Physico-chemical properties and carbohydrate-binding specificity of hemagglutination activity (HA) were compared in tissue lysates and haemolymph of unfed and bloodied females of five sandfly species. Sandfly gut lectins were found to be heat-labile, sensitive to dithiotreitol treatment, freezing/thawing procedures and were affected by divalent cations. The pH optimum of HA ranged between 7.0-7.5. Specificity of gut HA of all species studied was directed towards aminosugars and some glycoconjugates, mainly lipopolysaccharide from Escherichia coli K-235, heparin and fetuin. Gut HA of Phlebotomus papatasi (Scopoli, 1786) was strongly inhibited by lipophosphoglycan (LPG) from Leishmania major promastigotes. In females, that took blood, the HA was higher but the carbohydrate-binding specificity remained the same; this suggests that the same lectin molecule was present, at different levels, both in unfed and fed flies. High HA was found in ovaries of fed females of Lutzomyia longipalpis (Lutz et Nieva, 1912), P. papatasi and P. duhoscqi Neveu-Lemaire, 1906. In P. papatasi and P. duboscqi the HA was present also in the haemolymph and head lysates of both fed and unfed females. Carbohydrate-binding specificity of HA present in these tissues was similar with the gut lectin.
Maghemite (γ-Fe2O3) nanoparticles, 12 nm in size, were prepared by co-precipitation of Fe(II) and Fe(III) chlorides with ammonium hydroxide and oxidation with hydrogen peroxide. To achieve stability and biocompatibility, obtained particles were coated with silica, to which glucose and ascorbic acid were bound by different mechanisms. The composite particles were thoroughly characterized by transmission electron microscopy, dynamic light scattering, elemental analysis, and FT-Raman and fluorescence spectroscopy to determine composition, morphology, size and its distribution, ζ-potential, and scavenging of peroxyl and hydroxyl radicals. As the particles showed promising antioxidative properties, they may have a possible application as a stable magnetically controlled scavenger of reactive oxygen species., M. Moskvin, D. Horák., and Obsahuje bibliografii
Carcinopodacarus polymorphus gen. n. et sp. n. (Acariformes: Dermationidae: Dermationinae) is described from the guira cuckoo Guira guira (Gmelin) (Cuculiformes: Cuculidae) in Brazil. The new genus differs from the closest genus, Psittophagoides Fain, 1964, by the following features: in both sexes, the anterior spines of trochanters I and II are absent (vs present in Psittophagoides), setae d2 are distinctly developed (vs only alveoli), and genual setae mGI are absent (vs present); in males, the hysteronotal shield is split transversally at the level of trochanters III (vs hysteronotal shield entire); in females, the platelets situated posterior to the propodonotal shield are absent (vs present), the metapodosomal sclerites are present (vs absent), and the adanal shields are fused anteriorly to each other (vs separated from each other). In this species, andropolymorphism is detected for the first time for the family. It involves various characters but the most impressive feature is the structure of legs III. In hetero- and mesomorphic males, these legs are strongly hypertrophied and have a distinct ventral spur on femora III; in homeomorphic males, legs III are not modified and subequal to legs IV., Fabio Akashi Hernandes, Luiz Gustavo A. Pedroso, Andre V. Bochkov., and Obsahuje bibliografii
AT1 receptor (AT1R) blockade prevents physiological cardiac hypertrophy induced by resistance training. Also, our group showed that a single bout of resistance exercise (RE) activates the AKT/mTOR which was also inhibited by AT1R blocker. Here, we investigated whether IGF1-receptor (IGF1-R) and MAPKs were also activated after a single bout of RE. Wistar rats were divided into Sedentary (Sed), Sedentary treated with losartan (Sed+LOS), Exercise (EX), and Exercise treated with losartan (EX+LOS). Cardiac tissue was obtained 5 and 30 min after 4 sets of 12 repetitions of squat exercise (80 % 1RM). We demonstrated that a single bout of RE did not induce IGF1-R tyrosine phosphorylation. ERK1/2 and P38 phosphorylation levels were elevated in the EX 5min and EX 30min groups however, only ERK1/2 was inhibited by losartan treatment (AT1R blocker). Next, we showed that β-arrestin-2 expression increased 28 % in trained animals compared to sedentary group. Altogether, our results demonstrate that AT1R, but not IGF1-R, may exert the hypertrophic cardiac stimulus RE-induced. Also, activation of AKT/mTOR and ERK1/2 pathways may occur through the
β-arrestin-dependent pathway.
