Average distance in growing trees

Two kinds of evolving trees are considered here: the exponential trees, where subsequent nodes are linked to old nodes without any preference, and the Barab\'asi--Albert scale-free networks, where the probability of linking to a node is proportional to the number of its pre-existing links. In both cases, new nodes are linked to $m=1$ nodes. Average node-node distance $d$ is calculated numerically in evolving trees as dependent on the number of nodes $N$. The results for $N$ not less than a thousand are averaged over a thousand of growing trees. The results on the mean node-node distance $d$ for large $N$ can be approximated by $d=2\ln(N)+c_1$ for the exponential trees, and $d=\ln(N)+c_2$ for the scale-free trees, where the $c_i$ are constant. We derive also iterative equations for $d$ and its dispersion for the exponential trees. The simulation and the analytical approach give the same results.Comment: 6 pages, 3 figures, Int. J. Mod. Phys. C14 (2003) - in prin

New algorithm for the computation of the partition function for the Ising model on a square lattice

A new and efficient algorithm is presented for the calculation of the partition function in the $S=\pm 1$ Ising model. As an example, we use the algorithm to obtain the thermal dependence of the magnetic spin susceptibility of an Ising antiferromagnet for a $8\times 8$ square lattice with open boundary conditions. The results agree qualitatively with the prediction of the Monte Carlo simulations and with experimental data and they are better than the mean field approach results. For the $8\times 8$ lattice, the algorithm reduces the computation time by nine orders of magnitude.Comment: 7 pages, 3 figures, to appear in Int. J. Mod. Phys.

The relationship between seminal plasma aspartate aminotransferase activity, sperm osmotic resistance test value, and semen quality in boars

The relationship between the activity of aspartate aminotransferase (AspAT) in seminal plasma and the values of the osmotic resistance test (ORT) of acrosomal membranes and semen traits was examined on 120 young hybrid Pietrain and Duroc boars. The following semen quality traits were determined: the volume of the ejaculate, the percentage of spermatozoa with progressive motility, sperm concentration and the total number of spermatozoa in the ejaculate, percentage of spermatozoa with normal acrosome, the percentage of spermatozoa with major and minor morphological defects, ORT, and the activity of AspAT in seminal plasma. The activity of AspAT in seminal plasma was negatively correlated (p_0.01) with the spermatozoa concentration and total number per ejaculate, percentage of spermatozoa with progressive motility and percentage of spermatozoa with a normal acrosome, while positively with the percentage of spermatozoa with major (p≤0.001) and minor (p≤0.01) morphological defects. The ORT values negatively correlated with the percentage of spermatozoa with major (p≤0.05) and minor (p≤0.01) morphological defects, while positively (p≤0.001) with the percentage of spermatozoa with a normal acrosome

Cross-Sectional and Longitudinal Assessment of Arterial Stiffening with Age in European and Chinese Populations

As arteries become stiffer with aging, reflected waves move faster and augment late systolic pressure. Few studies have described the age-related changes in both peripheral and central systolic blood pressures in populations. We investigated the age dependency of peripheral (pSBP) and central (cSBP) systolic pressure and pressure amplification (i.e., difference between peripheral and central SBP) in randomly selected participants from European and Chinese populations. Data were collected in 1420 Europeans (mean age, 41.7 years) and 2044 (mean age, 45.1 years) Chinese. In cross-sectional analyses of the population samples cSBP consistently increased more with age than pSBP with the age-related increases being greater in women than men. Repeat assessment of pSBP and cSBP in 398 Europeans and 699 Chinese at a median interval approximately 4 years of follow-up confirmed that also within subjects cSBP rose steeper with aging than pSBP. In conclusion, with aging, pSBP approximates to cSBP. This might explain why in older subjects pSBP becomes the main predictor of cardiovascular complications

