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      • Rapid fecal cytokeratin-19 test and fecal occult blood test in screening for gastrointestinal diseases.

        Kim, Hyunjung,Kim, Yonggoo,Yoon, Sangsoon,Lim, Jihyang,Kim, Myungshin,Lee, Soonwook,Kang, Sunghan,Lee, Eun Jung,Kang, Chang Suk,Han, Kyungja Institute for Clinical Science] 2006 Annals of clinical and laboratory science Vol.36 No.3

        <P>To evaluate the screening power of the fecal cytokeratin-19 test (CK-19) and the fecal occult blood test (FOBT), we performed rapid fecal CK-19 and FOBT tests on 515 stool samples from patients with various GI diseases and 814 stool samples from control patients. The rapid fecal CK-19 test (developed by DiNonA Research Institute, Seoul, Korea) is based on gold immunochromatography and has a sensitivity of 1 ng/ml. The positive rate of the FOBT was 2.1% in controls, 14.0% in GI cancer patients, 3.5% in GI inflammation patients, 11.7% in bone marrow transplant (BMT) patients, and 6.0% in childhood diarrhea patients. Except for the GI inflammation patients, the patients' positive rates for FOBT were all higher than the controls (p <0.05). The positive rate of the fecal CK-19 test was 8.2% in controls, 42.1% in GI cancer patients, 66.0% in GI inflammation patients, 84.8% in BMT patients, and 19.9% in childhood diarrhea patients. In all of the patient groups, positive rates for the CK-19 test were higher than in the controls (p <0.05). The fecal CK-19 test was more frequently positive (42.1%) in GI cancer patients than the FOBT; if both tests were used, the sensitivity was 49.1%. The fecal CK-19 test (but not the FOBT) gave a higher positive rate in GI inflammation patients than the controls, suggesting that the CK-19 test could serve as a screening test for GI inflammation. The highest positive rate of the fecal CK-19 test was found in the BMT group, indicating that significant GI epithelial desquamation had occurred. Although the positive rate of the fecal CK-19 test in childhood diarrhea patients was higher than in the controls, it was much lower than in adults with GI inflammatory disease. Evidently, children with GI inflammation do not desquamate as much intestinal epithelium as adult patients with GI inflammation. This study shows that the rapid fecal GK-19 test, used in conjunction with the FOBT, may be a valuable screening technique for GI diseases and can assist physicians in the differential diagnosis of GI diseases.</P>

      • Donor-Specific HLA Class I and CREG Antibodies in Complement-Dependent Cytotoxicity-Negative Renal Transplants.

        Kim, Yonggoo,Yang, Chul Woo,Moon, In-Sung,Kim, Myungshin,Lim, Jihyang,Park, Yeon-Joon,Han, Kyungja,Oh, Eun-Jee Institute for Clinical Science] 2010 Annals of clinical and laboratory science Vol.40 No.4

        <P>Development of a solid-phase, single antigen panel reactive antibody test (SA-PRA) permits the analysis of antibody specificities. This study determined the impact of donor-specific antibodies (DSA) against class I HLA private antigens (DS-HLA) or HLA-A and -B cross-reactive group (DS-CREG) in kidney transplantation. Pre- and post-transplant sera of 133 renal allograft patients who had negative pretransplant complement-dependent cytotoxicity were tested for HLA class I antibody specificities by SA-PRA. Clinical relevance of the flow cytometric crossmatch test (FCXM) for the detection of class I DS-HLA or DS-CREG was analyzed. The sensitivity of FCXM to detect SA-PRA-defined class I DSA was 50% (5/10) and the specificity was 98.4% (121/123). Of 133 renal allograft recipients, including 26 patients with biopsy-proven acute antibody-mediated rejection (AMR), pretransplant DS-HLA or DS-CREG were detected in 10 patients. Pretransplant DSA were associated with AMR (p = 0.012) and a low calculated glomerular filtration rate (p = 0.036). In the analysis of post-transplant sera, the presence of either type of HLA antibodies and the de novo development of DSA were correlated with AMR (p <0.001). This study demonstrates that detection of DSA, including DS-HLA and DS-CREG, using the SA-PRA assay is useful to identify the renal allograft recipients with poor transplant outcome.</P>

      • A novel NOTCH2 mutation identified in a Korean family with Hajdu-Cheney syndrome showing phenotypic diversity.

