• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제25권4호
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• pp.375-378
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• 1999

우수한 항생제 요법이후 치성 감염으로 인한 Ludwig's angina의 합병증으로 인한 사망은 극히 드문 것으로 알려져 왔다. 본 교실에서는 고혈압의 기왕력을 지닌 57세 여환이 하악 전치부의 치근단 농양을 원인으로 하는 좌측 협간극의 감염으로 인하여 개구장애와 동통을 주소로 내원하여 입원치료중, Ludwig's angina 및 심경부감염으로 확산되고 입원 10일째 패혈증과 성인 호흡장애 증후군(ARDS)및 산발성 혈관내 응고증(DIC)의 진단하에 사망한 증례를 통하여 패혈증의 소견과 진단 및 그에 따른 처치 등에 대한 지견을 얻었기에 진단과 예방에 도움을 주고자 문헌고찰과 함께 보고하는 바이다.

• Biomolecules & Therapeutics
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• 제24권4호
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• pp.387-394
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• 2016

Sepsis, a serious clinical problem, is characterized by a systemic inflammatory response to infection and leads to organ failure. Toll-like receptor (TLR) signaling is intimately implicated in hyper-inflammatory responses and tissue injury during sepsis. Histone deacetylase (HDAC) inhibitors have been reported to exhibit anti-inflammatory properties. The aim of this study was to investigate the hepatoprotective mechanisms of trichostatin A (TSA), a HDAC inhibitor, associated with TLR signaling pathway during sepsis. The anti-inflammatory properties of TSA were assayed in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Polymicrobial sepsis was induced in mice by cecal ligation and puncture (CLP), a clinically relevant model of sepsis. The mice were intraperitoneally received TSA (1, 2 or 5 mg/kg) 30 min before CLP. The serum and liver samples were collected 6 and 24-h after CLP. TSA inhibited the increased production of tumor necrosis factor (TNF)-${\alpha}$ and interleukin (IL)-6 in LPS-stimulated RAW264.7 cells. TSA improved sepsis-induced mortality, attenuated liver injury and decreased serum TNF-${\alpha}$ and IL-6 levels. CLP increased the levels of TLR4, TLR2 and myeloid differentiation primary response protein 88 (MyD88) protein expression and association of MyD88 with TLR4 and TLR2, which were attenuated by TSA. CLP increased nuclear translocation of nuclear factor kappa B and decreased cytosolic inhibitor of kappa B ($I{\kappa}B$) protein expression, which were attenuated by TSA. Moreover, CLP decreased acetylation of $I{\kappa}B$ kinase (IKK) and increased association of IKK with $I{\kappa}B$ and TSA attenuated these alterations. Our findings suggest that TSA attenuates liver injury by inhibiting TLR-mediated inflammatory response during sepsis.

• 한국임상약학회지
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• 제30권3호
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• pp.161-168
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• 2020

Background: Recently, a study comprising adult patients with sepsis admitted in the intensive care unit (ICU) was conducted. The patients were treated with high doses of intravenous ascorbic acid, thiamine, and hydrocortisone; the clinical outcomes demonstrated significant therapeutic benefits. The mortality rate in children with sepsis is approximately 25%. However, the effects of additional treatment with ascorbic acid and thiamine ("vitamin protocol") in children are rarely investigated. Methods: A retrospective analysis was performed using medical records of patients diagnosed with sepsis and admitted to the pediatric ICU (PICU) between September 2016 and June 2019. The control group received treatment only as per sepsis protocol, whereas the treated group received both sepsis protocol and the vitamin protocol. The primary endpoint was change in Vasoactive-Inotropic Score (VIS) for 5 days. The secondary endpoints included the length of stay in the PICU, duration of using mechanical ventilators and vasopressors, and mortality rate. Results: The number of patients in the treated and control groups was 33 and 24, respectively. The treated group showed greater decrease in their VIS for 5 days than the control group (44.4 vs 18.6); however, the difference was not statistically significant. The length of stay in the PICU was significantly longer for the treated group than for the control group [10.0 days (Interquartile range (IQR), 6-18) vs 4.5 days (IQR, 4-10.3); p=0.004]. Conclusions: No significant treatment benefits were observed following vitamin protocol administration to the pediatric patients with sepsis. Further studies are necessary for improving the efficacy and safety of the vitamin protocol.

