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  1. Article ; Online: Targeting autophagy enhances BO-1051-induced apoptosis in human malignant glioma cells.

    Chu, Pei-Ming / Chen, Li-Hsin / Chen, Ming-Teh / Ma, Hsin-I / Su, Tsann-Long / Hsieh, Pei-Chen / Chien, Chian-Shiu / Jiang, Bo-Hua / Chen, Yu-Chih / Lin, Yi-Hui / Shih, Yang-Hsin / Tu, Pang-Hsien / Chiou, Shih-Hwa

    Cancer chemotherapy and pharmacology

    2012  Volume 69, Issue 3, Page(s) 621–633

    Abstract: Purpose: BO-1051 is an N-mustard derivative that is conjugated with DNA-affinic 9-anilinoacridine ... Since BO-1051 was reported to have strong anticancer activity, we investigated the effect and underlying ... mechanism of BO-1051 in human glioma cell lines.: Methods: Human glioma cell lines U251MG and U87MG were ...

    Abstract Purpose: BO-1051 is an N-mustard derivative that is conjugated with DNA-affinic 9-anilinoacridine. Since BO-1051 was reported to have strong anticancer activity, we investigated the effect and underlying mechanism of BO-1051 in human glioma cell lines.
    Methods: Human glioma cell lines U251MG and U87MG were studied with BO-1051 or the combination of BO-1051 and autophagic inhibitors. Growth inhibition was assessed by MTT assay. Apoptosis was measured by annexin V staining followed by flow cytometry and immunoblotting for apoptosis-related molecules. Induction of autophagy was detected by acridine orange labeling, electron microscopy, LC3 localization and its conversion. Transfection of shRNA was used to determine the involvement of Beclin1 in apoptotic cell death.
    Results: MTT assay showed that BO-1051 suppressed the viability of four glioma cell lines (U251MG, U87MG, GBM-3 and DBTRG-05MG) in a dose-dependent manner. The IC(50) values of BO-1051 for the glioma cells were significantly lower than the values for primary neurons cultures and normal fibroblast cells. Moreover, BO-1051 not only induced apoptotic cell death, but also enhanced autophagic flux via inhibition of Akt/mTOR and activation of Erk1/2. Importantly, suppression of autophagy by 3-methyladenine or bafilomycin A1 significantly increased BO-1051-induced apoptotic cell death in U251MG and U87MG cells. In addition, the proportion of apoptotic cells after BO-1051 treatment was enhanced by co-treatment with shRNA against Beclin1.
    Conclusions: BO-1051 induced both apoptosis and autophagy, and inhibition of autophagy significantly augmented the cytotoxic effect of BO-1051. Thus, a combination of BO-1051 and autophagic inhibitors offers a potentially new therapeutic modality for the treatment of malignant glioma.
    MeSH term(s) Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Autophagy/drug effects ; Blotting, Western ; Brain Neoplasms/drug therapy ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Cell Culture Techniques ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Glioma/drug therapy ; Glioma/metabolism ; Glioma/pathology ; Humans ; MAP Kinase Signaling System/drug effects ; Membrane Potential, Mitochondrial/drug effects ; Microscopy, Electron, Transmission ; Microscopy, Fluorescence ; Microscopy, Phase-Contrast ; Molecular Structure ; Nitrogen Mustard Compounds/chemistry ; Nitrogen Mustard Compounds/pharmacology ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; TOR Serine-Threonine Kinases/antagonists & inhibitors
    Chemical Substances Antineoplastic Agents ; BO-1051 ; Nitrogen Mustard Compounds ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2012-03
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 6820-2
    ISSN 1432-0843 ; 0344-5704 ; 0943-9404
    ISSN (online) 1432-0843
    ISSN 0344-5704 ; 0943-9404
    DOI 10.1007/s00280-011-1747-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Autophagy inhibition enhances apoptosis triggered by BO-1051, an N-mustard derivative, and involves the ATM signaling pathway.

