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Strong Genetic Influence (strong + genetic_influence)

Distribution by Scientific Domains

Psychology	50%

Selected Abstracts

Strong genetic influence on IPN vaccination-and-challenge trials in Atlantic salmon, Salmo salar L.

JOURNAL OF FISH DISEASES, Issue 8 2008
A Ramstad
Abstract Two series of experimental challenge trials were performed for evaluation of multivalent oil-adjuvanted vaccines with and without an infectious pancreatic necrosis virus (IPNV) antigen component. In both the trial series, Atlantic salmon were hatched, reared, vaccinated and subjected to temperature and light manipulation to induce smoltification. When ready for sea the fish were transported to the VESO Vikan experimental laboratory for bath or cohabitant challenge with IPNV. In the first series, four vaccination and bath challenge trials involving 2-year classes of experimental fish were conducted. In the second series, three groups of eyed eggs of Atlantic salmon allegedly differing in their innate resistance to IPNV were used (Storset, Strand, Wetten, Kjøglum & Ramstad 2007). Hatching, rearing and smoltification were synchronized for each group, and fish from each genetic group were randomly allocated IPN vaccine, reference vaccine or saline before being placed into parallel tanks for bath or cohabitant challenge. In the first series of trials, IPN-specific mortality commenced on day 10,12 after bath challenge. Replicates showed similar results. In trials 1 and 2 belonging to the same experimental fish year class, the average cumulative control mortality reached 60.6% and 79.5%, respectively, whereas in trials 3 and 4 belonging to the following year class the control mortality was consistently below 50%. In the second series of trials, the experimental fish originating from allegedly IPN susceptible parents consistently showed the highest cumulative mortality among the unvaccinated controls (>75%) whereas smolts derived from allegedly IPNV resistant parents showed only 26,35% control mortality. The IPN-vaccinated fish experienced significantly improved survival vs. the fish immunized with reference vaccine, with RPS values above 75% in the IPN susceptible strain. In the IPN resistant strain, the protection outcomes were variable and in part non-significant. The outcome of both the trial series suggests that control mortalities above 50% are necessary to reliably demonstrate specific protection with IPN vaccines. [source]

A common haplotype of the C-C chemokine receptor 2 gene and HLA-DRB1*0301 are independent genetic risk factors for Löfgren's syndrome

JOURNAL OF INTERNAL MEDICINE, Issue 5 2008
P. Spagnolo
Abstract. Aim., Sarcoidosis is a heterogeneous disorder with a strong genetic influence. Genetic factors are also thought to influence disease severity and outcome. We sought to determine whether polymorphisms within CCR2 gene predispose to Löfgren's syndrome , a clinically and genetically distinct sarcoidosis phenotype , and, importantly, whether this association is independent of the known association with the HLA-DRB1*0301 allele. Methods., We investigated 5 CCR2 variants and HLA-DRB1*0301 by sequence-specific primer (SSP) polymerase chain reaction (PCR) in 176 Spanish (76 Löfgren's syndrome, 100 controls) and 387 Swedish subjects (126 Löfgren's syndrome, 77 non-Löfgren sarcoidosis, 184 controls). Results., One of the deduced haplotypes (CCR2 haplotype 2) was associated with Löfgren's syndrome in both Spanish (OR: 2.03, uncorrected P = 0.02; permuted P = 0.041 vs. controls) and Swedish patients (OR: 3.02, uncorrected P = 0.0007; permuted P = 0.0027 vs. non-Löfgren sarcoidosis; OR: 2.46, uncorrected P = 0.0005; permuted P = 0.0031 vs. controls). HLA-DRB1*0301 allele frequency was also increased in Spanish (OR: 3.52, P = 0.0004 vs. controls) and Swedish patients with Löfgren's syndrome (OR: 10.98, P < 0.0001 vs. non-Löfgren sarcoidosis, OR: 7.71, P < 0.0001 vs. controls). Finally, multivariate analysis revealed that the CCR2 association was independent of HLA-DRB1*0301 in both Spanish (P = 0.02 vs. controls) and Swedish cohorts (P = 0.002 vs. non-Löfgren sarcoidosis, P = 0.001 vs. controls). Conclusions., This study confirms that CCR2 haplotype 2 and HLA-DRB1*0301 are independent genetic risk factors for Löfgren's syndrome. [source]

Genetic and environmental influence on language impairment in 4-year-old same-sex and opposite-sex twins

THE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 2 2004
Essi Viding
Background:, We investigated the aetiology of language impairment in 579 four-year-old twins with low language performance and their co-twins, members of 160 MZ twin pairs, 131 same-sex DZ pairs and 102 opposite-sex DZ pairs. Methods:, Language impairment in 4-year-olds was defined by scores below the 15th percentile on a general factor derived from an extensive language test battery. Language impairment of different degrees of severity was investigated by using multiple cut-offs below the 15th percentile. Results:, DeFries,Fulker extremes analysis indicated that language impairment as measured by the general language scale is under strong genetic influence. In addition, group differences heritability showed an increasing trend (from 38% to 76%) as a function of severity of language impairment. Although more boys are impaired than girls, incorporating opposite-sex DZ pairs into the analysis found neither quantitative nor qualitative differences between boys and girls in genetic and environmental aetiologies. Conclusions:, Language impairment at four years is heritable. This finding replicates previous research on language impairment and extends it by showing that language impairment is heritable in twins selected from a representative community sample. Despite the mean difference between boys and girls, genetic and environmental influences are quantitatively and qualitatively similar for language impairment for boys and girls. For both boys and girls, heritability appears to be greater for more severe language impairment, indicating stronger influence of genes at the lower end of language ability. [source]

Dyslexia: nature and nurture,

DYSLEXIA, Issue 3 2002
Richard K. Olson
Abstract This paper explores the balance of genetic and environmental influences on dyslexia in generally supportive educational environments. Evidence from family studies suggests and research with identical and fraternal twins confirms the presence of strong genetic influences on dyslexia, though the way dyslexia is defined influences the degree of genetic influence. The behavioural genetic evidence is supported with molecular genetic evidence from DNA analyses suggesting regions on several different chromosomes where genes related to dyslexia are likely to be found. The behavioural and molecular genetic analyses are also applied to different component word reading skills (orthographic coding and phonological decoding) as well as to related language skills (phoneme awareness) to better understand the genetic and cognitive pathways to dyslexia. Copyright © 2002 John Wiley & Sons, Ltd. [source]