• The Journal of Korean Medicine
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• v.22 no.1
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• pp.3-9
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• 2001

In the view of oriental medicine, the liver is the general of the army in its function of protecting against the enemy. So this concept is very closely associated to the immunological function. Its relations with immunological function are as follows. 1. The liver produces most of the proteins and converts them with hepatocytes, composes 80% in total reticuloendothelial system with Kuffer cells & endothelial cells and has typical structure of sinusoidal vessels closely related with the blood system. 2. The liver plays an important role in innate immunity with Kuffer cells as well as with the molecules that the liver produces, related to complementary systems. 3. In the embryonic period, the liver is associated with immune associated cell growth and their maturation. After birth, it is associated with removing old red blood cells and with systematically modulating immune system through hormone metabolism. 4. The liver controls the autoimmune disease resulting from immune complex by removing molecules like immune complex. 5. In the processing of blood 19A from the digestive system, the liver has an important role in protecting the body from unnecessary immune responses. 6. In the oriental medical view, liver plays a major role in the immune function by storing blood and dispersing stagnated hepatoqi with the help of the kidneys and spleen.

• Fisheries and Aquatic Sciences
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• v.15 no.1
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• pp.43-47
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• 2012

Growth hormone (GH) transgenesis in fish has the potential to improve aquaculture efficiency and capacity. However, many fast-growing transgenic fish have experienced side effects caused by excess GH expression. To overcome this unwanted issue associated with several GH transgenic mud loach Misgurnus mizolepis lines carrying GH construct driven by a strong ${\beta}$-actin regulator ($pml{\beta}$-actGH), we performed an alternative version of GH autotransgenesis using a weaker but more stable regulator, the mud loach lectin promoter. GH transgenesis with a pmlectGH construct consisting of the mud loach GH gene driven by the 2.3-kb lectin promoter exhibited significant growth stimulation. However, the extent of the growth acceleration in pmlectGH transgenics (six times maximum when assessed 2 months post hatching) was much less than that in transgenic individuals carrying the $pml{\beta}$-actGH construct. Additionally, the extraordinary gigantism that was common in $pml{\beta}$-actGH-transgenic mud loaches was diminished in transgenic loaches harboring the pmlectGH construct. Transgenic founders (pmlectGH) successfully transmitted their transgene into the next generation with up to 41% frequency. Growth stimulation also persisted in the transgenic F1 strains, with a seven-fold increase in maximum body weight at 6 months of age.

• Journal of Integrative Natural Science
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• v.4 no.2
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• pp.113-120
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• 2011

Brassinosteroids (BRs) are plant steroid hormones that play essential roles in growth and development. Mutations in BR-signaling pathways cause defective in growth and development like dwarfism, male sterility, abnormal vascular development and photomorphogenesis. Transition from vegetative to reproductive growth is a critical phase change in the development of a flowering plant. In a screen of activation-tagged Arabidopsis, we identified a mutant named abz126 that displayed longer hypocotyls when grown in the dark on MS media containing brassinazole (Brz), an inhibitor of BRs biosynthesis. We have cloned the mutant locus using adapter ligation PCR walking and identified that a single T-DNA had been integrated into the ninth exon of the GIGANTEA (GI) gene, involved in controling flowering time. This insertion resulted in loss-of-function of the GI gene and caused the following phenotypes: long petioles, tall plant height, many rosette leaves and late flowering. RT-PCR assays on abz126 mutant showed that the T-DNA insertion in GIGANTEA led to the loss of mRNA expression of the GI gene. In the hormone dose response assay, abz126 mutant showed: 1) an insensitivity to paclobutrazole (PAC), 2) an altered response with 6-benzylaminopurine (BAP) and 3) insensitive to Brassinolide (BL). Based on these results, we propose that the late flowering and tall phenotypes displayed by the abz126 mutant are caused by a loss-of-function of the GI gene associated with brassinosteroid hormone signaling.