    Chen, Li-Hsin / Loong, Che-Chuan / Su, Tsann-Long / Lee, Yi-Jang / Chu, Pei-Ming / Tsai, Ming-Long / Tsai, Ping-Hsin / Tu, Pang-Hsien / Chi, Chin-Wen / Lee, Hsin-Chen / Chiou, Shih-Hwa

    Biochemical pharmacology

    2011  Volume 81, Issue 5, Page(s) 594–605

    Abstract: In a previous study, BO-1051, an N-mustard linked with a DNA-affinic molecule, was shown to target ... as well as the underlying mechanism, of BO-1051. We found that BO-1051 simultaneously induced apoptosis ... and autophagy in hepatocellular carcinoma cell lines. DNA double strand breaks induced by BO-1051 ...

    Abstract In a previous study, BO-1051, an N-mustard linked with a DNA-affinic molecule, was shown to target various types of cancer cell lines. In the present study, we aimed to investigate the cytotoxicity, as well as the underlying mechanism, of BO-1051. We found that BO-1051 simultaneously induced apoptosis and autophagy in hepatocellular carcinoma cell lines. DNA double strand breaks induced by BO-1051 activated the ATM signaling pathway and subsequently resulted in caspase-dependent apoptosis. When autophagy was inhibited in its early or late stages, apoptosis was significantly enhanced. This result indicated autophagy as a cytoprotective effect against BO-1051-induced cell death. We further inhibited ATM activation using an ATM kinase inhibitor or ATM-specific siRNA and found that while apoptosis was blocked, autophagy also diminished in response to BO-1051. We not only determined a signaling pathway induced by BO-1051 but also clarified the linkage between DNA damage-induced apoptosis and autophagy. We also showed that BO-1051-induced autophagy acts as a cytoprotective reaction and downstream target of the ATM-signaling pathway. This research revealed autophagy as a universal cytoprotective response against DNA damage-inducing chemotherapeutic agents, including BO-1051, cisplatin, and doxorubicin, in hepatocellular carcinoma cell lines. Autophagy contributes to the remarkable drug resistance ability of liver cancer.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Ataxia Telangiectasia Mutated Proteins ; Autophagy/drug effects ; Carcinoma, Hepatocellular ; Cell Cycle Proteins/physiology ; Cell Line, Tumor ; DNA Damage ; DNA-Binding Proteins/physiology ; Humans ; Liver Neoplasms ; Nitrogen Mustard Compounds/pharmacology ; Protein-Serine-Threonine Kinases/physiology ; Signal Transduction ; Tumor Suppressor Proteins/physiology
    Chemical Substances Antineoplastic Agents ; BO-1051 ; Cell Cycle Proteins ; DNA-Binding Proteins ; Nitrogen Mustard Compounds ; Tumor Suppressor Proteins ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2011-03-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2010.12.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Enhancement of radiosensitivity in human glioblastoma cells by the DNA N-mustard alkylating agent BO-1051 through augmented and sustained DNA damage response.

    Chu, Pei-Ming / Chiou, Shih-Hwa / Su, Tsann-Long / Lee, Yi-Jang / Chen, Li-Hsin / Chen, Yi-Wei / Yen, Sang-Hue / Chen, Ming-Teh / Chen, Ming-Hsiung / Shih, Yang-Hsin / Tu, Pang-Hsien / Ma, Hsin-I

    Radiation oncology (London, England)

    2011  Volume 6, Page(s) 7

    Abstract: ... phenyl]urea (BO-1051) is an N-mustard DNA alkylating agent reported to exhibit antitumor activity. Here ... the IC50 and radiosensitivity of human glioma cell lines (U87MG, U251MG and GBM-3) following BO-1051. DNA ... the survival rate was determined using Kaplan-Meier method.: Results: BO-1051 inhibited growth of human gliomas ...

