8 research outputs found

    Microembolism after Endovascular Treatment of Unruptured Cerebral Aneurysms: Reduction of its Incidence by Microcatheter Lumen Aspiration

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    PurposeDiffusion-weighted MR images (DWI) obtained after endovascular treatment of cerebral aneurysms frequently show multiple high-signal intensity (HSI) dots. The purpose of this study was to see whether we could reduce their incidence after embolization of unruptured cerebral aneurysms by modification of our coiling technique, which involves the deliberate aspiration of the microcatheter lumen right after delivery of each detachable coil into the aneurysm sac.Materials and MethodsFrom January 2011 to June 2011, all 71 patients with unruptured cerebral aneurysms were treated using various endovascular methods. During the earlier period, 37 patients were treated using our conventional embolization technique (conventional period). Then 34 patients were treated with a modified coiling technique (modified period). DWI was obtained on the following day. We compared the occurrence of any DWI HSI lesions and the presence of the symptomatic lesions during the two time periods.ResultsThe incidence of the DWI HSI lesions differed significantly at 89.2% (33/37) during the conventional period and 26.5% (9/34) during the modified period (p < 0.0001). The incidence of symptomatic lesions differed between the two periods (29.7% during the conventional period vs. 2.9% during the modified period, p < 0.003).ConclusionAspiration of the inner content of the microcatheter right after detachable coil delivery was helpful for the reduction of the incidence of microembolisms after endovascular coil embolization for the treatment of unruptured cerebral aneurysms

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    The incidence of metabolic syndrome (MS) has increased significantly worldwide including U Korea over the past decade. Recent studies have shown that the MS develops during childhood and is highly prevalent among overweight children and adolescents. Thus, it is important for physicians to be acquainted with the definition, diagnostic criteria, epidemiology, and pathophysiology of MS for early identification and management of the MS in children and adolescents, which would be helpful to decrease the burden of type 2 diabetes and cardiovascular disease in adults. The aim of this review is to provide adequate guidelines for screening and managing strategies on MS based on recent findings. Proper and effective control of MS needs close cooperation among patients, physician, family members, school, society, and government, and it should be based on a thorough evaluation of medical system on obesity and MS.Barton M, 2010, PEDIATRICS, V125, P361, DOI 10.1542/peds.2009-2037*AM DIAB ASS, 2010, DIABETES CARE S1, V33, pS11, DOI DOI 10.2337/DC10-S011Park J, 2010, J KOREAN MED SCI, V25, P75, DOI 10.3346/jkms.2010.25.1.75Bray GA, 2009, LANCET, V374, P1677, DOI 10.1016/S0140-6736(09)61457-4Gonzalez-Suarez C, 2009, AM J PREV MED, V37, P418, DOI 10.1016/j.amepre.2009.07.012Lurbe E, 2009, J HYPERTENS, V27, P1719, DOI 10.1097/HJH.0b013e32832f4f6bSundaram SS, 2009, CURR OPIN PEDIATR, V21, P529, DOI 10.1097/MOP.0b013e32832cb16fHuang PL, 2009, DIS MODEL MECH, V2, P231, DOI 10.1242/dmm.001180Stanhope KL, 2009, J CLIN INVEST, V119, P1322, DOI 10.1172/JCI37385Lilly M, 2009, CAN FAM PHYSICIAN, V55, P363Steinberger J, 2009, CIRCULATION, V119, P628, DOI 10.1161/CIRCULATIONAHA.108.191394Johnson 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    Sesquiterpene Esters from Celastrus orbiculatus

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    Two Korean girls with complete androgen insensitivity syndrome diagnosed in infancy

