Observational studies have found a significant association between acid-suppressive drug use and incident asthma. However, the association between proton pump inhibitors (PPIs) and incident asthma in patients with coronary artery disease (CAD) is unclear. Thus, this study assessed the association between PPI use and incident asthma in patients with CAD. We conducted a retrospective cohort study using the National Health Insurance Research Database in Taiwan from 2004 to 2013. Each patient who took PPIs was assigned to the PPI group, whereas 1:1 sex-, age-, and drug index date-matched randomly selected patients without PPI prescription were assigned to the non-PPI group. We analyzed the risk of incident asthma using Cox proportional hazard regression models, including sex, age, urbanization, low income, and comorbidities. Sensitivity and subgroup analyses were also conducted. A total of 8499 cases were identified as PPI‐treated patients, and 8,499 subjects were included in the control group of PPI non‐users. After adjusting for sex, age, urbanization, low income, and comorbidities, PPI user was associated with a 1.18-fold (HR: 1.18; 95% CI: 1.05–1.34) increase for incident asthma in patients with CAD. We concluded that PPI use increased the risk of incident asthma in patients with CAD. The risk of incident asthma should be considered when weighing the benefits and risks of PPI and aspirin treatment in patients with CAD in clinical practice.

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BackgroundIt has been seemed that the gut microbiome alterations might be proposed as the metabolic disorder. However, the relationship between the microbiome and AMI has not been well validated. Methods The feces of the 44 subjects (AMI: 19; control: 25) were collected for fecal genomic DNAs extraction. The variable region V3–V4 of the 16S rRNA gene was sequencing by the platform of Illumina Miseq. The abundances of metabolites were analyzed by the Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolic pathways. ResultsThe abundance of bacteria was more enriched in the AMI group both in the observed operational taxonomic units (OTUs) and faith phylogenetic diversity (PD) (p-value=0.01 and <0.001 with 95% CI, individually). Selenomonadales was less enriched in the AMI group at the Family, Genus, and Species levels [all linear discriminant analysis (LDA) scores >2]. The seleno-compound was more abundant in the AMI group at the Family, Genus, and Species levels (all LDA scores >2).Conclusions This is the first study to demonstrate Selenomonadales and seleno-compound to be associated with the occurrence of AMI. Our findings provide an opportunity for a novel prevention and treatment of AMI.

Background Ischemic stroke is characterized by the loss of cerebral blood flow, which frequently leads to neurological deficits. Therefore, minimizing post-stroke functional disability is an important research topic. The fibrinogen-depleting agent lumbrokinase has been used to improve myocardial perfusion in symptomatic stable angina and to prevent secondary ischemic stroke. In this study, we aimed to clarify the neuroprotection of lumbrokinase on ischemic stroke and whether improve neurological dysfunction. We explored the neuroprotection and the underlying mechanisms of lumbrokinase in C57BL/6 mice subjected to permanent middle cerebral artery occlusion. Results Lumbrokinase at 1 mg/kg significantly attenuated the infarct volume and improved the neurological dysfunction. Lumbrokinase dramatically decreased the expressions of the endoplasmic reticulum (ER) transmembrane receptor protein inositol-requiring enzyme-1 (IRE1) and its downstream transcription factor, X-box binding protein-1, caspase-12, and nuclear factor kappa B activity. Moreover, lumbrokinase significantly inhibited apoptosis and autophagy and decreased the expression levels of the NOD-like receptor 3 inflammasome, caspase-1, and interleukin-1β compared with the vehicle treatment. Conclusions We suggest that post-stroke treatment with lumbrokinase protects against ischemic stroke by regulating ER stress through the IRE1 signaling pathways to inhibit apoptosis, autophagy, and inflammatory responses.