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  1. Article: Transcriptomic analysis of nitrogen metabolism pathways in

    Chen, Yanyan / Lin, Yijing / Zhu, Jingyi / Zhou, Jiayin / Lin, Haoyi / Fu, Yiting / Zhou, Yan

    Frontiers in microbiology

    2024  Volume 15, Page(s) 1323160

    Abstract: The acceleration of the nitrogen cycle and the nitrogen excess observed in some coastal waters has increased interest into understanding the biochemical and molecular basis of nitrogen metabolism in various microorganisms. To investigate nitrogen ... ...

    Abstract The acceleration of the nitrogen cycle and the nitrogen excess observed in some coastal waters has increased interest into understanding the biochemical and molecular basis of nitrogen metabolism in various microorganisms. To investigate nitrogen metabolism of a novel heterotrophic nitrification and aerobic denitrification bacterium
    Language English
    Publishing date 2024-02-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587354-4
    ISSN 1664-302X
    ISSN 1664-302X
    DOI 10.3389/fmicb.2024.1323160
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Relatlimab: a novel drug targeting immune checkpoint LAG-3 in melanoma therapy.

    Su, Jingjing / Fu, Yiting / Cui, Zitong / Abidin, Zain / Yuan, Jingsong / Zhang, Xinmiao / Li, Runmin / Zhao, Chunzhen

    Frontiers in pharmacology

    2024  Volume 14, Page(s) 1349081

    Abstract: Relatlimab is a type of human immunoglobulin G4 monoclonal blocking antibody. It is the world's first Lymphocyte-Activation Gene-3 (LAG-3) inhibitor and the third immune checkpoint inhibitor with clinical application, following PD-1 and CTLA-4. ... ...

    Abstract Relatlimab is a type of human immunoglobulin G4 monoclonal blocking antibody. It is the world's first Lymphocyte-Activation Gene-3 (LAG-3) inhibitor and the third immune checkpoint inhibitor with clinical application, following PD-1 and CTLA-4. Relatlimab can bind to the LAG-3 receptor which blocks the interaction between LAG-3 and its ligand to reduce LAG-3 pathway-mediated immunosuppression and promote T-cell proliferation, inducing tumor cell death. On 18 March 2022, the U.S. FDA approved the fixed-dose combination of relatlimab developed by Bristol Myers Squibb with nivolumab, under the brand name Opdualag for the treatment of unresectable or metastatic melanoma in adult and pediatric patients aged 12 and older. This study comprehensively describes the mechanism of action and clinical trials of relatlimab and a brief overview of immune checkpoint drugs currently used for the treatment of melanoma.
    Language English
    Publishing date 2024-01-10
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2023.1349081
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Advances in Research on microRNAs Related to the Invasion and Metastasis of Nasopharyngeal Carcinoma.

    Zhang, ShanShan / Wang, BaiQi / Zheng, LuLu / Fu, ZhuQiong / Fu, YiTing / Huang, WeiGuo / Cheng, AiLan

    Current molecular pharmacology

    2021  Volume 15, Issue 3, Page(s) 463–474

    Abstract: Nasopharyngeal Carcinoma (NPC), which is associated with latent Epstein-Barr virus infection in most cases, is a unique epithelial malignancy arising from the nasopharyngeal mucosal lining. Accumulating evidence is providing insights into the genetic and ...

    Abstract Nasopharyngeal Carcinoma (NPC), which is associated with latent Epstein-Barr virus infection in most cases, is a unique epithelial malignancy arising from the nasopharyngeal mucosal lining. Accumulating evidence is providing insights into the genetic and molecular aberrations that likely drive nasopharyngeal tumor development and progression. We review recent analyses of microRNAs (miRNAs), including Epstein-Barr virus-encoded miRNAs (EBV-encoded miRNAs) and dysregulated cellular miRNAs, that may be related to the metastasis of nasopharyngeal carcinoma. The studies summarized herein have greatly expanded our knowledge of the molecular biology of NPC involving miRNAs, and they may provide new biological targets for clinical diagnosis and reveal the potential of microRNA therapeutics. However, much remains to be uncovered.
    MeSH term(s) Epstein-Barr Virus Infections/genetics ; Herpesvirus 4, Human/genetics ; Humans ; MicroRNAs/genetics ; Nasopharyngeal Carcinoma/pathology ; Nasopharyngeal Neoplasms/pathology ; RNA, Viral
    Chemical Substances MicroRNAs ; RNA, Viral
    Language English
    Publishing date 2021-06-14
    Publishing country United Arab Emirates
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ISSN 1874-4702
    ISSN (online) 1874-4702
    DOI 10.2174/1874467214666210614150720
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Gestational cadmium exposure disrupts fetal liver development via repressing estrogen biosynthesis in placental trophoblasts.

