PKu8_refs.MYD F|7KKainu, T. A. Lindqvist, A. E. Sarna, S. J. Lundback, B. E. Sovijarvi, A. R.2008=FEV1 response to bronchodilation in an adult urban populationChest 2008/04/12Apr 10Background Most studies evaluating bronchodilation in flow-volume spirometry have been conducted in patients with obstructive airways diseases, but less is known about bronchodilation responses in the general population or in healthy subjects. Methods We evaluated an urban population sample of 628 adults (260 men, 368 women) aged 25-74 years with flow-volume spirometry using 0.4 mg of inhaled salbutamol aerosol with a spacer device for bronchodilation. On the basis of a structured interview, a subgroup of 219 healthy asymptomatic non-smokers was selected. Results In the population sample, the average increase of forced expiratory volume in one second (FEV1) from baseline after inhaled salbutamol was 77.2 ml (s.d. 109.7 ml) or 2.5% (3.9%). In healthy asymptomatic non-smokers, the mean change of FEV1 was 62.0 ml (89.7 ml) or 1.8% (2.6%). In the whole population, the 95(th) percentile limit of the increase of FEV1 was 8.5%, while it was 5.9% among healthy asymptomatic non-smokers. The absolute change of FEV1 correlated significantly with the baseline FVC (p<0.01). The ratio of FEV1 to forced vital capacity (FEV1/FVC) at baseline was the strongest influencing factor for bronchodilation response. Conclusions The results indicate that a significant increase of FEV1 from the baseline in a bronchodilation test is around 9% in an urban population. The level of the significant absolute increase of FEV1 seems to depend on FVC. Low baseline FEV1/FVC, reflecting airflow limitation, is the strongest determinant for FEV1 response to bronchodilation.Chest Chest. 2008 Apr 10;.0012-3692 (Print)184036713.924Division of Pulmonary Medicine, Department of Medicine, Helsinki University Central Hospital, P.O. Box 340, FIN-00029 HUS, Helsinki, Finland, Tel: +358-40-735 2763, Fax: +358-9-4717 4592; Research Unit of Pulmonary Diseases, Department of Medicine, Helsinki University Central Hospital and Clinical Research Institute Ltd, Helsinki, Finland; Department of Public Health, University of Helsinki, Helsinki, Finland; Unit for Lung and Allergy Research, National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Division of Clinical Physiology and Nuclear Medicine, Laboratory Department, Helsinki University Central Hospital, Helsinki, Finland./chest.07-2207 [pii] 10.1378/chest.07-||7^Mantere, O. Suominen, K. Valtonen, H. M. Arvilommi, P. Leppamaki, S. Melartin, T. Isometsa, E.2008;Differences in outcome of DSM-IV bipolar I and II disorders413-25Bipolar Disord103 2008/04/12MayObjectives: To investigate whether the course of bipolar disorder (BD) type II is more depressive than that of BD I, and, if so, to explore the underlying factors that cause this difference. Methods: In a prospective, naturalistic study of 191 secondary care psychiatric in- and outpatients diagnosed in an acute phase of BD I or II, 160 patients (85.1%) were followed for 18 months. Using a life chart, the exact timing of symptom states in follow-up was examined. Differences between BD I (n = 75) and II (n = 85) in duration of index phase and episode, time to full remission and recurrence, and time in any mood episode were investigated. Results: Patients with BD II spent a higher proportion of time ill (47.5% versus 37.7%; p = 0.02) and in depressive symptom states (58.0% versus 41.7%; p = 0.003) than BD I patients. This was a result of the higher proportion (61.7% versus 48.6%; p = 0.03) and mean number (1.69 versus 1.11; p = 0.006) of depressive illness phases in BD II, rather than of differences in the duration of depressive phases. Type of index phase strongly predicted the outcome. In linear regression models, both BD II and type of index phase predicted more time spent in depressive symptom states. Conclusions: In medium-term follow-up, BD II patients spend about 40% more time in depressive symptom states than BD I patients because a higher proportion of BD II patients have depressive phases and the frequency of these is higher. Differences in type of index phase may markedly confound differences in outcome between BD I and II.Mantere, Outi Suominen, Kirsi Valtonen, Hanna M Arvilommi, Petri Leppamaki, Sami Melartin, Tarja Isometsa, Erkki Denmark Bipolar disorders Bipolar Disord. 