Jeong Hun Kim

Seoul National University, Sŏul, Seoul, South Korea

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Publications (157)429.91 Total impact

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    ABSTRACT: The present study aimed to investigate the p53 expression pattern in tumor cells and in mature tumor vascular endothelium of retinoblastoma. Nuclear p53 accumulation was observed in most of the tumor cells in both the human and orthotopic retinoblastoma animal models using SNUOT-Rb1 and Y79 cells. In the orthotopic animal model, some of the tumor vascular endothelium also demonstrated nuclear p53 immunoreactivity, and the ratio of p53 positivity among the total mature tumor vascular endothelium was slightly higher in the Y79 cell model when compared with the SNUOT-Rb1 cell model. In addition, in the human retinoblastoma specimens, 32.9% of the tumor vascular endothelium showed p53 nuclear staining. In conclusion, some of the mature tumor vascular endothelium in both the human and orthotopic models of retinoblastoma share the same cytogenetic abnormality (an abnormal nuclear accumulation of p53) with retinoblastoma cells.
    Oncology reports. 06/2014;
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    ABSTRACT: Nanoparticles can be involved in biological activities such as apoptosis, angiogenesis, and oxidative stress by themselves. In particular, inorganic nanoparticles such as gold and silica nanoparticles are known to inhibit vascular endothelial growth factor (VEGF)-mediated pathological angiogenesis. In this study, we show that anti-angiogenic effect of inorganic nanospheres is determined by their sizes. We demonstrate that 20 nm size gold and silica nanospheres suppress VEGF-induced activation of VEGF receptor-2, in vitro angiogenesis, and in vivo pathological angiogenesis more efficiently than their 100 nm size counterparts. Our results suggest that modulation of the size of gold and silica nanospheres determines their inhibitory activity to VEGF-mediated angiogenesis.
    Nano Research 06/2014; · 7.39 Impact Factor
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    ABSTRACT: In diabetic retinopathy (DR), visual deterioration is related with retinal neovascularization and vascular hyperpermeability. Anti-vascular endothelial growth factor (VEGF) agents are currently utilized to suppress retinal neovascularization and macular edema (ME); however, there are still concerns on the widespread use of them because VEGF is a trophic factor for neuronal and endothelial cells in the retina. As an alternative treatment strategy for DR, it is logical to address hypoxia-related molecules to treat DR because the retina is in relative hypoxia as DR progresses. In this study, we demonstrate that destabilization of hypoxia-inducible factor-1α (HIF-1α) by SH-1242 and SH-1280, novel heat shock protein 90 (hsp90) inhibitors, leads to suppression of hypoxia-mediated retinal neovascularization and vascular leakage in diabetic retina. In vitro experiments showed that these inhibitors inhibited hypoxia-induced upregulation of target genes of HIF-1α and further secretion of VEGF. Furthermore, these inhibitors effectively suppressed expression of target genes of HIF-1α including vegfa in the retina of oxygen-induced retinopathy (OIR) mice. Interestingly, despite hsp90 inhibition, these inhibitors do not induce definite toxicity at the level of gene expression, cellular viability, and histologic integrity. We suggest that SH-1242 and SH-1280 can be utilized in the treatment of DR, as an alternative treatment of direct VEGF inhibition.
    Journal of molecular medicine (Berlin, Germany). 05/2014;
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    ABSTRACT: To analyse clinical characteristics and treatment outcomes of osteosarcoma that developed in survivors of bilateral retinoblastoma. Three institutions participated in this retrospective study. Among survivors of bilateral retinoblastoma who were diagnosed and treated between 1995 and 2012, 8 cases (4 male, 4 female) of osteosarcoma were identified. Medical records were thoroughly reviewed. Median age at diagnosis of bilateral retinoblastoma was 8.5 months (range 1.4-18.4 months). Treatment modalities for retinoblastoma were: enucleation+chemotherapy+radiotherapy (n=6); chemotherapy combined with focal therapy (n=1); and chemotherapy+radiotherapy (n=1). Median radiotherapy dose was 46.5 Gy (range 45-54 Gy). Median age at diagnosis of osteosarcoma was 8.9 years (range 5.4-20.3 years). Median interval between retinoblastoma and osteosarcoma was 8.2 years (range 5.0-20.0 years). Tumour locations were femur (n=5), tibia (n=1), mandible (n=1), and nasal cavity (n=1). Two patients presented with lung metastasis. Seven patients received multimodal treatment, and treatment was refused in 1 patient. After diagnosis of osteosarcoma, the patients were followed for a median of 17.3 months (range 4.4-56.4 months). The 2-year overall survival and event-free survival rates were 56.3±19.9% and 33.3±18.0%, respectively. At the time of analysis, 5 patients remained alive, and 2 of them were on therapy. Of the 3 surviving patients without evidence of disease, 2 received high dose chemotherapy with autologous peripheral blood stem cell support. Our data could be used as a basis for future studies aimed at reaching consensus about long term follow-up and treatment guidelines for this genetically susceptible group of patients.
