• Proceedings of the Korean Society for Emotion and Sensibility Conference
• /
• 2001.11a
• /
• pp.169-172
• /
• 2001

There are many people who suffer from simulation sickness when immersing in virtual reality. In this study, we analyzed two photoplethysmogram(PPG) parameters - a second derivative parameter and power spectral density ratios - in order to relate PPG parameters with simulation sickness. 36 young, healthy subjects were participated in the experiment, and each subject was equipped with a PPG electrode during his or her immersion. Simulation sickness section was defined as a 7 - second section which starts from the point where a subject reported simulation sickness, and normal section as a same-length section where no physical stimuli was presented to him or her. We compared the PPG parameters of the simulation sickness sections with the normal sections, - d/a ratio is believed to have lower value during vasodilation and higher value during vasoconstriction, however, we could not find much difference in the parameter between normal and simulation sickness sections. We also compared 1 to 10Hz power spectral density ratios in normal sections with in simulation sickness section, and found that 6 density ratios among them have different value. Therefore, the density ratios might be utilized as parameters to detect simulation sickness of subjects.

• Natural Product Sciences
• /
• v.11 no.1
• /
• pp.16-21
• /
• 2005

Nitric Oxide (NO), derived from L-arginine, is produced by two types (constitutive and inducible) of nitric oxide synthase (NOS: cNOS and iNOS). The NO produced in large amounts by the iNOS is known to be responsible for the vasodilation and hypotension observed in septic shock, cancer metastasis and inflammation. The inhibitors of iNOS, thus, may be useful candidates for the treatment of inflammatory diseases accompanied by the overproduction of NO. We prepared alcoholic extracts of herbal drugs which have been used for the treatment of inflammation in oriental medicine. We have screened the inhibitory activity of NO production in lipopolysaccharide (LPS)-activated macrophages after the treatment of these extracts. Among 82 kinds of extracts of herbal drugs, 35 extracts showed the potent inhibitory activity of NO production above 50% at the concentration of $50\;{\mu}g/mL$. The inhibitory activities of NO production were also evaluated for several solvent fractions at two different concentrations. Especially, hexane and EtOAc fractions of Alpinia officinarum, Angelica gigas, Ostericum koreanum, Saussurea lappa, Torilis japonica, and hexane fractions of Agrimonia pilosa, Machilus thunbergii, Hydrangea serrata, Magnolia obovata, Prunella vulgaris, Tussilago farfara, and EtOAC fractions of Perilla frutescence showed a significant activity at 10 and/or $25\;{\mu}g/mL$. In Western blot analysis, the hexane fractions ($5\;{\mu}g/mL$) of Magnolia obovata and Saussurea lappa, and EtOAc fractions ($20\;{\mu}g/mL$) of Hydrangea Serrata, Perilla frutescence and Torilis japonica inhibited the expression of iNOS protein in LPS-activated macrophages. These plants may be promising candidates for the study of the activity-guided purification of active compounds and might be useful for the treatment of inflammatory diseases and endotoxemia accompanying overproduction of NO.

• Restorative Dentistry and Endodontics
• /
• v.41 no.3
• /
• pp.202-209
• /
• 2016

Objectives: The purpose of this study was to investigate the involvement of TRPA1 in the cinnamaldehyde-induced pulpal blood flow (PBF) change in the feline dental pulp. Materials and Methods: Mandibles of eight cats were immobilized and PBF was monitored with a laser Doppler flowmetry at the mandibular canine tooth. To evaluate the effect of cinnamaldehyde on PBF, cinnamaldehyde was injected into the pulp through the lingual artery at a constant rate for 60 seconds. As a control, a mixture of 70% ethanol and 30% dimethyl sulfoxide (DMSO, vehicle) was used. To evaluate the involvement of transient receptor potential ankyrin 1 (TRPA1) in PBF change, AP18, a specific TRPA1 antagonist, was applied into the pulp through the Class V dentinal cavity followed by cinnamaldehyde-administration 3 minutes later. The paired variables of experimental data were statistically analyzed using paired t-test. A p value of less than 0.05 was considered as statistically significant. Results: Administration of cinnamaldehyde (0.5 mg/kg, intra-arterial [i.a.]) induced significant increases in PBF (p < 0.05). While administration of a TRPA1 antagonist, AP18 (2.5 - 3.0 mM, into the dentinal cavity [i.c.]) caused insignificant change of PBF (p > 0.05), administration of cinnamaldehyde (0.5 mg/kg, i.a.) following the application of AP18 (2.5 - 3.0 mM, i.c.) resulted in an attenuation of PBF increase from the control level (p < 0.05). As a result, a TRPA1 antagonist, AP18 effectively inhibited the vasodilative effect of cinnamaldehyde (p < 0.05). Conclusions: The result of the present study provided a functional evidence that TRPA1 is involved in the mechanism of cinnamaldehyde-induced vasodilation in the feline dental pulp.