2008 May;10(3):413-25.1398-5647 (Print)184026293.494Department of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, and Department of Psychiatry, Jorvi Hospital, Helsinki University Central Hospital, Espoo, Finland.3BDI502 [pii] 10.1111/j.1399-5618.2007.0050  F|7AHu, G. Antikainen, R. Jousilahti, P. Kivipelto, M. Tuomilehto, J.20083Total cholesterol and the risk of Parkinson disease Neurology 2008/04/11Apr 9OBJECTIVE: To examine the association between serum total cholesterol at baseline and the risk of Parkinson disease (PD). METHODS: Study cohorts included 24,773 Finnish men and 26,153 women aged 25 to 74 years without a history of PD and stroke at baseline. Hazard ratios (HRs) of incident PD were estimated for different levels of total cholesterol. RESULTS: During a mean follow-up period of 18.1 years, 321 men and 304 women developed incident PD. After adjustment for confounding factors (age, study years, body mass index, systolic blood pressure, education, leisure-time physical activity, smoking, alcohol consumption, coffee and tea consumption, and history of diabetes), the HRs of PD at different levels of total cholesterol (<5, 5-5.9, 6-6.9, and >/=7 mmol/L) were 1.00, 1.33, 1.53, and 1.84 (p for trend = 0.035) in men; 1.00, 1.55, 1.57, and 1.86 (p for trend = 0.113) in women; and 1.00, 1.42, 1.56, and 1.86 (p for trend = 0.002) in men and women combined (adjusted also for sex). In both sexes combined, the increased risk of PD associated with increasing levels of serum total cholesterol was present both in subjects aged 25-44 years and in subjects aged 45-54 years at baseline, and in never smokers and smokers; however, no association was found among subjects aged 55 years or older at baseline. CONCLUSION: This large prospective study suggests that high total cholesterol at baseline is associated with an increased risk of Parkinson disease.!Neurology Neurology. 2008 Apr 9;.1526-632X (Electronic)184010185.690From the Department of Health Promotion and Chronic Diseases Prevention (G.H., P.J., J.T.), National Public Health Institute, Helsinki; Department of Public Health (G.H., J.T.), University of Helsinki; Oulu City Hospital and Department of Public Health Science and General Practice (R.A.), University of Oulu; Department of Neuroscience and Neurology (M.K.), University of Kuopio; South Ostrobothnia Central Hospital (J.T.), Seinajoki, Finland; and Aging Research Center (M.K.), Karolinska Institutet, Stockholm, Sweden.I01.wnl.0000312511.62699.a8 [pii] 10.1212/01.wnl.0000312511.62699 T|7lKarlsson, L. Kiviruusu, O. Miettunen, J. Heila, H. Holi, M. Ruuttu, T. Tuisku, V. Pelkonen, M. Marttunen, M.2008cOne-Year Course and Predictors of Outcome of Adolescent Depression: A Case-Control Study in Finlande1-e10J Clin Psychiatry 2008/04/11Apr 8BACKGROUND: Clinical studies on the outcome of adolescent depression beyond treatment trials are scarce. OBJECTIVE: To investigate the impact of characteristics of the depressive episode and current comorbidity on the 1-year outcome of depression. METHOD: A sample of 174 consecutive adolescent psychiatric outpatients (aged 13 through 19 years) and 17 school-derived matched controls, all with unipolar depressive disorders at baseline, were reinterviewed for DSM-IV Axis I and Axis II disorders at 12 months. The study was conducted between January 1998 and May 2002. RESULTS: The outpatients had equal recovery rate and episode duration but shorter time to recurrence than the controls. Among the outpa-tients, Axis II comorbidity predicted shorter time to recurrence (p = .02). Longer time to recovery was predicted by earlier lifetime age at onset for depression (p = .02), poor psychosocial functioning (p = .003), depressive disorder diagnosis (p /=30 years using Bayesian spatial conditional autoregressive models. Registry of reimbursed medication for parkinsonism and a prescription database of purchase of these drugs were used to identify the study subjects. They were located by the map coordinates of the place of residence and aggregated into regular 100 km(2) grid cells. A total of 7,190 incident and 10,616 prevalent cases were found. The age-adjusted annual incidence was 32.6/100,000 (95% HDR 31.8-33.4) during the years 1995 to 2000 and prevalence was 268/100,000 (95% HDR 263-274) in 2000. The male to female