        Han, Mi Seon,Ko, Jung Min,Cho, Tae-Joon,Park, Woong-Yang,Cheong, Hae Il Institute for Clinical Science] 2015 Annals of clinical and laboratory science Vol.45 No.1

        <P>Hajdu-Cheney syndrome (HCS) and serpentine fibula-polycystic kidney syndrome (SFPKS) share many similarities, including craniofacial abnormalities, bony deformities, and renal involvement. Because mutations in exon 34 of NOTCH2 have been identified recently in both HCS and SFPKS patients, it has been suggested that these two syndromes be classed as the same disorder. A 3-year-old boy presented with polycystic kidneys and club feet detected during the fetal period; however, acroosteolysis and curved fibulae were not observed. His mother showed osteoporosis and had a history of compression fractures in the spine without renal anomalies. Although the same novel mutation in NOTCH2 was found in both the mother and her son, these patients displayed different clinical manifestations. In this report, we present a familial case of HCS in a boy and his mother that was suspected on physical examination and radiological findings. We speculate that HCS and SFPKS are a single disease entity with a wide spectrum of clinical manifestations associated with truncating mutations in exon 34 of NOTCH2.</P>

      • Time-Kill Synergy Tests of Tigecycline Combined with Imipenem, Amikacin, and Ciprofloxacin against Clinical Isolates of Multidrug-Resistant Klebsiella pneumoniae and Escherichia coli.

        Yim, Haejun,Woo, Heungjeong,Song, Wonkeun,Park, Min-Jeong,Kim, Hyun Soo,Lee, Kyu Man,Hur, Jun,Park, Man-Seung Institute for Clinical Science] 2011 Annals of clinical and laboratory science Vol.41 No.1

        <P>This study evaluated the activity of tigecycline combined with imipenem, amikacin, and ciprofloxacin against clinical isolates of multidrug-resistant Klebsiella pneumoniae and Escherichia coli co-producing extended-spectrum 관-lactamases and acquired AmpC 관-lactamases. Broth microdilution tests were performed for cefotaxime, ceftazidime, cefepime, imipenem, amikacin, ciprofloxacin, and tigecycline. Time-kill synergy studies were tested for tigecycline plus imipenem, tigecycline plus amikacin, and tigecycline plus ciprofloxacin. Imipenem (MIC(90) = 1 관g/ml for both K. pneumoniae and E. coli) and tigecycline (MIC(90) = 2 관g/ml for K. pneumoniae and 1 관g/ml for E. coli) were the most potent agents. Combination studies with tigecycline plus imipenem resulted in synergy against 18 K. pneumoniae and 3 E. coli isolates; tigecycline plus amikacin yielded synergy against 8 K. pneumoniae and 3 E. coli isolates; tigecycline plus ciprofloxacin yielded synergy against 7 K. pneumoniae and 2 E. coli isolates. No antagonism was observed with any combination. In the present study, imipenem, amikacin, and ciprofloxacin led to indifferent and some synergistic effects in combination with tigecycline, and none of them demonstrated antagonistic effects.</P>

      • Mutations of ACADS Gene Associated with Short-Chain Acyl-Coenzyme A Dehydrogenase Deficiency.

