PKq/: `{`{refs.MYDwF|7VLammi, N. Moltchanova, E. Blomstedt, P. A. Tuomilehto, J. Eriksson, J. G. Karvonen, M.2009PChildhood BMI trajectories and the risk of developing young adult-onset diabetes Diabetologia 2009/01/09Jan 8rAIMS/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.&Diabetologia Diabetologia. 2009 Jan 8.0012-186X (Print)191300405.822Diabetes Unit, Department of Health Promotion and Chronic Disease Prevention, National Public Health Institute, Mannerheimintie 166, 00300, Helsinki, Finland, niina.lammi@helsinki.fi.10.1007/s00125-008-||7Laatikainen, T. Janus, E. Kilkkinen, A. Heistaro, S. Tideman, P. Baird, A. Tirimacco, R. Whiting, M. Franklin, L. Chapman, A. Kao-Philpot, A. Dunbar, J.2009lChronic disease risk factors in rural australia: results from the greater green triangle risk factor surveys51-62Asia Pac J Public Health211 2009/01/07fThe aim of this article was to assess the level and prevalence of major chronic disease risk factors among rural adults. Two cross-sectional surveys were carried out in 2004 and 2005 in the southeast of South Australia and the southwest of Victoria. Altogether 891 randomly selected persons aged 25 to 74 years participated in the studies. Surveys included a self-administered questionnaire, physical measurements, and a venous blood specimen for lipid analyses. Two thirds of participants had cholesterol levels >/=5.0 mmol/L. The prevalence of high diastolic blood pressure (>/=90 mm Hg) was 22% for men and 10% for women in southeast of South Australia, and less than 10% for both sexes in southwest of Victoria. Two thirds of participants were overweight or obese (body mass index >/=25 kg/m(2)). About 15% of men and slightly less women were daily smokers. The abnormal risk factor levels underline the need for targeted prevention activities in the Greater Green Triangle region. Continuing surveillance of levels and patterns of risk factors is fundamentally important for planning and evaluating preventive activities.bLaatikainen, Tiina Janus, Edward Kilkkinen, Annamari Heistaro, Sami Tideman, Philip Baird, Andrew Tirimacco, Rosy Whiting, Malcolm Franklin, Lucinola Chapman, Anna Kao-Philpot, Anna Dunbar, James China Asia-Pacific journal of public health / Asia-Pacific Academic Consortium for Public Health Asia Pac J Public Health. 2009;21(1):51-62. Epub 2008 Dec 11.1010-5395 (Print)19124336NNational Public Health Institute, Helsinki, Finland. tiina.laatikainen@ktl.fi.51010539508327351 [pii] 10.1177/1010539508327351 [doi]eng , ,F|7MHamalainen, J. Isometsa, E. Sihvo, S. Kiviruusu, O. Pirkola, S. Lonnqvist, J.2009HTreatment of major depressive disorder in the Finnish general populationDepress Anxiety 2009/01/07Jan 5kBackground: Few general population studies of the treatment of major depressive disorder (MDD) have included the whole spectrum of treatments. We estimated the rates of different treatments and the effect of individual and disorder characteristics plus provider type on treatment received. Methods: In the Health 2000 Study, a representative sample (n=6,005) from the adult Finnish population (>/=30 years) were interviewed (CIDI) in 2000-2001 for the presence of DSM-IV mental disorders during the past 12 months. Logistic regression models were used to examine factors influencing the type of treatment: either pharmacotherapies (antidepressants, anxiolytics, sedatives/hypnotics, antipsychotics) or psychological treatment. Results: Of the individuals with MDD (n=288), currently 24% used antidepressants, 11% anxiolytics, 16% sedatives/hypnotics, 5% antipsychotics, and 17% reported having received psychological treatment. Overall, 31% received antidepressants or psychological treatment or both; 18% received minimally adequate treatment. Of those 33% (n=94) using health care services for mental reasons, 76% received antidepressants or psychological treatment or both; 54% received minimal adequate treatment. In logistic regression models, the use of antidepressants was associated with female sex, being single, severe MDD, perceived disability, and comorbid dysthymic disorder; psychological treatment with being divorced, perceived disability, and comorbid anxiety disorder. Conclusions: Due to the low use of health services for mental reasons, only one-third of subjects with MDD use antidepressants, and less than one-fifth receives psychological treatment. The treatments provided are determined mostly by clinical factors such as severity and comorbidity, in part by sex and marital status, but not education or income. Depression and Anxiety 0:1-11, 2008. (c) 2008 Wiley-Liss, Inc.3Depression and anxiety Depress Anxiety. 2009 Jan 5.1520-6394 (Electronic)191234561.893fDepartment of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, Finland.10.1002/da.||7 Vaarala, O.2008Leaking gut in type 1 diabetes701-6Curr Opin Gastroenterol246 2009/01/06NovPURPOSE OF REVIEW: Several studies have indicated that children with type 1 diabetes show altered intestinal immune system and, in particular, increased small intestinal permeability. This review discusses the recent research linking the gut and type 1 diabetes, which may reveal novel pathogenic pathways and new possibilities for disease prevention. RECENT FINDINGS: Recent studies indicate that not only patients with manifest type 1 diabetes show increased small intestinal permeability and high serum levels of zonulin, that is protein controlling epithelial tight junctions, but prediabetic, normoglycemic individuals with beta-cell autoimmunity show signs of leaking gut. Also studies in BioBreeding-rat model of autoimmune diabetes suggest that high permeability of the intestine precedes autoimmune diabetes. The enteropathy characterized by increased intestinal permeability and inflammation seems to be the basis for the development of beta-cell destruction, as for example zonulin agonist, which decreases the gut permeability, prevents the development of diabetes. SUMMARY: The leaking gut syndrome with subclinical inflammation is associated with beta-cell autoimmunity and type 1 diabetes. Furthermore, treatment of the leakiness has been reported to modulate development of autoimmune diabetes in animal models suggesting that intestinal environment plays a key role in the destruction of insulin-producing beta-cells in the pancreas.Vaarala, Outi Research Support, Non-U.S. Gov't United States Current opinion in gastroenterology Curr Opin Gastroenterol. 2008 Nov;24(6):701-6.1531-7056 (Electronic)191225193.271Laboratory for Immunobiology, Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland. outi.vaarala@ktl.fiA10.1097/MOG.0b013e32830e6d98 [doi] 00001574-200811000-00{~|77Klemola, P. Kaijalainen, S. Ylipaasto, P. Roivainen, M.2008JDiabetogenic effects of the most prevalent enteroviruses in Finnish sewage210-2Ann N Y Acad Sci1150 2009/01/06DecCommon enterovirus infections appear to initiate or facilitate the pathogenetic processes leading to type 1 diabetes (T1D) and also sometimes precipitate the clinical disease. We have recently demonstrated that (1) enterovirus-positive islet cells were seen on postmortem pancreatic specimens of several T1D patients but not in the corresponding samples of nondiabetic controls, and (2) several different enteroviruses can be associated with T1D. Enterovirus infections are transmitted from person to person by fecal-oral or respiratory routes, which means that infections usually start from the respiratory or gastrointestinal mucosa. Regardless of the clinical symptoms of the disease, viral replication continues in the submucosal lymphatic tissue for several weeks, up to a couple of months, and during that time the virus is excreted into the feces and translocated to the environment. Monitoring of sewage samples for enteroviruses can be used as a tool in epidemiologic studies of enterovirus. Finland has successfully used environmental control data in poliovirus surveillance for decades. About 24 samples have been collected annually from the Helsinki region, which covers about 20% of the population. In the present study, we have reanalyzed the sewage samples of the years 1993-2004 for nonpolio enteroviruses by inoculating them into five different continuous cell lines known to cover a wide range of serotypes. Isolated strains were identified by RT-PCR and VP1 sequencing. The most commonly detected serotypes were coxsackie B viruses (CBV1-5) and echoviruses (E6, 7, 11, 25, 30). Diabetogenic effects of the most prevalent enterovirus serotypes were studied in primary human beta cells.Klemola, Paivi Kaijalainen, Svetlana Ylipaasto, Petri Roivainen, Merja Research Support, Non-U.S. Gov't United States Annals of the New York Academy of Sciences Ann N Y Acad Sci. 2008 Dec;1150:210-2.1749-6632 (Electronic)191202971.731LEnterovirus Laboratory, National Public Health Institute, Helsinki, Finland./NYAS1150012 [pii] 10.1196/annals.14]KH||7gSimen-Kapeu, A. Kataja, V. Yliskoski, M. Syrjanen, K. Dillner, J. Koskela, P. Paavonen, J. Lehtinen, M.2008sSmoking impairs human papillomavirus (HPV) type 16 and 18 capsids antibody response following natural HPV infection745-51Scand J Infect Dis409 2008/12/17zAdolescent Adult Aged Antibodies, Viral/ blood Capsid/ immunology DNA, Viral/analysis Female Human papillomavirus 16/genetics/ immunology Human papillomavirus 18/genetics/ immunology Humans Immunoglobulin A/blood Immunoglobulin G/blood Middle Aged Papillomavirus Infections/ immunology/virology Smoking/ adverse effects Uterine Cervical Neoplasms/immunology/virology Young Adult4The natural history of oncogenic human papillomavirus (HPV) infections results from interactions of the virus, the host, and multiple cofactors. We studied the association between humoral immune response to HPV and smoking in 191 HPV infected women prospectively. Two follow-up samples (first and last) were analysed for serum cotinine levels, IgA and IgG antibodies to HPV16 and 18, and Chlamydia trachomatis using ELISA methods. HPV DNA analyses were also performed, and HPV16/18 antibodies were detectable in 23 of 40 (57.5%) HPV DNA-positive women. We performed age-stratified analyses and found that young smokers were less likely to develop HPV16/18 antibodies than non-smokers (OR: 0.2, 95% CI 0.0-0.9). Furthermore, they had a significantly decreased tendency of maintaining constant HPV16/18 IgG antibody positivity by the end of the follow-up (OR: 0.1, 95% CI 0.0-0.8). Smoking did not affect the development of HPV antibody responses in women over 30 y of age. Our results suggest that smoking may induce impaired antibody response in HPV16/18-infected young women.Simen-Kapeu, Aline Kataja, Vesa Yliskoski, Merja Syrjanen, Kari Dillner, Joakim Koskela, Pentti Paavonen, Jorma Lehtinen, Matti Research Support, Non-U.S. Gov't Sweden Scandinavian journal of infectious diseases Scand J Infect Dis. 2008;40(9):745-51.0036-5548 (Print)190862471.209VNational Public Health Institute, Youth Sexual Health Unit, Oulu, Finland. V Cz||7Jakkula, E. Rehnstrom, K. Varilo, T. Pietilainen, O. P. Paunio, T. Pedersen, N. L. deFaire, U. Jarvelin, M. R. Saharinen, J. Freimer, N. Ripatti, S. Purcell, S. Collins, A. Daly, M. J. Palotie, A. Peltonen, L.2008]The genome-wide patterns of variation expose significant substructure in a founder population787-94Am J Hum Genet836 2008/12/09Alleles Chromosomes, Human, Pair 22 Founder Effect Gene Frequency Genetic Variation Genome, Human Genome-Wide Association