61 Medizin und Gesundheit
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Major depressive disorder (MDD) is a common and severe disease characterized by mood changes, somatic alterations, and often suicide. MDD is treated with antidepressants, but the molecular mechanism of their action is unknown. We found that widely used antidepressants such as amitriptyline and fluoxetine induce autophagy in hippocampal neurons via the slow accumulation of sphingomyelin in lysosomes and Golgi membranes and of ceramide in the endoplasmic reticulum (ER). ER ceramide stimulates phosphatase 2A and thereby the autophagy proteins Ulk, Beclin, Vps34/Phosphatidylinositol 3-kinase, p62, and Lc3B. Although treatment with amitriptyline or fluoxetine requires at least 12 days to achieve sphingomyelin accumulation and the subsequent biochemical and cellular changes, direct inhibition of sphingomyelin synthases with tricyclodecan-9-yl-xanthogenate (D609) results in rapid (within 3 days) accumulation of ceramide in the ER, activation of autophagy, and reversal of biochemical and behavioral signs of stress-induced MDD. Inhibition of Beclin blocks the antidepressive effects of amitriptyline and D609 and induces cellular and behavioral changes typical of MDD. These findings identify sphingolipid-controlled autophagy as an important target for antidepressive treatment methods and provide a rationale for the development of novel antidepressants that act within a few days.
Background: Retinol binding protein 4 (RBP4), a protein secreted by adipocytes and bound in plasma to transthyretin (TTR), has been associated with obesity, the early phase of insulin resistance, metabolic syndrome, and type 2 diabetes mellitus. The objective of this study was to elucidate the relationship between RBP4, TTR, triglyceride (TG) and type 2 diabetes risk in rural Thailand. Results: RBP4 and TTR levels, as well as homeostatic model assessment of insulin resistance (HOMA-IR) values, were significantly elevated among subjects with high triglyceride levels (p < 0.01, p < 0.05, p < 0.05, respectively). Triglyceride levels correlated with RBP4 (r = 0.34, p < 0.001) and TTR (r= 0.26, p < 0.01) levels, as well as HOMA-IR values (r= 0.16, p < 0.05). After adjustment for age and gender, the risk of hypertriglyceridemia was 3.7 times greater (95% Cl =1.42 -9.73, p = 0.008) in the highest RBP4 tertile as compared to the lowest tertile. Similarly, the highest TTR and HOMA-IR tertiles had greater risk of hypertriglyceridemia at 3.5 (95% Cl = 1.30-9.20, p = 0.01) and 3.6 (95% CI = 1.33- 9.58, p = 0.01) times higher than the respective lowest tertiles. The correlation between TTR and blood glucose was statistically significant (r 0.18, p < 0.05), but not found this relationship in RBP4. Conclusions: The associations of RBP4 and TTR with hypertriglyceridemia and insulin resistance may have important implications for the risk of heart disease and stroke.
Chronic kidney disease (CKD) is associated with excessive mortality from cardiovascular disease (CVD). Endothelial dysfunction, an early manifestation of CVD, is consistently observed in CKD patients and might be linked to structural defects of the microcirculation including microvascular rarefaction. However, patterns of microvascular rarefaction in CKD and their relation to functional deficits in perfusion and oxygen delivery are currently unknown. In this in-vivo microscopy study of the cremaster muscle microcirculation in BALB/c mice with moderate to severe uremia, we show in two experimental models (adenine feeding or subtotal nephrectomy), that serum urea levels associate incrementally with a distinct microangiopathy. Structural changes were characterized by a heterogeneous pattern of focal microvascular rarefaction with loss of coherent microvascular networks resulting in large avascular areas. Corresponding microvascular dysfunction was evident by significantly diminished blood flow velocity, vascular tone, and oxygen uptake. Microvascular rarefaction in the cremaster muscle paralleled rarefaction in the myocardium, which was accompanied by a decrease in transcription levels not only of the transcriptional regulator HIF-1 alpha, but also of its target genes Angpt-2, TIE-1 and TIE-2, Flkt-1 and MMP-9, indicating an impaired hypoxia-driven angiogenesis. Thus, experimental uremia in mice associates with systemic microvascular disease with rarefaction, tissue hypoxia and dysfunctional angiogenesis.
Multi-element determination in human samples is very challenging. Especially in human intervention studies sample volumes are often limited to a few microliters and due to the high number of samples a high-throughput is indispensable. Here, we present a state-of-the-art ICP-MS/MS-based method for the analysis of essential (trace) elements, namely Mg, Ca, Fe, Cu, Zn, Mo, Se and I, as well as food-relevant toxic elements such as As and Cd. The developed method was validated regarding linearity of the calibration curves, method LODs and LOQs, selectivity and trueness as well as precision. The established reliable method was applied to quantify the element serum concentrations of participants of a human intervention study (LeguAN). The participants received isocaloric diets, either rich in plant protein or in animal protein. While the serum concentrations of Mg and Mo increased in participants receiving the plant protein-based diet (above all legumes), the Se concentration in serum decreased. In contrast, the animal protein-based diet, rich in meat and dairy products, resulted in an increased Se concentration in serum.
Background
Jump training (JT) can be used to enhance the ability of skeletal muscle to exert maximal force in as short a time as possible. Despite its usefulness as a method of performance enhancement in athletes, only a small number of studies have investigated its effects on muscle power in older adults.
