• Restorative Dentistry and Endodontics
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• v.19 no.2
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• pp.585-601
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• 1994

The purpose of this study was to evaluate the ability of several intracoronal base materials to prevent cervical leakage of a bleaching agent into the dentinal tubules and along the root canal. In this study, thirty-two anterior teeth were used. After lingual access was prepared in each tooth, tooth was instrumented with a step-back technique to a Nos. 40-50 using K-type files. All teeth were obturated with a lateral condensation technique. Excess gutta percha was removed with a warm instrument to the facial level of the CEJ. Teeth were divided into four groups : Teeth in control group were not filled with base material. Teeth in groups 1, 2, and 3 had 2mm of gutta percha removed with a warm instrument, then Dycal, Fuki II LC and Z-100 were filled with palstic instruments on the top of the gutta percha respectively. All teeth were bleached for 7 days, fresh bleach was added for another 7 days, then a 10 % methylene blue dye was placed inside the access preparation. They were stored at $37^{\circ}C$ and $100^{\circ}C$ humidity for 5 days. Each tooth was sectioned perpendicular to the long axis using a diamond disk. Initial cuts were made at the most coronal level of facial and lingual CEJ's, then another cuts continued appically in the levels of 0.5mm, 1.5mm, and 2.0mm respectively. The amount of dye leakage through the dentinal tubules was determined at each cut section. In addition, when the cut specimen was determined to be last penetration of any dye, this level was recorded as depth of apical leakage from the coronal terminus of the gutta percha, Dycal, Fuji II LC and Z-100. The acquired data were analyzed by Tukey's Multiple Range Test adn Cochran-Mantel-Haenszel Test to see if there was any statistically significant difference in dye penetration and linear apical leakage among the groups. The results were as follows : 1. Control group at levels of CEJ and 0.5mm, group 3 at level of 1.5mm, and group 2 AND 3 at level of 2.0mm showed the least dye penetration through the facial or lingual dentinal tubules, but there were no significant difference among three groups. 2. Group 2 at levels of CEJ and 0.5mm, group 3 at level of 1.5mm, and group 2 and 3 at level of 2.0mm showed the least dye penetration through the proximal dentinal tubules, but there were no significant difference among control group, group 2, and group 3. 3. Group 1 showed the greatest dye penetration through the facial or lingual and proximal dentinal tubules at all levels, and there were significant difference with other three groups. 4. Control group and group 1 showed 2mm apical dye leakage at facial or lingual and proximal aspects, group 2 showed 1.5mm, and group 3 showed 0.5mm.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.4
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• pp.425-434
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• 1997

Many reports represent that angiotensin II (ANG II) caused a dose dependent biphasic effects on fluid transport in the proximal tubule. However, respective roles of different signaling pathways in mediating these effects remain unsettled. The aim of the present study was to examine signaling pathways at high doses of ANG II on the $Na^+$ uptake of primary cultured rabbit renal proximal tubule cells(PTCs) in hormonally defined serum-free medium. High concentrations of ANG II $(>10^{-9}\;M)$ inhibited $Na^+$ uptake and increased $[Ca^{2+}]_i\;level$ in the PTCs. However, low concentrations of $(<10^{-11}\;ANG\;II)$ stimulated $Na^+$ uptake and did not affect $[Ca^{2+}]_i\;level$. 8-(N, N-diethylamino)-octyl-3,3,5- trimethoxybenzoate (TMB-8), ethylene glycol-bis$({/beta}-amino\;ethyl ether)-N,N,N'$, N'-tetra acetic acid (EGTA), and nifedifine partially blocked the inhibitory effects of ANG II on $Na^+$ uptake. When ANG II and bradykinin (BK) were treated together, $Na^+$ uptake was further reduced $(88.47{\pm}1.98%\;of\;that\;of\;ANG\;II,\;81.85{\pm}1.84%\;of\;that\;of\;BK)$. In addition, W-7 and KN-62 blocked the ANG II-induced inhibition of $Na^+$ uptake. Arachidonic acid reduced $Na^+$ uptake in a dose-dependent manner. When ANG II and arachidonic acid were treated together, inhibitory effects on $Na^+$ uptake significantly exhibited greater reduction than that of each group, respectively. When PTCs were treated by mepacrine $(10^{-6}\;M)$ and AACOCF3 $(10^{-5}\;M)$ for 1 hr before the addition of $(<10^{-9}\;ANG\;II)$, the inhibitory effect of ANG II was reversed. In addition, econazole $(>10^{-6}\;M)$ blocked ANG II-induced inhibition of $Na^+$ uptake. In conclusion, the $[Ca^{2+}]_i$ (calcium-calmodulin-dependent kinase) and phospholipase $A_2\;(PLA_2)$ metabolites are involved in the inhibitory effects of ANG II on $Na^+$ uptake in the PTCs.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.1
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• pp.83-91
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• 1999