Study/methods Homozygote Humans Linkage Disequilibrium Polymorphism, Single Nucleotide PopulationDecAlthough high-density SNP genotyping platforms generate a momentum for detailed genome-wide association (GWA) studies, an offshoot is a new insight into population genetics. Here, we present an example in one of the best-known founder populations by scrutinizing ten distinct Finnish early- and late-settlement subpopulations. By determining genetic distances, homozygosity, and patterns of linkage disequilibrium, we demonstrate that population substructure, and even individual ancestry, is detectable at a very high resolution and supports the concept of multiple historical bottlenecks resulting from consecutive founder effects. Given that genetic studies are currently aiming at identifying smaller and smaller genetic effects, recognizing and controlling for population substructure even at this fine level becomes imperative to avoid confounding and spurious associations. This study provides an example of the power of GWA data sets to demonstrate stratification caused by population history even within a seemingly homogeneous population, like the Finns. Further, the results provide interesting lessons concerning the impact of population history on the genome landscape of humans, as well as approaches to identify rare variants enriched in these subpopulations.Jakkula, Eveliina Rehnstrom, Karola Varilo, Teppo Pietilainen, Olli P H Paunio, Tiina Pedersen, Nancy L deFaire, Ulf Jarvelin, Marjo-Riitta Saharinen, Juha Freimer, Nelson Ripatti, Samuli Purcell, Shaun Collins, Andrew Daly, Mark J Palotie, Aarno Peltonen, Leena 1R01HL087679-01/HL/NHLBI NIH HHS/United States U54RR020278/RR/NCRR NIH HHS/United States Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't United States American journal of human genetics Am J Hum Genet. 2008 Dec;83(6):787-94.1537-6605 (Electronic)1906198611.092Department of Molecular Medicine, National Public Health Institute and Institute for Molecular Medicine Finland (FIMM), Helsinki, Finland.<S0002-9297(08)00590-9 [pii] 10.1016/j.ajhg.2008  ||7FSundell, L. Salomaa, V. Vartiainen, E. Poikolainen, K. Laatikainen, T.2008:Increased stroke risk is related to a binge-drinking habit3179-84Stroke3912 2008/10/041Adult Alcohol Drinking/ adverse effects/epidemiology Anthropometry Cause of Death Cerebral Hemorrhage/epidemiology Cohort Studies Educational Status Female Finland/epidemiology Habits Humans Male Middle Aged Prospective Studies Sampling Studies Smoking/epidemiology Stroke/ epidemiology/etiology/mortalityDecBACKGROUND AND PURPOSE: Heavy alcohol consumption increases the risk for all strokes, whereas moderate regular alcohol consumption is associated with a lower risk for ischemic stroke. The purpose of this study was to evaluate the effect of different drinking patterns on stroke risk, independent of average alcohol intake. METHODS: A prospective cohort study of 15 965 Finnish men and women age 25 to 64 years who participated in a national risk factor survey and had no history of stroke at baseline were followed up for a 10-year period. The first stroke event during follow-up served as the outcome of interest (N=249 strokes). A binge drinking pattern was defined as consuming 6 or more drinks of the same alcoholic beverage in men or 4 or more drinks in women in 1 session. Cox proportional-hazards models were adjusted for average alcohol consumption, age, sex, hypertension, smoking, diabetes, body mass index, educational status, study area, study year, and history of myocardial infarction. RESULTS: Binge drinking was an independent risk factor for total and ischemic strokes. Compared with non-binge drinkers, the hazard ratio for total strokes among binge drinkers was 1.85 (95% CI, 1.35 to 2.54) after adjusting for average alcohol consumption, age, and sex; the association was diluted after adjustment for other risk factors. Compared with non-binge drinkers, the risk for ischemic stroke was 1.99 (95% CI, 1.39 to 2.87) among binge drinkers; the association remained statistically significant after adjustment for potential confounders. CONCLUSIONS: This study found that a pattern of binge drinking is an independent risk factor for all strokes and ischemic stroke.Sundell, Laura Salomaa, Veikko Vartiainen, Erkki Poikolainen, Kari Laatikainen, Tiina Research Support, Non-U.S. Gov't United States Stroke; a journal of cerebral circulation Stroke. 2008 Dec;39(12):3179-84. Epub 2008 Oct 2.1524-4628 (Electronic)188327416.2964National Public Health Institute, Helsinki, Finland.=STROKEAHA.108.520817 [pii] 10.1161/STROKEAHA.108. ! 0F|7 aAntila, M. Partonen, T. Kieseppa, T. Suvisaari, J. Eerola, M. Lonnqvist, J. Tuulio-Henriksson, A.2008Cognitive functioning of bipolar I patients and relatives from families with or without schizophrenia or schizoaffective disorderJ Affect Disord 2009/01/02Dec 29BACKGROUND: Bipolar I disorder patients show cognitive impairments, and genetic vulnerability to other psychotic disorders may modify these impairments. We set out to assess cognitive functions and estimate their heritability in bipolar I disorder patients (bipolar families) and unaffected relatives in a group of families with bipolar I disorder only and in another group of families with both bipolar I disorder and schizophrenia or schizoaffective disorder (mixed families). METHODS: A neuropsychological test battery was administered to 20 bipolar patients and 36 relatives from bipolar families, 19 bipolar patients and 28 relatives from mixed families and 55 controls, all representing population-based samples. RESULTS: Irrespective of the family group, patients and relatives were impaired in psychomotor processing speed. Both patient groups were impaired in executive functioning, but the deficit was more severe in patients from mixed families. Patients from bipolar families scored lower than controls in nearly all measures of verbal memory. All relatives were slightly impaired in executive functioning. The heritability of cognitive functions was generally similar irrespective of psychopathology in the family. However, there were greater genetic effects in several cognitive tasks in mixed families. LIMITATIONS: The small sample size and familial type of bipolar disorder could limit the generalizability of the results. CONCLUSION: Impaired psychomotor processing speed and executive functions may represent markers of susceptibility to bipolar I disorder irrespective of psychopathology within the family. Generalized impairment in verbal memory, in turn, may associate more with bipolar disorder than to vulnerability to other psychotic disorders.<Journal of affective disorders J Affect Disord. 2008 Dec 29.0165-0327 (Print)191176103.144fDepartment of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, Finland.;S0165-0327(08)00462-X [pii] 10.1016/j.jad.2008.||7 MOjaniemi, K. K. Lintonen, T. P. Impinen, A. O. Lillsunde, P. M. Ostamo, A. I.2009hTrends in driving under the influence of drugs: a register-based study of DUID suspects during 1977-2007191-6Accid Anal Prev411 2008/12/31JanOur aim was to describe the incidence and trends of driving under the influence of drugs (DUID) and to examine the main drug findings and their trends in suspected DUID cases in Finland. A register-based study was conducted of all suspected DUID cases during 1977-2007. The data included 31,963 DUID offenders apprehended by the police with a positive finding for illicit/licit drug impairing driving performance. Toxicological results were analyzed in blood and/or urine specimens in one central laboratory. The incidence of suspected DUID cases increased 18-fold during 1977-2007. Most of the suspects were men (89.7%). However, the male-female ratio decreased from 13.9 to 7.3. The mean age decreased from 36.2 years in 1977 to 29.9 years in 2001 but has since reincreased. Most often found substances were benzodiazepines (75.7%), amphetamines (46.0%), cannabinoids (27.7%) and opioids (13.8%). Most common illicit drugs, amphetamines and cannabinoids, started to appear at the end of the 1980s. Poly-drug findings were common (77.1%). Suspected DUID cases have increased sharply after the introduction of a zero tolerance law, especially in regard to amphetamines. DUID is an increasing problem in Finland, and needs serious attention.Ojaniemi, Karoliina K Lintonen, Tomi P Impinen, Antti O Lillsunde, Pirjo M Ostamo, Aini I Research Support, Non-U.S. Gov't England Accident; analysis and prevention Accid Anal Prev. 2009 Jan;41(1):191-6. Epub 2008 Nov 17.1879-2057 (Electronic)19114154National Public Health Institute, Department of Mental Health and Alcohol Research, Mannerheimintie 166, Helsinki, Finland. karoliina.ojaniemi@ktl.fi;S0001-4575(08)00213-3 [pii] 10.1016/j.aap.2008.10.011 [doi]engzF|7 7Kanerva, M. Ollgren, J. Virtanen, M. J. Lyytikainen, O.2008gEstimating the annual burden of health care-associated infections in Finnish adult acute care hospitalsAm J Infect Control 2008/12/30Dec 24BACKGROUND: We estimated the burden of health care-associated infections (HAIs) occurring in Finnish adult acute care hospitals using national hospitalization data and estimates of HAI based on a recent national prevalence survey. METHODS: A total of 7531 non-HAI patients and 703 HAI patients (8.5%) identified in the prevalence survey were included in the study. Using the patients' national identity numbers and the prevalence survey date, we obtained data on hospitalizations, including discharge diagnoses from the National Hospital Discharge Registry (NHDR), and the dates and causes of death from the National Population Information System. We converted the prevalence of HAI into incidence using the Rhame-Sudderth formula, assessed the 28-day case fatality of the HAI patients, and then extrapolated the annual estimates of HAI burden from the total number of hospitalizations in adult acute care hospitals in 2005 (n = 804,456). We also assessed the sensitivity of the NHDR diagnoses in identifying HAIs. RESULTS: The estimated incidence of HAIs was 5.7% (95% confidence interval = 5.0% to 6.5%), and the 28-day case fatality was 9.8%. Thus, > 8500 hospitalizations per million population annually would result in at least 1 HAI and ~270 HAI-associated deaths within 28 days. The sensitivity of the NHDR diagnoses was 34% (range by infection type, 0% to 67%). CONCLUSION: Our disease burden estimates can be used in health care planning and resource allocation. The NHDR was not a reliable source for case finding of HAIs.mfor the Prevalence Survey Study Group American journal of infection control Am J Infect Control. 2008 Dec 24.1527-3296 (Electronic)191113671.907Department of Infectious Disease Epidemiology and Control, National Finnish Hospital Infection Program (SIRO), National Public Health Institute, Helsinki, Finland; Department of Medicine, Division of Infectious Diseases, Helsinki University Central Hospital, Helsinki, Finland.<S0196-6553(08)00745-1 [pii] 10.1016/j.ajic.2008.07.