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      • KCI등재

        Association of Osteoporosis-related Healthcare Costs with the Use of Tenofovir Disoproxil Fumarate and Tenofovir Alafenamide in Chronic Hepatitis B Patients: a Population-based National Cohort Study in Korea

        You Ran Noh(You Ran Noh),Hae Sun Suh(Hae Sun Suh) 대한약학회 2024 약학회지 Vol.68 No.1

        Long-term administration of tenofovir disoproxil fumarate (TDF) for chronic hepatitis B (CHB) may lead to bone mineral density loss. Tenofovir alafenamide (TAF) developed to address these concerns. This study aimed to investigate whether there is a significant difference in osteoporosis-related healthcare costs between CHB patients treated with TDF and TAF. This study is a retrospective cohort study using claims data from the Health Insurance Review and Assessment Service (HIRA) covering the entire population in Korea. The cohort included CHB patients treated with TDF or TAF from November 2017 to April 2022. We applied inverse probability of treatment weighting (IPTW) to balance baseline characteristics observed for one-year preceding prescription date. Osteoporosis-related costs per patient per year (PPPY) included all healthcare costs with an osteoporosis diagnosis code including outpatient and hospitalization costs. 7,172 and 3,837 patients were administered TDF and TAF respectively. After IPTW, TDF group had higher outpatient costs ($11.2) compared to TAF group ($6.1), but the difference was not statistically significant (p=0.1001). The total hospitalization cost was $24.6 in TDF group and $9.8 in TAF group, not statistically significant (p=0.1633). This largescale population-based study found no significant difference in osteoporosis-related healthcare costs between CHB patients treated with TDF and TAF.

      • SCISCIESCOPUS

        Small Heterodimer Partner Deficiency Increases Inflammatory Liver Injury Through C-X-C motif chemokine ligand 2-Driven Neutrophil Recruitment in Mice

        Noh, Jung-Ran,Kim, Yong-Hoon,Kim, Don-Kyu,Hwang, Jung Hwan,Kim, Kyoung-Shim,Choi, Dong-Hee,Lee, Seon-Jin,Lee, Hee Gu,Lee, Tae Geol,Weng, Hong-Lei,Dooley, Steven,Choi, Hueng-Sik,Lee, Chul-Ho ACADEMIC PRESS 2018 TOXICOLOGICAL SCIENCES Vol.163 No.1

        <P>Although detailed pathophysiological mechanisms of fulminant hepatitis remain elusive, immune cell recruitment with excessive cytokine production is a well-recognized hallmark of the disease. We determined the function of orphan nuclear receptor small heterodimer partner (SHP) in concanavalin A (ConA)-induced hepatitis model. Male CS7BL/6 J mice were injected intravenously with either a lethal dose (25 mg/kg) or a sub-lethal dose (15 mg/kg) of ConA. For the C-X-C motif chemokine ligand (CXCL) 2 neutralization study, mice were intravenously administered anti-mouse CXCL2 antibody (100 mu g/mouse). Thirty-six hours following lethal dose of ConA administration, 47% wild type (WI) mice were alive, whereas >85% of Shp knockout (KO) were dead. Shp KO mice were highly susceptible to ConA-induced liver injury and exhibited increased liver necrosis upon sublethal dose of ConA administration. FACS analysis and immunohistochemical staining showed significantly higher neutrophil infiltration in Shp KO mice, as compared with WT mice. We found that also in the WT situation, Shp expression gradually decreased, while Cxcl2 expression increased until 6 h, and vice versa at 24 h upon ConA-treatment, indicating an inverse correlation between Shp and Cxcl2 expression during ConA-induced hepatitis. Furthermore, in vivo neutralization of CXCL2 with neutralizing antibody reduces ConA-induced plasma ALT and AST levels, hepatocyte death and neutrophil infiltration in Shp KO mice. Collectively, these results confirm that lacking of SHP results in CXCL2-dependent neutrophil infiltration in ConA-induced liver damage. SHP plays a protective, anti-inflammatory role in liver during acute liver inflammation.</P>

      • SCIESCOPUSKCI등재

        Desalinated underground seawater of Jeju Island (Korea) improves lipid metabolism in mice fed diets containing high fat and increases antioxidant potential in t-BHP treated HepG2 cells

