비타민 D3 의 경구투여 또는 자외선 조사가 브로일러 병아리의 증체 및 비타민 D3 대사에 미치는 영향

장윤환(Y . H . Chiang),황선일(S . I . Hwang),김중달(J . D . Kim),M . F . Holick(M . F . Holick) 한국영양사료학회 1995 韓國營養飼料學會誌 Vol.19 No.6

Cyclobuxine D의 토끼 적출 장관에 대한 작용

이종화,박영현,조병헌,김종배,김정목,김유재,김천숙,차영덕,김영석 최신의학사 1988 最新醫學 Vol.31 No.1

Resource allocation for device-to-device communications underlaying LTE-advanced networks

Phunchongharn, P.,Hossain, E.,Kim, D. I. IEEE 2013 IEEE wireless communications Vol.20 No.4

<P>The Long Term Evolution-Advanced (LTEAdvanced) networks are being developed to provide mobile broadband services for the fourth generation (4G) cellular wireless systems. Deviceto- device (D2D) communications is a promising technique to provide wireless peer-to-peer services and enhance spectrum utilization in the LTE-Advanced networks. In D2D communications, the user equipments (UEs) are allowed to directly communicate between each other by reusing the cellular resources rather than using uplink and downlink resources in the cellular mode when communicating via the base station. However, enabling D2D communications in a cellular network poses two major challenges. First, the interference caused to the cellular users by D2D devices could critically affect the performances of the cellular devices. Second, the minimum quality-of-service (QoS) requirements of D2D communications need to be guaranteed. In this article, we introduce a novel resource allocation scheme (i.e. joint resource block scheduling and power control) for D2D communications in LTE-Advanced networks to maximize the spectrum utilization while addressing the above challenges. First, an overview of LTE-Advanced networks, and architecture and signaling support for provisioning of D2D communications in these networks are described. Furthermore, research issues and the current state-of-the-art of D2D communications are discussed. Then, a resource allocation scheme based on a column generation method is proposed for D2D communications. The objective is to maximize the spectrum utilization by finding the minimum transmission length in terms of time slots for D2D links while protecting the cellular users from harmful interference and guaranteeing the QoS of D2D links. The performance of this scheme is evaluated through simulations.</P>

Exendin-4 induction of cyclin D1 expression in INS-1 beta-cells: involvement of cAMP-responsive element.

Kim, M-J,Kang, J-H,Park, Y G,Ryu, G R,Ko, S H,Jeong, I-K,Koh, K-H,Rhie, D-J,Yoon, S H,Hahn, S J,Kim, M-S,Jo, Y-H Journal of Endocrinology, Ltd. [etc.] 2006 The Journal of endocrinology Vol.188 No.3

<P>Glucagon-like peptide-1 (GLP-1) and its analog exendin-4 (EX) have been considered as a growth factor implicated in pancreatic islet mass increase and beta-cell proliferation. This study aimed to investigate the effect of EX on cyclin D1 expression, a key regulator of the cell cycle, in the pancreatic beta-cell line INS-1. We demonstrated that EX significantly increased cyclin D1 mRNA and subsequently its protein levels. Although EX induced phosphorylation of Raf-1 and extracellular-signal-regulated kinase (ERK), both PD98059 and exogenous ERK1 had no effect on the cyclin D1 induction by EX. Instead, the cAMP-elevating agent forskolin induced cyclin D1 expression remarkably and this response was inhibited by pretreatment with H-89, a protein kinase A (PKA) inhibitor. Promoter analyses revealed that the cAMP-responsive element (CRE) site (at position -48; 5'-TAACGTCA-3') of cyclin D1 gene was required for both basal and EX-induced activation of the cyclin D1 promoter, which was confirmed by site-directed mutagenesis study. For EX to activate the cyclin D1 promoter effectively, CRE-binding protein (CREB) should be phosphorylated and bound to the putative CRE site, according to the results of electrophoretic mobility shift and chromatin immunoprecipitation assays. Lastly, a transfection assay employing constitutively active or dominant-negative CREB expression plasmids clearly demonstrated that CREB was largely involved in both basal and EX-induced cyclin D1 promoter activities. Taken together, EX-induced cyclin D1 expression is largely dependent on the cAMP/PKA signaling pathway, and EX increases the level of phosphorylated CREB and more potently trans-activates cyclin D1 gene through binding of the CREB to the putative CRE site, implicating a potential mechanism underlying beta-cell proliferation by EX.</P>

Optical subthreshold current method for extracting the interface states in MOS systems

Kim, M.S.,Nam, I.C.,Kim, H.T.,Shin, H.T.,Kim, T.E.,Park, H.S.,Kim, K.S.,Kim, K.H.,Choi, J.B.,Min, K.S.,Kim, D.J.,Kang, D.W.,Kim, D.M. IEEE 2004 IEEE electron device letters Vol.25 No.2

