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iets could improve the survival and growth of large yellow croaker larvae probably by promoting intestinal development, alleviating inflammation and enhancing appetite.

Strength-endurance mainly depends on the power output, which is often expressed relative to the individual’s maximal power capability (

). However, an individual can develop the same power, but in different combinations of force and velocity (force-velocity condition). Also, at matched power output, changing the force-velocity condition results in a change of the velocity-specific relative power (

), associated with a change in the power reserve. So far, the effect of these changing conditions on strength-endurance remains unclear.

We aimed to test the effects of force-velocity condition and power output on strength-endurance.

Fourteen sportsmen performed (i) force- and power-velocity relationships evaluation in squat jumps and (ii) strength-endurance evaluations during repeated squat jump tests in 10 different force-velocity-power conditions, individualized based on the force- and power-velocity relationships. Each condition was characterized by different (i) relative power (%

), (ii) velociance was almost fully dependent on the position of the exercise conditions relative to the individual force-velocity and power-velocity relationships (characterized by %

and

). Thus, the standardization of the force-velocity condition and the velocity-specific relative power should not be overlooked for strength-endurance testing and training, but also when setting fatiguing protocols.

Strength-endurance was almost fully dependent on the position of the exercise conditions relative to the individual force-velocity and power-velocity relationships (characterized by %Pmaxv and RFv). Thus, the standardization of the force-velocity condition and the velocity-specific relative power should not be overlooked for strength-endurance testing and training, but also when setting fatiguing protocols.Numerous recent studies have shown that patients with underlying cardiovascular disease (CVD) are at increased risk of more severe clinical course as well as mortality of COVID-19. Also, the available data suggests that COVID-19 is related to numerous de novo cardiovascular complications especially in the older population and those with pre-existing chronic cardiometabolic conditions. SARS-CoV-2 virus can cause acute cardiovascular injury, as well as increase the risk of chronic cardiovascular damage. As CVD seem to be the major comorbidity in critically unwell patients with COVID-19 and patients often die of cardiovascular complications, we review the literature and discuss the possible pathophysiology and molecular pathways driving these disease processes cytokine release syndrome, RAAS system dysregulation, plaque destabilization and coagulation disorders with the aim to identify novel treatment targets. In addition, we review the pediatric population, the major cause of the cardiovascular complications is pediatric inflammatory multisystem syndrome that is believed to be associated with COVID-19 infection. Due to the increasingly recognized CVD damage in COVID-19, there is a need to establish clear clinical and follow-up protocols and to identify and treat possible comorbidities that may be risk factors for the development of cardiovascular complications.Muscle damage affects the blood leukocyte profile. Resistance exercise (RE) with blood flow restriction (BFR) attenuates exercise-induced muscle damage (EIMD).

To evaluate muscle damage and the leukocyte profile in response to RE+BFR and to compare with high intensity RE.

Twenty volunteers performed the RE in the leg press apparatus in the following groups RE80, 80% of 1RM (3 × until concentric muscle failure); RE40+BFR, 40% of 1RM with BFR (same total work of RE80 group). The BFR applied was 80% of the total occlusion pressure.

There were no differences in the blood leukocyte profile among groups despite the lower exercise-induced muscle damage (EIMD) in the RE40+BFR group (RE80 10.07 ± 2.67 vs. RE40+BFR 8.25 ± 0.96; cell × 10

/mm

). Both groups showed leukocytosis (RE80 7.59 ± 1.48 vs. 10.07 ± 2.67 and RE40+BFR 6.57 ± 1.50 vs. 8.25 ± 0.96; cell × 10

/mm

) and lymphocytosis (RE80 2.48 ± 0.83 vs. 3.65 ± 1.31 and RE40+BFR 2.22 ± 0.23 vs. 3.03 ± 0.65; cell × 10

/mm

) immediately after exercise. signaling pathway Leukocytosis (ES 1.12 vs. ES 1.33) and lymphocytosis (ES 1.11 vs. ES 1.76) was greater in the RE40+BFR group.

RE associated with BFR was accompanied by a greater leukocytosis and lymphocytosis immediately after exercise, with no difference in neutrophils. This leukocyte blood profile may be related to less muscle damage, as well as faster muscle recovery after 24 and 48 h post-exercise.

RE associated with BFR was accompanied by a greater leukocytosis and lymphocytosis immediately after exercise, with no difference in neutrophils. This leukocyte blood profile may be related to less muscle damage, as well as faster muscle recovery after 24 and 48 h post-exercise.Idiopathic pulmonary fibrosis (IPF) is a fatal disease of the lower respiratory tract with restricted therapeutic options. Repetitive injury of the bronchoalveolar epithelium leads to activation of pulmonary fibroblasts, differentiation into myofibroblasts and excessive extracellular matrix (ECM) deposition resulting in aberrant wound repair. However, detailed molecular and cellular mechanisms underlying initiation and progression of fibrotic changes are still elusive. Here, we report the generation of a representative fibroblast reporter cell line (10-4A BFP ) to study pathophysiological mechanisms of IPF in high throughput or high resolution in vitro live cell assays. To this end, we immortalized primary fibroblasts isolated from the distal lung of Sprague-Dawley rats. Molecular and transcriptomic characterization identified clone 10-4A as a matrix fibroblast subpopulation. Mechanical or chemical stimulation induced a reversible fibrotic state comparable to effects observed in primary isolated fibroblasts. Finally, we generated a reporter cell line (10-4A BFP ) to express nuclear blue fluorescent protein (BFP) under the promotor of the myofibroblast marker alpha smooth muscle actin (Acta2) using CRISPR/Cas9 technology. We evaluated the suitability of 10-4A BFP as reporter tool in plate reader assays. In summary, the 10-4A BFP cell line provides a novel tool to study fibrotic processes in vitro to gain new insights into the cellular and molecular processes involved in fibrosis formation and propagation.