Aim: To character the specific metabolomics profiles in the sera of Chinese patients with mild persistent asthma and to explore potential metabolic biomarkers. Methods: Seventeen Chinese patients with mild persistent asthma and age-and sex-matched healthy controls were enrolled. Serum samples were collected, and serum metabolites were analyzed using GC-MS coupled with a series of multivariate statistical analyses. Results: Clear intergroup separations existed between the asthmatic patients and control subjects. A list of differential metabolites and several top altered metabolic pathways were identified. The levels of succinate (an intermediate in tricarboxylic acid cycle) and inosine were highly upregulated in the asthmatic patients, suggesting a greater effort to breathe during exacerbation and hypoxic stress due to asthma. Other differential metabolites, such as 3,4-dihydroxybenzoic acid and phenylalanine, were also identified. Furthermore, the differential metabolites possessed higher values of area under the ROC curve (AUC), suggesting an excellent clinical ability for the prediction of asthma. Conclusion: Metabolic activity is significantly altered in the sera of Chinese patients with mild persistent asthma. The data might be helpful for identifying novel biomarkers and therapeutic targets for asthma.

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The study was to investigate the association of endogenous erythropoietin (EPO) and coronary collateral development. Forty-nine patients (31 with chronic total occlusion (CTO), 18 with normal coronary artery) were consecutively enrolled. The serum EPO was positively related with Rentrop class. Increased serum EPO was one of the independent predictors of good collateral development (odds ratio 1.31; p = 0.025). A significantly positive correlation was seen between serum EPO and vascular endothelial growth factor (VEGF) levels (r = 0.96, p < 0.001). Circulatory EPO may be a useful biomarker for coronary collateral development and potential target for therapeutic angiogenesis in patients with CTO.

BACKGROUND Mushroom exposure is a global health issue. The manifestations of mushroom poisoning (MP) may vary. Some species have been reported as rhabdomyolytic, hallucinogenic, or gastrointestinal poisons. Critical or even fatal MPs are mostly attributable to Amanita phalloides , with the development of severe liver or renal failure. Myocardial injury and even cases mimicking ST-segment elevation myocardial infarction (STEMI) have been previously reported, while cardiac arrhythmia or cardiac arrest is not commonly seen. CASE SUMMARY We report a 68-year-old woman with MP who suffered from delirium, seizure, long QT syndrome on electrocardiogram (ECG), severe cardiac arrhythmias of multiple origins, and cardiac arrest. She was intubated and put on blood perfusion. Her kidney and liver functions were intact; creatine kinase-MB was mildly elevated, and then fell within normal range during her hospital stay. We sent the mushrooms she left for translation elongation factor subunit 1α, ribosomal RNA gene sequence, and internal transcribed spacer sequence analyses. There were four kinds of mushrooms identified, two of which were found to be toxic. CONCLUSION This is the first time that we found cardiac toxicity caused by Panaeolus subbalteatus and Conocybe lactea , which were believed to be toxic to the liver, kidney, and brain. We suggest that intensive monitoring and ECG follow-up are essential to diagnose prolonged QT interval and different forms of tachycardia in MP patients, even without the development of severe liver or renal failure. The mechanisms need to be further investigated and clarified based on animal experiments and molecular signal pathways.

The association between increases in both systemic and airway inflammation and acute exacerbation of COPD (AECOPD) has been reported by many studies. However, relatively little is known about the dynamics of inflammation resolution and their correlations with the improvement of clinical indices during treatment. In this study, a total of 93 consecutively hospitalized patients with AECOPD were recruited. Sputum and serum inflammatory markers were measured on the day of admission before treatment (day 0), day 4, 7 and 14 during treatment as well as 8 weeks after discharge. Clinical indices (lung function, dyspnea and COPD assessment test (CAT) scores) were also measured at those time points. By day 4, all airway inflammatory measures rapidly decreased and returned to baseline level. Notably, lung function and dyspnea improved to the baseline level by day 4 as well, consistent with the resolution of respiratory inflammation. However, despite the significant decrease by day 4, systemic inflammation did not reach baseline until day 14, concordant with the decrease in CAT score. In summary, we observed a time lag between the resolution of systemic and airway inflammation, which were correlated with the improvements of different clinical indices.

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