• The Journal of Korean Obstetrics and Gynecology
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• v.26 no.2
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• pp.178-187
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• 2013

Objectives: These cases are that of three girls who are diagnosed as precocious puberty. It seems that the incidence of precocious puberty is rapidly increasing these days. In addition to the psychosocial disturbances associated with precocious puberty, the premature pubertal growth spurt and the accelerated bone maturation result in reduced adult height. The aim of this study was to report the effect of Jowisengchung-tang in 3 cases of precocious puberty. Methods: Retrospective and comparative analysis of 3 children who had been diagnosed with preco cious puberty. Anthropometric measurements including height, weight, body fat, body fat percent, AHP and body mass index were measured. Endocrine investigations including estradiol, luteinizing hormone(LH), FSH were conducted. Pubertal stages were determined with a questionnaire using Tanner stages. Jowisengchung-tang was given to 3 precocious puberty girls. Results: After treatment, the hormone(estradiol index) and accompanying symptoms (breast bud with elevation of breast and papilla; enlargement of areola) were reduced compared with first visit day. Conclusions: We may conclude that Korean traditional treatment of Jowisengchung-tang is effective in patients with precocious puberty and menopausal symptoms.

• Proceedings of the Korean Society for Bioinformatics Conference
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• 2000.11a
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• pp.74-82
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• 2000

Prostate cancer initially responds and regresses in response to androgen depletion therapy, but most human prostate cancers will eventually recur, and re-grow as an androgen independent tumor. Once these tumors become hormone refractory, they usually are incurable leading to death for the patient. Little is known about the molecular details of how prostate cancer cells regress following androgen ablation and which genes are involved in the androgen independent growth following the development of resistance to therapy. Such knowledge would reveal putative drug targets useful in the rational therapeutic design to prevent therapy resistance and control androgen independent growth. The application of genome scale technologies have permitted new insights into the molecular mechanisms associated with these processes. Specifically, we have applied functional genomics using high density cDNA microarray analysis for parallel gene expression analysis of prostate cancer in an experimental xenograft system during androgen withdrawal therapy, and following therapy resistance, The large amount of expression data generated posed a formidable bioinformatics challenge. A novel template based gene clustering algorithm was developed and applied to the data to discover the genes that respond to androgen ablation. The data show restoration of expression of androgen dependent genes in the recurrent tumors and other signaling genes. Together, the discovered genes appear to be involved in prostate cancer cell growth and therapy resistance in this system. We have also developed and applied tissue microarray (TMA) technology for high throughput molecular analysis of hundreds to thousands of clinical specimens simultaneously. TMA analysis was used for rapid clinical translation of candidate genes discovered by cDNA microarray analysis to determine their clinical utility as diagnostic, prognostic, and therapeutic targets. Finally, we have developed a bioinformatic approach to combine pharmacogenomic data on the efficacy and specificity of various drugs to target the discovered prostate cancer growth associated candidate genes in an attempt to improve current therapeutics.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.42
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• pp.30.1-30.7
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• 2020

Background: Dental studies of precocious puberty have focused on examination of jaw and dentition growth. The aim of the study was to analyze the relationship between precocious puberty and maxillary dental developmental abnormalities (DDAs). Methods: This retrospective study was conducted on the Korean patients in whom dental panoramic and hand-wrist radiographs had been taken before they were 15 years of age. The maxillary DDAs were assessed as mesiodens, congenital missing teeth, peg-shape lateral incisors, or impacted teeth. The chronological ages of the control group members were within the normal range of the hand-wrist bone age. Others with a peak luteinizing hormone of ≥ 5 and < 5 IU/L were allocated to central precocious puberty (CPP) and peripheral precocious puberty (PPP), respectively. Results: Of the enrolled 270 patients, 195, 52, and 23 were allocated to the control, CPP, and PPP groups, respectively. The maxillary DDAs were significantly more prevalent in the CPP group than in the other groups. Among those with maxillary DDA, the mesiodens predominated. Age- and sex-adjusted multivariate analysis revealed maxillary DDA (odds ratio, 3.36; 95% CI, 1.60-7.05) and especially mesiodens (odds ratio, 5.52; CI, 2.29-13.28) to be significantly associated with CPP. Conclusions: Maxillary DDAs were significantly more prevalent in the CPP group than in the PPP or control groups. Among the many types of maxillary DDAs, mesiodens was significantly associated with CPP and may be considered a predictor of the development of CPP.

