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PURPOSE Although there have been studies emphasizing the re-education of North Korean (NK) doctors for post-unification of the Korean Peninsula, study on the content and scope of such re-education has yet to be conducted. Researchers intended to set the content and scope of re-education by a comparative analysis for the scores of the preliminary examination, which is comparable to the Korean Medical Licensing Examination (KMLE). METHODS The scores of the first and second preliminary exams were analyzed by subject using the Wilcoxon signed rank test. The passing status of the group of NK doctors for KMLE in recent 3 years were investigated. The multiple-choice-question (MCQ) items of which difficulty indexes of NK doctors were lower than those of South Korean (SK) medical students by two times of the standard deviation of the scores of SK medical students were selected to investigate the relevant reasons. RESULTS The average scores of nearly all subjects were improved in the second exam compared with the first exam. The passing rate of the group of NK doctors was 75%. The number of MCQ items of which difficulty indexes of NK doctors were lower than those of SK medical students was 51 (6.38%). NK doctors' lack of understandings for Diagnostic Techniques and Procedures, Therapeutics, Prenatal Care, and Managed Care Programs was suggested as the possible reason. CONCLUSION The education of integrated courses focusing on Diagnostic Techniques and Procedures and Therapeutics, and apprenticeship-style training for clinical practice of core subjects are needed. Special lectures on the Preventive Medicine are likely to be required also.

The role of eating frequency (EF) in obesity development has been debated, and few studies have investigated Asian populations. Diet quality might affect the association between EF and obesity. Therefore, we investigated the association between EF and obesity indicators in a representative sample of Korean adults with consideration to diet quality. This cross-sectional study used data of 6951 participants aged 19–93 years (male 49·8 %, female 50·2 %) from the Fourth Korean National Health and Nutrition Examination Survey. EF was assessed using a questionnaire, and diet quality was defined as mean adequacy ratio (MAR). To explore the association between EF and obesity indicators, we used multiple linear regression analyses with and without interaction terms between diet quality and EF. EF was inversely associated with each obesity indicator, including body fat percentage (BF%), BMI and waist circumference (WC), showing a significant linear trend (PPvalue of the interaction term EF×diet quality=0·008 in the regression model for BF%

Purpose Plasma lipoprotein-associated phospholipase A₂ (Lp-PLA₂) binds to low-density lipoprotein. The levels of Lp-PLA₂ reflect the plaque burden, and are upregulated in acute coronary syndrome (ACS). We investigated the diagnostic value of Lp-PLA2 levels and found that it might be a potential biomarker for ACS. Materials and methods We classified 226 study participants into three groups: patients without significant stenosis (control group), patients with significant stenosis with stable angina (SA group), and patients with ACS (ACS group). Results Lp-PLA₂ and high-sensitivity C-reactive protein (hs-CRP) levels were significantly greater in the ACS group than in the SA group (p=0.044 and p=0.029, respectively). Multivariate logistic regression analysis revealed that Lp-PLA₂ levels are significantly associated with ACS (odds ratio=1.047, p=0.013). The addition of Lp-PLA₂ to the ACS model significantly increased the global χ² value over traditional risk factors (28.14 to 35.602, p=0.006). The area under the receiver operating characteristic curve for Lp-PLA₂ was 0.624 (p=0.004). The addition of Lp-PLA₂ level to serum hs-CRP concentration yielded an integrated discrimination improvement of 0.0368 (p=0.0093, standard error: 0.0142) and improved the ability to diagnose ACS. Conclusion Lp-PLA₂ levels are related to plaque stability and might be a diagnostic biomarker for ACS.