Heritability and intrafamilial aggregation of arterial characteristics

BACKGROUND: We investigated the heritability and familial aggregation of various indexes of arterial stiffness and wave reflection and we partitioned the phenotypic correlation between these traits into shared genetic and environmental components. METHODS: Using a family-based population sample, we recruited 204 parents (mean age, 51.7 years) and 290 offspring (29.4 years) from the population in Cracow, Poland (62 families), Hechtel-Eksel, Belgium (36), and Pilsen, the Czech Republic (50). We measured peripheral pulse pressure (PPp) sphygmomanometrically at the brachial artery; central pulse pressure (PPc), the peripheral augmentation indexes (PAIxs) and central augmentation indexes (CAIxs) by applanation tonometry at the radial artery; and aortic pulse wave velocity (PWV) by tonometry or ultrasound. In multivariate-adjusted analyses, we used the ASSOC and PROC GENMOD procedures as implemented in SAGE and SAS, respectively. RESULTS: We found significant heritability for PAIx, CAIx, PPc and mean arterial pressure ranging from 0.37 to 0.41; P </= 0.0001. The method of intrafamilial concordance confirmed these results; intrafamilial correlation coefficients were significant for all arterial indexes (r >/= 0.12; P </= 0.02) with the exception of PPc (r = -0.007; P = 0.90) in parent-offspring pairs. The sib-sib correlations were also significant for CAIx (r = 0.22; P = 0.001). The genetic correlation between PWV and the other arterial indexes were significant (rhoG >/= 0.29; P < 0.0001). The corresponding environmental correlations were only significantly positive for PPp (rhoE = 0.10, P = 0.03). CONCLUSION: The observation of significant intrafamilial concordance and heritability of various indexes of arterial stiffness as well as the genetic correlations among arterial phenotypes strongly support the search for shared genetic determinants underlying these traits

DNA damage associated with ultrastructural alterations in rat myocardium after loud noise exposure.

Noise exposure causes changes at different levels in human organs, particularly the cardiovascular system, where it is responsible for increasing heart rate, peripheral vascular resistance, and blood pressure. In this study, we evaluated the effect of noise exposure on DNA integrity and ultrastructure of rat cardiomyocytes. The exposure to loud noise (100 dBA) for 12 hr caused a significant increase of DNA damage, accompanied by swelling of mitochondrial membranes, dilution of the matrix, and cristolysis. These alterations were concomitant with increased in situ noradrenaline levels and utilization. Genetic and ultrastructural alterations did not decrease 24 hr after the cessation of the stimulus. An elevated oxyradical generation, possibly related to altered sympathetic innervation, is hypothesized as responsible for the induction and persistence of noise-induced cellular damage

Influence of selected genetic polymorphisms of angiotensinogen, angiotensin-converting enzyme and type-1 angiotensin II receptor on arterial pressure and large artery stiffness parameters - depending on sodium intake