|||7 1Sarvikivi, E. Lyytikainen, O. Vaara, M. Saxen, H.2008jNosocomial bloodstream infections in children: an 8-year experience at a tertiary-care hospital in Finland1072-5Clin Microbiol Infect1411 2008/12/020Adolescent Bacterial Infections/ epidemiology/microbiology Blood/microbiology Child Cross Infection/ epidemiology/microbiology/mortality Finland/epidemiology Humans Infant, Newborn Intensive Care Units Mycoses/ epidemiology/microbiology Prevalence Risk Factors Sepsis/ epidemiology/microbiology/mortalityNovLaboratory-based surveillance at a Finnish paediatric tertiary-care centre during the period 1999-2006 identified 739 nosocomial bloodstream infections (BSIs) (1.6 BSIs/1000 patient-days). High rates were detected among haematology patients (4.9 BSIs/1000 patient-days) and neonatology patients (3.2 BSIs/1000 patient-days). Most BSIs (95%) were primary infections, and 75% of those were associated with a central line. The most common pathogens were coagulase-negative staphylococci (52%), Staphylococcus aureus (7%) and Candida species (6%). The overall mortality rate within 7 days after the first positive blood culture was 3%. Those who died were more likely to have been admitted to an intensive-care unit or to have undergone surgery.Sarvikivi, E Lyytikainen, O Vaara, M Saxen, H France Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases Clin Microbiol Infect. 2008 Nov;14(11):1072-5.1469-0691 (Electronic)190404792.980Department of Infectious Disease Epidemiology and Control, National Public Health Institute (KTL), Helsinki, Finland. emmi.sarvikivi@ktl.fi4CLM2079 [pii] 10.1111/j.1469-0691.2008.0 X||7 HIbrahem, S. Salmenlinna, S. Lyytikainen, O. Vaara, M. Vuopio-Varkila, J.2008pMolecular characterization of methicillin-resistant Staphylococcus epidermidis strains from bacteraemic patients1020-7Clin Microbiol Infect1411 2008/12/02~Adult Bacteremia/ epidemiology/ microbiology Bacterial Typing Techniques DNA Fingerprinting DNA, Bacterial/genetics Electrophoresis, Gel, Pulsed-Field Epidemiology, Molecular Finland/epidemiology Genotype Humans Infant, Newborn Intensive Care Units, Neonatal Methicillin Resistance Sequence Analysis, DNA Staphylococcus epidermidis/ classification/ genetics/isolation & purificationNovIn order to study the clonality of clinical methicillin-resistant Staphylococcus epidermidis (MRSE) strains and their staphylococcal cassette chromosome mec (SCCmec) elements, 60 isolates of MRSE from bacteraemic patients in three units of the Helsinki University Hospital, Finland were selected, covering the periods 1990-1993 and 1997-1998. The MRSE strains were analysed by pulsed-field gel electrophoresis (PFGE), multilocus sequence typing and SCCmec typing. Eleven PFGE types (FIN-SE-1-11) with sequence type ST2 (clonal complex 2; CC2) were identified. The previously established methicillin-resistant Staphylococcus aureus SCCmec criteria were applied to name the MRSE SCCmec complexes, and it was found that 7% of the isolates carried SCCmec type IA (ccrA1, class B), whereas the majority (93%) yielded six non-typeable SCCmec PCR patterns (P1-P6). Within each SCCmec PCR pattern, two ccr recombinase genes (ccrA2 and ccrA3) and two mec gene complexes (class A and class B) were detected. In addition, the ccrC gene was associated with three of the six patterns. In conclusion, the MRSE strains were genetically related to each other (ST2) but their SCCmec complexes were unique combinations of elements previously recognized among SCCmec types III and IV."Ibrahem, S Salmenlinna, S Lyytikainen, O Vaara, M Vuopio-Varkila, J Research Support, Non-U.S. Gov't France Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases Clin Microbiol Infect. 2008 Nov;14(11):1020-7.1469-0691 (Electronic)190404732.980|Department of Bacterial and Inflammatory Diseases, National Public Health Institute, Helsinki, Finland. salha.ibrahem@ktl.fi4CLM2080 [pii] 10.1111/j.1469-0691.2008.02 F 7(||7#Jallinoja, P. Pajari, P. Absetz, P.2008xRepertoires of lifestyle change and self-responsibility among participants in an intervention to prevent type 2 diabetes455-62Scand J Caring Sci223 2008/10/09Aged Diabetes Mellitus, Type 2/physiopathology/ prevention & control Female Humans Life Style Male Middle Aged Self Efficacy Weight Gain Weight LossSepThis paper analyses participants' accounts on their experiences of lifestyle change during and after the intervention to prevent type 2 diabetes. This paper explores whether the individual is seen as capable of autonomously seeking for a healthier lifestyle or as dependent on external controls and support. The study is based on focus group interview data collected among intervention participants one-and-a-half years after the intervention ended. Those who had been successful in the weight reduction and those whose weight had increased after the intervention were interviewed in separate interview groups. Both weight-losers and weight-gainers agreed with the health-related objectives of the intervention. Despite this agreement, we found three distinct repertoires concerning individuals' potential to proceed in and maintain lifestyle change. The hopelessness repertoire was used mainly by the weight-gainers to describe experiences where lifestyle change was seen to be very difficult. The struggle repertoire was used frequently especially by the weight-gainers but also by the weight-losers to describe struggling against external temptations and one's weaknesses. The self-governing individual repertoire was used most often by weight-losers to describe experiences where new, healthier lifestyle had to a significant extent become a routine and the individual was seen as in charge of his/her lifestyle. The study revealed that the interviewees hold an ambivalent stance towards self-responsibility. The individual was seen as both a sovereign actor and a dependent object of interventions. Most of our interviewees called for continuous controls and even surveillance but at the same time rejected the idea of authoritarian health education. This ambivalence was most clearly present in the struggle repertoire and could be a fruitful target of clarification in health interventions. For a major part of intervention participants, lifestyle change is characterized as a constant struggle and hence interventions should plan the continuation of a support system.Jallinoja, Piia Pajari, Pia Absetz, Pilvikki Research Support, Non-U.S. Gov't Sweden Scandinavian journal of caring sciences Scand J Caring Sci. 2008 Sep;22(3):455-62.1471-6712 (Electronic)188402290.652Department of Health Promotion and Chronic Disease Prevention, National Public Health Institute (KTL), Helsinki, Finland. piia.jallinoja@ktl.fi3SCS551 [pii] 10.1111/j.1471-6712.2007.0055 oP||7#Vaarala, O. Atkinson, M. A. Neu, J.2008The "perfect storm" for type 1 diabetes: the complex interplay between intestinal microbiota, gut permeability, and mucosal immunity2555-62Diabetes5710 2008/09/30Animals Diabetes Mellitus, Type 1/ immunology/microbiology/pathology Gastrointestinal Tract/ immunology/microbiology/pathology Humans Immunity, Mucosal/ immunology Intestinal Mucosa/ immunology/microbiology/pathology Models, BiologicalOctIt is often stated that type 1 diabetes results from a complex interplay between varying degrees of genetic susceptibility and environmental factors. While agreeing with this principal, our desire is that this Perspectives article will highlight another complex interplay potentially associated with this disease involving facets related to the gut, one where individual factors that, upon their interaction with each another, form a "perfect storm" critical to the development of type 1 diabetes. This trio of factors includes an aberrant intestinal microbiota, a "leaky" intestinal mucosal barrier, and altered intestinal immune responsiveness. Studies examining the microecology of the gastrointestinal tract have identified specific microorganisms whose presence appears related (either quantitatively or qualitatively) to disease; in type 1 diabetes, a role for microflora in the pathogenesis of disease has recently been suggested. Increased intestinal permeability has also been observed in animal models of type 1 diabetes as well as in humans with or at increased-risk for the disease. Finally, an altered mucosal immune system has been associated with the disease and is likely a major contributor to the failure to form tolerance, resulting in the autoimmunity that underlies type 1 diabetes. Herein, we discuss the complex interplay between these factors and raise testable hypotheses that form a fertile area for future investigations as to the role of the gut in the pathogenesis and prevention of type 1 diabetes.Vaarala, Outi Atkinson, Mark A Neu, Josef Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review United States Diabetes Diabetes. 2008 Oct;57(10):2555-62.1939-327X (Electronic)188202108.261Laboratory for Immunobiology, Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland. outi.vaarala@ktl.fi(57/10/2555 [pii] 10.2337/db08 1 l|?pPerala, J. Saarni, S. I. Ostamo, A. Pirkola, S. Haukka, J. Harkanen, T. Koskinen, S. Lonnqvist, J. Suvisaari, J.2008[Geographic variation and sociodemographic characteristics of psychotic disorders in Finland337-347Schizophrenia Research1062-3ArticleDecBackground: Geographical variation and sociodemographic characteristics may differ in affective and nonaffective psychotic disorders. We examined the geographical variation in the lifetime prevalence of psychotic disorders in a comprehensive general population study. Method: A nationally representative sample of 8028 Finns aged 30 or over was screened for psychotic and bipolar 1 disorders and interviewed with the Structured Clinical Interview for DSM-IV. Best-estimate DSM-IV diagnoses were formed by combining interview and case note data. Nationwide health care register data were used for the nonrespondents. Associations with sociodemographic features, place of birth and residence in urban or rural areas and in five regions, and migration between the regions were examined. Results: Schizophrenia and other nonaffective psychoses, but not affective psychoses, showed prominent regional variation, with highest odds found for schizophrenia among those born in the North (OR 7.72 95%CI 2.48-24.04) and the East (OR 3.99 95%CI 1.22-13.11). The risk of any psychotic disorder was lower for those born in urban areas (OR 0.73 95%CI 0.54-0.98), but no associations were found for separate diagnostic groups. Region of birth was the strongest determinant of geographical variation when both place of birth and residence were accounted for. Selective migration was not found. Education and income were higher and being employed more common in subjects with affective psychosis than in subjects with other psychotic disorders. Conclusions: Large area variation is more important than urban-rural disparity in psychotic disorders in Finland. Affective psychoses were different from nonaffective psychoses in terms of both regional variation and sociodemographic features. (C) 2008 Elsevier B.V. All rights reserved.://000261850300033Perala, Jonna Saarni, Samuli I. Ostamo, Aini Pirkola, Sami Haukka, Jari Harkanen, Tommi Koskinen, Seppo Lonnqvist, Jouko Suvisaari, Jaana 0920-9964ISI:0002618503000334.24010.1016/j.