• Biomedical Science Letters
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• v.11 no.2
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• pp.175-183
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• 2005

The two major isoflavones in soy, genistein and daidzein, are well known to prevent hormone-dependent cancers by their anti estrogenic activity. The exact molecular mechanisms for the protective action are, however, not provided yet. It has been reported that genistein and daidzein have a potential anticancer activity through their antiproliferative effect in many hormone-dependent cancer cell lines. Transforming growth $factor-\beta1(TGF-\beta1)$ has also been found to have cell growth inhibitory effect, especially in mammary epithelial cells. This knowledge led to a hypothetical mechanism that the soy isoflavones-induced growth inhibitory effect can be derived from the regulation of $TGF-\beta1$ and $TGF-\beta$ receptors. In order to test this hypothesis, the effects of the soy isoflavones at various concentrations and periods on the expression of $TGF-\beta1$and $TGF-\beta$ receptors were investigated by using Northern blot analysis in human breast carcinoma epithelial cell lines, an estrogen receptor positive cell line (MCF-7) and an estrogen receptor negative cell line (MDA-MB-231). As a result, only genistein has shown a profound dose-dependent effect on $TGF-\beta1$ expression in the $ER^+$ cell line within the range of doses tested, and the expression levels are correspondent to their inhibitory activities of cell growth. Moreover, daidzein showed down-regulated $TGF-\beta1$ expression at a low dose, the cell growth proliferation was promoted at the same condition. Therefore, antiproliferative activity of the soy isoflavones can be mediated by $TGF-\beta1$ expression, and the effects are mainly, if not all, occurred by ER dependent pathway. The expression of $TGF-\beta$ receptors was induced at a lower dose than the one for $TGF-{\beta}1$ induction regardless of the presence of ER, and the expression patterns are similar to those of the cell growth inhibition. These results indicated that the regulation of $TGF-\beta$ receptor expression as well, prior to $TGF-\beta1$ expression, may be involved in the antiproliferative activity of soy isoflavones. Little or no expression of $TGF-\beta$ receptors was found in the MCF-7 and MDA-MB-231 cells, suggesting refractory properties of the cells to growth inhibitory effect of the $TGF-\beta$. The soy isoflavones can seemingly restore the sensitivity of growth inhibitory responses to $TGF-\beta1$ by re-inducing $TGF-\beta$ receptors expression. In conclusions, our findings presented in this study show that the antitumorigenic activity of the soy isoflavones could be mediated by not only $TGF-\beta1$induction but $TGF-\beta$ receptor restoration. Thus, soy isoflavones could be good model molecules to develop new nonsteroidal antiestrogenic chemopreventive agents, associated with, regulation of $TGF-\beta$ and its receptors.

• Animal Bioscience
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• v.35 no.7
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• pp.989-998
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• 2022

