• 대한암한의학회지
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• 제17권1호
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• pp.1-7
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• 2012

Objective : The association of cancer survival and components of the systemic inflammatory response, combined to form inflammation-based prognostic scores (modified Glasgow Prognostic Score (GPS), Neutrophil Lymphocyte Ratio, Platelet Lymphocyte Ratio) is reviewed in this article. Methods and Results : With extensive research of papers in the PubMed, there is good evidence that preoperative measures of the systemic inflammatory response predict cancer survival, independent of tumor stage, in primary operable cancer. GPS also shows its prognostic value as a predictor of survival, independent of tumor stage, performance status and treatment in a variety of advanced cancer. GPS is associated with chemotherapy related toxicities as well as response to treatment and C-reactive protein shows its clinical value as a monitor of chemotherapy response. The systemic inflammatory response is closely related to cachexia and may be suitable measure for the clinical definition of cancer cachexia. Conclusion : Anticipated survival using the inflammation-based prognostic score is a major factor to be taken into consideration when deciding whether active intervention including surgery and chemotherapy or palliation therapy including acupuncture and herb medication is appropriate.

• Journal of Chest Surgery
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• 제37권11호
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• pp.922-924
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• 2004

호흡곤란을 주소로 55세 남자 환자가 입원하였다. 환자는 급성 심근 경색에 의한 심부전으로 진단 받은 후 체외순환 하에서 관상 동맥 우회술을 시행하였다. 수술 후 1일째 발열, 백혈구 증가증, 빈맥, 빈호흡 등의 증상을 보이기 시작하면서 전신혈관저항이 감소하고 전신성 염증반응 증후군이 발생하면서 쇽으로 이행하였다. 환자는 고용량(36$\mu$g/min)의 norepinephrine으로 치료하였으며 회복되어 퇴원하였다.

• Asian Pacific Journal of Cancer Prevention
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• 제14권9호
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• pp.5473-5476
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• 2013

Background: In our study, the LDH, albumin, hemoglobin, neutrophile, thrombocyte, lymphocyte counts and prognostic significance of neutrophile-lymphocyte and thrombocyte-lymphocyte ratios in NSCLC derived from these counts obtained during regular examinations of patients were examined. Materials and Methods: Histopathologically diagnosed non-small-cell-lung cancer patients between 2008 and 2010 were included in the study. Before the treatment, full blood count including routine lymphocyte count, blood biochemistry examinations including liver (AST, ALT, total protein, Albumin), LDH and kidney (BUN, Cre) function tests were performed. Results: A total of 156 patients, 76 of whom (48.7%) were female and 80 of whom (51.3%) were male were included. Mean hemoglobin level was determined as 12. Overall survival was found to be significantly dependent on whether patients were anemic or not (p: 0.005). Mean LDH level was determined as 233.4. There was nosurvival difference between patients with and without high LDH (p: 0.532). In patients where NLR showed systemic inflammatory response, overall survival was 10.8 months whereas this duration was 19.6 months in patients where the systemic inflammatory response was negative (p: 0.012). In patients where TLR showed systemic inflammatory response, overall survival was 13.6 months whereas this duration was 21.9 months in patients where the systemic inflammatory response was negative (p: 0.04). Conclusions: Molecular methods have been changing rapidly in today's world and they manage the treatment besides defining the prognosis of patients. However, easily accessible and cheap laboratory parameters should be considered in the prognosis of patients besides these new methods.

• Journal of Yeungnam Medical Science
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• 제40권4호
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• pp.435-441
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• 2023

Pheochromocytomas and paragangliomas (PPGLs) may secrete hormones or bioactive neuropeptides such as interleukin-6 (IL-6), which can mask the clinical manifestations of catecholamine hypersecretion. We report the case of a patient with delayed diagnosis of paraganglioma due to the development of IL-6-mediated systemic inflammatory response syndrome (SIRS). A 58-year-old woman presented with dyspnea and flank pain accompanied by SIRS and acute cardiac, kidney, and liver injuries. A left paravertebral mass was incidentally observed on abdominal computed tomography (CT). Biochemical tests revealed increased 24-hour urinary metanephrine (2.12 mg/day), plasma norepinephrine (1,588 pg/mL), plasma normetanephrine (2.27 nmol/L), and IL-6 (16.5 pg/mL) levels. ¹⁸F-fluorodeoxyglucose (FDG) positron emission tomography/CT showed increased uptake of FDG in the left paravertebral mass without metastases. The patient was finally diagnosed with functional paraganglioma crisis. The precipitating factor was unclear, but phendimetrazine tartrate, a norepinephrine-dopamine release drug that the patient regularly took, might have stimulated the paraganglioma. The patient's body temperature and blood pressure were well controlled after alpha-blocker administration, and the retroperitoneal mass was surgically resected successfully. After surgery, the patient's inflammatory, cardiac, renal, and hepatic biomarkers and catecholamine levels improved. In conclusion, our report emphasizes the importance of IL-6-producing PPGLs in the differential diagnosis of SIRS.

