Analysis of Scientific Papers Included in the

Background The purpose of our study was to analyze scientific papers published by SouthKorean plastic surgeons in journals included in the Science Citation Index Expanded (SCIE),and to evaluate the publication and research activities of Korean plastic surgeon.Methods We conducted a survey of SCIE papers in the field of plastic surgery published bySouth Korean authors between 2001 and 2010 using Web of Science software. We furtheranalyzed these results according to the number of publications per year, journals, institution,and type of papers. We also compared the total number of citations to published scientificpapers. We analyzed the rank of South Korea among other countries in representative journals.Results Overall, 667 papers were published by South Korean authors between 2001 and 2010.The number of publications increased dramatically from 2003 (n=31) to 2010 (n=139).Subsequently, the ten most productive Korean medical colleges were identified. All publishedpapers received 2,311 citations and the citation to paper ratio was 3.49. The rank of Koreaamong other countries in terms of the number of published papers remained in the top 10during the recent 10 years.Conclusions Publication output of Korean plastic surgeon over the last 10 years showed aremarkable growth in terms of quantity and quality. Currently, Korea is among the top sixcountries in representative plastic surgery journals. Korean plastic surgeons have playeda central role in this progress, and it is anticipated that they will continue to do so in thefuture

Analysis of Scientific Papers Included in the Sciences Citation Index Expanded Written by South Korean Plastic Surgeons: 2001-2010

BackgroundThe purpose of our study was to analyze scientific papers published by South Korean plastic surgeons in journals included in the Science Citation Index Expanded (SCIE), and to evaluate the publication and research activities of Korean plastic surgeon.MethodsWe conducted a survey of SCIE papers in the field of plastic surgery published by South Korean authors between 2001 and 2010 using Web of Science software. We further analyzed these results according to the number of publications per year, journals, institution, and type of papers. We also compared the total number of citations to published scientific papers. We analyzed the rank of South Korea among other countries in representative journals.ResultsOverall, 667 papers were published by South Korean authors between 2001 and 2010. The number of publications increased dramatically from 2003 (n=31) to 2010 (n=139). Subsequently, the ten most productive Korean medical colleges were identified. All published papers received 2,311 citations and the citation to paper ratio was 3.49. The rank of Korea among other countries in terms of the number of published papers remained in the top 10 during the recent 10 years.ConclusionsPublication output of Korean plastic surgeon over the last 10 years showed a remarkable growth in terms of quantity and quality. Currently, Korea is among the top six countries in representative plastic surgery journals. Korean plastic surgeons have played a central role in this progress, and it is anticipated that they will continue to do so in the future

AESIS-1, a Rheumatoid Arthritis Therapeutic Peptide, Accelerates Wound Healing by Promoting Fibroblast Migration in a CXCR2-Dependent Manner

In patients with autoimmune disorders such as rheumatoid arthritis (RA), delayed wound healing is often observed. Timely and effective wound healing is a crucial determinant of a patient’s quality of life, and novel materials for skin wound repair, such as bioactive peptides, are continuously being studied and developed. One such bioactive peptide, AESIS-1, has been studied for its well-established anti-rheumatoid arthritis properties. In this study, we attempted to use the anti-RA material AESIS-1 as a therapeutic wound-healing agent based on disease-modifying antirheumatic drugs (DMARDs), which can help restore prompt wound healing. The efficacy of AESIS-1 in wound healing was assessed using a full-thickness excision model in diabetic mice; this is a well-established model for studying chronic wound repair. Initial observations revealed that mice treated with AESIS-1 exhibited significantly advanced wound repair compared with the control group. In vitro studies revealed that AESIS-1 increased the migration activity of human dermal fibroblasts (HDFs) without affecting proliferative activity. Moreover, increased HDF cell migration is mediated by upregulating chemokine receptor expression, such as that of CXC chemokine receptor 2 (CXCR2). The upregulation of CXCR2 through AESIS-1 treatment enhanced the chemotactic reactivity to CXCR2 ligands, including CXC motif ligand 8 (CXCL8). AESIS-1 directly activates the ERK and p38 mitogen-activated protein kinase (MAPK) signaling cascades, which regulate the migration and expression of CXCR2 in fibroblasts. Our results suggest that the AESIS-1 peptide is a strong wound-healing substance that increases the movement of fibroblasts and the expression of CXCR2 by turning on the ERK and p38 MAPK signaling cascades

Transferrin induces interleukin-18 expression in chronic myeloid leukemia cell line, K-562