    The British journal of ophthalmology 05/2014; · 2.92 Impact Factor
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    ABSTRACT: Pericyte loss is an early characteristic change in diabetic retinopathy. Despite accumulating evidences that hyperglycemia induced angiopoietin 2 (Ang2) has a central role in pericyte loss, the precise molecular mechanism has not been elucidated. This study was to investigate the role of Ang2 in pericyte loss in diabetic retinopathy. We demonstrated that pericyte loss occurred with Ang2 increase in the diabetic mice retina, and the source of Ang2 could be endothelial cell. Ang2 induced pericyte apoptosis via p53 pathway under high glucose while Ang2 alone did not induce apoptosis. Integrin, not Tie-2 receptor, was involved for Ang2 induced pericyte apoptosis under high glucose as an Ang2 receptor. High glucose changed integrin expression pattern which increased integrin α3 and β1 in pericyte. Furthermore, in vitro, Ang2 induced pericyte apoptosis was effectively attenuated via p53 suppression by blocking integrin α3 and β1. In vivo, while intravitreal injection of Ang2 induced pericyte loss in C57/BL6 mice retina, intravitreal injection of anti-integrin α3 and β1 antibodies attenuated Ang2 induced pericyte loss. Taken together, Ang2 induced pericyte apoptosis under high glucose via α3β1 integrin. Glycemic control or blocking Ang2/integrin signaling could be a potential therapeutic target to prevent pericyte loss in early diabetic retinopathy.
    Diabetes 04/2014; · 7.90 Impact Factor
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    ABSTRACT: The aim of this study was to evaluate whether the clinical outcomes were associated with socioeconomic status (SES) in patients with acute myocardial infarction (AMI) who underwent percutaneous coronary intervention (PCI). The author analyzed 2,358 patients (64.9 ± 12.3 yr old, 71.5% male) hospitalized with AMI between November 2005 and June 2010. SES was measured by the self-reported education (years of schooling), the residential address (social deprivation index), and the national health insurance status (medical aid beneficiaries). Sequential multivariable modeling assessed the relationship of SES factors with 3-yr major adverse cardiovascular events (MACEs) and mortality after the adjustment for demographic and clinical factors. During the 3-yr follow-up, 630 (26.7%) MACEs and 322 (13.7%) all-cause deaths occurred in 2,358 patients. In multivariate Cox proportional hazards regression modeling, the only lower education of SES variables was associated with MACEs (hazard ratio [HR], 1.41; 95% confidence interval [CI], 1.04-1.91) and mortality (HR, 1.93; 95% CI, 1.16-3.20) in the patients with AMI who underwent PCI. The study results indicate that the lower education is a significant associated factor to increased poor clinical outcomes in patients with AMI who underwent PCI.
    Journal of Korean medical science 04/2014; 29(4):536-43. · 0.84 Impact Factor
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    ABSTRACT: Extracellular deposit of amyloid beta (Aβ) is a common pathologic feature in both age-related macular degeneration (AMD) and Alzheimer's disease, but the role of intracellular Aβ on the tight junction of the retinal pigment epithelium (RPE) is unknown. In this study, we investigated the intracellular Aβ expression and its role on the outer blood retinal barrier in the retina of 5XFAD mice, a mouse model of Alzheimer's disease. The retina of 5XFAD mice showed the pathologic features of AMD with intracellular Aβ in the RPE. As intracellular Aβ accumulated, zonular occludens-1 and occludin were markedly attenuated and lost their integrity as tight junctions in the RPE of 5XFAD mice. Also, Aβ42 uptake by ARPE-19 cells induced the tight junction breakdown of zonular occludens-1 and occludin without cell death. These results implicate that intracellular Aβ42 could play a role in the breakdown of the outer blood retinal barrier in 5XFAD mice. Thus, we suggested that 5XFAD mice could be a mouse model of dry AMD with regard to the Aβ42 related pathology.
