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This study examined the role of physical activity and changes in physical activity levels during childhood in long-term labor market outcomes. To address this important but under-researched theme, the study utilized data drawn from longitudinal research, the Cardiovascular Risk in Young Finns Study (YFS), and from registries compiled by Statistics Finland. The study consisted of children aged 9 (n = 1565) and 15 (n = 2445) at the time their physical activity was measured. Labor market outcomes, including employment status, average employment months, and average unemployment months, were calculated from 1997 to 2010, when the participants were aged 20 to 48 years. Regression models were used to assess the relationship between physical activity and labor market outcomes. The results show that the consequences of childhood physical activity may be far-reaching, as higher childhood physical activity was positively related to the probability of being employed and employment months and was negatively related to unemployment months. On average, a one-unit increase in physical activity index was related to a 1% higher probability of being employed, 0.10 more months of yearly employment, and 0.05 fewer months of yearly unemployment. The results also imply that persistently active individuals had the highest level of employment and the lowest level of unemployment compared with other activity groups. In conclusion, investments in childhood physical activity may not only promote health and well-being but may also correlate with better labor market outcomes later in life, providing both personal and societal benefits.

Health behaviors in youth can predict the same behaviors later in life, but the role of sport participation in predicting healthy lifestyle habits is unclear. This study aimed to investigate the association between participation in organized youth sport and adult healthy lifestyle habits. Data from the longitudinal Cardiovascular Risk in Young Finns Study (YFS) with a 28-year follow-up were used. The participation in sport-club training sessions was self-reported by 9-18-year-olds in 1983 and 1986 (n = 1285). During 2011, participants (aged 37-43-year old) reported their smoking status, alcohol consumption, fruit and vegetable consumption, and physical activity. Odd ratios (OR) were calculated using logistic regression, to examine how participation in organized youth sport was associated with having three or four versus fewer (0-2) healthy habits in adulthood. Participants who were active in youth sport in both 1983 and 1986 had almost two times greater odds of having three or four healthy habits in adulthood than those who were not active at both time points (OR: 1.75, 95%CI: 1.11-2.76). When the analyses were stratified by sex, the findings were statistically significant among women (OR: 2.13, 95%Cl: 1.13-3.99) but not men (OR: 1.27, 95%CI: 0.63-2.58). The results suggest that participation in organized youth sport could promote healthy lifestyle choices.

Objective The present study examined the impact of BP from childhood to mid-adulthood on retinal microvascular architecture. Methods The Cardiovascular Risk in Young Finns Study included children aged 3–18 years, from five Finnish University cities, with participants chosen randomly from the national population registrar from those areas. The age of participants included in the current analyses in childhood (1980) ranged from three to nine years and in mid-adulthood (2011) ranged from 34 to 40 years (complete data n = 657). Measures of retinal microvasculature architecture measured in adulthood included diameters, tortuosity, lengths, and LDR. Results Regression analysis showed a strong negative association between childhood systolic BP and adult arteriolar diameter (standardized regression coefficient [β] −0.300; p

Background Elevated white blood cells (WBC) in blood and C-reactive protein (CRP) in serum are often used as non-specific markers for bacterial etiology of infection in children. The aim of the present study was to evaluate how rapid WBC and CRP testing influences patient flow and cost in the pediatric emergency room (ER). Methods This study was a retrospective chart review. In all, 166 children who were treated during 3 months in the ER of a children's hospital, and in whom rapid tests for WBC and CRP were done, were included. The association between rapid testing and length of ER stay was evaluated, and the cost of rapid tests was compared with the corresponding cost if done in the hospital laboratory. Results Median ER stay was 147.5 min, if no examinations other than rapid CRP and WBC tests were done and if no emergency treatment was given, compared with 201.5 min for laboratory tests or emergency treatment given (P < 0.001). The respective figures were 142.5 min and 179.5 min in those 96 children discharged home (P = 0.003). The cost of rapid testing was only 41.5% of the corresponding laboratory cost. Conclusion The simultaneous rapid testing of CRP and WBC in children with presumable infection decreased cost and shortened the length of ER stay, if no other examinations or emergency treatment were needed. The cost of rapid testing was less than half of the corresponding cost in laboratory.