ratio was 1.45 (95% HDR 1.39-1.51) in incidence and 1.54 (95% HDR 1.47-1.61) in prevalence. There was strong evidence for geographic variation in incidence and prevalence. A zone with high incidence and prevalence was identified in the eastern and central part of Finland. There was no evidence for difference in incidence and prevalence between urban and rural areas. The marked (more than two-fold) geographic variation can hardly be caused solely by practices of the registration and collection of data on diagnosis or by methodological issues, but rather suggests to geographic variation in protective and predisposing factors of Parkinsonism in Finland. (c) 2008 Movement Disorder Society._Movement disorders : official journal of the Movement Disorder Society Mov Disord. 2008 Apr 8;.1531-8257 (Electronic)183989143.323sDepartment of Health Promotion and Chronic Disease Prevention, National Public Health Institute, Helsinki, Finland.10.1002/mds.22 B 3h||7Nyamdorj, R. Qiao, Q. Soderberg, S. Pitkaniemi, J. Zimmet, P. Shaw, J. Alberti, G. Nan, H. Uusitalo, U. Pauvaday, V. Chitson, P. Tuomilehto, J.2008Comparison of body mass index with waist circumference, waist-to-hip ratio, and waist-to-stature ratio as a predictor of hypertension incidence in Mauritius866-870 J Hypertens265 2008/04/10MayOBJECTIVE: Comparison of BMI with waist circumference, waist-to-hip ratio (WHR), and waist-to-stature ratio (WSR) as a predictor of hypertension incidence. METHODS: A total of 1658 men and 1976 women of Mauritian Indian and Mauritian Creole ethnicity, aged 25-74 years, free of hypertension, diabetes, cardiovascular disease, and gout at baseline in 1987 or 1992, were re-examined in 1992 and/or 1998 using the same survey methodology. Hazard ratios (HRs) for hypertension incidence were estimated applying an interval censored survival analysis (R program) using age as timescale based on baseline obesity indicators. RESULTS: A total of 787 incident hypertension cases were identified during the follow-up. HRs for hypertension incidence adjusting for baseline systolic blood pressure and cohort corresponding to a 1 SD increase in BMI, waist circumference, WHR, and WSR were 1.20 (1.24), 1.19 (1.21), 1.14 (1.10), and 1.20 (1.26) in Mauritian Indian men (women) and 1.23 (1.32), 1.34 (1.23), 1.41 (1.13), and 1.43 (1.33) in Mauritian Creoles, respectively, indicating that all obesity indicators significantly predicted hypertension incidence except for WHR in Mauritian Creole women. Paired homogeneity tests showed that there was no difference between BMI and the other three indicators for most of the comparisons with two exceptions: WSR was stronger than BMI (P = 0.002) in Mauritian Creole men but BMI was stronger than WHR (P = 0.047) in Mauritian Indian women in predicting the incident cases of hypertension. CONCLUSION: The relation of the development of hypertension with BMI was as strong as that with central obesity indicators in the population studied.<Journal of hypertension J Hypertens. 2008 May;26(5):866-870.0263-6352 (Print)183983274.021aDepartment of Public Health, University of Helsinki bDiabetes Unit, National Public Health Institute, Helsinki, Finland cDepartment of Medicine, Umea University Hospital, Umea, Sweden dInternational Diabetes Institute, Melbourne, Australia eDepartment of Endocrinology and Metabolic Medicine, Mint Wing, St Mary's Hospital, London, UK fMinistry of Health and Quality of Life, Port Louis, Mauritius.A10.1097/HJH.0b013e3282f624b7 [doi] 00004872-200805000-00 ] KF|7PPohjanvirta, R. Boutros, P. C. Moffat, I. D. Linden, J. Wendelin, D. Okey, A. B.2008[Genome-wide effects of acute progressive feed restriction in liver and white adipose tissueToxicol Appl Pharmacol 2008/04/09Feb 14`Acute progressive feed restriction (APFR) represents a specific form of caloric restriction in which feed availability is increasingly curtailed over a period of a few days to a few weeks. It is often used for control animals in toxicological and pharmacological studies on compounds causing body weight loss to equalize weight changes between experimental and control groups and thereby, intuitively, to also set their metabolic states to the same phase. However, scientific justification for this procedure is lacking. In the present study, we analyzed by microarrays the impact on hepatic gene expression in rats