• Title/Summary/Keyword: Induce resistance

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A Study on Crack Behavior of Chemically Prestressed Steel Fiber Reinforced Concrete (화학적 프리스트레스가 도입된 강섬유 보강 콘크리트의 균열거동에 대한 연구)

  • Shim, Byul;Kim, Young-Kyun;Song, Ha-Won
    • Proceedings of the Korea Concrete Institute Conference
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    • 2004.11a
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    • pp.121-124
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    • 2004
  • In this paper, a series of fracture tests are performed for the chemically prestressed steel fiber reinforced concrete (SFRC) manufactured with addition of expansive additives for the study of fracture behavior and characteristics. Cracking loads of the chemically prestressed SFRC are greater than that of normal concrete and those are also increased by increasing of steel fiber volume. Thus, it is necessary to obtain optimum steel fiber volume to induce chemically prestressing effectively to concrete members. The result of three-points bending tests shows that early-cracking resistance of the chemically prestressed SFRC is increased without increase of fracture energy. From the test, the tension softening curves are also obtained by poly-linear approximation method and simulated behaviors by using the determined tension softening curves agree with experimental results. And it is confirmed that cracking and ultimate behaviors of chemically prestressed SFRC can be predicted by using obtained fracture characteristics.

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A review of osteosarcopenic obesity related to nutritional intake and exercise

  • Lee, Namju
    • Journal of the Korean Applied Science and Technology
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    • v.36 no.3
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    • pp.797-803
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    • 2019
  • Recently, osteosarcopenic obesity (OSO) has been identified and notified world wide. Therefore, this study reviewed OSO related to lifestyle factors such as nutritional intake and exercise. Due to aging, OSO may be initiated by dietary factors and obesity related factors. Reduced muscle mass and increased fat mass may negatively impact bone health causing OSO. The complication of OSO development should be related to dietary imbalance combined with declined exercise and this may contribute to induce OSO by decreasing bone mass, muscle mass, and increasing obesity with aging. To prevent OSO, reaching peak bone mass and building optimal muscle and fat mass through exercise would be recommended. For treating OSO, balanced dietary intake and regular exercise through a whole life would be needed. In addition, sufficient carbohydrate and fat intake for minimizing protein catabolism would be recommended to prevent OSO. The combination of aerobic exercise and resistance training also would be an effective intervention for OSO population.

Senotherapeutics and Their Molecular Mechanism for Improving Aging

  • Park, Jooho;Shin, Dong Wook
    • Biomolecules & Therapeutics
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    • v.30 no.6
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    • pp.490-500
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    • 2022
  • Aging is defined as physiological dysfunction of the body and a key risk factor for human diseases. During the aging process, cellular senescence occurs in response to various extrinsic and intrinsic factors such as radiation-induced DNA damage, the activation of oncogenes, and oxidative stress. These senescent cells accumulate in many tissues and exhibit diverse phenotypes, such as resistance to apoptosis, production of senescence-associated secretory phenotype, cellular flattening, and cellular hypertrophy. They also induce abnormal dysfunction of the microenvironment and damage neighboring cells, eventually causing harmful effects in the development of various chronic diseases such as diabetes, cancer, and neurodegenerative diseases. Thus, pharmacological interventions targeting senescent cells, called senotherapeutics, have been extensively studied. These senotherapeutics provide a novel strategy for extending the health span and improving age-related diseases. In this review, we discuss the current progress in understanding the molecular mechanisms of senotherapeutics and provide insights for developing senotherapeutics.

Evaluation of physical properties of Zn-Al metal coating according to arc metal spray surface treatment method (아크 금속 용사 표면 처리 방법에 따른 Zn-Al 금속 용사 피막의 물리적 특성 평가)

  • Jang, Jong-Min;Kim, Yeung-Kwan;Lee, Han-Seung
    • Proceedings of the Korean Institute of Building Construction Conference
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    • 2022.11a
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    • pp.89-90
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    • 2022
  • Arc metal spraying is a widely used method for improving the performance of construction structures such as corrosion resistance and electromagnetic wave shielding. However, when arc metal spraying is applied to a concrete structure, adhesion performance may deteriorate. Therefore, the effect of each surface treatment method on the physical properties between the arc metal spray coating and concrete was reviewed by evaluating the deposition efficiency and adhesion performance according to the arc metal spray surface treatment method (surface reinforcing agent, roughening agent, and sealing agent). As a result, it is suggested as an optimal surface treatment condition to induce non-interface failure by using a roughening agent and to improve the properties of concrete and metal coatings by applying a surface reinforcing agent and sealing agent.