        Kim, Se Hwa,Park, Hyung-Doo,Sohn, Young Bae,Park, Sung Won,Cho, Sung Yoon,Ji, Suntae,Kim, Su Jin,Choi, Eun Wha,Kim, Chi Hwa,Ko, Ah-Ra,Yeau, Sunghee,Paik, Kyung-Hoon,Jin, Dong-Kyu Institute for Clinical Science] 2011 Annals of clinical and laboratory science Vol.41 No.1

        <P>Short-chain acyl-coenzyme A dehydrogenase deficiency (SCADD) is an autosomal recessive disorder of mitochondrial fatty acid oxidation associated with mutations in the ACADS gene (Acyl-CoA Dehydrogenase, Short-chain, OMIM #606885). SCADD is a heterogeneous condition that has been associated with various clinical phenotypes ranging from fetal metabolic decompensation in infancy to asymptomatic individuals. Here, the first Korean neonate diagnosed with SCADD by biochemical and genetic findings is reported. The patient has remained asymptomatic by avoiding hypoglycemia. An increased concentration of butylcarnitine was detected on newborn screening. Subsequent urine organic acid analysis showed increased urinary excretion of ethylmalonic acid. To confirm the presence of the genetic abnormality, all the coding exons of the ACADS gene and flanking introns were amplified by the polymerase chain reaction (PCR). Sequence analysis of the ACADS gene revealed novel homozygous missence mutations, c. 1031A>G (p.E344G) in exon 9. In summary, the first Korean patient with confirmed SCADD by genetic analysis is reported with novel mutation.</P>

      • Antitumor and normal cell protective effect of PKC412 in the athymic mouse model of ovarian cancer.

        Kim, Myungshin,Park, In-Yang,Lim, Jihyang,Kim, Yonggoo,Han, Ku Taek,Chung, Won Heui,Han, Kyungja Institute for Clinical Science] 2006 Annals of clinical and laboratory science Vol.36 No.4

        <P>N-benzoyl-staurosporine (PKC412) is a selective inhibitor of protein kinase C, and it inhibits the growth of human cancer cells. In this study, we examined the antitumor effect of PKC412, given singly and in combination with paclitaxel, on tumor regression and chemotherapeutic side effects by assessing tumor burden and cytokine production responses in vivo. Twenty-six nude mice intraperitoneally inoculated with SKOV3 cells were treated differently in 4 treatment groups: PKC412 plus paclitaxel (n = 7), paclitaxel-only (n = 6), PKC412-only (n = 6), and controls (n = 7). At autopsy, we found that PKC412 itself slightly reduced the mass of tumor but did not fully inhibit tumor formation. The incidence of evident disease was decreased when PKC412 was combined with paclitaxel (43%). From the body weight of the tumor-bearing mice, we observed that PKC412 plus paclitaxel treated mice were less wasted than paclitaxel-only treated mice (18.1 g vs 22.4 g, p = 0.001). We measured intracellular TNFalpha, IFNgamma, IL-4, and IL-10 in stimulated mouse splenocytes using flow cytometry to determine if PKC412 inhibited cytokine production in T cells. TNFalpha, IFNgamma, and IL-10 production were all significantly inhibited in the paclitaxel-treated mice. The inhibitory effects on cytokine production by paclitaxel were compensated with PKC412 combination (p = 0.008, 0.035, 0.014, respectively). From this study, we deduce that PKC412 may have clinical applications in promoting tumor regression in ovarian cancer when combined with paclitaxel. Moreover, PKC412 is able to prevent weight loss and immunosuppression induced by paclitaxel because it rescues normal proliferating cells from cytotoxic effects.</P>

      • Primary Plasma Cell Leukemia Associated with t(6;14)(p21;q32) and IGH Rearrangement: A Case Study and Review of the Literature.

        Cho, Sun Young,Lim, Gayoung,Oh, Seung Hwan,Lee, Hee Joo,Suh, Jin-Tae,Lee, Juhie,Lee, Woo-In,Lee, Hong Ghi,Yoon, Hwi-Joong,Park, Tae Sung Institute for Clinical Science] 2011 Annals of clinical and laboratory science Vol.41 No.3