    Neurobiology of aging 03/2014; · 5.94 Impact Factor
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    ABSTRACT: Retinal neovascularization in retinopathy of prematurity (ROP) is the most common cause of blindness for children. Despite evidence that hypoxia inducible factor (HIF)-1α -VEGF axis is associated with the pathogenesis of ROP, the inhibitors of HIF-1α have not been established as a therapeutic target in the control of ROP pathophysiology. We investigated the hypothesis that degradation of HIF-1α as a master regulator of angiogenesis in hypoxic condition, using β-lapachone, would confer protection against hypoxia-induced retinopathy without affecting physiological vascular development in mice with oxygen-induced retinopathy (OIR), an animal model of ROP. The effects of β-lapachone were examined after intraocular injection in mice with OIR. Intraocular administration of β-lapachone resulted in significant reduction in hypoxia-induced retinal neovascularization without retinal toxicity or perturbation of developmental retinal angiogenesis. Our results demonstrate that HIF-1α-mediated VEGF expression in OIR is associated with pathological neovascularization, not physiological angiogenesis. Thus, strategies blocking HIF-1α in the developing eye in the pathological hypoxia could serve as a novel therapeutic target for ROP.
    Journal of Cellular and Molecular Medicine 02/2014; · 4.75 Impact Factor
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    ABSTRACT: To evaluate the dose-effect relationship for single muscle advancement in consecutive esotropia and consecutive exotropia. Medical records from 22 patients with consecutive esotropia (n = 11) or exotropia (n = 11) were retrospectively reviewed. All patients had undergone either single lateral rectus or medial rectus advancement surgery. The alterations in muscle position and the angle deviation were measured in millimeters and prism diopters (PD) and the change in deviation was determined by subtracting the postoperative angle of deviation at 1 week from the preoperative angle. To quantify the clinical effect of muscle advancement, the ratio of the change in muscle position to the change in visual angle deviation was calculated (ie, the surgical dose-effect relationship). The mean deviation was 25.5 ± 10.4 PD preoperatively and 0 ± 6.9 PD at 1 week postoperatively. The success rate was 82% in the consecutive esotropia group and 91% in the consecutive exotropia group. The average correction ratio was 4.31 ± 0.96 PD/mm. In multiple regression analysis of total patients with consecutive strabismus and the consecutive esotropia group, the amount of muscle advancement and preoperative angle deviation were positively correlated with the correction ratio. In the consecutive exotropia group, there was no significant relationship between variables. Single muscle advancement generally provides enough correction for most consecutive strabismus cases. Surgical dose-effect relationship increases with preoperative angle deviation and amount of muscle advancement. Surgeons should consider reducing the amount of muscle advancement in patients with larger angle deviations, especially patients with consecutive esotropia. [J Pediatr Ophthalmol Strabismus 20XX;XX:XX-XX.].
    Journal of Pediatric Ophthalmology & Strabismus 02/2014; · 0.86 Impact Factor
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    ABSTRACT: To investigate the effect of protein kinase C (PKC)-ζ inhibition on vascular leakage in diabetic retinopathy, streptozotocin-induced diabetic mice were intravitreously injected with siPKC-ζ. According to the fluorescein angiography of the retinal vessels, suppression of PKC-ζ effectively attenuated vascular leakage in diabetic retina. Further evaluation on the retina with western blot analysis and immunohistochemistry revealed accompanying restoration of tight junction proteins on retinal vessels. As two major contributors to vascular leakage in diabetic retinopathy, vascular endothelial growth factor (VEGF) and advanced glycation end products (AGEs) were investigated on the tight junction protein expression in endothelial cells. Inhibition of PKC-ζ attenuated VEGF-induced decrease of tight junction proteins and accompanying hyperpermeability in human retinal microvascular endothelial cells (HRMECs). PKC-ζ inhibition also attenuated AGE-induced decrease of tight junction proteins in HRMECs. Our findings suggest that inhibition of PKC-ζ could be an alternative treatment option for compromised blood-retinal barrier in diabetic retinopathy.