    Fu, Yi-Ting / Zhang, Jin / Liu, Wei-Bo / Zhang, Yu-Feng / Zhang, Shuang / Tan, Lu-Lu / Lin, Qing / Ou-Yang, Kong-Wen / Xiong, Yong-Wei / Chang, Wei / Li, Hao / Yu, Jun-Ying / Zhang, Cheng / Xu, De-Xiang / Zhu, Hua-Long / Wang, Hua

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

    2023  Volume 176, Page(s) 113807

    Abstract: Cadmium (Cd), commonly found in diet and drinking water, is known to be harmful to the human liver. Nevertheless, the effects and mechanisms of gestational Cd exposure on fetal liver development remain unclear. Here, we reported that gestational Cd (150 ... ...

    Abstract Cadmium (Cd), commonly found in diet and drinking water, is known to be harmful to the human liver. Nevertheless, the effects and mechanisms of gestational Cd exposure on fetal liver development remain unclear. Here, we reported that gestational Cd (150 mg/L) exposure obviously downregulated the expression of critical proteins including PCNA, Ki67 and VEGF-A in proliferation and angiogenesis in fetal livers, and lowered the estradiol concentration in fetal livers and placentae. Maternal estradiol supplement alleviated aforesaid impairments in fetal livers. Our data showed that the levels of pivotal estrogen synthases, such as CYP17A1 and 17β-HSD, was markedly decreased in Cd-stimulated placentae but not fetal livers. Ground on ovariectomy (OVX), we found that maternal ovarian-derived estradiol had no major effects on Cd-impaired development in fetal liver. In addition, Cd exposure activated placental PERK signaling, and inhibited PERK activity could up-regulated the expressions of CYP17A1 and 17β-HSD in placental trophoblasts. Collectively, gestational Cd exposure inhibited placenta-derived estrogen synthesis via activating PERK signaling, and therefore impaired fetal liver development. This study suggests a protective role for placenta-derived estradiol in fetal liver dysplasia shaped by toxicants, and provides a theoretical basis for toxicants to impede fetal liver development by disrupting the placenta-fetal-liver axis.
    MeSH term(s) Pregnancy ; Female ; Humans ; Cadmium/toxicity ; Cadmium/metabolism ; Trophoblasts/metabolism ; Placenta/metabolism ; Liver/metabolism ; Estradiol ; Estrogens
    Chemical Substances Cadmium (00BH33GNGH) ; Estradiol (4TI98Z838E) ; Estrogens
    Language English
    Publishing date 2023-04-28
    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.2023.113807
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  5. Article: Gestational exposure to environmental cadmium induces placental apoptosis and fetal growth restriction via Parkin-modulated MCL-1 degradation

    Zhu, Hua-Long / Dai, Li-Min / Xiong, Yong-Wei / Shi, Xue-Ting / Liu, Wei-Bo / Fu, Yi-Ting / Zhou, Guo-Xiang / Zhang, Shuang / Gao, Lan / Zhang, Cheng / Zhao, Ling-Li / Xu, Xiao-Feng / Huang, Yi-chao / Xu, De-Xiang / Wang, Hua

    Journal of hazardous materials. 2022 Feb. 15, v. 424

    2022  

    Abstract: Heavy metal cadmium (Cd), a classical environmental pollutant, causes placental apoptosis and fetal growth restriction (FGR), whereby the mechanism remains unclear. Here, our human case-control study firstly showed that there was a positive association ... ...