• Molecules and Cells
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• 제44권12호
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• pp.893-899
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• 2021

BLT2 is a low-affinity receptor for leukotriene B₄, a potent lipid mediator of inflammation generated from arachidonic acid via the 5-lipoxygenase pathway. The aim of this study was to investigate whether BLT2 plays any role in sepsis, a systemic inflammatory response syndrome caused by infection. A murine model of cecal ligation and puncture (CLP)-induced sepsis was used to evaluate the role of BLT2 in septic inflammation. In the present study, we observed that the levels of ligands for BLT2 (LTB₄ [leukotriene B₄] and 12(S)-HETE [12(S)-hydroxyeicosatetraenoic acid]) were significantly increased in the peritoneal lavage fluid and serum from mice with CLP-induced sepsis. We also observed that the levels of BLT2 as well as 5-lipoxygenase (5-LO) and 12-LO, which are synthesizing enzymes for LTB₄ and 12(S)-HETE, were significantly increased in lung and liver tissues in the CLP mouse model. Blockade of BLT2 markedly suppressed the production of sepsis-associated cytokines (IL-6 [interleukin-6], TNF-α [tumor necrosis factor alpha], and IL-1β [interleukin-β] as well as IL-17 [interleukin-17]) and alleviated lung inflammation in the CLP group. Taken together, our results suggest that BLT2 cascade contributes to lung inflammation in CLP-induced sepsis by mediating the production of inflammatory cytokines. These findings suggest that BLT2 may be a potential therapeutic target for sepsis patients.

• The Korean Journal of Physiology and Pharmacology
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• 제12권2호
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• pp.79-81
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• 2008

The effects of decursinol on various models of sepsis were investigated. Intra-peritoneal pretreatment of mice with various doses of decursinol ($1{\sim}100$ mg/kg) effectively suppressed lethality induced in three mouse models of experimental sepsis, i.e., lipopolysaccharide (LPS)/D-galactosamine (GalN), high-dose LPS (20 mg/kg), and cecal ligation and puncture (CLP). Intra-peritoneal pretreatment of mice with decursinol (50 mg/kg) markedly enhanced the LPS/GalN -induced increase of plasma interleukin-10 (IL-10) levels, without affecting plasma TNF-${\alpha}$, IL-6 and IL-12 levels. These results suggest that decursinol could be effective for prevention or treatment of sepsis.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.301.3-302
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• 2002

Sepsis remains the leading cause of morbidity and mortality following trauma. Although hepatocellular dysfunction occurs during trauma and sepsis. the mechanism responsible for this remains unclear. We investigated the role of Kupffer cells in the alterations in microsomal drug metabolizing function during trauma and sepsis. Rats were subjected to trauma by femur fracture (FFx). After 72h, polymicrobial sepsis was induced by cecal ligation and puncture(CLP). (omitted)

• 한국동물위생학회지
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• 제35권3호
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• pp.191-195
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• 2012

Accumulated evidence indicate that Ginkgo biloba extract (EGb 761) acts as an antioxidant and scavenger of free radicals as well as influencing apoptotis. Earlier studies have employed the inflammatory agent lipopolysaccharide (LPS) to induce severe sepsis. In the present study, we examined whether the intraperitoneal injection of EGb 761 increases the survival rate of mice in the LPS-induced severe sepsis model. The survival rate was significantly increased by 30% in mice administered with 100 mg/kg of EGb 761 but not in mice administered with 50 mg/kg EGb 761. In addition, pre-treatment with EGb 761 increased the survival rate (30%) but post-treatment with EGb 761 did not. These results suggest that EGb 761 may have clinical potential in preventing sepsis induced mortality.

