Monitoring of multi-frequency polarization of gamma-ray bright AGNs

We started two observing programs with the Korean VLBI Network (KVN) monitoring changes in the flux density and polarization of relativistic jets in gamma-ray bright AGNs simultaneously at 22, 43, 86, 129 GHz. One is a single-dish weekly-observing program in dual polarization with KVN 21-m diameter radio telescopes beginning in 2011 May. The other is a VLBI monthly-observing program with the three-element VLBI network at an angular resolution range of 1.0--9.2 mas beginning in 2012 December. The monitoring observations aim to study correlation of variability in gamma-ray with that in radio flux density and polarization of relativistic jets when they flare up. These observations enable us to study the origin of the gamma-ray flares of AGNs.Comment: 4 pages, 4 figures, Proceedings of the conference "The innermost regions of relativistic jets and their magnetic fields", Granada, Spai

Genotypic Characterization of Vibrio vulnificus Clinical Isolates in Korea

AbstractObjectivesVibrio vunificus is known to cause septicemia and severe wound infections in patients with chronic liver diseases or an immuno-compromised condition. We carried out the molecular characterization of V. vulnificus isolates from human Vibrio septicemia cases based on pulsed-field gel electrophoresis (PFGE) using NotI and SfiI.Methods and ResultsPFGE was used to characterize a total of 78 strains from clinical cases after NotI or SfiI digestion. The geographical distribution of PFGE patterns for the strains from the southern part of Korea, a high-risk region for Vibrio septicemia, indicated that the isolates from southeastern Korea showed a comparatively higher degree of homology than those from southwestern Korea.ConclusionsWe report the genetic distribution of V. vulnficus isolated from Vibrio septicemia cases during 2000–2004 in Korea. This method has potential use as a subspecies-typing tool for V. vulnificus strains isolated from distant geographic regions

The Parkinsonian mimetic, 6-OHDA, impairs axonal transport in dopaminergic axons

6-hydroxydopamine (6-OHDA) is one of the most commonly used toxins for modeling degeneration of dopaminergic (DA) neurons in Parkinson's disease. 6-OHDA also causes axonal degeneration, a process that appears to precede the death of DA neurons. To understand the processes involved in 6-OHDA-mediated axonal degeneration, a microdevice designed to isolate axons fluidically from cell bodies was used in conjunction with green fluorescent protein (GFP)-labeled DA neurons. Results showed that 6-OHDA quickly induced mitochondrial transport dysfunction in both DA and non-DA axons. This appeared to be a general effect on transport function since 6-OHDA also disrupted transport of synaptophysin-tagged vesicles. The effects of 6-OHDA on mitochondrial transport were blocked by the addition of the SOD1-mimetic, Mn(III)tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP), as well as the anti-oxidant N-acetyl-cysteine (NAC) suggesting that free radical species played a role in this process. Temporally, microtubule disruption and autophagy occurred after transport dysfunction yet before DA cell death following 6-OHDA treatment. The results from the study suggest that ROS-mediated transport dysfunction occurs early and plays a significant role in inducing axonal degeneration in response to 6-OHDA treatment

Recurrent Hepatic Alveolar Echinococcosis: Report of The First Case in Korea with Unproven Infection Route

Human alveolar echinococcosis (AE), a hepatic disorder that resembles liver cancer, is a highly aggressive and lethal zoonotic infection caused by the larval stage of the fox tapeworm, Echinococcus multilocularis. E. multilocularis is widely distributed in the northern hemisphere; the disease-endemic area stretches from north America through Europe to central and east Asia, including northern parts of Japan, but it has not been reported in Korea. Herein, we represent a first case of AE in Korea. A 41-year-old woman was found to have a large liver mass on routine medical examination. The excised mass showed multinodular, necrotic, and spongiform appearance with small irregular pseudocystic spaces. Microscopically, the mass was composed of chronic granulomatous inflammation with extensive coagulation necrosis and parasite-like structure, which was revealed as parasitic vesicles and laminated layer delineated by periodic acid-Schiff (PAS) stain. Clinical and histologic features were consistent with AE. After 8 years, a new liver mass and multiple metastatic pulmonary nodules were found and the recurred mass showed similar histologic features to the initial mass. She had never visited endemic areas of AE, and thus the exact infection route is unclear