Wstęp Celem pracy było ustalenie związku polimorfizmów G-6A genu AGT, D/I genu ACE i A1166C genu AGT1R z wartościami ciśnienia tętniczego i usztywnienia dużych tętnic oraz ocena zależności między czynnikami genetycznymi i środowiskowymi i ich łącznego wpływu na analizowane parametry. Materiał i metody Badaniem objęto 52 rodziny (82 rodziców i 103 dzieci). U każdego uczestnika dokonano pomiarów ciśnienia tętniczego: obwodowego (metoda konwencjonalna i zapis 24-godzinny) i centralnego (analiza fali tętna), a także właściwości elastycznych dużych tętnic. U osób uczestniczących w badaniu oznaczono dobowe wydalanie sodu z moczem oraz wykonano analizy genetyczne. Wyniki Analizy dotyczące pojedynczych polimorfizmów wykazały zależność między polimorfizmem D/I genu ACE a 24-godzinnym i centralnym ciśnieniem skurczowym (SBPA, SBPC) i tętna (PPA, PPC). Ponadto wykazano obecność istotnych statystycznie interakcji między polimorfizmem D/I genu ACE a dobowym wydalaniem sodu z moczem w odniesieniu do SBPC, konwencjonalnego ciśnienia tętna (PPP), PPC oraz wzmocnienia fali aortalnej (AG). W analizie asocjacji przeprowadzonej między parametrami ciśnieniowymi i usztywnienia ścian naczyń a polimorfizmem D/I w tercylach dobowego wydalania sodu z moczem, w grupie osób homozygotycznych II w porównaniu z nosicielami allelu D, w trzecim tercylu wydalania sodu, obserwowano istotnie statystyczne wyższe wartości SBPC, PPP, PPA, PPC oraz AG, czego nie obserwowano w pierwszym i drugim tercylu. Wnioski W badanej populacji wykazano istotne interakcje między polimorfizmem D/I genu ACE a dobowym wydalaniem sodu z moczem w zakresie wpływu na ciśnienie tętnicze i sztywność tętnic. Allel D genu ACE wykazywał ochronną rolę w grupie osób z wysokim dobowym spożyciem sodu.Background In a population-based and family-based approach we investigated, to what extent blood pressure and large artery stiffness relate to the AGT G-6A, ACE D/I and AGT1R A1166C gene polymorphisms, as well as the interaction between genetic and environmental factors and their joint influence on the aforementioned parameters. Materials and methods We recruited 52 families (82 parents and 103 offspring). Peripheral pressures were derived from conventional and 24h-ambulatory blood pressure measurements, respectively. Central pressures and large artery stiffness parameters were assessed by pulse wave analysis. All participants collected a 24-h urine sample for the measurement of sodium excretion as well as blood sample for the evaluation of genetic analyses. Results In single gene analyzes, significant findings were revealed for ACE D/I polymorphism with respect to 24h-ambulatory and central systolic (SBPA, SBPC) and pulse (PPA, PPC) pressures. In further analyzes, we found an interaction between ACE D/I genotype and 24-h urinary sodium excretion in relation to SBPC, conventional pulse pressure (PPP), PPC and augmentation pressure (AG). In the third tertile of the distribution of sodium excretion we observed significantly increased SBPC, PPP, PPA, PPC and AG in ACE II homozygotes compared to D allele carriers, which was not observed in first and second tertile. Conclusions In the examined group, the interactions between D/I polymorphism of the ACE gene and daily sodium excretion in the urine were revealed, in relation to the parameters of blood pressure and arterial wall stiffness.The D allele of ACE gene showed a protective role in the group of subjects with high daily sodium intake

Influence of interaction between AGT G-6A, ACE D/I and AGTR1 A1166C gene polymorphisms on blood pressure and arterial stiffness