Objective: This study investigated the effects of intrauterine growth restriction (IUGR) during late pregnancy on the cell growth, proliferation, and differentiation in ovine fetal thymuses. Methods: Eighteen time-mated Mongolian ewes with singleton fetuses were allocated to three groups at d 90 of pregnancy: restricted group 1 (RG1, 0.18 MJ ME/body weight [BW]^0.75/d, n = 6), restricted group 2 (RG2, 0.33 MJ ME/BW^0.75/d, n = 6) and control group (CG, ad libitum, 0.67 MJ ME/BW^0.75/d, n = 6). Fetuses were recovered at slaughter on d 140. Results: The G0/G1 phase cell number in fetal thymus of the RG1 group was increased but the proliferation index and the expression of proliferating cell nuclear antigen (PCNA) were reduced compared with the CG group (p<0.05). Fetuses in the RG1 group exhibited decreased growth hormone receptor (GHR), insulin-like growth factor 2 receptor (IGF-2R), and their mRNA expressions (p<0.05). For the RG2 fetuses, there were no differences in the proliferation index and PCNA expression (p>0.05), but growth hormone (GH) and the mRNA expression of GHR were lower than those of the CG group (p<0.05). The thymic mRNA expressions of cyclin-dependent protein kinases (CDKs including CDK1, CDK2, and CDK4), CCNE, E2-factors (E2F1, E2F2, and E2F5) were reduced in the RG1 and RG2 groups (p<0.05), and decreased mRNA expressions of E2F4, CCNA, CCNB, and CCND were occurred in the RG1 fetuses (p<0.05). The decreased E-cadherin (E-cad) as a marker for epithelial-mesenchymal transition (EMT) was found in the RG1 and RG2 groups (p<0.05), but the OB-cadherin which is a marker for activated fibroblasts was increased in fetal thymus of the RG1 group (p<0.05). Conclusion: These results indicate that weakened GH/IGF signaling system repressed the cell cycle progression in G0/G1 phase in IUGR fetal thymus, but the switch from reduced E-cad to increased OB-cadherin suggests that transdifferentiation process of EMT associated with fibrogenesis was strengthened. The impaired cell growth, retarded proliferation and modified differentiation were responsible for impaired maturation of IUGR fetal thymus.

• Clinical and Experimental Reproductive Medicine
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• v.47 no.2
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• pp.94-100
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• 2020

The inverse correlation between maternal age and pregnancy rate represents a major challenge for reproductive endocrinology. The high embryo ploidy error rate in failed in vitro fertilization (IVF) cycles reflects genetic misfires accumulated by older oocytes over time. Despite the application of different follicular recruitment protocols during IVF, gonadotropin modifications are generally futile in addressing such damage. Even when additional oocytes are retrieved, quality is frequently poor. Older oocytes with serious cytoplasmic and/or chromosomal errors are often harvested from poorly perfused follicles, and ovarian vascularity and follicular oxygenation impact embryonic chromosomal competency. Because stimulation regimens exert their effects briefly and immediately before ovulation, gonadotropins alone are an ineffective antidote to long-term hypoxic pathology. In contrast, the tissue repair properties (and particularly the angiogenic effects) of platelet-rich plasma (PRP) are well known, with applications in other clinical contexts. Injection of conventional PRP and/or its components (e.g., isolated platelet-derived growth factors as a cell-free substrate) into ovarian tissue prior to IVF has been reported to improve reproductive outcomes. Any derivative neovascularity may modulate oocyte competence by increasing cellular oxygenation and/or lowering concentrations of intraovarian reactive oxygen species. We propose a mechanism to support intrastromal angiogenesis, improved follicular perfusion, and, crucially, embryo ploidy rescue. This last effect may be explained by mRNA upregulation coordinated by PRP-associated molecular signaling, as in other tissue systems. Additionally, we outline an intraovarian injection technique for platelet-derived growth factors and present this method to help minimize reliance on donor oocytes and conventional hormone replacement therapy.

• YAKHAK HOEJI
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• v.56 no.6
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• pp.352-357
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• 2012

FGFR3 is a member of the fibroblast growth factor receptor family which interacts with fibroblast growth factors, setting in motion a cascade of downstream signals, ultimately influencing mitogenesis and differentiation. This particular family member binds acidic and basic fibroblast growth hormone and plays a role in bone development and maintenance. Accumulated evidence suggests that aberrant regulation of FGFR3 and genetic alterations are implicated in the development and progression of various cancers. Despite a high incidence of FGFR3 over-expression, no such investigation has been performed in hepatocellular carcinoma. Thus, we investigated genetic alterations of the FGFR3 gene in 73 cases of hepatocellular carcinoma by single-strand conformational polymorphism (SSCP) and sequencing. One silent mutation (A369A) was found in the extracellular domain of FGFR3, and one genetic alteration in the immunoglobulin-like III domain of FGFR3 appeared to be polymorphism. Taken together, we concluded that over-expression of FGFR3 in hepatocellular carcinoma is not associated with genetic alterations of FGFR3 gene, and we suggest that there could be another underlying mechanism of aberrant FGFR3 expression in hepatocellular carcinoma.