|
New articles - Uudet artikkelit 23.5.2009 - ISI Web of Knowledge & PubMed Search Alert
|
|
Cardiovascular risk factors and dementia mortality: 40 years of follow-up in the Seven Countries Study
Alonso, A., Jacobs, D. R., Menotti, A., Nissinen, A., Dontas, A., Kafatos, A. and Kromhout, D. Journal of the Neurological Sciences. 2009; 280(1-2): 79-83. Article. IF 2.315 Previous research shows that cardiovascular risk factors in mid-adulthood could increase the risk of dementia later in life, but studies with very long follow-up are still scarce. We assessed whether cardiovascular risk factors measured in midlife were associated with dementia mortality during a 40-year follow-up. 10,211 men, aged 40-59 at baseline, from 13 cohorts of the Seven Countries Study were followed for 40 years. Information on cardiovascular risk factors was obtained at baseline from questionnaires and a physical examination. Dementia death was assigned if there was any mention of dementia on the death certificate. Associations between cardiovascular risk factors and death from dementia were estimated through Cox proportional hazards models. We identified 160 dementia deaths during the follow-up. Smoking, hypercholesterolemia, high blood pressure, low forced vital capacity and previous history of cardiovascular disease at baseline were associated with a higher risk of death from dementia in the follow-up. The hazard ratio (HR) of dementia death among heavy smokers was 1.58 (95% confidence interval (CI) 1.03, 2.43) compared to non-smokers. Similarly, the HR (95% CI) among those with systolic BP >= 160 or diastolic BP >= 95 mm Hg compared to normotensives (< 140/90) was 1.55 (1.02, 2.35). Individuals with the largest forced vital capacity had a lower risk of dying of dementia (HR 0.54, 95% CI 0.30, 0.98). Finally, total serum cholesterol was directly associated with higher risk of dementia mortality (p for trend = 0.03). In men, cardiovascular risk factors in midlife are associated with increased risk of dementia death later in life. (C) 2009 Elsevier B.V. All rights reserved. Association between antimicrobial consumption and resistance in Escherichia coli Bergman, M., Nyberg, S. T., Huovinen, P., Paakkari, P. and Hakanen, A. J. Antimicrob Agents Chemother. 2009; 53(3): 912-7. IF 4.390 During a 9-year study period from 1997 through 2005, the association between antimicrobial resistance rates in Escherichia coli and outpatient antimicrobial consumption was investigated in 20 hospital districts in Finland. A total of 754,293 E. coli isolates, mainly from urine samples, were tested for antimicrobial resistance in 26 clinical microbiology laboratories. The following antimicrobials were studied: ampicillin, amoxicillin-clavulanate, cephalosporins, fluoroquinolones, trimethoprim, trimethoprim-sulfamethoxazole, pivmecillinam, and nitrofurantoin. We applied a protocol used in earlier studies in which the level of antimicrobial consumption over 1 year was compared with the level of resistance in the next year. Statistically significant associations were found for nitrofurantoin use versus nitrofurantoin resistance (P < 0.0001), cephalosporin use versus nitrofurantoin resistance (P = 0.0293), amoxicillin use versus fluoroquinolone resistance (P = 0.0031), and fluoroquinolone use versus ampicillin resistance (P = 0.0046). Interestingly, we found only a few associations between resistance and antimicrobial consumption. The majority of the associations studied were not significant, including the association between fluoroquinolone use and fluoroquinolone resistance. A weighted multivariate signed-rank test for cluster-correlated data Haataja, R., Larocque, D., Nevalainen, J. and Oja, H. Journal of Multivariate Analysis. 2009; 100(6): 1107-1119. Article. IF 0.773 A weighted multivariate signed-rank test is introduced for an analysis of multivariate clustered data. Observations in different clusters may then get different weights. The test provides a robust and efficient alternative to normal theory based methods. Asymptotic theory is developed to find the approximate p-value as well as to calculate the limiting Pitman efficiency of the test. A conditionally distribution-free version of the test is also discussed. The finite-sample behavior of different versions of the test statistic is explored by simulations and the new test is compared to the unweighted and weighted versions of Hotelling's T-2 test and the multivariate spatial sign test introduced in [ D. Larocque, J. Nevalainen, H. Oja, A weighted multivariate sign test for cluster-correlated data, Biometrika 94 (2007) 267-283]. Finally, a real data example is used to illustrate the theory. (C) 2008 Elsevier Inc. All rights reserved. Holl, K., Lundin, E., Surcel, H. M., Grankvist, K., Koskela, P., Dillner, J., Hallmans, G., Wadell, G., Olafsdottir, G. H., Ogmundsdottir, H. M., Pukkala, E., Lehtinen, M., Stattin, P. and Lukanova, A. Int J Cancer. 