• 디지털융복합연구
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• 제13권1호
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• pp.407-414
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• 2015

이 연구는 순사망환자의 주진단에 관한 특성에 대해 분석하여 병원 의료의 질 수준 향상을 위한 기초자료로 활용하고자 시행하였다. 대전광역시 소재 K 대학병원에서 2011년, 2012년, 2013년 3년 동안 사망한 환자 1992명 중 순사망한 428명을 조사대상으로 선정하였으며, 분석방법으로는 카이제곱검정 및 fisher의 정확한 검정과 정준상관분석을 사용하였다. 분석한 결과, 일반적 특성과 주진단 상위 4위의 정준상관분석 결과, 주진단 중 상세불명 병원체의 폐렴(J18)과 살충제의 독작용(T60)에서 유의한 것으로 나타났다. 상세불명 병원체의 폐렴(J18)에서는 자동차보험, 15-29세 사이, 건강보험, 의료급여 등의 순으로 나타났으며(p<0.001), 살충제의 독작용(T60)에서는 건강보험, 의료급여, 자동차보험, 45-59세, 세종충남 등의 순으로 유의하게 나타났다(p<0.05). 결론적으로 노인인구의 사망을 감소시키기 위해 의료서비스의 질적 향상과 응급의료전달의 체계적인 구축시켜 순사망환자를 감소시켜나가는 것이 매우 중요하다고 할 수 있다.

• 동의신경정신과학회지
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• 제11권1호
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• pp.37-46
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• 2000

We investigated the effects of lemon pure essential oils on the heat shock-induced apoptosis in human astrocyte cell line CCF-STTG1. In previous studies, hear shock has been reported to induce the apoptosis or programmed cell death through the activation of caspase-3. Treatment of CCF-STTG1 cells with heat shock markedly induced apoptotic cell death as determined by flow cytometry. Interestingly, pretreatment of CCF-STTG1 cells with lemon pure essential oils inhibited the heat shock-induced apoptosis. Lemon also inhibited the heat shock-induced apoptosis in primary cultured rat astrocytes. To determine whether lemon inhibits the heat shock-induced activation of these apoptotic proteases, activation of CPP32 was assessed by Western blotting. Consistent with flow cytometry, DNA fragmentation and giemsa staining, heat shock-induced activation of CPP32 was blocked by lemon pure essential oil. PARP, cysteine protease substrates were fragmented as a consequence of apoptosis by heat shock. Lemon oil inhibited the PARP fragmentation. This essential oil also inhibited the heat shock-induced activation of caspase-3. These results suggest that lemon pure essential oils may modulate the apoptosis through the activation of the ICE-like caspases.

• Journal of Chest Surgery
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• 제27권9호
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• pp.752-758
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• 1994

From July 1983 to December 1992, 145 patients with mitral valvular disease underwent open heart surgery at Chonbuk National University Hospital. Of these patients, 89 patients[61.4%] required mitral valve replacement. 56 patients [38.6 %] had mitral valve repair. There were 32 women and 24 men and the mean age was 34.3 years[range 6 years to 62 years].There were 23 cases of pure mitral stenosis, 19 cases of mitral regurgitation and 14 cases of mixedmitral valvular disease. The mean duration of symptom was 4.53 years and mean mitral valvularorifice diameter[in cases of pure stenosis and mixed mitral valvular lesion] was 0.96 cm. According to the NYHA classification, the distribution of patients preoperatively was as follows; class IIa, 15 patients; class lib, 17 patients; class III, 22 patients; class IV, 2 patients. Four patients[7%] had an embolic history preoperatively. 24 patients[ 43 %] were in atrial fibrillation. In cases of pure mitral stenosis, the technique used included open mitral commissurotomy[21atients], open mitral commissurotomy with mitral annuloplasty[2 patients]. In mixed mitral valvular disease, open mitral commissurotomy[ll patients] and open mitral commissurotomy with mitral annuloplasty[l patient] were performed. In cases of mitral regurgitation, mitral annuloplasty[5 patients], mitral valvuloplasty[6 patients], mitral annuloplasty with valvuloplasty [3 patients] and ring annuloplasty [5 patients] were performed.There was one perioperative death related to acute renal failure and sepsis. One late death was occurred related to heart failure after 10 months postoperatively. One patient required reoperation due to restenosis and no embolic episode was occured. After operation, 34 patients were in NYHA functional class I, 20 patients were in class IIa.

• Journal of Chest Surgery
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• 제21권5호
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• pp.850-855
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• 1988

From July 1983 to June 1988, twenty six patients underwent mitral valve repair for pure mitral stenosis[21 patient] or for mitral stenosis with a mild degree of regurgitation[5 patient] at Chonbuk National University Hospital. All patients underwent open mitral commissurotomy and 17 patients required to additional procedures for relief of obstructive subvalvular lesion. There was no operative death. The patients were followed from one to sixty months[mean 24. 1Mo.] One late death occurred due to cardiac and renal failure 10 month postoperatively. Of the 25 surviving patients at the time of follow-up, 17 patients[68%] were in NYHA functional class I and 8 patients[32%] were in class II.