    Biochemical and Biophysical Research Communications 01/2014; · 2.28 Impact Factor
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    ABSTRACT: Angiogenesis-related blindness (ARB) includes age-related macular degeneration, diabetic retinopathy, and retinopathy of prematurity, all of which are based on pathologic angiogenesis. Current treatment options such as surgery, laser photocoagulation, and steroid have shown limitations because they do not directly resolve the pathologic events in the retina. Furthermore, recently approved and developed therapeutic drugs only focus on direct inhibition of growth factors and suppression of downstream signaling molecules of activated receptor proteins by orthosteric ligands. In this regard, allosteric regulation of receptors and ligands can be a valuable mechanism in the development of novel drugs for ARB. In this review, we briefly address the clinical significance of ARB for further discussion on allosteric regulation of pathologic angiogenesis for ARB. Interestingly, key molecules in the pathogenesis of ARB can be targets for allosteric regulation, sharing characteristics as allosteric proteins. With investigation of allostery by introducing well-established models for allosteric proteins and currently published novel allosteric modulators, we discuss the potential of allosteric regulation for ARB. In conclusion, we hope that allosteric regulation of pathologic angiogenesis in ARB can open new opportunities for drug development.
    Archives of Pharmacal Research 01/2014; · 1.54 Impact Factor
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    ABSTRACT: Age-related macular degeneration and diabetic retinopathy are leading causes of blindness. Vascular endothelial growth factor (VEGF) is known to be the main factor that induces pathological angiogenesis in these diseases. In this study, we investigate the therapeutic potential and safety profiles of high-affinity peptides targeting VEGF which are identified using an 'aptide' technology. We show that two VEGF-binding aptides, APTVEGF1 and APTVEGF2, demonstrate high binding affinity and specificity to VEGF. Furthermore, they suppress VEGF-induced activation of VEGF receptor-2, in vitro angiogenesis, and in vivo pathological choroidal and retinal neovascularization. Despite potent anti-angiogenic effects, both VEGF-binding aptides do not induce any definite toxicity at the level of cellular viability, histological integrity, and gene expression. Our data show the therapeutic potential of VEGF-binding peptides for the treatment of choroidal and retinal neovascularization.
    Biomaterials 01/2014; · 8.31 Impact Factor
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    ABSTRACT: In this study, we demonstrate that titanium dioxide nanoparticles suppress pathologic angiogenesis without definite toxicity. Titanium dioxide nanoparticles inhibited in vitro angiogenic processes and in vivo retinal neovascularization. Nevertheless, they did not induce significant toxicity at the level of gene expression, cellular viability, histologic integrity, and apoptotic activity. In general, local administration requires fewer nanoparticles than systemic application. Local delivery can be a safer platform to utilize nanoparticles for therapeutic uses.
    Nanomedicine: nanotechnology, biology, and medicine 01/2014; · 6.93 Impact Factor
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  • Byung Joo Lee, Jeong Hun Kim, Young Suk Yu
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    ABSTRACT: To address the surgical outcomes of pediatric patients with cataracts associated with posterior lenticonus who required cataract extraction and intraocular lens (IOL) implantation according to preoperative lens status. Department of Ophthalmology, Seoul National University Children's Hospital, Seoul, South Korea. Comparative case series. Patients who had cataract extraction and IOL implantation for posterior lenticonus were divided into 2 groups according to the preoperative lens status. Clinical features and visual outcomes in both groups were comparatively analyzed. Forty-seven eyes of 43 patients were studied. Thirty-five eyes had lens opacities localized to the posterior pole, and 12 eyes presented with total opacity of the lens. Preexisting posterior capsule defect was identified intraoperatively in 11 eyes with total lens opacity. Eyes with preexisting posterior capsule defects more frequently required ciliary sulcus fixation of the IOL (P=.01). The mean follow-up after cataract extraction was 66.9 months ± 35.9 (SD). The mean final corrected distance visual acuity of patients with total opacity (0.37 ± 0.57 logMAR) was better than that of patients with posterior polar opacity (0.56 ± 0.50 logMAR), with borderline significance (P=.05). A preexisting posterior capsule defect, found most often in eyes that presented with total lens opacity, could be an obstacle to capsular bag fixation of the IOL. Posterior lenticonus patients with total lens opacity had marginally significantly better visual outcomes than patients with posterior polar opacity. No author has a financial or proprietary interest in any material or method mentioned.