2009; 124(12): 2923-8. IF 4.555 According to the leading hypothesis on testicular cancer (TC) etiology exposure to a specific pattern of steroid hormones in utero, in particular, to high levels of estrogens and low levels of androgens is the major determinant of TC risk in the offspring. We performed a case-referent study nested within Finnish, Swedish and Icelandic maternity cohorts exploiting early pregnancy serum samples to evaluate the role of maternal endogenous steroid hormones with regard to the risk of TC. TC cases and referents were aged between 0 and 25 years. For each case-index mother pair, three or four matched referent-referent mother pairs were identified using national population registries. First trimester or early second trimester sera were retrieved from the index mothers of 73 TC cases and 286 matched referent mothers, and were tested for dehydroepiandrosterone sulfate (DHEAS), androstenedione, testosterone, estradiol, estrone, and sex hormone binding globulin (SHBG). Offspring of mothers with high DHEAS levels had a significantly decreased risk of TC (OR for highest vs. lowest DHEAS quartile, 0.18 (95% CI 0.06-0.58). In contrast, offspring of mothers with high androstenedione levels had an increased risk of TC (OR 4.1; 95% CI 1.2-12.0). High maternal total estradiol level also tended to be associated with an increased risk of TC in the offspring (OR 32; 95% CI 0.98-1,090). We report the first direct evidence that interplay of maternal steroid hormones in the early pregnancy is important in the etiology of TC in the offspring. Hyvärinen, K., Tuomainen, A. M., Laitinen, S., Bykov, I. L., Törmäkangas, L., Lindros, K., Kakela, R., Alfthan, G., Salminen, I., Jauhiainen, M., Kovanen, P. T., Leinonen, M., Saikku, P. and Pussinen, P. J. Infect Immun. 2009. IF 3.996 Periodontitis and Chlamydia pneumoniae infection are independent risk factors for cardiovascular diseases. The aim of the study was to investigate the effect of C. pneumoniae (Cpn) and Aggregatibacter actinomycetemcomitans (Aa) infection on hepatic inflammation and lipid homeostasis of apolipoprotein E-deficient mice. Mice were infected with viable C. pneumoniae intranasally three times for chronic or once for acute infection. Aa-group and Cpn+Aa-group received viable A. actinomycetemcomitans ten times intravenously. Hepatic alterations were assessed by histochemistry, lipid quantification, and the fatty acid profile analysis. The RNA expression levels and the presence of pathogens in the livers and lungs were detected by quantitative real-time PCR. Both pathogens were detected in the livers of the infected animals. Chronic C. pneumoniae induced marked changes in hepatic lipid homeostasis. A. actinomycetemcomitans infection resulted in inflammatory cell infiltration into the liver accompanied by elevated hepatic RNA expression levels of inflammation-related genes and higher serum amyloid A and lipopolysaccharide concentrations. Our results indicate that proatherogenic pathogens infect liver causing proinflammatory alterations and lipid disturbances. This may maintain chronic systemic inflammation attributable to the atherogenesis. Impinen, A., Rahkonen, O., Karjalainen, K., Lintonen, T., Lillsunde, P. and Ostamo, A. Traffic Inj Prev. 2009; 10(3): 220-6. BACKGROUND: Recidivism is a major problem in the prevention of DUI offenses. It is suggested that impairing substances used by drivers may relate to a higher risk of recidivism. This study aims to determine rearrest rates in different groups of arrested drivers focusing on different substances found in the blood. MATERIAL AND METHODS: The data utilized were obtained from the register of suspected DUI offenders maintained by the Finnish National Institute for Health and Welfare (THL). Data were available for the 15-year period between 1993 and 2007. The number of rearrests was traced from the individuals' ID codes. The mean blood alcohol concentration (BAC) of the DUI offenders was studied as well as their age at the time of the first arrest. Rearrest rates according to alcohol and drug