Qi power salt 투여가 심ㆍ폐기능 요인 및 혈청 Nitric oxide 생성에 미치는 영향

김학렬,박성률,이규성 한국운동과학회 2003 운동과학 Vol.12 No.4

김학렬, 박성률, 이규성. Qi power salt 투여가 심폐기능 요인 및 혈청 Nitric oxide 생성에 미치는 영향. 운동과학. 제12권 제4호, 597-612, 2003. 본 연구의 목적은 항산화제로서 Qi power salt 투여 유·무에 따른 심장, 페 기능 요인 및 무산소성역치(Anaerobic Threshold: AT)수준에서의 호흡, 순환 기능을 비교하는 것이며, Qi power salt 투여가 훈련된 운동선수들의 일시적 운동시 혈관 내피세포(Vascular Endothelium)에서 생성된 산화질소(Nitric Oxide; NO)에 미치는 영향을 평가하는 것이다. 스프린터와 지구성런너 집단의 안정시 및 최대운동시 호흡개스변인은 Qi power(QPS) 투여에 따른 유의한 차이가 없었다. 그러나 지구성런너 집단은 QPS 투여 후 최대운동지속시간(Exhaustion time, sec)에서 유의한 증가(p<.01)를 나타내었으나, 스프린터 집단에서 유의한 차이는 없는 것으로 나타났다. 또한 양집단간 차이검증에서 지구성런너들의 최대유산소성능력은 스프린터에 비해 유의하게 높은 수준(p<.0.01)을 나타내었다. QPS 투여와 비투여시 환기역치 수준에서의 호흡개스변인은 스프린터와 지구성런너 집단 모두에서 유의한 차이는 없는 것으로 나타났다. 그러나 양집단간 차이검증에서 QPS 투of와 비투여시 스프린터에 비해 지구성런너 집단은 유의하게 높은 수준을 나타내었다. 스프린터 집단 및 지구성런너 집단의 럴청 Nitric oxide(NO)농도는 QPS 투여시 안정시에 비해 투여30분후, 최대운동직후 및 회복30분에서도 유의한 차이는 없는 것으로 나타났다. 그러나 QPS 비투여시 에는 안정시에 비해 최대운동직후 유의하게 증가된 수준(p<.001)을 나타내었으며, 이러한 결과로서 회복30분과도 유의한 차이(p<.001)를 나타내었다. QPS 투여와 비투여에 따른 스프린터와 지구성런너틀의 집단간 차이를 검증한 결과, 안정시(p<.001)와 투여30분후(p<.001) 및 회복 30분(p<.001)에서 각각 집단간 차이를 나타내었으나, 최대운동직후 수준에서 유의한 차이는 없는 것으로 나타났다. 이상의 결과를 고려하여 볼 때 Qi power salt 투여는 지구성런너 및 스프린터 집단에서 최대 및 환기역치 수준의 호흡개스변인에 유의한 영향을 미치지 못하였으나, 혈청 NO 생성을 억제하는 효과를 나타냄으로서 이에 대한 지속적인 연구가 요구되는 바이다. Kim, H.L, Park S.y., Lee, KS. The effects of Qi power salt supplement in Cardio-vascular function and serum nitric oxide product. Exercise Science, 12(4): 597-612, 2003. The purpose of this study res compared with cardio-respiratory function to maximal aerobic power and ventilation threshold levels following Qi power salt supplement in sprinter and endurance runners. On the other hand, it was to evaluate a profile of serum nitric oxide product in endotherium as Qi power salt supplement, and compared to biochemical profiles between sprinter and endurance runners. Cardio-respiratory function in maximal state of sprinter and endurance runner group was not significant difference between QPS supplement and control. However, treadmill exhaustion time after QPS supplement was display a significantly increased levels(p<.01) in endurance runner group, but it was not significant difference in splinter group. Relative(P<.001) V0₂max(ml/kg/min, l/min) of endurance runner was shown a significantly high levels compared to sprinter. Cardio-respiratory variables in ventilation threshold levels during QPS supplement and control was not proved a significant difference in splinter and endurance runner group. However, endurance runner compared to sprinter group was shown a significantly high levels in QPS supplement and control. Serum nitric oxide concentration(uM) of sprinter and endurance runner was not shown a significantly difference in QPS supplement, but it was display a significantly Increased levels in exerciseafter immediately compared to baseline value in control Conclusively, the Qi power salt supplement in sprinter and endurance runner was not influence in respiratory, gas variables of maximal state and ventilation threshold, but it was a inhibition effect in serum nitric oxide production.