Experimental hypertension is associated with several functional alterations of vascular endothelium and smooth muscle, but relatively few studies have examined the control of arterial tone in isolated vascular preparations from patients with essential hypertension. Therefore, we compared functional characteristics in vitro of distal ring segments of the mesenteric artery from 17 hypertensive and 22 normotensive humans. Arterial constrictor responses induced by cumulative addition of Ca2+ in the presence of noradrenaline (NA) were more effectively inhibited by the Ca2+ entry blocker nifedipine (0.5 nM) in hypertensive than normotensive subjects (by 55.4±4.9, n=17 and 35.0±5.2%, n=22, respectively). Also the contractions elicited by high concentrations of KCl were more effectively inhibited by nifedipine in arterial rings from hypertensive than normotensive patients (by 38.9±3.7, n=17 and 20.2±4.6%, n=22, respectively). However, the concentration-response curves of contractions to NA, serotonin and KCl in the absence of nifedipine were similar between the study groups. The concentration-response curves of endothelium-dependent relaxations to acetylcholine and Ca2+ ionophore {"type":"entrez-nucleotide","attrs":{"text":"A23187","term_id":"833253","term_text":"A23187"}}A23187, as well as of endothelium-independent relaxations to the nitric oxide donor nitroprusside, β-adrenoceptor agonist isoprenaline and K+ channel opener cromakalim did not show any differences between the groups. Moreover, the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (0.1 mM) almost abolished the relaxations to acetylcholine and Ca2+ ionophore in both groups, indicating that these responses were largely mediated by nitric oxide. The function of arterial sodium pump was evaluated by relaxations elicited by the return of K+ upon contractions induced by K+-free solution. The rate of K+-relaxation was similar in hypertensive and normotensive arteries (for all these responses n=20–22 in the normotensive and 15–17 in the hypertensive group). These results suggest abnormal function of voltage-dependent Ca2+ channels in arterial smooth muscle of hypertensive patients, whereas vascular responses to endothelium-dependent and -independent vasodilators and classical contractile agents were similar between hypertensive and normotensive subjects. The present findings support the view that blockade of voltage-dependent Ca2+ channels is an effective means of reducing arterial tone in essential hypertension. Keywords: Arterial smooth muscle, endothelium, essential hypertension, nifedipine, nitric oxide Introduction Vascular endothelium plays an important role in the regulation of arterial tone via the production of powerful vasoactive mediators which include nitric oxide (NO), prostacyclin (PGI2) and the endothelium-derived hyperpolarizing and contractile factors (EDHF and EDCF, respectively) (Cohen & Vanhoutte, 1995; Moncada et al., 1991; Luscher & Vanhoutte, 1986). Both essential and experimental hypertension have been shown to be associated with alterations of endothelial function, which may contribute to the increased arterial resistance characteristic of hypertensive states (Moncada et al., 1991; Luscher, 1992; Panza et al., 1990; Linder et al., 1990; Zeiher et al., 1993; Watts et al., 1996). However, the responses of arterial smooth muscle to vasoconstrictor agents as well as to endothelium-independent relaxants have usually been found to remain unchanged in hypertensive humans (Falloon & Heagerty, 1994; Cockcroft et al., 1994). Endothelial function in humans has mainly been evaluated by the use of non-invasive and invasive in vivo techniques, the most widely used methods including the measurement of flow-induced changes in brachial artery diameter by ultrasound (Celermajer et al., 1994; Taddei et al., 1995), infusion of vasoactive agonists to the brachial artery and measurement of changes in flow by plethysmography (Panza et al., 1990; Linder et al., 1990; Taddei et al., 1995), and infusion of agonists into the coronary arteries during coronary angiography (Zeiher et al., 1993). When compared with the in vitro studies, a shortcoming of the experiments in vivo is the limited number of possible pharmacological compounds when investigating the control of arterial tone. Moreover, if functional alterations are observed in vivo, it is often difficult to define whether the changes are located in the endothelium or arterial smooth muscle. In spite of the intensive research in the field, only relatively few studies have examined in detail the function of the endothelium and arterial smooth muscle in essential hypertension. Therefore, the present study was designed to compare for the first time functional characteristics of a distal branch of the mesenteric artery (outer diameter 0.7–0.9 mm) from hypertensive and normotensive humans. Since only limited data is available concerning the roles of different endothelium-derived mediators in the vascular responses of humans, special attention was paid to the evaluation of the roles of NO, PGI2, EDHF and EDCF in the endothelium-mediated responses. The present findings support the view of an abnormal function of voltage-dependent Ca2+ channels in arterial smooth muscle of hypertensive patients, whereas no changes were observed in the vascular responses induced by endothelium-dependent and -independent vasodilators and classical vasoconstrictor agents between the hypertensive and normotensive subjects.

