3,470 research outputs found

    Effects of whole body vibration training on body composition, skeletal muscle strength, and cardiovascular health

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    Whole body vibration training (WBVT) has been used as a supplement to conventional exercise training such as resistance exercise training to improve skeletal muscle strength, specifically, in rehabilitation field. Recently, this exercise modality has been utilized by cardiovascular studies to examine whether WBVT can be a useful exercise modality to improve cardiovascular health. These studies reported that WBVT has not only beneficial effects on muscular strength but also cardiovascular health in elderly and disease population. However, its mechanism underlying the beneficial effects of WBVT in cardiovascular health has not been well documented. Therefore, this review highlighted the impacts of WBVT on cardiovascular health, and its mechanisms in conjunction with the improved muscular strength and body composition in various populations

    Effects of heated water-based versus land-based exercise training on vascular function in individuals with peripheral artery disease

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    Peripheral artery disease (PAD) is an atherosclerotic disease that is associated with poor vascular function, walking impairment, and reduced quality of life. Land-based exercise therapy (LBET) is frequently recommended to improve walking and reduce symptoms. Recently, evidence has suggested that heated-water exercise therapy (HWET) is an effective intervention for PAD. However, the efficacy of LBET versus HWET in PAD patients had not been elucidated. Therefore, we sought to compare effects of LBET with HWET on cardiovascular function, exercise tolerance, physical function, and body composition in PAD patients. PAD patients (n = 53) were recruited and randomly assigned to a LBET group (n = 25) or HWET group (n = 28). The LBET group performed treadmill walking, whereas the HWET group performed walking in heated water for 12 wk. Leg (legPWV) and brachial-to-ankle arterial stiffness (baPWV), blood pressure (BP), ankle-brachial index (ABI), 6-min walking distance (6MWD), claudication onset time (COT), physical function, and body composition were assessed before and after 12 wk. There were significant group-by-time interactions (P \u3c 0.05) for legPWV, BP, 6MWD, COT, body composition, and resting metabolic rate (RMR). Both groups significantly reduced (P \u3c 0.05) legPWV, BP, and body fat percentage, and HWET measures were significantly lower than LBET measures. Both groups significantly increased 6MWD, COT, and RMR, and HWET group measures were significantly greater than LBET measures. A time effect was noted for baPWV reduction in both groups (P \u3c 0.05). These results suggest that both LBET and HWET improve cardiovascular function, exercise tolerance, and body composition, and HWET showed considerably greater improvements compared with LBET in patients with PAD

    Tetra-μ-benzoato-bis­{[trans-1-(2-pyrid­yl)-2-(4-pyrid­yl)ethyl­ene]zinc(II)}

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    The paddle-wheel-type centrosymmetric dinuclear title complex, [Zn2(C7H5O2)4(C12H10N2)2], contains four bridging benzoate groups and two terminal trans-1-(2-pyrid­yl)-2-(4-pyrid­yl)ethyl­ene (L) ligands. The inversion center is located between the two ZnII atoms. The octa­hedral coordination around the ZnII atom, with four O atoms in the equatorial plane, is completed by an N atom of the L mol­ecule [Zn—N = 2.0198 (15) Å] and by the second ZnII atom [Zn⋯Zn = 2.971 (8) Å]. The ZnII atom is 0.372 Å out of the plane of the four coordinating O atoms

    NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor

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    AbstractDNA damage induced apoptosis suppressor (DDIAS), or human Noxin (hNoxin), is strongly expressed in lung cancers. DDIAS knockdown induced apoptosis in non-small cell lung carcinoma A549 cells in response to DNA damage, indicating DDIAS as a potential therapeutic target in lung cancer. To understand the transcriptional regulation of DDIAS, we determined the transcription start site, promoter region, and transcription factor. We found that DDIAS transcription begins at nucleotide 212 upstream of the DDIAS translation start site. We cloned the DDIAS promoter region and identified NFAT2 as a major transcription factor (Im et al., 2016 [1]). We demonstrated that NFATc1 regulates DDIAS expression in both pancreatic cancer Panc-1 cells and lung cancer cells
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