    Abstract Background: 1-{4-[Bis(2-chloroethyl)amino]phenyl}-3-[2-methyl-5-(4-methylacridin-9-ylamino)phenyl]urea (BO-1051) is an N-mustard DNA alkylating agent reported to exhibit antitumor activity. Here we further investigate the effects of this compound on radiation responses of human gliomas, which are notorious for the high resistance to radiotherapy.
    Methods: The clonogenic assay was used to determine the IC50 and radiosensitivity of human glioma cell lines (U87MG, U251MG and GBM-3) following BO-1051. DNA histogram and propidium iodide-Annexin V staining were used to determine the cell cycle distribution and the apoptosis, respectively. DNA damage and repair state were determined by γ-H2AX foci, and mitotic catastrophe was measure using nuclear fragmentation. Xenograft tumors were measured with a caliper, and the survival rate was determined using Kaplan-Meier method.
    Results: BO-1051 inhibited growth of human gliomas in a dose- and time-dependent manner. Using the dosage at IC50, BO-1051 significantly enhanced radiosensitivity to different extents [The sensitizer enhancement ratio was between 1.24 and 1.50 at 10% of survival fraction]. The radiosensitive G2/M population was raised by BO-1051, whereas apoptosis and mitotic catastrophe were not affected. γ-H2AX foci was greatly increased and sustained by combined BO-1051 and γ-rays, suggested that DNA damage or repair capacity was impaired during treatment. In vivo studies further demonstrated that BO-1051 enhanced the radiotherapeutic effects on GBM-3-beared xenograft tumors, by which the sensitizer enhancement ratio was 1.97. The survival rate of treated mice was also increased accordingly.
    Conclusions: These results indicate that BO-1051 can effectively enhance glioma cell radiosensitivity in vitro and in vivo. It suggests that BO-1051 is a potent radiosensitizer for treating human glioma cells.
    MeSH term(s) Animals ; Antineoplastic Agents, Alkylating/pharmacology ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Brain Neoplasms/radiotherapy ; Cell Line, Tumor ; DNA Damage/drug effects ; DNA, Neoplasm/drug effects ; DNA, Neoplasm/radiation effects ; Dose-Response Relationship, Drug ; Female ; Glioblastoma/genetics ; Glioblastoma/pathology ; Glioblastoma/radiotherapy ; Humans ; Mice ; Mice, Nude ; Models, Biological ; Nitrogen Mustard Compounds/pharmacology ; Radiation Tolerance/drug effects ; Radiation-Sensitizing Agents/pharmacology ; Up-Regulation/drug effects ; Xenograft Model Antitumor Assays
    Chemical Substances Antineoplastic Agents, Alkylating ; BO-1051 ; DNA, Neoplasm ; Nitrogen Mustard Compounds ; Radiation-Sensitizing Agents
    Language English
    Publishing date 2011-01-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1748-717X
    ISSN (online) 1748-717X
    DOI 10.1186/1748-717X-6-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Autophagy inhibition enhances apoptosis triggered by BO-1051, an N-mustard derivative, and involves the ATM signaling pathway

    Chen, Li-Hsin / Loong, Che-Chuan / Su, Tsann-Long / Lee, Yi-Jang / Chu, Pei-Ming / Tsai, Ming-Long / Tsai, Ping-Hsin / Tu, Pang-Hsien / Chi, Chin-Wen / Lee, Hsin-Chen / Chiou, Shih-Hwa

    Biochemical Pharmacology. 2011 Mar. 1, v. 81, no. 5

    2011  

    Abstract: In a previous study, BO-1051, an N-mustard linked with a DNA-affinic molecule, was shown to target ... as well as the underlying mechanism, of BO-1051. We found that BO-1051 simultaneously induced apoptosis ... and autophagy in hepatocellular carcinoma cell lines. DNA double strand breaks induced by BO-1051 ...