Angiotensin-converting enzyme inhibitors have been suggested to improve the function of arterial endothelium and smooth muscle not only through inhibition of angiotensin II formation and reduction of blood pressure, but also via additional pathways, e.g. potentiation of endogenous kinins and enhancement of endothelial autacoid formation. Therefore, we investigated whether 10-week-long quinapril therapy (10 mg kg -1 day -1 ) could beneficially influence the function of mesenteric arterial rings in vitro in deoxycorticosterone-NaCl-treated Wistar-Kyoto rats, a model of hypertension which is known to be resistant to angiotensin-converting enzyme inhibition. The quinapril treatment had no long-term blood pressure-lowering effect nor did it reduce the associated cardiac hypertrophy in deoxycorticosterone-NaCl hypertension. In noradrenaline-precontracted arterial rings the endothelium-dependent relaxations to acetylcholine and adenosine 5'-diphosphate as well as the endothelium-independent relaxations to nitroprusside and isoprenaline were clearly attenuated in the deoxycorticosterone-NaCl-treated rats. However, the quinapril therapy was without significant effect on any of these dilatory responses. In the presence of the nitric oxide synthase inhibitor N G -nitro-L-arginine methyl ester, the relaxations to acetylcholine in untreated and quinapril-treated hypertensive animals were practically absent, whereas in normotensive rats distinct relaxations to higher concentrations of acetylcholine were still present. Interestingly, when endothelium-dependent hyperpolarization was prevented by precontracting the preparations with potassium chloride, no differences were found in relaxations to acetylcholine and adenosine 5'-diphosphate between the study groups. Exogenous bradykinin induced small comparable contractions in endothelium-intact mesenteric arterial rings from all study groups. In conclusion, the 10-week-long quinapril therapy did not have any significant effects on arterial function in deoxycorticosterone-NaCI hypertensive rats. Therefore, the present results stress the roles of reduced blood pressure and diminished angiotensin II formation in the beneficial vascular effects of long-term angiotensin-converting enzyme inhibition in the present model of hypertension. Furthermore, since the relaxations to acetylcholine and adenosine 5'-diphosphate in the deoxycorticosterone-NaCl-treated rats were attenuated in the absence and presence of nitric oxide sj < nthase inhibition but not under conditions which prevented hyperpolarization, impaired endothelium-dependent relaxation to agonists can be attributed to diminished endothelium-dependent hyperpolarization in this model of hypertension.

Angiotensin-converting enzyme inhibitors have been shown to potentiate relaxations to kinins in several arteries, but the effects of long-term therapy on the responses to bradykinin in normotensive and hypertensive animals remain largely unknown. Therefore, the effects of 12-week-long ramipril therapy (1 mg kg-1 day-1) on responses of mesenteric arterial rings in vitro were studied in spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. Endothelium-dependent relaxations of noradrenaline-precontracted rings to acetylcholine were similar in normotensive rats and ramipril-treated hypertensive rats and more pronounced than in untreated hypertensive group. Higher concentrations of bradykinin (0.1-1 microM) induced slight contractions in noradrenaline-precontracted endothelium-intact rings of normotensive groups and untreated hypertensive group, whereas no response or a transient relaxation were observed in ramipril-treated hypertensive rats. Interestingly, in ramipril-treated hypertensive rats but not in the other groups, 20-min. pretreatment of arterial rings with ramiprilat unmasked or potentiated the relaxations to bradykinin, and these bradykinin-induced relaxations were effectively inhibited by the B2-kinin receptor antagonist Hoe-140. In conclusion, ramipril treatment clearly improved endothelium-dependent arterial relaxation to acetylcholine, and potentiated of even unmasked the dilatory response mediated via the endothelial B2-kinin receptor in spontaneously hypertensive rats. Since these enhancing effects on arterial relaxation in vitro could not be attributed to reduced breakdown of bradykinin, the present results suggest that long-term angiotensin-converting enzyme inhibition potentiated the actions of kinins at level of B2-kinin receptors.