findings were estimated using survival analysis methods. RESULTS: At the time of the first arrest, the drivers with a single DUI arrest were older and had a lower BAC than those who had a later arrest. The proportion of female drivers decreased as the number of rearrests increased. Drivers with drugs only or a combination of drugs and alcohol had a significantly higher rearrest rate than drivers with alcohol alone. Drivers with amphetamines only had the highest rearrest rates. Findings of benzodiazepine and opioids alone did not increase the risk of rearrest in the long run. Young age, male sex, high blood alcohol level, and arrest during the nighttime and during weekdays constituted a higher risk for rearrest. CONCLUSIONS: A third of those suspected of driving under the influence of alcohol and/or drugs are rearrested within 15 years. Drugs, especially amphetamines, are a risk factor for faster rearrest. These results show that the groups at risk of recidivism can be pinpointed. Interventions to prevent recidivism should be developed particularly for drugged drivers. Substance abuse beginning in adolescence seems to be a greater risk. Obesity and labour market success in Finland: The difference between having a high BMI and being fat Johansson, E., Böckerman, P., Kiiskinen, U. and Heliövaara, M. Economics & Human Biology. 2009; 7(1): 36-45. Article. This paper examines the relationship between obesity and labour market success in Finland, using various indicators of individual body composition along with body mass index (BMI). Weight, height, fat mass and waist circumference are measured by health professionals. We find that only waist circumference has a negative association with wages for women, whereas no obesity measure is significant in the linear wage models for men. However, all measures of obesity are negatively associated with women's employment probability and fat mass is negatively associated with men's employment probability. We also find that the use of categories for waist circumference and fat mass has a substantial influence on the results. For example, the category for high fat mass is associated with roughly 5.5% lower wages for men. All in all, the results indicate that in the absence of measures of body composition, there is a risk that labour market penalties associated with obesity are measured with bias. (C) 2009 Elsevier B.V. All rights reserved. Linkage and Linkage Disequilibrium Scan for Autism Loci in an Extended Pedigree from Finland Kilpinen, H., Ylisaukko-Oja, T., Rehnstrom, K., Gaal, E., Turunen, J. A., Kempas, E., von Wendt, L., Varilo, T. and Peltonen, L. Hum Mol Genet. 2009. IF 7.806 Population isolates, such as Finland, have proved beneficial in mapping rare causative genetic variants due to a limited number of founders resulting in reduced genetic heterogeneity and extensive linkage disequilibrium. We have here used this special opportunity to identify rare alleles in autism by genealogically tracing 20 autism families into one extended pedigree with verified genealogical links reaching back to the 17(th) century. In this unique pedigree we performed a dense microsatellite marker genome-wide scan of linkage and linkage disequilibrium, and followed initial findings with extensive fine-mapping. We identified a putative autism susceptibility locus at 19p13.3, and obtained further evidence for previously identified loci at 1q23 and 15q11-13. Most promising candidate genes were TLE2 and TLE6 genes clustered at 19p13 and ATP1A2 at 1q23. Korhonen, T., Kujala, U. M., Rose, R. J. and Kaprio, J. Twin Res Hum Genet. 2009; 12(3): 261-8. IF 1.525 Abstract We investigated prospectively whether physical activity level in adolescence predicts use of alcohol and illicit drugs in early adulthood. We studied 4,240 individual twins (1,870 twin pairs). We classified those who consistently reported frequent leisure physical activity at ages 16, 17 and 181/2 as persistent exercisers, those exercising less than three times monthly as persistently inactive, and all others as occasional exercisers. To control for familial confounds, within-family analyses compared activity-substance use associations in co-twins discordant for baseline physical activity. Individual-based analyses showed no clear association between baseline physical activity and subsequent weekly alcohol consumption. However, weekly alcohol intoxication (OR = 1.9, p = .002) and problems due to alcohol use (OR = 2.0, p < .001) were more common among persistently