    Journal of Cataract and Refractive Surgery 12/2013; · 2.75 Impact Factor
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    ABSTRACT: Ninjurin1 is a homotypic adhesion molecule that contributes to leukocyte trafficking in experimental autoimmune encephalomyelitis (EAE), an animal model of Multiple sclerosis (MS). However, in vivo gene-deficiency animal studies have not yet been done. Here, we constructed Ninjurin1 knockout (KO) mice and investigated the role of Ninjurin1 on leukocyte trafficking under inflammation conditions such as EAE and endotoxin-induced uveitis (EIU). Ninjurin1 KO mice attenuated EAE susceptibility by reducing leukocyte recruitment into the injury regions of the spinal cord and showed less adhesion of leukocytes on inflamed retinal vessels in EIU mice. Moreover, the administration of a custom-made antibody (Ab26-37) targeting the Ninjurin1 binding domain ameliorated the EAE symptoms, showing the contribution of its adhesion activity to leukocyte trafficking. In addition, we addressed the transendothelial migration (TEM) activity of bone-marrow derived macrophages (BMDMs) and Raw264.7 cells according to the expression level of Ninjurin1. TEM activity was decreased in Ninjurin1 KO BMDMs and siNinj1 Raw264.7 cells. Consistent with this, GFP-tagged mNinj1 overexpressing Raw264.7 cells increased their TEM activity. Taken together, we have clarified the contribution of Ninjurin1 to leukocyte trafficking in vivo and delineated its direct functions to TEM, emphasizing Ninjurin1 as a beneficial therapeutic target against inflammatory diseases such as MS.
    Journal of Biological Chemistry 12/2013; · 4.65 Impact Factor
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    ABSTRACT: Blood vessels exhibit highly regulated barrier function allowing selective passage of macromolecules. Abnormal vascular permeability caused by disorder in barrier function is often associated with various pathological states such as tumor progression or pulmonary fibrosis. There are no realistic in vitro models for measuring vascular permeability as most models are limited in mimicking anatomical structural properties of in vivo vessel barriers. This paper presents a reliable microfluidics-based chip for measuring permeability by engineering tubular perfusable microvessels. This platform is compatible with high resolution, live-cell time-lapse imaging and high throughput permeability measurements. The microvessels were formed by natural angiogenic process and thus exhibit reliable barrier properties with permeability coefficient of 1.55×10(-6)cm/s (for 70 kD FITC-dextran). The bioengineered microvessels showed properties similar to in vivo vessels in terms of cell-cell junction expression (ZO-1, Claudin-5 and VE-cadherin) and response to agonists such as histamine and TNF-α. We showed that hyperpermeability of the tumor microvessel could be normalized with anti-VEGF (bevacizumab) treatment, consistent with the mechanism of action for bevacizumab. The method developed here provide a relatively simple, robust method for assessing drug effects on permeability of microvessels with a number of potential applications in fundamental vascular biology as well as drug screening.
    Microvascular Research 12/2013; · 2.93 Impact Factor
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    ABSTRACT: The hyaloid vessel is a transient vascular network that nourishes the lens and the primary vitreous in the early developmental periods. In hyaloid vessels devoid of the support of astrocytes, we demonstrate that tight junction proteins, zonula occludens-1 and occludin, are regularly expressed at the junction of endothelial cells. To figure out the factor influencing the formation of tight junctions in hyaloid vessels, we further progress to investigate the interactions between endothelial cells and pericytes, two representative constituent cells in hyaloid vessels. Interestingly, endothelial cells interact with pericytes in the early postnatal periods and the interaction between two cell types provokes the up-regulation of transforming growth factor β1. Further in vitro experiments demonstrate that transforming growth factor 1 induces the activation of Smad2 and Smad3 and the formation of tight junction proteins. Taken together, in hyaloid vessels, pericytes seem to regulate the formation of tight junctions by the interaction with endothelial cells even without the support of astrocytes. Additionally, we suggest that the hyaloid vessel be a valuable system that can be utilized for the investigation of cell-cell interaction in the formation of tight junctions in developing vasculatures.
