• Journal of Korean Neurosurgical Society
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• 제29권11호
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• pp.1499-1504
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• 2000

Objectives : In general, conventional T2, T3 thoracoscopic sympathicotomy must be one of the most effective treatments for the essential palmar hyperhidrosis. However, this is offset by the occurrence of a high rate of side effects, such as embarrassing compensatory sweating and Hornor's syndrome. The authors have performed a selective T3 thoracoscopic sympathicotomy to our patients to see whether it provides successful results with less side effects. Its preliminary results were compared with those of conventional T2, T3 thoracoscopic sympathicotomy. Methods : The thoracoscopic sympathicotomy was performed in 54 patients suffering from essential palmar hyperhidrosis. Twenty-four patients underwent a conventional sympathicotmy(group A) from Jan 1997 to Dec 1997 and 30 patients a selective T3 sympathicotmy(group B) from Jan 1998 to Dec 1999. For assessment of postoperative success and of complications all patients charts were reviewed. Patients further received a postal questionnaire regarding long-term effect, satisfaction, and side-effects. Results : No recurrence was observed in both groups. The global rate of compensatory sweating was significantly(p ＝0.020) different in both groups : 11 patients(45.8%) in group A and 5 patients(16.73%) in group B. The Hornor's syndrome was observed only in 4 patients in group A. The preliminary results of the procedure in group A were considered fully-satisfying by 16 patients(66.6%), 6 patients(25%) were satisfied partially, and only 2 patients(8.3%) were dissatisfied, and those of the procedure in group B satisfying by 26 patients(86.6%), 4 patients(13.3.% ) were satisfied partially, and none dissatisfied. Conclusion : The selective T3 sympathicotomy results in a significant decrease in the rate of disturbing side effects comparing to conventional T2, T3 sympathicotomy and it dose not lead to recurrence. Our results contribute to recommendations of a selective T3 thoracoscopic sympathicotomy as treatment of choice in essential palmar hyperhidrosis.

• Radiation Oncology Journal
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• 제6권2호
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• pp.195-201
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• 1988

최근 폐암의 발생빈도는 높아지고 있으나, 아직까지 만족할 만한 치료 성적은 제시되시 많고 있으며, 현재로서는 가능한 한 초기에 발견하여 수술을 시행후 국소재발 위험군의 경우 방사선 치료를 시행하는 것이 최선의 방법으로 알려져있다. 이에 저자들은 1979년 3월부터 1986년 2월까지 서울대학교 병원에서 비소세포성 폐암 진단하에 근치적 절제수술 시행후 방사선 치료를 받은 60명의 환자를 대상으로 수술후 방사선 치료의 효과 및 예후인자에 대한 분석을 시행하여 다음과 같은 결과를 얻었다. 전체 환자 60명중 방사선 치료를 불완전하게 시행한 5명을 제외한 55명을 분석한 결과 전체 환자의 5년 생존율은 $39\%$였으며 무병생존율은 $29\%$였다. 환자의 예후를 결정하는 주요인자로서는 병기 및 국소 임파절 전이 여부였고, 1병기와 병리조직학적 분류 및 나이, 성별, 방사선 조사선량과 수술시 절제면의 종양 침범 여부는 예후에 큰 영향을 미치지 못하였다. 수술 시행후 방사선 치료를 받은 환자 군의 생존율은, 문헌상에 나타난 수술 단독 시행 환자군의 생존율과 비교해 볼 때 국소 임파절 전이가 있는 환자군에서 더 높은 결과를 보였으며, 임파절 전이가 없는 환자군에서는 큰 차이를 발견할 수 없었다. 국소 재발율도 임파절 전이가 있는 환자군에서는 수술 단독 시행 환자군보다 현저히 낮은 결과를 보여 수술후 방사선 치료가 임파절 전이가 있는 환자에게는 생존율의 증가 및 국소재발 억제의 효과를 나타냄을 관찰할 수 있었다.

• The Korean Journal of Physiology and Pharmacology
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• 제3권4호
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• pp.393-404
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• 1999