inactive participants. After excluding those reporting weekly intoxication at baseline, the risk for alcohol intoxication remained elevated among women occasionally (OR = 2.4, p = .017) or persistently (OR = 5.8, p < .001) inactive at baseline, but this association was not replicated within discordant twin pairs. Individual-based analyses showed that drug use in adulthood was more common among those persistently physically inactive in adolescence (OR = 3.7, p < .001) in comparison to those persistently active. This finding was replicated within discordant twin pairs. Among those with no drug experience during adolescence, persistent inactivity (OR = 1.9, p = .007) increased risk for drug use. We conclude that persistent physical inactivity in adolescence may increase the risk of later problems due to excess alcohol use. Sedentary lifestyle predicts illicit drug use even when controlling for familial factors. Childhood BMI trajectories and the risk of developing young adult-onset diabetes Lammi, N., Moltchanova, E., Blomstedt, P. A., Tuomilehto, J., Eriksson, J. G. and Karvonen, M. Diabetologia. 2009; 52(3): 408-14. IF 5.822 AIMS/HYPOTHESIS: The aim of this study was to examine the effects of childhood BMI growth dynamics on the risk of developing young adult-onset type 1 and type 2 diabetes. METHODS: Finnish national healthcare registers were used to identify individuals with diabetes diagnosed between 1992 and 1996 at 15-39 years of age. Non-diabetic control participants were chosen from the National Population Registry. Anthropometric measurements were obtained from the original child welfare clinic records. Only the case-control pairs with sufficient growth data recorded were included in the analyses (218/1,388 for type 1 diabetes [16%] and 64/1,121 for type 2 diabetes [6%]). Two developmental stages in BMI growth (the points of infancy maximum BMI and the BMI rebound) were examined, and conditional logistic regression was applied to the variables of interest. RESULTS: The risk for type 1 diabetes increased 1.19-fold per 1 kg/m(2) rise in the infancy maximum BMI (p = 0.02). In addition, there was a 1.77-fold increase in the risk for type 2 diabetes per 1 kg/m(2) rise in the level of BMI at the BMI rebound (p = 0.04). Higher values of BMI at these points corresponded to a larger BMI gain from birth to that developmental stage. Age at the infancy maximum BMI or age at the BMI rebound did not affect the risk for either type of diabetes. CONCLUSIONS/INTERPRETATION: The BMI gain in infancy among individuals who subsequently developed young adult-onset type 1 diabetes was faster than that of those who remained healthy. The excess BMI gain in individuals who developed young adult-onset type 2 diabetes could already be seen during early childhood. Markkanen Penttinen, P., Pelkonen, J., Tapanainen, M., Mäki-Paakkanen, J., Jalava, P. I. and Hirvonen, M. R. Inhal Toxicol. 2009. IF 1.831 Oxidative stress has been proposed to be one mechanism behind the adverse health outcomes associated with living in a damp indoor environment. In the present study, the capability of damp building-related microbes Streptomyces californicus and Stachybotrys chartarum to induce oxidative stress was evaluated in vitro. In addition, the role of oxidative stress in provoking the detected cytotoxic, genotoxic, and inflammatory responses was studied by inhibiting the production of reactive oxygen species (ROS) using N-acetyl-l-cysteine (NAC). RAW264.7 macrophages were exposed in a dose- and time-dependent manner to the spores of co-cultivated S. californicus and S. chartarum, to their separately cultivated spore-mixture, or to the spores of these microbes alone. The intracellular peroxide production and cytotoxicity were measured by flow cytometric analysis, nitric oxide production was analyzed by the Griess method, DNA damage was determined by the comet assay, and cytokine production was measured by an immunochemical ELISA (enzyme-linked immunosorbent assay). All the studied microbial exposures triggered oxidative stress and subsequent cellular damage in RAW264.7 macrophages. The ROS scavenger, NAC, prevented growth arrest, apoptosis, DNA damage, and cytokine production induced by the co-culture since it reduced the intracellular level of ROS within macrophages. In contrast, the DNA damage and cell cycle arrest induced by the spores of S. californicus alone could not be prevented by NAC. Bioaerosol-induced oxidative stress in macrophages may be an important mechanism behind the frequent respiratory symptoms and diseases suffered by residents of moisture damaged buildings. Furthermore, microbial interactions during co-cultivation stimulate the production of highly toxic compound(s) which may significantly increase oxidative damage. Predictors of mortality in beta-hemolytic streptococcal bacteremia: A population-based study Rantala, S., Vuopio-Varkila, J., Vuento, R., Huhtala, H. and Syrjänen, J. Journal of Infection. 