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정두련,송재훈,김은옥,류지소,이남용,이혁,백경란,김성민,배직현,우준희,김양수 대한감염학회 1997 감염 Vol.29 No.4
목적: 지역사회 획득 감염의 매우 흔한 원인균인 폐렴구균의 페니실린 및 다른 항균제에 대한 내성의 증가는 세계적으로 문제가 될 뿐 아니라 국내에서 더욱 큰 문제로 대두되고 있다. 본 연구는 항균제 내성 여부에 따른 폐렴구균 균혈증의 임상적 특성 및 위험 요인를 분석하여 항균제 내성의 임상적 의미를 조사하고자 시행되었다. 방법:1989년부터 1994년까지의 폐렴구균 균혈증 41례를 대상으로 하여 의무기록지를 조사하였다. 균주의 항균제 감수성 검사는 oxacillin 디스크 확산법으로 페니실린 내성 여부를 거사한 후, 한천 희석법을 이용하여 페니실린을 비롯한 11개의 항균제의 MIC (minimal inhibitory concentration)를 구하고 감수성 여부를 판정하였다. 결과: 41균주 중 68.3%가 페니실린에 대하여 내성(중등도 12.2%, 고도 56.1%)을 보였으며 다제내성률은 61%였다. 특히 소아에서는 100%(고도 88.2%)의 내성률을 보여 성인보다 내성률이 더 높았다. 페니실린 내성 균주는 대부분 다른 β-lactam 항균제에도 내성을 보였으며 특히 페니실린 고도 내성 균주는 cefotaxime, ceftriaxone에 대하여 100% 내성을 보였고 imipenem에 대해서도 95.5%의 중등도 내성률을 보였다. 혈청형은 19와 23이 많았고 그 외에 6이 있었다. 임상적 특성의 분석상 환자들의 연령분포는 3개월부터 82세까지였으며 기저질환을 가지고 있는 환자가 56%이었으며 지역사회 획득 감염이 71%였다. 균혈증의 일차감염원은 폐렴(22례, 54%)과 수막염(5례, 12%)이 가장 많았다. 페니실린 내성의 위험요인으로는 소아 연령만이 유의한 요인으로 분석되었다. 항균요법에 대한 반응을 볼 때 실패한 경우는 고도 내성 군의 20%에서만 있었으며 병원내 총사망률은 페니실린 감수성 군이 30%, 중등도 내성 군이 20%, 고도 내성 군이 13.6%로서 유의한 차이는 없었다. 결론: 페니실린 내성 폐렴구균은 국내에 만연하고 있으며 높은 다제내성률을 보였다. 이들은 대개 지역 사회 획득 감염을 일으키는데 균혈증의 경우 그 사망률은 내성 여부에 따른 차이를 보이지 않았다. 소아연령만이 페니실린 내성의 위험요인으로 분석되었다. Background: The emergence of penicillin-resistant Streptococcus pneumoniae (PRSP) poses serious therapeutic problem in clinical practice, especially in cases with bacteremia or meningitis. Methods: To investigate clinical characteristics of bacteremic pneumococcal diseases due to PRSP, we retrospectively analyzed 41 cases with cocumented bacteremic diseases seen in a tertiary care hospital between 1989 and 1994. Results: Agar dilution test of 41 strains isolated showed that 68.3% of S. pneumoniae were PRSP [high-level resistance(R) 56.1%, intermediate resistance(I) 12.2%]. High-level resistant strains were not susceptible to other β-lactam agents, whereas isolates of penicillin-susceptible S. pneumoniae(PSSP) were uniformly susceptible to all β-lactam agents. Predominant serogroups of PRSP were 19, 23, and 6. Bacteremic diseases caused by PRSP included pneumonia (22), meningitis (5), peritonitis (3), acute otitis media (2), acute tonsillitis (2), endocarditis (1), pyelonephritis(1), and primary bacteremia(5). Children were more likely to be infected with PRSP with high-level or intermediately resistant strains than were adults(P=0.0001), but no differences were seen between PRSP and PSSP regarding sex. previous antibiotic history, previous hospitalization, and underlying immunocompromised conditions. Most cases were community-acquired (R 78.3%, I 60%, S 61.5%). Fatality rates of patients infected with PRSP were not different significantly from PSSP (22.6% vs. 30%). However, most fatal cases had underlying immunocompromised conditions. Conclusion: PRSP is widely prevalent in Korea and shows resistance to most antibiotics. It causes community-acquired bacteremic diseases with poor outcomes, but there was no difference in mortality between patients infected with PRSP and PSSP. Pediatric age was the only risk factor for penicillin resistance.
