• The Journal of Korean Physical Therapy
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• v.20 no.3
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• pp.61-68
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• 2008

Purpose: Protein kinase C (PKC) is a member of a family of serine/threonine kinases that are activated by diacylglycerol (DG) and PKC stimulants. PKC play a key role in signal transduction, including muscle contraction, cell migration, apoptosis, cell proliferation and differentiation. However, the mechanism relating mitogen-activated protein kinases (MAPKs) and PKC, especially in the volume-dependent hypertensive state, remains unclear. Methods: In the present study, I investigated the relationship between PKC and MAPKs for isometric contraction, PKC translocation, and enzymatic activity from normotensive sham-operated rats (NSR) and aldosterone-analogue deoxycorticosterone acetate (DOCA) hypertensive rats (ADHR). Results: Systolic blood pressure was significantly increased in ADHR than in NSR. Physiological salt solution (PSS)-induced resting tension and the intracellular $Ca^{2+}$ concentration ([$Ca^{2+}{_i}$]) were different in the ADHR and NSR. The expression of PKC$\alpha$, PKC$\beta$II, PKC$\delta$, PKC$\varepsilon$ and PKC$\xi$ were different between the cytoplasmic and membranous fractions. However, expression of the PKC isoforms did not differ for the ADHR and NSR. The use of 12-deoxyphorbol 13-isobutyrate (DPB, a PKC stimulant) induced isometric contraction in $Ca^{2+}$-free medium, which was diminished in muscle strips from ADHR as compared to NSR. Increased vasoconstriction and phosphorylation induced by the use of 1 ${\mu}$M DPB were inhibited by treatment with 10 ${\mu}$M PD098059 and 10 ${\mu}$M SB203580, inhibitors of extracellular-regulated protein kinase 1/2 (ERK1/2) and p38 MAPK from ADHR, respectively. Conclusion: These results suggest that the development of aldosterone analogue-induced hypertension is associated with an altered blood pressure, resting tension, [$Ca^{2+}{_i}$], and that the $Ca^{2+}$-independent contraction evoked by PKC stimulants is due to the activation of ERK1/2 and p38 MAPK in volume-dependent hypertension. Therefore, it is suggested that PKC activity affects volume-dependent hypertension and the need to develop cardiovascular disease-specialized physical therapy.

• 한국생물공학회:학술대회논문집
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• 2000.04a
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• pp.378-381
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• 2000

The optimal conditions and properties for the immobilization of marine bacterium Pseudomonas aeruginosa BYK-2 have been determined. For the high productioon of biosurfactant, Na-alginate, PVA, modified PVA were used as a carrier. The optimal emulsifying activity on immobilized Pseudomonas aeruginosa BYK-2 showed 1036Unit (about 2.2g/L biosurfactant) in Basal salt medium(B.S.M.) at $25^{\circ}C$, 100rpm. Ca-alginate was selected the optimal bead among PVA, modified PVA and Ca-alginate. The optimal cell load in alginate bead was 10 gCWW/100g carrier. As the results of incubation of immobilized 5g Ca-alginate bead (conditions; 3% alginate, bead diameter: 2.3mm, 10% cell load) in 50m1 production medium, The emulsifying activity of 1407Unit, about 3.0g/L biosurfactant was obtained from immobilized cell after cultivation of 92hr at $25^{\circ}C$, 100rpm.

• Korean Journal of Environmental Biology
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• v.20 no.4
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• pp.303-308
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• 2002