• Imaging Science in Dentistry
• /
• v.49 no.4
• /
• pp.301-306
• /
• 2019

Purpose: This report presents a procedure for performing power Doppler ultrasound-guided sialography using the phenomenon of increased blood flow and illustrates its application to practical patient cases. Materials and Methods: The salivary gland was scanned using ultrasound equipment (GE LOGIQ5 Expert^® device; GE Medical Systems, Milwaukee, WI, USA) to identify pathological findings related to the patient's chief complaint. To identify the orifice of the main duct, it should be cannulated using a lacrimal dilator. After inserting the catheter into the cannulated main duct, the position of the catheter within the duct was confirmed by ultrasound. A contrast agent was injected until the patient felt fullness, and ultrasound (B-mode) was used to confirm whether the contrast agent filled the main canal and secondary and tertiary ducts. Then, power Doppler ultrasound was performed to determine whether the salivary gland had increased blood flow. Results: In 2 cases in this report, a power Doppler ultrasound scan showed a significant increase in blood flow after contrast medium injection, which was not observed on a preoperative scan. Conclusion: Power Doppler ultrasound was found to be a simple, safe, and effective tool for real-time sialography monitoring.

• International Journal of Vascular Biomedical Engineering
• /
• v.3 no.2
• /
• pp.1-9
• /
• 2005

Flow-induced dilation of blood vessel is the result of a series of bioreaction in vascular endothelial cells(VEC). Shear stress change by blood flow in human artery or vein is sensed by the mechanoreceptor and responsible for such a chain reaction. The inositol(1,4,5)-triphophate($IP_3$) is produced in the first stage to elevate permeability of the intercellular membrane to calcium ions by which the cytosolic calcium concentration is consequently increased. This intracellular calcium transient triggers synthesis of EDRF and prostacyclin. The mathematical model of this VEC calcium dynamics is reproduced from the literature. We then use the Computational Fluid Dynamics(CFD) technique to investigate the blood stream dictating the VEC calcium dynamics. The pulsatile blood flow in a stenosed blood vessel is considered here as a part of study on thrombogenesis. We calculate the pulsating shear stress (thus its temporal change) distributed over the stenosed artery that is implemented to the VEC calcium dynamics model. It has been found that the pulsatile shear stress induces larger intracellular $Ca^{2+}$ transient plus much higher amount of EDRF and prostacyclin release in comparison with the steady shear stress case. It is concluded that pulsatility of the physiological shear stress is important to keep the vasodilation function in the stenosed part of the blood vessel.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
• /
• v.30 no.6
• /
• pp.488-496
• /
• 2004

Oral & Maxillofacial surgery can lead to complications that result in abnormal sensation or movement. Inferior alveolar nerve(IAN) injury can result in dysesthesia, paresthsia of the lower lip and chin, so patients presenting with IAN damage suffer from sensory loss. But diagnosis of the nerve injury is largely limited to the subjective statements made by the patient. Distribution of sympathetic nerves parallels the distribution of the somatosensory nerves. Loss of sensory tone causes a concomitant loss of sympathetic activity, resulting in vasodilation of the cutaneous blood vessels that demonstrates greater heat loss. Digital infrared thermographic imaging(DITI) detects infra-red radiation given off by body. DITI can detect minute difference in temperature from different parts of the body and translates the amount of heat into quantitative data. The area of different temperature correlated with pain or disease can be visualized by corresponding color. The objective of this study was to determine the efficacy of DITI in objectively assessing IAN injury. The 19 normal subjects and the 14 patients underwent DITI scan. The normal subjects received unilateral IAN block anesthesia with 2 ml of 2% lidocaine (IAN bolck group) to evaluate temporary alteration in nerve function. Patient group were patients with unilateral IAN damage (dysesthesia or paresthesia) after surgical treatment(Mn. 3rd molar Extraction, etc.). The surgical procedure performed within 6 months of test. The results were as follows. 1. No significant differences in temperature were found between left and right sides of the lower lip and chin in the control group. 2. Significant temperature differences were found between the anesthetized and non-anesthetized sides of the lower lip and chin in the IAN block group. 3. Significant temperature differences were found between the involved and uninvolved sides of the lower lip and chin areas of the experimental group. The results of the study show that DITI can be an useful and effective means of objectively assessing and visualizing IAN damage.

• Nutritional Sciences
• /
• v.6 no.1
• /
• pp.25-30
• /
• 2003

The effects of soy-isoflavones, which are phytoestrogens derived from plants with a flavonoid structure, on cyclooxygenase -2 (COX-2) expression, PGE2 production, and mapkinases expression, were investigated in experimentally-induced atherogenic rats by feeding a high fat-high cholesterol diet. Female Sprague-Dawley rats were bilaterally ovariectomized; sham-operated animals were used as controls. Three weeks later, the animals were randomized to the following treatments for an eight-week experimental period: 17$\beta$-estradiol (200$\mu$ g/kg diet), low concentration of isoflavones (0.8g/kg diet), and high concentration of isoflavones (4.0g/kg diet). In the group supplemented with a high dose of isoflavones, COX-2 expression was down-regulated. This down-regulation was accompanied by a reduced expression of pERK1/2. In the second experiment using 48-week old female Sprague-Dawly rats, the effects of isoflavones and estrogen were compared in the basal estrogen-supplementation at the level of 600$\mu$ g/kg diet. Isoflavones induced the marked down-regulation of COX-2 protein and the decrease in $PGE_2$ production in estrogen supplemented states and this was followed by the down-regulation of p38 among mapkinases. The two different mapkinases are involved in the down-regulation of COX-2 depending on estrogen-deficient and estrogen supplemented states. This kind of COX-2 down-regulation by isoflavones was not observed in the different tissue, mammary glands. Further investigations on the relationship between COX-2 and biological activities such as vasodilation by isoflavonesin the absence or the presence of estrogen ave required in vivo system of female rats.

