Population genetic analyses of susceptibility to developing alcohol dependence

Marinković, Darko; Cvjetićanin, Suzana; Stanojević, Miroslav

doi:10.1080/16066350801900156

Cited by 12 publications

(20 citation statements)

References 9 publications

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“…comparison between ill and healthy individuals, pupils from special and regular schools, carriers of different blood types etc.) (BLAGOJEVIC et al, 1989;CVJETICANIN and MARINKOVIC, 2005a;CVJETICANIN and MARINKOVIC, 2009;MARINKOVIC et al, 1990;MARINKOVIC et al, 1994;MARINKOVIC et al, 2007;MARINKOVIC et al, 2008;MARKOVIC-DENIC et al, 1992;NIKOLIC et al, 2010;PETRICEVIC and CVJETICANIN, 2011).…”

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confidence: 99%

Morphogenetic variability and genetic loads among patients with different expression of developmental hip dysplasia

et al. 2017

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(p<0.05). Our results showed increase of genetic homozygosity in the groups of DDH female patients (44%), compared to male patients (39%), while in controls there was no difference between gender. Female DDH patients show a significant increase in average homozygosity of tested genetic markers (p<0.05) than male DDH patients. The enlargement of genetic loads correlates with severity of the disease (in studied groups of DDH patients) which may indicate some kind of predisposition for the degree of illness expression.

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confidence: 99%

Morphogenetic variability and genetic loads among patients with different expression of developmental hip dysplasia

et al. 2017

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“…In order to estimate the degree of recessive homozygosity and variability in the healthy control group and patients with RA, the homozygously recessive characteristics (HRC) test was applied (MARINKOVIC et al, 1990;MARINKOVIC, CVJETICANIN, 1991;MARINKOVIC, CVJETICANIN, 2013). The HRC test was used for assessing the proportion of clearly expressed homozygously recessive characteristics, which are considered as qualitative traits in every individual, indicating the degree of genetic homozygosity in humans MARINKOVIC et al, 2008;NIKOLIC et al, 2009;PETRICEVIC, CVJETICANIN, 2011;MARINKOVIC, CVJETICANIN, 2013;BRANKOVIC, CVJETICANIN, 2016). Considering that the HRCs tested are the markers of genes located on different chromosomes (CVJETICANIN, MARINKOVIC, 2009), insight into the prevalence of homozygous or heterozygous loci on different chromosomes could be determined.…”

Section: Study Methodsmentioning

confidence: 99%

“…The HRCs tested are the markers of genes that are located on different chromosomes (CVJETICANIN, MARINKOVIC, 2009). It is performed by direct observation of tested phenotype traits, and is a reliable method for the estimation of the individual and group homozygosity of populations (MARINKOVIC et al, 1990;MARINKOVIC, CVJETICANIN, 1991;MARINKOVIC, CVJETICANIN, 2013;MARINKOVIC et al, 2008;PETRICEVIC, CVJETICANIN, 2011;BRANKOVIC, CVJETICANIN, 2016;NIKOLIC et al, 2009;CVJETICANIN, MARINKOVIC, 2009). In order to maintain the same objectivity and equal criteria for determination of tested HRCs, one individual performed the testing.…”

Section: Study Methodsmentioning

confidence: 99%

Association of rheumatoid arthritis according to the degree of genetic homozygosity and gender: Pilot study

2019

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Rheumatoid arthritis (RA) is a chronic synovial inflammatory autoimmune disease with multifactorial origin. With epigenetic and genetic mechanisms playing a role in the development of RA, the aim of our study was to evaluate the anthropogenetic variability in tested individuals that were diagnosed with rheumatoid arthritis, and the possible influence of gender in expression of illness. 100 patients with rheumatoid arthritis (RA) and 100 healthy control individuals were evaluated. For the estimation of the degree of recessive homozygosity, the homozygously recessive characteristics (HRC) test was performed testing 20 HRCs. There was a significant difference in the individual variations of 20 HRCs between the individuals of the control group and patients with RA (X 2 =135.191; p<0.001). The mean values of the tested HRCs significantly differed between individuals of the control group and RA group (MVSDControl group-5.972.02, MVSDRA group-7.342.00, p=<0.001). There was a decrease in variability in the RA group versus the control group (VRA group=27.19%; VControl group=33.79%).There was significant difference in the frequencies of HRCs between those with and without RA in males (p<0.023) and in females (p<0.001). Our findings pointed to the higher degree of recessive homozygosity along with decreased variability in RA patients compared to a 1140

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“…Different frequencies of homozygously recessive characteristics in individuals of different groups being evaluated would be a manifestation of a kind of genetic load present in the selected samples of the studied population [13–16]. …”

Section: Methodsmentioning

confidence: 99%

Population genetic analyses of susceptibility to increased body weight

Nikolić¹,

Cvjetićanin²,

Petronić³

et al. 2012

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IntroductionObesity is a complex condition with multifactorial origin. Assuming that such a state is genetically controlled, the aim of our study was to evaluate the degree of genetic homozygosity among overweight and obese individuals by the homozygously recessive characteristics (HRC) test.Material and methodsWe analysed the presence, distribution and individual combination of 15 selected genetically controlled recessive phenotype traits in a sample of 140 individuals with increased body mass index (overweight individuals n = 100 and obese individuals n = 40) and a control group of normal weight individuals (n = 300).ResultsObese individuals have significantly higher mean values for genetic homozygosity than those with normal weight (normal weight: 3.61 ±1.48; obese: 4.13 ±1.47, p < 0.05) and difference in the presence of certain individual combinations of evaluated phenotype traits (Σχ2 = 76.9; p < 0.01). There was no difference in average homozygosity of such genetic markers between groups of normal weight and overweight individuals (normal weight: 3.61 ±1.48; overweight: 3.93 ±1.51, p > 0.05) and between groups of overweight and obese individuals (overweight: 3.93 ±1.51; obese: 4.13 ±1.47, p > 0.05). There is no difference in the presence of certain individual combinations of evaluated phenotype traits between overweight and obese individuals (Σχ2 = 20.6; p > 0.05).ConclusionsThere is a populational genetic difference in the degree of genetic homozygosity and variability between the group of normal weight and group of obese individuals, indicating a possible genetic component. Overweight and obese individuals have a genetic predisposition, but different expression of genetic loads could be one of the possible explanations for different susceptibility to increase of fat mass and body mass index.

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Population genetic analyses of susceptibility to developing alcohol dependence

Cited by 12 publications

References 9 publications

Morphogenetic variability and genetic loads among patients with different expression of developmental hip dysplasia

Morphogenetic variability and genetic loads among patients with different expression of developmental hip dysplasia

Association of rheumatoid arthritis according to the degree of genetic homozygosity and gender: Pilot study

Population genetic analyses of susceptibility to increased body weight

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