In the present study, we observed change in intracellular $Ca^{2+}$$([Ca^{2+}]_i)$ as measured with the fluorescent $Ca^{2+}-indicator$ fura-2 in association with force development of the rat basilar arteries during activation by$K^+$ depolarizing solution and U46619, a thromboxane analogue, in the absence and the presence of calcitonin-gent related peptide (CGRP). CGRP (30 and 100 nM) caused a concentration-dependent inhibition of U46619-induced contraction with decrease in $[Ca^{2+}]_i$, whereas it did not exert any effect on the $K^+$ (90 mM)-induced contraction and increase in $[Ca^{2+}]_i$, Further, $[Ca^{2+}]_i-force$ relationships were determined by plotting the ratio of $F_{340}/F_{380}$$([Ca^{2+}]_i)$ as a function of the force induced by U46619, and the results were compared with those obtained in the presence of CGRP. The curves obtained in the presence of CGRP (30 and 100 nM) were significantly moved to downward without right shift of the curves suggesting that CGRP inhibited the U46619-induced contraction only by mediation of reduction in $[Ca^{2+}]_i$ with out any change in the sensitivity of contractile apparatus to $Ca^{2+}$. The CGRP-induced attenuation of $[Ca^{2+}]_i$ and force development was significantly inhibited under pretreatment with CGRP $(8{\sim}37)$ fragment (100 nM), a CGRP1 receptor antagonist. Both the reduced contraction and reduction in $[Ca^{2+}]_i$ caused by CGRP were fully reversed by pretreatment with charybdotoxin (100 nM) and iberiotoxin (100 nM), large conductance $Ca^{2+}-activated$$K^+$ channel blockers, but not by apamin (300 nM), a small conductance $Ca^{2+}-activated$$K^+$ channel blocker, and glibenclamide ( 1 ${\mu}M$), an ATP-sensitive $K^+$ channel blocker. In conclusion, it is suggested that the CGRP1 receptor, upon activation by CGRP, are coupled to opening of $Ca^{2+}-activated$$K^+$ channel and cause to decrease in $[Ca^{2+}]_i$, thereby leading to vasodilation of the rat basilar artery. However, it is not defined that the mechanism underlying vasodilation whether the $K^+$ channel blockers, charybdotoxin and iberiotoxin directly block the CGRP receptors and that CGRP-evoked relaxation is dependent on the cyclic AMP or $K^+$ channel opening or both actions.
In order to achieve efficiency of laying eggs of silkworms, it is very important to eliminate noncocooning silkworms. This study is written on the basis of observation and analysis of mechanism of silkworms physiologically and anatomically. It is hoped that given herein will contribute to the effecting elimination work. Outline of the study summarize as follows: 1. It is observed through microscope that the silkworms which are seen normal state in the silk gland but no ability of cocoon making have polyhedrosis in the nerve, trachea and muscle near the tissue of the spinneret. 2. Relatively high proportion of non-cocooning silkworms are caused by the grasserie of the silkworms. 3. As a result of inoculation with purulent discharges against silkworms from first fooding through 8th day of 5th instar, number of cocooning silkworms were increased when inoculation are applied at laterer day of the instar. In the case of non-cocooning silkworms, meanwhile, resulted not big varriation when it is apllied in the early and middle of the period, but number of non-cocooning silkworm was reduced when the inoculation are given at laterer of the instar. Number of death during rearing and mounting are increased when earliest application of inoculation are carried out. 4. Symptom of grasserie was appeared more or less three days after application of the inoculation. Some silkworms which were inoculated just before mounting has ability of cocooning making even taken grasserie, in this case the silkworm can make thin cocoon. since the silkworm fall sick during cocoon making and unable of spinning soon. when the worm was affected by grasserie slightly, it was observed that the silkworm can spinning. It is supposed to be the light paralysis of spinneret is not very much influenced to spinning. 5. As a result of observation of original stock and hybrid including other 44 kinds of silkworm, many non-cocooning silkworms were found in the original stock especially originated from japanese than in hybrid. 6. A number of undulations are found in the middle division of the silk gland of non-cocooning silkworms. 7. According to the observation of the sizes of the body and digestive organs, normal natured silkworms and non-cocooning silkworms are more or less same in length, but the width, circumference of bodies and digestive organs were more larger in the later. If silkworm which was in the period of active eating of 5th instar was given shock of dropping to the floor, the silkworm receives little more shock when hit to side of the body than to head, and concrete floor than ondol and wooden floor.
