• Title/Summary/Keyword: protein release

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A Study of Hair Damage by Magic Straight Perm

  • Lim, Sun-Nye
    • Applied Microscopy
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    • v.42 no.3
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    • pp.129-135
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    • 2012
  • In this study, the changes in hair quality before and after Magic straight perm have been evaluated through a hair damage measurement method. For this, a healthy high school student's (age18 years) wavy hair was selected and permed on the left and right sides. Then, the changes caused by physical methods which were applied during the fl at iron-based Magic straight perm were evaluated based on the hair damage measurement method before and after the Magic straight perm. According to the protein release test after the Magic straight perm, 1.26% in average and 0.14% was observed in Cool Magic straight perm sample. In a field emission scanning electron microscopy (FE-SEM) test, saw teeth-shaped partial desquamation of cuticle cells and impurities were observed in the warm-treated hair sample. In atomic force microscope (AFM), line-profile is a method to represent roughness data on hair. According to analysis on 3-dimensional (3D) images, the hair with Cool Magic straight perm was lower than the hair with Warm Magic perm in terms of the color change of 3D images. In addition, vertical changes were observed in the hair with Cool Magic perm. As a result, irregular surface roughness was observed. This study proposed a method to minimize hair damage by cooling down the heat with the cool hair straightener as soon as the Warm Magic was finished.

Hair Damage and Wave Efficiency according to the Degree of Alkalinity in Permanent Wave

  • Jeong, Nam-Young;Lim, Sun-Nye;Choi, Chang-Nam
    • Applied Microscopy
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    • v.42 no.3
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    • pp.136-141
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    • 2012
  • Diversification and individualization are pursued to fulfill the increasing human desire for beauty. There are many methods to change human appearances; of these, a permanent wave is often applied to improve beauty. A permanent wave uses physical and chemical methods to break and reform the bonds of natural hair. Thus, research into the optimized conditions for permanent waves is necessary to minimize hair damage and improve the efficiency of the treatment. The object of this study is to examine the effect of varying the alkalinity (8%, 12%, and 16%) of the permanent wave treatment on the wave efficiency, degree of hair damage via tensile strength, and degree of hair protein release. The results indicate that the treatment with the highest alkalinity (16%) is more effective than that with 8% alkalinity; however, the degree of hair damage when treated with the 16% alkalinity wave is higher than with the 8% alkalinity wave. Additionally, hair proteins increasingly dissolve with increasing alkalinity of the permanent wave.

Effect of Solvent in Human Hair Dyeing with Natural Dye(II) (천연염료에 의한 모발염색에서 용매의 효과(II))

  • Choi, Chang-Nam;Yang, Hye-Youn;Jung, Nam-Young;Lim, Sun-Nye;Lee, Woong-Eui;Jang, Mi-Hwa
    • Textile Coloration and Finishing
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    • v.22 no.2
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    • pp.110-117
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    • 2010
  • Recently, there is a trend to utilize natural dyes in many dyeing fields. In this work, the effects of benzyl alcohol in human hair dyeing with cochineal, a natural dye, was investigated. We investigated the K/S value and color value of dyed hair, water retention of dyed hair, protein release-ability of dyed hair, and wash fastness of dyed hair according to dyeing time and temperature. The shade of dyed hair was reddish. By adding benzyl alcohol in cochineal dyeing, the dyeing rate was increased and the dyeing equilibrium was established at early stage. The water retention of dyed hair was increased and the protein release-ability of dyed hair was decreased, meaning that the hair was less damaged during dyeing, The dyed hair showed a good wash fastness.

Terpinen-4-ol Induces Autophagic and Apoptotic Cell Death in Human Leukemic HL-60 Cells

  • Banjerdpongchai, Ratana;Khaw-on, Patompong
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.12
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    • pp.7537-7542
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    • 2013
  • Background: Terpinen-4-ol, a monoterpene, is found as the main component of essential oil extracts from many plants. In this study apoptotic and autophagic types of cell death induced by terpinen-4-ol and associated mechanisms were investigated in human leukemic HL-60 cells. Materials and Methods: The cytotoxicity of human leukemic U937 and HL-60 cells was determined by MTT assay. Cytochrome c release, expression of Bax, Bcl-2, Bcl-xl and cleaved Bid were determined by Western blotting. Cell morphology was examined under a transmission electron microscope. LC3-I/II, ATG5 and Beclin-1 levels were detected by immunoblotting. Results: Terpinen-4-ol exhibited cytotoxicity to human leukemic HL-60 but not U937 cells. The apoptotic response to terpinen-4-ol in HL-60 cells was due to induction of cytochrome c release from mitochondria and cleavage of Bid protein after the stimulation of caspase-8. There was a slightly decrease of Bcl-xl protein level. The characteristic cell morphology of autophagic cell death was demonstrated with multiple autophagosomes in the cytoplasm. At the molecular level, the results from Western blot analysis showed that terpinen-4-ol significantly induced accumulation of LC3-I/II, ATG5 and Beclin-1, regulatory proteins required for autophagy in mammalian cells. Conclusions: Terpinen-4-ol induced-human leukemic HL-60 cell death was via both autophagy and apoptosis.