    Abstract In a previous study, BO-1051, an N-mustard linked with a DNA-affinic molecule, was shown to target various types of cancer cell lines. In the present study, we aimed to investigate the cytotoxicity, as well as the underlying mechanism, of BO-1051. We found that BO-1051 simultaneously induced apoptosis and autophagy in hepatocellular carcinoma cell lines. DNA double strand breaks induced by BO-1051 activated the ATM signaling pathway and subsequently resulted in caspase-dependent apoptosis. When autophagy was inhibited in its early or late stages, apoptosis was significantly enhanced. This result indicated autophagy as a cytoprotective effect against BO-1051-induced cell death. We further inhibited ATM activation using an ATM kinase inhibitor or ATM-specific siRNA and found that while apoptosis was blocked, autophagy also diminished in response to BO-1051. We not only determined a signaling pathway induced by BO-1051 but also clarified the linkage between DNA damage-induced apoptosis and autophagy. We also showed that BO-1051-induced autophagy acts as a cytoprotective reaction and downstream target of the ATM-signaling pathway. This research revealed autophagy as a universal cytoprotective response against DNA damage-inducing chemotherapeutic agents, including BO-1051, cisplatin, and doxorubicin, in hepatocellular carcinoma cell lines. Autophagy contributes to the remarkable drug resistance ability of liver cancer.
    Keywords DNA ; apoptosis ; autophagy ; cisplatin ; cytotoxicity ; doxorubicin ; drug resistance ; hepatoma ; signal transduction
    Language English
    Dates of publication 2011-0301
    Size p. 594-605.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2010.12.011
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: Enhancement of radiosensitivity in human glioblastoma cells by the DNA N-mustard alkylating agent BO-1051 through augmented and sustained DNA damage response

    Chen Ming-Teh / Yen Sang-Hue / Chen Yi-Wei / Chen Li-Hsin / Lee Yi-Jang / Su Tsann-Long / Chiou Shih-Hwa / Chu Pei-Ming / Chen Ming-Hsiung / Shih Yang-Hsin / Tu Pang-Hsien / Ma Hsin-I

    Radiation Oncology, Vol 6, Iss 1, p

    2011  Volume 7

    Abstract: ... phenyl]urea (BO-1051) is an N-mustard DNA alkylating agent reported to exhibit antitumor activity. Here ... 50 and radiosensitivity of human glioma cell lines (U87MG, U251MG and GBM-3) following BO-1051. DNA ... the survival rate was determined using Kaplan-Meier method. Results BO-1051 inhibited growth of human gliomas ...

    Abstract Abstract Background 1-{4-[Bis(2-chloroethyl)amino]phenyl}-3-[2-methyl-5-(4-methylacridin-9-ylamino)phenyl]urea (BO-1051) is an N-mustard DNA alkylating agent reported to exhibit antitumor activity. Here we further investigate the effects of this compound on radiation responses of human gliomas, which are notorious for the high resistance to radiotherapy. Methods The clonogenic assay was used to determine the IC 50 and radiosensitivity of human glioma cell lines (U87MG, U251MG and GBM-3) following BO-1051. DNA histogram and propidium iodide-Annexin V staining were used to determine the cell cycle distribution and the apoptosis, respectively. DNA damage and repair state were determined by γ-H2AX foci, and mitotic catastrophe was measure using nuclear fragmentation. Xenograft tumors were measured with a caliper, and the survival rate was determined using Kaplan-Meier method. Results BO-1051 inhibited growth of human gliomas in a dose- and time-dependent manner. Using the dosage at IC 50 , BO-1051 significantly enhanced radiosensitivity to different extents [The sensitizer enhancement ratio was between 1.24 and 1.50 at 10% of survival fraction]. The radiosensitive G 2 /M population was raised by BO-1051, whereas apoptosis and mitotic catastrophe were not affected. γ-H2AX foci was greatly increased and sustained by combined BO-1051 and γ-rays, suggested that DNA damage or repair capacity was impaired during treatment. In vivo studies further demonstrated that BO-1051 enhanced the radiotherapeutic effects on GBM-3-beared xenograft tumors, by which the sensitizer enhancement ratio was 1.97. The survival rate of treated mice was also increased accordingly. Conclusions These results indicate that BO-1051 can effectively enhance glioma cell radiosensitivity in vitro and in vivo . It suggests that BO-1051 is a potent radiosensitizer for treating human glioma cells.
    Keywords Medical physics. Medical radiology. Nuclear medicine ; R895-920 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
    Language English
    Publishing date 2011-01-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: Shrub Growth Improves Morphological Features of Nebkhas: A Case Study of

    Cheng, Long / Wu, Bo / Pang, Yingjun / Jia, Xiaohong

    Plants (Basel, Switzerland)

    2024  Volume 13, Issue 5

    Abstract: To understand the role of shrubs in nebkha development, a comparative analysis of nebkha morphology and shrub features was conducted in two different habitats at the southeast margin of the Tengger Desert, Northern China. Morphometric variables of ... ...