The anatomical location and somatotopic organization of the corticospinal tract (CST) in the corona radiata (CR) of the normal human brain have not been studied using diffusion tensor tractography so far. In this study, the anatomical location and somatotopic organization of the CST in the CR were evaluated by determining the highest probabilistic locations and distances between the upper and lower extremities in the slices of upper and lower CR in the brain. In the mediolateral direction, the average of the highest probabilistic locations for the upper and lower extremities were 40.27 and 37.16% at the upper CR level and 38.19 and 37.14% at the lower CR level, respectively. In the anteroposterior direction, the average of the highest probabilistic locations for the upper and lower extremities were 62.52 and 75.65% at the upper CR level and 60.19 and 68.12% at the lower CR level, respectively. The average distances between upper and lower extremities for the mediolateral direction were 2.41 mm at the upper CR level and 1.21 mm at the lower CR level. The average distances between upper and lower extremities for the anteroposterior direction were 5.23 mm at the upper CR level and 4.47 mm at the lower CR level, respectively. Our findings suggest that the anatomical location and somatotopic organization for the upper extremity are located anterolaterally to the lower extremity in the CR of a normal human brain and distances between the upper and lower extremities become decreased as the CST descends from the upper to the lower CR level.

Many studies have shown that asthma and obesity are linked and affect each other. Although obesity is an important risk factor for asthma, it is controversial whether asthma is a risk factor for obesity vice versa. Recent United States and European cohort studies have published papers reporting that pediatric asthma is a risk factor for obesity in school-aged children or adolescents. Previous studies have shown inconsistent results, suggesting that the 2 diseases are highly complex and that the relationships between them are strong. In order to understand the relationships between the 2 diseases, it is necessary to approach them from a new point of view such as energy metabolism relevance or autonomic nervous system control. (Allergy Asthma Respir Dis 2019;7:73-77)

Objective— Cardiac valvular endothelium is unique in its ability to undergo endothelial-to-mesenchymal transformation, a differentiation process that is essential for valve development and has been proposed as mechanism for replenishing the interstitial cells of mature valves. We hypothesized that the valvular endothelium contains endothelial cells that are direct precursors to osteoblastic valvular interstitial cells (VICs). Methods and Results— Clonal cell populations from ovine mitral valve leaflets were isolated by single cell plating. Mitral valvular endothelial and mesenchymal clones were tested for osteogenic, adipogenic, and chondrogenic differentiation, determined by the expression of lineage-specific markers. Mitral valvular endothelial clones showed a propensity for osteogenic, as well as chondrogenic differentiation that was comparable to a mitral valvular VIC clone and to bone marrow–derived mesenchymal stem cells. Osteogenic differentiation was not detected in nonvalvular endothelial cells. Regions of osteocalcin expression, a marker of osteoblastic differentiation, were detected along the endothelium of mitral valves that had been subjected in vivo to mechanical stretch. Conclusion— Mitral valve leaflets contain endothelial cells with multilineage mesenchymal differentiation potential, including osteogenic differentiation. This unique feature suggests that postnatal mitral valvular endothelium harbors a reserve of progenitor cells that can contribute to osteogenic and chondrogenic VICs.

Small cell lung cancer (SCLC) is the leading cause of cancer death, with a high propensity for aggressiveness and metastasis even in an early stage. Thus, identification of biomarkers as early diagnostics and treatment is needed. In this study, we investigated differentially regulated proteins between human SCLC tissues and normal bronchial epithelium by proteomic analysis using two-dimensional electrophoresis (2-DE) and MALDI-TOF mass spectrometry. Seven proteins and protein isoforms, including, γ-actin, tubulin α-1B, laminin B1, coactosin-like protein-1 (COTL-1), ubiquitin carboxyl-terminal esterase L1, ubiquitin-conjugating enzyme E2-25K, and carbonic anhydrase 1, were up-regulated more than 2 fold in SCLC tissues. In particular, up-regulated COTL-1 expression was validated by Western blot analysis, immunohistochemistry, and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Moreover, most SCLC tissues (93%; 28/30) were COTL-1-positive in immunohistochemistry, whereas only 16% (10/64) of nonsmall cell lung cancer (NSLC) tissues were. Taken together, this SCLC proteomic data may help in establishing a human SCLC proteome database. COTL-1 may be a biomarker or a therapeutic target in SCLC patients.

