• Title/Summary/Keyword: pPMA

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Oxygen Desaturation during Nutritive Sucking in Premature Infants with Bronchopulmonary Dysplasia : Its Effect on Feeding and Growth until 4 Months of Corrected Age (기관지폐 형성이상 미숙아의 젖병수유 시 저산소증: 생후 4개월까지 수유상태 및 성장에 미치는 영향)

  • Lim, Chang-Hwan;Lee, Joo-Young;Lee, Hyun-Seung;Lee, Jung-Hyun;Kim, So-Young;Sung, In-Kyung;Chun, Chung-Sik
    • Neonatal Medicine
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    • v.15 no.2
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    • pp.134-141
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    • 2008
  • Purpose : This study examined the occurrence of oxygen desaturation events during nutritive sucking in premature infants with bronchopulmonary dysplasia (BPD) and its effects on feeding and growth outcomes until 4 months of corrected age (CA). Methods : Thirty-four premature infants with BPD free from major cardiac, gastrointestinal, respiratory anomalies were included. By reviewing medical records, clinical characteristics, feeding conditions at 36 weeks of postmenstrual age (PMA), we focused on oxygen desaturation, and short-term outcomes in 14 infants with no or mild desaturation (group A) and in 20 infants with moderate or severe desaturation (group B). Results : Group B had lower birth weight and shorter gestational age at birth, longer duration of hospitalization, was discharged at higher weeks of PMA, and needed ventilatory assist and oxygen supplementation longer than group A (P<0.05). Group B started nutritive sucking later, with a greater decrease in $SpO_2$ during sucking, being more indicative of feeding problems at 40 weeks of PMA, but not at 4 months of CA. Percent of infant needing oxygen supplementation and percent of infants with growth failure were not different between groups at 40 weeks of PMA and 4 months of CA. Body weight and growth velocity differences noted at 40 weeks of PMA became insignificant at 4 months of CA. Conclusion : The severity of desaturation during nutritive sucking in premature infants with BPD influenced the infant's feeding and growth at 40 weeks of PMA. However, it disappeared at 4 months of CA.

Melatonin inhibits the Migration of Colon Cancer RKO cells by Down-regulating Myosin Light Chain Kinase Expression through Cross-talk with p38 MAPK

  • Zou, Duo-Bing;Wei, Xiao;Hu, Ruo-Lei;Yang, Xiao-Ping;Zuo, Li;Zhang, Su-Mei;Zhu, Hua-Qing;Zhou, Qing;Gui, Shu-Yu;Wang, Yuan
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.14
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    • pp.5835-5842
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    • 2015
  • Background: Melatonin, which is mainly produced by the pineal gland, has a good inhibitory effect on cell growth of multiple cancer types. However, the underlying molecular mechanisms of anti-tumor activity for colon cancer have not been fully elucidated. In this study, we investigated the effects of melatonin on migration in human colon cancer RKO cells and the potential molecular mechanisms. Materials and Methods: The viability of RKO cells was investigated by MTT assay after treatment with melatonin, SB203580 (p38 inhibitor) and phorbol 12-myristate 13-acetate (PMA, MAPK activator) alone or in combination for 48h. The effects of melatonin, and ML-7, a selective inhibitor of myosin light chain kinase (MLCK), and SB203580, and PMA on the migration of RKO cells were analyzed by in vitro scratch-wound assay. The relative mRNA levels of MLCK was assessed by real-time quantitative RT-PCR. Western blotting analysis was performed to examine the expression of MLCK, phosphorylation of myosin light chain (pMLC) and p38 (pp38). Results: The proliferation and migration of human colon cancer RKO cells were inhibited significantly after treatment with melatonin. The expression levels of MLCK and phosphorylation of MLC of RKO cells were reduced, and real-time quantitative RT-PCR showed that melatonin had significant effects on suppressing the expression of MLCK. Furthermore, the phosphorylation level of p38, which showed the same trend, was also reduced when cells were treated by melatonin. In addition, ML-7 (25umol/l) could down-regulate the phosphorylation of p38. Conclusions: Melatonin could inhibit the proliferation and migration of RKO cells, and further experiments confirmed that p38 MAPK plays an important role in regulating melatonin-induced migration inhibition through down-regulating the expression and activity of MLCK.

