• Asian-Australasian Journal of Animal Sciences
• /
• v.31 no.1
• /
• pp.3-12
• /
• 2018

Objective: DNA methylation plays a major role in regulating the expression of genes related to traits of economic interest (e.g., weight gain) in livestock animals. This study characterized and investigated the functional inferences of genome-wide DNA methylome in the loin (longissimus dorsi) muscle (LDM) of swine. Methods: A total of 8.99 Gb methylated DNA immunoprecipitation sequence data were obtained from LDM samples of eight Duroc pigs (four pairs of littermates). The reference pig genome was annotated with 78.5% of the raw reads. A total of 33,506 putative methylated regions (PMR) were identified from methylated regions that overlapped at least two samples. Results: Of these, only 3.1% were commonly observed in all eight samples. DNA methylation patterns between two littermates were as diverse as between unrelated individuals (p = 0.47), indicating that maternal genetic effects have little influence on the variation in DNA methylation of porcine LDM. The highest density of PMR was observed on chromosome 10. A major proportion (47.7%) of PMR was present in the repeat regions, followed by introns (21.5%). The highest conservation of PMR was found in CpG islands (12.1%). These results show an important role for DNA methylation in species- and tissue-specific regulation of gene expression. PMR were also significantly related to muscular cell development, cell-cell communication, cellular integrity and transport, and nutrient metabolism. Conclusion: This study indicated the biased distribution and functional role of DNA methylation in gene expression of porcine LDM. DNA methylation was related to cell development, cell-cell communication, cellular integrity and transport, and nutrient metabolism (e.g., insulin signaling pathways). Nutritional and environmental management may have a significant impact on the variation in DNA methylation of porcine LDM.

• Archives of Craniofacial Surgery
• /
• v.25 no.1
• /
• pp.11-16
• /
• 2024

Background: The pathogenesis of orofacial cleft (OFC) is multifactorial, involving both genetic and non-genetic factors, the latter of which play a key role in the development of these anomalies. This paper addresses the incidence of OFC in Indonesia, with a focus on identifying and examining the distribution of contributory factors, including parental medical history, pregnancy history, and environmental influences. Methods: The study was conducted through the collection of primary data. An interdisciplinary research team from Indonesia administered a standardized questionnaire to parents who had children with OFC and who had provided informed consent. The case group comprised 133 children born with cleft lip and/or palate, and the control was 133 noncleft children born full-term. The risk factors associated with OFC anomalies were analyzed using the chi-square test and logistic regression. All statistical analyses were performed using SPSS version 25. A p-value of 0.05 or less was considered to indicate statistical significance. Results: The study comprised 138 children, of whom 82 were boys (59.4%) and 56 were girls (40.6%). Among them, 45 patients (32.6%) presented with both cleft lip and cleft palate, 25 individuals (18.1%) had a cleft palate only, and 28 patients (20.3%) had a cleft lip only. OFC was found to be significantly associated with a maternal family history of congenital birth defects (p<0.05), complications during the first trimester (p<0.05), consumption of local fish (p<0.05), caffeine intake (p<0.05), prolonged medication use (p<0.05), immunization history (p<0.05), passive smoking (p<0.05), and X-ray exposure during pregnancy (p<0.05). Conclusion: The findings indicate close relationships between the incidence of OFC and maternal medical history, prenatal factors, and environmental influences.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.11 no.sup1
• /
• pp.1-6
• /
• 2008

Previous infant feeding guidelines recommended a delayed introduction of solids to beyond 6 months of age to prevent atopic diseases. However, scientific evidence supporting a delayed introduction of solids for prevention of atopic diseases is scarce and inconsistent. Current evidence does not support a major role for maternal dietary restrictions during pregnancy or lactation in the prevention of atopic disease. In studies of infants at high risk of developing atopic disease, there is evidence that exclusive breastfeeding for at least 4 months compared with feeding intact cow milk protein decreases the incidence of atopic dermatitis, cow milk allergy, and wheezing in early childhood. For infants at high risk of developing atopic disease who are not breastfed exclusively for 4 to 6 months, there is modest evidence that atopic dermatitis may be delayed or prevented by the use of extensively or partially hydrolyzed formulas, compared with cow milk formula, in early childhood. There is no convincing evidence that a delayed introduction of solid foods beyond 4 to 6 months of age prevents the development of atopic disease. For infants after 4 to 6 months of age, there are insufficient data to support a protective effect of any dietary intervention for the development of atopic disease.

