Differential Diagnosis of Human Sparganosis Using Multiplex PCR

Hyeong-Kyu Jeon,Kyu-Heon Kim,Woon-Mok Sohn,Keeseon S. Eom 대한기생충학열대의학회 2018 The Korean Journal of Parasitology Vol.56 No.3

Human sparganosis was diagnosed by morphological and genetic analyses in Korea. The complete mitochondrial genomes of Spirometra erinaceieuropaei and S. decipiens isolated in Korea have been recorded. Present study was performed to provide information to diagnose the etiologic agent of sparganosis by multiplex PCR using mitochondrial genome sequences of S. erinaceieuropaei and S. decipiens. In an effort to examine the differential diagnosis of spirometrid tapeworms, multiplex PCR assays were performed on plerocercoid larvae of S. erinaceieuropaei and S. decipiens. The PCR products obtained using species-specific primers were positively detected in all PCR assays on mixture of S. erinaceieuropaei and S. decipiens DNA. S. erinaceieuropaei-specific bands (239 bp and 401 bp) were obtained from all PCR assays using a mixture of S. erinaceieuropaei-specific primers (Se/Sd-1800F and Se-2018R; Se/Sd-7955F and Se-8356R) and S. erinaceieuropaei template DNA. S. decipiens-specific bands (540 bp and 644 bp) were also detected in all PCR assays containing mixtures of S. decipiens-specific primers (Se/Sd-1800F and Sd-2317R; Se/Sd-7955F and Sd-8567R) and S. decipiens template DNA. Sequence analyses on these species-specific bands revealed 100% sequence identity with homologous regions of the mtDNA sequences of S. erinaceieuropaei and S. decipiens. The multiplex PCR assay was useful for differential diagnosis of human sparganosis by detecting different sizes in species-specific bands.

Potential Effect of S-Nitrosylated Protein Disulfide Isomerase on Mutant SOD1 Aggregation and Neuronal Cell Death in Amyotrophic Lateral Sclerosis

Jeon, G. S.,Nakamura, T.,Lee, J. S.,Choi, W. J.,Ahn, S. W.,Lee, K. W.,Sung, J. J.,Lipton, S. A. HUMANA PRESS INC 2014 Molecular neurobiology Vol.49 No.2

Aggregation of misfolded protein and resultant intracellular inclusion body formation are common hallmarks of mutant superoxide dismutase (mSOD1)-linked familial amyotrophic lateral sclerosis (FALS) and have been associated with the selective neuronal death. Protein disulfide isomerase (PDI) represents a family of enzymatic chaperones that can fold nascent and aberrant proteins in the endoplasmic reticulum (ER) lumen. Recently, our group found that S-nitrosylated PDI could contribute to protein misfolding and subsequent neuronal cell death. However, the exact role of PDI in the pathogenesis of ALS remains unclear. In this study, we propose that PDI attenuates aggregation of mutant/misfolded SOD1 and resultant neurotoxicity associated with ER stress. ER stress resulting in PDI dysfunction therefore provides a mechanistic link between deficits in molecular chaperones, accumulation of misfolded proteins, and neuronal death in neurodegenerative diseases. In contrast, S-nitrosylation of PDI inhibits its activity, increases mSOD1 aggregation, and increases neuronal cell death. Specifically, our data show that S-nitrosylation abrogates PDI-mediated attenuation of neuronal cell death triggered by thapsigargin. Biotin switch assays demonstrate S-nitrosylated PDI both in the spinal cords of SOD1 (G93A) mice and human patients with sporadic ALS. Therefore, denitrosylation of PDI may have therapeutic implications. Taken together, our results suggest a novel strategy involving PDI as a therapy to prevent mSOD1 aggregation and neuronal degeneration. Moreover, the data demonstrate that inactivation of PDI by S-nitrosylation occurs in both mSOD1-linked and sporadic forms of ALS in humans as well as mice.

S6K1 Phosphorylation of H2B Mediates EZH2 Trimethylation of H3: A Determinant of Early Adipogenesis

Yi, S.,Um, S.,Lee, J.,Yoo, J.,Bang, S.,Park, E.,Lee, M.,Nam, K.,Jeon, Y.,Park, J.,You, J.,Lee, S.J.,Bae, G.U.,Rhie, J.,Kozma, Sara C.,Thomas, G.,Han, J.W. Cell Press 2016 Molecular Cell Vol.62 No.3

S6K1 has been implicated in a number of key metabolic responses, which contribute to obesity. Critical among these is the control of a transcriptional program required for the commitment of mesenchymal stem cells to the adipocytic lineage. However, in contrast to its role in the cytosol, the functions and targets of nuclear S6K1 are unknown. Here, we show that adipogenic stimuli trigger nuclear translocation of S6K1, leading to H2BS36 phosphorylation and recruitment of EZH2 to H3, which mediates H3K27 trimethylation. This blocks Wnt gene expression, inducing the upregulation of PPARγ and Cebpa and driving increased adipogenesis. Consistent with this finding, white adipose tissue from S6K1-deficient mice exhibits no detectable H2BS36 phosphorylation or H3K27 trimethylation, whereas both responses are highly elevated in obese humans or in mice fed a high-fat diet. These findings define an S6K1-dependent mechanism in early adipogenesis, contributing to the promotion of obesity.

