Genetic markers engendered by genome projects drew enormous interest in quantitative genetics, but knowledge on genetic architecture of complex traits is limited. Complexities in genetics will not allow us to easily clarify relationship between genotypes and phenotypes for quantitative traits. Quantitative genetics guides an important way in facing such challenges. It is our exciting task to find genes that affect complex traits. In this paper, landmark research and future prospects are discussed on genetic parameter estimation and quantitative trait locus (QTL) mapping as major subjects of interest.
The present study aimed to investigate the effects of maternal factors on body weight at hatching (day-old) and at six weeks of age in a commercial broiler line. A total of 6,765 records on body weight at day-old (BWTDO) and 115,421 records on body weight at six weeks of age (BWT6W), originated from a commercial broiler line during 14 generations, were used to estimate genetic parameters related to the effects of maternal traits on body weight of chicks immediately after hatch or six weeks thereafter. The data were analyzed using restricted maximum likelihood procedure (REML) and an animal model with DFREML software. Direct heritability ($h^{2}{_a}$), maternal heritability ($h^{2}{_m}$), and maternal environmental variance as the proportions of phenotypic variance ($c^{2}$) for body weight at day-old were estimated to be 0.050, 0.351, and 0.173, respectively. The respective estimated values for body weight at six weeks of age were 0.340, 0.022, and 0.030. The correlation coefficient between direct and maternal genetic effects for six-week-old body weight was found to be -0.335. Covariance components and genetic correlations were estimated using a bivariate analysis based on the best model determined by a univariate analysis. Between weights at hatching and at six week-old, the values of -0.07, 0.53 and 0.47 were found for the direct additive genetic variance, maternal additive genetic variance and permanent maternal environmental variance, respectively. The estimated correlation between direct additive genetic effect influencing weight at hatch and direct additive maternal effect affecting weight at six weeks of age was -0.21, whereas the correlation value of 0.15 was estimated between direct additive maternal effect influencing weight at hatch and direct additive genetic effect affecting weight at six-week-old. From the present findings, it can be concluded that the maternal additive genetic effect observed for weight at six weeks of age might be a factor transferred from genes influencing weight at hatch to weight at six-week-old.
The aim of this study was to estimate the factors that can be used as a predictive indicator of antler productivity in elk. Body weight and antler data from 115 stags raised at the Animal Genetic Resources Research Center in Korea were used in this study. The function for the average antler weight was derived by age, which was $y=-3.4693+5.3747x-0.8x^2+0.0424x^3$, and $R^2$ was 0.991. The analysis of the relationship between body weight at birth and the 1st and 2nd year and the antler weight after the 2nd year showed a correlation between them. There was a correlation between the antler weight of 1 and 2 year old stags and the weight of 2 year old stags as well; especially, both antler weights for the 1st and 2nd year were highly correlated with the antler weight of the 4th year. However, there was no relationship between the antler main beam length for the 1st and 2nd year and the antler weight after the 3rd year. Therefore, it is expected that a large amount of antler will be obtained in the future if proper management is carried out for young deer from birth to 2 years old. Additionally, the results of this study are expected to be useful for the development of a deer breeding program and the deer industry.
Background: The problem of cancer, especially lung cancer, is very acute in Bangladesh. The present study was conducted to evaluate the risk of lung cancer among Bangladeshi people based on hereditary, socio-economic and demographic factors. Materials and Methods: This study was carried out in 208 people (patients-104, controls-104) from January 2012 to September 2013 using a structured questionnaire containing details of lung cancer risk factors including smoking, secondhand smoke, tobacco leaf intake, age, gender, family history, chronic lung diseases, radiotherapy in the chest area, diet, obesity, physical activity, alcohol consumption, occupation, education, and income. Descriptive statistics and testing of hypotheses were used for the analysis using SPSS software (version 20). Results: According to this study, lung cancer was more prevalent in males than females. Smoking was the highest risk factor (OR=9.707; RR=3.924; sensitivity=0.8872 and P<0.0001) followed by previous lung disease (asthma, tuberculosis etc.) (OR=7.095; RR=1.508; sensitivity=0.316 and P<0.0001)) for male patients. Highly cooked food (OR=2.485; RR=1.126; sensitivity=0.418 and P=0.004)) and also genetic inheritance (OR=1.93; RR=1.335; sensitivity=0.163 and P=0.138) demonstrated significant correlation with lung cancer as risk factors after these two and alcohol consumption was not prevalent. On the other hand, for female patients, tobacco leaf intake represented the highest risk (OR=2.00; RR=1.429; sensitivity= 0.667 and P=0.5603) while genetic inheritance and highly cooked food also correlate with lung cancer but not so significantly. Socioeconomic status and education level also play important roles in causing lung cancer. Some 78.5% male and 83.3% of female cancer patients were rural residents, while 58.2% lived at the margin or below the poverty line. Most male (39.8%) and female (50.0%) patients had completed only primary level education, and 27.6% male and 33.3% female patients were illiterate. Smoking was found to be more prevalent among the less educated persons. Conclusions: The results obtained in this study indicate the importance of creating awareness about lung cancer risk factors among Bangladeshi people and making appropriate access to health services for the illiterate, poor, rural people.