of two APFR regimens that caused identical diminution of body weight (19%) but differed slightly in duration (4 vs. 10 days). In addition, white adipose tissue (WAT) was also subjected to the transcriptomic analysis on day-4. The data revealed that the two regimens led to distinct patterns of differentially expressed genes in liver, albeit some major pathways of energy metabolism were similarly affected (particularly fatty acid and amino acid catabolism). The reason for the divergence appeared to be entrainment by the longer APFR protocol of peripheral oscillator genes, which resulted in derailment of circadian rhythms and consequent interaction of altered diurnal fluctuations with metabolic adjustments in gene expression activities. WAT proved to be highly unresponsive to the 4-day APFR as only 17 mRNA levels were influenced by the treatment. This study demonstrates that body weight is a poor proxy of metabolic state and that the customary protocols of feed restriction can lead to rhythm entrainment.IToxicology and applied pharmacology Toxicol Appl Pharmacol. 2008 Feb 14;.0041-008X (Print)183946684.722MDepartment of Food and Environmental Hygiene, Faculty of Veterinary Medicine, P.O. Box 66, FI-00014, University of Helsinki, Finland; Finnish Food Safety Authority EVIRA, Research Unit of Kuopio, P.O. Box 92, FI-70701 Kuopio, Finland; National Public Health Institute, Laboratory of Toxicology, P.O. Box 95, FI-70701 Kuopio, Finland.<S0041-008X(08)00070-7 [pii] 10.1016/j.taap.2008.uc~|72Lahti, T. A. Haukka, J. Lonnqvist, J. Partonen, T.2008[Daylight saving time transitions and hospital treatments due to accidents or manic episodes74BMC Public Health8 2008/02/28>Accidents/ trends Adolescent Adult Aged Aged, 80 and over Bipolar Disorder/diagnosis/ epidemiology/etiology Child Circadian Rhythm Emergency Service, Hospital/ utilization Female Finland/epidemiology Humans International Classification of Diseases Male Middle Aged Models, Statistical Registries Sleep Deprivation TimeBACKGROUND: Daylight saving time affects millions of people annually but its impacts are still widely unknown. Sleep deprivation and the change of circadian rhythm can trigger mental illness and cause higher accident rates. Transitions into and out of daylight saving time changes the circadian rhythm and may cause sleep deprivation. Thus it seems plausible that the prevalence of accidents and/or manic episodes may be higher after transition into and out of daylight saving time. The aim of this study was to explore the effects of transitions into and out of daylight saving time on the incidence of accidents and manic episodes in the Finnish population during the years of 1987 to 2003. METHODS: The nationwide data were derived from the Finnish Hospital Discharge Register. From the register we obtained the information about the hospital-treated accidents and manic episodes during two weeks before and two weeks after the transitions in 1987-2003. RESULTS: The results were negative, as the transitions into or out of daylight saving time had no significant effect on the incidence of accidents or manic episodes. CONCLUSION: One-hour transitions do not increase the incidence of manic episodes or accidents which require hospital treatment.Lahti, Tuuli A Haukka, Jari Lonnqvist, Jouko Partonen, Timo Research Support, Non-U.S. Gov't England BMC public health BMC Public Health. 2008 Feb 26;8:74.1471-2458 (Electronic)183027341.603yDepartment of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, Finland. tuuli.lahti@ktl.fi11471-2458-8-74 [pii] 10.1186/1471-245,~|7 Yan, D. Olkkonen, V. M.2008-Characteristics of oxysterol binding proteins253-85 Int Rev Cytol265 2008/02/16Animals Biological Transport Cell Membrane/chemistry/ metabolism Golgi Apparatus Humans Lipid Metabolism/ physiology Receptors, Steroid/chemistry/ metabolism Saccharomyces cerevisiae/metabolism Signal Transduction/ physiology Sterols/chemistry/ metabolismProtein families characterized by a ligand binding domain related to that of oxysterol binding protein (OSBP) have been identified in eukaryotic species from yeast to humans. These proteins, designated OSBP-related (ORP) or OSBP-like (OSBPL) proteins, have been implicated in various cellular functions. However, the detailed mechanisms of their action have remained elusive. Data from our and other laboratories