• Journal of the Semiconductor & Display Technology
• /
• v.22 no.2
• /
• pp.96-103
• /
• 2023

This paper presents a robust position tracking controller for a motor used in semiconductor equipment, utilizing the motor angle measurement. Precise position control is challenging due to the presence of uncertainties in various motor applications. The proposed controller consists of a PD (Proportional-Derivative) controller and a PIO (Proportional-Integral Observer) to estimate the system's state and equivalent disturbance compensating for the uncertainties. Since the stability alternates as the observer gain increases, we have investigated it through the closedloop root locus under the system parameters change. The analysis has showed that the inertia of the motor is the main parameter that affects it, and by adjusting the control gain appropriately, the system can be rendered to be stable even when the inertia of the motor changes. The effectiveness of the proposed control algorithm is validated through computer simulations, followed by a comparison of its performance with the results of a previous study.

• Transactions on Control, Automation and Systems Engineering
• /
• v.1 no.1
• /
• pp.1-7
• /
• 1999

This paper gives a simulation study of a new fuzzy logic control(FLC) approach for the mold level control in continuous casting processes. The proposed FLC is PID type hybridizing the conventional fuzzy PI control and Fuzzy PD control with a simplified design scheme. It is shown that, compared with the conventional control, this new control strategy can achieve superior performance for steady-state response and is more robust against process parameter variations and disturbances.

• 제어로봇시스템학회:학술대회논문집
• /
• 2000.10a
• /
• pp.177-177
• /
• 2000

In this paper, we propose a two-input two-output fuzzy controller to improve the performance of transient response and to eliminate the steady state error. The outputs of this controller are the control input calculated by position-type fuzzy controller and the accumulated error scaling factor. Here, the accumulated error scaling factor is adjusted on-line by fuzzy rules according to the current trend of the controlled process. To show the usefulness of the proposed controller, it is applied to several systems that are difficult to get satisfactory response by conventional PD controllers or PI controllers.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.23 no.2
• /
• pp.416-425
• /
• 2009

Angiogenesis is important for promoting cardiovascular disease, wound healing, and tissue regeneration. We here investigated the pharmacological effects of Korea red ginseng water extract (KRGE) on angiogenesis and its underlying signal mechanism. This study showed that KRGE increased in vitro proliferation, migration, and tube formation of human umbilical endothelial cells, as well as stimulated in vivo angiogenesis. KRGE-induced angiogenesis was accompanied by phosphorylation of ERK1/2, Akt, and endothelial nitric oxide synthase (eNOS) as well as an increase in NO production. Inhibition of PI3K activity by wortmannin completely inhibited KRGE-induced angiogenesis and phosphorylation of Akt, ERK1/2, and eNOS, indicating that PI3K/Akt activation is an upstream event of KRGE-mediated angiogenic pathway. The MEK inhibitor PD98059 completely blocked KRGE-induced angiogenesis and ERK phosphorylation without affecting Akt and eNOS activation. However, the eNOS inhibitor NMA effectively inhibited tube formation, but partially blocked proliferation and migration as well as ERK phosphorylation without altering Akt and eNOS activation, revealing that eNOS/NO pathway is in part involved in ERK1/2 activation. This study first demonstrated the critical involvement of both ERK1/2 and eNOS activation in KRGE-induced angiogenesis, which lie on downstream of PI3K/Akt. Thus, these results indicate that KRGE requires activation of both the PI3K/Akt-dependent ERK1/2 and eNOS signal pathways and their cross-talk for its full angiogenic activity.

• Archives of Pharmacal Research
• /
• v.27 no.3
• /
• pp.324-333
• /
• 2004

To determine whether Insulin-like growth factor (IGF-I) treatment represents a potential means of enhancing the survival of cardiac muscle cells from adriamycin (ADR)-induced cell death, the present study examined the ability of IGF-I to prevent cell death. The study was performed utilising the embryonic, rat, cardiac muscle cell line, H9C2. Incubating cardiac muscle cells in the presence of adriamycin increased cell death, as determined by MTT assay and annexin V-positive cell number. The addition of 100 ng/mL IGF-I, in the presence of adriamycin, decreased apoptosis. The effect of IGF-I on phosphorylation of PI, a substrate of phosphatidylinositol 3-kinase (PI 3-kinase) or protein kinase B (AKT), was also examined in H9C2 cardiac muscle cells. IGF-I increased the phosphorylation of ERK 1 and 2 and $PKC{\;}{\zeta}{\;}kinase$. The use of inhibitors of PI 3-kinase (LY 294002), in the cell death assay, demonstrated partial abrogation of the protective effect of IGF-I. The MEK1 inhibitor-PD098059 and the PKC inhibitor-chelerythrine exhibited no effect on IGF-1-induced cell protection. In the regulatory subunit of PI3K-p85- dominant, negative plasmid-transfected cells, the IGF-1-induced protective effect was reversed. This data demonstrates that IGF-I protects cardiac muscle cells from ADR-induced cell death. Although IGF-I activates several signaling pathways that contribute to its protective effect in other cell types, only activation of PI 3-kinase contributes to this effect in H9C2 cardiac muscle cells.

