Effects of aerobic workout on the changes in the characteristics of dynamics of the center of gravity in different age categories

Introduction The quality and function of movements undergo deterioration due to weight gain. Aerobic training normalizes body weight, improves the health status, and in addition, it is expected to improve the dynamics of movements. The aims of this study were to prove the beneficial effects of recreational physical activities on the movements. Methods Participants were divided into five different age categories: second childhood, adolescence, mature age I, mature age II, and aging. Squatting and vertical jumping of the participants were measured at the beginning and at the end of a 5-month training program. These movements simulated ordinary daily movements. Changes in the body were determined by InBody230. APAS 3D system was used for movement analysis. Results The results showed significant improvements in body weight, fat mass, muscle mass, fat mass–body weight ratio, muscle mass–body weight ratio, body mass index, body fat percentage, and waist–hip ratio. During jumping, the lifting and sinking of the center of gravity’s (CG) position and its velocity and acceleration were improved. In case of squatting, the results showed significant improvements in the velocity and acceleration of dynamical characteristics of the CG. Other correlations were observed between changes in body composition and the dynamics of movements. Discussion The research proved that recreational training optimized body composition and improved the characteristics of CG’s dynamics. The study suggests considerable connection between body composition and the characteristics of the movements’ dynamics. From this point of view, our training program was the most effective in the working age groups

JDP2 overexpression provokes cardiac dysfunction in mice

The transcriptional regulator JDP2 (Jun dimerization protein 2) has been identified as a prognostic marker for patients to develop heart failure after myocardial infarction. We now performed in vivo studies on JDP2-overexpressing mice, to clarify the impact of JDP2 on heart failure progression. Therefore, during birth up to the age of 4 weeks cardiac-specific JDP2 overexpression was prevented by doxycycline feeding in transgenic mice. Then, JDP2 overexpression was started. Already after 1 week, cardiac function, determined by echocardiography, decreased which was also resembled on the cardiomyocyte level. After 5 weeks blood pressure declined, ejection fraction and cardiac output was reduced and left ventricular dilatation developed. Heart weight/body weight, and mRNA expression of ANP, inflammatory marker genes, collagen and fibronectin increased. Collagen 1 protein expression increased, and fibrosis developed. As an additional sign of elevated extracellular matrix remodeling, matrix metalloproteinase 2 activity increased in JDP2 mice. Thus, JDP2 overexpression is deleterious to heart function in vivo. It can be concluded that JDP2 overexpression provokes cardiac dysfunction in adult mice that is accompanied by hypertrophy and fibrosis. Thus, induction of JDP2 is a maladaptive response contributing to heart failure development

MicroRNA interactome analysis predicts post-transcriptional regulation of ADRB2 and PPP3R1 in the hypercholesterolemic myocardium

Little is known about the molecular mechanism including microRNAs (miRNA) in hypercholesterolemia-induced cardiac dysfunction. We aimed to explore novel hypercholesterolemia-induced pathway alterations in the heart by an unbiased approach based on miRNA omics, target prediction and validation. With miRNA microarray we identified forty-seven upregulated and ten downregulated miRNAs in hypercholesterolemic rat hearts compared to the normocholesterolemic group. Eleven mRNAs with at least 4 interacting upregulated miRNAs were selected by a network theoretical approach, out of which 3 mRNAs (beta-2 adrenergic receptor [Adrb2], calcineurin B type 1 [Ppp3r1] and calcium/calmodulin-dependent serine protein kinase [Cask]) were validated with qRT-PCR and Western blot. In hypercholesterolemic hearts, the expression of Adrb2 mRNA was significantly decreased. ADRB2 and PPP3R1 protein were significantly downregulated in hypercholesterolemic hearts. The direct interaction of Adrb2 with upregulated miRNAs was demonstrated by luciferase reporter assay. Gene ontology analysis revealed that the majority of the predicted mRNA changes may contribute to the hypercholesterolemia-induced cardiac dysfunction. In summary, the present unbiased target prediction approach based on global cardiac miRNA expression profiling revealed for the first time in the literature that both the mRNA and protein product of Adrb2 and PPP3R1 protein are decreased in the hypercholesterolemic heart

Exogenous coenzyme Q10 modulates MMP-2 activity in MCF-7 cell line as a breast cancer cellular model

