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  1. Article ; Online: A review on the use of extracellular vesicles for the delivery of drugs and biological therapeutics.

    Amina, Sundus Jabeen / Azam, Tasmia / Dagher, Fatima / Guo, Bin

    Expert opinion on drug delivery

    2024  Volume 21, Issue 1, Page(s) 45–70

    Abstract: Introduction: Exosomes, a type of extracellular vesicles, are effective tools for delivering small-molecule drugs and biological therapeutics into cells and tissues. Surface modifications with targeting ligands ensure precise delivery to specific cells, ...

    Abstract Introduction: Exosomes, a type of extracellular vesicles, are effective tools for delivering small-molecule drugs and biological therapeutics into cells and tissues. Surface modifications with targeting ligands ensure precise delivery to specific cells, minimizing accumulation in healthy organs and reducing the side effects. This is a rapidly growing area in drug delivery research and this review aims to comprehensively discuss the recent advances in the field.
    Area covered: Recent studies have presented compelling evidence supporting the application of exosomes as efficient delivery vehicles that escape endosome trapping, achieving effective in vivo delivery in animal models. This review provides a systemic discussion on the exosome-based delivery technology, with topics covering exosome purification, surface modification, and targeted delivery of various cargos ranging from siRNAs, miRNAs, and proteins, to small molecule drugs.
    Expert opinion: Exosome-based gene and drug delivery has low toxicity and low immunogenicity. Surface modifications of the exosomes can effectively avoid endosome trapping and increase delivery efficiency. This exciting technology can be applied to improve the treatments for a wide variety of diseases.
    MeSH term(s) Animals ; Pharmaceutical Preparations/metabolism ; Extracellular Vesicles ; Exosomes/metabolism ; Drug Delivery Systems ; Endosomes
    Chemical Substances Pharmaceutical Preparations
    Language English
    Publishing date 2024-01-31
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2167286-6
    ISSN 1744-7593 ; 1742-5247
    ISSN (online) 1744-7593
    ISSN 1742-5247
    DOI 10.1080/17425247.2024.2305115
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6012: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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  2. Article: Neratinib causes non-recoverable gut injury and reduces intestinal cytochrome P450 3A enzyme in mice.

    Tao, Gabriel / Dagher, Fatima / Ghose, Romi

    Toxicology research

    2022  Volume 11, Issue 1, Page(s) 184–194

    Abstract: Neratinib is a pan-HER tyrosine kinase inhibitor newly approved by FDA in 2017 to treat HER2-positive breast cancer, but the phase III trial of neratinib showed that 96% of the patients taking neratinib experienced diarrhea. So far very few mechanistic ... ...

    Abstract Neratinib is a pan-HER tyrosine kinase inhibitor newly approved by FDA in 2017 to treat HER2-positive breast cancer, but the phase III trial of neratinib showed that 96% of the patients taking neratinib experienced diarrhea. So far very few mechanistic studies explore neratinib-induced gastrointestinal (GI) toxicity. Hereby, we performed toxicity studies in mice to characterize the potential mechanism underlying this adverse effect. C57BL/6 J mice were separated into three groups A, B, C. Group A received vehicle; group B was orally dosed with 100 mg/kg neratinib once daily for 18 days. Group C was dosed with 100 mg/kg neratinib for 12 days and switched to vehicle for 6 days. Intestine and liver were collected for further analysis. Human intestine-derived cells were treated with neratinib
    Language English
    Publishing date 2022-01-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 2684701-2
    ISSN 2045-4538 ; 2045-452X
    ISSN (online) 2045-4538
    ISSN 2045-452X
    DOI 10.1093/toxres/tfab111
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Irinotecan decreases intestinal UDP-glucuronosyltransferase (UGT) 1A1 via TLR4/MyD88 pathway prior to the onset of diarrhea

    Tao, Gabriel / Dagher, Fatima / Li, Li / Singh, Rashim / Hu, Ming / Ghose, Romi

    Food and Chemical Toxicology. 2022 Aug., v. 166 p.113246-

    2022  

    Abstract: Irinotecan is a first-line treatment for colorectal cancer and the prodrug of 7-ethyl-10-hydroxy-camptothecin (SN-38). However, its fatal gastrointestinal (GI) toxicity raises serious concern. In liver, irinotecan generates its inactive metabolite, SN- ... ...