• Biomedical Science Letters
• /
• v.22 no.2
• /
• pp.60-64
• /
• 2016

In the pathogenesis of inflammatory diseases such as allergies, S100A8 acts as an important molecule and T lymphocytes are essential cytokine-releasing cells. In this study, we investigated the effect of S100A8 on release of cytokines, specifically MCP-1, IL-6, and IL-8 in T cells, and its associated signaling mechanism. S100A8 increased secretion of MCP-1, IL-6, and IL-8 in a time- and dose-dependent manner. Elevated secretion of MCP-1, IL-6, and IL-8 due to S100A8 was inhibited by the TLR4 inhibitor TLR4i, the PI3K inhibitor LY294002, the $PKC{\delta}$ inhibitor rottlerin, the ERK inhibitor PD98059, the p38 MAPK inhibitor SB202190, the JNK inhibitor SP600125, and the NF-${\kappa}B$ inhibitor BAY-11-7085. S100A8 induced phosphorylation of ERK, p38 MAPK, and JNK in a time-dependent manner, and activation was suppressed by TLR4i, LY294002, and rottlerin. S100A8 induced NF-${\kappa}B$ activation by $I{\kappa}-B{\alpha}$ degradation, and NF-${\kappa}B$ activity was suppressed by PD98059, SB202190, and SP600125. These results indicate that S100A8 induces cytokine release via TLR4. Study of PI3K, $PKC{\delta}$, MAPKs, and NF-${\kappa}B$ will contribute to elucidation of the S100A8-invovled mechanism.

• The Korean Journal of Physiology and Pharmacology
• /
• v.19 no.6
• /
• pp.499-506
• /
• 2015

Angiotensin II (Ang II), a key mediator of hypertensive, causes structural changes in the arteries (vascular remodeling), which involve alterations in cell growth, vascular smooth muscle cell (VSMC) hypertrophy. Ang II promotes fibrotic factor like IGFBP5, which mediates the profibrotic effects of Ang II in the heart and kidneys, lung and so on. The purpose of this study was to identify the signaling pathway of IGFBP5 on cell proliferation and migration of Ang II-stimulated VSMC. We have been interested in Ang II-induced IGFBP5 and were curious to determine whether a Pitavastatin would ameliorate the effects. Herein, we investigated the question of whether Ang II induced the levels of IGFBP5 protein followed by proliferation and migration in VSMC. Pretreatment with the specific Angiotensin receptor type 1 (AT1) inhibitor (Losartan), Angiotensin receptor type 2 (AT2) inhibitor (PD123319), MAPK inhibitor (U0126), ERK1/2 inhibitor (PD98059), P38 inhibitor (SB600125) and PI3K inhibitor (LY294002) resulted in significantly inhibited IGFBP5 production, proliferation, and migration in Ang II-stimulated VSMC. In addition, IGFBP5 knockdown resulted in modulation of Ang II induced proliferation and migration via IGFBP5 induction. In addition, Pitavastatin modulated Ang II induced proliferation and migration in VSMC. Taken together, our results indicated that Ang II induces IGFBP5 through AT1, ERK1/2, P38, and PI3K signaling pathways, which were inhibited by Pitavastatin. These findings may suggest that Pitavastatin has an effect on vascular disease including hypertension.

• Journal of Periodontal and Implant Science
• /
• v.50 no.6
• /
• pp.358-367
• /
• 2020