A Conclusive Review on Amyloid Beta Peptide Induced Cerebrovascular Degeneration and the Mechanism in Mitochondria

  • Merlin, Jayalal L.P.
    • Journal of Integrative Natural Science
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    • v.6 no.3
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    • pp.125-137
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    • 2013
  • Promising evidence suggests that amyloid beta peptide ($A{\beta}$), a key mediator in age-dependent neuronal and cerebrovascular degeneration, activates death signalling processes leading to neuronal as well as non-neuronal cell death in the central nervous system. A major cellular event in $A{\beta}$-induced apoptosis of non-neuronal cells, including cerebral endothelial cells, astrocytes and oligodendrocytes, is mitochondrial dysfunction. The apoptosis signalling cascade upstream of mitochondria entails $A{\beta}$ activation of neutral sphingomyelinase, resulting in the release of ceramide from membrane sphingomyelin. Ceramide then activates protein phosphatase 2A (PP2A), a member in the ceramide-activated protein phosphatase (CAPP) family. PP2A dephosphorylation of Akt and FKHRL1 plays a pivotal role in $A{\beta}$-induced Bad translocation to mitochondria and transactivation of Bim. Bad and Bim are pro-apoptotic proteins that cause mitochondrial dysfunction characterized by excessive ROS formation, mitochondrial DNA (mtDNA) damage, and release of mitochondrial apoptotic proteins including cytochrome c, apoptosis inducing factor (AIF), endonuclease G and Smac. The cellular events activated by $A{\beta}$ to induce death of non-neuronal cells are complex. Understanding these apoptosis signalling processes will aid in the development of more effective strategies to slow down age-dependent cerebrovascular degeneration caused by progressive cerebrovascular $A{\beta}$ deposition.

Differential Efflux of Mitochondrial Endonuclease G by hNoxa and tBid

  • Seo, Young-Woo;Park, Sun-Young;Yun, Cheol-Won;Kim, Tae-Hyoung
    • BMB Reports
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    • v.39 no.5
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    • pp.556-559
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    • 2006
  • The Bcl-2 family of proteins regulates mitochondrial functions during cell death by modulating the efflux of death-promoting proteins such as cytochrome c and endonuclease G. Upon the binding of death ligands to their receptors, caspase-8 cleaves Bid, a BH3-only protein, into tBid that causes the mitochondrial damages resulting in the release of cytochrome c and endonuclease G. Also, another BH3-only protein, hNoxa, has been shown to induce the efflux of cytochrome c from the mitochondria. Whether the efflux proteins from the mitochondria in response to tBid or hNoxa are the same or different, however, has not been addressed. We have demonstrated that endonuclease G activities are not detectable among the proteins released from isolated mitochondria by hNoxa but are detectable in that by tBid. These results suggest that the efflux of proteins from the mitochondria are differentially modulated by tBid and hNoxa.

Effects of Samul-Tang Extract on Vascular Endothelial Cells from Hydrogen Peroxide-induced Injury (사물탕(四物湯)이 혈관내피세포(血管內皮細胞)에 미치는 영향(影響))

  • Nam, Chang-Kyu;Kim, Young-Kyun;Moon, Byung-Soon
    • The Journal of Internal Korean Medicine
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    • v.20 no.1
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    • pp.83-98
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    • 1999
  • This study is designed to investigate the effects of Samul-Tang extract on the response of lactic dehydrogenase(LDH) release, cellular activity, lipid peroxidation, DNA synthesis and the changes of total protein of bovine pulmonary artery endothelial cells(PAEC) from hydrogen peroxide$(H_2O_2)$-induced injury. The results are as follows : 1. Samul-Tang significantly decreased $H_2O_2$-induced release of LDH from injured bovine PAEC. 2. Samul-Tang significantly repressed $H_2O_2$-induced cellular activity from injured bovine PAEC. 3. Samul-Tang significantly repressed $H_2O_2$-induced lipid peroxidation from injured bovine PAEC. 4. Samul-Tang significantly stimulated DNA synthesis in bovine PAEC. 5. Samul-Tang significantly repressed $H_2O_2$-induced changes of total protein volume from injured bovine PAEC. Above results suggest that Samul-Tang can protect bovine PAEC from $H_2O_2$-induced injury. These results can be effectively applied to the prevention and cure of cardiovascular and cerebrovascular diseases.

