1,122 research outputs found

    Ciliated muconodular papillary tumor of the lung: The risk of false-positive diagnosis in frozen section

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    AbstractCiliated muconodular papillary tumor (CMPT) is newly-defined low-grade malignant tumor, characterized as papillary tumor consisting of ciliated columnar, goblet, and basal cells. We present one case of pulmonary peripheral neoplasm misdiagnosed as mucinous adenocarcinoma. Pathologic findings showed, centrally, cystic papillary growth consisting of ciliated columnar, goblet, and basal cells, and peripherally, some tumor cells spread along the adjacent alveolar walls, in a lepidic fashion, and floating in pool of mucin. Tumor cells had bland nuclei, and no mitotic activity was observed. This had been initially misdiagnosed as mucinous adenocarcinoma in frozen section. We reviewed previous articles as well as permanent and frozen slides. In conclusion, in order to reduce the possibility of false positives, it is important to be aware that CMPT is a rare form of peripheral mucin-producing tumor with characteristic histologic findings

    β-catenin activated hepatocellular adenoma

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    Estimation of HIV Seroprevalence in Colorectal Hospitals by Questionnaire Survey in Korea, 2002–2007

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    AbstractObjectivesThe incidence of anal disease is higher among persons with human immunodeficiency virus (HIV) infection than among the general population. We surveyed the status of seroprevalence in colorectal hospitals in Korea.MethodsThe survey was conducted in colorectal hospitals in Korea from November to December 2008. The questionnaire was comprised of six topics about the status of HIV testing in colorectal hospitals. We gathered the data by website (http://hivqa.nih.go.kr/risk) or fax.ResultsAmong 774 colorectal hospitals contacted, 109 (14%) hospitals participated in the survey. Among these, 48 hospitals (44%) performed HIV tests in their own hospitals and 11 (23%) took HIV testing by rapid method. The main reason for recommending an HIV test was surgical operation (54%) followed by endoscope (11%) and health checkup (9%). The annual number of HIV tests increased from 58,647 (at 21 hospitals) in 2002 to 246,709 (at 58 hospitals) in 2007. HIV seroprevalence was >3.0 per 10,000 individuals during 2002–2005, decreased to 2.2 per 10,000 individuals in 2006 and rose to 2.8 per 10,000 individuals in 2007.ConclusionsHIV seroprevalence of colorectal hospitals was more than twice that of general hospitals in Korea. HIV surveillance systems based on colorectal hospitals for HIV/AIDS transmission prevention by early HIV diagnosis are needed

    Effect of moderate-intensity statin therapy on plaque inflammation in patients with acute coronary syndrome: A prospective interventional study evaluated by 18F-FDG PET/CT of the carotid artery

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    Background: Asian patients with acute coronary syndrome (ACS) are frequently prescribed moderate- -intensity statin in real practice, even during the early stage of ACS. Under assessment herein was the effect of moderate-intensity statin therapy on the resolution of plaque inflammation during the first month after ACS, a period with highest recurrent ischemic events, using dual time point 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT).Methods: This prospective study included statin-naïve patients with ACS and non-calcified carotid plaques (≥ 3 mm on ultrasound images). Baseline FDG PET/CT images of the carotid arteries of the patients were obtained. Then, all patients received atorvastatin (20 mg/day); follow-up FDG PET/CT images of the carotid arteries were then obtained after 1 month of therapy. The primary endpoint measurement was the change in the target-to-background ratio (TBR) of the carotid artery between the initial and follow-up FDG PET/CT scans.Results: Thirteen ACS patients completed the initial and follow-up FDG PET/CT scans. Moderate-intensity statin therapy failed to reduce plaque inflammation at 1 month after ACS (TBR 1.60 ± 0.20 at baseline vs. 1.50 ± 0.40 after therapy; p = 0.422) but significantly reduced serum low-density lipoprotein cholesterol (LDL-C) levels (mean LDL-C 101.2 ± 21.1 mg/dL at baseline vs. 70.7 ± 12.4 mg/dL after therapy; p < 0.001). Changes in the TBR and serum LDL-C levels were not correlated (r = –0.27, p = 0.243).Conclusions: Dual time point FDG PET/CT imaging demonstrates that moderate-intensity statin therapy was insufficient in suppressed plaque inflammation within the first month after ACS in Asian patients, even though achieving target LDL levels