        Noh, Jung-Ran,Gang, Gil-Tae,Kim, Yong-Hoon,Yang, Keum-Jin,Lee, Chul-Ho,Na, O-Su,Kim, Gi-Ju,Oh, Won-Keun,Lee, Young-Don The Korean Nutrition Society 2010 Nutrition Research and Practice Vol.2 No.4

        This study was performed to investigate the effect of desalinated underground seawater (named as 'magma seawater', MSW) of Jeju Island in Korea on lipid metabolism and antioxidant activity. MSW was collected from underground of Han-Dong in Jeju Island, and freely given to high fat diet (HFD)-fed C57BL/6 mice for 10 weeks. Although there were no significant differences in the body weight changes and plasma lipid levels, hepatic triglyceride levels were significantly lower in the MSW group than in the normal tap water (TW)-drunken control group. Furthermore, the activity of fatty acid synthase (FAS) was significantly decreased and carnitine palmitoyltransferase (CPT) activity was increased in MSW group compared to TW group. Similarly, real-time PCR analysis revealed that mRNA expressions of lipogenic genes were lowered in MSW groups compared to the control group. In a morphometric observation on the liver tissue, accumulation of fats was remarkably reduced in MSW group. Meanwhile, in vitro assay, tree radical scavenging activity measured by using diphenylpicrylhydrazyl (DPPH) was increased in MSW group. The 2'-7'-dichlorofluorescein diacetate (DCF-DA) staining followed with fluorescent microscopy showed a low intensity of fluorescence in MSW-treated HepG2 cells, compared to TW-treated HepG2 cells, which indicated that the production of reactive oxygen species by tert-butyl hydroperoxide (t-BHP) in HepG2 cells was decreased by MSW treatment. The antioxidant effect of MSW on t-BHP-induced oxidative stress in HepG2 cells was supported by the increased activities of intracellular antioxidant enzymes such as catalase and glutathione reductase. From these results, we speculate that MSW has an inhibitory effect on lipogenesis in liver and might play a protective role against cell damage by t-BHP-induced oxidative stress.

      • SCISCIESCOPUS

        Sulforaphane protects against acetaminophen-induced hepatotoxicity

        Noh, Jung-Ran,Kim, Yong-Hoon,Hwang, Jung Hwan,Choi, Dong-Hee,Kim, Kyoung-Shim,Oh, Won-Keun,Lee, Chul-Ho Elsevier 2015 Food and chemical toxicology Vol.80 No.-

        <P><B>Abstract</B></P> <P>Oxidative stress is closely associated with acetaminophen (APAP)-induced toxicity. Heme oxygenase-1 (HO-1), an antioxidant defense enzyme, has been shown to protect against oxidant-induced tissue injury. This study investigated whether sulforaphane (SFN), as a HO-1 inducer, plays a protective role against APAP hepatotoxicity <I>in vitro</I> and <I>in vivo</I>. Pretreatment of primary hepatocyte with SFN induced nuclear factor E2-factor related factor (Nrf2) target gene expression, especially HO-1 mRNA and protein expression, and suppressed APAP-induced glutathione (GSH) depletion and lipid peroxidation, which eventually leads to hepatocyte cell death. A comparable effect was observed in mice treated with APAP. Mice were treated with 300 mg/kg APAP 30 min after SFN (5 mg/kg) administration and were then sacrificed after 6 h. APAP alone caused severe liver injuries as characterized by increased plasma AST and ALT levels, GSH depletion, apoptosis, and 4-hydroxynonenal (4-HNE) formations. This APAP-induced liver damage was significantly attenuated by pretreatment with SFN. Furthermore, while hepatic reactive oxygen species (ROS) levels were increased by APAP exposure, pretreatment with SFN completely blocked ROS formation. These results suggest that SFN plays a protective role against APAP-mediated hepatotoxicity through antioxidant effects mediated by HO-1 induction. SFN has preventive action in oxidative stress-mediated liver injury.</P> <P><B>Highlights</B></P> <P> <UL> <LI> SFN pretreatment increases the cell viability against APAP-induced toxicity. </LI> <LI> SFN pretreatment protects depletion of cellular GSH after APAP treatment. </LI> <LI> SFN pretreatment enhances Nrf2 target gene expression, especially HO-1 after APAP treatment. </LI> <LI> SFN has protective effect against APAP overdose-induced liver injury <I>in vivo</I> model as well. </LI> </UL> </P>