2009; 58(4): 266-272. Proceedings Paper. IF 2.844 Objectives: Several factors associated with mortality in Lancefield group A beta-hemolytic streptococcal bacteremia have been described in population-based surveillance studies, whereas such reports on group B, C, and G streptococcal are scant. Methods: In this population-based study at 314 episodes of beta-hemolytic streptococcal bacteremia in adult patients in the Pirkanmaa area, Finland, during the 10-year period 1995-2004 were retrospectively reviewed. Results: The 30-day case-fatality rate was 13%, being highest in group C (22%); in group A it was 15%, in group B 7%, and in group G 15%. Confusion, unconsciousness and dyspnea as the first sign or symptom were associated with increased case-fatality, white fever seemed to be a protecting factor for death. Alcoholism and ultimately or rapidly fatal underlying disease were significantly associated with increased case-fatality. Among infections of the skin and soft-tissues, necrotizing fasciitis had the highest risk of death (38%), white patients with cellulitis had a case-fatality of 8%. A history of previous cellulitis seemed to protect against death (case-fatality of 3% as compared to 16% among those without such a history (p = 0.014)). Conclusion: A history of previous cellulitis seemed to be a protecting factor against death. Fever was also associated with a good prognosis. (c) 2009 The British Infection Society. Published by Elsevier Ltd. All rights reserved. Joint analysis of prevalence and incidence data using conditional likelihood Saarela, O., Kulathinal, S. and Karvanen, J. Biostatistics. 2009. IF 3.058 Disease prevalence is the combined result of duration, disease incidence, case fatality, and other mortality. If information is available on all these factors, and on fixed covariates such as genotypes, prevalence information can be utilized in the estimation of the effects of the covariates on disease incidence. Study cohorts that are recruited as cross-sectional samples and subsequently followed up for disease events of interest produce both prevalence and incidence information. In this paper, we make use of both types of information using a likelihood, which is conditioned on survival until the cross section. In a simulation study making use of real cohort data, we compare the proposed conditional likelihood method to a standard analysis where prevalent cases are omitted and the likelihood expression is conditioned on healthy status at the cross section. Tiainen, K., Sipila, S., Kauppinen, M., Kaprio, J. and Rantanen, T. Journal of Applied Physiology. 2009; 106(5): 1604-1610. Article. IF 3.632 Tiainen K, Sipila S, Kauppinen M, Kaprio J, Rantanen T. Genetic and environmental effects on isometric muscle strength and leg extensor power followed up for three years among older female twins. J Appl Physiol 106: 1604-1610, 2009. First published February 19, 2009; doi:10.1152/japplphysiol.91056.2008.-The purpose of this study was to examine changes in the contribution of genetic and environmental effects to isometric knee extensor strength and leg extensor power among 63- to 76-year-old female twins over a 3-yr follow-up. At baseline in 2000 the sample comprised 206 monozygotic (MZ) and 228 dizygotic (DZ) twin individuals, and at follow-up in 2003 the sample comprised 149 MZ and 164 DZ twin individuals. Genetic modeling showed that genetic effects explained 58% (95% CI: 46-68%) of the variance in muscle strength at baseline and 56% (95% CI: 41-68%) at follow-up, with no occasion-specific genetic effect. Nonshared environmental effects accounted for 42% (95% CI: 32-54%) of the variation at baseline and 15% (95% CI: 7-26%) at follow-up. In addition, new nonshared environmental effects explained the remaining variance, 29% (95% CI: 22-37%) of muscle strength at follow-up. For muscle power, the same genetic effects accounted for 67% (95% CI: 57-74%) of the variation at baseline and 48% (95% CI: 34-61%) at follow-up. Nonshared environmental effects in common at both measurement