It is not clear whether the fornix and cingulum are involved in cognition after putaminal hemorrhage (PH). We investigated structural changes and differences of the neural tracts, and the relationship between the integrity of the neural tracts and cognition not only at the affected but also at the unaffected side. Sixteen patients with left chronic putaminal hemorrhage and 20 healthy volunteers were enrolled. Using diffusion tensor tractography (DTT), we compared fiber number (FN), fractional anisotropy (FA), and apparent diffusion coefficient (ADC) of the neural tracts between patient and control groups. The relationship between the neural tract parameters and neuropsychological results was also analyzed. The left fornix FN was significantly lower than the right fornix FN in the patient group. Except for the cingulum FA, the neural tracts parameters for both the affected and unaffected hemispheres differed significantly between the groups. The fornix FA and ADC at the affected side were significantly correlated with intelligence quotient (IQ), mini-mental status examination (MMSE), and short-term memory. Interestingly, the fornix ADC at the unaffected side was significantly correlated with MMSE. However, none of the cingulum parameters was correlated with neuropsychological results. The fornix integrity is critical for cognitive impairment after putaminal hemorrhage.

Purpose: The purpose of this study is to evaluate the changing pattern of communication skills of medical students according to length and methods of training. Methods: We evaluated a 1-week communications training course in 2003, a 1-year course in 2004, and a 1-semester course in 2005 during development of our curriculum. We have conducted the 10-minute CPX on abdominal pain annually since 2002 to assess the clinical performance of medical students who have completed the 3rd year clerkship. We selected CPX videos that were appropriate for assessment. One hundred sixty-four videos were available (1-week didactics: 42 cases, 1-week training: 28 cases, 1-semester training: 50 cases, 1-year training: 44 cases). We developed a 10-item global rating checklist to assess communication skills. A 5-point Likert scale was used to evaluate each item (4-very likely, 0-least likely). Two expert standardized patient (SP) raters evaluated the communication skills of students independently. We analyzed the outcomes based on the training length and methods. The reliability (G coefficient) was 0.825 with 2 SPs and 1 station. Results: The communication skills of students improved with practice and longer training, especially with regard to opening the interview, expressing empathy, understanding the patient's perspective, and preparing for the physical examination. Rapport-building, organization of the interview, understandable explanation, nonverbal communication, active listening and consideration during the physical examination was unchanged between durations of training. The scores for empathetic expression, active listening and understanding the patient's perspective were low across all groups. Conclusion: We should concentrate our efforts to improve students' skills in empathetic expression, active listening and understanding the patient's perspective.

Background Recently, conventional interviews have been replaced with the multiple mini-interviews (MMI) for medical student selection in Korea. We first introduced the MMI as a new admissions tool in Korea. The aim of this study is to determine whether the MMI accurately predicts academic achievement on both written and performance-based examinations during the first 2 years of medical school. Methods The original scores of each station were standardized to T-scores in the candidates group. Three cohorts of students were included depending upon the year they entered medical school. Pearson’s correlations were calculated to estimate the correlations between MMI scores and academic achievements. Additional correlated factors were run through multiple stepwise linear regression analysis to estimate predictive validity. Results There were no differences between T-scores or grade point averages (GPA) among the cohorts. The correlation coefficients between total MMI scores and academic achievement in Year 1 and the Year 2 performance-based examinations ranged from 0.17 to 0.43. Station 1 significantly predicted academic achievement over the second year. Station 3 significantly predicted only performance-based examination performance over the second year. Conclusion MMI is a useful tool to assist with medical student selection. In particular, critical thinking, professionalism, and presentation and communication skills may be meaningful topics for predicting academic achievements, especially in performance-based subjects.