      • KCI등재

        Investigating the Leaching Rate of TiTe<sub>3</sub>O<sub>8</sub> Towards a Potential Ceramic Solid Waste Form

        Noh, Hye Ran,Lee, Dong Woo,Suh, Kyungwon,Lee, Jeongmook,Kim, Tae-Hyeong,Bae, Sang-Eun,Kim, Jong-Yun,Lim, Sang Ho Korean Radioactive Waste Society 2020 방사성폐기물학회지 Vol.18 No.4

        An important property of glass and ceramic solid waste forms is processability. Tellurite materials with low melting temperatures and high halite solubilities have potential as solid waste forms. Crystalline TiTe3O8 was synthesized through a solid-state reaction between stoichiometric amounts of TiO2 and TeO2 powder. The resultant TiTe3O8 crystal had a three-dimensional (3D) structure consisting of TiO6 octahedra and asymmetric TeO4 seesaw moiety groups. The melting temperature of the TiTe3O8 powder was 820℃, and the constituent TeO2 began to evaporate selectively from TiTe3O8 above around 840℃. The leaching rate, as determined using the modified American Society of Testing and Materials static leach test method, of Ti in the TiTe3O8 crystal was less than the order of 10-4 g·m-2·d-1 at 90℃ for durations of 14 d over a pH range of 2-12. The chemical durability of the TiTe3O8 crystal, even under highly acidic and alkaline conditions, was comparable to that of other well-known Ti-based solid waste forms.

      • Antiatherogenic Effect of Antioxidant Polyphenols from <i>Phellinus baumii </i> in Apolipoprotein E-Deficient Mice

        Noh, Jung-Ran,Lee, In-Kyoung,Kim, Yong-Hoon,Gang, Gil-Tae,Hwang, Jung Hwan,Ly, Sun-Yung,Yun, Bong-Sik,Lee, Chul-Ho S. Karger AG 2011 Annals of nutrition & metabolism Vol.59 No.2

        <P>Abstract</P><P><I>Aims:</I> The present study was carried out to investigate the antiatherosclerotic effect of antioxidant polyphenols from <I>Phellinus baumii</I> (PBE) in apolipoprotein E-deficient (apoE–/–) mice. <I>Methods and Results:</I> apoE–/– mice were randomly divided into three groups: mice on a normal chow diet comprised the normal group, mice on an atherogenic diet plus vehicle were the control group, and mice on an atherogenic diet plus PBE (500 mg/kg) comprised the PB500 group. After 8 weeks of treatment, the plasma lipids and cytokine levels were measured. Although no significant differences were found in cholesterol levels among groups, the triglyceride level was significantly decreased in the PBE-treated group compared with the control group. Plasma tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels were reduced by PBE treatment. Real-time PCR analysis of the aorta showed that PBE significantly prevented the upregulation of the vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, TNF-α, IL-6, and IL-1β expression. Furthermore, reduced macrophage infiltration, lipid accumulation and atherosclerotic lesions were observed in the aortic sinus and en face of the whole aorta in PBE-fed apoE–/– mice compared with atherogenic diet-fed control mice. <I>Conclusions:</I> Collectively, the findings of the present study suggest that the antiatherosclerotic effect of PBE is probably related to the inhibition of adhesion molecule and cytokine expression resulting in amelioration of lesion development.</P><P>Copyright © 2011 S. Karger AG, Basel</P>

      • KCI등재

        The First Successful Lung Transplantation in a Korean Child with Cystic Fibrosis

        Noh, Soo Ran,Lee, Eun,Yoon, Jisun,Jung, Sungsu,Yang, Song-I,Yu, Jinho,Hong, Soo-Jong KOREAN ACADEMY OF MEDICAL SCIENCE 2017 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.32 No.12

