• 제목/요약/키워드: Gyeongsang

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Effect of the Urease Accessory Genes on Activation of the Helicobacter pylori Urease Apoprotein

  • Park, Jeong-Uck;Song, Jae-Young;Kwon, Young-Cheol;Chung, Mi-Ja;Jun, Jin-Su;Park, Jeong-Won;Park, Seung-Gyu;Hwang, Hyang-Ran;Choi, Sang-Haeng;Baik, Seung-Chul;Kang, Hyung-Lyun;Youn, Hee-Shang;Lee, Woo-Kon;Cho, Myung-Je;Rhee, Kwang-Ho
    • Molecules and Cells
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    • 제20권3호
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    • pp.371-377
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    • 2005
  • The roles that accessory gene products play in activating the Helicobacter pylori urease apoprotein were examined. The activity of the urease apoprotein increased in the following order when it was expressed with the accessory genes: ureG < ureGH < ureFGH < ureEFGH < ureIEFGH. Moreover, stepwise additions of ureE and ureI to ureFGH significantly increased urease activity. Urease apoproteins coexpressed with ureFGH, ureEFGH, and ureIEFGH had similar low chymotrypsin susceptibilities. In vivo and in vitro activation studies showed that the cooperative effect of the accessory proteins involved processes in which the UreFGH complex, UreE, and UreI were implicated. Thus, the UreFGH complex may serve to alter the conformation of the apoprotein into one that is more competent to assemble a stable metallocenter, and that facilitates cooperative effects.

Helicobacter pylori Strain 51 (Korean Isolate): Ordered Overlapping BAC Library, Combined Physical and Genetic Map, and Comparative Analysis with H. pylori Strain 26695 and Strain J99

  • KANG HYUNG-LYUN;LEE WOO-KON;SONG JAE-YOUNG;CHOI SANG-HAENG;PARK SEONG-GYU;RYU BOK-DEOK;LEE EUN-JOO;KIM JI-SUN;PARK JEONG-UCK;BAIK SEUNG-CHUL;CHOI MYOUNG-BUM;YOUN HEE-SHANG;KO GYUNG-HYUCK
    • Journal of Microbiology and Biotechnology
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    • 제15권4호
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    • pp.844-854
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    • 2005
  • We constructed a defined physical and genetic map of H. pylori strain 51, previously isolated from a Korean patient with a duodenal ulcer, by combining a restriction analysis by pulse-field gel electrophoresis with the construction of a BAC library. A Notl-digest of H. pylori strain 51 genome yielded seven fragments, from which the genomic size was estimated to be 1,698$\pm$24 kb. The BAC library was constructed from 50 to 200 kb fragments of HindIII-digested genomic DNA. From 700 BAC clones, an ordered overlapping maxi-set of 82 BAC clones was assembled that covered the entire genome. The positions of 15 genes were localized in the strain 51 genome with 4-22 kb of resolution and were compared with their orthologues in strain 26695 and strain J99. The arrangement of the 15 genes was identical in strain 51 and strain J99, except for flaA and hpaA. The plasticity zone of strain 51, like that of strain J99, was located in the single region, and was shorter than those of strain 26695 and strain J99. The strain 51 plasticity zone consisted of ORFs common only to strain 51 and J99 or to strain 51 and 26695, as well as strain 51-specific ORFs. Three genetic translocations and/or inversions were found between orthologue ORFs in strain 51 and strain J99. These results show that the chromosomal organization of strain 51 differs from Western strains such as strain 26695 and strain J99.

Body Mass Index as a Predictor of Acute Kidney Injury in Critically Ill Patients: A Retrospective Single-Center Study

  • Ju, Sunmi;Lee, Tae Won;Yoo, Jung-Wan;Lee, Seung Jun;Cho, Yu Ji;Jeong, Yi Yeong;Lee, Jong Deog;Kim, Ju-young;Lee, Gi Dong;Kim, Ho Cheol
    • Tuberculosis and Respiratory Diseases
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    • 제81권4호
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    • pp.311-318
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    • 2018
  • Background: The aim of this study was to examine the influence of body mass index (BMI) on the development of acute kidney injury (AKI) in critically ill patients in intensive care unit (ICU). Methods: Data of patients admitted to medical ICU from December 2011 to May 2014 were retrospectively analyzed. Patients were classified into three groups according to their BMI: underweight (< $18.5kg/m^2$), normal ($18.5-24.9kg/m^2$), and overweight (${\geq}25kg/m^2$). The incidence of AKI was compared among these groups and factors associated with the development of AKI were analyzed. AKI was defined according to the Risk, Injury, Failure, Loss of kidney function, and End-stage (RIFLE) kidney disease criteria. Results: A total of 468 patients were analyzed. Their mean BMI was $21.5{\pm}3.9kg/m^2$, including 102 (21.8%) underweight, 286 (61.1%) normal-weight, and 80 (17.1%) overweight patients. Overall, AKI occurred in 82 (17.5%) patients. The overweight group had significantly (p<0.001) higher incidence of AKI (36.3%) than the underweight (9.8%) or normal group (15.0%). In addition, BMI was significantly higher in patients with AKI than that in those without AKI ($23.4{\pm}4.2$ vs. $21.1{\pm}3.7$, p<0.001). Multivariate analysis showed that BMI was significantly associated with the development of AKI (odds ratio, 1.893; 95% confidence interval, 1.224-2.927). Conclusion: BMI may be associated with the development of AKI in critically ill patients.

Risk Factor and Mortality in Patients with Pulmonary Embolism Combined with Infectious Disease

  • Lee, Gi Dong;Ju, Sunmi;Kim, Ju-Young;Kim, Tae Hoon;Yoo, Jung-Wan;Lee, Seung Jun;Cho, Yu Ji;Jeong, Yi Yeong;Jeon, Kyung Nyeo;Lee, Jong Deog;Kim, Ho Cheol
    • Tuberculosis and Respiratory Diseases
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    • 제83권2호
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    • pp.157-166
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    • 2020
  • Background: Infectious conditions may increase the risk of venous thromboembolism. The purpose of this study was to evaluate the risk factor for combined infectious disease and its influence on mortality in patients with pulmonary embolism (PE). Methods: Patients with PE diagnosed based on spiral computed tomography findings of the chest were retrospectively analyzed. They were classified into two groups: patients who developed PE in the setting of infectious disease or those with PE without infection based on review of their medical charts. Results: Of 258 patients with PE, 67 (25.9%) were considered as having PE combined with infectious disease. The sites of infections were the respiratory tract in 52 patients (77.6%), genitourinary tract in three patients (4.5%), and hepatobiliary tract in three patients (4.5%). Underlying lung disease (odds ratio [OR], 3.69; 95% confidence interval [CI], 1.926-7.081; p<0.001), bed-ridden state (OR, 2.84; 95% CI, 1.390-5.811; p=0.004), and malignant disease (OR, 1.867; 95% CI, 1.017-3.425; p=0.044) were associated with combined infectious disease in patients with PE. In-hospital mortality was higher in patients with PE combined with infectious disease than in those with PE without infection (24.6% vs. 11.0%, p=0.006). In the multivariate analysis, combined infectious disease (OR, 4.189; 95% CI, 1.692-10.372; p=0.002) were associated with non-survivors in patients with PE. Conclusion: A substantial portion of patients with PE has concomitant infectious disease and it may contribute a mortality in patients with PE.