• Molecules and Cells
• /
• v.43 no.1
• /
• pp.76-85
• /
• 2020

MARCH5 is a RING finger E3 ligase involved in mitochondrial integrity, cellular protein homeostasis, and the regulation of mitochondrial fusion and fission. To determine the function of MARCH5 during development, we assessed transcript expression in zebrafish embryos. We found that march5 transcripts were of maternal origin and evenly distributed at the 1-cell stage, except for the mid-blastula transition, with expression predominantly in the developing central nervous system at later stages of embryogenesis. Overexpression of march5 impaired convergent extension movement during gastrulation, resulting in reduced patterning along the dorsoventral axis and alterations in the ventral cell types. Overexpression and knockdown of march5 disrupted the organization of the developing telencephalon and diencephalon. Lastly, we found that the transcription of march5 was tightly regulated by the transcriptional regulators CHOP, C/EBPα, Staf, Znf143a, and Znf76. These results demonstrate the essential role of March5 in the development of zebrafish embryos.

• Asian Pacific Journal of Cancer Prevention
• /
• v.17 no.6
• /
• pp.2959-2964
• /
• 2016

The present study was conducted to investigate the prevalence of HPV infection in epithelial ovarian cancer (EOC) in Hunan province. DNA samples were collected from paraffin embedded ovarian tissue from 322 patients with EOC, 99 with ovarian benign tumors and 199 normal persons. The polymerase chain reaction and direct sequencing were used to identify the HPV types in the samples. The relationship between the infection of human papillomavirus (HPV) and the epithelial ovarian carcinoma (EOC) was investigated combined with clinical data. The prevalence of HPV18 and HPV33 in EOC group and benign group was higher than in the normal group. HPV18 and HPV33 may play a role in the development of both EOC and ovarian benign tumor and may participate in the development of EOC with traditional risk factors, family history and abortion, possibly exerting synergistic effects.

• Journal of Animal Science and Technology
• /
• v.59 no.1
• /
• pp.1.1-1.11
• /
• 2017

Background: Intrauterine environment plays a pivotal role in the origin of fatal diseases such as the metabolic syndrome. Diabetes is associated with low-grade inflammatory state and dysregulated adipokines production. The aim of this study is to investigate the effect of maternal diabetes on adipocytokines (adiponectin, leptin and TNF-${\alpha}$) production in F1 offspring in rats. Methods: The offspring groups were as follows: F1 offspring of control mothers under control diet (CD) (CF1-CD), F1 offspring of control mothers under high caloric diet (HCD) (CF1-HCD), F1 offspring of diabetic mothers under CD (DF1-CD), and F1 offspring of diabetic mothers under HCD (DF1-HCD). Every 5 weeks post-natal, 10 pups of each subgroup were culled to obtain blood samples for biochemical analysis. Results: The results indicate that DF1-CD and DF1-HCD groups exhibited hyperinsulinemia, dyslipidemia, insulin resistance and impaired glucose homeostasis compared to CF1-CD (p > 0.05). DF1-CD and DF1-HCD groups had high hepatic and muscular depositions of TGs. The significant elevated NEFA level only appeared in offspring of diabetic mothers that was fed HCD. DF1-CD and DF1-HCD groups demonstrated low serum levels of adiponectin, high levels of leptin, and elevated levels of TNF-${\alpha}$ compared to CF1-CD (p > 0.05). These results reveal the disturbed metabolic lipid profile of offspring of diabetic mothers and could guide further characterization of the mechanisms involved. Conclusion: Dysregulated adipocytokines production could be a possible mechanism for the transgenerational transmittance of diabetes, especially following a postnatal diabetogenic environment. Moreover, the exacerbating effects of postnatal HCD on NEFA in rats might be prone to adipcytokine dysregulation. Furthermore, dysregulation of serum adipokines is a prevalent consequence of maternal diabetes and could guide further investigations to predict the development of metabolic disturbances.

• Korean Journal of Agricultural Science
• /
• v.43 no.1
• /
• pp.52-60
• /
• 2016

In animal reproduction, the quality of oocytes and embryos has been evaluated by the expression of specific molecules. Follistatin (FST), which was isolated from follicular fluid, binds and bio-neutralizes the TGF-${\beta}$ superfamily members. Previous studies using the bovine model showed FST could be an important molecular determinant of embryo developmental competence. However, the effect of FST treatment on porcine embryo developmental competence has not been established. In this study, the effect of exogenous FST on porcine embryo developmental competence was investigated during in vitro culture. FST (10 ng/ml) treatment induced a significant decrease in the rate of cell arrest at the 4-cell stage. The expression levels of DNA-methyltransferase 1 (DNMT1), histone deacetylase 1 (HDAC1), and histone deacetylase 2 (HDAC2) were decreased in 4-cell stage embryos. FST treatment also resulted in significant improvements in developmental competence of embryos in terms of blastocyst formation rate and OCT-4 mRNA levels, the latter being related to pluripotency. In conclusion, during in vitro culture, FST treatment significantly ameliorated 4-cell block during embryonic development and improved embryo developmental competence. Therefore, FST treatment may potentially have a functional role in porcine embryogenesis that is broadly applicable to enhance in vitro embryo development.

