Basketball players possess a higher bone mineral density than matched non-athletes, swimming, soccer, and volleyball athletes: a systematic review and meta-analysis
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01.12.2020 |
Stojanović E.
Radovanović D.
Dalbo V.J.
Jakovljević V.
Ponorac N.
Agostinete R.R.
Svoboda Z.
Scanlan A.T.
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Archives of Osteoporosis |
10.1007/s11657-020-00803-7 |
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© 2020, International Osteoporosis Foundation and National Osteoporosis Foundation. Summary: Basketball athletes possess a higher bone mineral density (BMD) than matched non-athletes and swimming, soccer, and volleyball athletes. Differences appear to be exacerbated with continued training and competition beyond adolescence. The greater BMD in basketball athletes compared to non-athletes, swimming, and soccer athletes is more pronounced in males than females. Purpose: The aim of this study was to examine differences in total and regional bone mineral density (BMD) between basketball athletes, non-athletes, and athletes competing in swimming, soccer, and volleyball, considering age and sex. Methods: PubMed, MEDLINE, ERIC, Google Scholar, and Science Direct were searched. Included studies consisted of basketball players and at least one group of non-athletes, swimming, soccer, or volleyball athletes. BMD data were meta-analyzed. Cohen’s d effect sizes [95% confidence intervals (CI)] were interpreted as: trivial ≤ 0.20, small = 0.20–0.59, moderate = 0.60–1.19, large = 1.20–1.99, and very large ≥ 2.00. Results: Basketball athletes exhibited significantly (p < 0.05) higher BMD compared to non-athletes (small-moderate effect in total-body: d = 1.06, CI 0.55, 1.56; spine: d = 0.67, CI 0.40, 0.93; lumbar spine: d = 0.96, CI 0.57, 1.35; upper limbs: d = 0.70, CI 0.29, 1.10; lower limbs: d = 1.14, CI 0.60, 1.68; pelvis: d = 1.16, CI 0.05, 2.26; trunk: d = 1.00, CI 0.65, 1.35; and femoral neck: d = 0.57, CI 0.16, 0.99), swimming athletes (moderate-very large effect in total-body: d = 1.33, CI 0.59, 2.08; spine: d = 1.04, CI 0.60, 1.48; upper limbs: d = 1.19, CI 0.16, 2.22; lower limbs: d = 2.76, CI 1.45, 4.06; pelvis d = 1.72, CI 0.63, 2.81; and trunk: d = 1.61, CI 1.19, 2.04), soccer athletes (small effect in total-body: d = 0.58, CI 0.18, 0.97), and volleyball athletes (small effect in total-body: d = 0.32, CI 0.00, 0.65; and pelvis: d = 0.48, CI 0.07, 0.88). Differences in total and regional BMD between groups increased with age and appeared greater in males than in females. Conclusion: Basketball athletes exhibit a greater BMD compared to non-athletes, as well as athletes involved in swimming, soccer, and volleyball.
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Lung epithelium damage in COPD – An unstoppable pathological event?
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01.04.2020 |
Hadzic S.
Wu C.
Avdeev S.
Weissmann N.
Schermuly R.
Kosanovic D.
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Cellular Signalling |
10.1016/j.cellsig.2020.109540 |
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© 2020 Elsevier Inc. Chronic obstructive pulmonary disease (COPD) is a common term for alveolar septal wall destruction resulting in emphysema, and chronic bronchitis accompanied by conductive airway remodelling. In general, this disease is characterized by a disbalance of proteolytic/anti-proteolytic activity, augmented inflammatory response, increased oxidative/nitrosative stress, rise in number of apoptotic cells and decreased proliferation. As the first responder to the various environmental stimuli, epithelium occupies an important position in different lung pathologies, including COPD. Epithelium sequentially transitions from the upper airways in the direction of the gas exchange surface in the alveoli, and every cell type possesses a distinct role in the maintenance of the homeostasis. Basically, a thick ciliated structure of the airway epithelium has a major function in mucus secretion, whereas, alveolar epithelium which forms a thin barrier covered by surfactant has a function in gas exchange. Following this line, we will try to reveal whether or not the chronic bronchitis and emphysema, being two pathological phenotypes in COPD, could originate in two different types of epithelium. In addition, this review focuses on the role of lung epithelium in COPD pathology, and summarises underlying mechanisms and potential therapeutics.
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Hemodynamic factors associated with fetal cardiac remodeling in late fetal growth restriction: A prospective study
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01.09.2019 |
Rizzo G.
Mattioli C.
Mappa I.
Bitsadze V.
Khizroeva J.
Słodki M.
Makatsarya A.
D'Antonio F.