    Abstract Heavy metal cadmium (Cd), a classical environmental pollutant, causes placental apoptosis and fetal growth restriction (FGR), whereby the mechanism remains unclear. Here, our human case-control study firstly showed that there was a positive association of Parkin mitochondrial translocation, MCL-1 reduction, placental apoptosis, and all-cause FGR. Subsequently, Cd was administered to establish in vitro and in vivo models of placental apoptosis or FGR. Our models demonstrated that Parkin mitochondrial translocation was observed in Cd-administrated placental trophoblasts. Meaningfully, Parkin siRNA (siR) dramatically mitigated Cd-triggered apoptosis in placental trophoblasts. Mdivi-1 (M-1), an inhibitor for Parkin mitochondrial translocation, mitigated Cd-induced apoptosis in placental trophoblasts, which further ameliorated the effect of attenuated placental sizes in Cd-exposed mice. Furthermore, the interaction of MCL-1 with Parkin or Ub in Cd-stimulated cells was stronger than that in controls. MG132, an inhibitor for proteasome, abolished MCL-1 degradation in Cd-stimulated cells. Importantly, Parkin siR and M-1 memorably abolished the ubiquitin-dependent degradation of MCL-1 in placental trophoblasts. Interestingly, mito-TEMPO and melatonin, two mitochondria-targeted antioxidants, obviously rescued Cd-caused mitochondrial membrane potential (MMP) decrease, Parkin mitochondrial translocation, MCL-1 degradation, and apoptosis in placental trophoblasts. In conclusion, cadmium induces placental apoptosis and FGR via mtROS-mediated Parkin-modulated degradation of MCL-1.
    Keywords apoptosis ; cadmium ; case-control studies ; fetal development ; heavy metals ; humans ; maternal exposure ; melatonin ; membrane potential ; mitochondria ; mitochondrial membrane ; pollutants ; proteasome endopeptidase complex
    Language English
    Dates of publication 2022-0215
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 1491302-1
    ISSN 1873-3336 ; 0304-3894
    ISSN (online) 1873-3336
    ISSN 0304-3894
    DOI 10.1016/j.jhazmat.2021.127268
    Database NAL-Catalogue (AGRICOLA)

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  6. Article ; Online: Gestational exposure to environmental cadmium induces placental apoptosis and fetal growth restriction via Parkin-modulated MCL-1 degradation.

    Zhu, Hua-Long / Dai, Li-Min / Xiong, Yong-Wei / Shi, Xue-Ting / Liu, Wei-Bo / Fu, Yi-Ting / Zhou, Guo-Xiang / Zhang, Shuang / Gao, Lan / Zhang, Cheng / Zhao, Ling-Li / Xu, Xiao-Feng / Huang, Yi-Chao / Xu, De-Xiang / Wang, Hua

    Journal of hazardous materials

    2021  Volume 424, Issue Pt A, Page(s) 127268

    Abstract: Heavy metal cadmium (Cd), a classical environmental pollutant, causes placental apoptosis and fetal growth restriction (FGR), whereby the mechanism remains unclear. Here, our human case-control study firstly showed that there was a positive association ... ...

    Abstract Heavy metal cadmium (Cd), a classical environmental pollutant, causes placental apoptosis and fetal growth restriction (FGR), whereby the mechanism remains unclear. Here, our human case-control study firstly showed that there was a positive association of Parkin mitochondrial translocation, MCL-1 reduction, placental apoptosis, and all-cause FGR. Subsequently, Cd was administered to establish in vitro and in vivo models of placental apoptosis or FGR. Our models demonstrated that Parkin mitochondrial translocation was observed in Cd-administrated placental trophoblasts. Meaningfully, Parkin siRNA (siR) dramatically mitigated Cd-triggered apoptosis in placental trophoblasts. Mdivi-1 (M-1), an inhibitor for Parkin mitochondrial translocation, mitigated Cd-induced apoptosis in placental trophoblasts, which further ameliorated the effect of attenuated placental sizes in Cd-exposed mice. Furthermore, the interaction of MCL-1 with Parkin or Ub in Cd-stimulated cells was stronger than that in controls. MG132, an inhibitor for proteasome, abolished MCL-1 degradation in Cd-stimulated cells. Importantly, Parkin siR and M-1 memorably abolished the ubiquitin-dependent degradation of MCL-1 in placental trophoblasts. Interestingly, mito-TEMPO and melatonin, two mitochondria-targeted antioxidants, obviously rescued Cd-caused mitochondrial membrane potential (MMP) decrease, Parkin mitochondrial translocation, MCL-1 degradation, and apoptosis in placental trophoblasts. In conclusion, cadmium induces placental apoptosis and FGR via mtROS-mediated Parkin-modulated degradation of MCL-1.
    MeSH term(s) Animals ; Apoptosis ; Cadmium/toxicity ; Case-Control Studies ; Female ; Fetal Growth Retardation/chemically induced ; Mice ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Placenta ; Pregnancy ; Ubiquitin-Protein Ligases/genetics
    Chemical Substances Myeloid Cell Leukemia Sequence 1 Protein ; Cadmium (00BH33GNGH) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2021-09-20
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1491302-1
    ISSN 1873-3336 ; 0304-3894
    ISSN (online) 1873-3336
    ISSN 0304-3894
    DOI 10.1016/j.jhazmat.2021.127268
    Database MEDical Literature Analysis and Retrieval System OnLINE

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