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Maternal Separation Induced Visceral Hypersensitivity from Childhood to Adulthood
( Lisha Yi ),( Haiqin Zhang ),( Huihui Sun ),( Lu Zhou ),( Ying Chen ),( Liqian Xuan ),( Yuanxi Jiang ),( Shuchang Xu ) 대한소화기기능성질환·운동학회(구 대한소화관운동학회) 2017 Journal of Neurogastroenterology and Motility (JNM Vol.23 No.2
Background/Aims Early adverse life events (EALs) are relevant to irritable bowel syndrome in adulthood. Maternal separation (MS), as one of the EALs, has proved to induce visceral hypersensitivity in adult rats. However, the effect of MS on visceral hypersensitvity from the post-weaning period to adulthood remains unknown. Methods One hundred and ten neonatal Sprague-Dawley rats were randomly divided into 2 groups: rats in the MS group were exposed to 3 hours daily MS on postnatal day (PND) 2-14; the normal control (NC) group remained undisturbed. Visceral sensitivity was determined by measuring the visceromotor response to colorectal distention on PND21, 35, and 56. Anxiety-like behaviors were measured by the open field test. Results Compared with NC rats, MS rats showed significant visceral hypersensitivity from the post-weaning period to adult. The proportion of visceral hypersensitive rats decreased with age from 87.5% to 70.0% in the female MS group and from 90.0% to 66.7% in the male MS group. The relative VMR ratio of MS and NC on PND21 was higher than PND35 and PND56. MS rats showed decreased ability of movement and exploration to the novel environment in the post-weaning period, obesity in the prepubertal period, and more anxietylike behaviors in adulthood. Conclusions MS can significantly affect visceral sensitivity and behaviors of rats in different age stages, especially in the post-weaning period. Visceral hypersensitivity of MS rats is more pronounced in the post-weaning period and slightly restored in adults. Thus, visceral hypersensitivity in the post-weaning period might play a more meaningful pathophysiologic role in the formation of adult irritable bowel syndrome. (J Neurogastroenterol Motil 2017;23:306-315)
JUNG, SAMIL;YI, LISHA;JEONG, DONGJUN;KIM, JINSUN;AN, SUNGWHAN;OH, TAE-JEONG;KM, CHANG-HWAN;KIM, CHANG-JIN;YANG, YOUNG;KIM, KEUN IL;LIM, JONG-SEOK;LEE, MYEONG-SOK Sookmyung Women's University Research Institute of 2011 여성과 건강 Vol.6 No.2
The ADCYAP1 gene encodes an adenylate cyclase activating polypeptide 1. ADCYAP1 has been known to be involved in various biological processes. Multiple cytosine guanine dinucleotides (CpG island) are found in the ADCYAP1 promoter region. Transcriptional silencing by promoter hypermethylation is an important regulatory mechanism in tumorigenesis in many cancers. Therefore, the methylation level of the ADCYAP1 promoter was investigated in eight cervical cancer cell lines and human tissue samples with a distinctive degree of malignant transformation. While multiple CpG sites in the ADCYAPI promoter were highly methylated in CIN III and invasive carcinoma cells as well as seven cervical cancer cell lines, they were rarely methylated in normal cells. Importantly, methylation in the ADCYAP1 promoter seems to start from CIN I,relatively early stage of multistep carcinogenesis. This fact suggest that ADCYAP1 can be used as an effective and sensitive methylation biomarker for the early diagnosis of cervical cancer. Moreover, our data imply that the level of the ADCYAP1 promoter hypermethylation is correlated with cervical cancer development. We also show that ADCYAP1 gene expression was reactivated by the treatment of a DNA methyltransferase inhibitor of 5'-aza-2'deoxycytidine and/or a histone deacetylase inhibitor of trichostain A in cervical cancer cells suggesting that hypermethylation in the ADCYAP1 promoter is responsible for the transcriptional silencing of the ADCYAP1 gene in cervical cancer cells.