• Korean Journal of Pharmacognosy
• /
• v.37 no.2 s.145
• /
• pp.67-73
• /
• 2006

The butanol extracts of Agrimonia pilosa (BAP) induced dose-dependent vascular relaxation of phenylephrine-precontracted aorta, which was abolished by removal of functional endothelium. Pretreatment of the endothelium-intact aortic tissues with $N^G$-nitro-L-arginine methyl ester (L-NAME) and 1H-[1,2,4]-oxadiazole-[$4,3-{\alpha}$]-quinoxalin-1-one(ODQ) inhibited the relaxation induced by BAP. BAP-induced vascular relaxation was also markedly attenuated by addition of verapamiI, while the relaxant effect of BAP was not blocked by indomethacine, glibenclamide, tetraethylammonium (TEA), atropine, or propranolo. In addition, incubation of endothelium-intact aortic rings with BAP increased the vascular production of cGMP. These results suggest that BAP relaxes vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling pathway, which may be causally related with L-type $Ca^{2+}$ channels.

• Journal of Chest Surgery
• /
• v.28 no.8
• /
• pp.742-746
• /
• 1995

The present study was aimed at investigating possible transmitter mechanisms in the endothelial cell layer in regulating the tone of the vascular smooth muscle. The thoracic aorta was isolated from the anesthetized male white rabbits and its helical strips were prepared. Electrical field stimulation was delivered to platinum wire electrodes positioned parallel to the vessel segment preconstricted with phenylephrine [3.5x10-6 mol/L at a distance of 1.5-2.0 mm. The electrical stimulation [70 V, 5 msec, 0.5-200 Hz caused either relaxation only [34% or a biphasic response [prolonged relaxation following a weak and transient contraction, 66% . The relaxation response was frequency- dependent, and at 200 Hz a complete relaxation was noted. Mechanical rubbing of the endothelial layer abolished or greatly attenuated the relaxation. The relaxation was also markedly attenuated in the presence of NG-nitro- L-arginine methyl ester [10-3mol/L or procaine hydrochloride [3.5x10-4mol/L . Tetrodotoxin,guanethidine, atropine or indomethacin failed to block or enhance the relaxation response to electrical field stimulation. It is concluded that the vascular endothelium in the aorta contains diffusible substances that regulates the function of the smooth muscle layer, in which relaxation is more prominent than contraction. Their release by the electrical stimualtion in vitro may not involve classic neuronal transmitter release mechanisms or metabolism of arachidonic acids by cyclooxygenase. The release of the relaxing agents may require an increase in cytosolic calcium level. The chemical nature of the relaxant may be, to a large extent, nitric oxide.

• Journal of Chest Surgery
• /
• v.46 no.1
• /
• pp.14-21
• /
• 2013

Background: Reactive oxygen species (ROS) are known to be related to cardiovascular diseases. Many studies have demonstrated that angiotensin-converting enzyme inhibitors have beneficial effects against ROS. We investigated the antioxidant effect of captopril and enalapril in nitric oxide mediated vascular endothelium-dependent relaxations. Materials and Methods: Isolated rabbit abdominal aorta ring segments were exposed to ROS by electrolysis of the organ bath medium (Krebs-Henseleit solution) after pretreatment with various concentrations (range, $10^{-5}$ to $3{\times}10^{-4}$ M) of captopril and enalapril. Before and after electrolysis, the endothelial function was measured by preconstricting the vessels with norepinephrine ($10^{-6}$ M) followed by the cumulative addition of acetylcholine (range, $3{\times}10^{-8}$ to $10^{-6}$ M). The relevance of the superoxide anion and hydrogen peroxide scavenging effect of captopril and enalapril was investigated using additional pretreatments of diethyldithiocarbamate (DETCA, 0.5 mM), an inhibitor of Cu/Zn superoxide dismutase, and 3-amino-1,2,4-triazole (3AT, 50 mM), an inhibitor of catalase. Results: Both captopril and enalapril preserved vascular endothelium-dependent relaxation after exposure to ROS in a dose-dependent manner (p<0.0001). Pretreatment with DETCA attenuated the antioxidant effect of captopril and enalapril (p<0.0001), but pretreatment with 3AT did not have an effect. Conclusion: Both captopril and enalapril protect endothelium against ROS in a dose-dependent fashion in isolated rabbit abdominal aortas. This protective effect is related to superoxide anion scavenging.