Effect of Hot Water Treatment Times on Moisture Absorption and Germination of Albizzia julibrissin Seeds (열탕처리시간이 자귀나무 종자의 수분흡수 및 발아에 미치는 영향)

  • Seo, Byeong-Soo;Kim, Sun-Young;Park, Woo-Jin;Choi, Chung-Ho
    • Korean Journal of Plant Resources
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    • v.20 no.4
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    • pp.267-271
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    • 2007
  • This study was carried out to examine optimal hot water treatment time in Albizzia julibrissin seeds. Germination and moisture absorption characteristics among intact seeds, immersed seeds for 24 hours in distilled water and hot water treated seeds were surveyed. As result, treated seeds showed a highly significant difference with intact and immersed seeds (p<0.0l). Especially, treated seed for 2.0 minutes represented the highest percent of germination (PG). But mean germination time (MGT) did not have significant difference between non-treatment and treatments (p=0.502). Germination speed and germination performance index showed similar tendency with PG. In percent of moisture absorption (PMA) and moisture absorption rate constant (MARC) treatments had higher values than non-treatment whereas 2.0 minutes treatment was lower than non-treatment in initial moisture absorption rate (IMAR). In relation between germination properties and moisture absorption characteristics, all properties except MGT among germination properties had high correlations with PMA and MARC ($r=0.854{\sim}0.931$,p<0.01) whereas IMAR didn't have correlation.

Fumonisin B1 Induces Apoptosis in Sphingosine 1-Phosphate Lyase-null F9 Cells through Increase of Sphingolipids Levels

  • Pak, Seon-Mi;Park, Nam-Young;Park, Myung-Yong;Kim, Wan-Jong;Lee, Jong-Hwa;Oh, Sei-Kwan;Yoo, Hwan-Soo;Lee, Yong-Moon
    • Biomolecules & Therapeutics
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    • v.16 no.2
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    • pp.95-99
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    • 2008
  • Apoptosis is essential for a variety of pathophysiological progress. Apoptosis induction by various agents changes cellular morphology, DNA content and lipid membrane composition. Recently, sphingosine 1-phosphate (S1P) is avidly released from not only platelets and erythrocytes but vascular endothelium. Here we established S1P releasing cells by deleting S1P lyase (F9-12 cells). We observed apoptosis induction by the treatment of fumonisin B1 (FB1) in F9-12 cells but not in F9 wild-type cells. We measured high amounts of accumulated S1P and dihydroS1P (DHS1P) in FB1-induced apoptotic F9-12 cells. We also showed DHS1P release in an early stage of the apoptosis induction by FB1 but not by phorbol 12-myristate 13-acetate (PMA)-induced apoptosis, suggesting differential apoptotic processes.

Effects of Protein Kinase G on Phospholipase D Activity of Human Neutrophils (호중구에서 phospholipase D의 활성에 대한 protein kinase G의 영향)

  • 박지연;이민정;장민정;이선영;배외식;곽종영
    • Journal of Life Science
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    • v.13 no.6
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    • pp.903-910
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    • 2003
  • Phospholipase D (PLD) plays an important role as a signaling molecule in the activation of neutrophils. In this study, effect of nitric oxide (NO) and cGMP on the activation of PLD in human neutrophils was investigated. Sodium nitroprusside (SNP), an agent to produce NO spontaneously in cells, alone increased PLD activity and the maximal activation was obtained with 0.5 mM SNP. Dibutyryl-cAMP, an agent to increase an intracellular cAMP concentration inhibited formyl-Met-Leu-Phe (fMLP)-stimulated PLD activity but 8-bromo-cGMP (300 $\mu$M), an agent to increase an intracellular cGMP concentration did not affect basal and fMLP-stimulated PLD activity. NO-induced activation of PLD was not blocked by KT 5823, an inhibitor of cGMP-dependent protein kinase (PKG), suggesting that NO-induced PLD activation is not mediated by cGMP. NO also stimulated p38 mitogen activated protein kinase (MAPK) in human neutrophils, indicated by increased phosphorylation of p38 MAPK in Western blotting. NO-induced phosphorylation of p38 MAPK was not inhibited by KT 5823 or n-butanol. RhoA, an regulatory factor of PLD activation was trans-located from cytosolic fraction to plasma membranes by fMLP or phorbol ester, and fMLP-stimulated but not phorbol ester-stimulated translocation of RhoA was inhibited by cGMP. These results suggest that NO stimulates PLD activity through other unidentified facto.(s) than cGMP even though cGMP inhibits the artivation of RhoA.