Wstęp Celem badania było ustalenie związku polimorfizmów G-6A genu AGT, D/I genu ACE i A1166C genu AGTR1 z wartościami ciśnienia tętniczego i usztywnienia tętnic oraz ocena łącznego wpływu wymienionych polimorfizmów genetycznych na wybrane parametry. Materiał i metody Badaniem objęto 52 rodziny (82 rodziców i 103 dzieci). U każdego uczestnika dokonano pomiarów ciśnienia tętniczego: obwodowego (metoda konwencjonalna - SBPP, DBPP, PPP i 24-godzinny zapis - SBPA, DBPA, PPA) i centralnego (analiza fali tętna - SBPC>, DBPC, PPC) oraz własności elastycznych tętnic (wzmocnienie fali aortalnej - AG, obwodowy - AIxP i centralny - AIxC, wskaźniki wzmocnienia fali). Ponadto wśród osób uczestniczących w badaniu wykonano analizy genetyczne. Wyniki Analizy, dotyczące pojedynczych polimorfizmów, wykazały zależność między polimorfizmem D/I genu ACE a SBPA, SBPC, PPA i PPC. Ponadto, stwierdzono obecność istotnych statystycznie interakcji między polimorfizmami D/I genu ACE i A1166C genu AGTR1 w odniesieniu do SBPP (p = 0,02), SBPA (p = 0,03), SBPC (p = 0,03), PPP (p = 0,008), PPA (p = 0,02) oraz PPC (p = 0,007). W analizowanej populacji, u nosicieli allelu C genu AGTR1, SBPC było o 7,5 mm Hg (p = 0,0005), PPP o 7,7 mm Hg (p = 0,003), PPA o 3,0 mm Hg (p = 0,09) a PPC o 8,4 mm Hg (p = 0,0007) wyższe u homozygot II genu ACE w porównaniu z homozygotami DD. Dla parametrów usztywnienia tętnic, u nosicieli allelu C genu AGTR1 AG było o 3,7 mm Hg (p = 0,004), AIxP o 7,1% (p = 0,07) a AIxC o 5,7% (p = 0,03) wyższe u homozygot II genu ACE w porównaniu z homozygotami DD. Wnioski Uzyskane wyniki wskazują na łączne działanie polimorfizmów D/I genu ACE i A1166C genu AGTR1, z niekorzystnym wpływem allelu I genu ACE i allelu C genu AGTR1 na ciśnienie tętnicze oraz sztywność tętnic.Background In a population-based approach we investigated whether polymorphisms in the genes encoding AGT (G-6A), ACE (D/I) and AGTR1 (A1166C), alone or in combination, affected blood pressure and arterial stiffness parameters. Materials and methods We randomly recruited 52 families (82 parents and 103 offspring). Peripheral pressures were derived from conventional (SBPP, systolic blood pressure, DBPP, diastolic blood pressure, PPP pulse pressure) and 24h-ambulatory BP measurements (SBPA, DBPA, PPA), respectively. Central pressures (SBPC, DBPC, PPC), augmentation pressure (AG), peripheral (AIxP) and central (AIxC) augmentation indexes were assessed by pulse wave analysis. Polymorphisms of selected genes of the RAA system were detected in all participants. Results In single gene analyzes, significant findings were revealed for ACE D/I polymorphism with respect to SBPA, SBPC, PPA and PPC. In further analyzes, the interactions between D/I ACE and A1166C AGTR1 gene polymorphisms reached statistically significant values with regard to SBPP (p = 0.02), SBPA (p = 0.03), SBPC (p = 0.03), PPP (p = 0.008), PPA (p = 0.02) and PPC (p = 0.007). In the analyzed population, for AGTR1 C allele carriers, SBPC was 7.5 mm Hg (p = 0.0005), PPP 7.7 mm Hg (p = 0.003), PPA 3.0 mm Hg (p = 0.09) and PPC 8.4 mm Hg (p = 0.0007) higher for ACE II homozygotes in comparison to DD homozygotes. For AGTR1 C allele carriers, with respect to arterial wall stiffness parameters, AG was 3.7 mm Hg (p = 0.004), AIxP 7.1% (p = 0.07) and AIxC 5.7% (p = 0.03) higher for ACE II homozygotes, as compared to DD homozygotes. Conclusions The interactions between D/I polymorphism of the ACE gene and A1166C polymorphism of the AGTR1 gene revealing joint negative effect of ACE I allele and AGTR1 C allele, with respect to blood pressure and arterial stiffness

Influence of interaction between AGT G-6A, ACE D/I and AGTR1 A1166C gene polymorphisms on blood pressure and arterial stiffness