|?kLindh, E. Lind, S. M. Lindmark, E. Hassler, S. Perheentupa, J. Peltonen, L. Winqvist, O. Karlsson, M. C. I.2008?AIRE regulates T-cell-independent B-cell responses through BAFF 18466-18471OProceedings of the National Academy of Sciences of the United States of America10547ArticleNovAutoimmune polyendocrine syndrome type I (APS 1) results in multiple endocrine organ destruction and is caused by mutations in the autoimmune regulator gene (AIRE). APS I is characterized by circulating tissue-specific autoantibodies, and the presence of these antibodies is often predictive of organ destruction. The importance of AIRE in ensuring central tolerance by regulating the negative selection of autoreactive T cells has been shown clearly. However, in Aire(-/-) mice the phenotype (i.e., autoantibodies, liver infiltrates of B cells, splenomegaly, and marginal zone B-cell lymphoma) is predominantly B-cell mediated, suggesting an exaggerated activation of 8 cells. We have studied T-cell-independent B-cell responses in the absence of AIRE and found that Aire(-/-) mice have an increased response against T-cell-independent type II antigens. We linked this exaggerated response to the elevated serum levels of the B-cell-activating factor of the TNF family (BAFF) that were found both in APS I patients and in Aire(-/-) mice. Transfer of Aire(-/-) bone marrow into irradiated nude mice resulted in increased percentage of BAFF-expressing antigen-presenting cells compared with wt bone marrow, suggesting a T-cell-independent mechanism behind our findings. Furthermore, in vitro experiments showed that AIRE-deficient murine bone marrow-derived dendritic cells produced significantly more BAFF than wt cells when stimulated with IFN-gamma but not when stimulated with IL-10. Our results suggest a cell-intrinsic role for AIRE in peripheral dendritic cells by regulating IFN-gamma-receptor signaling and point toward complementary mechanisms by which AIRE is involved in maintaining tolerance.://000261489300077Lindh, Emma Lind, Sara M. Lindmark, Evelina Hassler, Signe Perheentupa, Jaakko Peltonen, Leena Winqvist, Ola Karlsson, Mikael C. I. 0027-8424ISI:0002614893000779.59810.1073/o|?AKivisto, J. E. Mattila, V. M. Arvola, T. Paavola, M. Parkkari, J.2008wSecular Trends in Poisonings Leading to Hospital Admission among Finnish Children and Adolescents between 1971 and 2005820-824Journal of Pediatrics1536ArticleDecObjective To investigate the secular trends in childhood poisonings leading to hospitalization in Finland. Study design All children and adolescents age 0 to 19 years hospitalized in Finland with the primary diagnosis of poisoning between 1971 and 2005 were identified using die International Classification of Diseases. Results During the study period, there were 41862 hospitalizations,with 96 427 hospital bed days for poisoning in 38 582 children and adolescents. The incidence of hospitalization declined from 91.3 admissions per 100 000 person-years in boys and 105.2 per person-years in girls in 1971 to 64.8 in boys and 83.5 in girls in 2005. In the 0- to 4-year age group, admissions declined by 51%. Hospitalizations for alcohol poisoning increased 1.7-fold (95% confidence interval = 1.4 to 2.2) in boys and 2.4-fold (95% confidence interval = 1.8 to 3.3) in girls. Alcohol poisoning was the primary diagnosis in 53% of those in the 10- to 14-year age group. Conclusions Poisoning remains an important cause of morbidity in Finnish children and adolescents despite the decreased overall incidence of poisonings leading to hospitalization between 1971 and 2005. The increasing trend of hospital admissions for alcohol poisoning, especially in 10- to 14-year-olds, is noteworthy. Effective primary prevention programs and adult supervision should be targeted at reducing alcohol consumption and alcohol-related poisonings in youth. (J Pediatr 2008;153:820-4)://000261659300022MKivisto, Juho E. Mattila, Ville M. Arvola, Taina Paavola, Meri Parkkari, Jari 0022-3476ISI:0002616593000224.01710.1016/|?PLeskela, U. Melartin, T. Rytala, H. Sokero, P. Lestela-Mielonen, P. Isometsa, E.2008iThe Influence of Major Depressive Disorder on Objective and Subjective Social Support A Prospective Study876-883%Journal of Nervous and Mental Disease19612ArticleDecThe impact of persistent depression on social support (SS) is not well known. In the Vantaa Depression Study (VDS), 193 patients with DSM-IV MDD were interviewed at baseline, at 6 and 18 months. Objective SS was measured with the Interview Measure of Social Relationships (IMSR), and subjective SS with the Perceived Social Support Scale-Revised (PSSS-R); the influence of time spent in major depressive episodes (MDEs) on SS at 18 months was investigated. Low objective SS was independently predicted by low baseline objective SS, male gender, and longer time spent in MDEs; low subjective SS by longer time spent in MDEs and lower baseline subjective SS. Along with clinical improvement, subjective SS improved but objective SS did not. The persistence of MDD seems to weaken both objective and subjective SS. Whether this results in progressively weakening objective and subjective SS, and thereby lowers the threshold for future depressive episodes, should be further investigated.://000261653500003eLeskela, Ulla Melartin, Tarja Rytsala, Heikki Sokero, Petteri Lestela-Mielonen, Paula Isometsa, Erkki 0022-3018ISI:0002616535000031.86310.1097/NMD.L;x|?Sund, R. Pukkala, E. Patja, K.2009[Cancer incidence among persons with fragile X syndrome in Finland: a population-based study85-90+Journal of Intellectual Disability Research53ArticleJanFragile X syndrome is a common inheritable cause of intellectual disability (ID) and is characterised by a large number of CGG repeats at the gene FMR1 located on the X-chromosome. It has been reported that this genetic mechanism may protect against malignant transformations. We extracted from the Finnish registry on persons with ID a cohort of 302 persons with a fragile X diagnosis during 1982-1986. Follow-up for cancer incidence was performed in the Finnish Cancer Registry until the end of the year 2005. There were 11 reported cancers during the mean follow-up of 21.4 years per person. The expected number of cancers based on the average Finnish population was 13.8 and no statistically significant protective effect was detected [standardised incidence ratios (SIR) 0.80, confidence interval (CI) 95% 0.40-1.4]. An increased risk for lip cancer was found (SIR 23, CI 95% 2.8-85). Confirmation of hypotheses about the mechanisms linking FXS and cancer needs further research.://000261620300010%Sund, R. Pukkala, E. Patja, K. Part 1 0964-2633ISI:0002616203000101.436 10.1111/j.1365-T|?Whincup, P. H. Kaye, S. J. Owen, C. G. Huxley, R. Cook, D. G. Anazawa, S. Barrett-Connor, E. Bhargava, S. K. Birgisdottir, B. S. E. Carlsson, S. de Rooij, S. R. Dyck, R. F. Eriksson, J. G. Falkner, B. Fall, C. Forsen, T. Grill, V. Gudnason, V. Hulman, S. Hypponen, E. Jeffreys, M. Lawlor, D. A. Leon, D. A. Minami, J. Mishra, G. Osmond, C. Power, C. Rich-Edwards, J. W. Roseboom, T. J. Sachdev, H. S. Syddall, H. Thorsdottir, I. Vanhala, M. Wadsworth, M. Yarbrough, D. E.2008<Birth Weight and Risk of Type 2 Diabetes A Systematic Review 2886-28970Jama-Journal of the American Medical Association30024ReviewDece Context Low birth weight is implicated as a risk factor for type 2 diabetes. However, the strength, consistency, independence, and shape of the association have not been systematically examined. Objective To conduct a quantitative systematic review examining published evidence on the association of birth weight and type 2 diabetes in adults. Data Sources and Study Selection Relevant studies published by June 2008 were identified through literature searches using EMBASE ( from 1980), MEDLINE ( from 1950), and Web of Science ( from 1980), with a combination of text words and Medical Subject Headings. Studies with either quantitative or qualitative estimates of the association between birth weight and type 2 diabetes were included. Data Extraction Estimates of association ( odds ratio [ OR] per kilogram of increase in birth weight) were obtained from authors or from published reports in models that allowed the effects of adjustment ( for body mass index and socioeconomic status) and the effects of exclusion ( for macrosomia and maternal diabetes) to be examined. Estimates were pooled using random- effects models, allowing for the possibility that true associations differed between populations. Data Synthesis Of 327 reports identified, 31 were found to be relevant. Data were obtained from 30 of these reports ( 31 populations; 6090 diabetes cases; 152 084 individuals). Inverse birth weight - type 2 diabetes associations were observed in 23 populations ( 9 of which were statistically significant) and positive associations were found in 8 ( 2 of which were statistically significant). Appreciable heterogeneity between populations (l(2)= 66%; 95% confidence interval [ CI], 51%- 77%) was largely explained by positive associations in 2 native North American populations with high prevalences of maternal diabetes and in 1 other population of young adults. In the remaining 28 populations, the pooled OR of type 2 diabetes, adjusted for age and sex, was 0.75 ( 95% CI, 0.70- 0.81) per kilogram. The shape of the birth weight - type 2 diabetes association was strongly graded, particularly at birth weights of 3 kg or less. Adjustment for current body mass index slightly strengthened the association ( OR, 0.76 [ 95% CI, 0.70-0.82] before adjustment and 0.70 [ 95% CI, 0.65- 0.76] after adjustment). Adjustment for socioeconomic status did not materially affect the association ( OR, 0.77 [ 95% CI, 0.70- 0.84] before adjustment and 0.78 [ 95% CI, 0.72- 0.84] after adjustment). There was no strong evidence of publication or small study bias. Conclusion In most populations studied, birth weight was inversely related to type 2 diabetes risk.://000261920900022gWhincup, Peter H. Kaye, Samantha J. Owen, Christopher G. Huxley, Rachel Cook, Derek G. Anazawa, Sonoko Barrett-Connor, Elizabeth Bhargava, Santosh K. Birgisdottir, Bryndi S. E. Carlsson, Sofia de Rooij, Susanne R. Dyck, Roland F. Eriksson, Johan G. Falkner, Bonita Fall, Caroline Forsen, Tom Grill, Valdemar Gudnason, Vilmundur Hulman, Sonia Hypponen, Elina Jeffreys, Mona Lawlor, Debbie A. Leon, David A. Minami, Junichi Mishra, Gita Osmond, Clive Power, Chris Rich-Edwards, Janet W. Roseboom, Tessa J. Sachdev, Harshpal Singh Syddall, Holly Thorsdottir, Inga Vanhala, Mauno Wadsworth, Michael Yarbrough, Donald E. 0098-7484ISI:000261o |?Tolppanen, A. M. Pulkkinen, L. Kuulasmaa, T. Kolehmainen, M. Schwab, U. Lindstroem, J. Tuomilehto, J. Uusitupa, M. Kuusisto, J.2008The genetic variation in the tenomodulin gene is associated with serum total and LDL cholesterol in a body size-dependent manner 1868-1872 International Journal of Obesity3212ArticleDec=We have reported that the sequence variation in the tenomodulin (TNMD) gene is associated with the risk of type 2 diabetes (T2DM), central obesity and serum levels of systemic immune mediators in the Finnish Diabetes Prevention Study (DPS), which is a longitudinal lifestyle intervention study on 522 middle-aged persons with impaired glucose tolerance (IGT). The aim of this study was to investigate whether the association with T2DM, observed in the DPS could be replicated in a larger, cross-sectional population-based random sample of 5298 men (3020 with normoglycaemia, 984 with impaired fasting glucose, 436 with IGT and 811 with T2DM) from the region of Kuopio, eastern Finland. To further explore the putative mechanisms linking TNMD to T2DM and metabolic syndrome, we studied the associations of TNMD sequence variation with lipid abnormalities characteristic to metabolic syndrome. The association with T2DM risk was not replicated, but significant associations were found with serum low-density lipoprotein and total cholesterol in a body mass index-dependent manner. These associations were also observed in the men of DPS, whereas in women these associations were not significant. These results from two independent study populations suggest that the genetic variation in TNMD could modulate cholesterol metabolism in obese men.://000261695400015|Tolppanen, A-M Pulkkinen, L. Kuulasmaa, T. Kolehmainen, M. Schwab, U. Lindstrom, J. Tuomilehto, J. Uusitupa, M. Kuusisto, J. 0307-0565ISI:0002616954000153.56010. |?Virtanen, H. E. Sundqvist, E. Main, K. M. Kiviranta, H. Tuomisto, J. T. Tuomisto, J. Vartiainen, T. Skakkebaek, N. E. Toppari, J.2008GCongenital cryptorchidism and dioxin levels in breast milk and placenta72-72Hormone Research70Meeting Abstract://000259785600232Virtanen, Helena E. Sundqvist, Erno Main, Katharina M. Kiviranta, Hannu Tuomisto, Jouni T. Tuomisto, Jouko Vartiainen, Terttu Skakkebaek, Niels E. Toppari, Jorma Suppl. 