• Journal of Life Science
• /
• v.33 no.6
• /
• pp.455-462
• /
• 2023

During pregnancy, maternal immune activation (MIA) from infection increases the risk of neurodevelopmental diseases, including schizophrenia and autism spectrum disorders. MIA induced by polyinosinic-polycytidylic acid (poly (I:C)) and lipopolysaccharide (LPS) in animal experiments has led to offspring with abnormal behaviors and brain development. In addition, it has recently been reported that microglia, which reside in the brain and function as immune cells, play an important role in behavioral abnormalities and brain development in MIA-induced offspring. However, the underlying mechanism remains unclear. In this study, we investigated whether microglia-specific inhibition of GPR56, a member of the G protein-coupled receptor (GPCR) family, causes behavioral abnormalities in brain development. First, MIA induction did not affect the microglia population, but when examining the expression of microglial GRP56 in MIA-induced fetuses, GPR56 expression was inhibited between embryonic days 14.5 (E14.5) and E18.5 regardless of sex. Furthermore, microglial GPR56-suppressed mice showed abnormal behaviors in the MIA-induced offspring, including sociability deficits, repetitive behavioral patterns, and increased anxiety levels. Although abnormal cortical development such as that in the MIA-induced offspring were not observed in the microglial GPR56-suppressed mice, their brain activity was observed through c-fos staining. These results suggest that microglia-specific GPR56 deficiency may cause abnormal behaviors and could be used as a biomarker for the diagnosis and/or as a therapeutic target of behavioral deficits in MIA offspring.

• Clinical and Experimental Reproductive Medicine
• /
• v.22 no.2
• /
• pp.163-170
• /
• 1995

Growth factors (GFs) produced by the embryo or by the maternal reproductive tract have been reported to regulate the embryonic development and differentiation. Among GFs, EGF as a mitogen plays a role in mitosis and functional differentiation of trophectoderm cells in mouse. The present study was carried out to investigate the effect of EGF on development of mouse embryos and to localize EGF in the mouse oocytes and embryos, which has been reported to be detected in the reproductive tract in mammals. To investigate the effect of EGF on the development of the embryo, mouse 2-cell embryos were cultured to blastocysts stage in Ham's F10 medium, treated with EGF(10-50 ng/ml) for 72 hrs. Immunocytochemistry was performed from oocyte to blastocyst stage with anti-EGF and anti-Mouse IgG, in order to determine the stage which EGF would be expressed in mouse. Exogenous EGF (more than 10 ng/ml) in the culture medium improved the developmental and hatching rates in the mouse embryos. As a result of immunocytochemistry, the embryonic EGF was expressed after the late 4-cell stage. EGF is thought to enhance preimplantation embryonic development and hatching. Exogenous EGF in the culture medium is thought to activate EGF receptor in the late 4-cell embryos and to enhance blastulation and hatching in mouse embryos. It is concluded that EGF enhances the developmental and hatching rates in the mouse embryos.

• Neonatal Medicine
• /
• v.16 no.2
• /
• pp.137-145
• /
• 2009

Purpose: The aim of this study was to determine the genotype frequencies of interleukin 10 (IL-10) gene polymorphisms and to investigate their association with the risk of respiratory distress syndrome (RDS) in preterm Korean infants. Methods: Two hundred fourteen preterm infants born at Ewha Womans University Mok Dong Hospital between November 2003 and July 2008 were studied. The cord blood of preterm neonates and the corresponding maternal blood were analyzed by PCR for IL-10 gene (IL-10 -1082A/G, -819T/C, and -592A/C) polymorphisms. The clinical data of patients were collected retrospectively by chart review. Results: The genotype frequencies of IL-10 genes in Korean mothers with preterm infants differ from other reports. The prevalence of two promoter SNPs of the IL-10 cytokine gene was similar but none had the IL-10-1082GG homozygote. Multiple logistic regression analysis demonstrated the risk of RDS to be significantly lower in the infants of the mothers with an IL-10-592AC/CC genotype than in those with an AA genotype (P=0.033). The risk of RDS was significantly lower in the mother with an IL-10-819TC/CC genotype than in those with a TT genotype (P=0.030). However, IL-10 polymorphisms in the cord blood were not significantly different in preterm infants with RDS compared with the preterm infants without RDS. When we compared the incidence of RDS and each IL-10A-1082G/T-819C/A-592C haplotype, the ACC haplotype had a protective effect on RDS (P=0.007). Conclusion: We conclude that the maternal IL-10-592A/C and IL-10-819T/C polymorphisms may have a role in the development of the RDS in preterm infants.