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    Androgen insensitivity syndrome (AIS) is a rare genetic disease caused by various abnormalities in the androgen receptor (AR). The AR is an essential steroid hormone receptor that plays a critical role in male sexual differentiation and development and preservation of the male phenotype. Mutations in the AR gene on the X chromosome cause malfunction of the AR so that a 46,XY karyotype male has some physical characteristics of a woman or a full female phenotype. Depending on the phenotype, AIS can be classified as complete, partial or mild. Here, we report 2 cases of complete AIS in young children who showed complete sex reversal from male to female as a result of AR mutations. They had palpable inguinal masses and normal female external genitalia, a blind-end vagina and absent Mรผllerian duct derivatives. They were both 46,XY karyotype and AR gene analysis demonstrated pathologic mutations in both. Because AIS is inherited in an X-linked recessive manner, we performed genetic analysis of the female family members of each patient and found the same mutation in the mothers of both patients and in the female sibling of case 2. Gonadectomy was performed in both patients to avoid the risk of malignancy in the undescended testicles, and estrogen replacement therapy is planned for their adolescence. Individuals with complete AIS are usually raised as females and need appropriate care

    Bone Mineral Density According to Age, Bone Age, and Pubertal Stages in Korean Children and Adolescents

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    To determine whether bone age (BA)-based bone mineral density (BMD) reference values are more accurate than chronological age-based BMD values in predicting the BMD of children who have a discrepancy between their chronological age and BA; we calculated BMD reference values for 514 healthy Korean children (262 girls and 252 boys) aged 5-20 yr by dual-energy X-ray absorptiometry. We found that children with BA chronological age discrepancy fitted better to the BA BMD reference curve than to the chronological age BMD reference curve. In contrast, most children without BA-chronological age discrepancy fitted well to both BA and chronological age BMD reference curves, because the 2 reference curves are very similar. In the linear regression analysis, BA-based equations for BMD had a higher R 2 value and lower standard error of estimate than chronological age-based equations. These results indicate that BA-based BMD values are more accurate in predicting BMD in children who have a discrepancy between their BA and chronological age.Gordon CM, 2008, J CLIN DENSITOM, V11, P43, DOI 10.1016/j.jocd.2007.12.005MOON JS, 2008, KOREAN J PEDIAT, V51, P1Baim S, 2008, J CLIN DENSITOM, V11, P6, DOI 10.1016/j.jocd.2007.12.002Buken B, 2007, FORENSIC SCI INT, V173, P146, DOI 10.1016/j.forsciint.2007.02.023Savaridas SL, 2007, J PEDIATR ORTHOPED, V27, P952, DOI 10.1097/bpo.0b013e31815b12f4Cui LH, 2007, J BONE MINER METAB, V25, P165, DOI 10.1007/s00774-006-0747-3Sheth RD, 2006, EPILEPSY BEHAV, V9, P601, DOI 10.1016/j.yebeh.2006.08.003Clark EM, 2006, J BONE MINER RES, V21, P1489, DOI 10.1359/JBMR.060601Ferrari SL, 2006, J BONE MINER RES, V21, P501, DOI 10.1359/JBMR.051215Cooper C, 2006, OSTEOPOROSIS INT, V17, P337, DOI 10.1007/s00198-005-2039-5Bachrach LK, 2005, ENDOCRIN METAB CLIN, V34, P521, DOI 10.1016/j.ecl.2005.04.001Pludowski P, 2005, J CLIN DENSITOM, V8, P48Jones G, 2005, BONE, V36, P352, DOI 10.1016/j.bone.2004.11.001Arabi A, 2004, BONE, V35, P1169, DOI 10.1016/j.bone.2004.06.015Freedman DS, 2002, PEDIATRICS, V110van der Sluis IM, 2002, ARCH DIS CHILD, V87, P341van der Sluis IM, 2002, J PEDIATR, V141, P204, DOI 10.1067/mpd.2002.125728Goulding A, 2001, J PEDIATR, V139, P509, DOI 10.1067/mpd.2001.116297Henderson CJ, 2000, ARTHRITIS RHEUM, V43, P531Bachrach LK, 1999, J CLIN ENDOCR METAB, V84, P4702, DOI 10.1210/jc.84.12.4702Semeao EJ, 1999, J PEDIATR, V135, P593, DOI 10.1016/S0022-3476(99)70058-2Bass S, 1999, J CLIN INVEST, V104, P795Ilich JZ, 1996, SKELETAL RADIOL, V25, P431BEUNEN GP, 1994, INT J OBESITY, V18, P542ALLEN DB, 1994, J ALLERGY CLIN IMMUN, V93, P967RECKER RR, 1992, JAMA-J AM MED ASSOC, V268, P2403KROGER H, 1992, BONE MINER, V17, P75TROUERBACH WT, 1991, BONE MINER, V13, P55GLASTRE C, 1990, J CLIN ENDOCR METAB, V70, P1330GREULICH WW, 1950, RADIOGRAPHIC ATLAS S

