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Sinae Kim,Jong Ho Lee,Siyoung Lee,Saerok Shim,Tam T. Nguyen,Jihyeong Hwang,Heijun Kim,Yeo-Ok Choi,Jaewoo Hong,Suyoung Bae,Hyun Jhung Jhun,Hokee Yum,이영민,Edward D. Chan,Liping Yu,Tania Azam,Yong-Dae Kim 대한면역학회 2020 Immune Network Vol.20 No.5
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) is a positive-sense single-stranded RNA (+ssRNA) that causes coronavirus disease 2019 (COVID-19). The viral genome encodes twelve genes for viral replication and infection. The third open reading frame is the spike (S) gene that encodes for the spike glycoprotein interacting with specific cell surface receptor – angiotensin converting enzyme 2 (ACE2) – on the host cell membrane. Most recent studies identified a single point mutation in S gene. A single point mutation in S gene leading to an amino acid substitution at codon 614 from an aspartic acid 614 into glycine (D614G) resulted in greater infectivity compared to the wild type SARS-CoV2. We were interested in investigating the mutation region of S gene of SARS-CoV2 from Korean COVID-19 patients. New mutation sites were found in the critical receptor binding domain (RBD) of S gene, which is adjacent to the aforementioned D614G mutation residue. This specific sequence data demonstrated the active progression of SARS-CoV2 by mutations in the RBD of S gene. The sequence information of new mutations is critical to the development of recombinant SARS-CoV2 spike antigens, which may be required to improve and advance the strategy against a wide range of possible SARS-CoV2 mutations.
The Link between Fusobacteria and Colon Cancer: a Fulminant Example and Review of the Evidence
Martina King,Hermione Hurley,Kevin R. Davidson,Edward C. Dempsey,Michelle A. Barron,Edward D. Chan,Amy Frey 대한면역학회 2020 Immune Network Vol.20 No.4
Systemic infections due to Fusobacterium may originate in the tonsillar/internal jugular veins or from the abdomen. We encountered a patient who presented with bacteremia, fulminant septic shock, and extensive soft tissue pyogenic infection due to Fusobacterium necrophorum. In addition, there was widespread metastatic colon cancer with the unique finding of pre-mortem co-localization of F. necrophorum and cancer cells at a site distant from the colon. We reviewed the literature of the association of F. necrophorum and colon cancer, and discuss the evidence of how each of these 2 distinct entities may mutually augment the development or progression of the other.
Schenkel Alan R.,Mitchell John D.,Cool Carlyne D.,Bai Xiyuan,Groshong Steve,Koelsch Tilman,Verma Deepshikha,Ordway Diane,Chan Edward D. 대한면역학회 2022 Immune Network Vol.22 No.3
Little is known of the lung cellular immunophenotypes in patients with non-tuberculous mycobacterial lung disease (NTM-LD). Flow-cytometric analyses for the major myeloid and lymphoid cell subsets were performed in less- and more-diseased areas of surgically resected lungs from six patients with NTM-LD and two with Pseudomonas aeruginosa lung disease (PsA-LD). Lymphocytes, comprised mainly of NK cells, CD4+ and CD8+ T cells, and B cells, accounted for ~60% of all leukocytes, with greater prevalence of T and B cells in more-diseased areas. In contrast, fewer neutrophils were found with decreased number in more-diseased areas. Compared to NTM-LD, lung tissues from patients with PsA-LD demonstrated relatively lower numbers of T and B lymphocytes but similar numbers of NK cells. While this study demonstrated a large influx of lymphocytes into the lungs of patients with chronic NTM-LD, further analyses of their phenotypes are necessary to determine the significance of these findings.
Xiyuan Bai,Shanae L. Aerts,Deepshikha Verma,Diane J. Ordway,Edward D. Chan 대한면역학회 2018 Immune Network Vol.18 No.3
Many studies have linked cigarette smoke (CS) exposure and tuberculosis (TB) infection and disease although much fewer have studied second-hand smoke (SHS) exposure. Our goal is to review the epidemiologic link between SHS and TB as well as to summarize the effects SHS and direct CS on various immune cells relevant for TB. PubMed searches were performed using the key words “tuberculosis” with “cigarette,” “tobacco,” or “second-hand smoke.” The bibliography of relevant papers were examined for additional relevant publications. Relatively few studies associate SHS exposure with TB infection and active disease. Both SHS and direct CS can alter various components of host immunity resulting in increased vulnerability to TB. While the epidemiologic link of these 2 health maladies is robust, more definitive, mechanistic studies are required to prove that SHS and direct CS actually cause increased susceptibility to TB.
이시영,최동기,곽아름,김시내,Tam Thanh Nguyen,길가애,김은혜,유광하,김인애,이영민,전현정,Edward D. Chan,Xiyuan Bai,김현우,김용성,김수현 대한면역학회 2017 Immune Network Vol.17 No.2
The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on a-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32g and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AATFc fusion protein inhibited IL-32g-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32g to PR3 was abrogated by AAT-Fc. The data suggest that the specific antiinflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.
Lee, Siyoung,Choi, Dong-Ki,Kwak, Areum,Kim, Sinae,Nguyen, Tam Thanh,Gil, Gaae,Kim, Eunhye,Yoo, Kwang Ha,Kim, In Ae,Lee, Youngmin,Jhun, Hyunjhung,Chan, Edward D.,Bai, Xiyuan,Kim, Hyunwoo,Kim, Yong-Sung 한국조명·전기설비학회 2017 한국조명·전기설비학회 학술대회논문집 Vol. No.
<P>The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on α-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32γ and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AAT-Fc fusion protein inhibited IL-32γ-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32γ to PR3 was abrogated by AAT-Fc. The data suggest that the specific anti-inflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.</P>