1 0301-0163ISI:00025978"|?Nikkari, S. T. Henttonen, A. Kunnas, T. Kahonen, M. Hutri-Kahonen, N. Juonala, M. Marniemi, J. Viikari, J. Raitakari, O. T. Lehtimaki, T.2008CEstrogen Receptor 2 Polymorphism and Carotid Intima-Media Thickness537-540Genetic Testing124ArticleDecAims: The present study was designed to investigate the effects of estrogen receptor 2 gene (ESR2) rs1256049 polymorphism to carotid artery intima-media thickness (CIMT), as part of the Cardiovascular Risk in Young Finns Study. Results: The frequencies of ESR2 genotypes G/G, G/A, and A/A were 85.1%, 14.3%, and 0.7%, respectively, in the whole study population (n = 2211). Compared with subjects with genotype GG, those with the A allele had higher mean CIMT (p = 0.004) and maximal CIMT (p = 0.005). Conclusions: In a Finnish population, the ESR2 rs1256049 polymorphism A allele is associated with preclinical atherosclerosis in young adulthood. Our results and those of others also suggest that some effects of this genetic variation may be population specific.://000261730600013Nikkari, Seppo T. Henttonen, Antti Kunnas, Tarja Kahonen, Mika Hutri-Kahonen, Nina Juonala, Markus Marniemi, Jukka Viikari, Jorma Raitakari, Olli T. Lehtimaki, Terho 1090-6576ISI:0002617306000131.21810.108xg@|?5Kiss, J. Jalkanen, S. Fulop, F. Savunen, T. Salmi, M.2008YIschemia-reperfusion injury is attenuated in VAP-1-deficient mice and by VAP-1 inhibitors 3041-3049European Journal of Immunology3811ArticleNovNeutrophils mediate the damage caused by ischemia-reperfusion both at the site of primary injury and in remote organs. Vascular adhesion protein-1 (VAP-1) is an ectoenzyme expressed on endothelial cells and it has been shown to regulate leukocyte extravasation. Here we show for the first time using VAP-1-deficient mice that VAP-1 plays a significant role in the intestinal damage and acute lung injury after ischemia-reperfusion. Separate inhibition of VAP-1 by small molecule enzyme inhibitors and a function-blocking monoclonal antibody in WT mice revealed that the catalytic activity of VAP-1 is responsible for its pro-inflammatory action. The use of transgenic humanized VAP-1 mice also showed that the enzyme inhibitors alleviate both the ischemia-reperfusion injury in the gut and neutrophil accumulation in the lungs. These data thus indicate that VAP-1 regulates the inflammatory response in ischemia-reperfusion injury and suggest that blockade of VAP-1 may have therapeutic value.://000261458000008BKiss, Jan Jalkanen, Sirpa Fulop, Ferenc Savunen, Timo Salmi, Marko 0014-2980ISI:0002614580000084.66210.1 j [t|?Dunbar, J. A. Reddy, P. Davis-Lameloise, N. Philpot, B. Laatikainen, T. Kilkkinen, A. Bunker, S. J. Best, J. D. Vartiainen, E. Lo, S. K. Janus, E. D.2008TDepression: An Important Comorbidity With Metabolic Syndrome in a General Population 2368-2373 Diabetes Care3112ArticleDec OBJECTIVE - There is a recognized association among depression, diabetes, and cardiovascular disease. The aim of this study was to examine in a sample representative of the general population whether depression, anxiety, and psychological distress are associated with metabolic syndrome and its components. RESEARCH DESIGN AND METHODS - Three cross-sectional surveys including clinical health measures were completed in rural regions of Australia during 2004-2006. A stratified random sample (n = 1,690, response rate 48%) of men and women aged 25-84 years was selected from the electoral roll. Metabolic syndrome was defined by the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, Adult Treatment Panel III (NCEP ATP III), and International Diabetes Federation (IDF) criteria. Anxiety and depression were assessed by the Hospital Anxiety and Depression Scale and psychological distress by the Kessler 10 measure. RESULTS - Metabolic syndrome was associated with depression but not psychological stress or anxiety. Participants with the metabolic syndrome had higher scores for depression (n = 409, mean score 3.41, 95% CI 3.12-3.70) than individuals without the metabolic syndrome (n = 936, mean 2.95, 95% CI 2.76-3.13). This association was also present in 338 participants with the metabolic syndrome and without diabetes (mean score 3.37, 95% CI 3.06-3.68). Large waist circumference and low HDL cholesterol showed significant and independent associations with depression. CONCLUSIONS - Our results show an association between metabolic syndrome and depression in a heterogeneous sample. The presence of depression in individuals with the metabolic syndrome has implications for clinical management.://000261552500028Dunbar, James A. Reddy, Prasuna Davis-Lameloise, Nathalie Philpot, Benjamin Laatikainen, Tiina Kilkkinen, Annamari Bunker, Stephen J. Best, James D. Vartiainen, Erkki Lo, Sing Kai Janus, Edward D. 0149-5992ISI:0002615525000287.85110|?Knaapila, A. Tuorila, H. Silventoinen, K. Wright, M. J. Kyvik, K. O. Cherkas, L. F. Keskitalo, K. Hansen, J. Martin, N. G. Spector, T. D. Kaprio, J. Perola, M.2008Genetic and Environmental Contributions to Perceived Intensity and Pleasantness of Androstenone Odor: An International Twin Study34-42Chemosensory Perception11ArticleMarXWe estimated the genetic and environmental components of variation in perceived intensity and pleasantness of androstenone, an odorous compound showing specific anosmia, by modeling twin data from Finland, Denmark, the UK, and Australia. The pooled data comprised 917 twin individuals (338 are male and 579 are female; aged from 10 to 83years) including 126 complete monozygous and 264 dizygous twin pairs as well as 137 twin individuals without their co-twin. They rated intensity and pleasantness of androstenone and citronellal (control) odors using nine categories. Additive genetic effects (heritability) contributed 28 and 21% to the variation in the perceived intensity and pleasantness of androstenone, respectively, but negligibly to variations in citronellal perception. A strong genetic correlation existed between the intensity and pleasantness of androstenone, whereas the environmental correlation was negligible. These results suggest that both intensity and pleasantness of androstenone are moderately influenced by genetic factors and that the traits are modified by an overlapping set of genes.://000261769700005Knaapila, Antti Tuorila, Hely Silventoinen, Karri Wright, Margaret J. Kyvik, Kirsten O. Cherkas, Lynn F. Keskitalo, Kaisu Hansen, Jonathan Martin, Nicholas G. Spector, Tim D. Kaprio, Jaakko Perola, Markus 1936-5802ISI:00026176970000510.1007/s12078-007-9005-x{4|?UCrohns, M. Saarelainen, S. Laitinen, J. Peltonen, K. Alho, H. Kellokumpu-Lehtinen, P.2008UEXHALED PENTANE AS A MARKER OF LIPID PEROXIDATION DURING RADIOTHERAPY FOR LUNG CANCER111-111Annals of Oncology19Meeting AbstractSep://000259973300303^Crohns, M. Saarelainen, S. Laitinen, J. Peltonen, K. Alho, H. Kellokumpu-Lehtinen, P. Suppl. 8 0923-7534ISI:00025997 phere.2008.07.085 080.x [doi]eng 2079.x [doi]eng 1128/cvi.00241-08 1515/cclm.2008.320  010 [pii]eng 00010.83561 20524 [doi]Eng -0331 [doi]eng  .2337/dc08-0175  0.1002/dmrr.904 00125-008-1189-3 1244-0 [doi]Eng 124/dmd.108.023457  sj.ejcn.1602882 002/eji.200838651 sigen.2007.02.001  9/gte.2008.0034  975740227610.734  56002322.015  1093/ije/dym225 1038/ijo.2008.217 11.006 [doi]Eng 92090002225.547 2788.2008.01116.x 0b013e31818ec6cf j.jpeds.2008.05.45  10.1093/jnci/djn386  pnas.0808205105  1.x [doi]eng  asis@ktl.fieng schres.2008.08.017 3454000152.499 520817 [doi]eng  06000101.525://000261822100014 Jakkula, Eveliina Rehnstroem, Karola Varilo, Teppo Pietilaeinen, Olli P. H. Paunio, Tiina Pedersen, Nancy L. deFaire, Ulf Jaervelin, Marjo-Riitta Saharinen, Juha Freimer, Nelson Ripatti, Samuli Purcell, Shaun Collins, Andrew Daly, Mark J. Palotie, Aarno Peltonen, Leena 0002-9297ISI:00026182210001411.09210.1016z|?Analitis, A. Katsouyanni, K. Biggeri, A. Baccini, M. Forsberg, B. Bisanti, L. Kirchmayer, U. Ballester, F. Cadum, E. Goodman, P. G. Hojs, A. Sunyer, J. Tiittanen, P. Michelozzi, P.2008^Effects of Cold Weather on Mortality: Results From 15 European Cities Within the PHEWE Project 1397-1408 American Journal of Epidemiology16812ArticleDecWeather-related health effects have attracted renewed interest because of the observed and predicted climate change. The authors studied the short-term effects of cold weather on mortality in 15 European cities. The effects of minimum apparent temperature on cause- and age-specific daily mortality were assessed for the cold season (October-March) by using data from 1990-2000. For city-specific analysis, the authors used Poisson regression and distributed lag models, controlling for potential confounders. Meta-regression models summarized the results and explored heterogeneity. A 1 degrees C decrease in temperature was associated with a 1.35% (95% confidence interval (CI): 1.16,1.53) increase in the daily number of total natural deaths and a 1.72% (95% CI: 1.44, 2.01), 3.30% (95% CI: 2.61, 3.99), and 1.25% (95% CI: 0.77, 1.73) increase in cardiovascular, respiratory, and cerebrovascular deaths, respectively. The increase was greater for the older age groups. The cold effect was found to be greater in warmer (southern) cities and persisted up to 23 days, with no evidence of mortality displacement. Cold-related mortality is an important public health problem across Europe. It should not be underestimated by public health authorities because of the recent focus on heat-wave episodes.://000261683100008Analitis, A. Katsouyanni, K. Biggeri, A. Baccini, M. Forsberg, B. Bisanti, L. Kirchmayer, U. Ballester, F. Cadum, E. Goodman, P. G. Hojs, A. Sunyer, J. Tiittanen, P. Michelozzi, P. 0002-9262ISI:0002616831000085.285|?5Yokoyama, Y. Sugimoto, M. Silventoinen, K. Kaprio, J.2008FWeight Growth Charts from Birth to 6 Years of Age in Japanese Triplets641-647 Twin Research and Human Genetics116ArticleDecWe analyzed the characteristics of weight growth and present the weight growth charts from birth to 6 years of age in Japanese triplets. The study included 366 mothers and their 1098 triplet children, who were born between 1978 and 2006. Data were collected through a mailed questionnaire sent to the mothers asking for information recorded in medical records. For these births, data on triplets' weight growth, gestational age, sex, parity, and maternal age at delivery were obtained from records in the Maternal and Child Health Handbooks, which is provided by the authorities after a report of pregnancy. Birthweight