We have reported that hypoxia stimulates EDRF(s) release from endothelial cells and the release may be augmented by previous hypoxia. As a mechanism, it was hypothesized that reoxygenation can stimulate EDRF(s) release from endothelial cells and we tested the hypothesis via bioassay experiment. In the bioassay experiment, rabbit aorta with endothelium was used as EDRF donor vessel and rabbit carotid artery without endothelium as a bioassay test ring. The test ring was contracted by prostaglandin $F_{2a}\;(3{\times}10^{-6}\;M)$ which was added to the solution perfusing through the aorta. Hypoxia was evoked by switching the solution aerated with 95% $O_2/5%\;CO_2$ mixed gas to one aerated with 95% $O_2/5%\;CO_2$ mixed gas. Hypoxia/reoxygenation were interexchanged at intervals of 2 minutes (intermittent hypoxia). In some experiments, endothelial cells were exposed to 10-minute hypoxia (continuous hypoxia) and then exposed to reoxygenation and intermittent hypoxia. In other experiments, the duration of reoxygenation was extended from 2 minutes to 5 minutes. When the donor aorta was exposed to intermittent hypoxia, hypoxia stimulated EDRF(s) release from endothelial cells and the hypoxia-induced EDRF(s) release was augmented by previous hypoxia/reoxygenation. When the donor aorta was exposed to continuous hypoxia, there was no increase of hypoxia-induced EDRF(s) release during hypoxia. But, after the donor aorta was exposed to reoxygenation, hypoxia-induced EDRF(s) release was markedly increased. When the donor aorta was pretreated with nitro-L-arginine $(10^{-5}$ M for 30 minutes), the initial hypoxia-induced EDRF(s) release was almost completely abolished, but the mechanism for EDRF(s) release by the reoxygenation and subsequent hypoxia still remained to be clarified. TEA also blocked incompletely hypoxia-induced and hypoxia/reoxygenation-induced EDRF(s) release. EDRF(s) release by repetitive hypoxia and reoxygenation was completely blocked by the combined treatment with nitro-L-arginine and TEA. Cytochrome P450 blocker, SKF-525A, inhibited the EDRF(s) release reversibly and endothelin antgonists, BQ 123 and BQ 788, had no effect on the release of endothelium-derived vasoactive factors. Superoxide dismutase (SOD) and catalase inhibited the EDRF(s) release from endothelial cells. From these data, it could be concluded that reoxygenation stimulates EDRF(s) release and hypoxia/reoxygenation can release not only NO but also another EDRF from endothelial cells by the production of oxygen free radicals.

• 한국산학기술학회논문지
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• 제21권5호
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• pp.384-390
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• 2020

유기인계 살충제를 음독하였을 경우 임상적으로 치명적인 결과를 가져올 수 있다. 이 연구는 유기인계 살충제 음독으로 인해 사망한 환자와 생존한 환자들의 내원 당시 중성구/림프구 비율을 비교 분석하여 사망률을 얼마나 예측할 수 있는지 알아보기 위해 시행되었다. 연구 자료는 전자의무기록에서 추출하였고, 2008년 1월부터 2018년 11월까지 유기인계 살충제를 음독하고 일개 응급실에 내원한 환자들(150명)을 생존 군(135명)과 사망 군(15명)으로 분류하고 후향적으로 비교 분석하였다. 환자들의 특성(나이, 성별, 기저질환 유무, 음독 후 병원까지 걸린 시간, 음독 양), 혈액검사 결과들과 의학적 중증도에 대한 개별 변수들을 먼저 비교한 후, 유의한 차이를 보이는 변수(나이, 혈중 백혈구 수, 아밀라아제 농도, 크레아티닌 농도, APACHE II점수 및 중성구/림프구 비율) 들에 대해 로지스틱 회귀분석을 시행하였다. 연구결과 나이, APACHE II 점수 및 중성구/림프구 비율이 사망 군에서 생존 군에 비해 유의하게 높았다. 이들 중 중성구/림프구 비율은 응급실에 내원하면 기본적으로 시행하는 전혈 검사를 통해 30분 이내에 신속하고 간단하게 얻을 수 있는 예측 인자이다. 본 연구를 통해 사망을 예측하는 도구로 중성구/림프구 비율이 유용하게 사용될 수 있으며, 특히, 수치가 10 이상으로 높은 경우 환자가 사망할 확률이 높음을 인지하고 집중 감시 및 치료를 해야 할 근거를 제시해 줄 수 있을 것으로 생각된다.

• Journal of Korean Neurosurgical Society
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• 제29권10호
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• pp.1365-1371
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• 2000

악성 임파종중에서 Non-Hodgkin 임파종이 척수 압박 증상을 일으키는 경우는 0.1~10.2%정도로 알려져 있으며, 이러한 척수 압박 증세가 임파종의 초기 증상으로 나타나는 경우는 특히 드문 것으로 알려져 있다. 척수 압박은 척추관내에 국한되어 있는 임파종에 의하거나 주변 임파절이나 척추로부터 전이된 경우에 발생하며, 다른 장기로의 침범 소견이 없는 원발성 척수 경막외 임파종의 경우, 조기에 외과적 감압이 이루어지고 보조요법으로 항암 치료 및 방사선 치료가 행해진다면 그 경과가 비교적 양호한 것으로 알려져 있다. 저자들은 요통을 전구 증상으로, 급성 하반신 부전마비 및 배뇨 장애 소견을 보여 본원에 내원후, 응급 감압술 및 조직병리검사 결과 B-세포성 Non-Hodgkin 임파종으로 확인된 두 명의 여자환자를 경험하였다. 수술후 두 환자의 증세는 모두 회복되었으며, 항암 치료 및 방사선 치료후 현재까지 추적 조사중이다. 이에 저자들은 초기 증상으로 경막외 척수 압박을 보인 원발성 Non-Hodgkin 임파종에 관해 문헌 고찰과 함께 보고하는 바이다.

