Decrease in QRS amplitude in juvenile female competitive athletes during the initial twenty-one months of intensive training

Background: The aim of this project was to study changes in QRS amplitude in junior female athletes during the initial twenty-one months of competitive training programme in aerobic gymnastics. Methods: Somatometric parameters, heart rate (HR), blood pressure (BP) and 12-lead ECGs were recorded in 12 female athletes, aged 13-17 years (average 13.8) at 3-month intervals over a period of 21 months. The Sokolow-Lyon index (SLI) and the maximum QRS spatial vector magnitude (QRSmax), approximated from RV5, RaVF and SV2 voltages, were analyzed. Results: The mean values of QRSmax and SLI decreased gradually during the study period. The difference between the mean QRSmax values at the beginning and at the end of the study period was -0.8 mV (30.8%), p < 0.001, and between the initial and final values of SLI was -0.6 mV (24%), p < 0.001. The somatometric parameters changed only slightly, HR and systolic BP values did not change significantly. Conclusions: This study showed that 21 months of competitive aerobic gymnastics training led to a decrease in the QRSmax magnitude. This finding is in contrast with the classical hypothesis on the ECG diagnostics of LVH and is in agreement with an alternative hypothesis on the relative voltage deficit during the early stage of LVH development. (Cardiol J 2007; 14: 260-265

Assembly of a polymer lab-on-chip device for impedimetric measurements of D-dimers in whole blood

This paper reports the development and characterisation of an assembly technology for a polymer lab-on-chip. The system consists of a 150 m deep hot embossed microfluidic channel in polycarbonate and Au electrodes fabricated separately by photolithography on polyethylenenaphthalate. The system is designed for impedimetric immunoassay detection in whole blood. Electrode layer and microfluidic substrate are joined by means of a 50 m thick double-sided medical grade adhesive tape, adjusted with an optical alignment system. The bond proved to be liquid tight at room temperature. An alignment accuracy of 34 m (+/- 19 m) evaluated over a set of 23 samples, was achieved. The effect of alignment accuracy of the intermediate adhesive film on whole blood flow properties in the device is studied. Already an alignment error of 70 m increases the flushing out time of whole blood by approximately 20 %

Posttranslational modifications of calcium/calmodulin-dependent protein kinase IIdelta and its downstream signaling in human failing hearts

BACKGROUND: In human failing hearts (HF) of different origin (coronary artery disease-CAD, dilated-DCM, restrictive and hypertrophic cardiomyopathy-OTHER), we investigated the active forms of Ca2+/calmodulin-dependent protein kinase IIdelta (p-Thr287-CaMKIIdelta, oxMet281/282-CaMKIIdelta) and their role in phenotypes of the disease. METHODS AND RESULTS: Although basic diagnostic and clinical markers indicating the attenuated cardiac contractility and remodeling were comparable in HF groups, CaMKIIdelta-mediated axis was different. P-Thr287-CaMKIIdelta was unaltered in CAD group, whereas it was upregulated in non-ischemic cardiomyopathic groups. No correlation between the upregulated p-Thr287-CaMKIIdelta and QT interval prolongation was detected. Unlike in DCM, oxMet281/282-CaMKIIdelta did not differ among HF groups. Independently of CaMKIIdelta phosphorylation/oxidation, activation of its downstreams-phospholamban and cardiac myosin binding protein-C was significantly downregulated supporting both diminished cardiac lusitropy and inotropy in all hearts. Content of sarcoplasmic reticulum Ca2+-ATPase 2a in all HF was unchanged. Protein phosphatase1beta was upregulated in CAD and DCM only, while 2A did not differ among groups. CONCLUSION: This is the first demonstration that the posttranslational activation of CaMKIIdelta differs in HF depending on etiology. Lower levels of downstream molecular targets of CaMKIIdelta do not correlate with either activation of CaMKIIdelta or the expression of major protein phosphatases in the HF. Thus, it is unlikely that these mechanisms exclusively underlie failing of the heart