Epigenetic regulation of the potential tumor suppressor gene, hLHX6.1, in human cervical cancer
JUNG, SAMIL;JEONG, DONGJUN;KIM, JINSUN;YI, LISHA;KOO, KEUNHOE;LEE, JAEHYOUK;KIM, CHANG-JIN;KIM, CHANG-HWAN;AN, SUNGWHAN;YANG, YOUNG;LIM, JONG-SEOK;KIM, KEUN IL;LEE, MYEONG-SOK Sookmyung Women's University Research Institute of 2011 여성과 건강 Vol.6 No.2
It is well known that the Homo sapiens LIM homeobox domain 6 gene (hLHX6), a putative transcription regulator, controls the differentiation and development of neural and lymphoid cells, particularly in the central nervous system. In this study, we investigated hLHX6.1 (an isoform of hLHX6), which functions as a tumor suppressor gene in the cervix. Firstly, the methylation levels of the h내X6 and hLHX6.1 promoters were investigated in 8 cervical cancer cell lines and human tissue samples with a distinctive degree of malignant transformation. In spite of the presence of multiple cytosine guanine dinucleotides (CpG islands) in 2 proximal promoters of the hLHX6 and hLHX6.1 genes, only the HLHX6.1 promoters were found to be mostly hyper¬methylated and associated with transcriptional silencing by promoter methylation, whereas the hLHX6 promoters were not. Methylation levels in the hLX6.1 promoter were also found to be strongly related to cervical cancer development. The level of hLHX6.1 gene expression was found to be relatively high in normal cells, in which the hLHX6.1 promoter was mostly unmethylated. However, the hLHX6.1 gene expression was down-regulated or undetectable in cervical cancer cell lines and cancer tissues, in which the hLHX6.1 promoter was hypermethylated. This epigenetic alteration in the hLHX6.1 promoter begins at a relatively early stage, suggesting its potential as a biomarker for the early diagnosis and prevention of cervical cancer. Moreover, the overexpression of the hLHX6.1 gene in cervical cancer cells suppressed the tumorigenic phenotype, as shown by soft agar colony formation and migration assays, suggesting that hLHX6.1 could be a new tumor suppressor gene in the cervix.
Jiaojiao Yi,Lin Yang,Lu Wang,Mingqin Xu,Lisha Liu 대한금속·재료학회 2022 METALS AND MATERIALS International Vol.28 No.1
A novel 3d transition metal high entropy alloy (TM HEA), CrCuFeTiV, was fabricated by arc-melting under a vacuum condition. Its phase component, microstructure, and compressive properties in the as-cast and annealed conditions were carefullyinvestigated. The experimental results showed that the alloys in both conditions consist of one BCC phase (CrV/FeTi-richregions), one FCC phase (Cu-rich), and one hexagonal Laves phase (Cr2Ti). It is suggested that the CrV-rich BCC phasepreferentially separates as dendritic centers. Subsequently, the Cr2Ti Laves phase and the FeTi-rich BCC phase solidify as adendritic outer layer. Finally, the FCC Cu-rich phase is squashed into the remaining interdendritic regions. Besides, the yieldstrength, ultimate strength, and hardness of the as-cast CrCuFeTiV alloy are 1686 MPa, 2205 MPa, and 624 HV, while thosefor the annealed alloy are 1510 MPa, 2035 MPa, and 618 HV, respectively. The obtained values are the highest among thetabulated fve-principle equiatomic Cu-containing 3d TM HEAs. The promising strength-hardness synergy of CrCuFeTiValloy is likely originated from the majority constitution of the BCC phase and Cr2Ti Laves phase.
The Role of Vimentin as a Methylation Bio-marker for Early Diagnosis of Cervical Cancer
Samil Jung,Lisha Yi,김진선,정동준,Taejeong Oh,Chang-Hwan Kim,Chang-Jin Kim,Jin Shin,Sungwhan An,이명석 한국분자세포생물학회 2011 Molecules and cells Vol.31 No.5
Multiple cytosine guanine dinucleotides (CpG island) are found in the VIM promoter region. The levels of VIM pro-moter methylation and VIM gene expression were investi-gated in 7 cervical cancer cell lines and 50 human tissue samples with a distinctive degree of malignant trans-for-mation. While multiple CpG sites in the VIM promoter were highly methylated in CIN III and invasive carcinoma cells, they were rarely methylated in normal cells. Our result shows that methylation in the VIM promoter appears to start from CIN I and CIN II, relatively early stages of multi-step carcinogenesis. This epigenetic alteration in VIM promoter suggests the availability as a biomarker for the early diagnosis and prevention of cervical cancer. We also show that hypermethylation in the VIM promoter is re-sponsible for transcriptional silencing of the VIM gene in cervical cancer cells. In addition, our result shows that exogenous overexpression of the VIM gene in SiHa cer-vical cancer cells slightly activated cell proliferation and migration as shown in soft agar colony formation and migration assays.