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Inhibitory effects of scoparone through regulation of PI3K/Akt and MAPK on collagen-induced human platelets

  • Lee, Dong-Ha
    • Journal of Applied Biological Chemistry
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    • v.63 no.2
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    • pp.131-136
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    • 2020
  • When blood vessels are damaged, a fast hemostatic response should occur to minimize blood loss and maintain normal circulation. Platelet activation and aggregation are essential in this process. However, excessive platelet aggregation or abnormal platelet aggregation may be the cause of cardiovascular diseases such as thrombosis, stroke, and atherosclerosis. Therefore, finding a substance capable of regulating platelet activation and suppressing agglutination reaction is important for the prevention and treatment of cardiovascular diseases. 6,7-Dimethoxy-2H-chromen-2-one (Scoparone), found primarily in the roots of Artemisia or Scopolia plants, has been reported to have a pharmacological effect on immunosuppression and vasodilation, but studies of platelet aggregation and its mechanisms are still insufficient. This study confirmed the effect of scoparone on collagen-induced human platelet aggregation, TXA2 production, and major regulation of intracellular granule secretion (ATP and serotonin release). In addition, the effect of scoparone on the phosphorylation of the phosphoproteins PI3K/Akt and mitogen-activated protein kinases (MAPK) involved in signal transduction in platelet aggregation was studied. As a result, scoparone significantly inhibited the phosphorylation of PI3K/Akt and MAPK, which significantly inhibited platelet aggregation through TXA2 production and intracellular granule secretion (ATP and serotonin release). Therefore, we suggest that scoparone is an antiplatelet substance that regulates the phosphorylation of phosphoproteins such as PI3K/Akt and MAPK and is of value as a preventive and therapeutic agent for platelet-derived cardiovascular disease.

Inhibitory Effect of Alpiniae officinarum Rhizoma Extract on Degranulation in RBL-2H3 Cells

  • Kim, Eunhee;Ahn, Sejin;Lee, Deug-Chan
    • Korean Journal of Plant Resources
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    • v.28 no.3
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    • pp.321-328
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    • 2015
  • Alpiniae officinarum Rhizoma (the rhizome of Alpinia officinarum Hance, known as lesser galangal), a family of Zingiberaceae, has been used to reduce pain of infection and inflammatory diseases in Asian countries. The present study was focused to evaluate the inhibitory degranulation effect of Alpiniae officinarum Rhizoma extract in RBL-2H3 rat basophilic leukemia cells. Cell viability was measured by MTT assay. RBL-2H3 cells were stimulated by phorbol 12-myristate 13-acetate and calcium ionophore A23187. Mast cell degranulation was analyzed by measuring release of β-hexosaminidase in RBL-2H3 cell. Gene expression was measured by qRT-PCR and signaling molecules were detected by immunoblotting. The Alpiniae officinarum Rhizoma extract suppressed β-hexosaminidase release in dose-dependent manner and inhibited cycloxygenase-2 and tumor necrosis factor-α gene expression. Furthermore, it was found that Alpiniae officinarum Rhizoma extract reduced mitogen-activated protein kinases, especially phosphorylated p38, at 0.75 ㎎/㎖ of Alpiniae officinarum Rhizoma extract concentrations. These data show that Alpiniae officinarum Rhizoma extract has immunosuppressive effect in mast cell induced allergic inflammation.

The Effect of Cobrotoxin on $NF-{\kappa}B$ binding Activity in Raw264.7 cells

  • Yoo, Jae-Ryong;Song, Ho-Sueb
    • Journal of Acupuncture Research
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    • v.22 no.2
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    • pp.133-139
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    • 2005
  • Cobrotoxin, a venom of Vipera lebetina turanica, is a group of basic peptidescomposed of 233 amino acids with six disulfide bonds formed by twelve cysteins. NF-kB is activated by subsequent release of inhibitory IkB and translocation of p50. Since sulfhydryl group is present in kinase domain of p50 subunit of NF-kB, cobrotoxin could modify NF-kB activity by protein-protein interaction. We therefore examined effect of cobrotoxin on NF-kB activities in lipopolysaccharide (LPS) and sodium nitroprusside (SNP)-stimulated Raw 264.7 mouse macrophages. Cobrotoxin suppressed the LPS and SNP-induced release of IkB and p50 translocation resulted in inhibition of DNA binding activity of NF-kB. Inhibition of NF-kB resulted in reduction of the LPS and SNP-induced production of inflammatory mediators NO and PGE2 generation. The inhibitory effect of cobrotoxin on the NF-kB activity were blocked by addition of reducing agents dithiothreitol and glutathione. These results demonstrate that cobrotoxin inhibits activation of NF-kB, and suggest that pico to nanomolar range of cobrotoxin could inhibit the expression of genes in the NF-kB signal pathway.

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