• 약학회지
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• 제51권6호
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• pp.383-388
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• 2007

It has been reported that sulfur-containing intermediates or products in the transsulfuration pathway including S-adenosylmethionine, 5'-methylthioadenosine, glutathione and taurine can prevent liver injury mediated by inflammation response induced by lipopolysaccharide (LPS) treatment. The present study examines the modulation of hepatic metabolism of sulfur amino acid in a model of acute sepsis induced by LPS treatment (5 mg/kg, iv). Serum TNF-alpha and hepatotoxic parameters were significantly increased in rats treated with LPS, indicating that LPS results in sepsis at the doses used in this study. LPS also induced oxidative stress determined by increases in malondialdehyde levels and decreases in total oxy-radical scavenging capacities. Hepatic methionine and glutathione concentrations were decreased, but S-adenosylho-mocysteine, cystathionine, cysteine, hypotaurine and taurine concentrations were increased. Hepatic protein expression of methionine adenosyltransferase, cystathionine beta-synthase and cysteine dioxygenase were induced, but gamma-glutamylcysteine ligase catalytic subunit levels were decreased. The results show that sepsis activates transsulfuration pathway from methionine to cysteine, suggesting an increased requirement for methionine during sepsis.

• The Korean Journal of Physiology and Pharmacology
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• 제26권6호
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• pp.511-518
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• 2022

Sepsis-associated myocardial injury, an invertible myocardial depression, is a common complication of sepsis. Neogambogic acid is an active compound in garcinia and exerts anthelmintic, anti-inflammatory, and detoxification properties. The role of neogambogic acid in sepsis-associated myocardial injury was assessed. Firstly, mice were pretreated with neogambogic acid and then subjected to lipopolysaccharide treatment to induce sepsis. Results showed that lipopolysaccharide treatment induced up-regulation of biomarkers involved in cardiac injury, including lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and troponin I (cTnI). However, pretreatment with neogambogic acid reduced levels of LDH, CK-MB, and cTnI, and ameliorated histopathological changes in the heart tissues of septic mice. Secondly, neogambogic acid also improved cardiac function in septic mice through reduction in left ventricular end-diastolic pressure, and enhancement of ejection fraction, fractional shortening, and left ventricular systolic mean pressure. Moreover, neogambogic acid suppressed cardiac apoptosis and inflammation in septic mice and reduced cardiac fibrosis. Lastly, protein expression of p-p38, p-JNK, and p-NF-κB in septic mice was decreased by neogambogic acid. In conclusion, neogambogic acid exerted anti-apoptotic, anti-fibrotic, and anti-inflammatory effects in septic mice through the inactivation of MAPK/NF-κB pathway.

• Clinical and Experimental Pediatrics
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• 제49권11호
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• pp.1167-1173
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• 2006

목 적 : 신생아 패혈증을 진단하기 위해 단독 그리고 복합적인 다양한 선별검사를 분석하기 위해 일신기독병원의 신생아집중치료실에서 2001년 4월 1일부터 2005년 12월 31일까지 68개월 동안 시행했다. 방 법 : 패혈증의 임상증상이 있는 100명의 신생아와 증상이 없는 정상 신생아를 대상으로 연구를 시행했다. 신생아 패혈증의 진단을 위해 CRP, 총 백혈구 수, 총 호중구 수, 미숙호중구/총호중구 비(I/T비), 혈소판 수, 호중구의 변성, 다형 핵 백혈구에 대한 GAC를 사용했다. 결 과 : CRP는 A군에서는 50례 중 40례에서(86%) 양성이었고 B군에서는 50례 중 37례에서(74%) 양성이었으며 특이도는 94%였다. 총 호중구 수는 민감도와 특이도가 각각 A군에서는 72%와 86%였고 B군에서는 62%와 86%로 단일 검사상 민감도가 두 번째로 높았다. A군에서 GAC와 혈소판 수에 대한 각각의 민감도는 74%와 64%였다. A군과 B군에 대해 검사를 개별적으로 시행했을 경우와 함께 시행했을 경우에 대한 민감도, 특이도, 그리고 예측도를 계산했다. 결 론 : CRP, 총 백혈구 수, 총 호중구 수, 혈소판 수, 호중구의 변성과 다형 핵 백혈구에 대한 GAC는 신생아 패혈증이 없는 배양 검사 상 음성인 경우를 알아내는데 높은 민감도를 나타냈다. 더욱이 3가지 검사를 함께 시행할 경우에 민감도가 증가했다.