69 research outputs found
Relative immaturity and ADHD : findings from nationwide registers, parent- and self-reports
BACKGROUND: We addressed if immaturity relative to peers reflected in birth month increases the likelihood of ADHD diagnosis and treatment.
METHODS: We linked nationwide Patient and Prescribed Drug Registers and used prospective cohort and nested case-control designs to study 6-69 year-old individuals in Sweden from July 2005 to December 2009 (Cohort 1). Cohort 1 included 56,263 individuals diagnosed with ADHD or ever used prescribed ADHD-specific medication. Complementary population-representative cohorts provided DSM-IV ADHD symptom ratings; parent-reported for 10,760 9-year-old twins born 1995-2000 from the CATSS study (Cohort 2) and self-reported for 6,970 adult twins age 20-47 years born 1959-1970 from the STAGE study (Cohort 3). We calculated odds ratios (OR:s) for ADHD across age for individuals born in November/December compared to January/February (Cohort 1). ADHD symptoms in Cohorts 2 and 3 were studied as a function of calendar birth month.
RESULTS: ADHD diagnoses and medication treatment were both significantly more common in individuals born in November/December versus January/February; peaking at ages 6 (OR: 1.8; 95% CI: 1.5-2.2) and 7 years (OR: 1.6; 95% CI: 1.3-1.8) in the Patient and Prescribed Drug Registers, respectively. We found no corresponding differences in parent- or self-reported ADHD symptoms by calendar birth month.
CONCLUSION: Relative immaturity compared to class mates might contribute to ADHD diagnosis and pharmacotherapy despite absence of parallel findings in reported ADHD symptom loads by relative immaturity. Increased clinical awareness of this phenomenon may be warranted to decrease risk for imprecise diagnostics and treatment. We speculate that flexibility regarding age at school start according to individual maturity could reduce developmentally inappropriate demands on children and improve the precision of ADHD diagnostic practice and pharmacological treatment.Swedish Research Council (2010-3184)Karolinska Institutet Center of Neurodevelopmental Disorders (KIND)Accepte
Childhood neurodevelopmental problems and adolescent bully victimization : population-based, prospective twin study in Sweden
Bully victimization is a common problem among children with neurodevelopmental
disorders, including attention deficit/hyperactivity disorder and autism spectrum
disorder. Previous research was mostly cross-sectional and seldom accounted for
co-morbid psychopathology, which makes it difficult to draw conclusions about
causality and specificity of any association. Using a genetically informative
prospective design, we investigated the association between various
neurodevelopmental problems (NDPs) in childhood and bully victimization in
adolescence, and the relative contributions of genetic and environmental factors
to this association. We obtained parent-reports of NDPs at age 9/12 years and
self-reported bully victimization at age 15 for 3,921 children participating in
the The Child and Adolescent Twin Study in Sweden (CATSS). Structural equation
modelling was used to control for NDP co-morbidity and bully victimization at
baseline. Cholesky decomposition was used to analyse genetic and environmental
contributions to observed associations. Because most of the NDPs were associated
to later bully victimization, a common effect of all NDPs was summarized into a
general NDP factor. Controlling for this general factor, only problems with
social interaction and motor control uniquely predicted subsequent bully
victimization in girls. General and unique associations were influenced by both
genetic and unique environmental factors. NDPs in general and social interaction
and motor problems in particular predicted later bully victimization. The
longitudinal design and twin analyses indicated that these associations might be
causal. Knowledge of these vulnerabilities may be important when designing risk
assessment and prevention strategies.The Swedish Council for Working Life and Social ResearchThe Research Council of the Swedish National Alcohol MonopolyThe Söderström-Königska FoundationFunds under the ALF agreementThe Swedish Research CouncilAccepte
The Swedish Twin Registry : establishment of a biobank and other recent developments
