Phenylalanine ammonia-lyase expression and pyranocoumarin accumulation in Angelica gigas plantlets exposed to light-emitting diodes

Angelica gigas (Dang Gui) is an important medicinal plant. In this study, we examined the accumulation of pyranocoumarin (decursin and decursinol angelate) and the expression of phenylalanine ammonia-lyase (PAL) in Korean angelica plantlet grown under different light-emitting diodes (LEDs) (red, orange, green, blue, and white). Three weeks after LED exposure (WAE), the transcript levels of phenylalanine ammonia-lyase mRNA in seedlings grown under orange LEDs were 4-, 18-, and 7-fold higher than those in seedlings grown under green, blue, and white LEDs, respectively. The decursinol angelate content was almost double than the decursin content. The highest levels of decursin (3.2 mg/g dry weight) and decursinol angelate (6 mg/g dry weight) were detected in plants grown under orange LEDs, at 2 WAE. Therefore, we suggest that orange LEDs may affect decursin and decursinol angelate accumulation. The findings of this study could help to determine an effective strategy for producing secondary metabolites in A. gigas using LED technology

The Relationship between Lewis/Secretor Genotypes and Serum Carbohydrate Antigen 19-9 Levels in a Korean Population

Background : The Lewis histo-blood group system consists of 2 major antigens-Le(a) and Le(b)-and a sialyl Lewis antigen-carbohyd rate antigen (CA) 19-9. We investigated the distribution of Lewis genotypes and evaluated the relationship between the Lewis/Secretor genotypes and the serum level of CA 19-9 in a Korean population to identify whether the serum CA 19-9 levels are influenced by the Lewis/Secretor genotypes. Methods : The study included 242 individuals who had no malignancies. Lewis genotyping was performed for the 59T>G, 508G>A and 1067T>A polymorphic sites. The Secretor genotype was determined through analysis of the 357C>T and 385A>T polymorphic sites and the fusion gene. Serum CA 19-9 level was analyzed using an electrochemiluminescence immunoassay. Results : Individuals carrying the 3 common genotypes-Le/Le, Le/le(59,508), and Le/le(59,1067)-accounted for 95% of the study population. In the Korean population, the allelic frequencies of Le, Le(59)le(59,508) and le(59,1067) were 0.731, 0.010, 0.223, and 0.035, respectiveiy. We found a significant difference in serum CA 19-9 concentrations among the 9 LewislSecretor genotype groups (P<0.001). The serum CA 19-9 levels in subjects with genotype groups 1 and 2 (Le/- and se/se) were higher than those with genotype groups 3-6 (Le/- and Se/-; 15.63 vs 6.64 kU/L, P<0.001). Conclusions : Le/Le(59,508), and Le/le(59,1067) are frequent Lewis genotypes in Koreans. Because serum CA 19-9 levels are significantly influenced by the LewislSecretor genotypes, caution is suggested when interpreting the serum CA 19-9 levels. (Korean J Lab Med 2010;30:51-7)SONG SY, 2008, KOREAN J HEMATOL, V43, P34Park KU, 2005, ANN HEMATOL, V84, P656, DOI 10.1007/s00277-005-1041-5Hayashi N, 2004, PATHOBIOLOGY, V71, P26, DOI 10.1159/000072959Hamajima N, 2002, J MOL DIAGN, V4, P103HAMAJIMA N, 2002, GASTRIC CANCER, V5, P194Liu TC, 2000, ANN HEMATOL, V79, P599Lamerz R, 1999, ANN ONCOL, V10, P145Vestergaard EM, 1999, CLIN CHEM, V45, P54Liu YH, 1999, J HUM GENET, V44, P181Kim MJ, 2002, YONSEI MED J, V43, P427SHIBATA A, 2003, GASTRIC CANCER, V6, P8Liu YH, 1999, J FORENSIC SCI, V44, P82Liu YH, 1998, HUM GENET, V103, P204Pang H, 1998, HUM GENET, V102, P675Narimatsu H, 1998, CANCER RES, V58, P512Liu YH, 1996, J FORENSIC SCI, V41, P1018Koda Y, 1996, AM J HUM GENET, V59, P343Kudo T, 1996, J BIOL CHEM, V271, P9830ROUQUIER S, 1995, J BIOL CHEM, V270, P4632KELLY RJ, 1995, J BIOL CHEM, V270, P4640NISHIHARA S, 1994, J BIOL CHEM, V269, P29271MOLLICONE R, 1994, J BIOL CHEM, V269, P20987

Hemolytic Disease of the Newborn Associated with Anti-Jr(a) Alloimmunization in a Twin Pregnancy: The First Case Report in Korea