    Abstract Irinotecan is a first-line treatment for colorectal cancer and the prodrug of 7-ethyl-10-hydroxy-camptothecin (SN-38). However, its fatal gastrointestinal (GI) toxicity raises serious concern. In liver, irinotecan generates its inactive metabolite, SN-38G via UDP-glucuronosyltransferase (UGT)1A1. Subsequently, SN-38G is excreted into GI tract where it is reactivated by microbiome to yield the toxic metabolite, SN-38. Activation of toll-like receptor (TLR)/myeloid differentiation primary response 88 (MyD88) by bacterial endotoxin decreases drug-metabolizing enzymes. In this study, we treated C57BL6/J mice with 50 mg/kg irinotecan once daily until observing grade 4 diarrhea. Mice were sacrificed on day0, day2 and day8. Based on the finding in C57BL6/J mice, we repeated the treatment in Tlr2⁻/⁻, Tlr4⁻/⁻ and Myd88⁻/⁻ mice to determine the impact of inflammation on UGT metabolism. Our toxicity study in C57BL6/J mice showed that mice started bloody diarrhea after 6 days’ injection of irinotecan. Ugt1a1 expression in GI tract started decreasing after 24h since first dose, before the onset of diarrhea. In Tlr4⁻/⁻ and Myd88⁻/⁻ mice, no Ugt1a1 reduction was observed in distal GI tract after irinotecan injection. In Tlr2⁻/⁻ mice, intestinal Ugt1a1 expression was down-regulated. Our results indicate that after two doses of irinotecan, mice started losing capability of detoxifying SN-38. TLR4 plays more important role in Ugt1a1 reduction than TLR2, despite that TLR2 and TLR4 share MyD88 as common adaptor protein. We concluded that irinotecan reduced intestinal Ugt1a1 via TLR4/MyD88 pathway, which eventually triggers the onset of diarrhea. Our finding unveils a novel mechanism underlying irinotecan-induced diarrhea and provides a new direction to prevent chemotherapy side effect.
    Keywords Toll-like receptors ; adverse effects ; colorectal neoplasms ; diarrhea ; digestive tract ; drug therapy ; endotoxins ; glucuronosyltransferases ; inflammation ; intestines ; liver ; metabolism ; metabolites ; microbiome ; toxicity ; toxicology ; Irinotecan ; UDP-glucuronosyltransferase1A1 ; Toll-like receptor ; Drug metabolism
    Language English
    Dates of publication 2022-08
    Publishing place Elsevier Ltd
    Document type Article ; Online
    ZDB-ID 782617-5
    ISSN 1873-6351 ; 0278-6915
    ISSN (online) 1873-6351
    ISSN 0278-6915
    DOI 10.1016/j.fct.2022.113246
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 4035: Show issues

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  4. Article ; Online: Irinotecan decreases intestinal UDP-glucuronosyltransferase (UGT) 1A1 via TLR4/MyD88 pathway prior to the onset of diarrhea.

    Tao, Gabriel / Dagher, Fatima / Li, Li / Singh, Rashim / Hu, Ming / Ghose, Romi

    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

    2022  Volume 166, Page(s) 113246

    Abstract: Irinotecan is a first-line treatment for colorectal cancer and the prodrug of 7-ethyl-10-hydroxy-camptothecin (SN-38). However, its fatal gastrointestinal (GI) toxicity raises serious concern. In liver, irinotecan generates its inactive metabolite, SN- ... ...

