http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Kim, Tae-Hyun,Kim, Hail,Park, Joo-Man,Im, Seung-Soon,Bae, Jin-Sik,Kim, Mi-Young,Yoon, Ho-Geun,Cha, Ji-Young,Kim, Kyung-Sup,Ahn, Yong-Ho American Society for Biochemistry and Molecular Bi 2009 The Journal of biological chemistry Vol.284 No.22
<P>Liver glucokinase (LGK) plays an essential role in controlling blood glucose levels and maintaining cellular metabolic functions. Expression of LGK is induced mainly regulated by insulin through sterol regulatory element-binding protein-1c (SREBP-1c) as a mediator. Since LGK expression is known to be decreased in the liver of liver X receptor (LXR) knockout mice, we have investigated whether LGK might be directly activated by LXRalpha. Furthermore, we have studied interrelationship between transcription factors that control gene expression of LGK. In the current studies, we demonstrated that LXRalpha increased LGK expression in primary hepatocytes and that there is a functional LXR response element in the LGK gene promoter as shown by electrophoretic mobility shift and chromatin precipitation assay. In addition, our studies demonstrate that LXRalpha and insulin activation of the LGK gene promoter occurs through a multifaceted indirect mechanism. LXRalpha increases SREBP-1c expression and then insulin stimulates the processing of the membrane-bound precursor SREBP-1c protein, and it activates LGK expression through SREBP sites in its promoter. LXRalpha also activates the LGK promoter by increasing the transcriptional activity and induction of peroxisome proliferator-activated receptor (PPAR)-gamma, which also stimulates LGK expression through a peroxisome proliferator-responsive element. This activation is tempered through a negative mechanism, where a small heterodimer partner (SHP) decreases LGK gene expression by inhibiting the transcriptional activity of LXRalpha and PPARgamma by directly interacting with their common heterodimer partner RXRalpha. From these data, we propose a mechanism for LXRalpha in controlling the gene expression of LGK that involves activation through SREBP-1c and PPARgamma and inhibition through SHP.</P>
β-cell serotonin production is associated with female sex, old age, and diabetes-free condition
Kim, Yeong Gi,Moon, Joon Ho,Kim, Kyuho,Kim, Hyeongseok,Kim, Juok,Jeong, Ji-Seon,Lee, Junguee,Kang, Shinae,Park, Joon Seong,Kim, Hail Academic Press 2017 Biochemical and biophysical research communication Vol. No.
<P><B>Abstract</B></P> <P>Serotonin is known to be present in pancreatic β-cells and to play several physiological roles, including insulin secretion, β-cell proliferation, and paracrine inhibition of α-cells. However, the serotonin production of different cell lines and islets has not been compared based on age, sex, and diabetes related conditions. Here, we directly compared the serotonin concentrations in βTC and MIN6 cell lines, as well as in islets from mice using ultra-performance liquid chromatography tandem mass spectrometry. The average serotonin concentration was 5–10 ng/mg protein in the islets of male and non-pregnant female mice. The serotonin level was higher in females than males at 8 weeks, although there was no difference at 1 year. Furthermore, we observed serotonin by immunofluorescence staining in the pancreatic tissues of mice and human. Serotonin was detected by immunofluorescence staining in a portion of β-cells from islets of old female mice, but not of male or young female mice. A similar pattern was observed in human pancreas as well. In humans, serotonin production in β-cells was associated with a diabetes-free condition. Thus, serotonin production in β-cells was associated with old age, female sex, and diabetes-free condition.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Actual serotonin concentrations in cell lines and islets are compared. </LI> <LI> Serotonin over-production in mouse β-cell is aged and female specific. </LI> <LI> Ovariectomy lowers serotonin concentrations in islets. </LI> <LI> Serotonin over-production in human β-cell is aged, female, and non-diabetes specific. </LI> </UL> </P>
( Kyungsoo Kim ),( Byoung-ki Kim ),( Hail Park ) 한국국제통상학회 2017 국제통상연구 Vol.22 No.2
This paper provides international evidence that the interplay between sophisticated interbank transactions and an interest rate-oriented monetary policy framework can increase the credit supply endogenously. Using country-level panel data collected from 18 countries with a floating exchange rate under an interest rate-oriented monetary policy framework, we find from a panel-VARX model that the impacts of non-core liability shocks on both monetary base and core asset are significantly positive. Policy implications of these findings are also discussed.