Objectives
The aims of this meta-analysis were to measure the effect of JT on muscular power in older adults (≥ 50 years), and to establish appropriate programming guidelines for this population.
Data Sources
The data sources utilised were Google Scholar, PubMed, and Microsoft Academic.
Study Eligibility Criteria
Studies were eligible for inclusion if they comprised JT interventions in healthy adults (≥ 50 years) who were free of any medical condition that could impair movement.
Study Appraisal and Synthesis Methods
The inverse variance random-effects model for meta-analyses was used because it allocates a proportionate weight to trials based on the size of their individual standard errors and facilitates analysis while accounting for heterogeneity across studies. Effect sizes (ESs), calculated from a measure of muscular power, were represented by the standardised mean difference and were presented alongside 95% confidence intervals (CIs).
Results
Thirteen training groups across nine studies were included in this meta-analysis. The magnitude of the main effect was ‘moderate’ (0.66, 95% CI 0.33, 0.98). ESs were larger in non-obese participants (body mass index [BMI] < 30 vs. ≥ 30 kg/m2; 1.03 [95% CI 0.34, 1.73] vs. 0.53 [95% CI − 0.03, 1.09]). Among the studies included in this review, just one reported an acute injury, which did not result in the participant ceasing their involvement. JT was more effective in programmes with more than one exercise (range 1–4 exercises; ES = 0.74 [95% CI − 0.49, 1.96] vs. 0.53 [95% CI 0.29, 0.78]), more than two sets per exercise (range 1–4 sets; ES = 0.91 [95% CI 0.04, 1.77] vs. 0.68 [95% CI 0.15, 1.21]), more than three jumps per set (range 1–14 jumps; ES = 1.02 [95% CI 0.16, 1.87] vs. 0.53 [95% CI − 0.03, 1.09]) and more than 25 jumps per session (range 6–200 jumps; ES = 0.88 [95% CI 0.05, 1.70] vs. 0.49 [95% CI 0.14, 0.83]).
Conclusions
JT is safe and effective in older adults. Practitioners should construct varied JT programmes that include more than one exercise and comprise more than two sets per exercise, more than three jumps per set, and 60 s of recovery between sets. An upper limit of three sets per exercise and ten jumps per set is recommended. Up to three training sessions per week can be performed.
Grabow, L, Young, JD, Alcock, LR, Quigley, PJ, Byrne, JM, Granacher, U, Škarabot, J, and Behm, DG. Higher quadriceps roller massage forces do not amplify range-of-motion increases nor impair strength and jump performance. J Strength Cond Res 32(11): 3059–3069, 2018—Roller massage (RM) has been reported to increase range of motion (ROM) without subsequent performance decrements. However, the effects of different rolling forces have not been examined. The purpose of this study was to compare the effects of sham (RMsham), moderate (RMmod), and high (RMhigh) RM forces, calculated relative to the individuals' pain perception, on ROM, strength, and jump parameters. Sixteen healthy individuals (27 ± 4 years) participated in this study. The intervention involved three 60-second quadriceps RM bouts with RMlow (3.9/10 ± 0.64 rating of perceived pain [RPP]), RMmod (6.2/10 ± 0.64 RPP), and RMhigh (8.2/10 ± 0.44 RPP) pain conditions, respectively. A within-subject design was used to assess dependent variables (active and passive knee flexion ROM, single-leg drop jump [DJ] height, DJ contact time, DJ performance index, maximum voluntary isometric contraction [MVIC] force, and force produced in the first 200 milliseconds [F200] of the knee extensors and flexors). A 2-way repeated measures analysis of variance showed a main effect of testing time in active (p < 0.001, d = 2.54) and passive (p < 0.001, d = 3.22) ROM. Independent of the RM forces, active and passive ROM increased by 7.0% (p = 0.03, d = 2.25) and 15.4% (p < 0.001, d = 3.73) from premeasure to postmeasure, respectively. Drop jump and MVIC parameters were unaffected from pretest to posttest (p > 0.05, d = 0.33–0.84). Roller massage can be efficiently used to increase ROM without substantial pain and without subsequent performance impairments.
Impact of self-assessment of return to work on employable discharge from multi-component cardiac rehabilitation. Retrospective unicentric analysis of routine data from cardiac rehabilitation in patients below 65 years of age. Presentation in the "Cardiovascular rehabilitation revisited" high impact abstract session during ESC Congress 2018.
Aging is a complex phenomenon that has detrimental effects on tissue homeostasis. The skeletal muscle is one of the earliest tissues to be affected and to manifest age-related changes such as functional impairment and the loss of mass. Common to these alterations and to most of tissues during aging is the disruption of the proteostasis network by detrimental changes in the ubiquitin-proteasomal system (UPS) and the autophagy-lysosomal system (ALS). In fact, during aging the accumulation of protein aggregates, a process mainly driven by increased levels of oxidative stress, has been observed, clearly demonstrating UPS and ALS dysregulation. Since the UPS and ALS are the two most important pathways for the removal of misfolded and aggregated proteins and also of damaged organelles, we provide here an overview on the current knowledge regarding the connection between the loss of proteostasis and skeletal muscle functional impairment and also how redox regulation can play a role during aging. Therefore, this review serves for a better understanding of skeletal muscle aging in regard to the loss of proteostasis and how redox regulation can impact its function and maintenance.