ZNF509S1 downregulates PUMA by inhibiting p53K382 acetylation and p53-DNA binding

Jeon, B.N.,Yoon, J.H.,Han, D.,Kim, M.K.,Kim, Y.,Choi, S.H.,Song, J.,Kim, K.S.,Kim, K.,Hur, M.W. Elsevier Science 2017 Biochimica et biophysica acta. Gene regulatory mec Vol.1860 No.9

Expression of the POK family protein ZNF509L, and -its S1 isoform, is induced by p53 upon exposure to genotoxic stress. Due to alternative splicing of the ZNF509 primary transcript, ZNF509S1 lacks the 6 zinc-fingers and C-terminus of ZNF509L, resulting in only one zinc-finger. ZNF509L and -S1 inhibit cell proliferation by activating p21/CDKN1A and RB transcription, respectively. When cells are exposed to severe DNA damage, p53 activates PUMA (p53-upregulated modulator of apoptosis) transcription. Interestingly, apoptosis due to transcriptional activation of PUMA by p53 is attenuated by ZNF509S1. Thus we investigated the molecular mechanism(s) underlying the transcriptional attenuation and anti-apoptotic effects of ZNF509S1. We show that ZNF509S1 modulation of p53 activity is important in PUMA gene transcription by modulating post-translational modification of p53 by p300. ZNF509S1 directly interacts with p53 and inhibits p300-mediated acetylation of p53 lysine K382, with deacetylation of p53 K382 leading to decreased DNA binding at the p53 response element 1 of the PUMA promoter. ZNF509S1 may play a role not only in cell cycle arrest, by activating RB expression, but also in rescuing cells from apoptotic death by repressing PUMA expression in cells exposed to severe DNA damage.

수수×수단그라스 교잡종 ( Sorghum bicolor ( L ) Moench ) 과 대두 ( Glycine Max ( L. ) Merr ) 간작이 생육특성 및 토양의 이화학적 성분에 미치는 영향

이상무,전병태 ( S . M . Lee,B . T . Jeon ) 한국축산학회 1996 한국축산학회지 Vol.38 No.2

Effects of sevoflurane on collagen production and growth factor expression in rats with an excision wound

LEE, H.-J.,KWON, J.-Y.,SHIN, S.-W.,BAEK, S.-H.,CHOI, K.-U.,JEON, Y.-H.,KIM, W.-S.,BAE, J.-H.,CHOI, H.-J.,KIM, H.-K.,BAIK, S.-W. Blackwell Publishing Ltd 2010 Acta anaesthesiologica Scandinavica Vol.54 No.7

<P>Background</P><P>Sevoflurane is a widely used inhalation anesthetic, but there are no studies on its effect on the wound-healing process. This study was undertaken to evaluate the effect of exposure time to sevoflurane on wound healing.</P><P>Method</P><P>Male Sprague–Dawley rats were used. Two circular full-thickness skin defects 8 mm in diameter were made on the dorsum of the rats. The animals were divided into six groups according to exposed gas type and time: S1 (sevoflurane, 1 h), S4 (sevoflurane, 4 h), S8 (sevoflurane, 8 h), O1 (oxygen, 1 h), O4 (oxygen, 4 h), and O8 (oxygen, 8 h). The surface area of the wounds was measured 0, 1, 3, and 7 days after surgery. Separately, the mean blood pressures (MBP) and arterial oxygen pressures (PaO<SUB>2</SUB>) were monitored during the sevoflurane exposure. Collagen type I production and transforming growth factor-β1 (TGF-β1) and basic fibroblast growth factor (bFGF) expression on the wound surface were analyzed. Routine histological analysis was also performed.</P><P>Result</P><P>Exposure duration to sevoflurane had no influence on MBP and PaO<SUB>2</SUB>. The reduction in wound size and collagen type I production was delayed in S8. The expression of TGF-β1 and bFGF on the wound surface in S8 was significantly attenuated in S8. The histology of the S8 demonstrated a delayed healing status.</P><P>Conclusions</P><P>Prolonged exposure to sevoflurane might alter the inflammatory phase of the wound-healing process by attenuation of growth factor expression such as TGF-β1 and bFGF and subsequently by reduced collagen production.</P>

Salmonella Typhi균의 분자역학적 연구

이복권,강연호,박미선,유재연,김성한,김준영,전형근 국립보건연구원 1999 국립보건원보 Vol.36 No.-

S-57 전자해도의 GML 변환 및 데이터베이스 관리

전성환(S.H.Jeon),이성대(S.D.Lee),곽용원(Y.W.Kwak),박철현(C.H.Park),박휴찬(H.C.Park) 한국정보과학회 2006 한국정보과학회 학술발표논문집 Vol.33 No.2C

