Publications by authors named "Xue Yan Peng"

Feline calicivirus (FCV; ) is a highly contagious RNA virus that causes upper respiratory tract infections and intestinal symptoms in cats. In 2023 and 2024, in Shanghai (SH), China, we collected oral swab samples from 189 domestic cats exhibiting symptoms of upper respiratory tract disease (URTD), to test for five designated respiratory pathogens. Among the 111 cats testing positive for these pathogens, the FCV-positivity rate was 52% (58/111).

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Objective: The lungs of patients with systemic sclerosis-associated interstitial lung disease (SSc-ILD) contain inflammatory myofibroblasts that arise in association with fibrotic stimuli and perturbed innate immunity. The cytosolic DNA-binding receptor cyclic GMP-AMP synthase (cGAS) is implicated in inflammation and fibrosis, but its involvement in SSc-ILD remains unknown. We examined cGAS expression, activity and therapeutic potential in SSc-ILD using human biospecimens, cultured fibroblasts, precision-cut lung slices and a well-accepted animal model.

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Objective: The lungs of patients with Systemic Sclerosis Associated Interstitial Lung Disease (SSc-ILD) contain inflammatory myofibroblasts arising in association with fibrotic stimuli and perturbed innate immunity. The innate immune DNA binding receptor Cyclic GMP-AMP synthase (cGAS) is implicated in inflammation and fibrosis, but its involvement in SSc-ILD remains unknown. We examined cGAS expression, activity, and therapeutic potential in SSc-ILD using cultured fibroblasts, precision cut lung slices (PCLS), and a well-accepted animal model.

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Rationale: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease for which current treatment options only slow clinical progression. Previously, we identified a subset of patients with IPF with an accelerated disease course associated with fibroblast expression of Toll-Like Receptor 9 (TLR9) mediated by interactions with its ligand mitochondrial DNA (mtDNA).

Objectives: We aimed to show that TLR9 activation induces fibroproliferative responses that are abrogated by its antagonism by using two commercially-available indirect inhibitors and a proprietary, selective direct small molecule inhibitor.

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Pulmonary fibrosis is a devastating lung disease with few therapeutic options. CHIT1 (chitinase 1), an 18 glycosyl hydrolase family member, contributes to the pathogenesis of pulmonary fibrosis through the regulation of TGF-β (transforming growth factor-β) signaling and effector function. Therefore, CHIT1 is a potential therapeutic target for pulmonary fibrosis.

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The title complex, [Ni(C(14)H(12)NO(2))(2)], lies about an inversion center. The Ni(II) atom is coordinated in a slightly distorted square-planar geometry by two O atoms and two N atoms from two 2-[imino-(phen-yl)meth-yl]-5-meth-oxy-phenolate ligands. The dihedral angle between the symmetry-unique phenyl and benzene rings is 73.

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