3-weeks old Commelina was transferred to and grown in Hoagland solution ($\pm$ 100 $\mu{M}$ $Cd^{2+}$, 100 $\mu{M}$ $Cd^{2+}$ ＋ 100$\mu{M}$ $Ca^{2+}$, 100 $\mu{M}$ $Cd^{2+}$ ＋ 200 $\mu{M}$ EGTA) for two weeks and then a number of physiological activities was investigated. $Cd^{2+}$ reduced total chlorophyll content up to 29% at a week and 75% at two weeks. In the treatment of $Cd^{2+}$ ＋ $Ca^{2+}$, the total chlorophyll content was reduced to 29% at a week and 80% at two weeks. $Cd^{2+}$ reduced 24% of Fv/Fm after two weeks. In case of $Cd^{2+}$ ＋ $Ca^{2+}$, Fv/Fm was reduced 55% at a week, but after two weeks, the plants were almost dead and Fv/Fm could not be measured. When EGTA was treated with $Cd^{2+}$, the value of Fv/Fm was not affected. There were no differences of water potential between the control and the treatment of $Cd^{2+}$+EGTA toy a week, but in other treatments. water potential was reduced. $Cd^{2+}$ reduced about 21% of water potential and $Cd^{2+}$ ＋ $Ca^{2+}$ reduced 43% of water potential after two weeks. $Cd^{2+}$ inhibited 21% of photosynthetic activity at a week and 32% at two weeks. In case of photosynthetic activity, $Cd^{2+}$ ＋ $Ca^{2+}$ inhibited 58% at a week and 73% at two weeks. $Cd^{2+}$+EGTA inhibited 15% of photosynthetic activity at a week and 21% at two weeks. Similar results were found in stomatal conductance. From the above results, it was observed that the treatment of $Ca^{2+}$ with $Cd^{2+}$ induced more reduction of a series of physiological responses than those of the treatment of $Cd^{2+}$ alone. Therefore, it could be concluded that $Ca^{2+}$ did not reduce the toxicity of $Cd^{2+}$, but enhanced $Cd^{2+}$ -induced physiological toxicities, but EGTA induced an decrease of $Cd^{2+}$ -induced physiological toxicities.

• Restorative Dentistry and Endodontics
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• v.22 no.1
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• pp.76-92
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• 1997

Porpilyromonas endodontalis is specifically involved in endodontic infections. The bacterium can be isolated almost exclusively only from infected rool canals. P. gingivalis also has been implicated in endodontic infection. Pathogemcity of P. gingival is is attributed to a variety of virulence factors, especially proteases, produced by the bacterium. Importance of P. endodontalis in endodontic infection has been revealed. However, the pathogenic property of P. endodontalis has not been extensively studied. The present study was undertaken to characterize the proteolytic activity of P. endodontalis and compare the activity with that of P. gingivalis which has the most potent and diverse proteases among oral bacteria. For this purpose, culture supematants(SUP) and cell extracts(CE) were obtained from these two bacteria and were subjected to zymography using 15% polyacrylamide gel copolymerized with gelatin, type I, IV collagens or albumin. Hydrolysis of the collagens was further investigated by the cleavage assay using native type I and IV collagens in solution-phase. The results were as follows: 1. P. endodontalis apparently has a proteolytic activity that is comparable with that of P. gingivalis. 2. SUP and CE obtained from P. endodontalis and P. gingival is showed the strongest activity for gelatin, followed by type I and IV collagens, and albumin. 3. In the zymography, no noticeable difference in proteolytic activity for gelatin and albumin between the SUP and CE was observed, but in the cleavage assay using native collagens, the SUP showed a stronger collagenolytic activity than the CE. 4. The gelatinolytic activity of both the SUP and CE from these two bacteria was diminished in the presence of $CaCl_2$ or reducing agents such as ${\beta}$-mercaptoethanol and dithiothreitol(DTT). 5. Type I(calf skin and human placenta) collagenolytic activity of P. endodontalis and P. gingivalis was reduced by DTT but not affected by $CaCl_2$. The inhibitory effect of DTT, however, was reduced to some extent by $CaCl_2$. 6. Type IV collagenolytic activity of these two bacteria was not affected by $CaCl_2$ but increased to some extent in association with the reducing agents. 7. Hydrolysis of albumin by P. endodontalis and P. gingivalis was demonstrated only in the presence of the reducing agents. The overall results indicate that with respect to proteolytic activity, P. endodontalis appears to be as potent as P. gingivalis, or maybe more, and its proteolytic characteristic is similar to that of P. gingivalis. This suggests that P. endodontalis has so potent proteolytic activity that can participate by itself in endodontic infections and apical periodontitis, causing tissue destruction.