suggest that binding of sterol ligands may be a unifying theme. Work with Saccharomyces cerevisiae ORPs suggests a function of these proteins in the nonvesicular intracellular transport of sterols, in secretory vesicle transport from the Golgi complex, and in the establishment of cell polarity. Mammals have more ORP genes, and differential splicing substantially increases the complexity of the encoded protein family. Functional studies on mammalian ORPs point in different directions: integration of sterol and sphingomyelin metabolism, sterol transport, regulation of neutral lipid metabolism, control of the microtubule-dependent motility of endosomes/lysosomes, and regulation of signaling cascades. We envision that during evolution, the functions of ORPs have diverged from an ancestral one in sterol transport, to meet the increasing demand of the regulatory potential in multicellular organisms. Our working hypothesis is that mammalian ORPs mainly act as sterol sensors that relay information to a spectrum of different cellular processes.Yan, Daoguang Olkkonen, Vesa M Research Support, Non-U.S. Gov't Review United States International review of cytology Int Rev Cytol. 2008;265:253-85.0074-7696 (Print)182758915.988kDepartment of Molecular Medicine, National Public Health Institute, Biomedicum, FI-00290 Helsinki, Finland.?S0074-7696(07)65007-4 [pii] 10.1016/S0074-7696(07)6500 K ;@||7 5Stenholm, S. Rantanen, T. Heliovaara, M. Koskinen, S.2008eThe mediating role of C-reactive protein and handgrip strength between obesity and walking limitation462-9J Am Geriatr Soc563 2008/01/09Aged Body Mass Index C-Reactive Protein/ metabolism Cross-Sectional Studies Female Finland Hand Strength/ physiology Health Surveys Humans Male Middle Aged Mobility Limitation Obesity/ blood/complications/ physiopathology Walking/ physiologyMarOBJECTIVES: To study the association between different obesity indicators and walking limitation and to examine the role of C-reactive protein (CRP) and handgrip strength in that association. DESIGN: A cross-sectional, population-based study. SETTING: The Health 2000 Survey with a representative sample of the Finnish population. PARTICIPANTS: Subjects aged 55 and older with complete data on body composition, CRP, handgrip strength, and walking limitation (N=2,208). MEASUREMENTS: Body composition, anthropometrics, CRP, medical conditions, handgrip strength, and maximal walking speed were measured in the health examination. Walking limitation was defined as maximal walking speed less than 1.2 m/s or difficulty walking half a kilometer. RESULTS: The two highest quartiles of body fat percentage and CRP and the two lowest quartiles of handgrip strength were all significantly associated with greater risk of walking limitation when chronic diseases and other covariates were taken into account. In addition, high CRP and low handgrip strength partially explained the association between high body fat percentage and walking limitation, but the risk of walking limitation remained significantly greater in persons in the two highest quartiles than in those in the lowest quartile of body fat percentage (odds ratio (OR)=1.75, 95% confidence interval (CI)=1.19-2.57 and OR=2.80, 95% CI 1.89-4.16). The prevalence of walking limitation was much higher in persons who simultaneously had high body fat percentage and low handgrip strength (61%) than in those with a combination of low body fat percentage and high handgrip strength (7%). Using body mass index and waist circumference as indicators of obesity yielded similar results as body fat percentage. CONCLUSION: Low-grade inflammation and muscle strength may partially mediate the association between obesity and walking limitation. Longitudinal studies and intervention trials are needed to verify this pathway.Stenholm, Sari Rantanen, Taina Heliovaara, Markku Koskinen, Seppo Research Support, Non-U.S. Gov't United States Journal of the American Geriatrics Society J Am Geriatr Soc. 2008 Mar;56(3):462-9. Epub 2007 Dec 27.1532-5415 (Electronic)181794813.331tDepartment of Health and Functional Capacity, National Public Health Institute, Turku, Finland. sari.stenholm@ktl.fi4JGS1567 [pii] 10.1111/j.1532-5415.2007.015 m [||7 $Hu, G. Jousilahti, P. Tuomilehto, J.2007Joint effects of history of hypertension at baseline and type 2 diabetes at baseline