    Immunohistochemical localization of insulin-like growth factor binding protein 2 in the central nervous system of SOD1(G93A) transgenic mice

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    In the present study, we performed immunohistochemical studies to investigate the changes of insulin-like growth factor binding protein 2 (IGFBP2) in the central nervous system of SOD1(G93A) mutant transgenic mice as an in vivo model of amyotrophic lateral sclerosis (ALS). Decreased immunoreactivity for IGFBP2 was observed in the cerebral cortex, hippocampus and brainstem of SOD1(G93A) transgenic mice. In the cerebral cortex, the number of IGFBP2-positive cells was decreased in the somatomotor area, somatosensory area, auditory area, visual area, entorhinal area, piriform area and prefrontal area. In the hippocampal formation, IGFBP2 immunoreactivity was significantly decreased in the CA1-3 areas and the dentate gyrus. In the brainstem, few IGFBP2-immunoreactive cells were observed in the medullary and pontine reticular formation, vestibular nucleus, trigeminal motor nucleus, facial nucleus, hypoglossal nucleus and raphe nucleus. In the spinal cord, IGFBP2 immunoreactivity was not significantly decreased in SOD1(G93A) transgenic mice. This study showing decreased IGFBP2 in different brain regions of SOD1(G93A) transgenic mice may provide clues for understanding differential susceptibility of neural structures in ALS.Kang DW, 2008, ANN ANAT, V190, P502, DOI 10.1016/j.aanat.2008.08.001Chesik D, 2007, CYTOKINE GROWTH F R, V18, P267, DOI 10.1016/j.cytogfr.2007.04.001GOODALL EF, 2006, EXPERT REV MOL MED, V8, P1, DOI 10.1017/S1462399406010854WILCZAK N, 2005, ENDOCRIN DEV, V9, P160Pirttila T, 2004, ACTA NEUROL SCAND, V109, P337, DOI 10.1111/j.1600-0404.2004.00223.xEkestern E, 2004, NEURODEGENER DIS, V1, P88, DOI 10.1159/000080049Chung YH, 2003, BRAIN RES, V994, P253, DOI 10.1016/j.brainres.2003.09.047Kaspar BK, 2003, SCIENCE, V301, P839Wilczak N, 2003, LANCET, V361, P1007Chowen JA, 2002, J NEUROENDOCRINOL, V14, P163, DOI 10.1046/j.0007-1331.2001.00758.xCleveland DW, 2001, NAT REV NEUROSCI, V2, P806Rowland LP, 2001, NEW ENGL J MED, V344, P1688Wang JM, 2000, BRAIN RES, V859, P381Torres-Aleman I, 1998, NEUROLOGY, V50, P772CLEMMONS DR, 1997, CYTOKINE GROWTH F R, V8, P45DErcole AJ, 1996, MOL NEUROBIOL, V13, P227Dore S, 1996, MOL BRAIN RES, V41, P128CollettSolberg PF, 1996, ENDOCRIN METAB CLIN, V25, P591JONES JI, 1995, ENDOCR REV, V16, P3LOGAN A, 1994, ENDOCRINOLOGY, V135, P2255GURNEY ME, 1994, SCIENCE, V264, P1772KERKHOFF H, 1994, ACTA NEUROPATHOL, V87, P411

    Acute Pancreatitis Complicating Spontaneous Acute Exacerbation of Chronic Hepatitis B Virus Infection: Case Report and Review of the Literature

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    Acute pancreatitis may complicate viral hepatitis B, as well as the other causes of viral hepatitis. There have been reports of acute pancreatitis complicating acute exacerbations of chronic hepatitis B virus infection, most of which were related to immunosuppressive treatment or organ transplantation. However, acute pancreatitis complicating spontaneous acute exacerbation of chronic hepatitis B virus infection is rare. We report a case of acute pancreatitis that developed while a spontaneous acute exacerbation of chronic hepatitis B virus infection was underway in a healthy carrier
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