Thyroid hormones are powerful modulators of heart function and susceptibility to arrhythmias via both genomic and non-genomic actions. We aimed to explore expression of electrical coupling protein connexin-43 (Cx43) in the heart of rats with altered thyroid status and impact of omega-3 polyunsaturated fatty acids (omega-3) supplementation. Adult male Lewis rats were divided into following six groups: euthyroid controls, hyperthyroid (treated with T3) and hypothyroid (treated with methimazol) with or without six-weeks lasting supplementation with omega-3 (20 mg/100 g/day). Left and right ventricles, septum and atria were used for immunoblotting of Cx43 and protein kinase C (PKC). Total expression of Cx43 and its phosphorylated forms were significantly increased in all heart regions of hypothyroid rats compared to euthyroid controls. In contrast, the total levels of Cx43 and its functional phosphorylated forms were decreased in atria and left ventricle of hyperthyroid rats. In parallel, the expression of PKC epsilon that phosphorylates Cx43, at serine 368, was increased in hypothyroid but decreased in hyperthyroid rat hearts. Omega-3 intake did not significantly affect either Cx43 or PKC epsilon alterations. In conclusion, there is an inverse relationship between expression of cardiac Cx43 and the levels of circulating thyroid hormones. It appears that increased propensity of hyperthyroid while decreased of hypothyroid individuals to malignant arrhythmias may be in part attributed to the changes in myocardial Cx43., B. Szeiffová Bačová, T. Egan Beňová, C. Viczenczová, T. Soukup, H. Rauchová, S. Pavelka, V. Knezl, M. Barančík, N. Tribulová., and Obsahuje bibliografii
The contrasting pattern of cardiac inotropy induced by human peptide endothelin-1 (ET-1) has not been satisfactorily explained. It is not clear whether ET-1 is primarily responsible for increased myocardial ET-1 expression and release with resultant inotropic effects, or for the induction of myocardial hypertrophy and heart failure. There are at least two subtypes of endothelin receptors (ETA and ETB) and the inotropic effects of ET-1 differ depending on the receptor involved. Along with some other groups, we reported significant subtype-ETB endothelin receptor down-regulation in human cardiac cells preincubated with endothelin agonists (Dřímal et al. 1999, 2000). The present study was therefore designed to clarify the subtype-selective mechanisms underlying the inotropic response to ET-1 and to its ETB-selective fragment (8-21)ET-1 in the isolated rat heart. The hearts were subjected to (1-21)ET-1 and to (8-21)ET-1, or to 30 min of stop-flow ischemia followed by 40 min of reperfusion, both before and after selective blockade of endothelin receptors.The present study revealed that both peptides, ET-1 and its (8-21)ET-1 fragment, significantly reduced coronary blood flow in nmolar and higher concentrations. The concomitant negative inotropy and chronotropy were marked after ET-1, while the infusion of the ET-1(8-21) fragment produced a slight but significant positive inotropic effect. Among the four endothelin antagonists tested in continuous infusion only the non-selective PD145065 and ETB1/B2-selective BQ788 (in mmolar concentrations) slightly reduced the early contractile dysfunction of the heart induced by ischemia, whereas ETA-selective PD155080 partially protected the rat heart on reperfusion., J. Dřímal, V. Knezl, J. Dřímal Jr , D. Dřímal, K. Bauerová , V. Kettmann, A.M. Doherty , M. Štefek., and Obsahuje bibliografii
Hypothermic incubation of chicken eggs leads to smaller embryos with enlarged hearts, originally described as hypertrophic. Over the years, however, accumulated evidence suggested that hyperplasia, rather than hypertrophy, is the predominant mechanism of cardiac growth during the prenatal period. We have thus set to reevaluate the hypothermia model to precise the exact cellular mechanism behind cardiac enlargement. Fertilized chicken eggs were incubated at either 37.5 °C (normothermia) or 33.5 °C from embryonic day (ED) 13 onward (hypothermia). Sampling was performed at ED17, at which point wet embryo and heart weight were recorded, and the hearts were submitted to histological examination. In agreement with previous results, the hypothermic embryos were 29% smaller and had hearts 18% larger, translating into a 67% increase in the heart to body weight ratio (P < 0.05 for all parameters). The cell size was essentially the same between control and hypothermic hearts in all regions analysed. Likewise, there was no significant relationship between the cell size and heart weight; however, in the hypothermic hearts, there was a trend showing positive correlation between cell sizes in different cardiac regions and heart weight. Proliferation rate, determined on the basis of anti-phosphohistone H3 immunofluorescence, showed an overall increase in the hypothermic group, reaching statistical significance (P = 0.02, t-test) in the right ventricle. The proliferation rate was similar among different regions of the same heart. However, the correlation between the proliferation rate and heart weight was only small (r2 = 0.007 and r2 = 0.234 for the normothermic and hypothermic group, respectively). We thus