The Swedish Twin Registry (STR) today contains more than 194,000 twins and more than 75,000 pairs have zygosity determined by an intra-pair similarity algorithm, DNA, or by being of opposite sex. Of these, approximately 20,000, 25,000, and 30,000 pairs are monozygotic, same-sex dizygotic, and opposite-sex dizygotic pairs, respectively. Since its establishment in the late 1950s, the STR has been an important epidemiological resource for the study of genetic and environmental influences on a multitude of traits, behaviors, and diseases. Following large investments in the collection of biological specimens in the past 10 years we have now established a Swedish twin biobank with DNA from 45,000 twins and blood serum from 15,000 twins, which effectively has also transformed the registry into a powerful resource for molecular studies. We here describe the main projects within which the new collections of both biological samples as well as phenotypic measures have been collected. Coverage by year of birth, zygosity determination, ethnic heterogeneity, and influences of in vitro fertilization are also described.VetenskapsrÄdetNIHSSFHjÀrt- och LungfondenAstma- och AllergiförbundetAccepte
âDet fĂ„r inte bli för mycket av det hĂ€r datoriserandet.â â En kvalitativ studie av digitaliseringens pĂ„verkan pĂ„ generationsskillnader, med fokus pĂ„ kommunikation
Titel âDet fĂ„r inte bli för mycket av det hĂ€r datoriserandet.â â En kvalitativ studie av digitaliseringens pĂ„verkan pĂ„
generationsskillnader, med fokus pÄ kommunikation
Författare Philip BernÄker & Julia Halldner
Uppdragsgivare JMG, Medieinriktningen pÄ lÀrarutbildningen, Göteborgs universitet
Kurs Examensarbete i Medie- och kommunikationsvetenskap vid institutionen för journalistik, medier och kommunikation
Göteborgs universitet
Termin VĂ„rterminen 2011
Handledare Jenny Wiik
Sidantal 40, inklusive bilaga
Antal ord 15 716
Syfte Att undersöka generationsskillnader gÀllande kommunikation i och med digitaliseringen. (UtifrÄn en lÀrares synvinkel)
Metod Kvalitativ undersökning i form av samtalsintervjuer
Material Sex stycken samtalsintervjuer med gymnasielÀrare i Göteborg
Huvudresultat Studien visar att lÀrarna anser att digitaliseringen Àr ett problem och att den har pÄverkat generationsskillnader negativt. LÀrarna
anser Ă€ven att kommunikationen har pĂ„verkats av digitaliseringen, bĂ„de positivt och negativt. Dock kommer ungdomar alltid ses pĂ„ ett visst sĂ€tt â lata, bekvĂ€ma och i behov av instruktioner. VĂ„r studie ökar medvetenheten kring problematiken som digitaliseringen har medfört
Ăter vi med ögonen i butiken? En studie om förpackningsdesign som möjlig konkurrensfördel för smĂ„skaliga livsmedelsföretag
Physiology and pathophysiology of central adenosine A1 and A2A receptors
The aim of this thesis was to further investigate the individual roles of
central adenosine A1 and A2A receptors in the physiological and
pathophysiological effects of adenosine. In addition, the characteristics
of different adenosine receptor ligands were studied. For these purposes
pharmacological tools as well as mice lacking adenosine A1 and/or A2A
receptors were used.
Both adenosine A1 receptor knock-out and adenosine A1/A2A receptor double
knock-out mice survived fetal life and developed no major defects. No
significant change in baseline motor activity was seen in these knock-out
mice.
In situ hybridization and receptor autoradiography confirmed that the
adenosine A1 receptor knock-out did not express any central adenosine A1
receptors. Adenosine A1 receptor heterozygotes expressed half the amount
of the receptor. The same was due for the adenosine A2A receptor
heterozygote regarding the adenosine A2A receptor expression. The
expression of adenosine A2A receptors was not affected by absence of the
adenosine A1 receptors.
Rats that were sleep-deprived for 3 or 6 hours had altered levels of both
adenosine A1 and A2A receptor mRNA. Adenosine A1 receptor mRNA was
up-regulated specifically in the horizontal limb of the diagonal band in
the basal forebrain. This up-regulation was not seen at the protein
level. On the contrary, adenosine A2A receptor mRNA was down-regulated,
and this was accompanied with a decrease in receptor binding after 3 but
not 6 hours of sleep-deprivation. The alterations of the adenosine A2A
receptor expression was observed only in the olfactory tubercle. The
sleep pattern and the response to sleep deprivation was studied in mice
lacking adenosine A1 receptors. These mice did unexpectedly not differ
from their wild-type siblings in these respects.