Angiotensin II (ANG II) has a biphasic effect on $Na^+$ transport in proximal tubule: low doses of ANG II increase the $Na^+$ transport, whereas high doses of ANG II inhibit it. However, the mechanisms of high dose ANG II-induced inhibition on $Na^+$ uptake are poorly understood. Thus the aim of the present study was to investigate signal transduction pathways involved in the ANG II-induced inhibition of $Na^+$ uptake in the primary cultured rabbit renal proximal tubule cells (PTCs) in hormonally defined serum-free medium. ANG II $(10^{-9}\;M)-induced$ inhibition of $Na^+$ uptake was blocked by losartan $(10^{-8}\;M,\;AT_1\;antagonist),$ but not by PD123319 $(10^{-8}\;M,\;AT_2\;antagonist)$ (P<0.05). ANG II-induced inhibition of $Na^+$ uptake was also completely abolished by neomycin $(10^{-4}\;M,$ PLC inhibitor), W-7 $(10^{-4}\;M,$ calmodulin antagonist), and $AACOCF_3\;(10^{-6}\;M,\;PLA_2\;inhibitor)$ (P<0.05). ANG II significantly increased $[^3H]arachidonic$ acid (AA) release compared to control. The ANG II-induced $[^3H]AA$ release was blocked by losartan, $AACOCF_3,$ neomycin, and W-7, but not by PD123319. ANG II-induced $[^3H]AA$ release in the presence of extracellular $Ca^{2+}$ was greater than in $Ca^{2+}-free$ medium, and it was partially blocked by TMB-8 $(10^{-4}\;M,$ intracelluar $Ca^{2+}$ mobilization blocker). However, in the absence of extracellular $Ca^{2+},$ it was completely blocked by TMB-8. In addition, econazole $(10^{-6}\;M,$ cytochrome P-450 monooxygenase inhibitor) and indomethacin $(10^{-6}\;M,$ cyclooxygenase inhibitor) blocked ANG II-induced inhibition of $Na^+$ uptake, but NGDA $(10^{-6}\;M,$ lipoxygenase inhibitor) did not affect it. In conclusion, $PLA_2-mediated$ AA release is involved in ANG II-induced inhibition of $Na^+$ uptake and is modulated by $[Ca^{2+}]_i$ in the PTCs.

• Kidney Research and Clinical Practice
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• v.36 no.2
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• pp.145-157
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• 2017

Background: Vitamin D is considered to exert a protective effect on various renal diseases but its underlying molecular mechanism remains poorly understood. This study aimed to determine whether paricalcitol attenuates inflammation and apoptosis during lipopolysaccharide (LPS)-induced renal proximal tubular cell injury through the prostaglandin $E_2$ ($PGE_2$) receptor EP4. Methods: Human renal tubular epithelial (HK-2) cells were pretreated with paricalcitol (2 ng/mL) for 1 hour and exposed to LPS ($1{\mu}g/mL$). The effects of paricalcitol pretreatment in relation to an EP4 blockade using AH-23848 or EP4 small interfering RNA (siRNA) were investigated. Results: The expression of cyclooxygenase-2, $PGE_2$, and EP4 were significantly increased in LPS-exposed HK-2 cells treated with paricalcitol compared with cells exposed to LPS only. Paricalcitol prevented cell death induced by LPS exposure, and the cotreatment of AH-23848 or EP4 siRNA offset these cell-protective effects. The phosphorylation and nuclear translocation of p65 nuclear factor-kappaB ($NF-{\kappa}B$) were decreased and the phosphorylation of Akt was increased in LPS-exposed cells with paricalcitol treatment. AH-23848 or EP4 siRNA inhibited the suppressive effects of paricalcitol on p65 $NF-{\kappa}B$ nuclear translocation and the activation of Akt. The production of proinflammatory cytokines and the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cells were attenuated by paricalcitol in LPS exposed HK-2 cells. The cotreatment with an EP4 antagonist abolished these anti-inflammatory and antiapoptotic effects. Conclusion: EP4 plays a pivotal role in anti-inflammatory and antiapoptotic effects through Akt and $NF-{\kappa}B$ signaling after paricalcitol pretreatment in LPS-induced renal proximal tubule cell injury.