<p>Abstract</p> <p>Background/Aims</p> <p>Matrix Metalloproteinases 2 is a key molecule in cellular invasion and metastasis. Mitochondrial ROS has been established as a mediator of MMP activity. Coenzyme Q₁₀contributes to intracellular ROS regulation. Coenzyme Q₁₀beneficial effects on cancer are still in controversy but there are indications of Coenzyme Q₁₀complementing effect on tamoxifen receiving breast cancer patients.</p> <p>Methods</p> <p>In this study we aimed to investigate the correlation of the effects of co-incubation of coenzyme Q10 and N-acetyl-L-cysteine (NAC) on intracellular H2O2 content and Matrix Metalloproteinase 2 (MMP-2) activity in MCF-7 cell line.</p> <p>Results and Discussion</p> <p>Our experiment was designed to assess the effect in a time and dose related manner. Gelatin zymography and Flowcytometric measurement of H2O2 by 2'7',-dichlorofluorescin-diacetate probe were employed. The results showed that both coenzyme Q10 and N-acetyl-L-cysteine reduce MMP-2 activity along with the pro-oxidant capacity of the MCF-7 cell in a dose proportionate manner.</p> <p>Conclusions</p> <p>Collectively, the present study highlights the significance of Coenzyme Q₁₀effect on the cell invasion/metastasis effecter molecules.</p

Hypercholesterolemia downregulates autophagy in the rat heart

Background: We have previously shown that efficiency of ischemic conditioning is diminished in hypercholesterolemia and that autophagy is necessary for cardioprotection. However, it is unknown whether isolated hypercholesterolemia disturbs autophagy or the mammalian target of rapamycin (mTOR) pathways. Therefore, we investigated whether isolated hypercholesterolemia modulates cardiac autophagy-related pathways or programmed cell death mechanisms such as apoptosis and necroptosis in rat heart. Methods: Male Wistar rats were fed either normal chow (NORM; n=9) or with 2% cholesterol and 0.25% cholic acid-enriched diet (CHOL; n=9) for 12 weeks. CHOL rats exhibited a 41% increase in plasma total cholesterol level over that of NORM rats (4.09mmol/L vs. 2.89mmol/L) at the end of diet period. Animals were sacrificed, hearts were excised and briefly washed out. Left ventricles were snap-frozen for determination of markers of autophagy, mTOR pathway, apoptosis, and necroptosis by Western blot. Results: Isolated hypercholesterolemia was associated with a significant reduction in expression of cardiac autophagy markers such as LC3-II, Beclin-1, Rubicon and RAB7 as compared to controls. Phosphorylation of ribosomal S6, a surrogate marker for mTOR activity, was increased in CHOL samples. Cleaved caspase-3, a marker of apoptosis, increased in CHOL hearts, while no difference in the expression of necroptotic marker RIP1, RIP3 and MLKL was detected between treatments. Conclusions: This is the first comprehensive analysis of autophagy and programmed cell death pathways of apoptosis and necroptosis in hearts of hypercholesterolemic rats. Our data show that isolated hypercholesterolemia suppresses basal cardiac autophagy and that the decrease in autophagy may be a result of an activated mTOR pathway. Reduced autophagy was accompanied by increased apoptosis, while cardiac necroptosis was not modulated by isolated hypercholesterolemia. Decreased basal autophagy and elevated apoptosis may be responsible for the loss of cardioprotection reported in hypercholesterolemic animals

Understanding mechanisms of asphaltene adsorption from organic solvent on mica

The adsorption process of asphaltene onto molecularly smooth mica surfaces from toluene solutions of various concentrations (0.01-1 wt %) was studied using a surface forces apparatus (SFA). Adsorption of asphaltenes onto mica was found to be highly dependent on adsorption time and asphaltene concentration of the solution. The adsorption of asphaltenes led to an attractive bridging force between the mica surfaces in asphaltene solution. The adsorption process was identified as being controlled by the diffusion of asphaltenes from the bulk solution to the mica surface with a diffusion coefficient on the order of 10-10 m2/s at room temperature, depending on the asphaltene bulk concentration. This diffusion coefficient corresponds to a hydrodynamic molecular radius of approximately 0.5 nm, indicating that asphaltene diffuses to mica surfaces as individual molecules at very low concentration (e.g., 0.01 wt %). Atomic force microscopy images of the adsorbed asphaltenes on mica support the results of the SFA force measurements. The results from the SFA force measurements provide valuable insights into the molecular interactions (e.g., steric repulsion and bridging attraction as a function of distance) of asphaltenes in organic media and hence their roles in crude oil and bitumen production