Adenosine A2A receptor knock-outs were more sensitive to hypoxia-ischemia
than wild-type mice. They developed an aggravated brain damage, which
resulted in altered behavior later in life. Adenosine A2A receptor
knock-outs exposed to hypoxia-ischemia showed altered behavior in the
open field test and performed less well in the rotarod test.
Chronic administration of the locomotor activity stimulating adenosine
A2A receptor antagonist SCH 58261 was given to rats. In contrast to
previous studies with the non-selective adenosine antagonist caffeine, no
tolerance developed to the motor stimulating effect after repeated
injections of the drug.
The locomotor effects of caffeine were analyzed in mice lacking adenosine
A1 receptors. The dose-response curve for caffeine seemed shifted to the
left, whereas response to high dose caffeine was unaltered in the
knock-out. No locomotor stimulating effect was observed in adenosine
A1/A2A receptor double knock-out mice in congruence with mice lacking
only the adenosine A2A receptor.
Finally, the selectivity of the adenosine receptor ligands DPCPX (A1
antagonist), SCH 58261(A2A antagonist), ZM 241385(A2A antagonist) and CGS
21680(A2A agonist) were tested by means of receptor binding in adenosine
receptor knock-out brains. DPCPX did not bind to brains from adenosine A1
receptor knock-outs, whereas SCH 58261 and ZM 241385 did not bind in
brains from adenosine A2A receptor knock-outs. CGS 21680 did however not
bind in the striatum from adenosine A2A receptor knock-outs, but
extra-striatal bindin
Subcortical brain volume differences in participants with attention deficit hyperactivity disorder in children and adults
Disrupted Attention to Otherâs Eyes is Linked to Symptoms of ADHD in Childhood
Attention-deficit/hyperactivity disorder (ADHD) is associated with impaired social interaction. Otherâs eyes are important for understanding the social world. Here, we examined concurrent and longitudinal links between attention to otherâs eyes and symptoms of ADHD and comorbid externalizing and internalizing symptoms. Eighty-two 8 to 13-year-old children (40% with ADHD) participated. The latency to a first gaze shift to and away from the eye region of human faces, when primed to look at either the eyes or the mouth, was recorded with eye tracking. Parents rated ADHD, externalizing and internalizing symptoms at the time of testing and at 2-year follow-up. The results show that longer looking at the eyes before reorienting was specifically associated with concurrent and future symptoms of inattention, even when accounting for comorbid symptoms. We conclude that the temporal microstructure of attention to otherâs eyes is altered in children with symptoms of ADHD, which may contribute to social impairments
Stimulant and non-stimulant attention deficit/hyperactivity disorder drug use:Total population study of trends and discontinuation patterns 2006-2009
The adenosine A1 receptor contributes to the stimulatory, but not the inhibitory effect of caffeine on locomotion: a study in mice lacking adenosine A1 and/or A2A receptors.
Caffeine has biphasic effects on locomotion, and blockade of the adenosine A(2A) receptor (A2AR) is necessary for the stimulatory effect of low doses of caffeine, but not for the locomotor depressant effect observed at high doses. We wanted to elucidate the role of the adenosine A(1) receptor (A1R) in mediating the locomotor effects of increasing doses of caffeine using wild-type mice (A1R(WT)), mice heterozygous for (A1R(HET)), and mice lacking the adenosine A(1) receptor (A1R(KO)). Caffeine had the typical biphasic dose-effect relationship in all three genotypes, but the stimulatory action of caffeine was facilitated in the A1R(KO) mice. In order to investigate the interaction between blockade of A1Rs and A2ARs, mice lacking both receptors (A1R(KO)/A2AR(KO)) were tested. Regardless of A1R genotype, animals lacking A2AR were not stimulated by caffeine, whereas animals heterozygous for A2AR were. As expected, the A1R is not crucial for the stimulatory effect of caffeine, but seems to modulate the effect of caffeine exerted via A2AR blockade. Furthermore, these results suggest that the inhibitory effect of high doses of caffeine is due neither to blockade of the A1R, nor of the A2AR, and an effect independent of these adenosine receptors is likely.Comparative StudyJournal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe
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