CHoi, Sang Rak;Kim, Yun Young;Jang, Eun Jin;Koo, Jin Suk
The Journal of Korean Medicine
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v.40
no.1
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pp.24-33
/
2019
Objectives: The purpose of this study is to analyze the causes of short stature through a clinical review of factors related to childhood height growth. So we can find the way to meet the needs of the heightism which is widely spread among modern people. Methods: Among 160 patients who came to Andong B oriental clinic for the purpose of growth therapy, 112 children whose height was smaller than other normal children were analyzed. When the children first came to the clinic, we checked their height and weight. The parents' height was recorded through a questionnaire. The relationship between obesity index and height growth was examined through growth plate test and Inbody test. We want to identify the genetic factors related to parental factors based on the data of the parent height. Results: For short stature children, weight was often normal or low. When we examined the relationship between parental genetic factors and child growth, we found that they were more influenced by father's height rather than mother's. We investigated the correlation between skeletal maturity and the five viscera. There was no apparent correlation between skeletal maturity and the five viscera but we found that there was some degree of relevance. Conclusions: For short stature children, the weight was often normal or low and parental genetic factors were more influenced by father than by mother. In the case of bone maturity it did not show a direct correlation between the five viscera.
Craniosynostosis is defined as the premature fusion of one or more of the cranial sutures. It leads not only to secondary distortion of skull shape but to various complications including neurologic, ophthalmic and respiratory dysfunction. Craniosynostosis is very heterogeneous in terms of its causes, presentation, and management. Both environmental factors and genetic factors are associated with development of craniosynostosis. Nonsyndromic craniosynostosis accounts for more than 70% of all cases. Syndromic craniosynostosis with a certain genetic cause is more likely to involve multiple sutures or bilateral coronal sutures. FGFR2, FGFR3, FGFR1, TWIST1 and EFNB1 genes are major causative genes of genetic syndromes associated with craniosynostosis. Although most of syndromic craniosynostosis show autosomal dominant inheritance, approximately half of patients are de novo cases. Apert syndrome, Pfeiffer syndrome, Crouzon syndrome, and Antley-Bixler syndrome are related to mutations in FGFR family (especially in FGFR2), and mutations in FGFRs can be overlapped between different syndromes. Saethre-Chotzen syndrome, Muenke syndrome, and craniofrontonasal syndrome are representative disorders showing isolated coronal suture involvement. Compared to the other types of craniosynostosis, single gene mutations can be more frequently detected, in one-third of coronal synostosis patients. Molecular diagnosis can be helpful to provide adequate genetic counseling and guidance for patients with syndromic craniosynostosis.
Development of hypertension is caused by complex contributions of genetic and environmental factors. In spite of the increased understanding of hypertension, genetic factors that contribute to hypertension largely remain elusive. ANO1 gene encoding a calcium-activated chloride channel has recently been reported to affect spontaneous hypertension in the animal model. In this report, we investigated possible association of the ANO1 gene with hypertension in human with ANO1 variants found in Korean population. Fourteen polymorphisms of ANO1 gene were analyzed to be associated with hypertension. Interestingly, the six polymorphisms that showed statistically significant association were all the male subjects. The highest significant SNP was rs7127129 (OR=1.14, CI: 1.02~1.28, additive P=0.023; OR=1.24, CI: 1.03~1.49, dominant P=0.025), and other five SNPs (rs2509153, rs11235473, rs10751200, rs10898827 and rs10899928) were also statistically associated with hypertension. Consequently, we found that the genetic variants of ANO1 present statistically significant associations with hypertension in human, especially, in male. To the best of our knowledge, this study is the first report describing association of genetic polymorphisms of ANO1 with hypertension in human.