    Acute Myocardial Infarction due to Polyarteritis Nodosa in a Young Female Patient

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    Coronary artery aneurysms are uncommon, are usually associated with atherosclerosis, and rarely involve all three major coronary arteries. The present report describes a rare case of a young female patient presenting with acute myocardial infarction (AMI). Coronary angiography revealed multiple severe aneurysmal and stenotic changes. Based on clinical feature and angiographic findings, it was strongly suspected that the patient had polyarteritis nodosa (PAN) complicated by AMI. The patient was treated with standard cardiac medications and immunosuppressive agents and has remained stable without further complications during a follow-up period of 6 months

    Circulating Autoantibodies in Patients with Aspirin-intolerant Asthma: An Epiphenomenon Related to Airway Inflammation

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    Several studies have suggested the involvement of an autoimmune mechanism in aspirin (ASA)-intolerant asthma. To test this hypothesis, we measured the levels of circulating autoantibodies, such as IgG and IgA to tissue transglutaminase (TGase), IgG to cytokeratins (CKs) 8, 18, and 19, Clq-binding immune complex (CIC), and antinuclear antibody (ANA), in the sera of 79 patients with ASA-intolerant asthma (Group I) and those of two control groups, consisting of 61 patients with ASA-tolerant asthma (Group II) and 88 healthy control subjects (Group III) by means of ELISA. Significantly higher prevalences of IgG antibodies to CK18 (13.9%) and CK19 (17.7%) were noted in Group I, as compared with Group III (p<0.05 for all) not with Group II. Regarding the prevalences of other autoantibodies, the levels of ANA (1.3%), IgG to TGase (3.8%), and CIC (24.7%) in Group I were not significantly different from those in Groups II and III. Significant correlations were found between positivities for the anti-CK18 and anti-CK19 autoantibodies and the PC20 methacholine values in the analysis of asthma Groups I and II vs. normal controls, (p=0.001 and p=0.003, respectively). Further studies are needed to explore the potential involvement of an autoantibody-mediated mechanism in the clinical manifestation of bronchial asthma

    Clinical Characteristics of Allergic Rhinitis According to Allergic Rhinitis and Its Impact on Asthma Guidelines

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    ObjectivesThe Allergic rhinitis and its impact on asthma (ARIA) guidelines were suggested for use to classify allergic rhinitis (AR). However, few studies have been performed in Asians. The objective of this study is to identify the clinical characteristics of AR in Korean patients according to the ARIA guidelines.MethodsFor the study, 610 patients who had been diagnosed with allergic rhinitis at Seoul National University Bundang Hospital and 545 patients who had been diagnosed with allergic rhinitis at 3 local clinics were included. All the patients were categorized into 4 groups, such as the mild intermittent, mild persistent, moderate-severe intermittent and moderate-severe persistent groups. The patients were given a questionnaire on allergic rhinitis-related symptoms and they underwent blood tests, including the blood eosinophil count and the serum total IgE level.ResultsThe most prevalent type was the moderate-severe persistent group (34.7%), and the moderate-severe intermittent group (17.1%) was the rarest. There were significant differences among the 4 groups for olfaction (P<0.001), self-awareness of rhinitis (P=0.013), a previous history of AR (P<0.001), self-awareness of asthma (P=0.001) and allergic conjunctivitis (P<0.001). On the allergy laboratory tests, there was a significant difference between the groups for the eosinophi count (P=0.004). The number of blood eosinophil was more in the persistent groups than in the intermittent groups.ConclusionAccording to the ARIA guidelines, the moderate-severe persistent group was the most prevalent for Korean patients. Blood eosinophilia and olfactory dysfunction were the most severe in the moderate-severe persistent group

    Circulating endothelial progenitor cells as a new marker of endothelial dysfunction or repair in acute stroke