    Molecules and Cells 11/2013; · 2.21 Impact Factor
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    ABSTRACT: Clusterin is a cytoprotective chaperone protein that is known to protect various retinal cells. It was also reported to be overexpressed in several types of malignant tumors, whose chemoresistance correlates with the expression of clusterin. Herein, we investigated the effect of clusterin on cisplatin-induced cell death of retinoblastoma cells. Firstly, evaluation of clusterin expression demonstrated that it was highly expressed in human retinoblastoma tissues and cell lines (SNUOT-Rb1 and Y79) particularly in the area between viable cells around vessels and necrotic zones in the relatively avascular area in human retinoblastoma tissues. Furthermore, the effects of cisplatin on retinoblastoma cells were evaluated. Cisplatin (1 µg/ml) significantly affected cell viability of SNUOT-Rb1 cells by inducing caspase-3-dependent apoptosis. Notably, the cell death due to cisplatin was prevented by 5 µg/ml of clusterin administered 4 h prior to cisplatin treatment by inhibiting cisplatin-induced apoptosis. Furthermore, overexpression of clusterin exerted its anti-apoptotic effect on cisplatin-induced apoptosis, and effectively prevented cisplatin-induced cell death. These data suggest that clusterin, found to be expressed in human retinoblastoma, may exert anti-apoptotic effects on cisplatin-induced apoptosis and prevent cell death. Therefore, clusterin can contribute to cisplatin resistance of retinoblastoma.
    Oncology Reports 10/2013; · 2.30 Impact Factor
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    ABSTRACT: Abstract Background: Adoption of smart devices for hospital use has been increasing with the development of health applications (apps) for patient point-of-care and hospital management. To promote the use of health apps, we describe the lessons learned from developing 12 health apps in the largest tertiary hospital in Korea. Materials and Methods: We reviewed and analyzed 12 routinely used apps in three categories-Smart Clinic, Smart Patient, and Smart Hospital-based on target users and functions. The log data for each app were collected from the date of release up until December 2012. Results: Medical personnel accessed a mobile electronic medical record app classified as Smart Clinic an average of 452 times per day. Smart Hospital apps are actively used to communicate with each other. Patients logged on to a mobile personal health record app categorized as Smart Patient an average of 222 times per day. As the mobile trend, the choice of supporting operating system (OS) is more difficult. By developing these apps, a monitoring system is needed for evaluation. Conclusions: We described the lessons learned regarding OS support, device choice, and developmental strategy. The OS can be chosen according to market share or hospital strategic plan. Smartphones were favored compared with tablets. Alliance with an information technology company can be the best way to develop apps. Health apps designed for smart devices can be used to improve healthcare. However, to develop health apps, hospitals must define their future goals and carefully consider all the aspects.
    Telemedicine and e-Health 08/2013; · 1.40 Impact Factor

Publication Stats

1k Citations
429.91 Total Impact Points


  • 2008–2014
    • Seoul National University
      • • Department of Ophthalmology
      • • Research Institute of Pharmaceutical Sciences
      Sŏul, Seoul, South Korea
    • Korea Research Institute of Standards and Science
      Daiden, Daejeon, South Korea
    • Anyang University
      Chemulpo, Incheon, South Korea
  • 2003–2014
    • Seoul National University Hospital
      • Department of Ophthalmology
      Sŏul, Seoul, South Korea
  • 2006–2013
    • Korea University
      • • Department of Biomedical Engineering
      • • Department of Food Bioscience and Technology
      • • Department of Electrical Engineering
      Seoul, Seoul, South Korea
  • 2005–2013
    • Yonsei University
      • • Department of Biotechnology
      • • Department of Biochemistry
      Seoul, Seoul, South Korea
  • 2012
    • Inje University
      Kŭmhae, South Gyeongsang, South Korea
    • University of Michigan
      • Life Sciences Institute
      Ann Arbor, MI, United States
  • 2011–2012
    • Inje University Paik Hospital
      • Department of Ophthalmology
      Goyang, Gyeonggi, South Korea
  • 2009–2012
    • Chonnam National University
      • Department of Cardiology
      Gwangju, Gwangju, South Korea