• The Korean Journal of Physiology and Pharmacology
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• 제10권4호
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• pp.217-222
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• 2006

Atherosclerosis is considered as a chronic inflammatory process. However, the nature of the oxidant signaling that regulates monocyte adhesion and its underlying mechanism is poorly understood. We investigated the role of reactive oxygen species on the vascular cell adhesion molecule-1 (VCAM-1) and monocyte adhesion in the cultured endothelial cells. $TNF-{\alpha}$ at a range of $1{\sim}30\;ng/ml$ induced VCAM-1 expression dose-dependently. BCECF-AM-labeled U937 cells firmly adhered on the surface of endothelial cells when the endothelial cells were incubated with $TNF-{\alpha}$ (15 ng/ml). Ten $\;{\mu}mol/L$ of SB203580, an inhibitor of p38 MAPK, significantly reduced $TNF-{\alpha}-induced$ VCAM-1 expression, compared to the JNK inhibitor ($40\;{\mu}mol/L$ of SP60015) or ERK inhibitor ($40\;{\mu}mol/L$ of U0126). Also, SB203580 significantly inhibited $TNF-{\alpha}-induced$ monocyte adhesion in HUVEC. Superoxide production was minimal in the basal condition, however, treatment of $TNF-{\alpha}$ induced superoxide production in the dihydroethidineloaded endothelial cells. Diphenyleneiodonium (DPI, $10\;{\mu}mol/L$), an inhibitor of NADPH oxidase, and rotenone $(1\;{\mu}mol/L)$, an inhibitor of mitochondrial complex I inhibited $TNF-{\alpha}-induced$ superoxide production, VCAM-1 expression and monocyte adhesion in the endothelial cells. Taken together, our data suggest that NADPH oxidase and mitochondrial ROS were involved in $TNF-{\alpha}-induced$ VCAM-1 and monocyte adhesion in the endothelial cells.

• The Korean Journal of Physiology and Pharmacology
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• 제13권1호
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• pp.27-32
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• 2009

The effects of oxidized low-density lipoprotein(OxLDL) and its major lipid constituent lysophosphatidylcholine(LPC) on $Ca^{2+}$ entry were investigated in cultured human umbilical endothelial cells(HUVECs) using fura-2 fluorescence and patch-clamp methods. OxLDL or LPC increased intracellular $Ca^{2+}$ concentration($[Ca^{2+}]_i$), and the increase of $[Ca^{2+}]_i$ by OxLDL or by LPC was inhibited by $La^{3+}$ or heparin. LPC failed to increase $[Ca^{2+}]_i$ in the presence of an antioxidant tempol. In addition, store-operated $Ca^{2+}$ entry(SOC), which was evoked by intracellular $Ca^{2+}$ store depletion in $Ca^{2+}$-free solution using the sarcoplasmic reticulum $Ca^{2+}$ pump blocker, 2, 5-di-t-butyl-l,4-benzohydroquinone(BHQ), was further enhanced by OxLDL or by LPC. Increased SOC by OxLDL or by LPC was inhibited by U73122. In voltage-clamped cells, OxLDL or LPC increased $[Ca^{2+}]_i$ and simultaneously activated non-selective cation(NSC) currents. LPC-induced NSC currents were inhibited by 2-APB, $La^{3+}$ or U73122, and NSC currents were not activated by LPC in the presence of tempol. Furthermore, in voltage-clamped HUVECs, OxLDL enhanced SOC and evoked outward currents simultaneously. Clamping intracellular $Ca^{2+}$ to 1 ${\mu}M$ activated large-conductance $Ca^{2+}$-activated $K^+(BK_{ca})$ current spontaneously, and this activated $BK_{ca}$ current was further enhanced by OxLDL or by LPC. From these results, we concluded that OxLDL or its main component LPC activates $Ca^{2+}$-permeable $Ca^{2+}$-activated NSC current and $BK_{ca}$ current simultaneously, thereby increasing SOC.