Background Medical students are usually under more stress than that experienced by non-medical students. Stress testing tools for Korean medical students have not been sufficiently studied. Thus, we adapted and modified the East Asian Student Stress Inventory (EASSI), a stress testing tool for Korean students studying abroad, and verified its usefulness as a stress test in Korean university students. We also compared and analyzed stress levels between medical and non-medical students. Methods A questionnaire survey was conducted on medical and non-medical students of a national university, and the responses of 224 students were analyzed for this study. Factor analysis and reliability testing were performed based on data collected for 25 adapted EASSI questions and those on the Korean version of the Global Assessment of Recent Stress Scale (GARSS). A correlation analysis was performed between the 13 modified EASSI questions and the GARSS, and validity of the modified EASSI was verified by directly comparing stress levels between the two student groups. Results The 13 questions adapted for the EASSI were called the modified EASSI and classified into four factors through a factor analysis and reliability testing. The Pearson's correlation analysis revealed a significant correlation between the modified EASSI and the Korean version of the GARSS, suggesting a complementary strategy of using both tests. Conclusion The validity and reliability of the EASSI were verified. The modified Korean EASSI could be a useful stress test for Korean medical students. Our results show that medical students were under more stress than that of non-medical students. Thus, these results could be helpful for managing stress in medical students.

In situ analysis of fetal semilunar valve leaflets has revealed cells coexpressing endothelial and mesenchymal markers along the endothelium, with diminished frequency seen in adult valves. To determine whether such cells are progenitor cells, we isolated clonal populations from human pulmonary valves. The clones expressed endothelial markers but showed potential to further differentiate into endothelium in response to vascular endothelial growth factor (VEGF)-A. When exposed to transforming growth factor (TGF)-β 2 , individual clones adopted a mesenchymal phenotype to varying degrees and expressed markers of endothelial to mesenchymal transformation (EMT). Both VEGF- and TGFβ 2 –induced phenotypic changes were partially reversible, indicating the plasticity of these cells. When challenged with VEGF or TGFβ 2 , a hierarchy of endothelial/mesenchymal potential could be seen among the clonal populations: cells initially closer to an endothelial phenotype showed a strong response to TGFβ 2 that could be inhibited by VEGF, whereas cells closer to a mesenchymal phenotype responded to TGFβ 2 but were resistant to endothelial-inducing effects of VEGF. These findings suggest the presence of bipotential valve progenitor cells with ability to differentiate into either endothelial or interstitial cells of the valve leaflet. Understanding the differentiation potential and function of these cells may be important for understanding heart valve disease and may also be applied to current paradigms for creating tissue-engineered heart valves.

This study was done to verify the validity and the reliability of the newly developed Computerized Dementia Screening Test (CDST) to be easily used in the primary care setting of Korea.Comparison of the results of CDST between 103 healthy control subjects and 41 patients who were diagnosed as having mild cognitive impairment or early dementia, having a clinical dementia rate of 0.5-1 from one health examination center and two neurology clinics in university hospitals.In order to estimate the criterion-related validity, logistic regression analysis for dementia was done using the four individual test results of CDST, age and educational level. The correlation between Korean Mini-Mental State Examination (K-MMSE) and the predicted probability of mild cognitive impairment and early dementia from the logistic regression was measured to verify its validity. The reliability of CDST was measured by test-retest reliability.The sensitivity and specificity of CDST were 75.6% and 94.2%, respectively, if the cut-off point was set to be 0.5 in the logistic regression model. The Pearson's Correlation Coefficient between K-MMSE and the predicted probability of mild cognitive impairment and early dementia from the logistic regression analysis was 0.59 (P0.001). The overall test-retest reliability using the predicted probability of dementia from the logistic regression analysis of CDST was 0.89 (P=0.01).The validity and reliability of CDST is adequate for use as a screening tool to identify mild cognitive impairment and early dementia in Korean primary care.

When the monocyte infiltrates a tissue, adhesion to the extracellular matrix provides structural anchors, and the cell may be deformed through these attachments. To test the hypothesis that human monocytes/macrophages are mechanically responsive, we studied the effects of small cyclic mechanical deformations on cultured human monocytes/macrophages. When monocytes/macrophages were subjected to 4% strain at 1 Hz for 24 hours, neither matrix metalloproteinase (MMP)-1 nor MMP-3 was induced; however, in the presence of phorbol myristate acetate, strain augmented MMP-1 expression by 5.1 ± 0.7-fold (P < 0.05) and MMP-3 expression by 1.6 ± 0.1-fold (P < 0.05). In contrast, MMP-9 expression was not changed by mechanical strain in the presence or absence of phorbol myristate acetate. Deformation rapidly induced the immediate early response genes c-fos and c-jun. In addition, mechanical deformation induced the transcription factor PU.1, an ets family member that is essential in monocyte differentiation, as well as mRNA for the M-CSF receptor. These studies demonstrate that human monocytes/macrophages respond to mechanical deformation with selective augmentation of MMPs, induction of immediate early genes, and induction of the M-CSF receptor. In addition to enhancing the proteolytic activity of macrophages within repairing tissues, cellular deformation within tissues may play a role in monocyte differentiation.