Park, Dong-Bum;Seo, Jeong-Taeg;Sohn, Heung-Kyu;Lee, Jong-Gap
Journal of the korean academy of Pediatric Dentistry
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v.25
no.2
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pp.352-367
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1998
Intracellular pH (pHi) plays an important role in the regulation of cellular processes by influencing the acitivity of various enzymes in cells. Therefore, almost every type of mammalian cell possesses an ability to regulate its pHi. One of the most prominent mechanisms in the regulation of pHi is $Na^+/H^+$ exchanger. This exchanger has been known to be activated when cells are stimulated by the binding of agonist to the muscarinic receptors. Therefore, the aims of this study were to compare the rates of $H^+$ extrusion through $Na^+/H^+$ exchanger before and during muscarinic stimulation and to investigate the possible existence of $HCO_3^-$ transporter which is responsible for the continuous supply of $HCO_3^-$ ion to saliva. Acinar cells were isolated from the rat mandibular salivary glands and loaded with pH-sensitive fluoroprobe, 2', 7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein(BCECF), for 30min at room temperature. Cells were attached onto the coverglass in the perfusion chamber and the changes in pHi were measured on the iverted microscope using spectrofluorometer. 1. By switching the perfusate from $HCO_3^-$-free to $HCO_3^-$-buffered solution, pHi decreased by $0.39{\pm}0.02$ pH units followed by a slow increase at an initial rate of $0.04{\pm}0.007$ pH units/min. The rate of pHi increase was reduced to $0.01{\pm}0.002$ pH units/min by the simultaneous addition of 1 mM amiloride and $100{\mu}M$ DIDS. 2. An addition and removal of $NH_4^+$ caused a decrease in pHi which was followed by an increase in pHi. The increase of pHi was almost completely blocked by 1mM amiloride in $HCO_3^-$-free perfusate which implied that the pHi increase was entired dependent on the activation of $Na^+/H^+$ exchanger in $HCO_3^-$-free condition. 3. An addition of $10{\mu}M$ carbachol increased the initial rate of pHi recovery from $0.16{\pm}0.01$ pH units/min to $0.28{\pm}0.03pH$ units/min. 4. The initial rate of pHi decrease induced by 1mM amiloride was also increased by the exposure of the acinar cells to $10{\mu}M$ carbachol ($0.06{\pm}0.008pH$ unit/min) compared with that obtained before carbachol stimulation ($0.03{\pm}0.004pH$ unit/min). 5. The intracellular buffering capacity ${\beta}1$ was $14.31{\pm}1.82$ at pHi 7.2-7.4 and ${\beta}1$ increased as pHi decreased. 6. The rate of $H^+$ extrusion through $Na^+/H^+$ exchanger was greatly enhanced by the stimulation of the cells with $10{\mu}M$ carbachol and there was an alkaline shift in the activity of the exchanger. 7. An intrusion mechanism of $HCO_3^-$ was identified in rat mandibular salivary acinar cells. Taken all together, I observed 3-fold increase in $Na^+/H^+$ exchanger by the stimulation of the acinar cells with $10{\mu}M$ carbachol at pH 7.25. In addition, I have found an additional mechanism for the regulation of pHi which transported $HCO_3^-$ into the cells.
