-CAD controls were enrolled. Samples of circulating leukocytes and plasma were collected. The mean LTL was measured using a polymerase chain reaction-based assay and expressed as the ratio of telomere repeat copies to single-copy gene (SCG) copies (T/S ratio). Reactive oxygen species (ROS) levels and total antioxidant capacity (T-AOC) were determined in plasma.ResultsBoth the T/S ratio (0.88±0.86 vs. 1.10±0.57, P=0.015) and telomere base pairs (4.97±1.37 kb vs. 5.32±0.91 kb, P=0.015) were significantly shorter in the PCAD group than in non-CAD controls. The T-AOC levels of the PCAD group were significantly lower than those of the non-CAD controls (0.482 mM [0.279, 0.603 mM]) vs. 0.778 mM [0.421, 0.924 mM], P=0.000). The ratio of T-AOC to ROS in the PCAD patients was significantly decreased compared to that of the non-CAD controls (0.1026±0. 1587 [Mm*ml/ng] vs. 0.1435±0.1946 [Mm*ml/ng], P=0.013).ConclusionThe results point to a potential link between reduced LTLs in patients with PCAD and early onset of atherosclerosis. The decline in antioxidant capacity may play an important role in accelerating the attrition of telomeres in PCAD patients.

Persistent room-temperature phosphorescence (p-RTP) of pure organic materials is attracting increasing attention. The design of efficient phosphors and understanding the origin of p-RTP, however, remain challenging. Herein, to gain further insights into pure organic p-RTP, we prepared a group of carbazole (CZ) and methyl benzoate (MBA) conjugates with a methyl ester unit at the para (4-MBACZ), meta (3-MBACZ), and ortho (2-MBACZ) sites. These isomers merely produce prompt fluorescence in solutions, but generate blue prompt/delayed fluorescence (DF) and orange p-RTP with lifetimes up to 865.2 ms in the crystalline state. Lifetimes of p-RTP are in the order of 2-MBACZ>3-MBACZ>4-MBACZ, which might be mainly ascribed to the combined effect of packing density, intermolecular interactions and steric hindrance. Meanwhile, upon mechanical grinding, while the emission color and profile of the luminogens do not significantly change, no (4-MBACZ) or shortened (3-MBACZ, 2-MBACZ) p-RTP is observed, accompanying the change from crystalline to amorphous states. Such p-RTP at amorphous states without external hosts is rarely reported, which demonstrates important implications for the molecular design and mechanism understanding towards p-RTP. Furthermore, their p-RTP attribute and different emission colors before and after ceasing the UV irradiation endow them promising applications in encryption and anticounterfeiting fields.

Lysyl oxidase-like 3 (LOXL3), a human disease gene candidate, is a member of the lysyl oxidase (LOX) family and is indispensable for mouse palatogenesis and vertebral column development. Our previous study showed that the loss of LOXL3 resulted in a severe cleft palate and spinal deformity. In this study, we investigated a possible role for LOXL3 in mouse embryonic lung development. LOXL3-deficient mice displayed reduced lung volumes and weights, diminished saccular spaces, and deformed and smaller thoracic cavities. Excess elastic fibres were detected in LOXL3-deficient lungs, which might be related to the increased LOXL4 expression. Increased transforming growth factor β1 (TGFβ1) expression might be involved in the up-regulation of LOXL4 in LOXL3-deficient lungs. We concluded that the loss of LOXL3 attenuates mouse embryonic lung development.