Optical subthreshold current method (OSCM) is proposed for characterizing the interface states in MOS systems using the current-voltage characteristics under a photonic excitation. An optical source with a subbandgap (E<SUB>ph</SUB>>E<SUB>g</SUB>) photonic energy (E<SUB>ph</SUB>=0.943 eV, P<SUB>opt</SUB>=+5 dBm), which is less than the silicon bandgap (E<SUB>g</SUB>=1.12;eV), is employed for the optical subthreshold current characterization of interface states in the photoresponsive energy band. We applied the OSCM method under a subbandgap photonic excitation to MOS systems with a poly-Si gate and verified a U-shaped distribution of interface trap density D<SUB>it</SUB>=10<SUP>10</SUP>∼10<SUP>12</SUP> eV<SUP>-1</SUP>cm<SUP>-2</SUP> for n- and p-type MOSFETs with W/L=30 μm/1.2 μm.

Development of transdermal vitamin D3 (VD3) delivery system using combinations of PLGA nanoparticles and microneedles

Kim, H. G.,Gater, D. L.,Kim, Y. C. Springer Science + Business Media 2018 Drug delivery and translational research Vol.8 No.1

<P>Although vitamin D3 (VD3), which is the main form of vitamin D, can be produced in human skin under the sunlight, vitamin D deficiency emerged as a major public health problem worldwide. Mainly, oral supplements or vitamin D-fortified foods are distributed to help supplementation of vitamin D. However, those oral methods are limitedly supplied in the Middle East countries, and oral absorption has low efficiency due to many barriers and various changes of conditions along the route. Then, it is recommended to take them every day in order to maintain the adequate serum level of vitamin D. Alternatively, transdermal delivery system could provide a convenient way to get sustained supplement of vitamin D by its advantages like avoiding first-pass effect of the liver and providing release for long periods of time. In this study, we introduced transdermal delivery system for sustained vitamin D release using coating microneedles that easily pierce the skin layer with enough mechanical strength and allow the localization of drugs within the dermal region. According to the experimental results, poly (lactic-co-glycolic acid) (PLGA) successfully encapsulated VD3 as a nanoparticle form with appropriate properties for transdermal delivery such as size distribution, skin compatibility, and effective release of encapsulated compound. Finally, PVD3 layers coated on solid microneedles were completely dissolved into intradermal region in porcine skin model and revealed better performance for VD3 release into plasma compared to ointment base transdermal method.</P>

d-pinitol regulates Th1/Th2 balance via suppressing Th2 immune response in ovalbumin-induced asthma

Lee, J.S.,Lee, C.M.,Jeong, Y.I.,Jung, I.D.,Kim, B.H.,Seong, E.Y.,Kim, J.I.,Choi, I.W.,Chung, H.Y.,Park, Y.M. North-Holland Pub ; Elsevier Science Ltd 2007 FEBS letters Vol.581 No.1

d-pinitol has been demonstrated to exert insulin-like and anti-inflammatory activities. However, its anti-allergic effect in the Th1/Th2 immune response is poorly understood. Recently, it was shown that T-bet and GATA-3 are master Th1 and Th2 regulatory transcription factors. In this study, we have attempted to determine whether d-pinitol regulates Th1/Th2 cytokine production, T-bet and GATA-3 gene expression in OVA-induced asthma model mice. We also examined to ascertain whether d-pinitol could influence eosinophil peroxidase (EPO) activity. After being sensitized and challenged with ovalbumin (OVA) showed typical asthmatic reactions. These reactions included an increase in the number of eosinophils in bronchoalveolar lavage (BAL) fluid, an increase in inflammatory cell infiltration into the lung tissue around blood vessels and airways, airway luminal narrowing, and the development of airway hyper-responsiveness (AHR). The administration of d-pinitol before the last airway OVA challenge resulted in a significant inhibition of all asthmatic reactions. Accordingly, this study may provide evidence that d-pinitol plays a critical role in the amelioration of the pathogenetic process of asthma in mice. These findings provide new insight into the immunopharmacological role of d-pinitol in terms of its effects in a murine model of asthma, and also broaden current perspectives in our understanding of the immunopharmacological functions of d-pinitol.

Integrin αvβ3-mediated transcriptional regulation of TIMP-1 in a human ovarian cancer cell line

Kim, D.S.,Jeon, O.H.,Lee, H.D.,Yoo, K.H.,Kim, D.S. Academic Press 2008 Biochemical and biophysical research communication Vol.377 No.2

