Annals of medicine
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It is essential to assess the cancer risk for patients with chronic obstructive pulmonary disease (COPD). Comparing gene expression data from patients with lung cancer (a total of 506 samples) and those with cancer-adjacent normal lung tissues (a total of 370 samples), we generated a qualitative transcriptional signature consisting of 2046 gene pairs. The signature was verified in an evaluation dataset comprising 18 subjects with severe disease and 52 subjects with moderate disease (Wilcoxon rank-sum test; p = 7.33 × 10-5). ⋯ KEY MESSAGESA cancer risk assessment signature was identified in patients with COPD. The signature is insensitive to batch effects and is well verified. COPD key genes identified in this study might play a crucial role in TCM treatment and cancer prevention.
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Clostridioides difficile (formerly known as Clostridium difficile) infection (CDI) is one of the most prevalent healthcare-associated infections in the United States (US). In the early 2000s, CDI emerged as a great threat with increasing prevalence, mortality, and severity, especially in advanced age. We investigated the US national trends in in-hospital CDI prevalence, mortality, severity, and age composition from 2003 to 2014. ⋯ Compared to the earlier years 2003-2008, overall CDI outcome improved in the later years 2008-2014. Younger patients increasingly contributed to CDI prevalence, mortality, and severity during 2003-2014. More studies to understand underlying driving forces of changes in CDI trends are warranted to mitigate CDI.
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Myeloid-derived suppressor cell (MDSC) mobilisation is an important immune event in acute myocardial infarction (AMI). The A2B adenosine receptor (A2BAR) plays key role in regulating MDSC function, but its specific involvement in MDSC mobilisation in AMI remains unclear. ⋯ Blocking A2BAR alleviates myocardial damage and improves myocardial systolic function through inhibition of spleen-derived MDSC mobilisation after AMI. Key MessagesSpleen-derived MDSC mobilisation aggravates myocardial inflammatory injury within 24 h of AMI.A2BAR promotes spleen-derived MDSC mobilisation within 24 h of AMI.Blocking A2BAR improves myocardial systolic function through inhibition of spleen-derived MDSC mobilisation.