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Journal of Perinatal Medicine |
10.1515/jpm-2019-0217 |
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© 2019 Walter de Gruyter GmbH, Berlin/Boston. Altered cardiac geometry affects a proportion of fetuses with growth restriction (FGR). The aim of this study was to explore the hemodynamic factors associated with cardiac remodeling in late FGR. This was a prospective study of singleton pregnancies complicated by late-onset FGR undergoing assessment of left (LV) and right (RV) ventricular sphericity-index (SI). The study population was divided in two groups according to the presence of cardiac remodelling, defined as LVSI <5th centile. The following outcomes were explored: Gestational age at birth, birthweight, caesarean section (CS) for fetal distress, umbilical artery (UA) pH and neonatal admission to special care unit. The differences between the 2 groups in UA pulsatility index (PI), middle cerebral artery (MCA) PI, uterine artery PI, cerebroplacental ratio (CPR) and umbilical vein (UV) flow corrected for fetal abdominal circumference (UVBF/AC) were tested. In total, 212 pregnancies with late FGR were enrolled in the study. An abnormal LV SI was detected in 119 fetuses (56.1%). Late FGR fetuses with cardiac remodeling had a lower birthweight (2390 g vs. 2490; P = 0.04) and umbilical artery pH (7.21 vs. 7.24; P = 0.04) and were more likely to have emergency CS (42.8% vs. 26.9%; P = 0.023) and admission to special care unit (13.4% vs. 4.3%; P = 0.03) compared to those with normal LVSI. No difference in either UA PI (p = 0.904), MCA PI (P = 0.575), CPR (P = 0.607) and mean uterine artery PI (P = 0.756) were present between fetuses with or without an abnormal LV SI. Conversely, UVBF/AC z-score was lower (-1.84 vs.-0.99; P ≤ 0.001) in fetuses with cardiac remodeling and correlated with LV (P ≤ 0.01) and RV SI (P ≤ 0.02). Fetal cardiac remodelling occurs in a significant proportion of pregnancies complicated by late FGR and is affected by a high burden of short-term perinatal compromise. The occurrence of LV SI is independent from fetal arterial Dopplers while it is positively associated with umbilical vein blood flow.
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Genetic re-engineering of polyunsaturated phospholipid profile of Saccharomyces cerevisiae identifies a novel role for Cld1 in mitigating the effects of cardiolipin peroxidation
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01.10.2018 |
Lou W.
Ting H.
Reynolds C.
Tyurina Y.
Tyurin V.
Li Y.
Ji J.
Yu W.
Liang Z.
Stoyanovsky D.
Anthonymuthu T.
Frasso M.
Wipf P.
Greenberger J.
Bayır H.
Kagan V.
Greenberg M.
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Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids |
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© 2018 Elsevier B.V. Cardiolipin (CL) is a unique phospholipid localized almost exclusively within the mitochondrial membranes where it is synthesized. Newly synthesized CL undergoes acyl remodeling to produce CL species enriched with unsaturated acyl groups. Cld1 is the only identified CL-specific phospholipase in yeast and is required to initiate the CL remodeling pathway. In higher eukaryotes, peroxidation of CL, yielding CLOX, has been implicated in the cellular signaling events that initiate apoptosis. CLOX can undergo enzymatic hydrolysis, resulting in the release of lipid mediators with signaling properties. Our previous findings suggested that CLD1 expression is upregulated in response to oxidative stress, and that one of the physiological roles of CL remodeling is to remove peroxidized CL. To exploit the powerful yeast model to study functions of CLD1 in CL peroxidation, we expressed the H. brasiliensis Δ12-desaturase gene in yeast, which then synthesized poly unsaturated fatty acids(PUFAs) that are incorporated into CL species. Using LC-MS based redox phospholipidomics, we identified and quantified the molecular species of CL and other phospholipids in cld1Δ vs. WT cells. Loss of CLD1 led to a dramatic decrease in chronological lifespan, mitochondrial membrane potential, and respiratory capacity; it also resulted in increased levels of mono-hydroperoxy-CLs, particularly among the highly unsaturated CL species, including tetralinoleoyl-CL. In addition, purified Cld1 exhibited a higher affinity for CLOX, and treatment of cells with H2O2 increased CLD1 expression in the logarithmic growth phase. These data suggest that CLD1 expression is required to mitigate oxidative stress. The findings from this study contribute to our overall understanding of CL remodeling and its role in mitigating oxidative stress.
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Regulatory element in fibrin triggers tension-activated transition from catch to slip bonds
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21.08.2018 |
Litvinov R.
Kononova O.
Zhmurov A.
Marx K.
Barsegov V.
Thirumalai D.
Weisel J.