We have previously reported that a disintegrin inhibits solid tumor growth and metastasis in mouse model [I.C. Kang, Y.D. Lee, D.S. Kim, A novel disintegrin salmosin inhibits tumor angiogenesis, Cancer Res. 59 (1999) 3754-3760; S.I. Kim, K.S. Kim, H.S. Kim, D.S. Kim, Y. Jang, K.H. Chung, Y.S. Park, Inhibitory effect of the salmosin gene transferred by cationic liposomes on the progression of B16BL6 tumors, Cancer Res. 63 (2003) 6458-462]. In this study, we have investigated the modulatory effect of a disintegrin, saxatilin, on the balance between MMP-9 and tissue inhibitor of metalloproteinase-1 (TIMP-1) in human ovarian cancer cell line MDAH 2774. Functional mechanism of the disintegrin-mediated transcriptional regulation of MMP-9 and TIMP-1 was examined in the ovarian cancer cell line. Saxatilin strongly induced TIMP-1 expression in dose- and time-dependent manners, while the disintegrin suppressed MMP-9 expression. Further analyses clearly indicated that interaction of the disintegrin and integrin αvβ3 results in the TIMP-1 promoter activation via c-fos to suppress TNF-α-induced cancer cell invasion. These results demonstrate that integrin αvβ3-mediated transcriptional regulation of MMP-9 and TIMP-1 is critical for suppressing the ovarian cancer cell invasion.

Potential roles of D-serine and serine racemase in experimental temporal lobe epilepsy

Ryu, H.J.,Kim, J.-E.,Yeo, S.-I.,Kim, D.-S.,Kwon, O.-S.,Choi, S.Y.,Kang, T.-C. Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of neuroscience research Vol.88 No.11

<P>To confirm the roles of D-serinergic gliotransmission in epilepsy, we investigated the relationship between spatiotemporally specific glial responses and the D-serine/serine racemase system in mesial temporal structures following status epilepticus (SE). In control animals, D-serine and serine racemase immunoreactivities were detected mainly in astrocytes. After SE, D-serine and serine racemase immunoreactivities were increased in astrocytes. Double-immunofluorescence study revealed that up-regulation of serine racemase immunoreactivity was relevant not to D-serine immunoreactivity but to nestin or vimentin immunoreactivity. Neither D-serine nor serine racemase was found in naïve or reactive microglia. In addition, phosphorylated N-methyl-D-aspartate (NMDA) receptor subunit 1 (pNR1-Ser896) immunoreactivity in the hippocampus was increased compared with controls. Increased D-serine immunoreactivity showed direct correlation with the phosphorylation of Ser896 of NR1. Given the findings of our previous study, these findings suggest that D-serine and serine racemase in astrocytes may play roles in neuronal hyperexcitability via a cooperative activation of NMDA receptors. Furthermore, serine racemase may be involved in migration and differentiation of immature astrocytes, which is relevant to reactive astrogliosis. © 2010 Wiley-Liss, Inc.</P>

Vitamin D deficiency impairs glucose-stimulated insulin secretion and increases insulin resistance by reducing PPAR-γ expression in nonobese Type 2 diabetic rats

Park, S.,Kim, D.S.,Kang, S. Butterworths ; Elsevier Science Ltd 2016 The Journal of nutritional biochemistry Vol.27 No.-

<P>Human studies have provided relatively strong associations of poor vitamin D status with Type 2 diabetes but do not explain the nature of the association. Here, we explored the physiological pathways that may explain how vitamin D status modulates energy, lipid and glucose metabolisms in nonobese Type 2 diabetic rats. Goto-Kakizaki (GK) rats were fed high-fat diets containing 25 (VD-low), 1000 (VD-normal) or 10,000 (VD-high) cholecalciferol-IU/kg diet for 8 weeks. Energy expenditure, insulin resistance, insulin secretory capacity and lipid metabolism were measured. Serum 25-OH-D levels, an index of vitamin D status, increased dose dependently with dietary vitamin D. VD-low resulted in less fat oxidation without a significant difference in energy expenditure and less lean body mass in the abdomen and legs comparison to the VD-normal group. In comparison to VD-low, VD-normal had lower serum triglycerides and intracellular fat accumulation in the liver and skeletal muscles which was associated with down-regulation of the mRNA expressions of sterol regulatory element binding protein-1c and fatty acid synthase and up-regulation of gene expressions of peroxisome proliferator-activated receptors (PPAR)-alpha and carnitine palmitoyltransferase-1. In euglycemic hyperinsulinemic clamp, whole-body and hepatic insulin resistance was exacerbated in the VD-low group but not in the VD-normal group, possibly through decreasing hepatic insulin signaling and PPAR-gamma expression in the adipocytes. In 3T3-L1 adipocytes 1,25-(OH)(2)-D (10 nM) increased triglyceride accumulation by elevating PPAR-gamma expression and treatment with a PPAR-gamma antagonist blocked the triglyceride deposition induced by 1,25-(OH)2-D treatment. VD-low impaired glucose-stimulated insulin secretion in hyperglycemic clamp and decreased beta-cell mass by decreasing beta-cell proliferation. In conclusion, vitamin D deficiency resulted in the dysregulation of glucose metabolism in GK rats by simultaneously increasing insulin resistance by decreasing adipose PPAR-gamma expression and deteriorating beta-cell function and mass. (C) 2015 Elsevier Inc. All rights reserved.</P>