• Molecules and Cells
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• v.28 no.3
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• pp.167-174
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• 2009

Genistein has been reported to potentiate glucose-stimulated insulin secretion (GSIS). Inhibitory activity on tyrosine kinase or activation of protein kinase A (PKA) was shown to play a role in the genistein-induced potentiation effect on GSIS. The aim of the present study was to elucidate the mechanism of genistein-induced potentiation of insulin secretion. Genistein augmented insulin secretion in INS-1 cells stimulated by various energygenerating nutrients such as glucose, pyruvate, or leucine/glutamine (Leu/Gln), but not the secretion stimulated by depolarizing agents such as KCl and tolbutamide, or $Ca^{2+}$ channel opener Bay K8644. Genistein at a concentration of $50{\mu}M$ showed a maximum potentiation effect on Leu/Gln-stimulated insulin secretion, but this was not sufficient to inhibit the activity of tyrosine kinase. Inhibitor studies as well as immunoblotting analysis demonstrated that activation of PKA was little involved in genistein-induced potentiation of Leu/Gln-stimulated insulin secretion. On the other hand, all the inhibitors of $Ca^{2+}$/calmodulin kinase II tested, significantly diminished genistein-induced potentiation. Genistein also elevated the levels of $[Ca^{2+}]_i$ and phospho-CaMK II. Furthermore, genistein augmented Leu/Gln-stimulated insulin secretion in CaMK II-overexpressing INS-1 cells. These data suggest that the activation of CaMK II played a role in genistein-induced potentiation of insulin secretion.

• Applied Chemistry for Engineering
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• v.7 no.5
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• pp.992-998
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• 1996

The $La_{0.8}Ca_{0.2}CoO_3$ prepared by a citrate process was shown to have higher oxygen reduction current density and specific activity than $LaCoO_3$, $La_{0.6}Ca_{0.4}CoO_3$. In the cyclic voltammogram, an oxygen desorption peak of a $La_{0.8}Ca_{0.2}CoO_3$+carbon electrode was larger than that of a only carbon electrode. $La_{0.8}Ca_{0.2}CoO_3$ sintered at $900^{\circ}C$ for 5 hours was shown high oxygen reduction current density because of the particle size distribution and sintering effect.

• Journal of Photoscience
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• v.3 no.3
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• pp.127-132
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• 1996

Calcium has a variety of functions in neuron and muscle cells and blood clotting, especially in the visual system where dark adapted rods cotransport with Na$^+$ into the cell. An influx of Ca$^{2+}$ flows out of the cell through the Na$^+$ - Ca$^{2+}$ exchanger. By using a modified Ussing chamber in order to bring in vivo environment close, we have concluded that Ca$^{2+}$ blocks the activity of guanylate cyclase; in consequence, having an effect on the amplitude of electroretinogram (ERG). We suggest that Ca$^{2+}$ moves between the photoreceptor and the vitreous humor by way of certain Ca$^{2+}$ transport mechanisms. Also, the effect of Zn$^{2+}$ in Ca$^{2+}$ - free ringer solution caused an elevation of amplitude in ERG and a reduction of threshold.

• Journal of Korean society of Dental Hygiene
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• v.17 no.2
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• pp.283-294
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• 2017