Sophora Flavescens Suppresses Degranulation and Pro-inflammatory Cytokines Production through the Inhibition of NF-${\kappa}B$ (p65) Activation in the RBL-2H3 cells

  • Lyu, Ji-Hyo;Park, Sang-Eun;Hong, Su-Hyun;Kim, Dong-Kyu;Ko, Woo-Shin;Hong, Sang-Hoon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.23 no.1
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    • pp.206-213
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    • 2009
  • Sophora flavescens, as a traditional herbal medicine, has been used to treat with a variety of disesases, In previous reports, S. flavescens and sophoraflavanone G (a prenylated flavonoid from S. flavescens) inhibited cytokines productions in LPS-induced Raw 264.7 macrophages cells and BV2 microglial cells. We examined on the anti-allergic effect of S. flavescens on the PMA plus A23187-induced rat leukemia (RBL-2H3) cells. S. flavescens inhibited the release of $\beta$-hexosaminidase and productions and expressions of tumor necrosis factor (TNF)-$\alpha$, interleukin (IL)-4 and cyclooxygenase (COX)-2 in a dose-dependent manner on stimulated RBL-2H3 cells, however, S. flavescens not affect cell viability. The protein expression level of nuclear factor (NF)-${\kappa}B$ (p65) was decreased in the nucleus and suppressed the degradation of inhibitory protein $I{\kappa}B-{\alpha}$ protein, the activation of extracellular signal-regulated kinases (ERK) mitogen-activated protein kinase (MAPK) by S. flavescens. These results suggest that S. flavescens could be involved anti-allergic effect by control of $NF-{\kappa}B$ (p65) translocation into the nucleus through inhibition of $I{\kappa}B-{\alpha}$ degradation and suppression of pro-inflammatory cytokines expression.

Biostable Poly(ethylene oxide)-b-poly(methacrylic acid) Micelles forpH-triggered Release of Doxorubicin

  • Choi, Young-Keun;Lee, Dong-Won;Yong, Chul-Soon;Choi, Han-Gon;Bronich, Tatiana K.;Kim, Jong-Oh
    • Journal of Pharmaceutical Investigation
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    • v.41 no.2
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    • pp.111-115
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    • 2011
  • pH-sensitive cross-linked polymeric micelles were synthesized by using block ionomer complexes of poly(ethylene oxide)-b-poly(methacrylic acid) (PEO-b-PMA) with calcium ions as micellar templates. An anticancer drug, doxorubicin (DOX) was conjugated on the cross-linked ionic cores of micelles via acid-labile hydrozone bonds. The resulting DOX-conjugated, pH-sensitive micelles are stable at physiological conditions, whereas the release of DOX was significantly increased at the acidic pH. Such micelles were internalized to lysosomes, and acidic pH in lysosomes triggers the release of DOX upon internalization in MCF-7 breast cancer cells. The released DOX entered the cell nucleus and eventually killed cancer cells. Therefore, these data demonstrate that the pH-sensitive micelles could be a promising nanocarrier for delivery of anticancer drug, DOX.

Effect of the Inhibition of PLA2 and PAF on the Neutrophilic Respiratory Burst and Apoptosis (호중구의 Respiratory Burst에 미치는 PLA2 및 PAF와 영향 : In vitro에서의 호중구의 산소기 생성 및 Apoptosis에 관한 연구)

  • Lee, Young-Man;Kim, Sang-Gyung;Park, Yoon-Yub
    • Tuberculosis and Respiratory Diseases
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    • v.48 no.6
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    • pp.887-897
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    • 2000
  • Background : Since the exact pathogenesis of sepsis-induced ARDS has not been elucidated, the mechanisms of enhanced neutrophilic respiratory burst were probed in endotoxin primed neutrophils associated with the roles of phospholipase A2(PLA2), platelet activating factor(PAF) and apoptosis. Methods : In isolated fresh human neutrophils, effects of the inhibition of PLA2 and PAF on the apoptosis were examined by the method of Annexin-FITC/dual PIflow cytometry. The roles of PLA2 and PAF on the neutrophilic respiratory burst were also examined by measuring oxidant generation in cytochrome-c reduction assay. Activities of the PLA2 and lysoPAF acetyltransferase (lysoPAF AT) of the neutrophils were determined to understand the effect of endotoxin on these enzymatic activities which may be related to the neutrophilic respiratory burst and apoptosis. In addition, the role roles of PLA2 and PAF in neutrophilic adhesion to bovine endothelial cells were examined in vitro by neutrophil adhesion assay. To investigate the effect of oxidants on pulmonary surfactant, cytochemical ultrastructural microscopy was performed. To inhibit PLA2 and PAF, non-specific PLA2 inhibitor mepacrine (100 nM) and WEB 2086 (100 nM) or ketotifen fumarate (10 ${\mu}g$/ml) were used respectively in all in vitro experimental sets. WEB 2086 is PAF receptor antagonist, and ketotifen fumarate is a lyso PAF AT inhibitor. Results: The mapacrine treatment, provided and the endotoxin (ETX) treatment, resulted in increased apoptosis of neutrophils (p<0.001) while treatments of WEB 2086 and ketotifen did not. The inhibition of PLA2 and PAF decreased (p<0.001) production of oxidants from PMA-stimulated neutrophils. While endotoxin increased the PLA2 activity of neutrophils (p<0.01), mepacrine supressed (p<0.001) the activity, provided after treatment of ETX. The lyso PAF actyltransferase activity (lyso PAF AT) increased (p<0.01) after treatment of ETX. In contrast, mepacrine, WEB 2086 and ketotifen showed a tendency of decreasing the activity after treatment of ETX. The treatment of ETX incresed (p<0.001) neutrophil adhesion to endothelial cells, which was reversed by inhibition of PLA2 and PAF (p<0.01). The binding of oxidants to pu1monary surfactant was identified histologically. Conclusions : The enhanced neutrophilic respiratory burst by ETX plays a pivotal role in the pathogenesis of ARDS in terms of oxidayive oxidative stress. Increased production of oxidants from neutrophils is mediated by the activations of PLA2 and lyso PAF AT.

