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Informative Studies (informative + studies)
Selected AbstractsPeer substance involvement modifies genetic influences on regular substance involvement in young womenADDICTION, Issue 10 2010Arpana Agrawal ABSTRACT Aims Peer substance involvement (PSI) is a robust correlate of adolescent substance use. A small number of genetically informative studies suggest that shared genetic and environmental factors contribute to this association. We examine mechanisms by which PSI influences the etiology of regular substance involvement (RSI), particularly in women. Design Population-based cohort study of twin women from the US Midwest. Participants 2176 twin women. Measurements To examine the relationship between self-reported PSI during adolescence and a composite RSI representing regular tobacco, alcohol and cannabis use during young adulthood, using genetically informative correlation, moderation and joint correlation-moderation models. Findings There was evidence for a significant additive genetic X environment interaction. PSI was moderately heritable (h2 = 0.25). Genetic, shared and non-shared influences on RSI overlapped with influences on PSI (genetic correlation of 0.43). Even after controlling for these shared genetic influences, RSI was more heritable in those reporting greater PSI. Conclusions While young women may select peers based on certain dispositional traits (e.g. permissiveness towards substance use), the social milieu constructed by PSI does modify the architecture of increased RSI in those individuals with increasing levels of PSI being associated with stronger expression of heritable influences. [source] Genetic and non-genetic influences on the development of co-occurring alcohol problem use and internalizing symptomatology in adolescence: a reviewADDICTION, Issue 7 2009Luca Saraceno ABSTRACT Aims Alcohol problem use during adolescence has been linked to a variety of adverse consequences, including cigarette and illicit drug use, delinquency, adverse effects on pubertal brain development and increased risk of morbidity and mortality. In addition, heavy alcohol-drinking adolescents are at increased risk of comorbid psychopathology, including internalizing symptomatology (especially depression and anxiety). A range of genetic and non-genetic factors have been implicated in both alcohol problem use as well as internalizing symptomatology. However, to what extent shared risk factors contribute to their comorbidity in adolescence is poorly understood. Design We conducted a systematic review on Medline, PsycINFO, Embase and Web of Science to identify epidemiological and molecular genetic studies published between November 1997 and November 2007 that examined risk factors that may be shared in common between alcohol problem use and internalizing symptomatology in adolescence. Findings Externalizing disorders, family alcohol problems and stress, as well as the serotonin transporter (5-HTT) S-allele, the monoamine oxidase A (MAOA) low-activity alleles and the dopamine D2 receptor (DDR2) Taq A1 allele have been associated most frequently with both traits. An increasing number of papers are focusing upon the role of gene,gene (epistasis) and gene,environment interactions in the development of comorbid alcohol problem use and internalizing symptomatology. Conclusions Further research in adolescents is warranted; the increasing availability of large longitudinal genetically informative studies will provide the evidence base from which effective prevention and intervention strategies for comorbid alcohol problems and internalizing symptomatology can be developed. [source] The association of use of sunbeds with cutaneous malignant melanoma and other skin cancers: A systematic reviewINTERNATIONAL JOURNAL OF CANCER, Issue 5 2007Article first published online: 27 NOV 200 Abstract Exposure to solar ultraviolet (UV) radiation is a known cause of skin cancer. Sunbed use represents an increasingly frequent source of artificial UV exposure in light-skinned populations. To assess the available evidence of the association between sunbed use and cutaneous malignant melanoma (melanoma) and other skin cancers, a systematic review of the literature till March 2006 on epidemiological and biological studies on sunbed use was performed in Pubmed, ISI Web of Science, Embase, Pascal, Cochrane library, Lilacs and Medcarib. Search for keywords in the title and in the abstract was done systematically and supplemented by manual searches. Only case,control, cohort or cross-sectional studies were selected. Data were abstracted by means of a standardized data-collection protocol. Based on 19 informative studies, ever-use of sunbeds was positively associated with melanoma (summary relative risk, 1.15; 95% CI, 1.00,1.31), although there was no consistent evidence of a dose,response relationship. First exposure to sunbeds before 35 years of age significantly increased the risk of melanoma, based on 7 informative studies (summary relative risk, 1.75; 95% CI, 1.35,2.26). The summary relative risk of 3 studies of squamous cell carcinoma showed an increased risk. For basal cell carcinoma, the studies did not support an association. The evidence does not support a protective effect of the use of sunbeds against damage to the skin from subsequent sun exposure. Young adults should be discouraged from using indoor tanning equipment and restricted access to sunbeds by minors should be strongly considered. © 2006 Wiley-Liss, Inc. [source] Ancestral roles of eukaryotic frataxin: mitochondrial frataxin function and heterologous expression of hydrogenosomal Trichomonas homologues in trypanosomesMOLECULAR MICROBIOLOGY, Issue 1 2008Shaojun Long Summary Frataxin is a small conserved mitochondrial protein; in humans, mutations affecting frataxin expression or function result in Friedreich's ataxia. Much of the current understanding of frataxin function comes from informative studies with yeast models, but considerable debates remain with regard to the primary functions of this ubiquitous protein. We exploit the tractable reverse genetics of Trypanosoma brucei in order to specifically consider the importance of frataxin in an early branching lineage. Using inducible RNAi, we show that frataxin is essential in T. brucei and that its loss results in reduced activity of the marker Fe,S cluster-containing enzyme aconitase in both the mitochondrion and cytosol. Activities of mitochondrial succinate dehydrogenase and fumarase also decreased, but the concentration of reactive oxygen species increased. Trypanosomes lacking frataxin also exhibited a low mitochondrial membrane potential and reduced oxygen consumption. Crucially, however, iron did not accumulate in frataxin-depleted mitochondria, and as T. brucei frataxin does not form large complexes, it suggests that it plays no role in iron storage. Interestingly, RNAi phenotypes were ameliorated by expression of frataxin homologues from hydrogenosomes of another divergent protist Trichomonas vaginalis. Collectively, the data suggest trypanosome frataxin functions primarily only in Fe,S cluster biogenesis and protection from reactive oxygen species. [source] The prodromal phase of sporadic Parkinson's disease: Does it exist and if so how long is it?,MOVEMENT DISORDERS, Issue 13 2008Christopher H. Hawkes MD Abstract It is frequently assumed that idiopathic Parkinson's disease starts with several nonmotor symptoms and signs, but the evidence for this stage in the disease process is of variable quality. This review evaluates the more robust prospective or pathologically confirmed publications to establish whether there is a premotor period and if so what is its duration. The most informative studies are considered to be those concerned with olfaction, dysautonomia, and sleep disorder. Estimates for the duration of the prodromal phase vary from months to decades. It is concluded that there probably is an early phase in the disease where a variety of nonmotor features develop, but the sequence and time of onset of such features is not well established. © 2008 Movement Disorder Society [source] A molecular correlate of clinicopathology in transthyretin amyloidosis,THE JOURNAL OF PATHOLOGY, Issue 1 2009Mark B Pepys Abstract The mechanisms responsible for amyloid deposition at different times and in different organs, even in individuals with the same amyloidogenic mutation, are not known. The demonstration, in hereditary systemic transthyretin Val30Met amyloidosis, that such differences are consistently associated with amyloid fibrils composed of different length transthyretin fragments sheds new light on this question and will open the way to further informative studies. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] | ||||||||||