• KSBB Journal
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• v.7 no.2
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• pp.85-91
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• 1992

The role of NAA(1-Naphthaleneacetic acid) and BA(6-Benzyladenine) in the adventitious shoot regeneratlon from Populus leaf segments and changes in the pattern of RNA and protein synthesis were investigated. The adventitious shoot regeneration octured at the basal cut end of Populus leaf segments. This process was effected by many factors, including wounding culture conditions, light and plant growth regulators etc. The highest adventitious shoot regeneration frequency was obtained at $0.01mg/\ell$ NAA with $0.2mg/\ell$ BA. In this condition adventitious shoot starved to regenerate on the 13th day of oullure. The most optimal hormone composition for RNA and protein synthesis was $0.01mg/\ell$ NAA with $0.2mg/\ell$ BA. The content of RNA and protein was greater at the proximal part. In the course of adventitious shoot regeneration, the proteins associated with polar-regeneration appeared at the proximal part of populus leaf segment.

• Journal of Korean Foot and Ankle Society
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• v.8 no.2
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• pp.117-120
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• 2004

Purpose: The purpose of this study was to evaluate the effect and short-term results of the modified Mau osteotomy designed by the author. Materials and Methods: Seventeen feet treated with newly designed osteotomy from 2003 to 2004 were included. We performed metatarsal osteotomy and distal soft tissue procedure on 17 feet (12 patients) and additional Akin osteotomy on 6 feet (4 patients). An oblique osteotomy was made from the neck in the dorsum, aiming proximal to the base of the first metatarsal with vertical short arm on the base. We performed long arm of osteotomy parellel to the acrylic plate which was supposed as ground plane. Preoperative radiographs and follow up radiographs at three month were used for radiologic evaluation. Results: Mean hallux valgus angle was $43.6^{\circ}$ and mean intermetatarsal angle was $20.4^{\circ}$ on preoperative weight bearing radiograph. Mean amount of correction of the hallux valgus angle was $37.5^{\circ}$ and intermetatarsal angle was $14.2^{\circ}$ at three months after operation. There was no fixation loss or malunion, and the clinical result was subjectively exellent. Conclusion: More proximal rotational axis can achieve sufficient intermetatarsal angle correction, and vertical arm can provide more stable contact. So this newly modified Mau osteotomy was considered as a good alternative procedure in the treatment of severe hallux valgus.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.1
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• pp.35-43
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• 1997

Cis-dichlorodiammine platin${\mu}M$II (Cisplatin), an effective chemotherapeutic agent, induces acute renal failure by unknown mechanisms. To investigate direct toxic effects of cisplatin on the renal proximal tubular transport system, LLC-$PK_1$ cell line was selected as a cell model and the sugar transport activity was evaluated during a course of cisplatin treatment. Cells grown to confluence were treated with cisplatin for 60 min, washed, and then incubated for up to 5 days. At appropriate intervals, cells were tested for sugar transport activity using ${\alpha}-methyl-D-[^{14}C]glucopyranoside$ (AMG) as a model substrate. In cells treated with 100 ${\mu}M$ cisplatin, the AMG uptake was progressively impaired after 3 days. The viability of cells was not substantially changed with cisplatin of less than 100 ${\mu}M$, but it decreased markedly with 150 and 200 ${\mu}M$. In cisplatin-treated cells, the $Na^+$ -dependent AMG uptake was drastically inhibited with no change in the $Na^+$ -independent uptake. Kinetic analysis indicated that Vmax was suppressed, but Km was not altered. The $Na^+$ -dependent phlorizin binding was also decreased in cisplatin-treated cells. However, the AMG efflux from preloaded cells was not apparently retarded by cisplatin treatment. These data indicate that the cisplatin treatment impairs $Na^+$ -hexose cotransporters in LLC-$PK_1$ cells and suggest strongly that defects in transporter function at the luminal plasma membrane of the proximal tubular cells constitute an important pathogenic mechanism of cisplatin nephrotoxicity.