The spectra of the $Co^{II}CyDTA$(CyDTA: cyclohexyldiaminetetraacetic acid) complex have been measured in aqueous solution of pH = 6-13.2. The red shift of the spectrum in the more basic solution was ascribed to the transformation of $CoCyDTA^{2-}$ into $CoCyDTA(OH)^{3-}$. The equilibrium constant, $K_{OH} = [CoCyDTA(OH)^{3-}]/[CoCyDTA^{2-}][OH^-]$ was $75M^{-1}$ at $40^{\circ}C$. The electron transfer reactions of $CoCyDTA^{2-}$ and $CoCyDTA(OH)^{3-}$ with $Fe(CN)_6^{3-}$ have been studied using spectrophotometric technique in the range of pH applied to the determination of equilibrium constant. The pseudo first-order rate constants observed ($k_{obs}$) were not changed upto pH = 10.8, but increased with increasing pH in the range of pH = $10.8{\sim}13.0$. The rate law reduced in the range of pH = 6-13 was $k_{obs} = (k_3[CoCyDTA^{2-}] + k_4[CoCyDTA(OH)^{3-}])/(1+K_1[CoCyDTA^{2-}])$. The rate constants of the reactions (3a) and (3b), $k_3$ and $k_4$ respectively have been determined to be 0.529 and $4.500M^{-1}sec^{-1}$ at $40^{\circ}C$. The activation entropies (147{\pm}1.1JK^{-1} mol^{-1}$ at pH = 10.8) and activation volumes $(6.25cm^3mol^{-1}, pH = 10.8)$ increased with increasing pH, while the activation enthalpy (12.44 ${\pm}$ 0.20 kcal/mole) was independent of pH. Using the pH effect on the rate constants, the activation entropies and the activation volumes, the mechanism of the electron transfer reaction for $Co^{II}-Fe^{III}$ system was discussed.
Youn Seon Min;Oh Young Kee;Kim Joo Heon;Park Mi Ja;Seong In Ock;Kang Kimun;Chai Gyuyong
Radiation Oncology Journal
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v.23
no.1
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pp.51-60
/
2005
Purpose : Selective inhibition of multiple molecular targets may improve the antitumor activity of radiation. Two specific inhibitors of selective cyclooxygenase-2 (COX-2) and epidermal growth factor receptor (EGFR) were combined with radiation on the HeLa cell line. To investigate cooperative mechanism with selective COX-2 inhibitor and EGFR blocker, in vitro experiments were done. Materials and Methods : Antitumor effect was obtained by growth inhibition and apoptosis analysis by annexin V-Flous method. Radiation modulation effects were determined by the clonogenic cell survival assay. Surviving fractions at 2 Gy ($SF_2$) and dose enhancement ratio at a surviving fraction of 0.25 were evaluated. To investigate the mechanism of the modulation of radiosensitivity, the cell cycle analyses were done by flow cytometry. The bcl-2 and bax expressions were analyzed by western blot. Results : A cooperative effect were observed on the apoptosis of the HeLa ceil line when combination of the two drugs, AG 1478 and NS 398 with radiation at the lowest doses, apoptosis of $22.70\%$ compare with combination of the one drug with radiation, apoptosis of $8.49\%$. In cell cycle analysis, accumulation of cell on $G_0/G_l$ phase and decrement of S phase fraction was observed from 24 hours to 72 hours after treatment with radiation, AG 1478 and NS 398. The combination of NS 398 and AG 1478 enhanced radiosensitivity on a concentration-dependent manner in HeLa cells with dose enhancement ratios of 3.00 and $SF_2$ of 0.12 but the combination of one drug with radiation was not enhanced radlosensitivity with dose enhancement ratios of 1.12 and SF2 of 0.68 (p=0.005). The expression levels of bcl-2 and bax were reduced when combined with AG 1478 and NS 398. Conclusion : Our results indicate that the selective COX-2 inhibitor and EGFR blocker combined with radiation have potential additive or cooperative effects on radiation treatment and may act through various mechanisms including direct inhibition of tumor cell proliferation, suppression of tumor cell cycle progression and inhibition of anti-apoptotic proteins.
