[다층_석정호 수상소감] 요동치는 흔들림을 되찾을 계기

석정호 고요아침 2019 열린시학 Vol.24 No.3

[다층_석정호 수상작] 메롱 말매미 외 1편

석정호 고요아침 2019 열린시학 Vol.24 No.3

[다층_석정호 신작] 꽃

석정호 고요아침 2019 열린시학 Vol.24 No.3

봄밤

석정호 고요아침 2018 열린시학 Vol.23 No.2

靜脈內 Neostigmine이 Atopine 前處理 犬의 血壓에 미치는 影響

昔廷鎬 충남대학교 의과대학 지역사회의학연구소 1980 충남의대잡지 Vol.7 No.2

In this experiment, by-intravenously administered neostigmine the blood pressure was increased initially, decreased and increased in nonpretreated dogs, but increased response was appeared only in atropinized dogs, and the increased pressor response was inhibited by hexamethonium, regitine and reserpine. By intraventricular neostigmine the blood pressure was decreased only. These results indicate that the pressor response of neostigmine is due to stimulation on the sympathetic ganglia and not related to central effect.

Elecsys 2010을 이용한 골대사지표검사의 평가

석정호,조은해,이수연,김종원 대한진단검사의학회 2006 Annals of Laboratory Medicine Vol.26 No.3

배경 : 골대사 지표는 골다공증에 의한 골절의 위험도 및 골다공증의 치료의 효과를 판정하는데 있어서 유용한 도구로 사용된다. 본 검사실에서는 Elecsys 2010 (Roche Diagnostics Corp.,Indianapolis, USA)으로 측정한 혈청 골대사 지표의 성능을 평가하였다.방법 : 골대사지표인 혈청 PTH, 오스테오칼신, 혈청 CTX에대한 Elecsys 2010의 분석능을 평가하였고 검체는 정도관리물질과환자 검체를 이용하였다. 상관성 검증을 위하여 방사선면역측정법으로 PTH를 그리고 ELISA로 혈청 오스테오칼신과 S-NTX를측정하였다. 또한 건강한 4,569명의결과치를 참고하여 혈청 오스테오칼신과 S-CTX에 대한 성별과 연령에 따른 한국인에서의 참고치를 설정하였다.결과 : 정밀도에 있어서 검사중 변이계수와 총 변이계수는, 저농도의 S-CTX (5.42%) 외에는 모두 5%내로 유지되었으며, 모든 항목에서 우수한 직선성을 보였다(r2≥0.99, P<0.01). Elecsys2010을 이용한 혈청 오스테오칼신과 PTH도 기존의 방법에 의한결과치와 좋은 상관관계를 나타내었다(혈청 오스테오칼신, r=0.95,P<0.01; PTH, r=0.96, P<0.01). S-CTX와 S-NTX도 유의한상관관계를 나타내었다(r=0.76, P<0.01). 혈청오스테오칼신(ng/mL)과 S-CTX (ng/mL)의 참고치는 다음과 같았다(성인 남성:9.58-33.62과 0.18-0.89; 31-50세 여성, 8.00-31.46과 0.11-0.81;50세 이상 여성, 8.30-43.50과 0.11-1.00).

주요우울장애에서 시상하부-뇌하수체-부신피질 축 변화의 진단적 함의

석정호 대한우울조울병학회 2014 우울조울병 Vol.12 No.1

Functional changes of hypothalamic-pituitary-adrenal (HPA) axis have been gathering attention from many investigators since HPA axis is a main neuroendocrine system in acute and chronic stress responses. HPA axis dysfunction may be one of the important pathophysiologic mechanisms in the development of major depressive disorder (MDD). Various laboratory tests including dexamethasone suppression test (DST) and cortisol awakening response assessing HPA axis functional reactivity have been conducted to investigate diagnostic validities in MDD. Major depressive disorder is a heterogeneous clinical syndrome in which various subtypes of major depressive disorder exist. Although researchers have not reached an unequivocal conclusion about HPA axis function changes in MDD, they have found differences in HPA axis hyperactivity among melancholic and atypical depression and Cushing’s disease. Functional changes in HPA axis may have diagnostic implications in differentiating subtypes of MDD. In addition, pituitary response to corticotropin releasing hormone may be associated with phenotypic difference of hypercortisolism between melancholic depression and Cushing’s disease. Further integration about this issue should be pursued in the future.

ong-term Activation of c-Jun N-terminal Kinase through Receptor Interacting Protein is Associated with DNA Damage-induced Cell Death

석정호,박경아,변희선,원민호,신상희,최병렬,이현지,김영래,홍장희,박종선,허강민 대한약리학회 2008 The Korean Journal of Physiology & Pharmacology Vol.12 No.4

Activation of c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase family, is an important cellular response that modulates the outcome of the cells which are exposed to the tumor necrosis factor (TNF) or the genotoxic stress including DNA damaging agents. Although it is known that JNK is activated in response to genotoxic stress, neither the pathways to transduce signals to activate JNK nor the primary sensors of the cells that trigger the stress response have been identified. Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-β-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation. Our findings revealed that this sustained JNK activation was not mediated by the TNF (tumor necrosis factor) receptor signaling, but it required a functional ATM (ataxia telangiectasia) activity. In addition, JNK inhibitor SP-600125 significantly blocked the Adr-induced cell death, but it did not affect the cell death induced by MNNG. These findings suggest that the sustained activation of JNK mediated by RIP plays an important role in the DNA damage-induced cell death, and that the duration of JNK activation relays a different stress response to determine the cell fate.

우울장애 환자에서 주의력 관련 신경망의 기능 이상

석정호 대한우울조울병학회 2009 우울조울병 Vol.7 No.1

Attention deficit is a major cognitive symptom in major depressive disorder. Studies on attention deficit of the patients with depressive disorder have shown various results depending on difficulty or characteristics of the tasks, the severity of depressive symptoms and accompanying features. Recently functional neuroimaging studies with neurocognitive activation paradigm enable us to investigate the neural network dysfunction associated with attention deficit in patients with depressive disorder. Reviews of relevant articles and literatures revealed that the attention deficit of depressive patients is prominent in effortful information processing task and not in automatic information-processing task. This characteristic may be originated from mild reduction of cognitive resources and the narrowed-focus related to depressive cognitive biases. Findings of neuroimaging studies have found that prefrontal hypoactivity and limbic hyperactivity with compensatory cerebellar hyperactivity may be associated with attention deficit in the patients with depressive disorder. Based on these advances in understanding of the neural network dysfunction, development of treatment strategies and neuroscientific researches validating the efficiency of each treatment should be followed.

갑각류 골격근의 Sarcoplasmic Reticulum에서 칼슘유리

석정호,정정구,허강민,이재흔 大韓藥理學會 1994 대한약리학잡지 Vol.30 No.1

갑각류 골격근의 SR에서 칼슘유리 channel protein complex의 성격을 규명하기 위해 민물가재 및/또는 바다가재의 SR vesicles을 분리하여 <TEX>$^{45}Ca$</TEX> 유리, <TEX>$[^3H]ryanodine$</TEX>결합, 및 immunoblot 실험을 실시하여 다음과 같은 결과를 얻었다. 1.민물가재 SR의 <TEX>$[^3H]ryanodine$</TEX>결합 실험에서 민물가재 SR의 maximal binding site및 affinity모두 바다가재에서 보다 낮았으나, high affinity binding site이었다. Extravesicles 칼슘농도를 증가시켰을 때 <TEX>$[^3H]ryanodine$</TEX>결합은 약간 증가되었으나, AMP나 AMP와 caffeine을 동시에 첨가하였을 때는 현저히 증가되었다(p<0.05). 이런 증가 현상은 <TEX>$MgCl_2$</TEX>나 tetracaine으로 유의성 있게 억제되었으나(p<0.001), ruthenium red에 의해서는 약간 억제되었다. 2.민물가재 SR을 전기영동하였을 때 바다가재의 ryanodine receptor band (HMWBr)와 비슷하나 포유류의 것(HMWBS) 보다는 약간 빠른 mobility를 나타낸다. 3.바다가재 HMWBr에 대한 polyclonal Ab를 이용한 민물가재, 바다가재 및 토끼 골격근의 칼슘유리 channel간의 면역학적 교차반응에서 민물가재와 바다가재의 칼슘유리 channel 간에는 교차반응이 있었으나, 포유류의 것과는 아무런 반응이 없었다. 4.민물가재 SR에서 <TEX>$^{45}Ca$</TEX>유리는 extravesicles의 칼슘농도 증가에 따라서 증가되었고, 낮은 외부 칼슘 농도에서 바다가재 보다 빠르게 일어났으나, AMP와 caffeine에 의해 영향을 받지 않았고, <TEX>$MgCl_2$</TEX>와 tetracaine으로 약간(<TEX>$3{\sim}8%$</TEX>) 그리고 고농도의 ruthenium red로 중등도(23%) 억제되었다. 이상의 실험성적으로 갑각류 칼슘유리 channel protein은 포유류의 것과는 기능적으로나 면역학적으로 매우 다른 특징을 가지고 있고, 민물가재와 바다가재 칼슘유리 channel은 서로 유사한 특징을 갖지만, 민물가재의 칼슘유리 channel이 바다가재의 것보다 외부칼슘에 예민한 기능을 갖는 것으로 사료된다. To characterize the SR Ca-release channel protein complex of crustacean, <TEX>$^{45}Ca-release,\;[^3H]ryanodine$</TEX> binding, and immunoblot studies were carried out in the crayfish and/or lobster skeletal sarcoplasmic reticulum. Bmax and affinity of crayfish SR to ryanodine were lower than those of lobster SR. AMP (5mM) increased <TEX>$[^3H]ryanodine$</TEX> binding significantly in both vesicles (P<0.05). <TEX>$Mg^{2+}$</TEX>(5mM) or tetracaine(1mM) inhibited <TEX>$[^3H]ryanodine$</TEX> binding significantly in both vesicles (P<0.001), but ruthenium red <TEX>$(10\;{\mu}M)$</TEX> inhibited it moderately. In SDS polyacrylamide gel electrophoretic analysis of crayfish SR vesicles, there was a high molecular weight band that showed similar mobility with Ca-release channel protein of lobster skeletal SR, but more rapid mobility (HMWBr) than that of rabbit skeletal SR (HMWBS). Immunoblot analysis showed that polyclonal Ab to lobster skeletal SR Ca-release channel protein was react with HMWBr of crayfish skeletal SR, but not with that of HMWBs of rabbit skeletal SR. <TEX>^{45}Ca-release</TEX> from crayfish skeletal SR vesicles was increased by the increase of extravesicular calcium from <TEX>$1{\mu}M$</TEX> to 1mM. This Ca-release phenomenon was similar, but more sensitive in the low concentration of <TEX>$Ca^{2+}$</TEX>, compared to that from lobster SR vesicles. AMP (5mM) or caffeine (10mM) did not affect to <TEX>$^{45}Ca-release.\;^{45}Ca-release$</TEX> was inhibited slightly (<TEX>$3{\sim}8%\;by\;Mg^{2+}$</TEX>) (5mM) or tetracaine (1mM), and moderately (23%) by high concentration of ruthenium red <TEX>$(300\;{\mu}M)$</TEX>. From the above results, it is suggested that SR Ca-release channel protein of crustacean has different properties from that of the rabbit, and similar properties between crayfish and lobster in functional and immunological aspects, but Ca-release via crayfish channel may be more sensitive to calcium.