proved to be the strongest contribution on weight of triplets from 1 to 6 years of age. In addition, gestational age was also a significant contributing factor to weight from birth to 6 years of age. Moreover, males had a higher weight from birth to 6 years of age than females. Compared to the 50th percentile of the growth standard for the general population of Japan, the weight deficit of the triplets was more than 40% at birth (male, -1.28 kg; female, -1.28 kg), decreased within the first 1 year of age, and fluctuated between 4% and 9% until 6 years of age (male, -1.82 kg; female, -1.78 kg). In conclusion, triplets have lower birth weight than singletons and in spite of the rapid catch-up growth during first year of life they are behind singletons even in mid-childhood. This study provides growth curves for use in triplets.://000261530600010DYokoyama, Yoshie Sugimoto, Masako Silventoinen, Karri Kaprio, Jaakko 1832-4274ISI:00026153  |? ;Battie, M. C. Videman, T. Levalahti, E. Gill, K. Kaprio, J.2008nGenetic and Environmental Effects on Disc Degeneration by Phenotype and Spinal Level A Multivariate Twin Study 2801-2808Spine3325ArticleDec}Study Design. A classic twin study with multivariate analyses was conducted. Objective. We aimed to further clarify the presence and magnitude of genetic influences on disc degeneration, and to better understand the phenomenon of disc degeneration through comparisons of genetic and environmental influences on specific degenerative signs and different lumbar levels. Summary of Background Data. Previous studies suggest a substantial genetic influence on disc degeneration, but raise important questions about which disc phenotypes are or are not largely genetically influenced and differential effects on spinal levels. Methods. The study sample consisted of 152 monozygotic and 148 dizygotic male twin pairs, 35 to 70 years of age, from the population-based Finnish Twin Cohort. Lumbar magnetic resonance imaging was conducted with quantitative or qualitative assessments of disc signal, bulging, and height narrowing at each lumbar level. Data on possible confounding factors were obtained from an extensive, structured interview. Quantitative genetic modeling was conducted using MPlus. Results. Heritability estimates varied from 29% to 54%, depending on the particular disc degeneration phenotype and lumbar level. The same genetic influences affected signal intensity and disc height (genetic correlations of -0.60 - -0.66) or bulging (-0.71 - -0.72) to a great degree at either the lower or upper lumbar levels and genetic influences on disc height narrowing and bulging were virtually the same. (0.92-0.97). Conversely, genetic correlations (and environmental correlations) were substantially lower for upper and lower lumbar levels, implying largely independent effects. Conclusion. Genetic and environmental influences on disc degeneration seem to be of similar importance. Disc signal, narrowing, and bulging had a primarily common genetic pathway, suggesting a common genetic etiopathogenesis. Conversely, genetic and environmental influences differed substantially for upper versus lower lumbar levels, emphasizing the importance of examining these levels separately in studies of associated genes, other constitutional factors, and environmental influences.://000261345400015LBattie, Michele C. Videman, Tapio Levalahti, Esko Gill, Kevin Kaprio, Jaakko 0362-2436ISI:000261  |?!Lee, J. E. Spiegelman, D. Hunter, D. J. Albanes, D. Bernstein, L. van den Brandt, P. A. Buring, J. E. Cho, E. English, D. R. Freudenheim, J. L. Giles, G. G. Graham, S. Horn-Ross, P. L. Hakansson, N. Leitzmann, M. F. Mannisto, S. McCullough, M. L. Miller, A. B. Parker, A. S. Rohan, T. E. Schatzkin, A. Schouten, L. J. Sweeney, C. Willett, W. C. Wolk, A. Zhang, S. M. Smith-Warner, S. A.2008jFat, Protein, and Meat Consumption and Renal Cell Cancer Risk: A Pooled Analysis of 13 Prospective Studies 1695-1706(Journal of the National Cancer Institute10023ArticleDecYResults of several case-control studies suggest that high consumption of meat (all meat, red meat, or processed meat) is associated with an increased risk of renal cell cancer, but only a few prospective studies have examined the associations of intakes of meat, fat, and protein with renal cell cancer. We conducted a pooled analysis of 13 prospective studies that included 530 469 women and 244 483 men and had follow-up times of up to 7-20 years to examine associations between meat, fat, and protein intakes and the risk of renal cell cancer. All participants had completed a validated food frequency questionnaire at study entry. Using the primary data from each study, we calculated the study-specific relative risks (RRs) for renal cell cancer by using Cox proportional hazards models and then pooled these RRs by using a random-effects model. All statistical tests were two-sided. A total of 1478 incident cases of renal cell cancer were identified (709 in women and 769 in men). We observed statistically significant positive associations or trends in pooled age-adjusted models for intakes of total fat, saturated fat, monounsaturated fat, polyunsaturated fat, cholesterol, total protein, and animal protein. However, these associations were attenuated and no longer statistically significant after adjusting for body mass index, fruit and vegetable intake, and alcohol intake. For example, the pooled age-adjusted RR of renal cell cancer for the highest vs the lowest quintile of intake for total fat was 1.30 (95% confidence interval [CI] = 1.08 to 1.56; P-trend = .001) and for total protein was 1.17 (95% CI = 0.99 to 1.38; P-trend = .02). By comparison, the pooled multivariable RR for the highest vs the lowest quintile of total fat intake was 1.10 (95% CI = 0.92 to 1.32; P-trend = .31) and of total protein intake was 1.06 (95% CI = 0.89 to 1.26; P-trend = .37). Intakes of red meat, processed meat, poultry, or seafood were not associated with the risk of renal cell cancer. Intakes of fat and protein or their subtypes, red meat, processed meat, poultry, and seafood are not associated with risk of renal cell cancer.://000261462400009Lee, Jung Eun Spiegelman, Donna Hunter, David J. Albanes, Demetrius Bernstein, Leslie van den Brandt, Piet A. Buring, Julie E. Cho, Eunyoung English, Dallas R. Freudenheim, Jo L. Giles, Graham G. Graham, Saxon Horn-Ross, Pamela L. Hakansson, Niclas Leitzmann, Michael F. Mannisto, Satu McCullough, Marjorie L. Miller, Anthony B. Parker, Alexander S. Rohan, Thomas E. Schatzkin, Arthur Schouten, Leo J. Sweeney, Carol Willett, Walter C. Wolk, Alicja Zhang, Shumin M. Smith-Warner, Stephanie A. 0027-8874ISI:00026146240000915.678|?"Raitakari, O. T. Juonala, M. Ronnemaa, T. Keltikangas-Jarvinen, L. Rasanen, L. Pietikainen, M. Hutri-Kahonen, N. Taittonen, L. Jokinen, E. Marniemi, J. Jula, A. Telama, R. Kahonen, M. Lehtimaki, T. Akerblom, H. K. Viikari, J. S. A.2008<Cohort Profile: The Cardiovascular Risk in Young Finns Study 1220-1226%International Journal of Epidemiology376ArticleDec://000261461700007Raitakari, Olli T. Juonala, Markus Ronnemaa, Tapani Keltikangas-Jarvinen, Liisa Rasanen, Leena Pietikainen, Matti Hutri-Kahonen, Nina Taittonen, Leena Jokinen, Eero Marniemi, Jukka Jula, Antti Telama, Risto Kahonen, Mika Lehtimaki, Terho Akerblom, Hans K. Viikari, Jorma S. A. 0300-5771ISI:0002614617000075.15110.|?#oShetty, S. Weston, C. J. Oo, Y. H. Youster, J. Hubscher, S. Salmi, M. Jalkanen, S. T. Lalor, P. F. Adams, D. H.2008sC-TYPE LECTIN RECEPTORS SUPPORT LYMPHOCYTE ADHESION TO SINUSOIDAL ENDOTHELIUM IN CHRONIC INFLAMMATORY LIVER DISEASE1606 Hepatology484Meeting AbstractOct://000259757402276Shetty, Shishir Weston, Chris J. Oo, Ye. H. Youster, Janine Hubscher, Stefan Salmi, Marko Jalkanen, Sirpa T. Lalor, Patricia F. Adams, David H. Suppl. S 0270-9139ISI:00025(d|?$:Palo, J. U. Hedman, M. Ulmanen, I. Lukka, M. Sajantila, A.2007GHigh degree of Y-chromosomal divergence within Finland-forensic aspects120-124'Forensic Science International-Genetics12Proceedings PaperJunuAmong the Finns, the levels of autosomal STR and mtDNA variation have been reported to be relatively high and evenly distributed throughout the country. In contrast, the Y-STR variation is markedly lower than observed in most other European populations, showing notable geographical substructure within Finland. There are striking interregional differences-the western, middle and eastern parts of Finland segregate clearly, with phi(ST) values comparable to the highest divergences among European populations. The low Y-STR diversity reduces the discriminative power of Y-chromosomal markers among Finns, and, furthermore, the geographical substructure complicates the assessment of profile probabilities in forensic settings. Here, the Y-STR diversity pattern in Finland is for the first time evaluated from the forensic viewpoint. (c) 2007 Elsevier Ireland Ltd. All rights reserved.://000261500100009UPalo, Jukka U. Hedman, Minttu Ulmanen, Ismo Lukka, Matti Sajantila, Antti Sp. Iss. SI 1872-4973ISI:0002615001000092.01510.1016/j.f  |?%WYlonen, S. K. Salminen, I. Lyssenko, V. Virtanen, S. M. Groop, L. Aro, A. Saloranta, C.2008The Pro12Ala polymorphism of the PPAR-gamma 2 gene affects associations of fish intake and marine n-3 fatty acids with glucose metabolism 1432-1439&European Journal of Clinical Nutrition6212ArticleDecBackground/Objectives: Data on associations between marine n-3 fatty acids and glucose metabolism are inconsistent. Therefore, we explored effects of the Pro12Ala polymorphism in peroxisome proliferator-activated receptor (PPAR)-gamma 2 gene on associations of fish intake and dietary and plasma eicosapentaenoic and docosahexaenoic acid with glucose metabolism. The design comprises of the cross-sectional analysis. Subjects/Methods: The Pro12Ala variant in the PPAR-gamma 2 (PPARG) gene was genotyped in 571 non-diabetic relatives of subjects with type II diabetes. The dietary intake was measured by a 3-day food record, and the plasma cholesterol ester fatty acid composition was analysed with gas chromatography. Associations of dietary and plasma variables with insulin resistance and fasting and 2-h glucose and free fatty acid concentrations were analysed with multiple linear regression analysis. Results: In men, there was a significant interaction between PPARG polymorphism and plasma docosahexaenoic acid on fasting free fatty acid concentration (P = 0.036), and genotype-stratified models showed an inverse association in Pro homozygotes only (P = 0.028). In women, the proportion of plasma eicosapentaenoic acid was higher in Ala-allele carriers compared to Pro homozygotes (1.67 vs 1.44% respectively, P = 0.006). A significant interaction between PPARG polymorphism and fish intake on 2-h glucose was found in women (P = 0.021), and genotype-stratified models suggested an inverse association in Ala-allele carriers only (P = 0.039). Conclusions: The findings suggest that PPARG polymorphism might affect the plasma proportion of eicosapentaenoic acid and modulate the associations of fish intake and marine n-3 fatty acids with glucose metabolism and fasting free fatty acids.://000261330800011WYlonen, S. K. Salminen, I. Lyssenko, V. Virtanen, S. M. Groop, L. Aro, A. Saloranta, C. 0954-3007ISI:0002613308000112.32610.1038/-|?