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    BACKGROUND AND PURPOSE: Understanding on distinct subsets of endothelial progenitor cells may provide insights of endothelial dysfunction or repair in the acute ischemic event. Recent in vitro data have reported the colony-forming unit (CFU) and outgrowth cell population as a subset of endothelial progenitor cells. In this study, we undertook to validate the significance of CFU number and outgrowth cell yield in acute stroke. METHODS: Mononuclear cells were isolated from the peripheral blood of 75 patients with acute stroke, 45 patients with chronic stroke, and 40 age-matched healthy volunteers. CFU numbers were counted after culturing them for 7 days, and outgrowth cell appearance was measured during the 2 months of culture. Endothelial progenitor cell function was also evaluated by matrigel plate assays. Independent parameters predicting CFU number and outgrowth cell yield were assessed using logistic regression analysis. RESULTS: The CFU numbers and tube formation abilities in matrigel assays were significantly reduced in patients with acute stroke compared with patients with chronic stroke or healthy control subjects. Moreover, patients with large artery atherosclerosis had much lower CFU numbers and functional activities than ones with cardioembolism. Outgrowth cells were isolated from 10% of healthy control subjects and 22% of patients with chronic stroke during the cultures, but from 71% of patients with stroke. Multivariate analysis identified glycosylated hemoglobin and National Institutes of Health Stroke Scale on admission as significant independent predictors of a low CFU number and a high isolation frequency of outgrowth cells, respectively. CONCLUSIONS: CFU number may thus represent an accumulated endothelial progenitor cell dysfunctional status, whereas outgrowth cell appearance may reflect the resilience of the systemic circulation to acute ischemic stress

    Increased Circulating Endothelial Microparticles and Carotid Atherosclerosis in Obstructive Sleep Apnea

