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1582. Surface modification of cyclic olefin copolymers for osteochondral defect repair can increase pro-destructive potential of human chondrocytes in vitro
- Creator:
- Polanská, M., Hana Hulejová, Miroslav Petrtýl, Bastl, Z., Ilona Spirovová, Kruliš, Z., Zdeněk Horák, David Veigl, and Ladislav Šenolt
- Format:
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, chondrocyty, biokompatibilita, chondrocytes, biocompatibility, osteochondral defects, 14, and 612
- Language:
- English
- Description:
- Materials on the basis of cycloolefin copolymers (COC) are suitable for subchondral defect repairs. The objective of this study was to evaluate the influence of surface modification of COC and COC/LLDPE blends on the viability and gene expression of chondrocytes. Human chondrocytes were incubated on the surface of the studied materials. Half of the materials were plasmatically modified with a subsequent type II collagen application. The gene expression of matrix metalloproteinases (MMP-1,-3,-13), pro-inflammatory cytokines (IL-1, TNF-alpha) and apoptotic molecules (BAX, Bcl-2) was evaluated using quantitative Taq-Man PCR after 48 h incubation. Chondrocyte viability was evaluated by the MTT test after 2, 4 and 8 days of incubation. The synthesis of MMPs was measured by ELISA assay in cell culture medium after 48 h of incubation. Chondrocytes incubated on plasmatically modified in contrast to unmodified materials demonstrated significantly increased gene expression of IL-1 (p<0.05), MMP-1 and MMP-3 (p<0.05 for both comparisons) as well as MMP-13 (p<0.001). Increased gene expression was confirmed by significantly increased production of active forms of particular MMPs into the cell culture medium. Unlike surface unmodified polymers, the modified materials showed timedependent reduction of chondrocyte viability. The gene expression of TNF-α and apoptotic molecules by chondrocytes was not significantly changed by different materials. Cycloolefin copolymers and their blends may represent suitable materials for tissue engineering, however, their surface modification followed by collagen type II application may, at least under in vitro conditions, reduce the viability of chondrocytes and induce their pro-destructive behavior. The potential benefit or disadvantage of surface modifications of materials for osteochondral defect repairs needs to be further elucidated., M. Polanská ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1583. Susceptibility to ischemia-induced arrhythmias and the effect of preconditioning in the diabetic rat heart
- Creator:
- Ravingerová, T., Štetka, R., Dezider Pancza, Oľga Uličná, Atila Ziegelhöffer, and Ján Styk
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, experimental diabetes, myocardial ischemia, preconditioning, arrhythmias, rat heart, 14, and 612
- Language:
- English
- Description:
- Diabetic heart is suggested to exhibit either increased or decreased resistance to ischemic injury. Ischemic preconditioning suppresses arrhythmias in the normal heart, whereas relatively little is known about its effects in the diseased myocardium. Our objective was to investigate whether development of diabetes mellitus modifies the susceptibility to ischemia-induced arrhythmias and affects preconditioning in the rat heart. Following 1 and 9 weeks of streptozotocin-induced (45 mg/kg, i.v.) diabetes, the hearts were Langendorff-perfused at constant pressure of 70 mm Hg and subjected to test ischemia induced by 30 min occlusion of the left anterior descending (LAD) coronary artery. Preconditioning consisted of one cycle of 5 min ischemia and 10 min reperfusion, prior to test ischemia. Susceptibility to ischemia-induced arrhythmias was lower in 1-week diabetics: only 42 % of diabetic hearts exhibited ventricular tachycardia (VT) and 16 % had short episodes of ventricular fibrillation (VF) as compared to VT 100 % and VF 70 % (including sustained VF 36 %) in the non-diabetics (P<0.05). Development of the disease was associated with an increased incidence of VT (VT 92 %, not significantly different from non-diabetics) and longer total duration of VT and VF at 9-weeks, as compared to 1-week diabetics. Preconditioning effectively suppressed arrhythmias in the normal hearts (VT 33 %, VF 0 %). However, it did not provide any additional antiarrhythmic protection in the acute diabetes. On the other hand, in the preconditioned 9-weeks diabetic hearts, the incidence of arrhythmias tended to decrease (VT 50 %, transient VF 10 %) and their severity was reduced. Diabetic rat hearts are thus less susceptible to ischemia-induced arrhythmias in the acute phase of the disease. Development of diabetes attenuates increased ischemic tolerance, however, diabetic hearts in the chronic phase can benefit more from ischem preconditioning, due to its persisting influence., T. Ravingerová, R. Štetka, D. Pancza, O. Uličná, A. Ziegelhöffer, J. Styk., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1584. Synthesis of water-soluble star polymers based on cyclodextrins
- Creator:
- Kotrchová, L and Tomáš Etrych
- Format:
- print, bez média, and svazek
- Type:
- model:article and TEXT
- Subject:
- polymery, léky, polymers, drugs, Drug delivery system, HPMA copolymers, RAFT polymerization, Star polymers, 14, and 612
- Language:
- English
- Description:
- Novel star polymers based on the water-soluble N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer and cyclodextrin were synthesized and the physico-chemical behavior of these precursors was studied. Semitelechelic HPMA copolymers were grafted onto the cyclodextrin core, thus forming star-like structure. Both prepared systems were designed as possible polymer carriers for the controlled release of cytostatic drugs, which after the drug release and degradation will be eliminated from the organism. Two synthesis approaches were used to obtain similar polymer carriers with different degradation rates. All the polymers were prepared by reversible additionfragmentation chain-transfer polymerization, which guarantees low dispersity of the prepared systems., L. Kotrchová, T. Etrych., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
1585. Synthetic polymer scaffolds for soft tissue engineering
- Creator:
- Olga Janoušková
- Format:
- print, bez média, and svazek
- Type:
- model:article and TEXT
- Subject:
- tkáňové inženýrství, tissue engineering, synthetic 3D scaffolds, soft tissue regeneration, 14, and 612
- Language:
- English
- Description:
- Tissue engineering (TE) and regenerative medicine are progressively developed areas due to many novel tissue replacements and implementation strategies. Increasing knowledge involving the fabrication of biomaterials with advanced physicochemical and biological characteristics, successful isolation and preparation of stem cells, incorporation of growth and differentiation factors, and biomimetic environments gives us a unique opportunity to develop various types of scaffolds for TE. The current strategies for soft tissue reconstitution or regeneration highlight the importance of novel regenerative therapies in cases of significant soft tissue loss and in cases of congenital defects, disease, trauma and ageing. Various types of biomaterials and scaffolds have been tested for soft tissue regeneration. The synthetic types of materials have gained great attention due to high versatility, tunability and easy functionalization for better biocompatibility. This article reviews the current materials that are usually the most used for the fabrication of scaffolds for soft TE; in addition, the types of scaffolds together with examples of their applications for the regenerative purposes of soft tissue, as well as their major physicochemical characteristics regarding the increased applicability of these materials in medicine, are reviewed., O. Janoušková., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
1586. Systemic administration of an antagomir designed to inhibit miR-92, a regulator of angiogenesis, failed to modulate skeletal anabolic response to mechanical loading
- Creator:
- Sengul, A., Santisuk, R., Xing, W., and Kesavan, C.
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, microRNA, mechanical loading, angiogenesis, mice, microRNA-92, 14, and 612
- Language:
- English
- Description:
- The goal of this study is to evaluate if promotion of angiogenesis by systemic treatment with an antagomir against miR-92a, a well established inhibitor of angiogenesis, will maximize the benefits of exercise on bone. Ten week old female C57BL6/J mice were subjected to two weeks of external load by four point bending. During the first week of mechanical loading (ML), mice were injected (2.7 mg/kg of bodyweight) with antagomir against miR-92 or control antagomir (3 alternate days via retro-orbital). No difference in tissues weights (heart, kidney, liver) were found in mice treated with miR-92 vs. control antagomir suggesting no side effects. Two weeks of ML increased tibia TV, BV/TV and density by 6-15 %, as expected, in the control antagomir treated mice. Similar increases in the above parameters (7-16 %) were also seen in mice treated miR-92 antagomir. Administration of miR-92 antagomir was effective in reducing levels of mir-92 in heart, liver and skeletal muscle and in contrast, expression levels of two other microRNA’s miR-93 and miR-20a remain constant, thus suggesting specificity of the antagomir used. Surprisingly, we failed to detect significant changes in the expression levels of vascular genes (VEGF, CD31 and Tie2) in heart, liver or skeletal muscle. Based on these findings, we conclude that systemic administration of antagomir against miR-92 while reduced expression levels of miR-92 in the tissues; it did not significantly alter either angiogenic or osteogenic response, thus suggesting possible redundancy in miR-92 regulation of angiogenesis., A. Sengul, ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1587. Systems analysis in hypertension: complementary role of physiologists and geneticists
- Creator:
- Josef Zicha, Ivana Vaněčková, and Jaroslav Kuneš
- Format:
- print, bez média, and svazek
- Type:
- article, úvodníky, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, fyziologie, genetika, hypertension, physiology, genetics, 14, and 612
- Language:
- English
- Description:
- J. Zicha, I. Vaněčková, J. Kuneš. and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1588. T2D risk haplotypes of the TCF7L2 gene in the czech population sample: the association with free fatty acids composition
- Creator:
- Josef Včelák, Daniela Vejražková, Markéta Vaňková, Lukášová, P., Bradnová, O., Hálková, T., Bešťák, J., Kateřina Andělová, Hana Kvasničková, Petra Hoskovcová, Karel Vondra, Jana Vrbíková, and Běla Bendlová
