BackgroundChronic obstructive pulmonary disease (COPD) is a complex condition, whose diagnosis requires spirometric assessment. However, considering its heterogeneity, subjects with similar spirometric parameters do not necessarily have the same functional status. To overcome this limitation novel biomarkers for COPD have been investigated. Therefore, we aimed to explore the potential value of N-glycans as COPD biomarkers and to examine the individual variation of plasma protein and immunoglobulin G (IgG) glycosylation profiles in subjects with COPD and healthy controls.MethodsBoth the total plasma protein and IgG N-glycome have been profiled in the total of 137 patients with COPD and 95 matching controls from Croatia. Replication cohort consisted of 61 subjects with COPD and 148 controls recruited at another Croatian medical centre.ResultsPlasma protein N-glycome in COPD subjects exhibited significant decrease in low branched and conversely, an increase in more complex glycan structures (tetragalactosylated, trisialylated, tetrasialylated and antennary fucosylated glycoforms). We also observed a significant decline in plasma monogalactosylated species, and the same change replicated in IgG glycome. N-glycans also showed value in distinguishing subjects in different COPD GOLD stages, where the relative abundance of more complex glycan structures increased as the disease progressed. Glycans also showed statistically significant associations with the frequency of exacerbations and demonstrated to be affected by smoking, which is the major risk factor for COPD development.ConclusionsThis study showed that complexity of glycans associates with COPD, mirroring also the disease severity. Moreover, changes in N-glycome associate with exacerbation frequency and are affected by smoking. In general, this study provided new insights into plasma protein and IgG N-glycome changes occurring in COPD and pointed out potential novel markers of the disease progression and severity.Electronic supplementary materialThe online version of this article (10.1186/s12967-018-1695-0) contains supplementary material, which is available to authorized users.

SARS-CoV-2 has been circulating in population worldwide for the past year and a half, and thus a vast amount of scientific literature has been produced in order to study the biology of the virus and the pathophysiology of COVID-19, as well as to determine the best way to prevent infection, treat the patients and eliminate the virus. SARS-CoV-2 binding to the ACE2 receptor is the key initiator of COVID-19. The ability of SARS-CoV-2 to infect various types of cells requires special attention to be given to the cardiovascular system, as it is commonly affected. Thorough diagnostics and patient monitoring are beneficial in reducing the risk of cardiovascular morbidity and to ensure the most favorable outcomes for the infected patients, even after they are cured of the acute disease. The multidisciplinary nature of the fight against the COVID-19 pandemic requires careful consideration from the attending clinicians, in order to provide fast and reliable treatment to their patients in accordance with evidence-based medicine principles. In this narrative review, we reviewed the available literature on cardiovascular implications of COVID-19; both the acute and the chronic.

Background and Aims COPD is progressive lung disease with known higher cardiovascular (CV) risk, mainly attributed to smoking of cigarettes as the main etiological factor of disease. The aim of this study was to compare CV risk in patients with COPD to control groups of smokers and non‐COPD and to investigate the relation of lung function variables, COPD severity, and smoking with Systemic Coronary Risk Estimation (SCORE) risk calculation, arterial stiffness (AS) values, and biological systemic inflammatory markers. Methods A total of 208 subjects were included in this study: 61 subjects diagnosed with COPD, 83 smokers without COPD, and 64 nonsmokers without COPD. Medical history and clinical data were recorded, including assessment of pulmonary function and AS, calculation of ankle‐brachial index, blood analysis, and CV risk assessment by SCORE risk calculation. Results Subjects with COPD had significantly higher values of SCORE calculation of risk, central aortic pressure, AS, and markers of systemic inflammation compared to control groups of smokers and nonsmokers without COPD ( p < 0.001). Furthermore, statistically significant increase in hs‐CRP concentration was found between the COPD group and the control group of non‐COPD smokers ( p < 0.001), and a statistically significantly higher SCORE calculation was found in the COPD group compared to control groups of smokers and nonsmokers without COPD ( p < 0.001). Conclusion The results of the research support further identification and research of biological markers and simple specific tests such as arteriography that will enable progress in personalized treatment of patients with COPD and better primary and secondary prevention of comorbidities with the aim of improved treatment outcome.

Our findings indicate significant tobacco use among medical students in Croatia. There is an urgent need to reduce this harmful behaviour through more comprehensive public health initiatives, provision of support for cessation among health professionals who smoke and provision of training to health professionals to assist their patients with cessation.