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Red Ginseng Extract Reduced Metastasis of Colon Cancer Cells In Vitro and In Vivo

  • Seo, Eun-Young;Kim, Woo-Kyoung
    • Journal of Ginseng Research
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    • v.35 no.3
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    • pp.315-324
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    • 2011
  • This study investigated the effect of red ginseng extract on metastasis of colon cancer cells in vitro and in vivo. Wound healing migration, cell motility, invasion, and activity, protein expression, and mRNA expression of matrix metalloproteinases (MMPs) were examined in SW480 human colon cancer cells. SW480 cells were cultured with or without $100{\mu}g/L$ PMA in the absence or presence of various concentrations (100, 200, or $300{\mu}g/mL$) of red ginseng extract. Red ginseng extract treatment caused signifi cant suppression of cell motility and invasion (p<0.05) in SW480 cells. Red ginseng extract inhibited MMP-2 and MMP-9 activity and their protein and mRNA expression in a dose-dependent manner (p<0.05) in SW480 cells. For experimental metastasis, BALB/c mice were injected intravenously with CT-26 mouse colon cancer cells in the tail vein, and were orally administered various concentrations (0, 75, 150, or 300 mg/kg body weight) of red ginseng extract for 3 weeks. Numbers of pulmonary nodules were signifi cantly decreased in mice that were fed red ginseng extract (p<0.05). Plasma MMP-2 and MMP-9 activity signifi cantly decreased in response to treatment with red ginseng extract in mice (p<0.05). These data suggest that red ginseng extract may be useful for prevention of cancer invasion and metastasis through inhibition of MMP-2 and MMP-9 pathways.

Redifferentiation of Dedifferentiated Chondrocytes on Chitosan Membranes and Involvement of PKCα and P38 MAP Kinase

  • Lee, Yoon Ae;Kang, Shin-Sung;Baek, Suk-Hwan;Jung, Jae-Chang;Jin, Eun Jung;Tak, Eun Nam;Sonn, Jong Kyung
    • Molecules and Cells
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    • v.24 no.1
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    • pp.9-15
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    • 2007
  • To investigate the effects of chitosan on the redifferentiation of dedifferentiated chondrocytes, we used chondrocytes obtained from a micromass culture system. Micromass cultures of chick wing bud mesenchymal cells yielded differentiated chondrocytes, but these dedifferentiated during serial monolayer subculture. When the dedifferentiated chondrocytes were cultured on chitosan membranes they regained the phenotype of differentiated chondrocytes. Expression of protein kinase $C{\alpha}$ ($PKC{\alpha}$) increased during chondrogenesis, decreased during dedifferentiation, and increased again during redifferentiation. Treatment of the cultures with phorbol 12-myristate 13-acetate (PMA) inhibited redifferentiation and down-regulated $PKC{\alpha}$. In addition, the expression of p38 mitogen-activated protein (MAP) kinase increased during redifferentiation, and its inhibition suppressed redifferentiation. These findings establish a culture system for producing chondrocytes, point to a new role of chitosan in the redifferentiation of dedifferentiated chondrocytes, and show that $PKC{\alpha}$ and p38 MAP kinase activities are required for chondrocyte redifferentiation in this model system.