Objectives: The purpose of the study was to investigate the effect of calcium concentration in saliva on dental caries activity after consuming calcium. Methods: A total of 59 adult women aged 20 to 40 years were surveyed for calcium intake. The daily average calcium intake was analyzed through dietary records of the subjects. The subjects were divided into two groups based on daily average calcium intake. Salivary pH and concentrations of minerals in the saliva were obtained from A group and B group. Calcium ($Ca^{2+}$) and magnesium ($Mg^{2+}$) concentrations in saliva were measured by HPLC-Ion chromatography using 15 mM sulfuric acid. The dental caries activity test was quantified by salivary buffer capacity test and plaque pH test. Results: The mean $Ca^{2+}$ concentrations of A group was $12.75{\mu}g/m$, the mean $Ca^{2+}$ concentrations in the B group was $16.30{\mu}g/mL$ (p<0.05) and respectively, $Mg^{2+}$ concentrations were found to be $0.48{\mu}g/mL$ and $0.51{\mu}g/mL$. Calcium intake and calcium concentration in saliva showed a significant correlation (r=0.380). Conclusions: The mean $Ca^{2+}$ concentrations in saliva was higher in the high calcium intake group. Therefore, calcium intake in saliva was correlated with dental caries.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.1
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• pp.37-43
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• 2005

Our previous report demonstrated that chick myoblasts are equipped with $Ca^{2+}$-permeable stretchactivated channels and $Ca^{2+}-activated$ potassium channels ($K_{Ca}$), and that hyperpolarization-induced by $K_{Ca}$ channels provides driving force for $Ca^{2+}$ influx through the stretch-activated channels into the cells. Here, we showed that acetylcholine (ACh) also hyperpolarized the membrane of cultured chick myoblasts, suggesting that nicotinic acetylcholine receptor (nAChR) may be another pathway for $Ca^{2+}$ influx. Under cell-attatched patch configuration, ACh increased the open probability of $K_{Ca}$ channels from 0.007 to 0.055 only when extracellular $Ca^{2+}$ was present. Nicotine, a nAChR agonist, increased the open probability of $K_{Ca}$ channels from 0.008 to 0.023, whereas muscarine failed to do so. Since the activity of $K_{Ca}$ channel is sensitive to intracellular $Ca^{2+}$ level, nAChR seems to be capable of inducing $Ca^{2+}$ influx. Using the $Ca^{2+}$ imaging analysis, we were able to provide direct evidence that ACh induced $Ca^{2+}$ influx from extracellular solution, which was dramatically increased by valinomycin-mediated hyperpolarization. In addition, ACh hyperpolarized the membrane potential from $-12.5{\pm}3$ to $-31.2{\pm}5$ mV by generating the outward current through $K_{Ca}$ channels. These results suggest that activation of nAChR increases $Ca^{2+}$ influx, which activates $K_{Ca}$ channels, thereby hyperpolarizing the membrane potential in chick myoblasts.

• Biomolecules & Therapeutics
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• v.7 no.3
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• pp.227-233
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• 1999

The effects of 2-bromo-3-(3,5-tert-butyl-4-hydroxylphenyl)-1,4-naphthalenedione(TPN2), a synthetic vitamin K derivative, on platelet aggregation and its action mechanisms were investigated in rat platelet. TPN2 inhibited the platelet aggregation induced by collagen($10\mu\textrm{g}$/ml), thrombin(0.1 U/ml), A23187($10\mu\textrm{M}$) and arachidonic acid($100\mu\textrm{M}$) in concentration-dependent manner with $IC_{50}$ values of 6.5$\pm$1.3, 59.3$\pm$4.5, 13.0$\pm$2.37 and 2.9$\pm$$1.0\mu\textrm{M}$, respectively. Collagen-induced serotonin release was significantly reduced by TPN2. The elevation of intracellular free $Ca^{2+}$ concentration ([$Ca^{2+}$]i) by collagen stimulation was greatly decreased by the pretreatment of TPN2, which was due to the inhibition of calcium release from intracellular store and influx from outside of the cell. TPN2 also significantly reduced the thromboxane $A_2$($TXA_2$) formation in a concentration-dependent manner. The collagen-induced arachidonic acid (AA) release in [$^3H$]-AA incorporated platelet, an indicative of the phospholipase $A_2$ activity, was decreased by TPN2 pretreatment. TPN2 significantly inhibited the activity of thromboxane synthase, but did not affect the cyclooxygenase activity. From these results. it is suggested that TPN2 exert its antiplatelet activity through the inhibition of the intra-cellular $Ca^{2+}$ mobilization and the decrease of the $TXA_2$ synthesis.