Ph.D., University of Kansas (2018)
B.S., China Pharmaceutical University (2013)

Stanford Advisors

All Publications

  • Precision environmental health monitoring by longitudinal exposome and multi-omics profiling. Genome research Gao, P., Shen, X., Zhang, X., Jiang, C., Zhang, S., Zhou, X., Schüssler-Fiorenza Rose, S. M., Snyder, M. 2022


    Conventional environmental health studies have primarily focused on limited environmental stressors at the population level, which lacks the power to dissect the complexity and heterogeneity of individualized environmental exposures. Here, as a pilot case study, we integrated deep-profiled longitudinal personal exposome and internal multi-omics to systematically investigate how the exposome shapes a single individual's phenome. We annotated thousands of chemical and biological components in the personal exposome cloud and found they were significantly correlated with thousands of internal biomolecules, which was further cross-validated using corresponding clinical data. Our results showed that agrochemicals and fungi predominated in the highly diverse and dynamic personal exposome, and the biomolecules and pathways related to the individual's immune system, kidney, and liver were highly associated with the personal external exposome. Overall, this data-driven longitudinal monitoring study shows the potential dynamic interactions between the personal exposome and internal multi-omics, as well as the impact of the exposome on precision health by producing abundant testable hypotheses.

    View details for DOI 10.1101/gr.276521.121

    View details for PubMedID 35667843

  • Human exposome assessment platform. Environmental epidemiology (Philadelphia, Pa.) Merino Martinez, R., Muller, H., Negru, S., Ormenisan, A., Arroyo Muhr, L. S., Zhang, X., Trier Moller, F., Clements, M. S., Kozlakidis, Z., Pimenoff, V. N., Wilkowski, B., Boeckhout, M., Ohman, H., Chong, S., Holzinger, A., Lehtinen, M., van Veen, E., Bala, P., Widschwendter, M., Dowling, J., Tornroos, J., Snyder, M. P., Dillner, J. 1800; 5 (6): e182


    The Human Exposome Assessment Platform (HEAP) is a research resource for the integrated and efficient management and analysis of human exposome data. The project will provide the complete workflow for obtaining exposome actionable knowledge from population-based cohorts. HEAP is a state-of-the-science service composed of computational resources from partner institutions, accessed through a software framework that provides the world's fastest Hadoop platform for data warehousing and applied artificial intelligence (AI). The software, will provide a decision support system for researchers and policymakers. All the data managed and processed by HEAP, together with the analysis pipelines, will be available for future research. In addition, the platform enables adding new data and analysis pipelines. HEAP's final product can be deployed in multiple instances to create a network of shareable and reusable knowledge on the impact of exposures on public health.

    View details for DOI 10.1097/EE9.0000000000000182

    View details for PubMedID 34909561

  • Decoding personal biotic and abiotic airborne exposome. Nature protocols Jiang, C., Zhang, X., Gao, P., Chen, Q., Snyder, M. 2021


    The complexity and dynamics of human diseases are driven by the interactions between internal molecular activities and external environmental exposures. Although advances in omics technology have dramatically broadened the understanding of internal molecular and cellular mechanisms, understanding of the external environmental exposures, especially at the personal level, is still rudimentary in comparison. This is largely owing to our limited ability to efficiently collect the personal environmental exposome (PEE) and extract the nucleic acids and chemicals from PEE. Here we describe a protocol that integrates hardware and experimental pipelines to collect and decode biotic and abiotic external exposome at the individual level. The described protocol has several advantages over conventional approaches, such as exposome monitoring at the personal level, decontamination steps to increase sensitivity and simultaneous capture and high-throughput profiling of biotic and abiotic exposures. The protocol takes ~18 h of bench time over 2-3 d to prepare samples for high-throughput profiling and up to a couple of weeks of instrumental time to analyze, depending on the number of samples. Hundreds to thousands of species and organic compounds could be detected in the airborne particulate samples using this protocol. The composition and complexity of the biotic and abiotic substances are heavily influenced by the sampling spatiotemporal factors. Basic skillsets in molecular biology and analytical chemistry are required to carry out this protocol. This protocol could be modified to decode biotic and abiotic substances in other types of low or ultra-low input samples.

    View details for DOI 10.1038/s41596-020-00451-8

    View details for PubMedID 33437065

  • The Exposome in the Era of the Quantified Self ANNUAL REVIEW OF BIOMEDICAL DATA SCIENCE, VOL 4 Zhang, X., Gao, P., Snyder, M. P., Altman, R. B. 2021; 4: 255-277
  • Targeting Heat Shock Protein 70 to Ameliorate c-Jun Expression and Improve Demyelinating Neuropathy ACS CHEMICAL NEUROSCIENCE Zhang, X., Li, C., Fowler, S. C., Zhang, Z., Blagg, B. J., Dobrowsky, R. T. 2018; 9 (2): 381-+


    Increased expression of the c-jun transcription factor occurs in a variety of human neuropathies and is critical in promoting Schwann cell (SC) dedifferentiation and loss of the myelinated phenotype. Using cell culture models, we previously identified KU-32 as a novobiocin-based C-terminal heat shock protein 90 (Hsp90) inhibitor that decreased c-jun expression and the extent of demyelination. Additional chemical optimization has yielded KU-596 as a neuroprotective novologue whose mechanistic efficacy to improve a metabolic neuropathy requires the expression of Hsp70. The current study examined whether KU-596 therapy could decrease c-jun expression and improve motor function in an inducible transgenic model of a SC-specific demyelinating neuropathy (MPZ-Raf mice). Treating MPZ-Raf mice with tamoxifen activates the MAPK kinase pathway, increases c-jun expression and produces a profound demyelinating neuropathy characterized by a loss of motor function and paraparesis. KU-596 therapy did not interfere with MAPK activation but reduced c-jun expression, significantly improved motor performance, and ameliorated the extent of peripheral nerve demyelination in both prevention and intervention studies. Hsp70 was necessary for the drug's neuroprotective efficacy since MPZ-Raf × Hsp70 knockout mice did not respond to KU-596 therapy. Collectively, our data indicate that modulating Hsp70 may provide a novel therapeutic approach to attenuate SC c-jun expression and ameliorate the onset of certain demyelinating neuropathies in humans.

    View details for DOI 10.1021/acschemneuro.7b00377

    View details for Web of Science ID 000426144000028

    View details for PubMedID 29120605

    View details for PubMedCentralID PMC5821551