Transferrin is an iron carrier protein involved in iron uptake and the regulation of cell growth. Although highly proliferative cells express transferrin and its receptor. little is known about the role of transferrin in the cellular response to cytokine production. The non-iron-bound form of transferrin (apo-transferrin) was administered to human chronic myeloid leukemia cell line, K-562 cells to assess Whether it could induce interleukin-18 (IL-18). Apo-transferrin enhanced IL-18 mRNA and protein and. moreover, IL-18 secretion was increased by treatment with apo-transferrin. In conclusion, apo-transferrin regulates IL-18 expression and we suggest that it is involved in cytokine production. (C) 2008 Elsevier Ltd. All rights reserved.Park S, 2007, CELL MOL IMMUNOL, V4, P329Kim KE, 2007, ONCOGENE, V26, P1468, DOI 10.1038/sj.onc.1209926Jung MK, 2006, IMMUNOL LETT, V107, P125, DOI 10.1016/j.imlet.2006.08.004Kim J, 2006, BIOCHEM BIOPH RES CO, V344, P1284, DOI 10.1016/j.bbrc.2006.04.016Lesnikov VA, 2006, APOPTOSIS, V11, P79, DOI 10.1007/s10495-005-3086-2Gomme PT, 2005, DRUG DISCOV TODAY, V10, P267Bergman M, 2004, CLIN IMMUNOL, V113, P340, DOI 10.1016/j.clim.2004.08.011XIULIAN D, 2004, J CELL PHYSL, V201, P45Zhang B, 2003, LEUKEMIA RES, V27, P813, DOI 10.1016/S0145-2126(03)00005-5Garcia CI, 2003, GLIA, V42, P406, DOI 10.1002/glia.10227Lopez M, 2003, BRIT J HAEMATOL, V120, P829Qian ZM, 2002, PHARMACOL REV, V54, P561Mehindate K, 2001, J NEUROCHEM, V77, P1386Liu BL, 2000, CYTOKINE, V12, P1519He QY, 2000, BIOCHEM J, V350, P909Cho D, 2000, CANCER RES, V60, P2703Munder M, 1998, J EXP MED, V187, P2103Carlevaro MF, 1997, J CELL BIOL, V136, P1375Gu Y, 1997, SCIENCE, V275, P206Yeoman LC, 1996, ONCOL RES, V8, P273KOBUNE M, 1994, HEPATOLOGY, V19, P1468SIRBASKU DA, 1991, BIOCHEMISTRY-US, V30, P7466

Lipo-PGE1 suppresses collagen production in human dermal fibroblasts via the ERK/Ets-1 signaling pathway

<div><p>Dysregulation of collagen production contributes to various pathological processes, including tissue fibrosis as well as impaired wound healing. Lipo-prostaglandin E1 (Lipo-PGE1), a lipid microsphere-incorporated prostaglandin E1, is used as a vasodilator for the treatment of peripheral vascular diseases. Lipo-PGE1 was recently shown to enhance human dermal fibroblast (HDF) migration and <i>in vivo</i> wound healing. No published study has characterized the role of Lipo-PGE1 in collagen regulation in HDFs. Here, we investigated the cellular signaling mechanism by which Lipo-PGE1 regulates collagen in HDFs. Collagen production was evaluated by the Sircol collagen assay, Western blot analysis of type I collagen and real time PCR. Unexpectedly, Lipo-PGE1 decreased mRNA expression of collagen 1A1, 1A2, and 3A1. Lipo-PGE1 markedly inhibited type I collagen and total soluble collagen production. In addition, Lipo-PGE1 inhibited transforming growth factor-β-induced collagen expression via Smad2 phosphorylation. To further investigate whether extracellular signal-regulated kinase (ERK)/Ets-1 signaling, a crucial pathway in collagen regulation, is involved in Lipo-PGE1-inhibited collagen production, cells were pretreated with an ERK-specific inhibitor, PD98059, prior to the addition of Lipo-PGE1. Lipo-PGE1-inhibited collagen mRNA expression and total soluble collagen production were recovered by pretreatment with PD98059. Moreover, Lipo-PGE1 directly induced the phosphorylation of ERK. Furthermore, silencing of Ets-1 recovered Lipo-PGE1-inhibited collagen production and PD98059 blocked Lipo-PGE1-enhanced Ets-1 expression. The present study reveals an important role for Lipo-PGE1 as a negative regulator of collagen gene expression and production via ERK/Ets-1 signaling. These results suggest that Lipo-PGE1 could potentially be a therapeutic target in diseases with deregulated collagen turnover.</p></div

