Zobrazení zdroje stránky Danielsenlevine0211

95pg/mL; 0.40-2.12). The prevalence of obesity was higher among non-dynapenic participants (45.3%; 95% CI, 37.7-53). In dynapenic older adults, obesity was predominant in males (53.6%) and subjects with normal muscle strength had higher serum levels of TNF-β (0.63pg/mL; 0.30-1.30) and lower hand-grip strength (24kg; 20.00-28.00). Using a multivariate quantile regression analysis, we found a strong and negative association between IL-10 and muscle strength.<br /><br /> This study can help to understand the association of inflammation, obesity and muscle strength to promote interventions in order to avoid or delay the negative outcomes associated with dynapenia and sarcopenia in older adults.<br /><br />This study can help to understand the association of inflammation, obesity and muscle strength to promote interventions in order to avoid or delay the negative outcomes associated with dynapenia and sarcopenia in older adults.The deleterious effects of aging on force production are observable from the age of 40 upwards, depending on the measure. Neural mechanisms contributing to maximum force production and rate of force development have been suggested as descending drive from supraspinal centers, spinal motoneuron excitability, and corticospinal inhibition of descending drive; all of which influence motor unit recruitment and/or firing rate. Resistance-trained Master athletes offer a good source of information regarding the inevitable effects of aging despite the countermeasure of systematic resistance-training. However, most evidence of neural adaptation is derived from longitudinal intervention studies in previously untrained (i.e. resistance-training naïve) older adults. There is good evidence for the effect of resistance-training on the end-point of neural activation, i.e. [https://www.selleckchem.com/products/nx-5948.html selleck products] motor unit behavior, but little to no data on the generation of descending drive from e.g. transcranial magnetic stimulation or cortical imaging studies in older adults. This, along with tracking master athletes over several years, would provide valuable information and could be the focus of future research.<br /><br /> The effects of sargahydroquinoic acid (SHQA) on cellular senescence and the underlying mechanisms were investigated using human umbilical vascular endothelial cells (HUVECs).<br /><br /> SHQA or DMSO was supplemented into the medium. Low dose of H<br /><br /> O<br /><br /> was used to induce premature senescence. Replicative senescence was achieved by continuously culturing cells until they reached a plateau phase. Senescence biomarkers, including p53, p21, and p16 proteins, and SA-β-Gal activity were measured.<br /><br /> Pretreatment of SHQA significantly suppressed the oxidative stress-induced protein expression of p53, p21, and p16, as well as the activity of SA-β-Gal. Additionally, SHQA also delayed the replicative senescence as indicated by an increased population doubling number, reduced protein expression of p53, p21, and p16, as well as a decreased SA-β-Gal activity. SHQA inhibited the phosphorylation of Akt, mTOR, and downstream targets of mTOR, such as p-S6K, which was elevated by premature senescence and replicative senescence. In the absence of senescence stimuli, SHQA also inhibited the Akt/mTOR signaling pathway and promoted autophagy.<br /><br /> SHQA suppressed senescence induced by oxidative stress and replication through inhibiting the Akt/mTOR pathway. With the potential of acting as an Akt/mTOR inhibitor, SHQA might be useful for developing anti-ageing therapy.<br /><br />SHQA suppressed senescence induced by oxidative stress and replication through inhibiting the Akt/mTOR pathway. With the potential of acting as an Akt/mTOR inhibitor, SHQA might be useful for developing anti-ageing therapy.<br /><br /> Aging is often associated with low-grade systemic inflammation and reduced anabolic hormone levels. To investigate whether lifelong exercise training can decrease the age-related low-grade inflammation and anabolic hormone levels, we examined hormonal and inflammatory parameters among highly-trained male masters athletes and age-matched non-athletes.<br /><br /> From 70 elite power and endurance master athletes - EMA (51.3±8.0yr), 32 young controls - YC (23.7±3.9yr) and 24 untrained age-matched controls - MAC (47.2±8.0yr) venous blood was drawn to measure inflammatory parameters (interleukin-6 [IL-6], tumor necrosis factor-α [TNF-α] and interleukin-10 [IL-10]) and circulating hormones (luteinizing hormone [LH], total testosterone, estradiol, sex hormone-binding globulin [SHBG] and free androgen index [FAI]).<br /><br /> EMA showed a better anti-inflammatory status than MAC (higher IL-10 and IL-10/IL-6 ratio and lower IL-6), but a lower anti-inflammatory status than YC (higher TNF-α) (p&lt;0.05). The MAC group had lower testosterone levels compared to the YC and EMA group (p&lt;0.05), and lower estradiol levels and testosterone/LH ratio compared to YC (p&lt;0.05). In the control groups (MAC and YC), testosterone correlated negatively with age and proinflammatory parameters, and positively with anti-inflammatory parameters.<br /><br /> Elite master athletics elevated levels of anti-inflammatory cytokines above that seen in non-athlete peers and mitigated the age-related reduction in testosterone levels.<br /><br />Elite master athletics elevated levels of anti-inflammatory cytokines above that seen in non-athlete peers and mitigated the age-related reduction in testosterone levels.Age is a major risk factor for abdominal aortic aneurysm (AAA), for which treatment options are limited to surgical intervention for large AAA and watchful waiting for small aneurysms. However, the factors that regulate the expansion of aneurysms are unclear. Development of new therapeutic strategies to prevent or treat small aneurysms awaits a more thorough understanding of the etiology of AAA formation and progression with aging. A variety of structural and functional changes have been reported in aging vasculature, but emerging evidence implicates senescent cells in the formation of AAA through their paracrine effects on vascular wall cell populations. Here we show that aging is associated with transcriptional changes in abdominal aortic tissue consistent with loss of smooth muscle cells, leukocyte adhesion, inflammation, and accumulation of senescent cells in the vascular wall and surrounding perivascular adipose tissue. Furthermore, aged mice demonstrated anatomical and histopathological features of AAA development in response to administration of angiotensin II over 28 days.