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Synthesis of Novel 18F-Labeled-Nitroimidazole-Based Imaging Agents for Hypoxia: Recent Advances

  • Anh Thu Nguyen;Hee-Kwon Kim
    • The Korean Journal of Nuclear Medicine Technology
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    • v.27 no.2
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    • pp.83-93
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    • 2023
  • Hypoxia indicates the condition of low oxygen levels in tissues. In oncology, hypoxia can induce cancer progression and metastasis, as well as cause resistance to cancer therapies. The detection of hypoxia by using molecular imaging, particularly, positron emission tomography (PET) has been extensively studied due to many advantages. Nitroimidazoles, the moieties that can be trapped in hypoxic tissues due to selective reduction, have been used to design and synthesize of hypoxia-targeting radiopharmaceuticals. This review provides a summary of synthetic routes towards 18F-labeled-nitroimidazole radiotracers for PET imaging of hypoxia.

Transgenic Rice Plants Expressing an Active Tobacco Mitogen-activated Protein Kinase Kinase Induce Multiple Defense Responses

  • Jeong, Jin-A;Yoo, Seung-Jin;Yang, Douck-Hee;Shin, Seo-Ho;Lee, Myung-Chul;Cho, Baik-Ho;Yang, Kwang-Yeol
    • The Plant Pathology Journal
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    • v.24 no.4
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    • pp.375-383
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    • 2008
  • It is well known that NtMEK2, a tobacco MAPK kinase, is the upstream kinase of both salicylic acid-induced protein kinase and wound-induced protein kinase. In addition, expression of $NtMEK2^{DD}$, a constitutively active mutant of NtMEK2, is known to induce multiple defense responses in tobacco. In this study, transgenic rice plants that contained an active or inactive mutant of NtMEK2 under the control of a steroid inducible promoter were generated and used to determine if a similar MAPK cascade is involved in disease resistance in rice. The expression of $NtMEK2^{DD}$ in transgenic rice plants resulted in HR-like cell death. The observed cell death was preceded by the activation of endogenous rice 48-kDa MBP kinase, which is also activated by Xanthomonas oryzae pv. oryzae, the bacterial blight pathogen of rice. In addition, prolonged activation of the MAPK induced the generation of hydrogen peroxide and up-regulated the expression of defense-related genes including the pathogenesis-related genes, peroxidases and glutathione S-transferases. These results demonstrate that NtMEK2 is functionally replaceable with rice MAPK kinase in inducing the activation of the downstream MAPK, which in turn induces multiple defense responses in rice.

Saponins from Rubus parvifolius L. Induce Apoptosis in Human Chronic Myeloid Leukemia Cells through AMPK Activation and STAT3 Inhibition

  • Ge, Yu-Qing;Xu, Xiao-Feng;Yang, Bo;Chen, Zhe;Cheng, Ru-Bin
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.13
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    • pp.5455-5461
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    • 2014
  • Background: Saponins are a major active component for the traditional Chinese medicine, Rubus parvifolius L., which has shown clear antitumor activities. However, the specific effects and mechanisms of saponins of Rubus parvifolius L. (SRP) remain unclear with regard to human chronic myeloid leukemia cells. The aim of this study was to investigate inhibition of proliferation and apoptosis induction effects of SRP in K562 cells and further elucidate its regulatory mechanisms. Materials and Methods: K562 cells were treated with different concentrations of SRP and MTT assays were performed to determine cell viability. Apoptosis induction by SRP was determined with FACS and DAPI staining analysis. Western blotting was used to detect expression of apoptosis and survival related genes. Specific inhibitors were added to confirm roles of STAT3 and AMPK pathways in SRP induction of apoptosis. Results: Our results indicated that SRP exhibited obvious inhibitory effects on the growth of K562 cells, and significantly induced apoptosis. Cleavage of pro-apoptotic proteins was dramatically increased after SRP exposure. SRP treatment also increased the activities of AMPK and JNK pathways, and inhibited the phosphorylation expression level of STAT3 in K562 cells. Inhibition of the AMPK pathway blocked the activation of JNK by SRP, indicating that SRP regulated the expression of JNK dependent oon the AMPK pathway. Furthermore, inhibition of the latter significantly conferred resistance to SRP pro-apoptotic activity, suggesting involvement of the AMPK pathway in induction of apoptosis. Pretreatment with a STAT3 inhibitor also augmented SRP induced growth inhibition and cell apoptosis, further confirming roles of the STAT3 pathway after SRP treatment. Conclusions: Our results demonstrated that SRP induce cell apoptosis through AMPK activation and STAT3 inhibition in K562 cells. This suggests the possibility of further developing SRP as an alternative treatment option, or perhaps using it as adjuvant chemotherapeutic agent for chronic myeloid leukemia therapy.