Filefish muscle in the form of thin plate $(5{\times}10{\times}0.4\;cm)$ was dried in a forced air dryer at $47.5^{\circ}C$ to study the relation between dehydration mechanism and water activity. The dryer was designed in such a way that the temperature, relative humidity and velocity of air could be controlled. The whole dehydration process of the filefish muscle was divided into two different drying rate periods, constant and falling rate period. During the constant drying rate period, the drying rate was proportional to the square root of air velocity under the conditions of constant temperature and relative humidity of air. The falling rate period was further divided into two different falling drying rate periods, first and second falling rate period. The first falling rate period was an unsaturated surface drying period caused by partial unsaturation of the drying surface with capillary condensed free water diffused from the internal part of the filefish muscle. At this stage he drying rate was mainly dependent on the relative humidity at constant air temperature, and case-hardening phenomenon started at the end of this stage. The moisture content and the water activity at which the second falling rate period started were not constant, because the drying rate of the first falling rate period was strongly dependent on the air humidity. The second falling rate period was again divided into two drying rate periods, former and latter period. The drying rates of both of these periods were independent on the external air humidity. During the former period of the second falling rate period, the dehydration was proceeded by diffusion and vaporization of capillary condensed free water in filefish muscle. The diffusion coefficient of water was $2.89{\times}10^{-10}m^2/sec\;at\;47.5^{\circ}C$. At this stage, the case-herdening continued until the water activity reduced to 0.7. The latter period of the second falling rate period started at the water activity of 0.45. The dedydration was proceeded by diffusion and vaporization of bound water, which adsorbed in multimolecular layers, through the hardened drying surface. The number of molecular layers was 4, and the diffusion coefficient of water during this stage was $4.38{\times}10^{-11}m^2/sec\;at\;47.5^{\circ}C$.
Park, J.E.;Ryu, G.H.;Lee, I.Y.;Lee, H.K.;Shin, H.S.;Lee, J.O.;Kim, K.U.
Korean Journal of Weed Science
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v.14
no.2
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pp.94-100
/
1994
This experiment was conducted to determine selective mechanism of cyhalofop-butyl ester ((((R-butyl 2-(4-(4-cyano-2-fluorophenoxy) phenoxy) propionate)) between rice and Echinochloa crus-galli. 100ppm of cyhalofop-butyl ester inhibited over 90% of seedling growth of E. crus-galli when applied at 3 leaf stage and complete inhibition was observed at 180ppm applied at the 4 leaf stage, but rice(Chucheongbyeo) was not inhibited by cyhalofop-butyl ester even at 230ppm, regardless of its growth stages(3, 4, 5 and 6 leaf stages). Cyhalofop-butyl ester applied through stem at 10 and 50ppm moved most rapidly to the meristem and resulted in the highest injury on plant height, root length and fresh weight of E. crus-galli. compared with root or leaf application. Seedlings of rice and E. crus-galli at 3 or 4 leaf stage were dipped in 180ppm of cyhalofop-butyl ester solution for 1 minute and aboveground parts of E. crus-galli and rice were removed immediataly after dipping treatment. Regrowth of E. crus-galli was inhibited by the herbicide by 41.7%, but no inhibition was observed in rice. Further, content of chlorophyll reduced to 18.7% of the untreated control, showing appearence of almost being killed, but no effect on chlorophyll content of rice was observed.