and during follow-up on the risk of coronary heart disease3059-66 Eur Heart J2824 2007/11/06Adult Aged Coronary Disease/etiology/ mortality Diabetes Mellitus, Type 2/complications/ mortality Diabetic Angiopathies/complications/ mortality Epidemiologic Methods Female Humans Hypertension/complications/ mortality Incidence Male Middle AgedDecAIMS: To evaluate the joint associations of history of hypertension at baseline and type 2 diabetes at baseline and during follow-up on the incidence of coronary heart disease (CHD) and CHD mortality. METHODS AND RESULTS: Study cohorts included 49 775 Finnish subjects aged 25-74 without history of CHD and stroke. The multivariable-adjusted hazard ratios (HRs) of CHD incidence were 1.25, 1.69, 1.25, 1.83, 1.85, 2.39, 2.15, and 3.31 (P-value for trend <0.001), respectively, among men with hypertension I (blood pressure 140-159/90-94 mmHg or using antihypertensive drugs at baseline but blood pressure <160/95 mmHg) only, with hypertension II (blood pressure > or =160/95 mmHg) only, with incident diabetes during follow-up only, with both hypertension I and incident diabetes, with both hypertension II and incident diabetes, with history of diabetes at baseline only, with both hypertension I and history of diabetes, and with both hypertension II and history of diabetes compared with men without either of these diseases. The corresponding HRs of CHD incidence among women were 1.52, 2.37, 2.45, 3.78, 4.56, 5.63, 6.10, and 7.41 (P-value for trend <0.001), respectively. The impact on CHD mortality associated with the different strata of hypertension and diabetes was almost the same or a little stronger compared with that on the CHD incidence. CONCLUSION: Hypertension and type 2 diabetes increase the CHD risk independently, and their combination increases the risk dramatically, particularly in women.Hu, Gang Jousilahti, Pekka Tuomilehto, Jaakko Research Support, Non-U.S. Gov't England European heart journal Eur Heart J. 2007 Dec;28(24):3059-66. Epub 2007 Nov 2.0195-668X (Print)179818267.286Department of Health Promotion and Chronic Diseases Prevention, National Public Health Institute, Helsinki, Finland. hu.gang@ktl.fi+ehm501 [pii] 10.1093/eurheartj/ {|||7 Veckman, V. Julkunen, I.2008OStreptococcus pyogenes activates human plasmacytoid and myeloid dendritic cells296-304 J Leukoc Biol832 2007/10/30kAdult Antigens, CD/analysis CD4-Positive T-Lymphocytes/cytology/immunology Cell Differentiation Chemokines/biosynthesis/secretion Cytokines/biosynthesis/secretion Dendritic Cells/classification/ immunology HLA-D Antigens/biosynthesis Humans Influenza A Virus, H3N2 Subtype/immunology Myeloid Cells/immunology Streptococcus pyogenes/ immunology Th1 Cells/secretionFebHuman peripheral blood contains two major dendritic cell (DC) populations, namely CD11c(-)CD123+ plasmacytoid DCs (PDCs) and CD11c+CD123(-) myeloid DCs (MDCs). Although the activation of these DC types by various TLR ligands has been relatively well-characterized, less is known about the ability of whole live bacteria to induce PDC and MDC activation. In the present report, we have compared the activation of human PDCs and MDCs in response to major human bacterial pathogen Streptococcus pyogenes (group A streptococci) and influenza A virus. S. pyogenes stimulation resulted in the maturation of both DC types, as evidenced by enhanced expression of costimulatory molecules and production of proinflammatory cytokines and chemokines. Furthermore, S. pyogenes-stimulated PDCs and MDCs activated naive CD4+ T cells and enhanced their Th1 cytokine production. Influenza A virus infection induced rapid PDC activation, whereas MDCs were extremely sensitive to influenza A virus-induced cell death. The most significant differences between DC types were seen in the production of IL-10 and IL-12, which were only produced by S. pyogenes-stimulated MDCs. Although S. pyogenes was able to induce PDC activation, only influenza A virus infection resulted in detectable IFN-alpha production. Our results show that depending on the infecting microbe, the functions of PDCs and MDCs may be partially overlapping, suggesting a considerable flexibility of the human DC system.Veckman, Ville Julkunen, Ilkka Comparative Study Research Support, Non-U.S. Gov't United States Journal of leukocyte biology J Leukoc Biol. 2008 