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ZnCl inhibits postharvest disease on pear and crabapple by inducing autophagy of Penicillium expansum.
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Institute of Food Bioscience and Technology, College of Biosystems Engineering and Food Science, Zhejiang University, Hangzhou, 310058, Zhejiang, China. Electronic address:
Penicillium expansum is a phytopathogen causing postharvest disease of many fruits, which has led to enormous losses. Therefore, it is of great significance to take efficient methods to control this notorious phytopathogen. In this study, zinc, an essential trace element for human body, has been found to be able to effectively inhibit the P.
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Service de Médecine interne et polyvalente, Centre Hospitalier du Haut-Anjou, Château-Gontier, France; Université d'Angers, Inserm, CNRS, MITOVASC, Equipe MitoLab, SFR ICAT, F-49000 Angers, France. Electronic address:
Infections are increasingly recognised as a major cause of morbidity and mortality in patients with vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic (VEXAS) syndrome. We conducted a systematic review to characterise the infectious burden of VEXAS syndrome and propose preventive strategies. We included 57 studies (813 patients) showing that infections in patients with VEXAS syndrome were frequent, severe in 40-60% of cases, and fatal in 6-15% of cases.
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Vacuoles, E1 enzyme, X-linked, autoinflammatory, and somatic (VEXAS) syndrome is a newly identified disorder caused by an acquired monogenic somatic UBA1 gene mutation, affecting nuclear and cytoplasmic ubiquitination. This mutation triggers immune dysregulation, leading to diverse clinical and pathological features resembling inflammatory rheumatic diseases. Blood abnormalities stem from myeloid precursor dysfunction, presenting as elevated concentrations of inflammatory markers and cytokines, leukopenia, and macrocytosis.
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VEXAS (Vacuoles, E1 enzyme, X-linked, Autoinflammatory, Somatic) syndrome is a haemato-rheumatoid disease caused by somatic UBA1 mutations in hematopoietic stem cells (HSCs). The pathogenic cell type(s) responsible for the syndrome are unknown and murine models recapitulating the disease are lacking. We report that loss of Uba1 in various mouse hematopoietic cell types resulted in pleiotropic consequences and demonstrate that murine mutants with about 70% loss of Uba1 in neutrophils induced non-lethal VEXAS-like symptoms.
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