• The Korean Journal of Physiology and Pharmacology
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• 제22권1호
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• pp.1-15
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• 2018

Inflammasomes are intracellular multiprotein complexes that coordinate anti-pathogenic host defense during inflammatory responses in myeloid cells, especially macrophages. Inflammasome activation leads to activation of caspase-1, resulting in the induction of pyroptosis and the secretion of pro-inflammatory cytokines including interleukin $(IL)-1{\beta}$ and IL-18. Although the inflammatory response is an innate host defense mechanism, chronic inflammation is the main cause of rheumatic diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), and $Sj{\ddot{o}}gren^{\prime}s$ syndrome (SS). Since rheumatic diseases are inflammatory/autoimmune disorders, it is reasonable to hypothesize that inflammasomes activated during the inflammatory response play a pivotal role in development and progression of these diseases. Indeed, previous studies have provided important observations that inflammasomes are actively involved in the pathogenesis of inflammatory/autoimmune rheumatic diseases. In this review, we summarize the current knowledge on several types of inflammasomes during macrophage-mediated inflammatory responses and discuss recent research regarding the role of inflammasomes in the pathogenesis of inflammatory/autoimmune rheumatic diseases. This avenue of research could provide new insights for the development of promising therapeutics to treat inflammatory/autoimmune rheumatic diseases.

• Pediatric Infection and Vaccine
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• 제24권2호
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• pp.102-107
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• 2017

목적: 가와사키병의 환아뿐만 아니라, 다른 전신 염증 질병의 환아들에 관상동맥 병변(coronary arterial lesion [CAL])의 발생이 보고되었다. 본 연구에서는 전형적인 전신염증반응증후군(systemic inflammatory response syndrome [SIRS])의 소견을 보이는 패혈증 마우스 모델에서 가와사키병 환아에게 관찰되는 CAL이 발생하는지 확인하고자 하였다. 방법: 생후 6주 C57BL/6 마우스에 내독소를 복강내주사하여 SIRS를 보이는 패혈증 모델을 유도하였다. 대조군과 패혈증군의 주요 장기의 조직학적 소견을 비교하였고 패혈증 마우스에서 CAL을 찾기 위한 시도를 하였다. 결과: 대조군과 비교하여, 염증세포의 침윤이 패혈증 마우스의 심장, 간, 신장에 상대적으로 증가하였다. 패혈증 마우스의 심장에서 심근(심근염)과 심장 주위 연조직에 림프구 침윤을 확인하였다. 또한, 패혈증 마우스의 관상동맥을 관찰하였지만, CAL을 확인할 수는 없었다. 결론: 본 연구에서 패혈증 마우스 모델에서 CAL의 존재를 확인하는 것은 실패하였다. 하지만, SIRS를 유발하는 많은 종류의 원인 질병에서 CAL이 발생한다는 것은 잘 알려져 있다. 가와사키병을 포함한 다양한 전신 염증 질병에 나타나는 CAL의 임상적 의미에 대한 연구가 필요할 것이다.

• Archives of Pharmacal Research
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• 제15권2호
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• pp.169-175
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• 1992

Anti-inflammatory glucocorticoid (GC) derivatives have been clinically used in immune-malfunctional diseases for their immunosuppressive activity. However, there is still a lack of knowledge on the relationship between anti-inflammatory and immunosuppressive activities. In order to compare immunosuppressive activities with the known anti-inflammatory activities of the GC derivatives, eight clinically used GC derivatives including hydrocortisone, prednislone, 6$\alpha$-methyl prednisolone, triamcinolone, dexamethasone, betamethasone, triamcinolone acetonide and fluocinolone acetonide were selected, and lymphoblastosis inhibition and plaque-forming cell (PFC) response in mice were studied as immunological parameters. In Con A-induced lymphoblatosis inhibition invitro, all derivatives showed potent inhibition $IC_{50}$ values of the derivaties except methyl prednisolone and triamcinolone were less than $10^{-7}$M and good dose dependency was obtained. This result was well correlated with that of their anti-inflammatory potencies obtained. This result was well correlated with that of their anti-inflammatory potencies and their receptor binding affinities. However, in PFC response, consistent result were not obtained. Total numbers of PFCs per spleen were decreased by some derivatives, but numbers of PFCs per $10^6$ cells were not decreased by systemic administration of but numbers of PFCs per $10^6$ cells were not decreased by systemic administration of GC at the dose of 0.05 mg/mouse. Furthermore, at the dose of 0.1 mg/mouse, numbers of PFCs per $10^6$ cells were found to be increased, although total PFCs per spleen were decreased.

