• The Korean Journal of Physiology and Pharmacology
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• 제10권5호
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• pp.289-295
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• 2006

Sodium fluoride (NaF) has been shown to be cytotoxic and elicit inflammatory response in human. However, the cellular mechanisms underlying NaF-induced cytotoxicity in periodontal tissues have not yet been elucidated. This study is aimed to investigate the mechanisms of NaF-induced apoptosis in human gingival fibroblast (HGF). NaF decreased the cell viability of HGF in a dose- and time-dependent manner. NaF gave rise to apoptotic morphological changes including cell shrinkage, chromatin condensation, and DNA fragmentation. However, NaF did not affect the production of ROS. In addition, NaF augumented cytochrome c release from mitochondria into the cytosol, and enhanced caspase -9 and -3 activities., cleavage (85 kDa fragments) of poly (ADP-ribose) polymerase (PARP) and upregulation of voltage-dependent anion channel (VDAC) 1. These results demonstrated that NaF-induced apoptosis in HGF may be mediated with mitochondria. Furthermore, NaF elevated caspase-8 activity and upregulated Fas-ligand (Fas-L), suggesting involvement of death receptor mediated pathway in NaF-induced apoptosis. Expression of Bcl-2, an anti-apoptotic Bcl-2 family, was downregulated, whereas expression of Bax, a pro-apoptotic Bcl-2 family, was not affected in NaF-treated HGF. These results suggest that NaF induces apoptosis in HGF through both mitochondria- and death receptor-mediated pathway mediated by Bcl-2 family.

• Childhood Kidney Diseases
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• 제17권2호
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• pp.137-142
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• 2013

전신형 PHA 1은 ENaC의 ${\alpha}$ (SCNN1A), ${\beta}$ (SCNN1B), ${\gamma}$ (SCNN1G) 아단위를 암호화하는 유전자의 변이로 경상피나트륨 수송의 결함으로 발생하게 되며 신생아기에 생명을 위협하는 염분 소실, 고칼륨혈증, 대사성 산증이 발생하게 된다. 또한 신장 뿐 아니라 대장, 침샘, 땀샘 및 호흡기상피 등의 다양한 표적 기간에서 전신적으로 알도스테론에 대한 저항성이 나타난다. 최근 전신형 PHA 1의 임상상과 유전자형 및 이환된 환아들의 장기 추적 결과에 대한 보고가 되고 있으나 질환의 희소성으로 임상 표현형을 설명하기는 어려운 실정이다. 저자들은 사망을 초래할 수 있는 심각한 전해질 이상을 보인 환아에서 PHA를 의심하여 염분 및 양이온 교환수지를 투여하여 효과적으로 전해질 교정이 되어 추적관찰 중이며, 유전자 검사를 통해 missense mutation을 나타낸 전신형 PHA1을 경험하였기에 보고하는 바이다.

• The Korean Journal of Physiology and Pharmacology
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• 제9권4호
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• pp.239-246
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• 2005

In the central nervous system, nitric oxide (NO) is associated with many pathological diseases such as brain ischemia, neurodegeneration and inflammation. The epigallocatechin gallate (EGCG), a major compound of green tea, is recognized as protective substance against neuronal diseases. This study is aimed to investigate the effect of EGCG on NO-induced cell death in PC12 cells. Administration of sodium nitroprusside (SNP), a NO donor, decreased cell viability in a dose- and time-dependent manner and induced genomic DNA fragmentation with cell shrinkage and chromatin condensation. EGCG diminished the decrement of cell viability and the formation of apoptotic morphologenic changes as well as DNA fragmentation by SNP. EGCG played as an antioxidant that attenuated the production of reactive oxygen species (ROS) by SNP. The cells treated with SNP showed downregulation of Bcl-2, but upregulation of Bax. EGCG ameliorated the altered expression of Bcl-2 and Bax by SNP. The release of cytochrome c from mitochondria into cytosol and expression of voltage -dependent anion channel (VDAC)1, a cytochrome c releasing channel in mitochondria, were increased in SNP-treated cells, whereas were attenuated by EGCG. The enhancement of caspase-9, preceding mitochondria-dependent pathway, caspase-8 and death receptor-dependent pathway, as well as caspase-3 activities were suppressed by EGCG. SNP upragulated Fas and Fas-L, which are death receptor assembly, whereas EGCG ameliorated the expression of Fas enhanced by SNP. These results demonstrated that EGCG has a protective effect against SNP-induced apoptosis in PC12 cells, through scavenging ROS and regulating the mitocondria- and death receptor-mediated signal pathway. The present study suggest that EGCG might be a natural neuroprotective substance.

• The Korean Journal of Physiology and Pharmacology
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• 제13권6호
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• pp.517-526
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• 2009

The present study was attempted to investigate whether polyphenolic compounds isolated from wine, which is brewed from Rubus coreanum Miquel (PCRC), may affect the release of catecholamines (CA) from the isolated perfused adrenal medulla of the spontaneously hypertensive rats (SHRs), and to establish its mechanism of action. PCRC $(20\sim180\;{\mu}g/ml)$ perfused into an adrenal vein for 90 min relatively dose-dependently inhibited the CA secretory responses to ACh (5.32 mM), high $K^+$ (56 mM), DMPP $(100\;{\mu}M)$ and McN-A-343 $(100\;{\mu}M)$. PCRC itself did not affect basal CA secretion (data not shown). Also, in the presence of PCRC $(60\;{\mu}g/ml)$, the CA secretory responses to veratridine (a selective $Na^+$ channel activator $(10\;{\mu}M)$, Bay-K-8644 (a L-type dihydropyridine $Ca^{2+}$ channel activator, $10\;{\mu}M$), and cyclopiazonic acid (a cytoplasmic $Ca^{2+}$-ATPase inhibitor, $10\;{\mu}M$) were significantly reduced, respectively. In the simultaneous presence of PCRC $(60\;{\mu}g/ml)$ and L-NAME (an inhibitor of NO synthase, $30\;{\mu}M$), the inhibitory responses of PCRC on the CA secretion evoked by ACh, high $K^+$, DMPP, and Bay-K-8644 were considerably recovered to the extent of the corresponding control secretion compared with that of PCRC-treatment alone. The level of NO released from adrenal medulla after the treatment of PCRC $(60\;{\mu}g/ml)$ was greatly elevated compared with the corresponding basal level. Taken together, these results demonstrate that PCRC inhibits the CA secretion from the isolated perfused adrenal medulla of the SHRs evoked by stimulation of cholinergic receptors as well as by direct membrane-depolarization. It seems that this inhibitory effect of PCRC is mediated by blocking the influx of calcium and sodium into the adrenal medullary chromaffin cells of the SHRs as well as by inhibition of $Ca^{2+}$ release from the cytoplasmic calcium store at least partly through the increased NO production due to the activation of NO synthase.

• Journal of Electrochemical Science and Technology
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• 제11권2호
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• pp.187-194
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• 2020

Two types of sodium cobalt pyrophosphates, triclinic Na_3.12Co_2.44(P₂O₇)₂ and orthorhombic Na₂CoP₂O₇, are compared as high-voltage cathode materials for Na-ion batteries. Na₂CoP₂O₇ shows no electrochemical activity, delivering negligible capacity. In contrast, Na_3.12Co_2.44(P₂O₇)₂ exhibits good electrochemical performance, such as high redox potential at ca. 4.3 V (vs. Na/Na⁺) and stable capacity retention over 50 cycles, although Na_3.12Co_2.44(P₂O₇)₂ delivered approximately 40 mA h g^-1. This is attributed to the fact that Na₂CoP₂O₇ (~3.1 Å) has smaller diffusion channel size than Na_3.12Co_2.44(P₂O₇)₂ (~4.2 Å). Moreover, the electrochemical performance of Na_3.12Co_2.44(P₂O₇)₂ is examined using Na cells and Li cells. The overpotential of Na cells is smaller than that of Li cells. This is due to the fact that Na_3.12Co_2.44(P₂O₇)₂ has a smaller charge transfer resistance and higher diffusivity for Na⁺ ions than Li⁺ ions. This implies that the large channel size of Na_3.12Co_2.44(P₂O₇)₂ is more appropriate for Na⁺ ions than Li⁺ ions. Therefore, Na_3.12Co_2.44(P₂O₇)₂ is considered a promising high-voltage cathode material for Na-ion batteries, if new electrolytes, which are stable above 4.5 V vs. Na/Na⁺, are introduced.

• Korean Chemical Engineering Research
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• 제48권6호
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• pp.791-794
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• 2010

축전식 전기탈이온(Capacitive deionization: CDI) 시스템을 실제공정에 적용하기 위하여 대용량 제작이 가능하며 높은 처리 효율을 갖는 셀 구조 연구가 필요하다. 본 연구에서는 대용량 제작을 위하여 낮은 수압으로 운전할 수 있는 병렬형 구조와 처리효율을 증가시키기 위하여 집중형 유로를 동시에 적용하여 설계하고 성능 평가하였다. 설계한 유로 구조의 유입수 흐름을 확인하기 위하여 유체역학적 모델링이 가능한 COMSOL프로그램을 사용하여 집중형 유로가 형성되는 것을 확인하였고, 염 제거 효율을 확인하기 위하여 단위 셀과 20층으로 용량 증축된 스택을 사용하여 CDI운전을 통한 제거효율을 확인하였다. 그 결과 $210cm^2$ 면적의 단위 셀에서는 18 ml/min의 유량조건에서 1.1 psi의 수압으로 70.8%의 제거효율을 보였으며, 20층으로 용량 증축된 셀에서는 유량을 20배로 늘린 360 ml/min의 유량조건에서 1.3~1.5 psi의 수압으로 75.6%의 제거효율을 확인할 수 있었다. 연구된 유로 설계는 대용량 시스템을 제작하는데 있어서 적합한 병렬형 구조이며 효율적인 탈염을 할 수 있는 집중형 유로로 설계되어 실제공정에 적용할 수 있는 구조임을 확인할 수 있었다.

• The Korean Journal of Pain
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• 제33권2호
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• pp.108-120
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• 2020

From the perspective of the definition of pain, pain can be divided into emotional and sensory components, which originate from potential and actual tissue damage, respectively. The pharmacologic treatment of the emotional pain component includes antianxiety drugs, antidepressants, and antipsychotics. The anti-anxiety drugs have anti-anxious, sedative, and somnolent effects. The antipsychotics are effective in patients with positive symptoms of psychosis. On the other hand, the sensory pain component can be divided into nociceptive and neuropathic pain. Non-steroidal anti-inflammatory drugs (NSAIDs) and opioids are usually applied for somatic and visceral nociceptive pain, respectively; anticonvulsants and antidepressants are administered for the treatment of neuropathic pain with positive and negative symptoms, respectively. The NSAIDs, which inhibit the cyclo-oxygenase pathway, exhibit anti-inflammatory, antipyretic, and analgesic effects; however, they have a therapeutic ceiling. The adverse reactions (ADRs) of the NSAIDs include gastrointestinal problems, generalized edema, and increased bleeding tendency. The opioids, which bind to the opioid receptors, present an analgesic effect only, without anti-inflammatory, antipyretic, or ceiling effects. The ADRs of the opioids start from itching and nausea/vomiting to cardiovascular and respiratory depression, as well as constipation. The anticonvulsants include carbamazepine, related to sodium channel blockade, and gabapentin and pregabalin, related to calcium blockade. The antidepressants show their analgesic actions mainly through inhibiting the reuptake of serotonin or norepinephrine. Most drugs, except NSAIDs, need an updose titration period. The principle of polypharmacy for analgesia in case of mixed components of pain is increasing therapeutic effects while reducing ADRs, based on the origin of the pain.

• 대한약리학회지
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• 제25권1호
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• pp.23-30
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• 1989

함께 투여되는 마약성진통제에 따라 효능제 또는 길항제(mixed agonist-antagonist)로 작용하는 buprenorphine을 사용하여 개구리 좌골신경에 존재하는 아편수용체의 성질을 검토하였다. 실험은 sucrose-gap apparatus를 사용하여 활동전압에 대한 영향을 관찰하였으며 약물의 상호작용을 검토하고자 meperidine 또는 naloxone을 사용하여 다음과 같은 결과를 얻었다. 1) Buprenorphine은 현저하게 개구리 좌골신경의 활동전압을 저하시켰다. 2) 두 개의 최고작용농도를 보였는데 저농도에서는 $10^{-8}\;M$, 또 고농도에서는 $10^{-4}\;M$에서 현저하게 작용을 나타내었다. 3) Buprenorphine은 meperidine의 활동전압 저하작용을 의의있게 억제하였다. 4) Naloxone에 의하여 Buprenorphine의 저하 작용이 억제되었다. 위의 실험결과로 Buprenorphine은 순수 마약성진통제의 작용을 억제하여 차단제로 작용하는 한편 또한 효능제로 활동전압을 의의있게 억제하였다. 이로써 개구리 좌골신경에 있는 아편수용체는 세포막에 또는 세포막 주위에서 $Na^+-Channel$이 활성화되는 데 중요한 역할을 하는 것으로 간주되며 이 수용체는 또한 Naloxone에 매우 민감한 반응을 나타낸다.

• 공업화학
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• 제9권7호
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• pp.1090-1097
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• 1998

국부 마취제로 이용되는 lidocaine 화합물들이 마취 효과를 나타내는 과정을 알아보기 위하여 세포벽을 구성하는 지질 이중막의 모사 시스템으로 공기/물 계면에 형성된 지질 단분자 막을 이용하여 lidocaine 화합물들이 지질 단분자 막의 팽창에 미치는 영향을 연구하였다. Lidocaine이 신경 세포와 접하게 되면 세포벽을 구성하는 지질 이중막을 팽창시켜 이중막에 함침된 단백질을 압축하여 이를 통한 이온 통과가 차단되어 신경 전달이 마비된다는 가설과, 단백질 이온 통로에 존재하는 lidocaine receptor에 직접 흡착되어 이온 통로를 막는다는 가설이 구체적 실험 없이 제안되었다. 본 연구에서는 두 가설 타당성을 증명하고자 리피드 단분자 막팽창에 lidocaine이 미치는 영향을 조사하였다. 실험 결과 유용성인 lidocaine은 phosphatidyl choline, sphingomyelin, DS-PL95E, lipoid의 단분자 막을 수축시켰으며 phosphatidyl ethanolamine은 특정 조성 범위에서만 단분자 막을 팽창시켰다. 반면 수용성인 lidocaine-HCl 염은 실험에 사용된 모든 지질의 단분자 막을 팽창시켰다.

• Clinical and Experimental Pediatrics
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• 제54권2호
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• pp.90-93
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• 2011

Pseudohypoaldosteronism type 1 (PHA1) is a rare form of mineralocorticoid resistance characterized in newborns by salt wasting with dehydration, hyperkalemia and failure to thrive. This disease is heterogeneous in etiology and includes autosomal dominant PHA1 owing to mutations of the NR3C2 gene encoding the mineralocorticoid receptor, autosomal recessive PHA1 due to mutations of the epithelial sodium channel (ENaC) gene, and secondary PHA1 associated with urinary tract diseases. Amongst these diseases, autosomal dominant PHA1 shows has manifestations restricted to renal tubules including a mild salt loss during infancy and that shows a gradual improvement with advancing age. Here, we report a neonatal case of PHA1 with a NR3C2 gene mutation (a heterozygous c.2146_2147insG in exon 5), in which the patient showed failure to thrive, hyponatremia, hyperkalemia, and elevated plasma renin and aldosterone levels. This is the first case of pseudohypoaldosteronism type 1 confirmed by genetic analysis in Korea.