S-57 포맷으로 기술된 전자해도는 바다에 대한 디지털 지도로서 해안선, 수심, 항로표시 등과 같은 다양한 정보를 표현하고 있다. 이러한 전자해도는 주로 선박의 항해라는 특수한 목적으로만 사용되어 왔고, 전용의 시스템을 통해서만 이용할 수 있는 단점이 있다. 또한, S-57이라는 특수한 포맷으로 기술되어 있기 때문에 다양한 활용이 어렵다는 문제점을 가지고 있다. 이러한 전자해도를 손쉽게 이용하고 해양정보시스템의 기반 데이터로 활용하기 위해서는 범용의 표준 포맷으로 변환할 필요가 있다. 이러한 범용 표준으로 OGC(Open Geospatial Consortium)에서는 지리정보를 효과적으로 표현할 수 있는 XML(eXtensible Markup Language) 기반의 GML(Geography Markup Language) 표준을 발표하였다. 이에 본 논문에서는 선박의 항해에만 제한적으로 사용되던 전자해도를 손쉽고 다양한 활용이 가능하도록 GML로 변환하고 관리하는 방법을 제한한다. 즉, S-57 포맷의 전자해도를 GML 포맷으로 변환하고, 변환된 GML을 데이터베이스로 관리하는 시스템을 설계하고 구현하였다.

Development of a Saccharomyces cerevisiae strain for the production of 1,2-propanediol by gene manipulation

Jeon, E.,Lee, S.,Kim, D.,Yoon, H.,Oh, M.,Park, C.,Lee, J. IPC Science and Technology Press ; Elsevier Scienc 2009 Enzyme and microbial technology Vol.45 No.1

The main goal of this research was to achieve a more efficient production of 1,2-propanediol (1,2-PD) using mutated Saccharomyces cerevisiae. 1,2-PD cannot be produced by wild type S. cerevisiae. To develop a S. cerevisiae mutant that could produce 1,2-PD, the mgs gene of E. coli-K12 MG1655 and the dhaD gene of Citrobacter freundii were inserted into yeast expression vectors such as pESC-URA and pESC-TRP and transformed into the wild type of S. cerevisiae. As a result, the batch fermentation of S. cerevisiae YPH500, harboring an mgs gene inserted pJES27 vector, resulted in a yield of 0.17g/L. On the other hand, the methylglyoxal synthase of the recombinant S. cerevisiae YPH500, harboring a dhaD gene inserted pJES29 vector, was inactive and produced no detectable amount of 1,2-PD. Therefore, in order to achieve a maximum yield of 1,2-PD, we selected the pESC-TRP vector that is able to co-express the dhaD gene with the pJES27 vector. By inserting the dhaD gene into the pESC-TRP vector, the pJES30 vector was constructed. The maximal yield of 1,2-PD achieved in a 1% galactose batch fermentation by pJES27 and pJES30 harboring S. cerevisiae was 0.45g/L.

Ribosomal protein S6 is a selective mediator of TRAIL-apoptotic signaling

Jeon, Y-J,Kim, I K,Hong, S-H,Nan, H,Kim, H-J,Lee, H-J,Masuda, E S,Meyuhas, O,Oh, B-H,Jung, Y-K Nature Publishing Group 2008 Oncogene Vol.27 No.31

TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is a potent inducer of apoptosis in tumor cells and holds a promise as a therapeutic agent against cancer. To elucidate the death signaling evoked by TRAIL, we performed a functional genetic screening and rescued TRAIL-resistant Jurkat clones harboring ribosomal protein S6 (rpS6) cDNA in anti-sense frame. Reduction of rpS6 expression in Jurkat and HeLa cells attenuated apoptosis induced by TRAIL, but not those by other cell death signals, including tumor necrosis factor-α and cycloheximide, etoposide, doxorubicin, tunicamycin and staurosporine. Death receptor (DR) 4, but not DR5, was downregulated in rpS6 knockdown cells. Conversely, the sensitivity to TRAIL was increased by the ectopic expression of wild-type rpS6 and further by phospho-defective rpS6 mutant (S6-SS235,6AA), but not by phospho-mimic rpS6 mutant (S6-SS235,6DD). Also, unphosphorylatable rpS6 knock-in mouse embryo fibroblasts (rpS6<SUP>P−/−</SUP> MEFs) were more sensitive to TRAIL than control MEFs. In addition, SKHep-1 tumor cells, which express less phospho-rpS6 and are more sensitive to TRAIL than other tumor cells, became effectively desensitized to TRAIL after rpS6 knockdown. These results suggest that rpS6, especially in its unphosphorylated form, is a selective mediator of TRAIL-induced apoptosis.Oncogene (2008) 27, 4344–4352; doi:10.1038/onc.2008.73; published online 24 March 2008