    Abstract To understand the role of shrubs in nebkha development, a comparative analysis of nebkha morphology and shrub features was conducted in two different habitats at the southeast margin of the Tengger Desert, Northern China. Morphometric variables of 184
    Language English
    Publishing date 2024-02-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2704341-1
    ISSN 2223-7747
    ISSN 2223-7747
    DOI 10.3390/plants13050624
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: A comparative study on fundamental movement skills among children with autism spectrum disorder and typically developing children aged 7-10.

    Dong, Liangshan / Fan, Rong / Shen, Bo / Bo, Jin / Pang, Yanli / Song, Yu

    Frontiers in psychology

    2024  Volume 15, Page(s) 1287752

    Abstract: Background: Autism Spectrum Disorder (ASD) is a neurodevelopmental condition with unique differences in social interaction, communication, and a spectrum of behavioral characteristics. In the past, motor disturbance in individuals with ASD has not been ... ...

    Abstract Background: Autism Spectrum Disorder (ASD) is a neurodevelopmental condition with unique differences in social interaction, communication, and a spectrum of behavioral characteristics. In the past, motor disturbance in individuals with ASD has not been considered a significant core deficit due to the predominant focus on sociability and communication issues. However, recent studies indicate that motor deficits are indeed associated with the fundamental symptoms of ASD. As there is limited research on the motor behavior of children with ASD, particularly in China, the objective of this study is to investigate the development of fundamental movement skills (FMS) in children with ASD and compare them to typically developing children.
    Method: The study recruited 108 children with ASD (87 boys, 21 girls) aged 7-10 years from two special education rehabilitation centers in Wuhan, China. For comparison, a control group of 108 typically developing children, matched by age and gender, was randomly selected from three local primary schools. FMS were assessed using the Movement Assessment Battery for Children - Second Edition (MABC-2), which evaluates manual dexterity, aiming and catching, as well as static and dynamic balance. Group differences on MABC-2 percentile scores were analyzed using descriptive statistics and Mann-Whitney U test. Effect sizes were also calculated for practical significance.
    Results: Findings from the study showed that a significant majority, around 80%, of children with ASD either displayed motor challenges or were at risk of developing such delays. When comparing to their typically developing peers, children with ASD scored notably lower in areas of manual dexterity, ball skills, and both static and dynamic balance (with all these findings being statistically significant at
    Conclusion: In addition to addressing the other skill development areas outlined in the diagnostic manual for ASD, clinicians diagnosing and treating children with ASD should also assess the presence of motor skill development. For individuals with ASD who have co-existing motor difficulties, it is essential to offer evidence-based interventions tailored to their specific needs.
    Language English
    Publishing date 2024-03-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2563826-9
    ISSN 1664-1078
    ISSN 1664-1078
    DOI 10.3389/fpsyg.2024.1287752
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Empowering Medical Data Analysis

    Guan Bo / Wang Shanshan / Zhang Qing / Pang Bo / Zuo Yan

    IEEE Access, Vol 12, Pp 1650-

    An Advanced Deep Fusion Model for Sorting Medicine Document

    2024  Volume 1659

    Abstract: To enhance the accuracy of medical document classification, we propose an advanced deep fusion model for sorting medicine document. Specifically, we enhance text representation using the bidirectional encoder representation from transformers (BERT). BERT ...