Purpose: The aim of this study was to investigate the efficacy and validity of subgingival bacterial sampling using a retraction cord, and to evaluate how well this sampling method reflected changes in periodontal conditions after periodontal therapy. Methods: Based on clinical examinations, 87 subjects were divided into a healthy group (n=40) and a periodontitis group (n=47). Clinical measurements were obtained from all subjects including periodontal probing depth (PD), bleeding on probing (BOP), clinical attachment loss (CAL), and the plaque index. Saliva and gingival crevicular fluid (GCF) as a subgingival bacterial sample were sampled before and 3 months after periodontal therapy. The salivary and subgingival bacterial samples were analyzed by reverse-transcription polymerase chain reaction to quantify the following 11 periodontal pathogens: Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Tannerella forsythus (Tf), Treponema denticola (Td), Prevotella intermedia (Pi), Fusobacterium nucleatum (Fn), Pavimonas micra (Pm), Campylobacter rectus (Cr), Prevotella nigrescens (Pn), Eikenella corrodens (Ec), and Eubacterium nodatum (En). Results: Non-surgical periodontal therapy resulted in significant decreases in PD (P<0.01), CAL (P<0.01), and BOP (P<0.05) after 3 months. Four species (Pg, Tf, Pi, and Pm) were significantly more abundant in both types of samples in the periodontitis group than in the healthy group. After periodontal therapy, Cr was the only bacterium that showed a statistically significant decrease in saliva, whereas statistically significant decreases in Cr, Pg, and Pn were found in GCF. Conclusions: Salivary and subgingival bacterial sampling with a gingival retraction cord were found to be equivalent in terms of their accuracy for differentiating periodontitis, but GCF reflected changes in bacterial abundance after periodontal therapy more sensitively than saliva.

• Biomolecules & Therapeutics
• /
• v.27 no.4
• /
• pp.363-372
• /
• 2019

Daidzein isolated from soybean (Glycine max) has been widely studied for its antioxidant and anti-inflammatory activities. However, the protective effects of 7,8,4'-trihydroxyisoflavone (THIF), a major metabolite of daidzein, on 6-hydroxydopamine (OHDA)-induced neurotoxicity are not well understood. In the current study, 7,8,4'-THIF significantly inhibited neuronal cell death and lactate dehydrogenase (LDH) release induced by 6-OHDA in SH-SY5Y cells, which were used as an in vitro model of Parkinson's disease (PD). Moreover, pretreatment with 7,8,4'-THIF significantly increased the levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) and decreased malondialdehyde (MDA) activity in 6-OHDA-induced SH-SY5Y cells. In addition, 7,8,4'-THIF significantly recovered 6-OHDA-induced cleaved caspase-3, cleaved caspase-9, cleaved poly-ADP-ribose polymerase (PARP), increased Bax, and decreased Bcl-2 levels. Additionally, 7,8,4'-THIF significantly restored the expression levels of phosphorylated c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase 1/2 (ERK 1/2), phosphatidylinositol 3-kinases (PI3K)/Akt, and glycogen synthase kinase-3 beta ($GSK-3{\beta}$) in 6-OHDA-induced SH-SY5Y cells. Further, 7,8,4'-THIF significantly increased the reduced tyrosine hydroxylase (TH) level induced by 6-OHDA in SH-SY5Y cells. Collectively, these results suggest that 7,8,4'-THIF protects against 6-OHDA-induced neuronal cell death in cellular PD models. Also, these effects are mediated partly by inhibiting activation of the MAPK and PI3K/Akt/$GSK-3{\beta}$ pathways.

• Journal of Periodontal and Implant Science
• /
• v.52 no.2
• /
• pp.116-126
• /
• 2022

Purpose: This study evaluated the efficacy of treating periodontitis using subgingival nano-hydroxyapatite powder with an air abrasion device (NHAPA) combined with scaling and root planing (SRP). Methods: A total of 28 patients with stage III periodontitis (grade B) were included in this study, although 1 was lost during follow-up and 3 used antibiotics. The patients were divided into a test group and a control group. All patients first received whole-mouth SRP using hand instruments, and a split-mouth approach was used for the second treatment. In the test group, the teeth were treated with NHAPA for 15 seconds at 70% power per pocket. Subgingival plaque samples were obtained from the 2 deepest pockets at the test and control sites before treatment (baseline) and 3 months after treatment. The full-mouth plaque index (PI), gingival index (GI), papillary bleeding index (PBI), bleeding on probing (BOP), probing depth (PD) and clinical attachment level (CAL) were recorded at baseline and at 1- and 3-month post-treatment. Real-time polymerase chain reaction was used to determine the colonisation of Treponema denticola (Td), Porphyromonas gingivalis (Pg), and Aggregatibacter actinomycetemcomitans in the subgingival plaque. Results: From baseline to the first month, the test group showed significantly larger changes in BOP and CAL (43.705%±27.495% and 1.160±0.747 mm, respectively) than the control group (36.311%±27.599% and 0.947±0.635 mm, respectively). Periodontal parameters had improved in both groups at 3 months. The reductions of PI, GI, BOP, PD, and CAL in the test group at 3 months were greater and statistically significant. The total bacterial count and Td and Pg species had decreased significantly by the third month in both groups (P<0.05). Conclusions: Applying NHAPA in addition to SRP improves clinical periodontal parameters more than SRP alone. Subgingival NHAPA may encourage clot adhesion to tooth surfaces by increasing surface wettability.