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    Background and Purpose Endothelial impairment is a linking mechanism between obstructive sleep apnea (USA) and cardiovascular diseases Profiles of endothelial micropanicles (EMPs) and endothelial progenitor cells (EPCs) reflect the degree of endothelial impairment The aims of this study were to measure the levels of EMI`s and progenitor cells in USA, determine the correlations between these factors and USA severity and the deuce of atherosclerosis, and document any changes in these factors after therapy Methods Subjects with (n=82) and without (n=22) OSA were recruited prospectively We measured the number of colony-forming units (CM) in cell cultuie as the endothelial progenitor cell index, and the number of EMPs using flow cytometry with CD31 [platelet endothelial cell adhesion molecule (PECAM)], CD42 (platelet glycoprotem), annexm V, and CD62E (E-selectin) antibodies at baseline and Act 4-6 weeks of continuous positive airway pressure (CPA P) therapy Carotid int ima-media thickness (IMT) was regarded as a marker of atherosclerosis Results The levels of PECAM(+)CD42(-) (p<0 001). PECAM(+)annexin V(+) (p<0 001), and E-selectin(+) micropamcles (p=0 001) were higher in USA subjects than in non-USA subjects The number of CRJ did not differ between the two groups OSA severity independently predicted the levels of PECAM(+)CD42(-) (p=0 02) and PECA(+)annexin V(+) (p=0 004) Carotid IMT was correlated with USA severity (p<0 001), PECAM(+)CD42: (p=0 03), and PECAM(+)annexin (p=0 01) Neither USA severity nor carotid IMT was correlated with either the number of CFI) or E-selectin(+) CPAP therapy decreased the occurrence of E-selecte (p<0 001) in 21 of the USA subjects, but had no effect on the other micioparticles of the number CFU Conclusions USA led to the overproduction of EMI`s, which moderately correlated with USA seventy and the degree of atherosclerosis, and partly responded to therapy The endothelial impairment might contribute to future cardiovascular events J Clin Neurol 2010;6`89-98This research was supported by the Stem Cell Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, Republic of Korea (#SC4120).de Lima AMJ, 2010, RESPIRATION, V79, P370, DOI 10.1159/000227800Jung KH, 2009, ANN NEUROL, V66, P191, DOI 10.1002/ana.21681Ayers L, 2009, EUR RESPIR J, V33, P574, DOI 10.1183/09031936.00107408Akinnusi ME, 2009, AM J RESP CRIT CARE, V179, P328Christou K, 2009, SLEEP MED, V10, P87, DOI 10.1016/j.sleep.2007.10.011Barcelo A, 2008, THORAX, V63, P946, DOI 10.1136/thx.2007.093740Dorkova Z, 2008, CHEST, V134, P686, DOI 10.1378/chest.08-0556Robinson GV, 2008, THORAX, V63, P855, DOI 10.1136/thx.2007.088096Somers VK, 2008, CIRCULATION, V118, P1080, DOI 10.1161/CIRCULATIONAHA.107.189375Hirschi KK, 2008, ARTERIOSCL THROM VAS, V28, P1584, DOI 10.1161/ATVBAHA.107.155960Daniel L, 2008, NEPHROL DIAL TRANSPL, V23, P2129, DOI 10.1093/ndt/gfn029Martin K, 2008, LUNG, V186, P145, DOI 10.1007/s00408-008-9073-yAmabile N, 2008, AM J RESP CRIT CARE, V177, P1268, DOI 10.1164/rccm.200710-1458OCHeiss C, 2008, J AM COLL CARDIOL, V51, P1760, DOI 10.1016/j.jacc.2008.01.040Chu K, 2008, STROKE, V39, P1441, DOI 10.1161/STROKEAHA.107.499236Jelic S, 2008, CIRCULATION, V117, P2270, DOI 10.1161/CIRCULATIONAHA.107.741512Lee ST, 2008, NEUROLOGY, V70, P1510Bakouboula B, 2008, AM J RESP CRIT CARE, V177, P536, DOI 10.1164/rccm.200706-840OCLopez-Jimenez F, 2008, CHEST, V133, P793, DOI 10.1378/chest.07-0800de la Pena M, 2008, RESPIRATION, V76, P28, DOI 10.1159/000109643WON CHJ, 2008, P AM THORAC SOC, V5, P193Kloner RA, 2007, CIRCULATION, V116, P1306, DOI 10.1161/CIRCULATIONAHA.106.678375El Solh AA, 2007, AM J RESP CRIT CARE, V175, P1186, DOI 10.1164/rccm.200611-1598OCIBER C, 2007, AASM MANUAL SCORINGMONTSERRAT JM, 2007, AM J RESP CRIT CARE, V176, P6Pirro M, 2006, ARTERIOSCL THROM VAS, V26, P2530, DOI 10.1161/01.ATV.0000243941.72375.15Ryan S, 2006, AM J RESP CRIT CARE, V174, P824, DOI 10.1164/rccm.200601-066OCBoulanger CM, 2006, HYPERTENSION, V48, P180, DOI 10.1161/01.HYP.0000231507.00962.b5Arteaga RB, 2006, AM J CARDIOL, V98, P70, DOI 10.1016/j.amjcard.2006.01.054Robinson GV, 2006, EUR RESPIR J, V27, P1229, DOI 10.1183/09031936.06.00062805Werner N, 2005, NEW ENGL J MED, V353, P999Mezentsev A, 2005, AM J PHYSIOL-HEART C, V289, pH1106, DOI 10.1152/ajpheart.00265.2005Minoguchi K, 2005, AM J RESP CRIT CARE, V172, P625, DOI 10.1164/rccm.200412-1652OCMassa M, 2005, BLOOD, V105, P199, DOI 10.1182/blood-2004-05-1831Kim J, 2004, AM J RESP CRIT CARE, V170, P1108, DOI 10.1164/rccm.200404-519OCJy W, 2004, J THROMB HAEMOST, V2, P1842Tramontano AF, 2004, BIOCHEM BIOPH RES CO, V320, P34, DOI 10.1016/j.bbrc.2004.05.127Ip MSM, 2004, AM J RESP CRIT CARE, V169, P348, DOI 10.1164/rccm.200306.767OCBarba C, 2004, LANCET, V363, P157Bernal-Mizrachi L, 2003, AM HEART J, V145, P962, DOI 10.1016/S0002-8703(03)00103-0Jimenez JJ, 2003, THROMB RES, V109, P175, DOI 10.1016/S0049-3848(03)00064-1Hill JM, 2003, NEW ENGL J MED, V348, P593Preston RA, 2003, HYPERTENSION, V41, P211, DOI 10.1161/01.HYP.0000049760.15764.2DSabatier F, 2002, DIABETES, V51, P2840, DOI 10.2337/diabetes.51.9.2840El-Solh AA, 2002, CHEST, V121, P1541Boulanger CM, 2001, CIRCULATION, V104, P2649Barbe F, 2001, ANN INTERN MED, V134, P1015Chin K, 2000, AM J MED, V109, P562Lusis AJ, 2000, NATURE, V407, P233Ohga E, 1999, J APPL PHYSIOL, V87, P10YOUNG T, 1993, NEW ENGL J MED, V328, P1230JOHNS MW, 1991, SLEEP, V14, P540
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