Cornus controversa is a long-lived woody species mostly distributed in East Asia. Random amplified polymorphic DNA (RAPD) markers were used to investigate the genetic diversity and population structure of Korean populations of this species. A high level of genetic variation was found in seven populations of C. controversa. The mean genetic diversity (H) was 0.222 across populations, varying from 0.200 to 0.238. Eighty of the 93 loci (86.0%) showed detectable polymorphism in at least one population. Total genetic diversity values ($H_T$) varied between 0.192 and 0.231, giving an average overall polymorphic loci of 0.212. The interlocus variation of genetic diversity within populations ($H_S$) was high (0.167). Mean of genetic diversity in C. controversa was higher than average values for species with similar life history traits. The sexual reproduction, perennial habitat, and longevity are proposed as possible factors contributing to high genetic diversity. On a per locus basis, the proportion of total genetic variation due to differences among populations ($G_{ST}$) ranged from 0.169 to 0.278 with a mean of 0.216, indicating that about 21.6% of the total genetic variation was among populations. An indirect estimate of the number of migrants per generation (Nm=1.893) indicated that gene flow was extensive among Korean populations of C. controversa.
Shin, Mi Na;Lee, Kyung Hea;Lee, Hye Sang;Sasaki, Satoshi;Oh, Hea Young;Lyu, Eun Soon;Kim, Mi Kyung
Nutrition Research and Practice
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v.7
no.5
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pp.400-408
/
2013
Obesity may be the consequence of various environmental or genetic factors, which may be highly correlated with each other. We aimed to examine whether grandmaternal and maternal obesity and environmental risk factors are related to obesity in daughters. Daughters (n = 182) recruited from female students, their mothers (n = 147) and their grandmothers (n = 67) were included in this study. Multivariable logistic regression was used to analyze the association between the daughter's obesity and maternal, grandmaternal, and environmental factors. Maternal heights of 161-175cm (OD: 8.48, 95% CI: 3.61-19.93) and 156-160 cm (2.37, 1.14-4.91) showed positive associations with a higher height of daughter, compared to those of 149-155 cm. Mothers receiving a university or a higher education had a significant OR (3.82, 1.27-11.50) for a higher height of daughter compared to those having a low education (elementary school). Mother having the heaviest weight at current time (59-80 kg, 3.78, 1.73-8.28) and the heaviest weight at 20 years of age (51-65 kg, 3.17, 1.53-6.55) had significant associations with a higher height of daughters, compared to those having the lightest weight at the same times. There was no association between the height, weight, and BMI of daughters and the characteristics and education of her grandmothers. In conclusion, although genetic factors appear to influence the daughter's height more than environmental factors, the daughter's weight appears to be more strongly associated with individual factors than the genetic factors.
Speech and language are uniquely human-specific traits, which contributed to humans becoming the predominant species on earth. Disruptions in the human speech and language function may result in diverse disorders. These include stuttering, aphasia, articulation disorder, spasmodic dysphonia, verbal dyspraxia, dyslexia and specific language impairment. Among these disorders, stuttering is the most common speech disorder characterized by disruptions in the normal flow of speech. Twin, adoption, and family studies have suggested that genetic factors are involved in susceptibility to stuttering. For several decades, multiple genetic studies including linkage analysis were performed to connect causative gene to stuttering, and several genetic studies have revealed the association of specific gene mutation with stuttering. One notable genetic discovery came from the genetic studies in the consanguineous Pakistani families. These studies suggested that mutations in the lysosomal enzyme-targeting pathway genes (GNPTAB, GNPTG and NAPGA) are associated with non-syndromic persistent stuttering. Although these studies have revealed some clues in understanding the genetic causes of stuttering, only a small fraction of patients are affected by these genes. In this study, we summarize recent advances and future challenges in an effort to understand genetic causes underlying stuttering.
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