• Journal of Microbiology and Biotechnology
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• 제24권8호
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• pp.1133-1142
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• 2014

Interleukin-32 (IL-32) is a cytokine and inducer of various proinflammatory cytokines such as $TNF{\alpha}$, IL-$1{\beta}$, and IL-6 as well as chemokines. There are five splicing variants (${\alpha}$, ${\beta}$, ${\gamma}$, ${\delta}$, and ${\varepsilon}$) and IL-$32{\gamma}$ is the most active isoform. We generated human IL-$32{\gamma}$ transgenic (IL-$32{\gamma}$ TG) mice to express high level of IL-$32{\gamma}$ in various tissues, including immune cells. The pathology of sepsis is based on the systemic inflammatory response that is characterized by upregulating inflammatory cytokines in whole body, particularly in response to gram-negative bacteria. We investigated the role of IL-$32{\gamma}$ in a mouse model of experimental sepsis by using lipopolysaccharides (LPS). We found that IL-$32{\gamma}TG$ mice resisted LPS-induced lethal endotoxemia. IL-$32{\gamma}$ reduced systemic cytokines release after LPS administration but not the local immune response. IL-$32{\gamma}TG$ increased neutrophil influx into the initial foci of the primary injected site, and prolonged local cytokines and chemokines production. These results suggest that neutrophil recruitment in IL-$32{\gamma}TG$ occurred as a result of the local induction of chemokines but not the systemic inflammatory cytokine circulation. Together, our results suggest that IL-$32{\gamma}$ enhances an innate immune response against local infection but inhibits the spread of immune responses, leading to systemic immune disorder.

• Biomolecules & Therapeutics
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• 제29권3호
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• pp.295-302
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• 2021

Microglial priming is the process of microglial proliferation and activation in response to neurodegeneration and abnormal protein accumulation. Priming makes microglia susceptible to secondary inflammatory stimuli and causes exaggerated inflammatory responses. In the present study, we established a microglial priming model in mice by administering a single injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 20 mg/kg). MPTP induced microglial activation without dopaminergic degeneration; however, subsequent treatment with a sub-toxic dose of lipopolysaccharides (LPS) induced an amplified inflammatory response and caused nigrostriatal dopaminergic degeneration. These pathological and inflammatory changes, including microglial activation and dopaminergic cell loss in the substantia nigra (SN) area were reversed by papaverine (PAP) administration. In addition, MPTP/LPS enhanced interleukin-1β (IL-1β) expression and processing via nod-like receptor protein 3 (NLRP3) inflammasome activation in the SN region of mice. However, PAP treatment suppressed inflammasome activation and subsequent IL-1β maturation. Moreover, PAP inhibited nuclear factor-κB (NF-κB) and enhanced cAMP-response element binding protein (CREB) activity in the SN of MPTP/LPS mice. These results suggest that PAP inhibits the activation of NLRP3 inflammasome by modulating NF-κB and CREB signaling pathways, which results in reduced microglial activation and neuronal cell death. Thus, PAP may be a potential candidate for the treatment of Parkinsons's disease, which is aggravated by systemic inflammation.

• Nutrition Research and Practice
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• 제4권4호
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• pp.259-269
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• 2010

Resistance training (RT) is associated with reduced risk of low grade inflammation related diseases, such as cardiovascular disease and type 2 diabetes. The majority of the data studying cytokines and exercise comes from endurance exercise. In contrast, evidence establishing a relationship between RT and inflammation is more limited. This review focuses on the cytokine responses both following an acute bout, and after chronic RT. In addition, the effect of RT on low grade systemic inflammation such as individuals at risk for type 2 diabetes is reviewed. Cytokines are secreted proteins that influence the survival, proliferation, and differentiation of immune cells and other organ systems. Cytokines function as intracellular signals and almost all cells in the body either secrete them or have cytokine receptors. Thus, understanding cytokine role in a specific physiological situation such as a bout of RT can be exceedingly complex. The overall effect of long term RT appears to ameliorate inflammation, but the specific effects on the inflammatory cytokine, tumor necrosis factor alpha are not clear, requiring further research. Furthermore, it is critical to differentiate between chronically and acute Interleukin-6 levels and its sources. The intensity of the RT and the characteristics of the training protocol may exert singular cytokine responses and as a result different adaptations to exercise. More research is needed in the area of RT in healthy populations, specifically sorting out gender and age RT acute responses. More importantly, studies are needed in obese individuals who are at high risk of developing low grade systemic inflammatory related diseases. Assuring adherence to the RT program is essential to get the benefits after overcoming the first acute RT responses. Hence RT could be an effective way to prevent, and delay low grade systemic inflammatory related diseases.