• Asian-Australasian Journal of Animal Sciences
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• v.21 no.12
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• pp.1800-1806
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• 2008

Cytokines play a central role in the mucosal immune response and are involved in regulation of nutrient absorption, metabolism and animal growth. This study investigated the effect of diet manipulation with specialized protein or peptide sources on expression of cytokine (IL-1, IL-6, IL-10, and TNF-${\alpha}$) mRNA abundance in different intestinal regions and at different ages post-weaning in piglets. A total of 48 (17 days of age, $6.16{\pm}0.34kg\;BW$) weanling pigs were fed either a corn-soy/whey protein basal diet, the basal diet supplemented with spray-dried plasma protein (SDPP), or the basal diet supplemented with $Peptiva^{(R)}$, a hydrolyzed marine plant protein. A fourth treatment group was fed the SDPP diet, but the feed intake level was limited (SDPP-LF). Pigs were killed at 3 and 10 d, and intestinal cytokine mRNA was measured by real-time PCR using the relative quantification method. The SDPP-LF group exhibited an increased TNF-${\alpha}$ mRNA abundance compared with the ad libitum SDPP group (p<0.05). The TNF-${\alpha}$ and IL-10 mRNA abundance increased from the proximal to distal part of the intestine, and the mRNA abundance was greater (p<0.01) in the distal intestine as compared with the proximal and middle intestine. The cytokines IL-1-${\beta}$, IL-10 and TNF-${\alpha}$ mRNA abundance also increased from d3 to d10 postweaning (p<0.01). In summary, restricted feeding increased the TNF-${\alpha}$ mRNA abundance in the small intestine, however neither SDPP nor peptide supplementation affected cytokine mRNA expression. Abundance of mRNA for most cytokines examined in this study increased with age post-weaning, suggesting that during 10 d after weaning the mucosal immune system is still under development.

• Journal of Korean Physical Therapy Science
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• v.4 no.2
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• pp.399-403
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• 1997

The purpose of this study was to determine the efficacy of electrode placement on procaine iontophoresis. Thirty-three healthy students with an age range of 19 to 34 years, were participated in this study. The subjects were randomly assigned into 3 groups. Each subjects received iontophoresis on the proximal 1/3 of volar surface of dominant forearm with soft cotton pad($3.5{\times}3.5cm$) soaked in 2 ml of 4% procaine hydrochloride (pH 5.1) at 4 mA for 10 minutes(total current 40 mA min) of anodal DC. In transversal electrode placement(TEP) group, dispersive electrode was placed on the proximal 1/3 of dorsal surface of the forearm. In longitudinal electrode placement (LEP) group and control group, dispersive electrode were placed on the distal 1/3 of volar surface of the forearm. After procaine iontophoresis, duration of anesthesia were evaluated at five minutes intervals on five random locations in the iontophoretically area using a 21-gauge sterile hypodermic needle pressed with 1 mm invagination until return the sharp pin-pricking pain sensation. The data were ana lysed with one-way ANOVA to determine signific~nt differences between groups. The results showed significantly differences in the local anesthetic duration between the 3 groups(p<0.001). The anesthetic durations of TEP group and LEP group were significantly longer when compared with control group(p<0.05). Anesthetic durations of TEP group and LEP group were not significantly difference, but anesthetic duration of LEP group tends to longer than TEP group. In view of these results, clinicians should consider the electrode placement method when performing the iontophoresis.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.2
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• pp.135-143
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• 2018

Tumor necrosis $factor-{\alpha}$ ($TNF{\alpha}$) and the angiotensin system are involved in inflammatory diseases and may contribute to acute kidney injury. We investigated the mechanisms by which $TNF{\alpha}$-converting enzyme (TACE) contributes to lipopolysaccharide (LPS)-induced renal inflammation and the effect of TACE inhibitor treatment on LPS-induced cellular injury in human renal proximal tubule epithelial (HK-2) cells. Mice were treated with LPS (10 mg/kg, i.p.) and HK-2 cells were cultured with or without LPS ($10{\mu}g/ml$) in the presence or absence of a type 1 TACE inhibitor ($1{\mu}M$) or type 2 TACE inhibitor ($10{\mu}M$). LPS treatment induced increased serum creatinine, $TNF{\alpha}$, and urinary neutrophil gelatinase-associated lipocalin. Angiotensin II type 1 receptor, mitogen activated protein kinase (MAPK), and TACE increased, while angiotensin-converting enzyme-2 (ACE2) expression decreased in LPS-induced acute kidney injury and LPS-treated HK-2 cells. LPS induced reactive oxygen species and the down-regulation of ACE2, and these responses were prevented by TACE inhibitors in HK-2 cells. TACE inhibitors increased cell viability in LPS-treated HK-2 cells and attenuated oxidative stress and inflammatory cytokines. Our findings indicate that LPS activates renin angiotensin system components via the activation of TACE. Furthermore, inhibitors of TACE are potential therapeutic agents for kidney injury.