• 한국수학교육학회지시리즈B:순수및응용수학
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• 제11권4호
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• pp.275-285
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• 2004

In this paper, the time series models for the number of reported death claims of compulsory automobile liability insurance in Korea are studied. We found that IMA${(0, 1, 1)}\;{\times}\;{(0, 1, 1)}_{12}$ would the most appropriate model for the number of reported claims by the Box-Jenkins method.

• Journal of Chest Surgery
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• 제23권2호
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• pp.253-259
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• 1990

Between January, 1970 and August, 1989, a total of 81 patients whose age were more than 20 years of life, received total correction for tetralogy of Fallot. This report analyzed 70 patients among them and excluded the remaining 11 patients whose clinical data could not be found. Their mean age was 25.750.39 years[range 20 \ulcorner50]. The clinical manifestations were cyanosis and clubbing [64 pts], frequent URI[40 pts], anoxic spell [19 pts], infective endo-carditis[4 pts], brain abscess[3 pts], pulmonary tuberculosis[3 pts] and CHF, chest tightness, nephrotic syndrome, left hemiplegia, and tamponade. The types of right ventricular outflow tract obstruction were combined[46 pts], pure infundibular [21 pts] and pure valvular[3 pts]. Associated cardiovascular anomalies were PFO [27 pts], ASDi8 pts], LSVC[8 pts], aortic regurgitation [5 pts], right aortic arch, coronary artery anomalies, PDA and dextrocardia. Hospital mortality was 5.7%. The causes of death ware low cardiac output [2 pts], aggravation of CRF[1 pts] and brain damage[1 pts]. There was one late death because of residual intracardiac shunt and congestive heart failure. During the follow-up period, 16 patients were lost and the remaining 49 patients were asymptomatic and leading normal lives. Residual intracardiac shunt was detected in 5 patients with radionuclide single pass study but all of them had Qp / Qs ratio less than 1.5.

• Clinical and Experimental Reproductive Medicine
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• 제26권2호
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• pp.171-178
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• 1999

The follicular fluid (FF) of ovary contains various biological active products which affected on the growth of follicles and the fertilization of oocyte in physiological reproductive process of mammals. This study was designed to determine the effects of human FF on fertilization of oocyte and embryonal development in vitro culture. The FF was prepared as clear without blood contamination by needle aspiration from mature follicles of human at the time of oocytes retrieval for in vitro fertilization (IVF). As the medium for culture in vitro of embryonal cells, human tubal fluid (HTF) supplemented with follicular fluids at concentrations of 10%, 40% and pure FF were used. These effects were compared to control group of cultured embryos in HTF supplemented with 0.4% BSA (bovine serum albumin). For IVF, 64 eggs in control group, 67 eggs in 10% FF, 57 eggs in 40% FF and 64 eggs in pure FF were respectively allocated. And the rates of fertilization were almost similar in all groups as resulting 82.81% in control, 85.07% in 10% FF, 87.71% in 40% FF and 81.25% in pure FF. On the examination for embryonal cleavage from fertilized eggs, the rates of developing to 4 cell stage was similar in all groups, as results 98.11% in control, 98.27% in 10% FF and 98% in 40% FF but 78.84% in pure FF. And the rates of developing to 8-16 cell stage were significantly reduced as 44% in 40% FF and 44.23% in pure FF (p<0.05) compare to 71.69% in control media. As likewise, the rates of developing to morular stage were also significantly reduced to 36% (p<0.05) and 21.15% (p<0.01) respectively in 40% FF and pure FF. And the rates to blastocystic stage of embryo was lowest as 7.69% in pure FF (Table 1). The quality of embryonal cells on cleavage to the 8-16 cell stage was poorer, higher concentrations of FF. The rates of grade 1 in pure FF, as 23.07%, was lowest compare to those of other groups, in which the rates of grade 1 in control, 10% FF and 40% FF were 58.49%, 47.36% and 34% respectively. And on the contrary, the rate of grade 4 in pure FF was highest as 23.07%, while those were 5.66% in control, 8.77% in 10% FF and 20% in 40% FF (Table 2). On the viability of embryos, the rate of embryonal cell death was more rise, at the higher concentrations as well as longer exposure in the follicular fluid. At 48 hours after in vitro culture of embryos, the rate of survival embryos in pure FF was markedly lowered as 44.23%, compare to that of control (p<0.05). But there was not significant difference between the rates of survival embryos in each group beside the pure FF, which the rates were 77.35% in control, 70.17% in 10% FF and 60% in 40% FF respectively. And at 72 hours after in vitro culture, the rates of survival embryos were also significantly dropped to 21.15% in pure and 36% in 40% at concentration of FF compare to 62.26% in control (p<0.05, p<0.01). Finally, the rate of embryonal death at 96 hours after in vitro culture was highest as 82.69% in pure FF among all groups which those were 35.84 in control, 56.14% in 10% FF and 64% in 40% FF respectively (Fig. 1, 2, 3). In conclusion, this study suggests that the FF has no effects, in particular, to the in vitro fertilization of oocytes but exerted a bad effect to the cleavage, quality and viability of the embryonal cells during in vitro culture. However, the FF is harmful on embryonal development at conditions in higher concentration and especially on the embryos after $8{\sim}16$ cell stage.