&[Celius, T. Roblin, S. Harper, P. A. Matthews, J. Boutros, P. C. Pohjanvirta, R. Okey, A. B.2008eAryl Hydrocarbon Receptor-Dependent Induction of Flavin-Containing Monooxygenase mRNAs in Mouse Liver 2499-2505Drug Metabolism and Disposition3612ArticleDec1Flavin-containing monooxygenases (FMOs) are important in detoxication but generally are considered not to be inducible by xenobiotics. Our recent microarray studies revealed induction of FMO2 and FMO3 mRNAs by 2,3,7,8-tetrachlorodibenzo-p-dioxin ( TCDD) in liver of mice with wild-type aryl hydrocarbon receptor (AHR) but not in Ahr-null mice. The aim of the present study was to delineate mechanisms of FMO regulation. In adult male mice, basal FMO3 mRNA is low but was induced 6-fold at 4 h and 6000-fold at 24 h. The ED50 was approximately 1 mu g/kg for FMO2 and FMO3, similar to that for the classic AHR-regulated gene, Cyp1a1. In adult female mice basal FMO3 mRNA is high and was not induced at 4 h but was elevated 8-fold at 24 h. FMO5 mRNA was significantly down-regulated by TCDD in both male and female adult mice. Juvenile mice show no sex difference in response to TCDD; FMO3 was induced 4 to 6-fold by TCDD in both sexes. Chromatin immunoprecipitation demonstrated recruitment of AHR and aryl hydrocarbon nuclear translocator proteins to Fmo3 regulatory regions, suggesting that induction by TCDD is a primary AHR-mediated event. Although FMO2 and FMO3 mRNAs were highly induced by TCDD in adult males, overall FMO catalytic activity increased only modestly. In contrast to the striking up-regulation of FMO2 and FMO3 in mouse liver, TCDD has little effect on FMO mRNA in rat liver. However, FMO2 and FMO3 mRNAs were highly induced in transgenic mice that express wild-type rat AHR, indicating that lack of induction in rat is not due to an incompetent AHR in this species.://000261345000015sCelius, Trine Roblin, Steven Harper, Patricia A. Matthews, Jason Boutros, Paul C. Pohjanvirta, Raimo Okey, Allan B. 0090-9556ISI:0002613450000153.90710.1 ; +|?']Arnlov, J. Zethelius, B. Riserus, U. Basu, S. Berne, C. Vessby, B. Alfthan, G. Helmersson, J.2009Serum and dietary beta-carotene and alpha-tocopherol and incidence of type 2 diabetes mellitus in a community-based study of Swedish men: report from the Uppsala Longitudinal Study of Adult Men (ULSAM) study97-105 Diabetologia521ArticleJanAims/hypothesis To investigate the association of serum concentrations and dietary intake of beta-carotene and alpha-tocopherol with type 2 diabetes incidence. Methods Serum beta-carotene, a-tocopherol, lifestyle factors (BMI, physical activity and smoking) and metabolic factors (insulin sensitivity [homeostasis model assessment], acute insulin response and impaired fasting glucose) were analysed in 846 50-year-old non-diabetic Swedish men (participants in the Uppsala Longitudinal Study of Adult Men). Diabetes was identified in 245 participants at reinvestigations after 10, 20 and 27 years. At the 20 year reinvestigation, dietary intake of beta-carotene and alpha-tocopherol, insulin sensitivity (euglycaemic-hyperinsulinaemic clamp) and insulin secretion (early insulin response in OGTT) were determined. Results The highest tertile of serum beta-carotene at age 50 (>0.335 mu mol/l) was associated with 59% lower risk of diabetes during follow-up compared with the lowest tertile (<0.210 mu mol/l) after adjustment for lifestyle and metabolic factors (p<0.01). The highest tertile of lipid-corrected serum alpha-tocopherol at age 50 (>3.67 mu mol/mmol) was associated with 46% lower risk of diabetes compared with the lowest tertile (<3.25 mu mol/mmol) independently of metabolic factors (p<0.05). Moreover, lower serum beta-carotene and alpha-tocopherol concentrations were independently associated with impaired insulin sensitivity (p<0.001), but not with early insulin response, in a subsample of non-diabetic individuals 20 years later. Dietary intake of beta-carotene and alpha-tocopherol independently predicted type 2 diabetes during 7 years of follow-up. Conclusions/interpretation Serum concentrations and dietary intakes of beta-carotene and alpha-tocopherol independently predicted insulin resistance and type 2 diabetes incidence during 27 years of follow-up in a community-based study of men. This result supports the importance of impaired antioxidant status for the development of insulin resistance and type 2 diabetes.://000261375400015]Arnlov, J. Zethelius, B. Riserus, U. Basu, S. Berne, C. Vessby, B. Alfthan, G. Helmersson, J. 0012-186XISI:0002613754000155.82210.1007/s^O|?(.Honkanen, J. Skarsvik, S. Knip, M. Vaarala, O.2008}Poor in vitro induction of FOXP3 and ICOS in type 1 cytokine environment activated T-cells from children with type 1 diabetes635-641(Diabetes-Metabolism Research and Reviews248ArticleNov-DecBackground Type 1 diabetes (T1D) is characterised by loss of tolerance to beta-cell antigens, and the insulin-producing beta-cells in the pancreatic islets are destroyed by the host's own immune system. immunological risk factors associated with T1D are related to the defects in the polarization of T-cells and in the function of regulatory T (Treg)-cells. We set out to study whether an impaired induction of regulatory mechanisms during the generation of T-cell responses upon stimulation is associated with T1D. Methods Naive T-cells were isolated from 18 children with recent T1D (0-14days from diagnosis; mean age 9.3 years), 11 children who had had T1D for at least 1 year (mean age 10.6) and 14 non-diabetic children (mean age 8.1). CD45RA+ T-cells were stimulated with PHA for 72 h in type 1 cytokine [interleukin (IL)-12 and anti-IL-4] or type 2 cytokine (IL-4 and anti-IL-12) environment. T-cell polarization and regulation related markers were analysed by quantitative reverse transcription polymerase chain reaction (QRT-PCR) (Th1 promoting T-bet, Th2 promoting GATA-3 and regulation related FOXP3, ICOS and NFATc2). Results Children with recently diagnosed T1D showed decreased induction of FOXP3, ICOS and NFATc2 in T-cells activated in type 1 cytokine milieu (p = 0.007, p = 0.001, and p = 0.02), whereas no differences between the diabetic and healthy children were seen in the up-regulation of activation markers, T-bet and GATA-3. Conclusions The poor induction of factors that mediate down-modulation of T-cell responses upon stimulation in type 1 cytokine environment may contribute to the development of autoreactive type I responses in T1D. Copyright (C) 2008 John Wiley & Sons, Ltd.://000261302800007<Honkanen, Jarno Skarsvik, Susanne Knip, Mikael Vaarala, Outi 1520-7552ISI:0002613028000073.0871H7|?)FValkonen, T. Blomgren, J. Kauppinen, T. M. Martikainen, P. Maenpaa, E.2008The effects of regional socioeconomic and cultural characteristics on the spatial patterns of the Second Demographic Transition in Finland 2043-2056Demographic Research19Proceedings PaperDectThe article studies to what extent regional socioeconomic and cultural characteristics explain spatial patterns in the Second Demographic Transition in Finland. The country's 75 functional regions are used as area units. A summary indicator of the transition based on divorce and cohabitation is used as the dependent variable. The results show that the spatial pattern is mainly determined according to the regional level of urbanization, but the effect is mediated by cultural characteristics (secularization and support for the socialist and green parties). The cultural characteristics have only a modest independent effect.://000261618600001UValkonen, Tapani Blomgren, Jenni Kauppinen, Timo M. Martikainen, Pekka Maenpaa, Elina 1435-9871ISI:00026161860|?*;Aasvee, K. Kurvinen, E. Sundvall, J. Jauhiainen, M. Tur, I.2008Aggregation of lipoprotein and inflammatory parameters in families with a history of premature myocardial infarction: the Tallinn Myocardial Infarction Study 1602-1608*Clinical Chemistry and Laboratory Medicine4611ArticleNovBackground: The offspring of individuals with a history of premature myocardial infarction are at increased risk of premature coronary attacks. The aim of this study was to determine parent/offspring associations of coronary risk factors in families affected by premature myocardial infarction and to compare these to corresponding control families. Methods: The cohort of cases consisted of 71 male survivors of myocardial infarction and their 128 descendants (aged 7-18 years). As control families, 85 randomly selected healthy males with their 66 descendants were investigated. Besides traditional risk factors, serum high sensitive C-reactive protein (hsCRP), apolipoprotein (apo) E phenotypes and lipoprotein(a) were analyzed. Results: In the offspring of the patients, fibrinogen and atherogenic lipoprotein parameters were higher than in the corresponding controls, but hsCRP, lipoprotein(a) and anthropometric data did not differ between the groups. The adult-offspring positive correlations were detected in fibrinogen and in almost all measured lipoprotein fractions in the affected families; amongst the controls, the association was observed only for triglyceride levels. Multiple logistic regression analysis demonstrated independent association of offspring apoB, apoA-I and fibrinogen levels with a family history of premature myocardial infarction. Conclusions: The most informative predictors of future coronary attacks during childhood are apoB-100 and apoB/apoA-I ratio; serum hsCRP and lipoprotein(a) do not have predictive value in childhood.://000261386100019KAasvee, Katrin Kurvinen, Elvira Sundvall, Jouko Jauhiainen, Matti Tur, Inna 1434-6621ISI:0002613861000191.74110.|?+BLundberg, A. Wikberg, L. A. Ilonen, J. Vaarala, O. Bottcher, M. F.2008`Lipopolysaccharide-Induced Immune Responses in Relation to the TLR4(Asp299Gly) Gene Polymorphism 1878-1883Clinical and Vaccine Immunology1512ArticleDecAltered microbial exposure is a possible explanation for the increase of allergies in the Western world. However, genetic factors influence microbially induced immune responses. We have investigated the TLR4(Asp299Gly) gene polymorphism and its possible association with receptor expression of circulating peripheral blood monocytes and the in vitro cytokine responses and phosphorylation of intracellular signaling proteins in peripheral blood mononuclear cells (PBMC) stimulated with lipopolysaccharide (LPS) from Escherichia coli and Salmonella enterica serotype Typhimurium. We studied 34 of the predominant haplotype TLR4 Asp299 (AA) and 8 heterozygote Asp299Gly (AG) individuals. TLR4 expression levels were similar in the two genotype groups. Serovar Typhimurium LPS induced interleukin-12p70 from PBMC, and the degree of phosphorylation of the intracellular signaling protein I kappa B alpha in PBMC was lower in the AG than the AA group (P = 0.03 and P = 0.04, respectively). These results were not seen, however, when PMBC were stimulated with E. coli-derived LPS. Based on these results, we propose that TLR4(Asp299Gly) gene polymorphism and the bacterial origin of LPS should be considered when environmental LPS exposure is evaluated in disease risk or protection.://000261384800019ZLundberg, Anna Wikberg, Lars Andersson Ilonen, Jorma Vaarala, Outi Bottcher, Malin Fageras 1556-6811ISI:0002613848000191.99510.4|?,Salo, S. Verta, M. Malve, O. Korhonen, M. Lehtoranta, J. Kiviranta, H. Isosaari, P. Ruokojarvi, P. Koistinen, J. Vartiainen, T.2008Contamination of River kymijoki sediments with polychlorinated dibenzo-p-dioxins, dibenzofurans and mercury and their transport to the Gulf of Finland in the Baltic Sea 1675-1683 Chemosphere7310ArticleNovKymijoki, the fourth largest river in Finland, has been heavily polluted by pulp mill effluents as well as the chemical industry. Up to 24000ton of wood preservative, chlorophenol known as Ky-5, was manufactured in the upper reaches of the river, an unknown amount of which was discharged into the river between 1940 and 1984. Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) occurred as impurities in the final Ky-5 product. The PCDD/F concentrations and burden in the river sediments were studied and the transport of PCDD/Fs from contaminated sites downstream and into the Gulf of Finland in the Baltic Sea was estimated. More than 190 sediment cores were sampled to estimate the volume of contaminated sediments and the total PCDD/F burden. The transport of PCDD/Fs was estimated using sediment traps placed at several sites. The survey revealed that sediments in the river were heavily polluted by PCDD/Fs, the main toxic congener being 1,2,3,4,6,7,8-heptachlorodibenzofuran, a major contaminant in the Ky-5 product. The mean total concentration at the most polluted river site downstream from the main source was 42000 mu g kg(-1) d.w. (106 mu g I-TEQkg(-1)). The elevated concentrations in the coastal region and the present estimated transport from the River Kymijoki confirm earlier assessments that the river is a major source of PCDD/F for the Gulf of Finland. (C) 2008 Elsevier Ltd. All rights reserved.://000261561600015Salo, Simo Verta, Matti Malve, Olli Korhonen, Markku Lehtoranta, Jouni Kiviranta, Hannu Isosaari, Pirjo Ruokojarvi, Paivi Koistinen, Jaana Vartiainen, Terttu 0045-6535ISI:0002615616000152.739!10.1016/j.chemosL;z|?-Fondelli, M. C. Chellini, E. Yli-Tuomi, T. Cenni, I. Gasparrini, A. Nava, S. Garcia-Orellana, I. Lupi, A. Grechi, D. Mallone, S. Jantunen, M.2008BFine particle concentrations in buses and taxis in Florence, Italy 8185-8193Atmospheric Environment4235ArticleNovOn October 2004, a sampling survey was carried out in Florence to estimate urban fine particle exposure concentrations inside commuting vehicles during workdays characterized by heavy traffic. Portable samplers were positioned inside four regularly scheduled diesel-powered buses and four taxis during eight weekdays. Each sampler consisted of a 2.5 mu m size pre-separator cyclone, a direct-reading data logging photometer (pDR-1200), and a 4 L min(-1) filter sampler for the determination of PM2.5 mass concentration. Based on reflectance analysis measurements, a PM2.5 Black Smoke Index was determined for each filter, and the elemental composition of the PM2.5 was analyzed by Particle Induced X-ray Emission (PIXE). PM2.5 mass concentrations inside the vehicles correlated well with the urban ambient air PM2.5 concentrations measured at the fixed-site monitoring stations. The PM2.5 excess above the urban ambient level was on average 32 mu g m(-3) (range: 22-52 mu g m(-3)) and 20 mu g m(-3) (range: 11-29 mu g m(-3)) in buses and taxis, respectively. The PM2.5-bound sulfur concentration was also higher in the buses than in the taxis. Based on daily Time-Microenvironment-Activity-Diary (TMAD) data. the Florentines spend on average 9.7% of their day in traffic, and the corresponding average exposure is approximately 12% of their daily PM2.5 personal exposure. The obtained data could be used to plan interventions to minimize the PM2.5 citizen exposures in commuting. (C) 2008 Elsevier Ltd. All rights reserved.://000261301200006Fondelli, M. Cristina Chellini, Elisabetta Yli-Tuomi, Tarja Cenni, Isabella Gasparrini, Antonio Nava, Silvia Garcia-Orellana, Isabel Lupi, Andrea Grechi, Daniele Mallone, Sandra Jantunen, Matti 1352-2310ISI:0002613012000062.54910.1016/j.atm U C{H|?.FFranc, M. Moffat, I. Boutros, P. Tuomisto, J. Pohjanvirta, R. Okey, A.2008ePatterns of dioxin-altered mRNA expression in livers of dioxin-sensitive versus dioxin-resistant rats809-830Archives of Toxicology8211ArticleNovsDioxins exert their major toxicologic effects by binding to the aryl hydrocarbon receptor (AHR) and altering gene transcription. Numerous dioxin-responsive genes previously were identified both by conventional biochemical and molecular techniques and by recent mRNA expression microarray studies. However, of the large set of dioxin-responsive genes the specific genes whose dysregulation leads to death remain unknown. To identify specific genes that may be involved in dioxin lethality we compared changes in liver mRNA levels following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in three strains/lines of dioxin-sensitive rats with changes in three dioxin-resistant rat strains/lines. The three dioxin-resistant strains/lines all harbor a large deletion in the transactivation domain of the aryl hydrocarbon receptor (AHR). Despite this deletion, many genes exhibited a "Type-I" response-that is, their responses were similar in dioxin-sensitive and dioxin-resistant rats. Several genes that previously were well established as being dioxin-responsive or under AHR regulation emerged as Type-I responses (e.g. CYP1A1, CYP1A2, CYP1B1 and Gsta3). In contrast, a relatively small number of genes exhibited a Type-II response-defined as a difference in responsiveness between dioxin-sensitive and dioxin-resistant rat strains. Type-II genes include: malic enzyme 1, ubiquitin C, cathepsin L, S-adenosylhomocysteine hydrolase and ferritin light chain 1. In silico searches revealed that AH response elements are conserved in the 5'-flanking regions of several genes that respond to TCDD in both the Type-I and Type-II categories. The vast majority of changes in mRNA levels in response to 100 mu g/kg TCDD were strain-specific; over 75% of the dioxin-responsive clones were affected in only one of the six strains/lines. Selected genes were assessed by quantitative RT-PCR in dose-response and time-course experiments and responses of some genes were assessed in Ahr-null mice to determine if their response was AHR-dependent. Type-II genes may lie in pathways that are central to the difference in susceptibility to TCDD lethality in this animal model.://000261422200004vFranc, Monique A. Moffat, Ivy D. Boutros, Paul C. Tuomisto, Jouni T. Tuomisto, Jouko Pohjanvirta, Raimo Okey, Allan B. 0340-5761ISI:0002614222000041.75610.1007}k{|?/Lu, A. T. Ogdie, M. N. Jarvelin, M. R. Moilanen, I. K. Loo, S. K. McCracken, J. T. McGough, J. J. Yang, M. H. Peltonen, L. Nelson, S. F. Cantor, R. M. Smalley, S. L.2008`Association of the Cannabinoid Receptor Gene (CNR1) With ADHD and Post-Traumatic Stress Disorder 1488-1494EAmerican Journal of Medical Genetics Part B-Neuropsychiatric Genetics147B8ArticleDecAttention deficit hyperactivity disorder (ADHD) is a highly heritable disorder affecting some 5-10% of children and 4-5% of adults. The cannabinoid receptor gene (CNR1) is a positional candidate gene due to its location near an identified ADHD linkage peak on chromosome 6, its role in stress and dopamine regulation, its association with other psychiatric disorders that co-occur with ADHD, and its function in learning and memory. We tested SNP variants at the CNR1 gene in two independent samples-an unselected adolescent sample from Northern Finland, and a family-based sample of trios (an ADHD child and their parents). In addition to using the trios for association study, the parents (with and without ADHD) were used as an additional case/control sample of adults for association tests. ADHD and its co-morbid psychiatric disorders were examined. A significant association was detected for a SNP haplotype (C-G) with ADHD (P = 0.008). A sex by genotype interaction was observed as well with this haplotype posing a greater risk in males than females. An association of an alternative SNIP haplotype in this gene was found for post-traumatic stress disorder (PTSD) (P=0.04 for C-A, and P = 0.01 for C-G). These observations require replication, however, they suggest that the CNR1 gene may be a risk factor for ADHD and possibly PTSD, and that this gene warrants further investigation for a role in neuropsychiatric disorders. (c) 2008 Wiley-Liss, Inc.://000261415800023Lu, Ake T. Ogdie, Matthew N. Jarvelin, Marjo-Ritta Moilanen, Irma K. Loo, Sandra K. McCracken, James T. McGough, James J. Yang, May H. Peltonen, Leena Nelson, Stanley F. Cantor, Rita M. Smalley, Susan L. Sp. Iss. SI 1552-4841ISI:0002614158000234.22410|?0XSalminen, M. Vahlberg, T. Sihvonen, S. Piirtolal, M. Isoahol, R. Aamio, P. Kivela, S. L.2008Effects of risk-based multifactorial fall prevention program on maximal isometric muscle strength in community-dwelling aged: a randomized controlled trial487-493(Aging Clinical and Experimental Research205ArticleOctuBackground and aims: The aim of this study was to assess the effects of risk-based multifactorial fall prevention program on maximal isometric strength in the community-dwelling aged. Methods: 591 subjects were randomized in two age groups (65-74 and >= 75 yrs), intervention group (IG) (n=293) and control group (CG) (n=298). A 12-month program consisted of individual geriatric assessment, individual guidance on fall prevention, home hazards assessment, physical exercises in groups, lectures, psychosocial activity groups, and home exercises. Strength was measured on an adjustable dynamometer chair. Results: Among women, the extension strength of the left knee increased by 7% in IG and 2% in CG (p=0.006), and that of the right knee by 7% and 4% (p=0.057), respectively. Subgroup analyses in the two age groups revealed a significant difference between groups among men aged 65-74 yrs, in favour of CG subjects, whose flexion strength of the left knee increased by 14% whereas the corresponding increase in IG was only 1% (p=0.042). Among women aged 65-74 yrs, the extension strength of right (increase of 8% in IG, 4% in CG) (p=0.046) and left knees (9% and 3%) (p=0.008) and flexion strength of right (10% and 4%) (p=0.042) and left knees (10% and 4%) (p=0.041) increased more in IG than in CG. Conclusions: The 12-month fall prevention program increased maximal isometric muscle strength among women only, especially those aged 65-74 years. We suggest that more intensive exercise, including the use of extra weights or resistance, is needed to increase muscle strength in men. (Aging Clin Exp Res 2008; 20: 487-493) (c) 2008, Editrice Kurtis.://000261510300015uSalminen, Marika Vahlberg, Tero Sihvonen, Sanna Piirtolal, Maarit Isoahol, Rairno Aamio, Pertti Kivelae, Sirkka-Liisa 1594-0667ISI:0002615103000151.311 .11.005 [doi]eng 004 [doi]Eng 10.1093/aje/kwn266 osenv.2008.07.054 .1002/ajmg.b.30693 47.012 [doi]eng 33003034.875 /s00204-008-0303-0PKzx-:I/**refs.FRM 0B< !// !HPRIMARYyearIndex 6ByP/) idreference_type text_stylesauthoryear title pages secondary_title volume numbernumber_of_volumessecondary_authorplace_published publishersubsidiary_authoredition keywords type_of_workdate2)  abstractlabelurltertiary_titletertiary_author notes isbn custom_1 custom_2 custom_3 custom_4alternate_titleaccession_number call_number short_title custom_5 custom_6sectionoriginal_publicationH) reprint_editionreviewed_itemauthor_addressimagecaption custom_7 electronic_resource_number link_to_pdf translated_author translated_titlename_of_databasedatabase_providerresearch_notes language access_datelast_modified_date !! 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