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  • 1
    In: Evidence-Based Complementary and Alternative Medicine, Hindawi Limited, Vol. 2016 ( 2016), p. 1-17
    Abstract: Objective . The aim of this systematic review is to evaluate the efficacy and safety of herbal medicines in the management of metabolic syndrome. Materials and Methods . On December 9, 2015, we searched PubMed, EMBASE, Cochrane Library, SCOPUS, AMED, CNKI, KoreaMed, KMBASE, OASIS, and J-STAGE with no restriction on language or published year. We selected randomized controlled trials that involved patients with metabolic syndrome being treated with herbal medicines as intervention. The main keywords were “Chinese herbal medicines”, “metabolic syndrome”, and “randomized controlled trials”. Herbal substances which were not based on East Asian medical theory, combination therapy with western medicines, and concurrent diseases other than metabolic syndrome were excluded. The risk of bias was assessed by Cochrane’s “Risk of Bias” tool. The protocol or review was registered in PROSPERO (an international prospective register of systematic reviews) ( CRD42014006842 ). Results . From 1,098 articles, 12 RCTs were included in this review: five trials studied herbal medicines versus a placebo or no treatment, and seven trials studied herbal medicines versus western medicines. Herbal medicines were effective on decreasing waist circumference, blood glucose, blood lipids, and blood pressure. Conclusion . This study suggests the possibility that herbal medicines can be complementary and alternative medicines for metabolic syndrome.
    Type of Medium: Online Resource
    ISSN: 1741-427X , 1741-4288
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2016
    detail.hit.zdb_id: 2148302-4
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  • 2
    In: Stem Cells International, Hindawi Limited, Vol. 2016 ( 2016), p. 1-11
    Abstract: Although hypoxic environments have been known to regulate the migratory ability of bone marrow-derived mesenchymal stem cells (BM-MSCs), which is a critical factor for maximizing the therapeutic effect, the underlying mechanisms remain unclear. Therefore, we aimed to confirm the effect of hypoxia-inducible factor-1 α (HIF-1 α ) on the migration of BM-MSCs and to analyze the interaction between HIF-1 α and integrin-mediated signals. Hypoxia-activated HIF-1 α significantly increased BM-MSC migration. The expression of integrin α 4 was decreased in BM-MSCs by increased HIF-1 α under hypoxia, whereas the expression of Rho-associated kinase 1 (ROCK1) and Rac1/2/3 was increased. After downregulation of HIF-1 α by YC-1, which is an inhibitor of HIF-1 α , BM-MSC migration was decreased via upregulation of integrin α 4 and downregulation of ROCK1 and Rac1/2/3. Knockdown of integrin α 4 by integrin α 4 siRNA (siITGA4) treatment increased BM-MSC migration by upregulation of ROCK1, Rac1/2/3, and matrix metalloproteinase-2 regardless of oxygen tension. Moreover, siITGA4 treatment increased HIF-1 α expression and augmented the translocation of HIF-1 α into the nucleus under hypoxia. Taken together, the alternative expression of HIF-1 α induced by microenvironment factors, such as hypoxia and integrin α 4 , may regulate the migration of BM-MSCs. These findings may provide insights to the underlying mechanisms of BM-MSC migration for successful stem cell-based therapy.
    Type of Medium: Online Resource
    ISSN: 1687-966X , 1687-9678
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2016
    detail.hit.zdb_id: 2573856-2
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  • 3
    In: BioMed Research International, Hindawi Limited, Vol. 2022 ( 2022-5-5), p. 1-19
    Abstract: Although many anticancer drugs have been developed for triple-negative breast cancer (TNBC) treatment, there are no obvious therapies. Moreover, the combination of epidermal growth factor receptor- (EGFR-) targeted therapeutics and classical chemotherapeutic drugs has been assessed in clinical trials for TNBC treatment, but those are not yet approved. Our serial studies for newly developed herbal medicine named SH003 provide evidence of its broad effectiveness in various cancers, especially on TNBC. The current study demonstrates a synergic effect of combinatorial treatment of SH003 and docetaxel (DTX) by targeting EGFR activation. The combinatorial treatment reduced the viability of both BT-20 and MDA-MB-231 TNBC cells, displaying the synergism. The combination of SH003 and DTX also caused the synergistic effect on apoptosis. Mechanistically, the cotreatment of SH003 and DTX inhibited phosphorylation of EGFR and AKT in both BT-20 and MDA-MB-231 cells. Moreover, our xenograft mouse tumor growth assays showed the inhibitory effect of the combinatorial treatment with no effect on body weight. Our immunohistochemistry confirmed its inhibition of EGFR phosphorylation in vivo. Collectively, combinatorial treatment of SH003 and DTX has a synergistic anticancer effect at a relatively low concentration by targeting EGFR in TNBC, indicating safety and efficacy of SH003 as adjuvant combination therapy with docetaxel. Thus, it is worth testing the combinatorial effect in clinics for treating TNBC.