Proceedings of the Korean Institute of Intelligent Systems Conference
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1993.06a
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pp.975-976
/
1993
This talk presents the overview of the author's research and development activities on fuzzy inference hardware. We involved it with two distinct approaches. The first approach is to use application specific integrated circuits (ASIC) technology. The fuzzy inference method is directly implemented in silicon. The second approach, which is in its preliminary stage, is to use more conventional microprocessor architecture. Here, we use a quantitative technique used by designer of reduced instruction set computer (RISC) to modify an architecture of a microprocessor. In the ASIC approach, we implemented the most widely used fuzzy inference mechanism directly on silicon. The mechanism is beaded on a max-min compositional rule of inference, and Mandami's method of fuzzy implication. The two VLSI fuzzy inference chips are designed, fabricated, and fully tested. Both used a full-custom CMOS technology. The second and more claborate chip was designed at the University of North Carolina(U C) in cooperation with MCNC. Both VLSI chips had muliple datapaths for rule digital fuzzy inference chips had multiple datapaths for rule evaluation, and they executed multiple fuzzy if-then rules in parallel. The AT & T chip is the first digital fuzzy inference chip in the world. It ran with a 20 MHz clock cycle and achieved an approximately 80.000 Fuzzy Logical inferences Per Second (FLIPS). It stored and executed 16 fuzzy if-then rules. Since it was designed as a proof of concept prototype chip, it had minimal amount of peripheral logic for system integration. UNC/MCNC chip consists of 688,131 transistors of which 476,160 are used for RAM memory. It ran with a 10 MHz clock cycle. The chip has a 3-staged pipeline and initiates a computation of new inference every 64 cycle. This chip achieved an approximately 160,000 FLIPS. The new architecture have the following important improvements from the AT & T chip: Programmable rule set memory (RAM). On-chip fuzzification operation by a table lookup method. On-chip defuzzification operation by a centroid method. Reconfigurable architecture for processing two rule formats. RAM/datapath redundancy for higher yield It can store and execute 51 if-then rule of the following format: IF A and B and C and D Then Do E, and Then Do F. With this format, the chip takes four inputs and produces two outputs. By software reconfiguration, it can store and execute 102 if-then rules of the following simpler format using the same datapath: IF A and B Then Do E. With this format the chip takes two inputs and produces one outputs. We have built two VME-bus board systems based on this chip for Oak Ridge National Laboratory (ORNL). The board is now installed in a robot at ORNL. Researchers uses this board for experiment in autonomous robot navigation. The Fuzzy Logic system board places the Fuzzy chip into a VMEbus environment. High level C language functions hide the operational details of the board from the applications programme . The programmer treats rule memories and fuzzification function memories as local structures passed as parameters to the C functions. ASIC fuzzy inference hardware is extremely fast, but they are limited in generality. Many aspects of the design are limited or fixed. We have proposed to designing a are limited or fixed. We have proposed to designing a fuzzy information processor as an application specific processor using a quantitative approach. The quantitative approach was developed by RISC designers. In effect, we are interested in evaluating the effectiveness of a specialized RISC processor for fuzzy information processing. As the first step, we measured the possible speed-up of a fuzzy inference program based on if-then rules by an introduction of specialized instructions, i.e., min and max instructions. The minimum and maximum operations are heavily used in fuzzy logic applications as fuzzy intersection and union. We performed measurements using a MIPS R3000 as a base micropro essor. The initial result is encouraging. We can achieve as high as a 2.5 increase in inference speed if the R3000 had min and max instructions. Also, they are useful for speeding up other fuzzy operations such as bounded product and bounded sum. The embedded processor's main task is to control some device or process. It usually runs a single or a embedded processer to create an embedded processor for fuzzy control is very effective. Table I shows the measured speed of the inference by a MIPS R3000 microprocessor, a fictitious MIPS R3000 