Ryu, Jae-Ryeon,Kim, Young-Shin,Kim, Hyeong-In,Lee, Heui-Jung,Lee, Won-Ho,Yoo, Mi-Ae 부산대학교 유전공학연구소 1996 분자생물학 연구보 Vol.12 No.-
D-raf, a Drosophila homolog of Raf - 1, functions as a signal transducer in cell proliferation and differentiation. The reporter plasmid p5'-1103 Draf-lacZ fused the Draf gene regulatory region (-1103~+300 with respect to the translation initiation site) with the lacZ gene in a P-element vector was constructed. Expression of the Draf-lacZ fusion gene was demonstrated in Kc cells by transient expression assay. Transgenic lines bearing Draf-lacZ fusion gene were established by P-element mediated transformation with the reporter plasmid. Spatial pattern of the Draf-lacZ expression in transgenic embryos and ovaries was similar to the distribution of the endogenous D-raf transcripts examined by in situ hybridization in previous study. We first report the expression of D-rsf gene in larval fat body analogous to the vertebrate liver and in testis and anterior ejaculatory duct of adult male. And our results show that the regulatory region is sufficient for expression of the D-raf gene. Draf-lacZ transgenic flies obtained in this study promise to be useful for studying multiple roles and regulation of expression of D-raf gene.
Ryu, Jae-Ryeon,Choi, Thae-Yeong,Kwon, Eun-Jeong,Lee, Won-Ho,Nishida, Yasuyoshi,Hayashi, Yuko,Matsukage, Akio,Yamaguchi, Masamitsu,Yoo, Mi-Ae 부산대학교 유전공학연구소 1997 분자생물학 연구보 Vol.13 No.-
The DRE/DREF system plays an important role in transcription of DNA replication genes such as those encoding the 180 and 73 kDa subunits of DNA polymeraseαas well as that encoding PCNA. In this study, we found two sequences homologous to DRE(5'-TATCGATA-3')in the 5'-flanking region(-370 to-357 with respect to the transcription initiation site) of the D-raf gene and confirmed transcription activity through gel mobility shift assay, transient CAT assays, and spatial patterns of lacZ expression in transgenic larval tissues carrying D-raf gene is another target of the Zerknu¨llt(Zen)protein with observation of D-raf repression by Zen protein in cultured cells anf its ectopic expression in the dorsal region of the homozygous zen mutant embryo. The evdience of DRE/DREF involvement in regulation of the D-raf gene obtained in this study strongly supports the idea that the DRE/DREF system is responsible for the coordinated regulation of cell proliferation-related genes in Drosophila.
ACN9 Regulates the Inflammatory Responses in Human Bronchial Epithelial Cells
( Jae Hoon Jeong ),( Jeeyoung Kim ),( Jeongwoon Kim ),( Hye-ryeon Heo ),( Jin Seon Jeong ),( Young-joon Ryu ),( Yoonki Hong ),( Seon-sook Han ),( Seok-ho Hong ),( Seung-joon Lee ),( Woo Jin Kim ) 대한결핵 및 호흡기학회 2017 Tuberculosis and Respiratory Diseases Vol.80 No.3
Background: Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. Methods: We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9 . We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. Results: ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. Conclusion: Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.
ACN9 Regulates the Inflammatory Responses in Human Bronchial Epithelial Cells
Jeong, Jae Hoon,Kim, Jeeyoung,Kim, Jeongwoon,Heo, Hye-Ryeon,Jeong, Jin Seon,Ryu, Young-Joon,Hong, Yoonki,Han, Seon-Sook,Hong, Seok-Ho,Lee, Seung-Joon,Kim, Woo Jin The Korean Academy of Tuberculosis and Respiratory 2017 Tuberculosis and Respiratory Diseases Vol.80 No.3
Background: Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. Methods: We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9. We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. Results: ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. Conclusion: Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.