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Proceedings of the National Academy of Sciences of the United States of America |
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© 2018 National Academy of Sciences. All Rights Reserved. Fibrin formation and mechanical stability are essential in thrombosis and hemostasis. To reveal how mechanical load impacts fibrin, we carried out optical trap-based single-molecule forced unbinding experiments. The strength of noncovalent A:a knob-hole bond stabilizing fibrin polymers first increases with tensile force (catch bonds) and then decreases with force when the force exceeds a critical value (slip bonds). To provide the structural basis of catch–slip-bond behavior, we analyzed crystal structures and performed molecular modeling of A:a knob-hole complex. The movable flap (residues γ295 to γ305) containing the weak calcium-binding site γ2 serves as a tension sensor. Flap dissociation from the B domain in the γ-nodule and translocation to knob ‘A’ triggers hole ‘a’ closure, resulting in the increase of binding affinity and prolonged bond lifetimes. The discovery of biphasic kinetics of knob-hole bond rupture is quantitatively explained by using a theory, formulated in terms of structural transitions in the binding pocket between the low-affinity (slip) and high-affinity (catch) states. We provide a general framework to understand the mechanical response of protein pairs capable of tension-induced remodeling of their association interface. Strengthening of the A:a knob-hole bonds at 30- to 40-pN forces might favor formation of nascent fibrin clots subject to hydrodynamic shear in vivo.
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Matrix metalloproteinases: Role in cardiac remodeling in patients with connective tissue dysplasia
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01.01.2018 |
Djazaeva M.
Gladkikh N.
Reshetnikov V.
Yagoda A.
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Medical News of North Caucasus |
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© 2018 Stavropol State Medical University. All Rights Reserved. 57 men and 43 women, aged 22.0±4.2 years were examined to determine the clinical and prognostic value of matrix metalloproteinases in heart remodeling in CTD. Serum concentrations of MMP-1, MMP-9, TIMP-1 were determined by ELI-SA («Cloud-Clone Corp.», China). Imbalance of MMP-1, MMP-9 and their inhibitor - TIMP-1 was revealed in patients with CTD. Significant increase in MMP-1 level was registered in cases of MVP with myxomatous degeneration and mitral regurgitation of II degree. Risk of cardiac remodeling progression at three-year follow-up increases in cases of elevated of MMP-1/TIMP-1 coefficient. Identified changes in the MMPs system in patients with CTD may be used as additional criteria of severity and determination of probability of progression of heart connective tissue structures remodeling.
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Effects of fixed combination of indacaterol/glycopyrronium in chronic obstructive pulmonary disease: State-of-the art review
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01.01.2018 |
Avdeev S.
Trushenko N.
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Pulmonologiya |
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© 2018 Medical Education. All rights reserved. Long-acting bronchodilators (long-acting β 2 -agonists (LABA), long-acting anticholinergics (LAMA) and their combinations) are the basic drugs for treatment of stable chronic obstructive pulmonary disease (COPD). Indacaterol/glycopyrronium (IND/GLY) is the first fixed LABA/LAMA combination acquired significant evidence of its efficacy for improvement lung function, symptoms, and quality of life, and decrease in the rate of acute exacerbations of COPD. The aim of this review was to reassess clinical efficacy of IND/GLY in treatment of COPD with regard to recent data and to outline the further role of this combination in therapy of COPD.
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The effects of angiotensin-converting enzyme inhibitors in heart recipients: A single center experience
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01.01.2018 |
Shevchenko A.
Faradzhov R.
Izotov D.
Koloskova N.
Nikitina E.
Gichkun O.
Orlov V.
Tunyaeva I.
Mironkov B.
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Vestnik Transplantologii i Iskusstvennykh Organov |
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© 2018 Russian Transplant Society. All Rights Reserved. Aim. To study the effect of ACE inhibitors (ACEI) in heart recipients on the prognosis and myocardial remodeling. Materials and methods. Three hundred and eighty-six patients who received orthotopic heart transplantation (HT) were consequently enrolled to the study from February 2009 to November 2016. Results. Thirty days after the HT, ACEIs were assigned to 141 recipients. Arterial hypertension was diagnosed in all cardiac recipients who received ACEI and among 48 patients (19.5%) from non-ACEI group. Patients receiving ACEI had significantly better event-free survival than control group (p = 0.045) during the follow-up for 1361,6 ± 36,9 days. Left ventricle (LV) end-diastolic dimension did not change over the time in both groups, whereas LV posterior wall thickness in non-ACEI group significantly increased from 1.35 ± 0.03 cm to 1,23 ± 0.05 cm (p < 0.05). Conclusion. Cardiac recipients who received ACE inhibitors had better survival and less transplant left ventricle progression, that could reflect beneficial effects of renin-aldosterone-angiotensin system inhibition after heart transplantation.
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