Mechanical forces and biochemical stimuli may interact to regulate cellular responses. In this study, we tested the hypothesis that very small mechanical strains interact with growth factors in the regulation of matrix metalloproteinase (MMP)-1. Human vascular smooth muscle cells (VSMCs) were cultured on a precoated silicone membrane in a device that imposes a highly uniform biaxial strain. VSMCs cultured on fibronectin were treated with cyclic 1-Hz strains of 0, 1, or 4%, and MMPs were assayed by Western analysis or gelatin zymography. Small strains did not induce MMP-1 in VSMCs, but strain was a potent inhibitor of platelet-derived growth factor (PDGF)- or tumor necrosis factor-alpha-induced synthesis of MMP-1. In contrast, MMP-2 and TIMP-2 levels were not changed by PDGF and/or mechanical strain. VSMCs strained on the 120-kDa chymotryptic fragment of fibronectin or RGD peptides suppressed PDGF-induced expression of MMP-1, indicating that this effect is not mediated by the heparin-binding domain or connecting segment-1 of fibronectin. Northern analysis of ets-1, a transcriptional activator of MMP-1 expression, showed that strain down-regulated ets-1 expression, whereas c-fos expression was augmented. Thus, small deformations can selectively suppress MMP-1 synthesis by VSMCs, demonstrating the exquisite sensitivity of the cell to mechanical stimuli.

Background Since the generation of reactive oxygen species (ROS) and release of inflammatory mediators play a major role in UVB-induced inflammation, vigorous attempts have been made for the pharmacological management of these molecules as well as for uncovering the molecular signaling pathways. Homoisoflavanone (5,7-dihydroxy-3-(3-hydroxy-4-methoxybenzyl)-chroman-4-one, HIF) extracted from Cremastra appendiculata has anti-angiogenic activities, but its effect on inflammation was unknown. Objective To investigate the anti-inflammatory effects of HIF on the skin and the underlying molecular mechanisms. Methods HaCaT cells were irradiated by UVB (10 mJ/cm 2 ) with or without HIF. Prostaglandin E 2 (PGE 2 ) level was measured by enzyme immunoassay. Activation of MAPK and production of cyclooxygenase-2 (COX-2) were determined by Western blot analysis. Localization of nuclear factor kappa B (NF-κB) was assessed by immunofluorescence microscopy. Hairless mice were stimulated with UVB or chemical stimulants to induce inflammatory responses in skin. Results Pretreatment with HIF inhibited the production of intracellular ROS induced by UVB irradiation in HaCaT cells. Further analysis revealed a decrease in the level of MAPK activation and down-regulation of COX-2 expression. In addition, HIF attenuated the nuclear localization of NF-κB, resulting in the suppression of inflammatory molecules such as IL-6, IL-8, and TNF-α. Finally, topical treatment with HIF inhibited ear edema induced by UVB, 12- O -tetradecanoylphorbol-13-acetate (TPA), arachidonic acid (AA), or croton oil. Conclusion HIF has a strong protective effect against proinflammatory responses, implying the possibility of preventive application for inflammatory skin diseases.