• The Korean Journal of Physiology and Pharmacology
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• 제22권6호
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• pp.689-696
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• 2018

Increasing evidence implicates changes in $[Ca^{2+}]_i$ and oxidative stress as causative factors in amyloid beta ($A{\beta}$)-induced neuronal cell death. Cyanidin-3-glucoside (C3G), a component of anthocyanin, has been reported to protect against glutamate-induced neuronal cell death by inhibiting $Ca^{2+}$ and $Zn^{2+}$ signaling. The present study aimed to determine whether C3G exerts a protective effect against $A{\beta}_{25-35}$-induced neuronal cell death in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using MTT assay for cell survival, and caspase-3 assay and digital imaging methods for $Ca^{2+}$, $Zn^{2+}$, MMP and ROS. Treatment with $A{\beta}_{25-35}$ ($20{\mu}M$) for 48 h induced neuronal cell death in cultured rat pure hippocampal neurons. Treatment with C3G for 48 h significantly increased cell survival. Pretreatment with C3G for 30 min significantly inhibited $A{\beta}_{25-35}$-induced $[Zn^{2+}]_i$ increases as well as $[Ca^{2+}]_i$ increases in the cultured rat hippocampal neurons. C3G also significantly inhibited $A{\beta}_{25-35}$-induced mitochondrial depolarization. C3G also blocked the $A{\beta}_{25-35}$-induced formation of ROS. In addition, C3G significantly inhibited the $A{\beta}_{25-35}$-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid ${\beta}$-induced neuronal cell death by reducing multiple apoptotic signals.

• Toxicological Research
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• 제12권2호
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• pp.289-293
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• 1996

Our previous studies demonstrated that quinone (menadione) is cytotoxic to rat platelets. In an attempt to assess the relative contributions of redox cycling and/or arylation in quinone-induced cytotoxicity, we have studied three quinones with different mechanisms: 2, 3-dimethoxy-1, 4-naphthoquinone (DMNQ; pure redox cycler), menadione (both redox cycler and arylator), and 1, 4-benzoquinone (pure arylator). The order of redox cycling capacity in platelet rich plasma (PRP) isolated from rats was menadione>DMNQ>1, 4-benzoquonone, which was consistent with the previous studies using isolated hepatocytes. 1, 4-Benzoquinone was more toxic to rat platelets than menadione, while DMNQ did not cause cell death at all. Lactate dehydrogenase inhibition studies revealed that 1, 4-benzoquinone inhibited significantly in a time-dependent manner, while menadione and DMNQ did not at all. These results suggested that arylation by quinone compounds might play a critical role in quinone-induced cytotoxicity in rat platelets.

• The Korean Journal of Physiology and Pharmacology
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• 제22권3호
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• pp.311-319
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• 2018

Mitochondrial calcium overload is a crucial event in determining the fate of neuronal cell survival and death, implicated in pathogenesis of neurodegenerative diseases. One of the driving forces of calcium influx into mitochondria is mitochondria membrane potential (${\Delta}{\psi}_m$). Therefore, pharmacological manipulation of ${\Delta}{\psi}_m$ can be a promising strategy to prevent neuronal cell death against brain insults. Based on these issues, we investigated here whether nobiletin, a Citrus polymethoxylated flavone, prevents neurotoxic neuronal calcium overload and cell death via regulating basal ${\Delta}{\psi}_m$ against neuronal insult in primary cortical neurons and pure brain mitochondria isolated from rat cortices. Results demonstrated that nobiletin treatment significantly increased cell viability against glutamate toxicity ($100{\mu}M$, 20 min) in primary cortical neurons. Real-time imaging-based fluorometry data reveal that nobiletin evokes partial mitochondrial depolarization in these neurons. Nobiletin markedly attenuated mitochondrial calcium overload and reactive oxygen species (ROS) generation in glutamate ($100{\mu}M$)-stimulated cortical neurons and isolated pure mitochondria exposed to high concentration of $Ca^{2+}$ ($5{\mu}M$). Nobiletin-induced partial mitochondrial depolarization in intact neurons was confirmed in isolated brain mitochondria using a fluorescence microplate reader. Nobiletin effects on basal ${\Delta}{\psi}_m$ were completely abolished in $K^+-free$ medium on pure isolated mitochondria. Taken together, results demonstrate that $K^+$ influx into mitochondria is critically involved in partial mitochondrial depolarization-related neuroprotective effect of nobiletin. Nobiletin-induced mitochondrial $K^+$ influx is probably mediated, at least in part, by activation of mitochondrial $K^+$ channels. However, further detailed studies should be conducted to determine exact molecular targets of nobiletin in mitochondria.