        <P>Cystic fibrosis (CF) is an autosomal recessive inherited multisystem disorder caused by mutations of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein. Respiratory failure remains the most frequent cause of morbidity and mortality. Lung transplantation is the only option to treat end-stage lung disease. Very few cases of CF occur in Koreans. We report the case of a 12-year-old girl with respiratory failure due to CF who underwent lung transplantation. She had been diagnosed with CF 8 years previously after being treated for recurrent <I>Pseudomonas aeruginosa</I> pneumonia and malnutrition based on sweat chloride concentrations and the CFTR protein gene mutation test. Progression to end-stage lung disease and respiratory failure led to registration with the Korean Network for Organ Sharing. She underwent successful double lung transplantation in 2014. Although she has diabetes mellitus and chronic kidney disease, she has a better quality of life and a prolonged life expectancy.</P>

      • SCISCIESCOPUS

        Preventative Effects of <i>Platycodon grandiflorum</i> Treatment on Hepatic Steatosis in High Fat Diet-Fed C57BL/6 Mice

        Noh, Jung-Ran,Kim, Yong-Hoon,Gang, Gil-Tae,Yang, Keum-Jin,Kim, Sang-Kyum,Ryu, Shi-Yong,Kim, Young-Sup,Lee, Chul-Ho,Lee, Hyun-Sun Pharmaceutical Society of Japan 2010 Biological & pharmaceutical bulletin Vol.33 No.3

        <P><I>Platycodon grandiflorum</I> (PG) (Korean name, <I>Doraji</I>; Chinese name, <I>Jiegeng</I>; and Japanese name, <I>Kikyo</I>) is a perennial plant in the Campanulaceae family that contains triterpenoid saponins, carbohydrates, and fibers. This study was carried out to investigate effects of root of PG on fatty liver inhibition in high fat diet (HFD)-fed C57BL/6 mice. C57BL/6 mice were divided into control, total extract of PG (T-PG, 500 mg/kg) and saponin fraction (S-PG, 50 mg/kg)-treated groups. Significant decreases in body weight, associated with fat mass reduction, were observed in PG-treated groups (<I>p</I><0.05). Hepatic lipid content and score index calculated from morphometric observations on fatty liver were significantly decreased in the PG-treated groups (<I>p</I><0.05). Moreover, activities of fatty acid synthase (FAS) and carnitine palmitoyl-transferase (CPT) were significantly suppressed and increased as compared with the control group, respectively (<I>p</I><0.05). mRNA expressions of the sterol regulatory element binding protein (SREBP1c) and stearoyl-CoA desaturase (SCD1) gene were suppressed in the T-PG and S-PG groups (<I>p</I><0.05). From these findings, we speculate that fatty liver inhibition effects of PG extract and its saponins appear to be conferred by hepatic lipogenesis and acceleration of energy expenditure, along with modulation of liver FAS and CPT activities in HFD-fed C57BL/6 mice.</P>

      • SCIESCOPUSKCI등재

        Clinical Microbiology and Biomedical Sciences : Comparative Proteomic Analyses of Synovial Fluids and Serums from Rheumatoid Arthritis Patients

        ( Ran Noh ),( Sung Goo Park ),( Ji Hyeon Ju ),( Seung Wook Chi ),( Sun Hong Kim ),( Chong Kil Lee ),( Jeong Hoon Kim ),( Byoung Chul Park ) 한국미생물 · 생명공학회 2014 Journal of microbiology and biotechnology Vol.24 No.1

        Rheumatoid arthritis (RA) is a chronic and systemic inflammatory disorder that primarily affects the flexible joints and may also affect a number of tissues and organs. The progression of RA involves an inflammatory response of the capsule around the joint, swelling of synovial cells with excess synovial fluid (SF), and the development of fibrous tissue in the synovium. Since the progressive pathology of the disease often leads to the irreversible destruction of articular cartilage and ankylosis of the joint, early diagnosis of RA is essential. Thus, we undertook a comparative proteomic approach to investigate novel biomarkers for early diagnosis using SFs and serums from RA patients. As a result, we identified 32 differentially expressed spots in SFs and 34 spots in serums. The differential expression of the STEAP4 and ZNF 658 proteins were validated using immunoblotting of the SFs and serums, respectively. These data suggest that differentially expressed proteins in SFs and serums could be used as RA-specific biomarkers for the diagnosis and monitoring of RA. Furthermore, these findings advance our understanding of the molecular etiopathogenesis of RA.

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