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.

Trichostatin A induces apoptosis in lung cancer cells viasimultaneous activation of the death receptor-mediated andmitochondrial pathway

김학렬,김은정,양세훈,정은택,박채니,이재형,윤명자,소홍섭,박래길 생화학분자생물학회 2006 Experimental and molecular medicine Vol.38 No.6

Trichostatin A (TSA), originally developed as an antifungal agent, is one of potent histone deace-tylase (HDAC) inhibitors, which are known to cause growth arrest and apoptosis induction of trans-formed cells, including urinary bladder, breast, prostate, ovary, and colon cancers. However, the effect of HDAC inhibitors on human non-small cell lung cancer cells is not clearly known yet. Herein, we demonstrated that treatment of TSA resulted in a significant decrease of the viability of H157 cells in a dose-dependent manner, which was revealed as apoptosis accompanying with nuclear fragmen-tation and an increase in sub-G0/G1 fraction. In addition, it induced the expression of Fas/FasL, which further triggered the activation of caspase-8. Catalytic activation of caspase-9 and decreased expression of anti-aptototic Bcl-2 and Bcl-XL pro-teins were observed in TSA-treated cells. Catalytic activation of caspase-3 by TSA was further con-firmed by cleavage of pro-caspase-3 and intracellular substrates, including poly (ADP-ribose) polymerase (PARP) and inhibitor of caspase-activated deoxy-ribonuclease (ICAD). In addition, a characteristic phenomenon of mitochondrial dysfunction, inc-luding mitochondrial membrane potential transition and release of mitochondrial cytochrome c into the cytosol was apparent in TSA-treated cells. Taken together, our data indicate that inhibition of HDAC by TSA induces the apoptosis of H157 cells through signaling cascade of Fas/FasL-mediated extrinsic and mitocondria-mediated intrinsic caspases path-way.

하악골에 발생한 원발성 골내암종의 치험례

김학렬,류동목,오정환,Kim, Hak-Ryeol,Ryu, Dong-Mok,Oh, Jung-Hwan 대한구강악안면외과학회 2007 대한구강악안면외과학회지 Vol.33 No.3

Primary intraosseous carcinoma (PIOC) is a rare odontogenic carcinoma defined as a squamous cell carcinoma arising within a jaw having no initial connection with the oral mucosa, and probably developing from residues of the odontogenic epithelium. PIOC appears more common in male than female, especially at posterior portion of the mandible. Radiographic features of PIOC show irregular patterns of bone destruction with ill defined margins. It could be sometimes misdiagnosed as the cyst or benign tumor because it shows well defined margins. If it couldn't be done appropriate treatment initially, PIOC shows extremely aggressive involvement, extensive local destruction and spreads to the overlying soft tissue. Therefore accurate diagnosis in early state is necessary. The diagnosis criteria proposed for PIOC are : (1) absence of ulcer formation, except when caused by other factors, (2) histologic evidence of squamous cell carcinoma without a cystic component or other odontogenic tumor cell, and (3) absence of another primary tumor on chest radiograph obtained at the time of diagnosis and during a follow-up period of more than 6 month(Suei et al., 1994).

F-68 : Free Paper Presentation ; Inhibition of Autophagy Enhances Apoptotic Potential of Pemetrexed and Simvastatin in Malignant Mesothelioma and Lung Cancer Cells

김학렬,김옥희,김영숙,황기은,정은택 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-

Background: Pemetrexed is a multitarget antifolate for the treatment of malignant mesothelioma and non-small cell lung cancer (NSCLC) and has been shown to stimulate autophagy. In this study, we determined whether combination treatment with pemetrexed and simvastatin can induce autophagy in malignant mesothelioma and NSCLC cells. Furthermore, we determined whether inhibition of autophagy can drive malignant mesothelioma and NSCLC cells into apoptosis. Methods: Malignant mesothelioma cells MSTO-211 and NSCLC cells A549 were treated with pemetrexed and simvastatatin alone and in combination. Autophagy was assessed by transmission electron microscopy and confocal microscopy for GFP-LC3 and acridine orange. Autophagic induction by pemetrexed and simvastatatin was also investigated using autophagic inhibitors or inducers, the proportion of apoptotic cells was further determined by Annexin V assay. Results: Combination of pemetrexed and simvastatatin induced more caspase dependent apoptosis and autophagy than either drug in malignant mesothelioma and NSCLC cells. 3-methyladenine (3-MA), bafilomycin A, E64d/pepstatin A, and ATG5 siRNA increased apoptotic potential of pemetrexed and simvastatatin whereas rapamycin and LY294002 decreased caspase dependent apoptosis of pemetrexed and simvastatatin. Conclusions: Combination of pemetrexed and simvastatatin augments their apoptosis and autophagy in malignant mesothelioma and NSCLC cells. Inhibition of autophagy was shown to enhance apoptosis, suggesting a novel therapeutic strategy against malignant mesothelioma and lung cancer.Background: Pemetrexed is a multitarget antifolate for the treatment of malignant mesothelioma and non-small cell lung cancer (NSCLC) and has been shown to stimulate autophagy. In this study, we determined whether combination treatment with pemetrexed and simvastatin can induce autophagy in malignant mesothelioma and NSCLC cells. Furthermore, we determined whether inhibition of autophagy can drive malignant mesothelioma and NSCLC cells into apoptosis. Methods: Malignant mesothelioma cells MSTO-211 and NSCLC cells A549 were treated with pemetrexed and simvastatatin alone and in combination. Autophagy was assessed by transmission electron microscopy and confocal microscopy for GFP-LC3 and acridine orange. Autophagic induction by pemetrexed and simvastatatin was also investigated using autophagic inhibitors or inducers, the proportion of apoptotic cells was further determined by Annexin V assay. Results: Combination of pemetrexed and simvastatatin induced more caspase dependent apoptosis and autophagy than either drug in malignant mesothelioma and NSCLC cells. 3-methyladenine (3-MA), bafilomycin A, E64d/pepstatin A, and ATG5 siRNA increased apoptotic potential of pemetrexed and simvastatatin whereas rapamycin and LY294002 decreased caspase dependent apoptosis of pemetrexed and simvastatatin. Conclusions: Combination of pemetrexed and simvastatatin augments their apoptosis and autophagy in malignant mesothelioma and NSCLC cells. Inhibition of autophagy was shown to enhance apoptosis, suggesting a novel therapeutic strategy against malignant mesothelioma and lung cancer.

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.

미국흰불나방(Hyphantria cunea Drury)의 Trehalase 에 관한 연구

김학렬,한원동,윤치영 고려대학교 한국곤충연구소 1987 昆蟲硏究誌 Vol.13 No.1

미국 흰불나방(Hyphantria cunea D.)의 trehalase isozyme 분포, 소화관내 분포, 변태단계애 따른 활성의 변화 및 섭식과 활성과의 관계등을 조사하여 다음과 같은 결과를 얻었다. 1. Trehalase는 40K의 분자량이 동일한 3개의 isozyme, 즉 TR-1, 2, 3가 존재하며, TR-1과 TR-2는 지방체와 혈림프에 TR-2 및 TR-3는 소화관에 존재하였다. 2. 변태 단계에 따른 trehalase의 활성 변화에 있어서, 소화관에서는 7령 중기에 최대 활성을 보이며, 용시기에도 일부 활성이 존재하며, 이는 TR-2에 기인되는 것임을 확인하였다. 혈림프에 존재하는 trehalase는 유충기에 낮은 활성을 보이다가 용시기에 증가하였다. 3. 소화관 조직에서의 trehalase는 대부분이 중장조직에서 나타나나 장관(gut lumen)에서는 중장 뿐만 아니라 후장에서도 높은 활성을 보여주었다. 4. Starvation시에 지속적인 trehalase 활성의 감소를 보여 주었으며, 재섭식시에는 2일이내에 정상적인 활성 수준으로 회복되었다. Trehalase of H. cunea were isolated to determine their isozyme localization and their organ distribution. The activity changes and relationship between feeding and stavation were also studied. There were three isozymes of trehalase with M.W.40,000 and TR-1, 2 were localized in fat body and haemolymph, while TR-2, 3 in alimentary canal. In the developmental change of trehalase activities in alimentary canal, trehalase showed high activity in late instar larva and somewhat lower activities in pupal stage due to TR-2 isozyme. Trehalase mainly occurred in midgut tissue, but its activities in the gut in including their contents were mainly distributed in midgut and hindgut. The activities of trehalase significantly decreased during starvation and repaired by subsequent feeding.

F-64 : Free Paper Presentation ; Celecoxib and Sulindac Inhibits TGF-β1-induced Epithelial-mesenchymal Transition and Suppresses Lung Cancer Migration and Invasion via Down-regulation of SIRT-1

김학렬,김영숙,황기은,정은택 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-

Background: Non-steroidal anti-inflammatory drugs (NSAIDs) has been reported to suppress lung cancer invasion and metastasis. We investigated the role of NSAIDs as an inhibitor of TGF-β1-induced EMT, and the underlying mechanisms of suppressing lung cancer migration and invasion by celexib and sulindac. Methods: We evaluated the efficacy of NSAIDs in TGF-β1-induced EMT. Electric cell-substrate impedance sensing (ECIS) was used to evaluate the migration and invasion. The matrix metalloproteinase (MMP) gelatinolytic activity was determined by gelatin zymography. SIRT1 was knocked down or overexpressed to determine its role in preventing TGF-β1-induced EMT by NSAIDs. Results: Celecoxib was more effective in preventing TGF-β1-induced EMT, as compared with sulindac, indicating upregulation of E-cadherin, and downregulation of N-cadherin, mesenchymal and transcription factors. ECIS assay showed that NSAIDs could inhibit TGF-β1-enhanced migration and invasion of A549 cells. Increment in MMP-9 expression following activation of TGF-β1 was also observed. However, treatment with NSAIDs inhibited MMP-9 expression. SIRT1 downregulation enhanced reverse of TGF-β1-induced EMT by celecoxib or sulindac. In contrast, SIRT1 upregulation had a relevant role in TGF-β1-induced EMT. Conclusions: Celecoxib and sulindac can inhibit TGF-β1-induced EMT and suppress migration and invasion via down-regulation of SIRT-1. SIRT1 is positive regulator of TGF-β1-induced EMT and potential therapeutic target to reverse EMT and to prevent lung cancer progression.Background: Non-steroidal anti-inflammatory drugs (NSAIDs) has been reported to suppress lung cancer invasion and metastasis. We investigated the role of NSAIDs as an inhibitor of TGF-β1-induced EMT, and the underlying mechanisms of suppressing lung cancer migration and invasion by celexib and sulindac. Methods: We evaluated the efficacy of NSAIDs in TGF-β1-induced EMT. Electric cell-substrate impedance sensing (ECIS) was used to evaluate the migration and invasion. The matrix metalloproteinase (MMP) gelatinolytic activity was determined by gelatin zymography. SIRT1 was knocked down or overexpressed to determine its role in preventing TGF-β1-induced EMT by NSAIDs. Results: Celecoxib was more effective in preventing TGF-β1-induced EMT, as compared with sulindac, indicating upregulation of E-cadherin, and downregulation of N-cadherin, mesenchymal and transcription factors. ECIS assay showed that NSAIDs could inhibit TGF-β1-enhanced migration and invasion of A549 cells. Increment in MMP-9 expression following activation of TGF-β1 was also observed. However, treatment with NSAIDs inhibited MMP-9 expression. SIRT1 downregulation enhanced reverse of TGF-β1-induced EMT by celecoxib or sulindac. In contrast, SIRT1 upregulation had a relevant role in TGF-β1-induced EMT. Conclusions: Celecoxib and sulindac can inhibit TGF-β1-induced EMT and suppress migration and invasion via down-regulation of SIRT-1. SIRT1 is positive regulator of TGF-β1-induced EMT and potential therapeutic target to reverse EMT and to prevent lung cancer progression.

대학교 신입생들에서 지각된 스트레스 및 취약성 변인과 신체화 경향의 관계에 관한 연구

김학렬,조준호,조용래,Kim, Hack-Ryul,Cho, Jun-Ho,Cho, Yong-Rae 한국정신신체의학회 1997 정신신체의학 Vol.5 No.1

For the purpose of examining the relationship between perceived stress, vulnerability variables, and somatization tendency, the self-report questionnaires of perceived stress, styles of stress coping(passive and active copings), self-perception, gender, and somatization tendency were administered to university entrants(n=2,024). The results were as follows: 1) Perceived stress, styles of stress coping(passive and active copings), self-perception, and gender accounted for 15.56% of the total variance in somatization tendency. As a result of comparing the relative contributions of all predictor variables to somatization tendency, the highest was perceived stress, and the next in order were passive coping style, self-perception, and gender, whereas direct effect of active coping style was not significant. 2) The two-way and three-way interaction effects of perceived stress X vulnerability variables were not significant. 3) The two-way and three-way interaction effects of gender X psychosocial variables were not significant. To conclude, perceived stress and vulnerability variables independently contribute to somatization tendency in university entrants, and furthermore it is suggested that vulnerability variables as well as perceived stress must be considered to account for somatization tendency.

F-70 : Free Paper Presentation ; Synergistic Effect of Sulindac and Simvastatin on Apoptosis in Lung Cancer A549 Cells through AKT-dependent Downregulation of Survivin

김학렬,권수진,김영숙,황기은,정은택 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-

Background: Non-steroidal anti-inflammatory drugs (NSAIDs) and statins are potential chemopreventive agents. The mechanism underlying the deregulation of survivin by NSAIDs and statins in non-small cell lung cancer (NSCLC) has not been elucidated. We investigated the synergistic interaction of sulindac and simvastatin in lung cancer cells. Methods: Cell viability was measured by the MTT assay. The expression of apoptotic markers, AKT, and survivin in response to sulindac and simvastatin was examined by western blotting. DNA fragmentation by apoptosis was analyzed by flow cytometry in A549 cells. ROS generation was measured by flow cytometry using H2DCFDA and MitoSOX Red, and the effects of pretreatment with N-acetylcysteine were tested. The effects of AKT on survivin expression in sulindac and simvastatin-treated cells were assessed. Survivin was knocked down or overexpressed to determine its role in apoptosis induced by sulindac and simvastatin. Results: Sulindac and simvastatin synergistically augmented apoptosis and intracellular ROS production in A549 cells. Inhibition of AKT by siRNA or LY294002 inhibited survivin, whereas AKT overexpression markedly increased survivin expression even in the presence of sulindac and simvastatin. In addition, survivin siRNA enhanced sulindac and simvastatin-induced apoptosis. In contrast, survivin upregulation protected against sulindac and simvastatin-induced apoptosis.Background: Non-steroidal anti-inflammatory drugs (NSAIDs) and statins are potential chemopreventive agents. The mechanism underlying the deregulation of survivin by NSAIDs and statins in non-small cell lung cancer (NSCLC) has not been elucidated. We investigated the synergistic interaction of sulindac and simvastatin in lung cancer cells. Methods: Cell viability was measured by the MTT assay. The expression of apoptotic markers, AKT, and survivin in response to sulindac and simvastatin was examined by western blotting. DNA fragmentation by apoptosis was analyzed by flow cytometry in A549 cells. ROS generation was measured by flow cytometry using H2DCFDA and MitoSOX Red, and the effects of pretreatment with N-acetylcysteine were tested. The effects of AKT on survivin expression in sulindac and simvastatin-treated cells were assessed. Survivin was knocked down or overexpressed to determine its role in apoptosis induced by sulindac and simvastatin. Results: Sulindac and simvastatin synergistically augmented apoptosis and intracellular ROS production in A549 cells. Inhibition of AKT by siRNA or LY294002 inhibited survivin, whereas AKT overexpression markedly increased survivin expression even in the presence of sulindac and simvastatin. In addition, survivin siRNA enhanced sulindac and simvastatin-induced apoptosis. In contrast, survivin upregulation protected against sulindac and simvastatin-induced apoptosis.

운동생리 분야 : 유산소성 트레이닝 ( 5week ) 후 흰쥐 혈청에서의 크레아틴 포스포키나제 ( CPK ) , 젖산탈수소효소 ( LDH ) 및 젖산탈수소 동위효소의 변화

김학렬,김양수,김창근,안응남,손태열,안의수 한국체육학회 1991 국제스포츠 학술대회 Vol.1991 No.-