Capsiate, one of the major capsaicinoids, is nonpungent and present in sweet pepper. We investigated the effects of capsiate on the ultraviolet B (UVB)-induced inflammatory response in skin and its molecular mechanisms. Capsiate-pretreated human keratinocytes inhibited intracellular reactive oxygen species (ROS), which activate the mitogen-activated protein kinase and nuclear factor-kappaB (NF-kappaB) pathways. Therefore, we determined the effects of capsiate on these pathways. Capsiate inhibited UVB-induced cyclooxygenase-2 (COX-2) expression, extracellular signal-related kinase 1/2 phosphorylation, nuclear translocation of NF-kappaB, and the expression of proinflammatory cytokines and potent angiogenic factors, including vascular endothelial cell growth factor and matrix metalloproteinase-2 (MMP-2) and MMP-9. In addition, capsiate inhibited UVB-induced epidermal growth factor receptor (EGFR) activation, which reduces the levels of proinflammatory cytokines and angiogenic factors. We also investigated the photoprotective effects of capsiate in vivo. Topical treatment with capsiate significantly decreased UVB-induced skin damage and inhibited the expression of COX-2, proinflammatory cytokines, and angiogenic factors, including platelet/endothelial cell adhesion molecule-1 and intercellular adhesion molecule-1. Inhibition of Src kinase activity and ROS may inhibit the EGFR activation. Therefore, capsiate may protect the skin from UVB-induced adverse effects and these results provide a molecular basis for understanding its effects on inflammation and angiogenesis.

We have reported that vascular endothelial growth factor (VEGF)-A induces the proliferation of human pulmonary valve endothelial cells (HPVECs) through nuclear factor in activated T cells (NFAT)c1 activation [1]. Here we show that VEGF-A increases the migration of HPVECs through NFATc1 activation, suggesting that VEGF-A/NFATc1 regulates the migration of HPVECs. To learn how this pathway may be involved in post-natal valvular repair, HPVECs were treated with VEGF-A, with or without cyclosporine A to selectively block VEGF–NFATc1 signaling. Down Syndrome critical region 1 (DSCR1) and heparin-binding EGF-like growth factor (HB-EGF) are two genes identified by DNA microarray as being up-regulated by VEGF-A in a cyclosporine-A-sensitive manner. DSCR1 silencing increased the migration of ovine valve endothelial cells, whereas HB-EGF silencing inhibited migration. This differential effect suggests that VEGF-A/NFATc1 signaling might be a crucial coordinator of endothelial cell migration in post-natal valves.

The endothelium of the cardiac valves is unique compared the rest of the vasculature in its ability to undergo an endothelial-to-mesenchymal transformation (EMT) in vitro in response to transforming growth factor-beta (TGF-beta). EMT is a critical event during embryonic valve development, and both VEGF-A and Notch1 have been shown to function in this process. Here we investigate the effects of VEGF-A and Notch1 on EMT in clonal endothelial cell (EC) populations isolated from adult aortic valve leaflets. VEGF-A inhibited TGF-beta-induced EMT. Endothelial growth, however, was not affected by VEGF-A or TGF-beta. A positive role for Notch1 was revealed in three experiments: (1) TGF-beta induced Notch1 mRNA in valve ECs, (2) a gamma-secretase inhibitor of Notch1 signaling blocked EMT, and (3) overexpression of a ligand-independent form of Notch1 induced EMT. These results demonstrate, for the first time, that VEGF-A and Notch1 play opposing roles in regulating EMT in post-natal valve endothelium.

Purpose: We aimed to evaluate the use and safety of double dose oseltamivir for patients manifesting severe respiratory symptoms or showing no improvement of clinical symptoms after 72 hours’ treatment with the usual oseltamivir dosage. Methods: We analyzed the clinical features of 2009 influenza A H1N1 inpatients who had been admitted to a university hospital’s Department of Pediatrics between August 2009 and January 2010. The Influenza A H1N1 diagnoses were confirmed by real-time reverse transcriptase polymerase chain reaction. Results: The study participants numbered 157 (mean age, 5.0 years; male-to-female ratio, 1.1:1). Among them, twenty (mean age, 5.2 years) were administered double dose oseltamivir. This double dose group showed higher peak body temperatures and more abnormal radiologic results than the other, usual-dose group. The mean time duration between high fever and afebrile status after initiation of double-dose oseltamivir administration was 2.1 days, whereas that within the usual-dose group was 1.7 days. There were no adverse effects in the patients treated with double-dose oseltamivir. Conclusion: Double-dose oseltamivir was well tolerated in patients with severe 2009 influenza A H1N1 infection.(Allergy Asthma Respir Dis 2014;2:64-69)