Jung, Samil,Yi, Lisha,Jeong, Dongjun,Kim, Jinsun,An, Sungwhan,Oh, Tae-Jeong,Kim, Chang-Hwan,Kim, Chang-Jin,Yang, Young,Kim, Keun Il,Lim, Jong-Seok,Lee, Myeong-Sok National Hellenic Research Foundation 2011 ONCOLOGY REPORTS Vol.25 No.1
<P>The ADCYAP1 gene encodes an adenylate cyclase activating polypeptide 1. ADCYAP1 has been known to be involved in various biological processes. Multiple cytosine guanine dinucleotides (CpG island) are found in the ADCYAP1 promoter region. Transcriptional silencing by promoter hypermethylation is an important regulatory mechanism in tumorigenesis in many cancers. Therefore, the methylation level of the ADCYAP1 promoter was investigated in eight cervical cancer cell lines and human tissue samples with a distinctive degree of malignant transformation. While multiple CpG sites in the ADCYAP1 promoter were highly methylated in CIN III and invasive carcinoma cells as well as seven cervical cancer cell lines, they were rarely methylated in normal cells. Importantly, methylation in the ADCYAP1 promoter seems to start from CIN I, relatively early stage of multistep carcinogenesis. This fact suggest that ADCYAP1 can be used as an effective and sensitive methylation biomarker for the early diagnosis of cervical cancer. Moreover, our data imply that the level of the ADCYAP1 promoter hypermethylation is correlated with cervical cancer development. We also show that ADCYAP1 gene expression was reactivated by the treatment of a DNA methyltransferase inhibitor of 5'-aza-2'deoxycytidine and/or a histone deacetylase inhibitor of trichostain A in cervical cancer cells suggesting that hypermethylation in the ADCYAP1 promoter is responsible for the transcriptional silencing of the ADCYAP1 gene in cervical cancer cells.</P>
The role of hLHX6-HMR as a methylation biomarker for early diagnosis of cervical cancer
Jung, Samil,Jeong, Dongjun,Kim, Jinsun,Yi, Lisha,Koo, Keunhoe,Lee, Jaehyouk,Lee, Soon-Duck,Park, Jin-Wha,Chang, Boogi,Kim, Chang-Hwan,Kim, Chang-Jin,Lee, Myeong-Sok Spandidos Publications 2010 ONCOLOGY REPORTS Vol.23 No.6
<P>The homo sapiens LIM homeobox domain LHX6 gene, hLHX6, is a putative transcription regulator with homeo-domain. Multiple cytosine guanine dinucleotides (CpG island) are found in the genomic sequences between exon 4a and exon 5 of the gene encoding hLHX6s (alternative short iso-form of hLHX6 gene). This specific CpG island, hLHX6-HMR, is found frequently hypermethylated in 7 cervical cancer cell lines as shown in MSP, BSP, and COBRA assays. Methylation densities were also investigated with human tissue samples with a distinctive degree of malignant transformation. Our data showed that the hLHX6-HMR was rarely or partly methylated in the normal and CIN I cells, respectively. In contrast, it was frequently hypermethylated in CIN II, CIN III, and invasive carcinoma cells. In summary, this methylation study led to two conclusions. First, hLHX6-HMR hypermethylation is exclusively associated with cervical carcinogenesis. Second, the epigenetic change in hLHX6-HMR seems to start at CIN I, relatively early stage of cervical cancer development. Therefore, hLHX6-HMR can be used as an effective and sensitive methylation biomarker for early diagnosis of cervical cancer.</P>