Demulsification mechanism of asphaltene-stabilized water-in-oil emulsions by a polymeric ethylene oxide-propylene oxide demulsifier

The demulsification mechanism of asphaltene-stabilized water-in-toluene emulsions by an ethylene-oxide-propylene oxide (EO-PO) based polymeric demulsifier was studied. Demulsification efficiency was determined by bottle tests and correlated to the physicochemical properties of asphaltene interfacial films after demulsifier addition. From bottle tests and droplet coalescence experiments, the demulsifier showed an optimal performance at 2.3 ppm (mass basis) in toluene. At high concentrations, the demulsification performance deteriorated due to the intrinsic stabilizing capacity of the demulsifier, which was attributed to steric repulsion between water droplets. Addition of demulsifier was shown to soften the asphaltene film (i.e., reduce the viscoelastic moduli of asphaltene films) under both shear and compressional interfacial deformations. Study of the macrostructures and the chemical composition of asphaltene film at the toluene-water interface after demulsifier addition demonstrated gradual penetration of the demulsifier into the asphaltene film. Demulsifier penetration in the asphaltene film changed the asphaltene interfacial mobility and morphology, as probed with Brewster angle and atomic force microscopy

Isolated hypercholesterolemia leads to steatosis in the liver without affecting the pancreas

Abstract Background Lipid accumulation in the liver and pancreas is primarily caused by combined hyperlipidemia. However, the effect of isolated hypercholesterolemia without hypertriglyceridemia is not fully described. Therefore, our aim was to investigate whether hypercholesterolemia alone leads to alterations both in hepatic and pancreatic lipid panel and histology in rats. Methods Male Wistar rats were fed with 2% cholesterol +0.25% cholate-supplemented diet or standard chow for 12 weeks. Blood was collected at weeks 0, 4, 8 and 12 to measure serum cholesterol and triglyceride levels. At week 12, both the pancreas and the liver were isolated for further histological and biochemical analysis. Hepatic and plasma fatty acid composition was assessed by gas chromatography. Expression of mRNA of major enzymes involved in saturated/unsaturated fatty acid synthesis was analyzed by qPCR. In separate experiments serum enzyme activities and insulin levels were measured at week 9. Results At week 12, rats fed with 2% cholesterol +0.25% cholate-supplemented diet were characterized by elevated serum cholesterol (4.09 ± 0.20 vs. 2.89 ± 0.22 mmol/L, *p < 0.05) while triglyceride (2.27 ± 0.05 vs. 2.03 ± 0.03 mmol/L) and glucose levels (5.32 ± 0.14 vs. 5.23 ± 0.10 mmol/L) remained unchanged. Isolated hypercholesterolemia increased hepatic lipid accumulation, hepatic cholesterol (5.86 ± 0.22 vs. 1.60 ± 0.15 ng/g tissue, *p < 0.05) and triglyceride contents (19.28 ± 1.42 vs. 6.78 ± 0.71 ng/g tissue, *p < 0.05), and hepatic nitrotyrosine level (4.07 ± 0.52 vs. 2.59 ± 0.31 ng/mg protein, *p < 0.05). The histology and tissue lipid content of the pancreas was not affected. Serum total protein level, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities remained unchanged in response to isolated hypercholesterolemia while serum alkaline phosphatase activity (ALP) significantly increased. Plasma insulin levels did not change in response to isolated hypercholesterolemia suggesting an intact endocrine function of the pancreas. Isolated hypercholesterolemia caused a significantly increased hepatic and serum fatty acid level associated with a marked alteration of fatty acid composition. Hepatic expression of Δ9-desaturase (SCD1) was increased 4.92×, while expression of Δ5-desaturase and Δ6-desaturase were decreased (0.447× and 0.577×, respectively) due to isolated hypercholesterolemia. Conclusions Isolated hypercholesterolemia leads to hepatic steatosis and marked alterations in the hepatic lipid profile without affecting the pancreas. Altered fatty acid profile might mediate harmful effects of cholesterol in the liver