    Abstract To enhance the accuracy of medical document classification, we propose an advanced deep fusion model for sorting medicine document. Specifically, we enhance text representation using the bidirectional encoder representation from transformers (BERT). BERT is a bidirectional model that considers context information in input sequences. This capability is particularly valuable for medical document, as medical information often requires understanding in a global context, such as diagnoses, medical history, and treatment plans. Furthermore, BERT can learn the semantics of words and phrases, comprehending the different meanings of the same word in distinct contexts, which is crucial for representing medical document. For example, In the context of cardiology, stroke often refers to a cerebrovascular accident, which is a condition where blood flow to the brain is disrupted, leading to neurological impairment. This type of stroke is related to the brain and is a significant concern in the field of cardiology due to its impact on the circulatory system. In dermatology, stroke might be used to refer to a type of skin condition, such as stroking the skin. However, this context is less common and not related to the cerebrovascular meaning. Subsequently, we employ both Convolutional Neural Network (ConvNet) and Bidirectional Long Short Term Memory (Bi-LSTM) to extract local features and global long-term dependencies, respectively. Their outputs are then fused to extract useful document features at multiple levels, effectively capturing the documental structure. The proposed deep fusion model leverages the complementary strengths of these components, enhancing the model’s generalization ability and mitigating the risk of over-fitting. Ultimately, by comparing our approach with state-of-the-art methods in medical document classification, we demonstrate the effectiveness of the proposed methodology.
    Keywords Medicine data analysis ; word embedding ; deep learning ; deep fusion model ; Electrical engineering. Electronics. Nuclear engineering ; TK1-9971
    Subject code 006
    Language English
    Publishing date 2024-01-01T00:00:00Z
    Publisher IEEE
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article: The role of Cyclin Dependent Kinase Inhibitor 3 (

    Zhang, Chuanlong / Shen, Qian / Gao, Mengqi / Li, Junchen / Pang, Bo

    Heliyon

    2024  Volume 10, Issue 4, Page(s) e26061

    Abstract: Background: Although many experiments and clinical studies have proved the link between the expression of : Objective: Explore the extensive tumor-promoting effects of : Methods: We systematically reviewed the literature on : Results: We found ... ...

    Abstract Background: Although many experiments and clinical studies have proved the link between the expression of
    Objective: Explore the extensive tumor-promoting effects of
    Methods: We systematically reviewed the literature on
    Results: We found that
    Conclusion: CDKN3
    Language English
    Publishing date 2024-02-08
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2835763-2
    ISSN 2405-8440
    ISSN 2405-8440
    DOI 10.1016/j.heliyon.2024.e26061
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Progress in pretreatment of methadone: an update since 2015

    Pang, Bo / Jiang, Yinru

    Preparative Biochemistry & Biotechnology. 2023 Feb. 1, v. 53, no. 2 p.109-119

    2023  

    Abstract: Methadone, a µ-opioid receptor agonist, is widely used in pain-relieving and treating opioid dependence. If not strictly controlled, as an opioid substitute, it can lead to abuse and cause more severe withdrawal responses than heroin. Also, overdose or ... ...

    Abstract Methadone, a µ-opioid receptor agonist, is widely used in pain-relieving and treating opioid dependence. If not strictly controlled, as an opioid substitute, it can lead to abuse and cause more severe withdrawal responses than heroin. Also, overdose or abuse of this drug in clinical use may provide severe side effects such as apnea, circulatory collapse, cardiac arrest, and even death. For these reasons, simple, rapid, and efficient methods have been developed for the pretreatment of methadone. This review presents a comprehensive conclusion of the pretreatment methods used for methadone in various sample matrices, focusing on the developments since 2015. Traditionally used pretreatment methods like solid-phase extraction and liquid-liquid extraction are discussed and newly developed methods like solid-phase microextraction and liquid-liquid microextraction along with new materials applied are focused.
    Keywords agonists ; apnea ; biochemistry ; biotechnology ; cardiac arrest ; death ; heroin ; liquid-phase microextraction ; methadone ; overdose ; solid phase microextraction ; Extraction ; pretreatment ; review
    Language English
    Dates of publication 2023-0201
    Size p. 109-119.
    Publishing place Taylor & Francis
    Document type Article ; Online
    ZDB-ID 1322522-4
    ISSN 1532-2297 ; 1082-6068
    ISSN (online) 1532-2297
    ISSN 1082-6068
    DOI 10.1080/10826068.2022.2056900
    Database NAL-Catalogue (AGRICOLA)

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