Jr(a) is a high-frequency antigen found in all ethnic groups. However, the clinical significance of the anti-Jr(a) antibody has remained controversial. Most studies have reported mild hemolytic disease of the newborn and fetus (HDNF) in Jr(a)-positive patients. Recently, fatal cases of HDNF have also been reported. We report the first case of HDNF caused by anti-Jr(a) alloimmunization in twins in Korea. A 33-yr-old nulliparous woman with no history of transfusion or amniocentesis was admitted at the 32nd week of gestation because of vaginal bleeding caused by placenta previa. Anti-Jr(a) antibodies were detected in a routine laboratory examination. An emergency cesarean section was performed at the 34th week of gestation, and 2 premature infant twins were delivered. Laboratory examination showed positive direct antiglobulin test and Jr(a+) phenotype in the red blood cells and the presence of anti-Jr(a) antibodies in the serum in both neonates. The infants underwent phototherapy for neonatal jaundice; this was followed by conservative management. They showed no further complications and were discharged on the 19th postpartum day. Preparative management to ensure the availability of Jr(a-) blood, via autologous donation, and close fetal monitoring must be performed even in cases of first pregnancy in Jr(a-) women. (Korean J Lab Med 2010;30:511-5)Arriaga F, 2009, TRANSFUSION, V49, P813, DOI 10.1111/j.1537-2995.2009.02118.xPeyrard T, 2008, TRANSFUSION, V48, P1906, DOI 10.1111/j.1537-2995.2008.01787.xROBACK JD, 2008, TECHNICAL MANUAL, P411CHUNG HJ, 2007, KOREAN J BLOOD TRANS, V18, P111Ishihara Y, 2006, FETAL DIAGN THER, V21, P269, DOI 10.1159/000091354Daniels GL, 2004, VOX SANG, V87, P304Kwon MY, 2004, TRANSFUSION, V44, P197Bellver-Pradas J, 2001, AM J OBSTET GYNECOL, V184, P75STROUP M, 1970, P 23 ANN M AM ASS BL, P86KIM DW, 1995, ELS APPL ELECT MAT, V6, P185MIYAZAKI T, 1994, VOX SANG, V66, P51OGASAWARA K, 1990, ACTA HAEMATOL JAPON, V53, P1131GARRATTY G, 1990, TRANSFUS MED REV, V4, P297NANCE SJ, 1987, TRANSFUSION, V27, P449BACON J, 1986, TRANSFUSION, V26, P543LEVENE C, 1986, TRANSFUSION, V26, P119TAKABAYASHI T, 1985, TOHOKU J EXP MED, V145, P97TOY P, 1981, VOX SANG, V41, P40ORRICK LR, 1980, AM J OBSTET GYNECOL, V137, P135NAKAJIMA H, 1978, VOX SANG, V35, P265VEDO M, 1978, TRANSFUSION, V18, P569TRITCHLER JE, 1977, TRANSFUSION, V17, P177KENDALL AG, 1976, TRANSFUSION, V16, P646

Effect of the Presence of Brain-Derived Neurotrophic Factor Val66Met Polymorphism on the Recovery in Patients With Acute Subcortical Stroke

Objective : To investigate the effect of brain-derived neurotrophic factor (BDNF) Valmet polymorphism on the recovery after subcortical stroke, using the modified Rankin Scale (mRS). Methods : Subcortical stroke patients with copies of BDNF Valmet polymorphism (n=7) were compared to their controls (n=7) without a copy of BDNF Valmet polymorphism after matching for initial severity, location and type of stroke. The mRS scores at 1 and 3 months after discharge from the neurorehabilitation unit were compared between the groups. Results : A repeated measures ANOVA for mRS revealed significant interaction between time and group (F(2, 24) =37.2, p<0.001) and a significant effect of time (F(2, 24)=10.8, p<0.001), thereby reflecting significant differences between the Met allele (+) group and the Met allele (-) group. There was a significant difference in mRS scores at 3 months post-discharge between the two groups (p=0.01) although no difference was evident in mRS scores at 1 month post-discharge between the two groups. There were significant improvements between mRS scores on admission and mRS scores at 1 month post-discharge (p=0.02), and between mRS scores at 1 month post-discharge and mRS scores at 3 months post-discharge (p=0.004) in the Met allele (-) group. Conclusion : BDNF Valmet polymorphism may be associated with worse functional outcome in Korean patients with subcortical stroke. Therefore, BDNF Valmet polymorphism should be considered as an important prognostic factor for recovery and responses to rehabilitation therapies after stroke in Korean patients. There is a need for developing different rehabilitation strategies for the population with BDNF Valmet polymorphism. Further studies assessing different outcomes for various functional domains of stroke recovery are needed to clarify the role of BDNF Valmet polymorphism.This research was supported by SK Chemicals Co. through Seoul National University R&DB Foundation (Grant No. 800-2010095).OAIID:oai:osos.snu.ac.kr:snu2013-01/102/0000005165/4SEQ:4PERF_CD:SNU2013-01EVAL_ITEM_CD:102USER_ID:0000005165ADJUST_YN:YEMP_ID:A075663DEPT_CD:801CITE_RATE:0FILENAME:첨부된 내역이 없습니다.DEPT_NM:의학과EMAIL:[email protected]:

Performance Evaluation of the GlucoDr Plus Glucometer

Background: Because strict glucose control is important for reducing the complications of diabetes, the self-monitoring of blood glucose is one of the fundamental treatment modalities. Many glucometers have been developed. In the present study, we evaluated a new glucometer: GlucoDr (TM) Plus (Allmedicus, Anyang, Gyeonggi-do, Republic of Korea). Methods: The evaluation was performed based on Clinical and Laboratory Standards Institute guidelines. Interferences by ascorbic acid, uric acid, maltose, and acetaminophen were examined, and the performance of the unit was compared to those of six other glucometers. The effects of hematocrit, of oxygen partial pressure (PaO(2)), and of multiple users were also evaluated. Results: Within-run, between-run, between- day, and total imprecision (coefficients of variation) were 0.99-4.98%. Satisfactory linearity was found for glucose concentrations of 32.5-786.5 mg/dL (R(2) = 0.9985). A comparison with the reference laboratory method showed close concordance over the entire range of concentrations evaluated (R(2) = 0.9869). No significant effects were noted due to added interferents, hematocrit, and PaO(2). Conclusions: The GlucoDr Plus showed acceptable performance in terms of precision and linearity. It was minimally affected by various interferents. GlucoDr Plus is suitable for the self-monitoring of blood glucose by patients with diabetes.Schleis TG, 2007, PHARMACOTHERAPY, V27, P1313Tsujimura S, 2006, BIOSCI BIOTECH BIOCH, V70, P654D`Orazio P, 2006, CLIN CHEM LAB MED, V44, P1486, DOI 10.1515/CCLM.2006.275Nathan DM, 2005, NEW ENGL J MED, V353, P2643Wild S, 2004, DIABETES CARE, V27, P1047*CLIN LAB STAND I, 2004, EP5A2 CLSI*CLIN LAB STAND I, 2003, EP6A CLSI*INT ORG STAND, 2003, 151972003E ISO*CLIN LAB STAND I, 2002, EP7A CLISTang ZP, 2001, CRIT CARE MED, V29, P1062Tang ZP, 2000, AM J CLIN PATHOL, V113, P75Turner RC, 1998, LANCET, V352, P837*CLIN LAB STAND I, 1995, EP9A CLSI1994, DIABETES CARE, V17, P81MERENSTEIN GB, 1993, PEDIATRICS, V92, P4741993, N ENGL J MED, V329, P977BARRETT AE, 1979, J CLIN PATHOL, V32, P893

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

Real-Time PCR Method for HPV DNA Detection

Human papillomavirus (HPV) infection is an important etiologic factor in cervical carcinogenesis. Various HPV DNA detection methods have been evaluated for clinicopathological level. For the specimens with normal cytological finding, discrepancies among the detection methods were frequently found and adequate interpretation can be difficult. 6,322 clinical specimens were submitted and evaluated for real-time PCR and Hybrid Capture 2 (HC2). 573 positive or &quot;Not Detected but Amplified&quot; (NDBA) specimens by real-time PCR were additionally tested using genetic analyzer. For the reliability of real-time PCR, 325 retests were performed. Optimal cut-off cycle threshold ( ) value was evaluated also. 78.7% of submitted specimens showed normal or nonspecific cytological finding. The distributions of HPV types by real-time PCR were not different between positive and NDBA cases. For positive cases by fragment analysis, concordance rates with real-time PCR and HC2 were 94.2% and 84.2%. In NDBA cases, fragment analysis and real-time PCR showed identical results in 77.0% and HC2 revealed 27.6% of concordance with fragment analysis. Optimal cut-off value was different for HPV types. NDBA results in real-time PCR should be regarded as equivocal, not negative. The adjustment of cut-off value for HPV types will be helpful for the appropriate result interpretation

Usefulness of Multiplex Real-Time PCR for Simultaneous Pathogen Detection and Resistance Profiling of Staphylococcal Bacteremia