Induction of Apoptosis by Combination Treatment with Luteolin and TRAIL in T24 Human Bladder Cancer Cells (T24 방광암세포에서 Luteolin과 TRAIL의 복합 처리에 따른 Apoptosis 유도)

  • Park, Hyun Soo;Choi, Yung Hyun
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.42 no.9
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    • pp.1363-1369
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    • 2013
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can selectively induce apoptosis by targeting cancer cells. However, some cancer cells are resistant to TRAIL-induced cytotoxicity. One method of overcoming TRAIL resistance is combination treatment with reagents to sensitize cells to TRAIL. Luteolin, a flavonoid, has been shown to have anti-cancer effects by inducing apoptosis and cell cycle arrest in various cancer cell lines in vitro. In this study, we investigated the effects of combination treatment with non-toxic concentration of TRAIL and luteolin in T24 human bladder cancer cells. Combined treatment with luteolin and TRAIL significantly inhibits cell proliferation via activation of caspases by inducing Bid truncation, up-regulation of Bax and down-regulation of X-linked inhibitor of apoptosis protein (XIAP). However, the apoptotic effects of combination treatment with luteolin and TRAIL were significantly inhibited by specific caspases inhibitors. Taken together, these results indicate that combination treatment with TRAIL and luteolin can induce apoptosis in TRAIL-resistant cancer cells through down-regulation of XIAP and modulation of tBid and Bax expression.

Hypoxia-inducible factor 1α inhibitor induces cell death via suppression of BCR-ABL1 and Met expression in BCR-ABL1 tyrosine kinase inhibitor sensitive and resistant chronic myeloid leukemia cells

  • Masanobu Tsubaki;Tomoya Takeda;Takuya Matsuda;Akihiro Kimura;Remi Tanaka;Sakiko Nagayoshi;Tadafumi Hoshida;Kazufumi Tanabe;Shozo Nishida
    • BMB Reports
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    • v.56 no.2
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    • pp.78-83
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    • 2023
  • Chronic myeloid leukemia (CML) has a markedly improved prognosis with the use of breakpoint cluster region-abelson 1 (BCR-ABL1) tyrosine kinase inhibitors (BCR-ABL1 TKIs). However, approximately 40% of patients are resistant or intolerant to BCR-ABL1 TKIs. Hypoxia-inducible factor 1α (HIF-1α) is a hypoxia response factor that has been reported to be highly expressed in CML patients, making it a therapeutic target for BCR-ABL1 TKI-sensitive CML and BCR-ABL1 TKI-resistant CML. In this study, we examined whether HIF-1α inhibitors induce cell death in CML cells and BCR-ABL1 TKI-resistant CML cells. We found that echinomycin and PX-478 induced cell death in BCR-ABL1 TKIs sensitive and resistant CML cells at similar concentrations while the cell sensitivity was not affected with imatinib or dasatinib in BCR-ABL1 TKIs resistant CML cells. In addition, echinomycin and PX-478 inhibited the c-Jun N-terminal kinase (JNK), Akt, and extracellular-regulated protein kinase 1/2 (ERK1/2) activation via suppression of BCR-ABL1 and Met expression in BCR-ABL1 sensitive and resistant CML cells. Moreover, treatment with HIF-1α siRNA induced cell death by inhibiting BCR-ABL1 and Met expression and activation of JNK, Akt, and ERK1/2 in BCR-ABL1 TKIs sensitive and resistant CML cells. These results indicated that HIF-1α regulates BCR-ABL and Met expression and is involved in cell survival in CML cells, suggesting that HIF-1α inhibitors induce cell death in BCR-ABL1 TKIs sensitive and resistant CML cells and therefore HIF-1α inhibitors are potential candidates for CML treatment.

Botrytis cinerea hypovirulent strain △BcSpd1 induced Panax ginseng defense

  • Shuhan Zhang;Junyou Han;Ning Liu;Jingyuan Sun;Huchen Chen;Jinglin Xia;Huiyan Ju;Shouan Liu
    • Journal of Ginseng Research
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    • v.47 no.6
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    • pp.773-783
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    • 2023
  • Background: Gray mold, caused by Botrytis cinerea, is one of the major fungal diseases in agriculture. Biological methods are preferred over chemical fungicides to control gray mold since they are less toxic to the environment and could induce the resistance to pathogens in plants. In this work, we try to understand if ginseng defense to B. cinerea could be induced by fungal hypovirulent strain △BcSpd1. BcSpd1 encodes Zn(II)2Cys6 transcription factor which regulates fungal pathogenicity and we recently reported △BcSpd1 mutants reduced fungal virulence. Methods: We performed transcriptomic analysis of the host to investigate the induced defense response of ginseng treated by B. cinerea △BcSpd1. The metabolites in ginseng flavonoids pathway were determined by UPLC-ESI-MS/MS and the antifungal activates were then performed. Results: We found that △BcSpd1 enhanced the ginseng defense response when applied to healthy ginseng leaves and further changed the metabolism of flavonoids. Compared with untreated plants, the application of △BcSpd1 on ginseng leaves significantly increased the accumulation of p-coumaric acid and myricetin, which could inhibit the fungal growth. Conclusion: B. cinerea △BcSpd1 could effectively induce the medicinal plant defense and is referred to as the biological control agent in ginseng disease management.