유용단백질 생산을 위한 곤충세포의 현탁배양기술

김학렬,정인식 경희대학교 유전공학연구소 1990 遺傳工學論文集 Vol.2 No.-

이상에서 곤충세포의 특성,배지 및 곤충세포 현탁배양시의 고려사항등에 관해서 간략히 기술해보았다 결론적으로 곤충세포를 이용한 유용물질의 상업적 생산을 위해서는 곤충세포의 효율적인 현탁배양 기술이 매우 중요한 요소가 된다고 할수 있다 따라서 현탁배양시의 hydrodynamics와 세포의 생리특성간의 상호관계에 대한 기초적인 이해를 바탕으로 앞으로는 값싸고 조성이 복잡하지 않은 곤충세포 배지의 개발과 고농도 세포배양을 위한 process-intensive한 생물반응기의 개발 등 현탁배양 기술의 향상에 대한 연구가 필요하다고 사료된다

박해기 수원지역 신앙선조들의 삶과 죽음

김학렬 수원교회사연구소 2005 상교우서 Vol.- No.8

배추흰나비(Pieris rapae L.)의 혈림프내 β - N - acetylglucosaminidase 에 관하여

김학렬,윤치영 고려대학교 한국곤충연구소 1986 昆蟲硏究誌 Vol.12 No.1

전기영동 및 면역학적 방법을 이용하여 배추희나비(Pieris rapae L.)의 혈림프 β-N-acetylglucosaminidase의 몇가지 特性을 調査하였다. 1. Haemolymph β-N-acetylglucosaminidase는 2種의 구성소단위로 되어 있으며 분자량은 각각 7.8×104, 7.4×104 dalton이었다. 2. Haemolymph enzyme과 면역학적으로 동일한 효소가 moulting fluid 내에도 존재하였다. 3. 5齡 幼蟲에서 羽化 前까지 全時期에 걸쳐 혈림프에는 효소의 量的 변화는 없었으나, 효소활성은 前踊初에서 증가하여 化 直後 최대의 활성을 나타내었으며 그 이후 급격히 감소하였다. 4. 抗 haemolymph β-N-acetylglucosaminidase에 대하여 fat body, gut, testis 그리고 integument는 precpitin line을 형성하였으나 saliva는 형성하지 않았다. 즉 면역적으로 동일한 haemolymph enzyme은 fat body, gut, testis 및 integument에는 존재하였으나 saliva에서는 존재하지 않았다.

대량객혈시 동맥색전술에 있어서 색전물질의 효능비교

김학렬,양세훈,정은택,노지영,노병석 대한결핵 및 호흡기학회 1997 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.85 No.0

가족성 원발성 폐섬유화증 2가계

김학렬,양동규,오연목,심태선,임채만,이상도,고윤석,김우성,김원동,김동순 대한결핵 및 호흡기학회 2002 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.95 No.0

NCI-H157 폐암 세포주에서 활성산소종의 생성과 미토콘드리아 기능변화를 통한 Arsenic Trioxide와 Sulindac 병합요법의 세포고사효과

김학렬,양세훈,정은택 대한결핵및호흡기학회 2005 Tuberculosis and Respiratory Diseases Vol.59 No.1

Background : Arsenic trioxide (As2O3) has been used to treat acute promyelocytic leukemia, and it induces apop tosis in a variety of solid tumor cell lines including non-small cell lung cancer cells. However, nonsteroidal anti- inflammatory drugs (NSAID) can enhance tumor response to chemotherapeutic drugs or radiation. It was previously demonstrated that a combination treatment with As2O3 and sulindac induces the apoptosis of NCI-H157 human lung carcinoma cells by activating the caspase cascade. This study aimed to determine if a combination treatment augmented its apoptotic potential through other pathways except for the activation of the caspase cascade. Material and Methods : The NCI-H157 cells were treated with As2O3, sulindac and antioxidants such as glutathione (GSH) and N-acetylcysteine (NAC). The cell viability was measured by a MTT assay, and the level of intracellular hydrogen peroxide (H2O2) generation was monitored fluorimetrically using a scopoletin-horse radish peroxidase (HRP) assay. Western blotting and mitochondrial membrane potential transition analysis were performed in order to define the mechanical basis of apoptosis. Results : The viability of the cells was decreased by a combination treatment of As2O3 and sulindac, and the cells were protected using antioxidants in a dose-dependent manner. The increased H2O2 generation by the combination treatment was inhibited by antioxidants. The combination treatment induced changes in the mitochondrial transmembrane potential as well as the expression of the Bcl-2 family proteins, and increased cytochrome c release into the cytosol. However, the antioxidants inhibited the effects of the combination treatment. Conclusion : Combination treatment with As2O3 and sulindac induces apoptosis in NCI-H157 human lung carcinoma cells via ROS generation with a mitochondrial dysfunction. (Tuberc Respir Dis 2005; 59: 30-38)

흉막 국균증(Pleural Aspergillosis) 치험 1례

김학렬,정은택 圓光大學校 醫科學硏究所 1997 圓光醫科學 Vol.13 No.1-2

Pleural aspergillosis is not associated with pulmonary aspergillosis. However, it could occur in patients who have a chronic pneumothorax and bronchopleural fistula with pulmonary tuberculosis history. The treatment requires a thoracoplastic operation following a pleuropneumonectomy. This procedure includes the administering of an antifungal agent such as Amphotericin B or Nystatin via parenteral or intrapleural infusion for several months. Our report includes a) a study on a patient who came to us, and was found to have aspergillosis during a microscopic examination and cultivation test of pleural discharge, and who had been diagnosed with pneumothorax, bronchopleural fistula and pulmonary tuberculosis history twelve years earlier. The patient was then given a pleural decortication prior to and following which antifungal agent was administered, b) a research of applicable literature.

Transcriptional regulation, stabilization, and subcellular redistribution of MRP1 by GSK 3αβ: novel insights on modes of cadmiuminduced cell death stimulated by MRP1

김학렬,김영숙,황기은,정은택,오선희 대한결핵 및 호흡기학회 2015 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.120 No.-

Objectives: Cadmium (Cd) resistance is associated with the suppression of autophagy in H460 cells, which is regulated byglycogen synthase kinase (GSK) 3αβ. However, the involvement of multidrug resistance (MDR) in this signals and its mechanisms remain to be elucidated. Methods: We used Cd-resistant cells (RH460) to demonstrate that the induction of MDR-associated protein (MRP1) in response to Cd is enhanced in H460 cells compared to RH460. Results: Treating RH460 cells with Cd induced large cytoplasmic vacuoles, which was inhibited by 3-MA. MRP1 was redistributedfrom the perinuclear to the cytoplasmic compartment following exposure to Cd. Cd-induced MRP1, GSK3αβ, and LC3-II were suppressed by GSK3 inhibitor, but increased by lithium. Furthermore, MRP1 was upregulated by okadaic acid and downregulated by vanadate, suggesting that MRP1 was stabilized by GSK3αβ. In addition, co-immunoprecipitation and co-localization analyzes revealed a interaction between MRP1 and GSK3αβ. Knockdown of GSK3β decreased Cd induced MRP1, whereas its overexpression upregulated MRP1. MRP1 also co-localized with LAMP-2, and the subsequent release of cathepsins into the cytosol. In mice chronically injected with Cd, MRP1 localized to the perinuclear region of bronchial and alveolar epithelial cells. Conclusions: Cd toxicity is regulated by the transcriptional regulation, stabilization, and subcellular redistribution of MRP1 via the posttranslational modification of GSK3αβ. Therefore, GSK3αβ plays a critical role in MRP1-induced cell death.

Different effects of STAT5b and AKT activation by celecoxib in high and low doses on TGF-β1-induced epithelial-mesenchymal transition

김학렬,김영숙,조경화,황기은,정은택 대한결핵 및 호흡기학회 2015 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.120 No.-

Background: Cox-2 serves as a positive regulator of EMT. However, the addition of celecoxib to chemotherapy in clinical trials failed to benefit the survival of NSCLC patients. In this study, to re-evaluate the therapeutic potentials of celecoxib for NSCLC, we herein attempted to examine the cellular impacts of celecoxib, on NSCLC cells, in particular on EMT process. Methods: We evaluated the efficacy of celecoxib depending on the amount of dose in TGF-β1-induced EMT. EMT-related molecular alterations were detected by western blotting and ECIS. In addition, STAT5b and AKT were knocked down or overexpressed to determine its role in preventing TGF-β1-induced EMT by celecoxib. Results: Celecoxib in high dose was effective in preventing TGF-β1-induced EMT, as indicated by upregulation of E-cadherin, and downregulation of mesenchymal markers and transcription factors. On the other hand, celecoxib in low dose rather promoted TGF-β1-induced EMT. We found from phopho-kinase array kit that the different effects resulted from the two different doses of celecoxib, 2 μM and 20 μM, used were related to STAT 5b and AKT proteins. In addition STAT5b or AKT downregulation enhanced reverse of TGF-β1-induced EMT by high dose of celecoxib. In contrast, AKT upregulation had a relevant role in TGF-β1-induced EMT. Conclusions: Different doses of celecoxib used showed the opposite effects on TGF-β1-induced EMT through STAT5b and AKT pathway. We show for the first time the molecular mechanisms underlying the efficacy of celecoxib in NSCLC cells.