Staphylococci are the leading cause of nosocomial blood stream infections. Fast and accurate identification of staphylococci and confirmation of their methicillin resistance are crucial for immediate treatment with effective antibiotics. A multiplex real-time PCR assay that targets mecA, femA specific for S. aureus, femA specific for S. epidermidis, 16S rRNA for universal bacteria, and 16S rRNA specific for staphylococci was developed and evaluated with 290 clinical blood culture samples containing Grampositive cocci in clusters (GPCC). For the 262 blood cultures identified to the species level with the MicroScan WalkAway system (Siemens Healthcare Diagnostics, USA), the direct real-time PCR assay of positive blood cultures showed very good agreement for the categorization of staphylococci into methicillin-resistant S. aureus (MRSA), methicillin-susceptible S. aureus (MSSA), methicillin-resistant S. epidermidis (MRSE), methicillin-susceptible S. epidermidis (MSSE), methicillin-resistant non-S. epidermidis CoNS (MRCoNS), and methicillin-susceptible non-S. epidermidis CoNS (MSCoNS) ( = 0.9313). The direct multiplex real-time PCR assay of positive blood cultures containing GPCC can provide essential information at the critical point of infection with a turnaround time of no more than 4 h. Further studies should evaluate the clinical outcome of using this rapid real-time PCR assay in glycopeptide antibiotic therapy in clinical settings

MYC quantitation in cell-free plasma DNA by real-time PCR for gastric cancer diagnosis

Background: Detection of tumor-associated genetic alterations in plasma of cancer patients has recently been suggested to be an accurate method for detecting early or recurrent cancer. Methods: We performed quantitative real-time PCR for MYC and GAPDH in tissue and plasma samples of 57 patients with gastric cancer and in plasma of 79 cancer-free individuals. We also performed two-color MYC fluorescence in situ hybridization (FISH) in tissue from the 57 patients with gastric cancer. Results: The tissue MYC/GAPDH ratio by real-time PCR was significantly correlated with MYC status by FISH (p<0.001). The mean ratio of plasma MYC/GAPDH was 5.226+/-3.578 (range: 1.25-18.35) in gastric cancer patients, and 2.436+/-0.881 (range: 1.00-5.00) in the healthy volunteers (p<0.001). We used receiver-operating characteristics (ROC) curve analysis to select two optimal plasma MYC/GAPDH cut-offs of 2.725 and 5.225. The sensitivity and specificity were 75.4% and 76.9% at 2.725, 38.6% and 100% at 5.225, respectively. The plasma MYC/GAPDH ratio from cancer patients was significantly correlated with the tissue MYC/GAPDH ratio (p=0.009), and tissue MYC status by FISH (p=0.024). Conclusions: These findings suggest that the plasma MYC/GAPDH ratio, as determined by real-time PCR, may be an alternative non-invasive approach for detecting gastric cancer. Clin Chem Lab Med 2009; 47:530-6.Kim MA, 2007, HUM PATHOL, V38, P1386, DOI 10.1016/j.humpath.2007.02.005Sai S, 2007, ANTICANCER RES, V27, P2747Mitsui F, 2007, MODERN PATHOL, V20, P622, DOI 10.1038/modpathol.3800777Vita M, 2006, SEMIN CANCER BIOL, V16, P318, DOI 10.1016/j.semcancer.2006.07.015Corzo C, 2006, CANCER GENET CYTOGEN, V165, P151, DOI 10.1016/j.cancergencyto.2005.08.013Crew KD, 2006, WORLD J GASTROENTERO, V12, P354Calcagno DQ, 2005, ANTICANCER RES, V25, P4069Gotoh T, 2005, J CLIN ONCOL, V23, P5205, DOI 10.1200/JCO.2005.02.014Tse C, 2005, CLIN CHEM, V51, P1093, DOI 10.1373/clinchem.2004.044305Kindich R, 2005, CLIN CHEM, V51, P649, DOI 10.1373/clinchem.2004.045013Lee TL, 2002, CLIN CANCER RES, V8, P1761Usadel H, 2002, CANCER RES, V62, P371*AM JOINT COMM CAN, 2002, AJCC CANC STAG MAN, P99Livak KJ, 2001, METHODS, V25, P402, DOI 10.1006/meth.2001.1262Lee HS, 2001, CANCER, V92, P1427Lo YMD, 2001, CLIN CANCER RES, V7, P1856Koo SH, 2000, CANCER GENET CYTOGEN, V117, P97AALTONEN LA, 2000, INT AGENCY RES CANC, P37Castells A, 1999, J CLIN ONCOL, V17, P578Hara T, 1998, LAB INVEST, V78, P1143Landis SH, 1998, CA-CANCER J CLIN, V48, P6Suzuki S, 1997, J SURG ONCOL, V66, P173Nawroz H, 1996, NAT MED, V2, P1035Henriksson M, 1996, ADV CANCER RES, V68, P109PARK JG, 1990, CANCER RES, V50, P2773STROUN M, 1989, ONCOLOGY, V46, P318LAUREN P, 1965, ACTA PATHOL MIC SC, V64, P31