Evaluating the Effectiveness of Cryopreserved Acellular Dermal Matrix in Immediate Expander-Based Breast Reconstruction: A Comparison Study

Background CGCryoDerm was first introduced in 2010 and offers a different matrix preservation processes for freezing without drying preparation. From a theoretical perspective, CGCryoDerm has a more preserved dermal structure and more abundant growth factors for angiogenesis and recellularization. In the current study, the authors performed a retrospective study to evaluate freezing- and freeze-drying-processed acellular dermal matrix (ADM) to determine whether any differences were present in an early complication profile. Methods Patients who underwent ADM-assisted tissue expander placement for two stage breast reconstruction between January of 2013 and March of 2014 were retrospectively reviewed and divided into two groups based on the types of ADM-assisted expander reconstruction (CGDerm vs. CGCryoDerm). Complications were divided into four main categories and recorded as follows: seroma, hematoma, infection, and mastectomy skin flap necrosis. Results In a total of 82 consecutive patients, the CGCryoDerm group had lower rates of seroma when compared to the CGDerm group without statistical significance (3.0% vs. 10.2%, P=0.221), respectively. Other complications were similar in both groups. Reconstructions with CGCryoDerm were found to have a significantly longer period of drainage when compared to reconstructions with CGDerm (11.91 days vs. 10.41 days, P=0.043). Conclusions Preliminary findings indicate no significant differences in early complications between implant/expander-based reconstructions using CGCryoderm and those using CGDerm

Lipo-PGE1 inhibited collagen gene expression and production induced by TGF- β.

<p>(A) HDFs were pretreated with 10 ng/mL TGF-β for 2 h, before addition of 5 ng/mL Lipo-PGE1. After 24 h, total RNA was extracted and real-time RT-PCR was performed. Bars indicate mean ± SD of three independent experiments, each with triplicate samples. *<i>P</i><0.05 <i>vs</i>. control, ^§<i>P</i><0.05 <i>vs</i>. TGF-β-treated group. (B) The total collagen concentration in conditioned medium was determined by the Sircol assay after 48 h of culture. Data are mean ± SD. *<i>P</i><0.05 <i>vs</i>. control, ^§<i>P</i><0.05 <i>vs</i>. TGF-β-treated group. (C) Effects of Lipo-PGE1 on TGF-β-induced type I collagen expression. HDF cells were pretreated with TGF- β (10 ng/ml) for 2 h, and then incubated with 5 ng/mL Lipo-PGE1 for 36 h. Type I collagen production was analyzed by Western blot analysis. (D) Lipo-PGE1 inhibited TGF-β-induced phosphorylation of Smad2. HDF cells were treated with Lipo-PGE1, and then challenged with TGF- β (10 ng/ml). After 36 hours, whole cell lysates were probed with antibodies against Smad2, phospho-Smad2 in Western blots. The band intensities were quantitated and data are mean ± SD. *<i>P</i><0.01 <i>vs</i>. control, ^§<i>P</i><0.01 <i>vs</i>. TGF-β-treated group.</p

Activation of the ERK pathway is involved in Lipo-PGE1-induced collagen inhibition.

<p>(A) HDFs were pretreated with or without a specific inhibitor of ERK1/2 (PD98059) for 1 h and then incubated with 5 ng/mL Lipo-PGE1. Total RNA was extracted and cDNA was synthesized for real-time RT-PCR. Data are mean ± SD of three independent experiments. *<i>P</i><0.05 <i>vs</i>. control; ^§<i>P</i><0.05 <i>vs</i>. Lipo-PGE1-treated group. (B) Cells were pretreated with or without a specific inhibitor of ERK1/2 (PD98059) for 1 h and then treated with 5 ng/mL Lipo-PGE1. Total collagen was determined by the Sircol assay. A representative of three independently performed experiments is shown. <i>Bars</i>, mean ± SE. *<i>P</i><0.05 <i>vs</i>. control, ^§<i>P</i><0.05 <i>vs</i>. Lipo-PGE1-treated group. (C) Cells were treated with 5 ng/mL Lipo-PGE1 for 1 min, 5 min, 10 min, 30 min and 60 min. After cell lysis, the level of ERK1/2 phosphorylation was determined by Western blot analysis. The levels of total ERK were used to confirm equal loading of the cell lysates.</p