DEL 적혈구에 의한 항-D 동종면역

Extremely weak D variants called DEL are serologically detectable only by adsorption-elution techniques. A nucleotide change of exon 9 in RHD gene, RHD (K409K, 1227G>A) allelic variant is present in almost all the DEL individuals of East Asians. No DEL phenotype has yet been shown to induce a primary alloanti-D immunization in East Asia. A 68-yr-old D-negative Korean man was negative for anti-D at admission, and he developed alloanti-D after transfusion of red blood cells (RBC) from 4 apparently D-negative donors. Four donors who typed D-negative by routine serologic test were analyzed by real-time PCR for RHD gene and RHD (K409K). One donor was found to have RHD (K409K), This is the first case in which DEL RBCs with RHD (K409K) induced a primary alloanti-D immunization in Asian population. Because the DEL phenotype can induce an anti-D immunization in D-negative recipients, further discussion is needed whether RhD negative donors should be screened by molecular method and what an efficient genotyping method is for detecting the RHD gene carriers in Korea. (Korean J Lab Med 2009;29:361-5)Polin H, 2009, TRANSFUSION, V49, P676, DOI 10.1111/j.1537-2995.2008.02046.xFlegel WA, 2009, TRANSFUSION, V49, P465, DOI 10.1111/j.1537-2995.2008.01975.xSun CF, 2008, ANN CLIN LAB SCI, V38, P258Richard M, 2007, TRANSFUSION, V47, P852, DOI 10.1111/j.1537-2995.2007.01199.xLuettringhaus TA, 2006, TRANSFUSION, V46, P2128, DOI 10.1111/j.1537-2995.2006.01042.xYasuda H, 2005, TRANSFUSION, V45, P1581, DOI 10.1111/j.1537-2995.2005.00579.xWagner T, 2005, TRANSFUSION, V45, P520Gassner C, 2005, TRANSFUSION, V45, P527Kim JY, 2005, TRANSFUSION, V45, P345WAGNER FF, 2001, BMC GENET, V2, P10Avent ND, 2000, BLOOD, V95, P375Aubin JT, 1997, BRIT J HAEMATOL, V98, P356Okuda H, 1997, J CLIN INVEST, V100, P373Avent ND, 1997, BLOOD, V89, P2568HWANG YS, 1996, KOREAN J BLOOD TRANS, V7, P233DANIELS G, 1995, HUMAN BLOOD GROUPSMAK KH, 1993, TRANSFUSION, V33, P348LINCHU M, 1988, TRANSFUSION, V28, P350

JNK pathway is involved in the inhibition of inflammatory target gene expression and NF-kappaB activation by melittin

<p>Abstract</p> <p>Background</p> <p>Bee venom therapy has been used to treat inflammatory diseases including rheumatoid arthritis in humans and in experimental animals. We previously found that bee venom and melittin (a major component of bee venom) have anti-inflammatory effect by reacting with the sulfhydryl group of p50 of nuclear factor-kappa B (NF-κB) and IκB kinases (IKKs). Since mitogen activated protein (MAP) kinase family is implicated in the NF-κB activation and inflammatory reaction, we further investigated whether activation of MAP kinase may be also involved in the anti-inflammatory effect of melittin and bee venom.</p> <p>Methods</p> <p>The anti-inflammatory effects of melittin and bee venom were investigated in cultured Raw 264.7 cells, THP-1 human monocytic cells and Synoviocytes. The activation of NF-κB was investigated by electrophoretic mobility shift assay. Nitric oxide (NO) and prostaglandin E₂(PGE₂) were determined either by Enzyme Linked Immuno Sorbent Assay or by biochemical assay. Expression of IκB, p50, p65, inducible nitric oxide synthetase (iNOS), cyclooxygenase-2 (COX-2) as well as phosphorylation of MAP kinase family was determined by Western blot.</p> <p>Results</p> <p>Melittin (0.5–5 μg/ml) and bee venom (5 and 10 μg/ml) inhibited lipopolysaccharide (LPS, 1 μg/ml) and sodium nitroprusside (SNP, 200 μM)-induced activation of c-Jun NH2-terminal kinase (JNK) in RAW 264.7 cells in a dose dependent manner. However, JNK inhibitor, anthra [1,9-cd]pyrazole-6 (2H)-one (SP600215, 10–50 μM) dose dependently suppressed the inhibitory effects of melittin and bee venom on NF-κB dependent luciferase and DNA binding activity via suppression of the inhibitory effect of melittin and bee venom on the LPS and SNP-induced translocation of p65 and p50 into nucleus as well as cytosolic release of IκB. Moreover, JNK inhibitor suppressed the inhibitory effects of melittin and bee venom on iNOS and COX-2 expression, and on NO and PGE₂generation.</p> <p>Conclusion</p> <p>These data show that melittin and bee venom prevent LPS and SNP-induced NO and PGE₂production via JNK pathway dependent inactivation of NF-κB, and suggest that inactivation of JNK pathways may also contribute to the anti-inflammatory and anti-arthritis effects of melittin and bee venom.</p