    Abstract Irinotecan is a first-line treatment for colorectal cancer and the prodrug of 7-ethyl-10-hydroxy-camptothecin (SN-38). However, its fatal gastrointestinal (GI) toxicity raises serious concern. In liver, irinotecan generates its inactive metabolite, SN-38G via UDP-glucuronosyltransferase (UGT)1A1. Subsequently, SN-38G is excreted into GI tract where it is reactivated by microbiome to yield the toxic metabolite, SN-38. Activation of toll-like receptor (TLR)/myeloid differentiation primary response 88 (MyD88) by bacterial endotoxin decreases drug-metabolizing enzymes. In this study, we treated C57BL6/J mice with 50 mg/kg irinotecan once daily until observing grade 4 diarrhea. Mice were sacrificed on day0, day2 and day8. Based on the finding in C57BL6/J mice, we repeated the treatment in Tlr2
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Antineoplastic Agents, Phytogenic/pharmacology ; Camptothecin/toxicity ; Diarrhea/chemically induced ; Diarrhea/metabolism ; Glucuronosyltransferase/metabolism ; Irinotecan/adverse effects ; Mice ; Myeloid Differentiation Factor 88/genetics ; Myeloid Differentiation Factor 88/metabolism ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 4/metabolism ; Uridine Diphosphate
    Chemical Substances Adaptor Proteins, Signal Transducing ; Antineoplastic Agents, Phytogenic ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; Tlr4 protein, mouse ; Toll-Like Receptor 2 ; Toll-Like Receptor 4 ; Uridine Diphosphate (58-98-0) ; Irinotecan (7673326042) ; UGT1A1 enzyme (EC 2.4.1.-) ; Glucuronosyltransferase (EC 2.4.1.17) ; Camptothecin (XT3Z54Z28A)
    Language English
    Publishing date 2022-06-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 782617-5
    ISSN 1873-6351 ; 0278-6915
    ISSN (online) 1873-6351
    ISSN 0278-6915
    DOI 10.1016/j.fct.2022.113246
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 529: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Corrigendum to "Irinotecan decreases intestinal UDP-glucuronosyltransferase (UGT) 1A1 via TLR4/MyD88 pathway prior to the onset of diarrhea" [Food Chem. Toxicol. 166 (2022) 113246].

    Tao, Gabriel / Dagher, Fatima / Li, Li / Singh, Rashim / Hu, Ming / Ghose, Romi

    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

    2022  Volume 171, Page(s) 113547

    Language English
    Publishing date 2022-12-08
    Publishing country England
    Document type Published Erratum
    ZDB-ID 782617-5
    ISSN 1873-6351 ; 0278-6915
    ISSN (online) 1873-6351
    ISSN 0278-6915
    DOI 10.1016/j.fct.2022.113547
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 529: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article: Dietary phytochemical and metabolic disease prevention: Focus on plant proteins.

    Yang, Song-Hong / Tao, Gabriel / Yang, Liu / Wu, Xiaohui / Liu, Jing-Wen / Dagher, Fatima / Ou, Shi-Yi / Song, Yuan / Huang, Jun-Qing

    Frontiers in nutrition

    2023  Volume 10, Page(s) 1089487

    Abstract: Plant-based functional foods have attracted increasing research interest to validate their use in preventing metabolic disease. Since it is increasingly recognized that inflammation, oxidative stress, and circadian rhythm play vital roles in various ... ...

    Abstract Plant-based functional foods have attracted increasing research interest to validate their use in preventing metabolic disease. Since it is increasingly recognized that inflammation, oxidative stress, and circadian rhythm play vital roles in various metabolic diseases, including diabetes, obesity and non-alcoholic liver disease, plant proteins, protein hydrolysates, and food extracts that intervene in these biological processes are promising dietary supplements to prevent metabolic diseases. Here, we reviewed the recent research on plant-based foods used for metabolic disease prevention and provided new perspectives regarding the current study gaps and future directions in this field.
    Language English
    Publishing date 2023-01-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2776676-7
    ISSN 2296-861X
    ISSN 2296-861X
    DOI 10.3389/fnut.2023.1089487
    Database MEDical Literature Analysis and Retrieval System OnLINE

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