Wstęp Celem badania było ustalenie związku polimorfizmów G-6A genu AGT, D/I genu ACE i A1166C genu AGTR1 z wartościami ciśnienia tętniczego i usztywnienia tętnic oraz ocena łącznego wpływu wymienionych polimorfizmów genetycznych na wybrane parametry. Materiał i metody Badaniem objęto 52 rodziny (82 rodziców i 103 dzieci). U każdego uczestnika dokonano pomiarów ciśnienia tętniczego: obwodowego (metoda konwencjonalna — SBPP, DBPP, PPP i 24-godzinny zapis — SBPA, DBPA, PPA) i centralnego (analiza fali tętna — SBPC, DBPC, PPC) oraz własności elastycznych tętnic (wzmocnienie fali aortalnej — AG, obwodowy — AIxP i centralny — AIxC, wskaźniki wzmocnienia fali). Ponadto wśród osób uczestniczących w badaniu wykonano analizy genetyczne. Wyniki Analizy, dotyczące pojedynczych polimorfizmów, wykazały zależność między polimorfizmem D/I genu ACE a SBPA, SBPC, PPA i PPC. Ponadto, stwierdzono obecność istotnych statystycznie interakcji między polimorfizmami D/I genu ACE i A1166C genu AGTR1 w odniesieniu do SBPP (p = 0,02), SBPA (p = 0,03), SBPC (p = 0,03), PPP (p = 0,008), PPA (p = 0,02) oraz PPC (p = 0,007). W analizowanej populacji, u nosicieli allelu C genu AGTR1, SBPC było o 7,5 mm Hg (p = 0,0005), PPP o 7,7 mm Hg (p = 0,003), PPA o 3,0 mm Hg (p = 0,09) a PPC o 8,4 mm Hg (p = 0,0007) wyższe u homozygot II genu ACE w porównaniu z homozygotami DD. Dla parametrów usztywnienia tętnic, u nosicieli allelu C genu AGTR1 AG było o 3,7 mm Hg (p = 0,004), AIxP o 7,1% (p = 0,07) a AIxC o 5,7% (p = 0,03) wyższe u homozygot II genu ACE w porównaniu z homozygotami DD. Wnioski Uzyskane wyniki wskazują na łączne działanie polimorfizmów D/I genu ACE i A1166C genu AGTR1, z niekorzystnym wpływem allelu I genu ACE i allelu C genu AGTR1 na ciśnienie tętnicze oraz sztywność tętnic.Background In a population-based approach we investigated whether polymorphisms in the genes encoding AGT (G-6A), ACE (D/I) and AGTR1 (A1166C), alone or in combination, affected blood pressure and arterial stiffness parameters. Materials and methods We randomly recruited 52 families (82 parents and 103 offspring). Peripheral pressures were derived from conventional (SBPP, systolic blood pressure, DBPP, diastolic blood pressure, PPP pulse pressure) and 24h-ambulatory BP measurements (SBPA, DBPA, PPA), respectively. Central pressures (SBPC, DBPC, PPC), augmentation pressure (AG), peripheral (AIxP) and central (AIxC) augmentation indexes were assessed by pulse wave analysis. Polymorphisms of selected genes of the RAA system were detected in all participants. Results In single gene analyzes, significant findings were revealed for ACE D/I polymorphism with respect to SBPA, SBPC, PPA and PPC. In further analyzes, the interactions between D/I ACE and A1166C AGTR1 gene polymorphisms reached statistically significant values with regard to SBPP (p = 0.02), SBPA (p = 0.03), SBPC (p = 0.03), PPP (p = 0.008), PPA (p = 0.02) and PPC (p = 0.007). In the analyzed population, for AGTR1 C allele carriers, SBPC was 7.5 mm Hg (p = 0.0005), PPP 7.7 mm Hg (p = 0.003), PPA 3.0 mm Hg (p = 0.09) and PPC 8.4 mm Hg (p = 0.0007) higher for ACE II homozygotes in comparison to DD homozygotes. For AGTR1 C allele carriers, with respect to arterial wall stiffness parameters, AG was 3.7 mm Hg (p = 0.004), AIxP 7.1% (p = 0.07) and AIxC 5.7% (p = 0.03) higher for ACE II homozygotes, as compared to DD homozygotes. Conclusions The interactions between D/I polymorphism of the ACE gene and A1166C polymorphism of the AGTR1 gene revealing joint negative effect of ACE I allele and AGTR1 C allele, with respect to blood pressure and arterial stiffness