Feb;83(2):296-304. Epub 2007 Oct 26.0741-5400 (Print)179653374.572Department of Viral Diseases and Immunology, National Public Health Institute, Mannerheimintie 166, FI-00300 Helsinki, Finland. ville.veckman@ktl.fi+jlb.0707457 [pii] 10.1189/jlb.07 ? /||7 DPehrsson, A. Gunnar, T. Engblom, C. Seppa, H. Jama, A. Lillsunde, P.2008Roadside oral fluid testing: comparison of the results of drugwipe 5 and drugwipe benzodiazepines on-site tests with laboratory confirmation results of oral fluid and whole blood140-8Forensic Sci Int1752-3 2007/07/21Amphetamines/analysis Automobile Driving/ legislation & jurisprudence Benzodiazepines/analysis Cocaine/analysis Dopamine Uptake Inhibitors/analysis Forensic Toxicology Gas Chromatography-Mass Spectrometry Humans Narcotics/analysis Reagent Strips Saliva/ chemistry Sensitivity and Specificity Substance Abuse Detection/ instrumentation/ methods Substance-Related Disorders/diagnosis Tetrahydrocannabinol/analysisMar 5Drugged drivers pose a serious threat to other people in traffic as well as to themselves. Reliable oral fluid screening devices for on-site screening of drugged drivers would be both a useful and convenient means for traffic control. In this study we evaluated the appropriateness of Drugwipe 5 and Drugwipe Benzodiazepines oral fluid on-site tests for roadside drug screening. Drivers suspected of driving under the influence of drugs were screened with the Drugwipe tests. Oral fluid and whole blood samples were collected from the drivers and tested for amphetamine-type stimulant drugs, cannabis, opiates, cocaine and benzodiazepines by immunological methods, GC and GC-MS. The performance evaluations of the tests were made by comparing the results of the Drugwipe tests with laboratory GC-MS confirmation results of oral fluid or whole blood. In addition to the performance evaluations of the Drugwipe tests based on laboratory results, a questionnaire on the practical aspects of the tests was written for the police officers who performed the tests. The aim of the questionnaire was to obtain user comments on the practicality of the tests as well as the advantages and weak points of the tests. The results of the performance evaluations were: for oral fluid (sensitivity; specificity; accuracy) amphetamines (95.5%; 92.9%; 95.3%), cannabis (52.2%; 91.2%; 85.1%), cocaine (50.0%; 99.3%; 98.6%), opiates (100%; 95.8%; 95.9%), benzodiazepines (74.4%; 84.2%; 79.2%) and for whole blood accordingly, amphetamines (97.7%; 86.7%; 95.9%), cannabis (68.3%; 87.9%; 84.9%), cocaine (50.0%; 98.5%; 97.7%), opiates (87.5%; 96.9%; 96.6%) and benzodiazepines (66.7%; 87.0%; 74.4%). Although the Drugwipe 5 successfully detected amphetamine-type stimulant drugs and the police officers were quite pleased with the current features of the Drugwipe tests, improvements must still be made regarding the detection of cannabis and benzodiazepines.Pehrsson, Anna Gunnar, Teemu Engblom, Charlotta Seppa, Heikki Jama, Ahlam Lillsunde, Pirjo Research Support, Non-U.S. Gov't Ireland Forensic science international Forensic Sci Int. 2008 Mar 5;175(2-3):140-8. Epub 2007 Jul 20.1872-6283 (Electronic)176408371.397fNational Public Health Institute, Drug Research Unit, Mannerheimintie 166, FI-00300 Helsinki, Finland.AS0379-0738(07)00574-9 [pii] 10.1016/j.forsciint.2007.05  ||7Kilpinen, H. Ylisaukko-Oja, T. Hennah, W. Palo, O. M. Varilo, T. Vanhala, R. Nieminen-von Wendt, T. von Wendt, L. Paunio, T. Peltonen, L.20086Association of DISC1 with autism and Asperger syndrome187-96Mol Psychiatry132 2007/06/21BAsperger Syndrome/ genetics Autistic Disorder/ genetics Child, Preschool DNA-Binding Proteins/genetics Family Health Female Finland Genetic Predisposition to Disease Humans Infant Linkage Disequilibrium/ genetics Male Microsatellite Repeats/genetics Nerve Tissue Proteins/ genetics Polymorphism, Single Nucleotide/geneticsFeb The DISC1 gene at 1q42 has generated considerable interest in various psychiatric diseases, since a balanced translocation interrupting the gene was found to cosegregate with schizophrenia and related mental illnesses in a large Scottish pedigree. To date, linkage and association findings to this locus have been replicated in several study samples ascertained for psychotic disorders. However, the biological function of DISC1 in neuronal development would suggest a potential role for