P424Short-term ACE Inhibition upregulates cardiac expression of SERCA2a and protects against ventricular arrhythmias in healthy rats

Introduction: Chronic angiotensin converting enzyme inhibitor (ACEIs) treatment can suppress arrhythmogenesis. To examine whether the effect is more immediate and independent of suppression of pathological remodelling, we tested the antiarrhythmic effect of short-term ACE inhibition in healthy normotensive rats. Methods and results: Wistar rats were administered with enalaprilat (ENA, i.p., 5 mg/kg every 12 h) or vehicle (CON) for two weeks. Cellular shortening was measured in isolated, electrically paced cardiomyocytes. Standard 12-lead electrocardiography was performed and, hearts of anesthetized open-chest rats were subjected to 6-min ischemia followed by 10-minute reperfusion to examine susceptibility to ventricular arrhythmias. Expressions of calcium regulating proteins (SERCA2a, cardiac sarco/endoplasmic reticulum Ca2+-ATPase; CSQ, calsequestrin; TRD, triadin; PLB, phospholamban; FKBP12.6, FK506-binding protein) were measured by Western blot and mRNA levels of L-type calcium channel (Cacna1c), ryanodine receptor (Ryr2) and potassium channels Kcnh2 and Kcnq1 were measured by qRT-PCR. ENA decreased systolic as well as diastolic blood pressure (by 20%, and by 31%, respectively, for both P<0.05) but enhanced shortening of cardiomyocytes at basal conditions (by 34%, P<0.05) and under beta-adrenergic stimulation (by 73%, P<0.05). Enalaprilat shortened QTc interval duration (CON: 78±1 ms vs. ENA: 72±2 ms; P<0.05) and significantly decreased the total duration of ventricular fibrillations (VF) and the number of VF episodes (P<0.05). Reduction in arrhythmogenesis was associated with a pronounced upregulation of SERCA2a and increased Cacna1c mRNA levels. Conclusion: Short-term ACEI treatment can provide protection against I/R injury-induced ventricular arrhythmias in healthy myocardium and this effect is associated with increased SERCA2a expression. CON ENA Calcium regulating proteins SERCA2a 100±20 304±13* CSQ 100±6 105±7 TRD 100±16 117±10 PLB 100±9 109±16 FKBP12 100±12 93±

Zmniejszenie amplitudy zespołu QRS u młodych kobiet uprawiających sport podczas początkowego okresu intensywnego treningu fizycznego trwającego 21 miesięcy

Wstęp: Celem niniejszego badania była ocena zmian wartości amplitudy napięcia zespołu QRS u młodych kobiet uprawiających sport podczas 21-miesięcznego okresu intensywnego treningu rywalizacyjnego w zakresie aerobiku gimnastycznego. Metody: Przez okres 21 miesięcy w grupie uprawiających sport 12 młodych kobiet w wieku 13-17 lat (średnio 13,8 roku) w co 3-miesięcznych odstępach analizowano parametry antropometryczne, częstość akcji serca, ciśnienie tętnicze oraz wybrane wskaźniki 12-odprowadzeniowego badania elektrokardiograficznego. Analizie poddano wyliczone wcześniej: wskaźnik Sokołowa- Lyona (SLI) oraz wartość tak zwanego maksymalnego wektora przestrzennego zespołu QRS (QRSmax), ocenionego na podstawie wartości amplitudy załamków: R w odprowadzeniu V5 (RV5), R w odprowadzeniu aVF (RaVF) oraz S w odprowadzeniu V2 (SV2). Wyniki: Średnia wartość QRSmax oraz SLI stopniowo zmniejszyła się podczas trwania okresu treningu. Różnica między średnią wartością QRSmax na początku oraz na końcu badania wynosiła: -0,8 mV (30,8%, p < 0,001), zaś pomiędzy początkową i końcową wartością SLI: -0,6 mV (24%, p < 0,001). Parametry antropometryczne uległy jedynie niewielkiej zmianie, częstość akcji serca oraz skurczowe ciśnienie tętnicze nie zmieniły się w istotny sposób. Wnioski: W badaniu wykazano, że wdrożenie trwającego 21 miesięcy rywalizacyjnego treningu w zakresie aerobiku gimnastycznego spowodowało zmniejszenie wartości maksymalnego wektora przestrzennego zespołu QRS. Wyniki te są odmienne niż klasyczna hipoteza, na której opiera się elektrokardiograficzna diagnostyka przerostu lewej komory oraz zgodne z założeniami hipotezy alternatywnej, mówiącej o relatywnym obniżeniu wartości woltażu podczas wstępnej fazy rozwoju przerostu lewej komory. (Folia Cardiologica Excerpta 2007; 2: 477&#8211;484