Interest Rate-oriented Monetary Policy Framework and Financial Procyclicality
( Kyung Soo Kim ),( Byoung Ki Kim ),( Hail Park ) 한국경제학회 2012 The Korean Economic Review Vol.28 No.2
This paper shows that the current interest rate-oriented monetary policy framework if combined with sophisticated interbank transactions a la Adrian and Shin (2009), can foster or accelerate financial procyclicality since the central bank`s high-powered money can be used as a funding source for financial intermediaries. Interbank transactions that involve maturity transformations pave a silky way for the flow of high-powered money to end up as lending for the ultimate borrowers. This paper also provides some empirical evidence using Korean financial data. In particular, we find that the growth of non-core liabilities, as a close proxy for interbank liabilities, has substantial explanatory power for the growths of core assets, monetary base, and broad money. This paper explores the implications of the findings in terms of the central bank`s responsibility for asset price misalignments and financial stability.
Moon Joon Ho,Lee Joonyub,Kim Kyun Hoo,Kim Hyun Jung,Kim Hyeongseok,Cha Hye-Na,Park Jungsun,Lee Hyeonkyu,Park So-young,Jang Hak Chul,Kim Hail 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Pregnancy imposes a substantial metabolic burden on women, but little is known about whether or how multiple pregnancies increase the risk of maternal postpartum diabetes. In this study, we assessed the metabolic impact of multiple pregnancies in humans and in a rodent model. Mice that underwent multiple pregnancies had increased adiposity, but their glucose tolerance was initially improved compared to those of age-matched virgin mice. Later, however, insulin resistance developed over time, but insulin secretory function and compensatory pancreatic β cell proliferation were impaired in multiparous mice. The β cells of multiparous mice exhibited aging features, including telomere shortening and increased expression of Cdkn2a. Single-cell RNA-seq analysis revealed that the β cells of multiparous mice exhibited upregulation of stress-related pathways and downregulation of cellular respiration- and oxidative phosphorylation-related pathways. In humans, women who delivered more than three times were more obese, and their plasma glucose concentrations were elevated compared to women who had delivered three or fewer times, as assessed at 2 months postpartum. The disposition index, which is a measure of the insulin secretory function of β cells, decreased when women with higher parity gained body weight after delivery. Taken together, our findings indicate that multiple pregnancies induce cellular stress and aging features in β cells, which impair their proliferative capacity to compensate for insulin resistance.
Cho Gahyang,Hyun Kwangbeom,Choi Jieun,Shin Eunji,Kim Bumsoo,Kim Hail,Kim Jaehoon,Yong-Mahn Han 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Neurogenin 3 (NGN3) is a key transcription factor in the cell fate determination of endocrine progenitors (EPs) in the developing pancreas. Previous studies have shown that the stability and activity of NGN3 are regulated by phosphorylation. However, the role of NGN3 methylation is poorly understood. Here, we report that protein arginine methyltransferase-1 (PRMT1)-mediated arginine 65 methylation of NGN3 is required for the pancreatic endocrine development of human embryonic stem cells (hESCs) in vitro. We found that inducible PRMT1-knockout (P-iKO) hESCs did not differentiate from EPs into endocrine cells (ECs) in the presence of doxycycline. Loss of PRMT1 caused NGN3 accumulation in the cytoplasm of EPs and decreased the transcriptional activity of NGN3. We found that PRMT1 specifically methylates NGN3 arginine 65 and that this modification is a prerequisite for ubiquitin-mediated degradation. Our findings demonstrate that arginine 65 methylation of NGN3 is a key molecular switch in hESCs permitting their differentiation into pancreatic ECs.
김학혜 中央醫學社 1976 中央醫學 Vol.30 No.1
Reported a clinical study of 82 cases of newborn infants with aspiration pneumonia who admitted to pediatric department, Ewha Woman’s University Hospital from 1968 Jan. to 1974 Dec. Obtained following results 1) Sex incidence was male 48(45.8%), female 34(41.5% , no difference. 2) 23(38%) of these infants were born prematurity, 20(24.4%) were born at term, 3(3. 7%) were post mature. 3) 26.5% of the infants were delivered by cesarean in production of aspiration. 4) Abnormality during pregnancy of mother revealed toxemia (53.8%), placenta previa (15.4%), viginal bleeding (23.1%) abruptio placenta (7.7 %) , and premature rupture of membranes (29.3%). 5) The chief complaints on admission were cyanosis (70. 7 °% ), weak crying (52.3%), grunting (34.1%), subcostal retraction (21.9 % ), respiratory difficulty (14.6%), apneic spell (10.9%), and meconium stained (23.1%) in orders. 6) Positive gastric juice culture were E. coli (42.9%), Staphylococus aureus(32.2 %), Streptococcus, Pseudomonas, Aerobacter, Proteus in orders. 7) 23 patients showed under 6 points in one min. Apgar score. 8) Breathing was faster than 80 per min. in 28(34. 1%) cases and was 40 to 80 per min. in 39(47.6%). 11 patients died. 9) Treatment of infants involved isolation in an incubator, artificial ventilation, oxygenation, administration of antibiotics. 13 died among 82 cases.