Background —Unstable atherosclerotic lesions typically have an abundant inflammatory cell infiltrate, including activated T cells, macrophages, and mast cells, which may decrease plaque stability. The pathophysiology of inflammatory cell recruitment and activation in the human atheroma is incompletely described. Methods and Results —We hypothesized that differential gene expression with DNA microarray technology would identify new genes that may participate in vascular inflammation. RNA isolated from cultured human aortic smooth muscle cells treated with tumor necrosis factor-α (TNF-α) was examined with a DNA microarray with 8600 genes. This experiment and subsequent Northern analyses demonstrated marked increases in steady-state eotaxin mRNA (>20 fold), a chemokine initially described as a chemotactic factor for eosinophils. Because eosinophils are rarely present in human atherosclerosis, we then studied tissue samples from 7 normal and 14 atherosclerotic arteries. Immunohistochemical analysis demonstrated overexpression of eotaxin protein and its receptor, CCR3, in the human atheroma, with negligible expression in normal vessels. Eotaxin was predominantly located in smooth muscle cells. The CCR3 receptor was localized primarily to macrophage-rich regions as defined by immunopositivity for CD 68; a minority of mast cells also demonstrated immunopositivity for the CCR3 receptor. Conclusions —Eotaxin and its receptor, CCR3, are overexpressed in human atherosclerosis, suggesting that eotaxin participates in vascular inflammation. These data demonstrate how genomic differential expression technology can identify novel genes that may participate in the stability of atherosclerotic lesions.

Abstract —Vascular smooth muscle cells must monitor and respond to their mechanical environment; however, the molecular response of these cells to mechanical stimuli remains incompletely defined. By applying a highly uniform biaxial cyclic strain to cultured cells, we used DNA microarray technology to describe the transcriptional profile of mechanically induced genes in human aortic smooth muscle cells. We first identified vascular endothelial growth factor (VEGF) as a mechanically induced gene in these cells; VEGF served as a positive control for these experiments. We then used a DNA microarray with 5000 genes with putative functions to identify additional mechanically induced genes. Surprisingly, relatively few genes are mechanically induced in human aortic smooth muscle cells. Only 3 transcripts of 5000 were induced >2.5-fold: cyclooxygenase-1, tenascin-C, and plasminogen activator inhibitor-1. Downregulated transcripts included matrix metalloproteinase-1 and thrombomodulin. The transcriptional profile of mechanically induced genes in human aortic smooth muscle cells suggests a response of defense against excessive deformation. These data also demonstrate that in addition to identifying large clusters of genes that respond to a given stimulus, DNA microarray technology may be used to identify a small subset of genes that comprise a highly specific molecular response.

Background The underlying rationale of platelet rich plasma (PRP) therapy is that an injection of concentrated PRP at the site of injury may promote tissue repair via cytokine release from platelets. The molecular mechanisms of PRP therapy in the skin wound healing process are not well understood at present, and would benefit from clarification. Methods PRP was stimulated with angonists for 5 min, and cytokine profile analysis was performed. To investigate the wound healing activity of PRP, cell proliferation and migration analyses were performed in skin cells. The effects of PRP were analyzed on the expression and activity of matrix metalloproteinase (MMP)-1, -2, -9, and the activation of transcription factors. Results Thrombin was found to be a strong stimulator of PRP activation to release growth factors and chemokines. PRP induced cell proliferation and migration in HUVECs, HaCaT cells, and HDFs, as well as MMP-1and MMP-9 expression in HaCaT cells, but PRP did not have a significant effect on the expression or activity of MMPs in HDFs. The transcription factors, including signal transducer and activator of transcription-3 (STAT-3) were found to be phosphorylated following PRP treatment in HaCaT cells. Conclusion In this study, we have identified the cytokine profile of activated PRP after agonist stimulation. We have shown that PRP plays an active role in promoting the proliferation and migration of skin cells via the regulation of MMPs, and this may be applicable to the future development of PRP therapeutics to enhance skin wound healing.