        <P>Because plasma cell leukemia (PCL) is a rare and distinct variant among plasma cell dyscrasias, recent clinical and cytogenetic studies have been performed in different ethnic groups to define the characteristics of these PCL patients. As far as we know, IGH rearrangements involving t(11;14) and (14;16) are significantly more frequent in PCL than in myeloma patients. However, PCL cases associated with t(6;14)(p21;q32) or IGH-CCND3 rearrangement are extremely rare in the literature; only one PCL case with t(6;14) has been documented. A 61-year-old female was admitted due to fatigue, weight loss, and exertional dyspnea. Plasmacytoid cells were counted up to 76% at a peripheral blood film, but bone marrow aspiration failed because of dry-tapping. Flow cytometric analysis showed positive for CD138 and cytoplasmic kappa light chain. Chromosome analysis revealed t(6;14)(p21;q32), which was confirmed by an IGH split-out probe in FISH analysis. Immunofixation electrophoresis also presented monoclonal bands identified as IgG and kappa light chain. Finally, she was diagnosed as primary PCL associated with t(6;14) and IGH rearrangement. Although considerable advances have been made in the understanding of the biology and molecular pathogenesis of PCL, further clinical, laboratory, and genetic studies of PCL associated with such a rare IGH rearrangement would be necessary in the future. To the best of our knowledge, this is the first report of PCL associated with t(6;14) as a sole chromosomal abnormality.</P>

      • Korean Monozygotic Twins with Lethal Acantholytic Epidermolysis Bullosa Caused by Two Novel DSP Mutations

        Kim, S. J.,Ko, J. M.,Shin, S. H.,Kim, E.-K.,Kim, H.-S.,Lee, K.-A. INSTITUTE FOR CLINICAL SCIENCE 2017 Annals of clinical and laboratory science Vol.47 No.2

        <P>Desmoplakin is an essential cytoplasmic plaque protein in desmosomes, and it is the major linker between intercellular junctions in the skin and heart. The role of desmoplakin is anchoring transmembrane cadherins to cytoplasmic intermediate filaments. The desmoplakin gene (DSP) is located on chromosome 6, and six common allelic disorders are associated with this gene, including autosomal-dominant or -recessive disorders that affect the skin, heart, hair, and nails. In particular, lethal acantholytic epidermolysis bullosa (LAEB) is an autosomal recessively inherited and extremely rare genetic skin disorder, and only three molecularly confirmed families with LAEB have been reported previously. Generalized oozing erosion of the entire skin is the main clinical feature, which leads to excessive transcutaneous fluid loss and neonatal death. Histopathologically, this disorder is classified as a suprabasal subtype of epidermolysis bullosa simplex. In this study, we report for the first time in Korea on monozygotic twins with LAEB caused by two novel nonsense mutations in the DSP gene. Both of the twins exhibited severe and rapid progressive whole body skin erosion, and they died shortly after birth because of multiorgan failure followed by excessive fluid loss.</P>

      • Rare Korean Cases of Very-long-chain Acyl-CoA Dehydrogenase Deficiency with a Novel Recurrent Mutation

        Ko, J. M.,Seo, J.,Choi, M.,Song, J.,Lee, K.-A.,Shin, C. H. INSTITUTE FOR CLINICAL SCIENCE 2016 Annals of clinical and laboratory science Vol.46 No.1

        <P>Very-long-chain acyl-CoA dehydrogenase deficiency (VLCADD; OMIM#201475) is a rare metabolic disorder of mitochondrial fatty acid oxidation. VLCADD includes three clinical forms that are grouped based on disease severity. Here, we present two unrelated patients suspected of having VLCADD based on a newborn screening test. One patient was diagnosed in the neonatal period and, to date, has not shown any symptoms or signs associated with VLCADD; in contrast, diagnosis was delayed in the other patient after events of hypoketotic hypoglycemia and steatohepatitis. Repeated biochemical analyses and a liver biopsy implied VLCADD, and direct sequencing analysis led to the discovery of three novel mutations, including an identical missense variant (p.Ser207Pro) on ACADVL. Our patients were the first cases of the milder form of VLCADD, and the identical mutation detected might represent a founder mutation in the Korean population and be associated with the milder phenotype of VLCADD.</P>

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