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  • PROJ 16S rRNA gene diversity during DOES incubation under different HHP

    Yu Zhang, Shanghai Jiaotong University,2023.03.13

    Description

    The microbial diversity of hadal sediment from the Mariana Trench with increasing high hydrostatic pressure (HHP; 0.1, 40, 70, 90 and 115 MPa) during incubation using the (deep ocean experimental simulator) DOES system at a flow rate of 0.3 mL/min.

    OEP004015

  • PROJ Metagenomics during DOES incubation under different HHP

    Yu Zhang, Shanghai Jiao Tong University,2023.03.15

    Description

    The metagenomics of hadal sediment from the Mariana Trench with increasing high hydrostatic pressure (HHP; 0.1, 40, 70, 90 and 115 MPa) during incubation using the (deep ocean experimental simulator) DOES system at a flow rate of 0.3 mL/min. A constant supply of 100 µmol/L NO3- and oxygen are maintained in the system.

    OEP004042

  • PROJ Metatranscriptomics during DOES incubation under different HHP

    Yu Zhang, School of Oceanography, Shanghai Jiao Tong University,2023.03.15

    Description

    The metatranscriptomics of hadal sediment from the Mariana Trench with increasing high hydrostatic pressure (HHP; 0.1, 40, 70, 90 and 115 MPa) during incubation using the (deep ocean experimental simulator) DOES system at a flow rate of 0.3 mL/min. A constant supply of 100 µmol/L NO3- and oxygen are maintained in the system.

    OEP004045

  • PROJ Heterologous expression and activity assay of clade I and II N2O reductase genes using WP3 strain at 0.1, 20 and 40 MPa

    Yu Zhang, ,2023.04.11

    Description

    The nos gene clusters includes Tat-dependent (clade I) and Sec-dependent (clade II) clades. Activity detection of microbial Sec-nosZ and Tat-nosZ enzymes from the hadal sediments under different hydrostatic pressures.

    OEP004102

  • PROJ Differentiation of islet organoids (S5D3)

    Zhiying Liao, Guangzhou laboratory,2024.03.01

    Description

    To assess the impact of FGF7 on ACE2 expression during both the early developmental stages, our study comprised three main experimental groups: Group 1 (G1) served as the control without additional modifications to the differentiation protocol. Group 2 (G2) received 50 ng/mL FGF7 at S5. Group 3 (G3) was supplied with both 50 ng/mL FGF7 and FGFRi (5 μM alofanib and 5 μM PD) at S5. Each group had three reproducible samples.

    OEP005097

  • PROJ ICC WES

    Shaolai Zhou, Fudan University, Zhongshan Hospital,2024.01.31

    Description

    OEP005036

  • PROJ Newly-designed primers for hadal ecosystem

    Yu Zhang, Shanghai Jiaotong University,2020.12.06

    Description

    The hadal microbial community is largely distinct from shallower marine as well as other well investigated ecosystem. We designed newly candidate primers for bacterial and archaeal communities of the hadal trench to show a more realistic picture.

    OEP001350

  • PROJ Genomic data analysis of 80 Yao samples

    Shuhua Xu, Shanghai Institute of Nutrition and Health, CAS,2023.06.07

    Description

    OEP004182

  • PROJ Loss of Setd2 induces systemic inflammation via embryo-derived Kupffer-like cell differentiation to drive malignant transformation

    Yuanliang Zhang, Shanghai Institute of Hematology,2023.12.07

    Description

    SETD2, a specific histone H3 lysine 36 tri-methyltransferase, is recurrently mutated in hematopoietic malignancies. Setd2 deficiency impairs the self-renewal and competitive potential of hematopoietic stem/progenitor cells (HSPCs), while it promotes a myelodysplastic syndrome-like (MDS) transformation. Nevertheless, the precise oncogenic advantages conferred upon HSPCs by Setd2 loss remain inadequately elucidated. Here, we observed that diseased HSPCs, with completely loss of self-renewal capabilities, can differentiate into embryo-derived Kupffer-like cells, characterized by heightened competitive ability, proliferation, and exacerbated inflammatory effects. The Kupffer-like cells sustain persistent systemic inflammation, thereby forcing the malignant transformation process. Notably, macrophage depletion effectively ameliorates the inflammatory state and alleviates MDS-like symptoms. Mechanistically, loss of Setd2 induces substantial alterations in DNA methylation patterns and chromatin accessibility, which instigate the activation of Irf8 synergistically and/or independently. Consequently, our study posits the notion that the long-lived inflammatory cells differentiated from HSPCs compensate the impaired self-renewal and induce malignant transformation independently.

    OEP004811

  • PROJ OEP004177

    Boya Zhang, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine,2023.06.02

    Description

    OEP004177