conclude that hyperplasia is the predominant response mechanism in this volume-overload model; mechanistically, decreased heart rate at lower temperature increases the end-diastolic and stroke volume, minimizing the drop in cardiac output through the Frank-Starling mechanism. and Corresponding author: David Sedmera
Cardiac micropotentials are considered to have a predictive value in critical ventricular tachycardia or sudden death. These micropotentials are obtained by numeric filtration of the result of sequential averaging of about 200 systoles (i.e. of measurement at about 3 min interval) which is significantly influenced by known intraindividual ECG variability. It follows from our previous studies that the non-dipolar residue (i.e. the sum of all components of an equivalent source of the heart electrical field with the exception of the first three dominant dipolar components) corresponds by its nature to the cardiac micropotentials, i.e. to late potentials. Verification of this hypothesis utilizing singular value decomposition and replacing the sequential averaging by "surface" averaging of the matrix of synchronously measured ECGs is the aim of this project. The results of the present study can be considered as a confirmation of this hypothesis. These results provide a better understanding of the structure of the body surface potential distribution and for clinical purposes they make it possible to attain cardiac micropotentials (late potentials) from one systole.
Our aim was to evaluate whether endothelial overexpressing of the bradykinin B1 receptor could be associated with altered left ventricular and myocardial performance. Echocardiography and hemodynamic were employed to assess left ventricular morphology and function in Sprague Dawley transgenic rats overexpressing the endothelial bradykinin B1 receptor (Tie2B1 rats). The myocardial inotropism was evaluated on papillary muscles contracting in vitro. In Tie2B1 animals, an enlarged left ventricular cavity and lower fractional shortening coupled with a lower rate of pressure change values indicated depressed left ventricular performance. Papillary muscle mechanics revealed that both Tie2B1 and wild-type rat groups had the same contractile capacities under basal conditions;
however, in transgenic animals, there was accentuated inotropism due to post-pause potentiation. Following treatment with the Arg9-BK agonist, Tie2B1 papillary muscles displayed a reduction in myocardial inotropism. Endothelial B1 receptor overexpression has expanded the LV cavity and worsened its function. There was an exacerbated response of papillary muscle in vitro to a prolonged resting pause, and the use of a B1 receptor agonist impairs myocardial inotropism.
The matrix metalloproteinases (MMPs) play a key role during cardiac remodeling. The aim of the study was to investigate the changes in collagenous proteins and MMPs in the model of non-ischemic, anthracycline-induced chronic cardiomyopathy in rabbits using both biochemical and histological approaches. The study was carried out in three groups of Chinchilla male rabbits: 1) daunorubicin (3 mg/kg, once weekly for 10 weeks), 2) control (saline in the same schedule), 3) daunorubicin with the cardioprotectant dexrazoxane (60 mg/kg, before each daunorubicin). Morphological changes in the myocardium of daunorubicin-treated animals were characterized by focal myocardial interstitial fibrosis of different intensity. The subsequent proliferation of the fibrotic tissue was marked by an increased content of both collagen types I and III, which resulted in their typical coexpression in the majority of bundles of fibers forming either smaller or larger scars. Biochemical analysis showed a significantly increased concentration of hydroxyproline, mainly in the pepsin-insoluble fraction of collagenous proteins, in the daunorubicin-treated group (1.42±0.12 mg/g) as compared with the control (1.03±0.04 mg/g) and dexrazoxane (1.07±0.07 mg/g) groups. Dexrazoxane co-administration remarkably reduced the cardiotoxic effects of daunorubicin to the extent comparable with the controls in all evaluated parameters. Using zymography, it was possible to detect only a gelatinolytic band corresponding to MMP-2 (MMP-9 activity was not detectable). However, no significant changes in MMP-2 activity were determined between individual groups. Immunohistochemical analysis revealed increased MMP-2 expression in both cardiomyocytes and fibroblasts. Thus, this study has revealed specific alterations in the collagen network in chronic anthracycline cardiotoxicity in relationship to the expression and activity of major MMPs., M. Adamcová ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy