• The Korean Journal of Pain
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• 제21권1호
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• pp.27-32
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• 2008

Background: Experimental evidence indicates that ginseng modulate the nociceptive transmission. Authors examined the role of adrenergic and cholinergic receptors on the antinociceptive action of Korean red ginseng against the formalin-induced pain at the spinal level. Methods: Catheters were inserted into the intrathecal space of male Sprague-DawIey rats. Fifty ${\mu}l$ of 5% formalin solution was injected to the hindpaw for induction of pain and formalin-induced pain (flinching response) was observed. The role of spinal adrenergic and cholinergic receptors on the effect of Korean red ginseng was assessed by antagonists (Prazosin, yohimbine, atropine and mecamylamine). Results: Intrathecal Korean red ginseng produced a dose-dependent suppression of the flinching response in the rat formalin test. All of prazosin, yohimbine, atropine and mecamylamine antagonized the antinociception of Korean red ginseng. Conclusions: Spinal Korean red ginseng is effective against acute pain and facilitated pain state evoked by formalin injection. All of alpha 1, alpha 2, muscarinic and nicotinic receptors may play an important role in the antinociceptive action of Korean red ginseng at the spinal level.

• The Korean Journal of Physiology and Pharmacology
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• 제4권4호
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• pp.275-281
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• 2000

Cholecystokinin (CCK) is a gastrointestinal hormone which plays an important role in satiety and gastric motility. It is also widely distributed throughout the central nervous system, where it appears to be involved in the central control of anxiety, feeding behavior and nociception. Two distinct CCK receptor types, $CCK_A$ and $CCK_B,$ have been found in the brain. Both CCK receptors coexist in the rat nucleus tractus solitarius (NTS), which is the primary center for the coordination of peripheral and central activities related to gastrointestinal, cardiovascular and respiratory functions. In order to study ionic actions of CCK on each type of receptor, we investigated the effects of CCK-8S on neurons located in the NTS of the rat using whole-cell patch-clamp recordings in brainstem slices. Application of CCK-8S, under current clamp, produced a membrane depolarization accompanied by action potential firing. This CCK-evoked excitation was dose-dependent $(10\;nM{\sim}10\;{\mu}M)$ and observed in more than 60% of NTS neurons. Under voltage clamp conditions, CCK-8S induced an inward current with a notably increased spontaneous excitatory synaptic activity. However, CCK-8S did not significantly change the amplitude of pharmacologically isolated and evoked EPSP(C)s. Using selective $CCK_A$ and $CCK_B$ receptor antagonists, we observed two different effects of CCK-8S, which suggest $CCK_A$ receptor-mediated inhibitory and $CCK_B$ receptor-mediated excitatory effects in the NTS. These results may help to explain the ability of CCK to modulate gastrointestinal and other reflex systems in the NTS.

• Transactions on Electrical and Electronic Materials
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• 제4권3호
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• pp.10-14
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• 2003

In this paper, we have introduced the x-ray detector built with a CsI:Na scintillation layer deposited on amorphous selenium. To determine the thickness of the CsI:Na layer, we have estimated the transmission spectra and the absorption of continuous x-rays in diagnostic range by using computer simulation (MCNP 4C). A x-ray detector with 65 ${\mu}m$-CsI:Na/30 ${\mu}m$-Se layer has been fabricated by a thermal evaporation technique. SEM and PL measurements have been performed. The dark current and x-ray sensitivity of the fabricated detector has been compared with that of the conventional a-Se detector with 100 ${\mu}m$ thickness. Experimental results show that both detectors exhibit a similar dark current, which was of a low value below $400 pA/cm^2$ at 10 V/${\mu}m$. However, the CsI:Na-Se detector indicates high x-ray sensitivity, roughly 1.3 times that of a conventional a-Se detector. Furthermore, a CsI:Na-Se detector with an aluminium reflective layer shows a 1.8 times higher x-ray sensitivity than an a-Se detector. The hybrid type detector proposed in this work exhibits a low dark current and high x-ray sensitivity, and, in particular, excellent linearity to the x-ray exposure dose.

• 한국인터넷방송통신학회논문지
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• 제17권6호
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• pp.127-135
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• 2017

대부분의 최신 자동차들은 편안하고 안전한 운전 환경을 위해 다양한 종류의 ECU들을 탑재하고 있다. ECU들 사이의 효율적인 통신을 위해 대부분의 자동차 제조사들은 Controller Area Network(CAN) 프로토콜을 사용하고 있다. 그러나 CAN은 데이터 인증을 제공하지 않는다. 이러한 취약점 때문에 CAN은 메시지 재생공격에 취약하다. 본 논문은 자동차 내부 네트워크에 적용 가능한 현실적인 메시지 인증 기법을 제안한다. CAN 데이터 프레임의 제한적인 공간을 고려하여, 데이터와 메시지 인증 코드 (MAC)를 동시에 전송하기 위해서는 짧은 길이의 MAC을 사용하는 것이 가장 적합하다. 그러나 짧은 길이의 MAC은 암호학적 안전성을 충분히 보장하지 않기 때문에 안전성을 보장하기 위한 추가적인 조치가 필요하다. 본 연구에서 제안한 메시지 인증 기술은 CAN의 제한된 데이터 페이로드를 고려하기 때문에 차량 내부의 안전한 네트워크를 설치하는데 유용하게 활용될 수가 있다.

• Asian Pacific Journal of Cancer Prevention
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• 제13권4호
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• pp.1505-1510
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• 2012

To aim of this was to observe emodin-mediated cytotoxicity and its influence on Rad51 and ERCC1 expressionin non-small cell lung cancer (NSCLC). NSCLC cells were cultured in vitro with emodin at various concentrations (0, 25, 50, 75 and $100\;{\mu}mol/L$) for 48h and the proliferation inhibition rate was determined by the MTT method. Then, NSCLC were treated with emodin (SK-MES-1 $40\;{\mu}mol/L$, A549 $70\;{\mu}mol/L$) or $20\;{\mu}mol/L$ U0126 (an ERK inhibitor) for 48 h, or with various concentrations of emodin for 48 h and the protein and mRNA expressions of ERCC1 and Rad51 were determined by RT-PCR and Western blot assay, respectively. Emodin exerted a suppressive effect on the proliferation of NSCLC in a concentration dependent manner. Protein and mRNA expression of ERCC1 and Rad51 was also significantly decreased with the dose. Vacuolar degeneration was observed in A549 and SK-MES-1 cell lines after emodin treatment by transmission electron microscopy. Emodin may thus inhibited cell proliferation in NSCLC cells by downregulation ERCC1 and Rad51.

• Journal of Chest Surgery
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• 제33권3호
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• pp.268-272
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• 2000

Thoracic sympathicotomy has been used safely and successfully to treat essential hyperhidrosis. However, it has been difficult to treat compansatory hyperhidrosis after thoracic sympathicotomy and focal hyperhidrosis. The sweat glands were innervated by post-ganglionic sympathetic fibers with acetylcholic serving as the transmitter. Botulinum A toxin has been reported to block neuro-transmission at the cholinergic autonomic nerve terminals. Prospecting its effect for the sweat gland, we treated 5 patients with focal hyperhidrosis with botulinum A toxin. Three patients received bilateral thoracic sympathectomy (1 case) and sympathicotomy(2 case) via VAT. The hyperhidrosis area was marked with betadine and was subdivided into squares of 2$\times$2 cm(4$\textrm{cm}^2$) each. Botulinum A toxin was injected intracutaneously in a dosage of 2.5U/0.1ml(100U/4ml) /4$\textrm{cm}^2$. A total dose of 100U of Botulinum A toxin was injected into the affected sites. Subjective assessment of sweat production by the patients using a visual analogue scale showed a 20~70% improvement. During the follow-up period, no toxic effects were observed.

• 한국진공학회:학술대회논문집
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• 한국진공학회 1999년도 제17회 학술발표회 논문개요집
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• pp.192-192
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• 1999

SIMS(Secondary Ion Mass Spectrometry)는 다른 표면 분석장비와 비교하여^g , pp m,^g , pp b 단위의 미량분석이 가능한 장비로서, 특히 depth Profiling을 위한 dynamic SIMS는 Mass Spectrometer의 종류에 따라 Quadrupole SIMS (Q-SIMS)와, Magnetic Sector SIMS (M-SIMS)로 분류된다. 한편, Q-SIMS와 달리 M-SIMS의 경우, Transmission을 높여 주기 위해 Sample Holder에 수 keV의 bias를 걸어 주는데, 이로 인하여 분석 원소에 대한 Sensitivity가 향상되어 지는 반면, RSF의 변화와 같은 분석상의 Artifact가 발생하게 된다. 일반적으로 Q-SIMS의 경우에는 RSF의 RSD(Relative Standard Deviation)가 1%이내에서 보고되고 있지만 M-SIMS에 있어서는 이러한 Deviation이 M-SIMS보다 크게 나타난다. 이 차이는 주로 Sample Holder와 Immersion Lens 사이에 형성되는 Magnetic Field의 왜곡과 Spectrometer의 문제로부터 발생한다. 본 논문에서는 Sample Holder의 종류 및 holder so window 위치에 따라 RSF의 차이를 측정하고 그 data를 RS/1 통계 Package를 이용하여 계량적으로 검증하였으며, 그 차이의 원인과 대책을 제시하고자 한다. 실험에 사용된 Sample은 Si(100) p-type Wafer에 Boron을 이온 주입하여 제작하였다. 이온 주입 장비는 Varian E-500HP이며, 5.0E13 ions/cm2의 dose양을 80keV의 Energy로 각각 7도와 22도의 Tilt와 Twist Angle로 이온 주입을 하였다. SIMS분석에 사용된 Sample Holder는 각각 3 Hole, 9 Hole Type HOlder이며, 분석은 Cameca IMS-6f를 사용하여 B에 대한 Matrix Peak으로 28Si++를 얻었다. 실험 결과 3 Hole Type Sample Holder의 경우 RSF의 RSD는 5.84%, 9Hle Type Sample Holder의 경우는 14.3%로 나타났으나 분석 Window의 위치에 따르는 Grouping을 실시한 결과, 3 Hole Type Sample Holder의 경우 1.2%, 9Hole Type Sample Holder의 경우 9.8%로 RSF의 변화가 감소하였다. 이러한 Deviation은 Sample Holder를 Mount시킬 때 세 개의 Screw를 이용하여 Immersion Lens와의 평형을 잡아주기 때문에 발생하며, 이 Munting을 정확히 해줌으로써 RSF의 변화를 줄일 수 있으나, 실제로 완벽한 Mounting이 불가능하기 때문에 RSF를 일정하게 하기 위해서는 Sample Holder so Window의 취치를 일정하게 설정한 후 분석을 실시해야 한다고 판단된다.

• Asian Pacific Journal of Cancer Prevention
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• 제14권10호
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• pp.5905-5910
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• 2013

Background: To investigate the preventive and therapeutic potential of garlic oil on human pancreatic carcinoma cells. Methods: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay was performed to study the effects of garlic oil on three human pancreatic cancer cell lines, AsPC-1, Mia PaCa-2 and PANC-1. Cell cycle progression and apoptosis were detected by flow cytometry (FCM), staining with PI and annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI), respectively. Morphologic changes of pancreatic cancer cells were observed under transmission electron microscopy (TEM) after treatment with garlic oil at low inhibitory concentrations ($2.5{\mu}M$ and $10{\mu}M$) for 24 hours. Results: Proliferation of the AsPC-1, PANC-1, and Mia PaCa-2 cells was obviously inhibited in the first 24 hours with the MTT assay. The inhibition effect was more significant after 48 hours. When cells were exposed to garlic oil at higher concentrations, an early change of the apoptotic tendency was detected by FCM and TEM. Conclusion: Garlic oil could inhibit the proliferation of AsPC-1, PANC-1, and Mia PaCa-2 cells in this study. Moreover, due to programmed cell death, cell cycle arrest, or both, pro-apoptosis effects on AsPC-1 cells were induced by garlic oil in a dose and time dependent manner in vitro.

• Asian Pacific Journal of Cancer Prevention
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• 제14권2호
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• pp.747-752
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• 2013

Oncostatin M (OSM) is a multifunctional cellular regulator acting on a wide variety of cells, which has potential roles in the regulation of gene activation, cell survival, proliferation and differentiation. Previous studies have shown that OSM can induce morphological and/or functional differentiation and maturation of many tumor cells. However, the action of OSM on the induction of differentiation of human hepatocellular carcinoma (HCC) has not been reported. Here, we investigated the effects of different concentrations of OSM on human HCC cell line SMMC-7721 growth, proliferation, cell cycling, apoptosis and differentiation in vitro. Cell growth was determined via MTT assay, proliferation by cell cycle analysis, apoptosis by flow cytometry, morphology by transmission electronic microscopy, and cell function by detection of biochemical markers. Our results demonstrated that OSM strongly inhibited the growth of SMMC-7721 cells in a dose-dependent manner, associated with decreased clonogenicity. Cell cycle analysis revealed a decreased proportion of cells in S phase, with arrest at G0/G1. The apotosis rate was increased after OSM treatment compared to the control. These changes were associated with striking changes in cellular morphology, toward a more mature hepatic phenotype, accompanied by significant reduction of the expression of AFP and specific activity of ${\gamma}$-GT, with remarkable increase in secretion of albumin and ALP activity. Taken together, our findings indicate that OSM could induce the differentiation and reduce cell viability of SMMC-7721 cells, suggesting that differentiation therapy with OSM offers the opportunity for therapeutic intervention in HCC.

• Journal of Microbiology
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• 제43권2호
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• pp.133-143
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• 2005

Shigellosis is a global human health problem. Four species of Shigella i.e. S. dysenteriae, S. flexneri, S. boydii and S. sonnei are able to cause the disease. These species are subdivided into serotypes on the basis of O-specific polysaccharide of the LPS. Shigella dysenteriae type 1 produces severe disease and may be associated with life-threatening complications. The symptoms of shigellosis include diarrhoea and/or dysentery with frequent mucoid bloody stools, abdominal cramps and tenesmus. Shigella spp. cause dysentery by invading the colonic mucosa. Shigella bacteria multiply within colonic epithelial cells, cause cell death and spread laterally to infect and kill adjacent epithelial cells, causing mucosal ulceration, inflammation and bleeding. Transmission usually occurs via contaminated food and water or through person-to-person contact. Laboratory diagnosis is made by culturing the stool samples using selective/differential agar media. Shigella spp. are highly fragile organism and considerable care must be exercised in collecting faecal specimens, transporting them to the laboratories and in using appropriate media for isolation. Antimicrobial agents are the mainstay of therapy of all cases of shigellosis. Due to the global emergence of drug resistance, the choice of antimicrobial agents for treating shigellosis is limited. Although single dose of norfloxacin and ciprofloxacin has been shown to be effective, they are currently less effective against S. dysenteriae type 1 infection. Newer quinolones, cephalosporin derivatives, and azithromycin are the drug of choice. However, fluoroquinolone-resistant S. dysenteriae type 1 infection have been reported. Currently, no vaccines against Shigella infection exist. Both live and subunit parenteral vaccine candidates are under development. Because immunity to Shigella is serotype-specific, the priority is to develop vaccine against S. dysenteriae type 1 and S. flexneri type 2a. Shigella species are important pathogens responsible for diarrhoeal diseases and dysentery occurring all over the world. The morbidity and mortality due to shigellosis are especially high among children in developing countries. A recent review of literature (KotIoff et al.,1999) concluded that, of the estimated 165 million cases of Shigella diarrhoea that occur annually, $99\%$ occur in developing countries, and in developing countries $69\%$ of episodes occur in children under five years of age. Moreover, of the ca.1.1 million deaths attributed to Shigella infections in developing countries, $60\%$ of deaths occur in the under-five age group. Travellers from developed to developing regions and soldiers serving under field conditions are also at an increased risk to develop shigellosis.