Zilan
Zheng
Sponsor: Jeffrey Williams, Ph.D. Ag & Resource Economics The freight rate for containers from Shanghai to LA surged after the pandemic hit, yet the increased demand for medical supplies and Americans' shifted purchasing habits were not the sole reason behind it. The other possible reason was that the severe congestion at the Port of Los Angeles decreased the overall supply of containers in the round trip between Shanghai and LA. The constraints that lead to congestion at the Port of Los Angeles include reduced terminal space, an inefficient trucking system, skilled labor shortages, and outdated technology at the port. However, other factors that different between import peaks in 2018 and 2021 have exaggerated the congestion at the Port of Los Angeles during the pandemic. This paper develops a simulation model to investigate how congestion builds upon congestion. The model incorporates the scenarios of vessel redirection and decreased processing efficiency when the port is congested, and it indicates that the real processing capacity of a port is significantly lower than the theoretical one. The findings obtained from this paper could provide useful insights for risk resilience at ports and mitigation of such disruption in the future. A Novel Function of MARCKS in Macrophage Activation and Pulmonary Fibrosis
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Authors:
Zilan Zheng
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Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with poor prognosis and no effective treatment characterized by the accumulation of fibroblasts leading to disrupted gas exchange, responsible for respiratory failure then death. Macrophages, a type of innate immune cells, have been implicated to play a significant role in driving fibrosis; therefore, targeting macrophage polarization influencing IPF progression have recently emerged as a promising therapeutic strategy. A single-cell transcriptomic study has recently discovered upregulation of a membrane-bound protein, Myristoylated Alanine Rich C-Kinase Substrate (MARCKS), in both monocytic cells and alveolar macrophages isolated from IPF patients. We generated macrophage-specific MARCKS-knockout mice and carried out a bleomycin-induced pulmonary fibrosis model using these mice to investigate the functional role of macrophages' MARCKS in mediating lung fibrosis. By using Masson's trichrome staining and immunohistochemical assays, histopathological analysis of lung tissues showed that bleomycin administration induced severe lung damage and collagen deposition concomitant with increased macrophage infiltration into fibrotic lungs in wild-type mice, whereas MARCKS-knockout mice displayed significantly lower degrees of fibrosis, macrophage infiltration, and hydroxyproline contents upon bleomycin exposure. These results suggest that MARCKS functions in lung macrophage-mediated fibrosis progression and it may serve as a therapeutic target for pulmonary fibrosis.
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UC Davis / MED: Int Med Nephrology (sac) / 2023
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Zilan Zheng