points explained 33% (95% CI: 25-43%) of the total variation at baseline and 11% (95% CI: 5-21%) at follow-up. The remaining variance of muscle power at follow-up was accounted for by time-specific environmental effects. Results indicated that the contribution of genetic effects to isometric muscle strength was stable, whereas for leg extensor power the proportion of genetic effects decreased during the follow-up. We observed new specific environmental effects underlying follow-up muscle strength and power, which effects could be due to the onset of new disease processes or changes in lifestyle. Vaarasmaki, M., Pouta, A., Elliot, P., Tapanainen, P., Sovio, U., Ruokonen, A., Hartikainen, A. L., McCarthy, M. and Jarvelin, M. R. American Journal of Epidemiology. 2009; 169(10): 1209-1215. Article. IF 5.285 The association between maternal gestational diabetes (GDM) and manifestations of metabolic syndrome among Caucasian adolescents was studied with data from the population-based Northern Finland 1986 Birth Cohort. This is a longitudinal cohort study from early pregnancy until offspring age 16 years and includes data from a risk group-based GDM screen of pregnant mothers by an oral glucose tolerance test. Metabolic outcomes were compared between the offspring of women with GDM (OGDM; n = 95) and reference group offspring (n = 3,909). The prevalence of overweight was significantly higher in the OGDM group (18.8 vs. 8.4%; P < 0.001) than in the reference group. The median body mass index (20.8 vs. 20.2 kg/m(2), 95% confidence interval (CI) for the percentage difference adjusted for sex: 3.5%, 9.5%), waist circumference (73.3 vs. 71.5 cm, 95% CI: 3.2%, 7.5%), and fasting insulin (10.20 vs. 9.30 milliunits/L, 95% CI: 5.9%, 26.0%) were higher, and homeostatic model assessment-insulin sensitivity (74.7 vs. 82.3, 95% CI: -20.6%, -5.4%) was lower in the OGDM group. These differences were similar after an additional adjustment for birth weight and gestational age. The differences in waist circumference, insulin, and homeostatic model assessment-insulin sensitivity were attenuated but remained statistically significant after additional adjustment for body mass index at 16 years. These findings highlight the importance of prevention strategies among children born to women with GDM. Associations between alpha-Tocopherol, beta-Carotene, and Retinol and Prostate Cancer Survival Watters, J. L., Gail, M. H., Weinstein, S. J., Virtamo, J. and Albanes, D. Cancer Research. 2009; 69(9): 3833-3841. Article. IF 7.672 Previous studies suggest that carotenoids and tocopherols (vitamin E compounds) may be inversely associated with prostate cancer risk, yet little is known about how they affect prostate cancer progression and survival. We investigated whether serum alpha-tocopherol, P-carotene, and retinol concentrations, or the alpha-tocopherol and beta-carotene trial supplementation, affected survival of men diagnosed with prostate cancer during the alpha-Tocopherol, beta-Carotene Cancer Prevention Study, a randomized, double-blind, placebo-controlled primary prevention trial testing the effects of beta-carotene and alpha-tocopherol supplements on cancer incidence in adult male smokers in southwestern Finland (n = 29,133). Prostate cancer survival was examined using the Kaplan-Meier method with deaths from other causes treated as censoring, and using Cox proportional hazards regression models with hazard ratios (HR) and 95% confidence intervals (CI) adjusted for family history of prostate cancer, age at randomization, benign prostatic hyperplasia, age and stage at diagnosis, height, body mass index, and serum cholesterol. As of April 2005, 1,891 men were diagnosed with prostate cancer and 395 died of their disease. Higher serum alpha-tocopherol at baseline was associated with improved prostate cancer survival (HR, 0.67; 95% CI, 0.45-1.00), especially among cases who had received the alpha-tocopherol intervention of the trial and who were in the highest quintile of alpha-tocopherol at baseline (HR, 0.51; 95% CI, 0.20-0.90) or at the 3-year follow-up measurement (HR, 0.26; 95% CI, 0.09-0.71). Serum beta-carotene, serum retinol, and supplemental beta-carotene had no apparent effects on survival. These findings suggest that higher alpha-tocopherol (and not beta-carotene or retinol) status increases overall prostate cancer survival. Further investigations, possibly including randomized studies, are needed to confirm this observation. [Cancer Res 2009;69(9):3833-41] |