• The Korean Journal of Physiology
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• 제24권1호
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• pp.123-129
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• 1990

A comparative study of acid-base balance has been made between acidemia-induced hyperkalemia and hyperkalemia-induced acidemia. A group of rabbits was infused 0.1 N hydrochloric acid solution and metabolic acidosis was induced. Another group was administered 20 mM potassium chloride solution and hyperkalemia was induced. The third group was infused 0.1 N hydrochloric acid and 20 mM potassium chloride solution, simultaneously. Acid-base data and plasma potassium ion concentration were monitored every thirty minutes in these three groups of rabbits. Following results were obtained: 1 ) Along with the infusion of hydrochloric acid, acute metabolic acidosis was induced in the rabbits. Plasma bicarbonate ion concentration decreased primarily in this group. As a respiratory compensation, there was a tendency of reduction of arterial $Pco_{2}$. The alteration of data became larger along with the amount of administration and the time elapsed. However, hyperkalemia was not so severe compared with the second group. 2) In potassium chloride infused group, plasma potassium ion concentration increased along with the time elapsed and the amount of infusion. And the alteration of acid-base data was parrallel to the level of potassium ion concentration, above all depression of pH was prominent. 3) Above data suggest that when acute metabolic acidosis was induced, exchange of intracellular potassium ion with extracellular hydrogen ion seems significant for the regulation of extracellular acid-base balance. And when hyperkalemia was induced with the infusion of potassium chloride solution, the exchange of intracellular hydrogen ion with extracellular potassium ion also seems significant for the regulation of extracellular potassium balance. 4) In the group of rabbits infused hydrochloric acid and potassium simultaneously, disturbances of acid-base balance and potassium balance were much more severe than two other groups. In these mixed disturbances, the process of compensatory mechanism might be inhibited and one disturbance might aggregate each other. 5) Through above data it has been postulated that in acid-base disturbance potassium balance can be sacrificed as a compensatory mechanism, and vice versa in disturbance of potassium balance. And our data also suggest that hydrogen ion and potassium ion are compensatory pair, one another.

• Asian Pacific Journal of Cancer Prevention
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• 제16권7호
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• pp.2819-2826
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• 2015

Combinations of multiple biomarkers representing distinct aspects of metastasis may have better prognostic value for breast cancer patients, especially those in late stages. In this study, we evaluated the protein levels of N-${\alpha}$-acetyltransferase 10 protein (Naa10p), synuclein-${\gamma}$ (SNCG), and phosphatase of regenerating liver-3 (PRL-3) in 365 patients with breast cancer by immunohistochemistry. Distinct prognostic subgroups of breast cancer were identified by combination of the three biomarkers. The Naa10p+SNCG-PRL-3-subgroup showed best prognosis with a median distant metastasis-free survival (DMFS) of 140 months, while the Naa10p-SNCG+PRL-3+subgroup had the worst prognosis with a median DMFS of 60.5 months. Multivariate analysis indicated Naa10p, SNCG, PRL-3, and the TNM classification were all independent prognostic factors for both DMFS and overall survival (OS). The three biomarker combination of Naa10p, SNCG and PRL-3 performed better in patients with lymph node metastasis, especially those with more advanced tumors than other subgroups. In conclusion, the combined expression profile of Naa10p, SNCG and PRL-3, alone or in combination with the TNM classification system, may provide a precise estimate of prognosis of breast cancer patients.

• Asian Pacific Journal of Cancer Prevention
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• 제16권7호
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• pp.3035-3042
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• 2015

Background: Isorhamnetin (Iso), a novel and essential monomer derived from total flavones of Hippophae rhamnoides that has long been used as a traditional Chinese medicine for angina pectoris and acute myocardial infarction, has also shown a spectrum of antitumor activity. However, little is known about the mechanisms of action Iso on cancer cells. Objectives: To investigate the effects of Iso on A549 lung cancer cells and underlying mechanisms. Materials and Methods: A549 cells were treated with $10{\sim}320{\mu}g/ml$ Iso. Their morphological and cellular characteristics were assessed by light and electronic microscopy. Growth inhibition was analyzed by MTT, clonogenic and growth curve assays. Apoptotic characteristics of cells were determined by flow cytometry (FCM), DNA fragmentation, single cell gel electrophoresis (comet) assay, immunocytochemistry and terminal deoxynucleotidyl transferase nick end labeling (TUNEL). Tumor models were setup by transplanting Lewis lung carcinoma cells into C57BL/6 mice, and the weights and sizes of tumors were measured. Results: Iso markedly inhibited the growth of A549 cells with induction of apoptotic changes. Iso at $20{\mu}g/ml$, could induce A549 cell apoptosis, up-regulate the expression of apoptosis genes Bax, Caspase-3 and P53, and down-regulate the expression of Bcl-2, cyclinD1 and PCNA protein. The tumors in tumor-bearing mice treated with Iso were significantly smaller than in the control group. The results of apoptosis-related genes, PCNA, cyclinD1 and other protein expression levels of transplanted Lewis cells were the same as those of A549 cells in vitro. Conclusions: Iso, a natural single compound isolated from total flavones, has antiproliferative activity against lung cancer in vitro and in vivo. Its mechanisms of action may involve apoptosis of cells induced by down-regulation of oncogenes and up-regulation of apoptotic genes.