microprocessor with min and max instructions, and a UNC/MCNC ASIC fuzzy inference chip. The software that used on microprocessors is a simulator of the ASIC chip. The first row is the computation time in seconds of 6000 inferences using 51 rules where each fuzzy set is represented by an array of 64 elements. The second row is the time required to perform a single inference. The last row is the fuzzy logical inferences per second (FLIPS) measured for ach device. There is a large gap in run time between the ASIC and software approaches even if we resort to a specialized fuzzy microprocessor. As for design time and cost, these two approaches represent two extremes. An ASIC approach is extremely expensive. It is, therefore, an important research topic to design a specialized computing architecture for fuzzy applications that falls between these two extremes both in run time and design time/cost. TABLEI INFERENCE TIME BY 51 RULES {{{{Time }}{{MIPS R3000 }}{{ASIC }}{{Regular }}{{With min/mix }}{{6000 inference 1 inference FLIPS }}{{125s 20.8ms 48 }}{{49s 8.2ms 122 }}{{0.0038s 6.4㎲ 156,250 }} }}
Vascular smooth muscle cell (VSMC) apoptosis has been identified in various vascular diseases, including atherosclerosis and restenosis after angioplasty, and has been known to precipitate atherosclerotic plaque instability and rupture. Oxysterols are known as inducers of apoptosis in VSMC, and 7-ketocholesterol (7KC) is the major nonenzymically formed oxysterol in atherosclerotic lesions. The precise mechanism underlying VSMC apoptosis is still poorly understood. In this study, we investigated whether 7KC causes apoptosis, and characterized its apoptotic mechanisms in primary cultured rat aortic VSMC. Cell viability was assessed by MTT assay and trypan blue assay. Apoptosis was assessed by flow cytometry, immunofluorescence, immunoprecipitation, and Western blot analyses. 7KC markedly decreased the VSMC viability in a time- and concentration-dependent manner, and increased the production of 4-hydroxynonenal (HNE), a major end-product of lipid peroxidation, which also decreased the VSMC viability. Pretreatment with 2,4-dinitrophenylhydrazine, a well-known reagent of lipid peroxidation-derived aldehydes, significantly restored the 7KC-decreased viability of VSMC. Furthermore, HNE, as well as 7KC, reduced the level of total Akt, a major mediator of cell survival. The 7KC-decreased level of total Akt was significantly restored by pretreatments with 2,4-dinitrophenylhydrazine and N-acetylcysteine. Lactacystin, a proteasome inhibitor, protected VSMC against apoptosis and Akt degradation, but did not inhibit HNE production. In the immunoprecipitation assay, 7KC increased HNE-modified Akt. From the results, it seems that, in atherosclerotic lesions, 7KC induces HNE production in VSMC, and this HNE binds to Akt, proceeding to proteasomal degradation of Akt, through which mechanism the atherosclerotic plaque instability may be facilitated.
Lee, Min Ho;Kim, Jeongyong;Cho, Yoonjung;Kim, Do Hyun;Yang, Ji Yeong;Kwon, Hye Jin;Park, Min;Woo, Hyun Jun;Kim, Sa-Hyun;Kim, Jong-Bae
Korean Journal of Clinical Laboratory Science
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v.51
no.1
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pp.71-77
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2019
Menadione is known as an anti-tumor factor. Many studies have reported the potential anti-cancer role of menadione against a range of cancer cell lines. In this study, the anti-cancer effects of menadione and the underlying molecular signaling involved in apoptosis was investigated in gastric cancer cell lines. The menadione treatment decreased the cell viability of MKN45 gastric cancer cells. The decreased cell viability was attributed to the induction of apoptosis, which was confirmed by the results indicating the activation of caspase-3 and -7 and the cleavage of PARP in Western blotting. The upstream regulatory molecules involved in apoptosis were investigated further and it was discovered that menadione reduced the expression of survivin, an inhibitor of upstream apoptosis proteins. In addition, a transcription factor ${\beta}$-catenin, which is known to regulate survivin expression, was down-regulated by menadione. A previous report showed that menadione inhibited XIAP expression to induce apoptosis and induced G2/M cell cycle arrest in AGS cells. This study elucidated another inhibitory mechanism of menadione against gastric cancer cells in a different cell line. Although further studies will be needed, the inhibitory mechanism demonstrated in this study will help better understand the anti-cancer effects of menadione.
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