Positioning Europe for the EPITRANSCRIPTOMICS challenge

The genetic alphabet consists of the four letters: C, A, G, and T in DNA and C,A,G, and U in RNA. Triplets of these four letters jointly encode 20 different amino acids out of which proteins of all organisms are built. This system is universal and is found in all kingdoms of life. However, bases in DNA and RNA can be chemically modified. In DNA, around 10 different modifications are known, and those have been studied intensively over the past 20 years. Scientific studies on DNA modifications and proteins that recognize them gave rise to the large field of epigenetic and epigenomic research. The outcome of this intense research field is the discovery that development, ageing, and stem-cell dependent regeneration but also several diseases including cancer are largely controlled by the epigenetic state of cells. Consequently, this research has already led to the first FDA approved drugs that exploit the gained knowledge to combat disease. In recent years, the ~150 modifications found in RNA have come to the focus of intense research. Here we provide a perspective on necessary and expected developments in the fast expanding area of RNA modifications, termed epitranscriptomics.SCOPUS: no.jinfo:eu-repo/semantics/publishe

Amlodipine at high dose increases preproendothelin-1 expression in the ventricles and aorta of normotensive rats.

BACKGROUND: High doses of dihydropyridine calcium channel blockers can activate the sympathetic nervous system and the renin-angiotensin system. Both noradrenaline and angiotensin II stimulate preproendothelin-1 gene expression, yet the effects of high doses of dihydropyridines on preproendothelin-1 expression in vivo remain unknown. OBJECTIVES: To investigate the effects of high doses of dihydropyridines on preproendothelin-1 expression in the ventricles and aorta of normotensive rats. METHODS: Sprague-Dawley rats were treated with amlodipine 5 or 20 mg/kg per day (Amlo 5 or Amlo 20) in drinking water for 5 days or 5 weeks. Systolic blood pressure and heart rate were measured by tail-cuff plethysmography. Gene expression was examined by reverse transcriptase polymerase chain reaction. RESULTS: Amlo 5 increased heart rate during the first week only and had no effect on blood pressure and ventricular weight and gene expression. Amlo 20 reduced blood pressure transiently and increased heart rate consistently. It did not change relative left ventricular weight (corrected for body weight) after 5 days, but increased it after 5 weeks; it increased relative right ventricular weight at both time points. Aorta weight (mg/mm) was decreased after 5 weeks of treatment with both dosages of amlodipine. Preproendothelin-1 mRNA levels were increased by Amlo 20 in the ventricles and aorta and, concomitantly, renin mRNA was increased in the kidney. Less consistently, interleukin-6 mRNA also increased in ventricles, whereas cardiotrophin-1 mRNA remained unchanged. The sensitivity of isolated aorta to the contractile effect of noradrenaline was decreased by Amlo 5, but not by Amlo 20. CONCLUSIONS: In Sprague-Dawley rats, high-dose amlodipine, while promoting neurohormonal activation, induced overexpression of preproendothelin-1 mRNA in the ventricles and aorta. Endothelin-1 overexpression could contribute to the lack of inhibitory effect of high-dose amlodipine on ventricular mass in normotensive rats