this gene also in other, early onset neuropsychiatric disorders. Here we have addressed the allelic diversity of the DISC1, DISC2 and TRAX genes, clustered in 1q42, in Finnish families ascertained for infantile autism (97 families, n(affected)=138) and Asperger syndrome (29 families, n(affected)=143). We established association between autism and a DISC1 intragenic microsatellite (D1S2709; P=0.004). In addition, evidence for association to Asperger syndrome was observed with an intragenic single nucleotide polymorphism (SNP) of DISC1 (rs1322784; P=0.0058), as well as with a three-SNP haplotype (P=0.0013) overlapping the HEP3 haplotype, that was previously observed to associate with schizophrenia in Finnish families. The strongest associations were obtained with broad diagnostic categories for both disorders and with affected males only, in agreement with the previous sex-dependent effects reported for DISC1. These results would further support the involvement of DISC1 gene also in the etiopathogenesis of early onset neuropsychiatric disorders.Kilpinen, H Ylisaukko-Oja, T Hennah, W Palo, O M Varilo, T Vanhala, R Nieminen-von Wendt, T von Wendt, L Paunio, T Peltonen, L Research Support, Non-U.S. Gov't England Molecular psychiatry Mol Psychiatry. 2008 Feb;13(2):187-96. Epub 2007 Jun 19.1359-4184 (Print)1757960811.804bDepartment of Molecular Medicine, National Public Health Institute, Biomedicum, Helsinki, Finland.)4002031 [pii] 10.1038/sj.mp.400 F 7||73Haukka, J. Suvisaari, J. Hakkinen, L. Lonnqvist, J.2008(Growth pattern and risk of schizophrenia63-70 Psychol Med381 2007/05/18>Adolescent Adult Age Factors Body Height/genetics/physiology Body Mass Index Body Weight/genetics/physiology Child Child Development/physiology Child Health Services/statistics & numerical data Child of Impaired Parents/psychology/statistics & numerical data Confounding Factors (Epidemiology) Female Finland/epidemiology Genetic Predisposition to Disease/epidemiology/genetics Growth/genetics/ physiology Humans Linear Models Longitudinal Studies Male Models, Genetic Nuclear Family/psychology Risk Factors Schizophrenia/diagnosis/ epidemiology/genetics Siblings/psychologyJanBACKGROUND: Foetal nutrition and growth seem to affect the risk of developing schizophrenia. Exposure to famine during foetal development and low birthweight increase the risk. However, few studies have investigated the association between schizophrenia and adult height and weight or patterns of growth. METHOD: The study population consisted of two subpopulations: families with at least one member with schizophrenia, and families of offspring of mothers with psychotic disorder, and controls. Using a seven-parameter model of height growth curves, we compared the parameters of persons who later developed schizophrenia and their unaffected siblings from the same families. We also studied how growth curve parameters differed in children with genetic risk for schizophrenia and controls, and whether weight, height and body mass index (BMI) at different ages predicted later development of schizophrenia. RESULTS: The predicted growth curves based on a parametric model were nearly identical for persons with schizophrenia and their unaffected siblings. Adult height of daughters of mothers with psychoses was borderline significantly (p=0.0536) lower compared to controls, while no difference was detected among sons (p=0.3283). CONCLUSIONS: No association between growth characteristics and schizophrenia in families with at least one member with schizophrenia was found. Family-related factors should be taken into account as possible confounders in future studies on growth and schizophrenia.Haukka, J Suvisaari, J Hakkinen, L Lonnqvist, J Comparative Study England Psychological medicine Psychol Med. 2008 Jan;38(1):63-70. Epub 2007 May 17.0033-2917 (Print)175069263.816~Department of Mental Health and Alcohol Research, KTL, National Public Health Institute, Helsinki, Finland. jari.haukka@ktl.fi7S0033291707000839 [pii] 10.1017/S0033291707000 2.x [doi]eng 8-8-74 [doi]eng 2207 [doi]Eng ehm501 [doi]eng .022 [doi]eng 7-4 [doi]eng 67.x [doi]eng 3388 [pii]Eng 007 [pii]Eng07457 [doi]eng 2031 [doi]eng 024 [doi]Eng .a8 [doi]Eng 839 [doi]eng 02.002 [doi]EngPKi8I/**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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