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, TCF7L2, haplotypes, type 2 diabetes, gestational diabetes, genetics, polycystic ovary syndrome, diabetes risk, free fatty acids, polyunsaturated fatty acids, 14, and 612
- Language:
- English
- Description:
- The association of transcription factor 7-like 2 (TCF7L2) gene variants with the pathogenesis of T2D, gestational diabetes and polycystic ovary syndrome (PCOS) was examined. The study involved 1460 individuals: 347 T2D patients (D); 261 gestational diabetics (G); 147 offspring of T2D (O); 329 women with PCOS, and 376 controls (C). The SNPs: rs7901695; rs7903146; rs12255372 in the TCF7L2 gene were genotyped. Anthropometric and biochemical parameters, oGTT derived indices were assessed. In addition, free fatty acids (FFAs) were evaluated in 183 non-diabetic women. The CTT haplotype showed the strongest association with T2D with OR 1.57, p=0.0003. The frequency of the CTT/CTT haplotype was decreasing in following order: D 10.6, O 9.5, G 6.1, C 5.3 and PCOS 4.9 [%]. Among CTT carriers, significantly decreased levels of oGTT-stimulated insulin and C-peptide as well as proportions of fasting PUFAs were observed. The carriership of CTG/TCG was associated with gestational diabetes, OR 2.59, p=0.036. The association of TCF7L2 haplotypes with T2D and gestational diabetes but not with PCOS was confirmed. Novel association of TCF7L2 with FFAs composition was found., J. Včelák ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1589. T45G and G276T adiponectin gene polymorphisms in primary aldosteronism and healthy controls in an east slovak population
- Creator:
- Jochmanová, I., Viera Habalová, Helena Hatriková, Andrea Galovičová, and Ivica Lazúrová
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, primary aldosteronism, adiponectine gene polymorphism, metabolic syndrome, triglycerides, 14, and 612
- Language:
- English
- Description:
- Metabolic complications are frequent in primary aldosteronism (PA) and adiponectin gene polymorphisms seem to confer a genetic risk for metabolic alterations. Aim of the study was to evaluate the prevalence of metabolic symptoms in patients with PA compared to controls and the prevalence of two single nucleotide polymorphisms (SNPs), T45G and G276T, in the adiponectin gene and their relationship to metabolic syndrome (MS). The study involved 47 patients with PA and 90 controls selected from general population. Body mass index (BMI), and selected biochemical parametres were examined, and the mentioned SNPs were genotyped in all subjects. PA pati ents had a significantly higher BMI (p < 0.0001), blood glucose level (p < 0.01), and triglycerides (p < 0.0005) compared to controls. There were no significant differences in the prevalence of the studied genotypes of adiponectin gene polymorphisms. The 276GT genotype was linked with lower levels of triglycerides (p ≤ 0.05), while 276GG was related to higher levels of triglycerides (p=0.01). A similar but non- significant tendency was observed in relation to cholesterol levels. We can conclude that PA patients with the 276GT genotype have lower triglycerides levels, but there are not significant differences in the distribution of genotypes and alleles among PA patients and controls in an East Slovak population., I. Jochmanová, ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1590. Targeted deletion of MMP-9 attenuates myocardial contractile dysfunction in heart failure
- Creator:
- Moshal, K. S., Rodriguez, W. E., Sen, U., and Tyagi, Suresh C.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, biofyzika, srdeční selhání, physiology, biophysics, heart failure, endothelial-myocyte uncoupling, ventricular contraction, volume overload, left ventricle (LV) rings, aortocaval shunt, 14, and 612
- Language:
- English
- Description:
- Chronic volume overload (VO) on the left ventricle (LV) augments redox stress and activates matrix metalloproteinase (MMP) which causes the endocardial endothelial-myocyte (EM) disconnection leading to myocardial contractile dysfunction. VO-induced MMP-9 activation impairs cardiac functions, in part by endothelial endocardial apoptosis, but the role of MMP-9 on EM functions remains obscure. We conjecture that chronic VO activates MMP-9 and causes EM uncoupling. Arteriovenous fistula (AVF) was created in genetically identical wild type (WT) mice (FVB/NJ) and MMP-9 knockout mice (MMP-9KO, FVB.Cg-MMP9tm1Tvu/J). Sham-operated mice were used as controls. Before experimentation the phenotype analysis of MMP-9KO mice was carried out. In-gel-gelatin zymography for MMP-9 activation was performed on LV homogenates. The EM functions were determined on LV rings using tissue myobath. We report a decrease in MMP-9 activity in left ventricular myocardial extracts in MMP-9 deficient mice after AVF. The responses to drugs affecting cardiac functions (acetylcholine (Ach), nitroprusside and bradykinin) were attenuated in AVF mice suggesting the impairment of EM coupling. Interestingly, the EM functions were restored in the MMP-9 deficient mice after AVF. We suggest a direct cause-and-effect relationship between MMP-9 activation and EM uncoupling in LV myocardium after chronic VO and the possible involvement of MMP-9 in myocardial contractile performance., K. S. Moshal, W. E. Rodriguez, U. Sen, S. C. Tyagi., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public