    Type of Medium: Online Resource
    ISSN: 2314-6141 , 2314-6133
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2698540-8
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  • 4
    Online Resource
    Online Resource
    Hindawi Limited ; 2021
    In:  Evidence-Based Complementary and Alternative Medicine Vol. 2021 ( 2021-8-10), p. 1-10
    In: Evidence-Based Complementary and Alternative Medicine, Hindawi Limited, Vol. 2021 ( 2021-8-10), p. 1-10
    Abstract: Docetaxel-based therapy has been applied to kill cancers including lung and breast cancers but frequently causes peripheral neuropathy such as mechanical allodynia. Lack of effective drugs for chemotherapy-induced peripheral neuropathy (CIPN) treatment leads us to find novel drugs. Here, we investigated whether and how novel anticancer herbal prescription SH003 alleviates mechanical allodynia in mouse model of docetaxel-induced neuropathic pain. Docetaxel-induced mechanical allodynia was evaluated using von Frey filaments. Nerve damage and degeneration in paw skin of mice were investigated by immunofluorescence staining. Neuroinflammation markers in bloodstream, lumbar (L4-L6) spinal cord, and sciatic nerves were examined by ELISA or western blot analysis. Docetaxel (15.277 mg/kg) was intravenously injected into the tail vein of C57BL/6 mice, and mechanical allodynia was followed up. SH003 (557.569 mg/kg) was orally administered at least 60 min before the mechanical allodynia test, and von Frey test was performed twice. Docetaxel injection induced mechanical allodynia, and SH003 administration restored withdrawal threshold. Meanwhile, degeneration of intraepidermal nerve fibers (IENF) was observed in docetaxel-treated mice, but SH003 treatment suppressed it. Moreover, docetaxel injection increased levels of TNF-α and IL-6 in plasma and expressions of phospho-NF-κB and phospho-STAT3 in both of lumbar spinal cord and sciatic nerves, while SH003 treatment inhibited those changes. Taken together, it is worth noting that TNF-α and IL-6 in plasma and phospho-NF-κB and phospho-STAT3 in spinal cord and sciatic nerves are putative biomarkers of docetaxel-induced peripheral neuropathy (DIPN) in mouse models. In addition, we suggest that SH003 would be beneficial for alleviation of docetaxel-induced neuropathic pain.
    Type of Medium: Online Resource
    ISSN: 1741-4288 , 1741-427X
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2148302-4
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  • 5
    Online Resource
    Online Resource
    Hindawi Limited ; 2012
    In:  The Scientific World Journal Vol. 2012 ( 2012), p. 1-6
    In: The Scientific World Journal, Hindawi Limited, Vol. 2012 ( 2012), p. 1-6
    Abstract: As one of the effective control devices of air pollutants, the wet electrostatic precipitator (ESP) is an effective technique to eliminate acid mist and fine particles that are re-entrained in a collection electrode. However, its collection efficiency can deteriorate, as its operation is subject to water-induced corrosion of the collection electrode. To overcome this drawback, we modified the wet ESP system with the installation of a PVC dust precipitator wherein water is supplied as a replacement of the collection electrode. With this modification, we were able to construct a compact wet ESP with a small specific collection area (SCA, 0.83 m 2 /(m 3 /min)) that can acquire a high collection efficiency of fine particles (99.7%).
    Type of Medium: Online Resource
    ISSN: 1537-744X
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2012
    detail.hit.zdb_id: 2075968-X
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  • 6
    In: BioMed Research International, Hindawi Limited, Vol. 2015 ( 2015), p. 1-9
    Abstract: Graphene is receiving increased attention due to its potential widespread applications in future. However, the health effects of graphene have not yet been well studied. Therefore, this study examined the pulmonary effects of graphene oxide using male Sprague-Dawley rats and a single 6-hour nose-only inhalation technique. Following the exposure, the rats were allowed to recover for 1 day, 7 days, or 14 days. A total of three groups were compared: control (fresh air), low concentration ( 0.46 ± 0.06  mg/m 3 ), and high concentration ( 3.76 ± 0.24  mg/m 3 ). The exposure to graphene oxide did not induce significant changes in the body weights, organ weights, and food consumption during the 14 days of recovery time. The microalbumin and lactate dehydrogenase levels in the bronchoalveolar lavage (BAL) fluid were not significantly changed due to the exposure. Similarly, total cell count, macrophages, polymorphonuclear leukocytes, and lymphocytes were not significantly altered in the BAL fluid. Plus, the histopathological examination of the rat lungs only showed an uptake of graphene oxide in the alveolar macrophages of the high-concentration group. Therefore, these results demonstrate that the single inhalation exposure to graphene oxide induce minimal toxic responses in rat lungs at the concentrations and time points used in the present study.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2015
    detail.hit.zdb_id: 2698540-8
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