The results indicated that high TH17/Treg ratio exists inrheumatic MVD. This imbalance may play a role in the pathogenesis, and TH17/Treg balance may be a promising therapeutic approach in RHD.
Decreased adropin levels were found in the nocturnal hypertensive and non-dipper groups. Adropin and hsCRP were found to be independently associated with a non-dipping pattern. We suggest that decreased levels of adropin in non-dipper hypertensive patients might be associated with a longer duration of exposure to high BP. These results point to a possible future role of adropin in identifying hypertensive patients at higher risk of target organ damage.
Objective:SCUBE1 [signal peptide-CUB (complement C1r/C1 s)-EGF (epidermal growth factor)-like domain-containing protein 1] might function as a novel platelet-endothelial adhesion molecule and play pathological roles in cardiovascular biology. Acute myocardial infarction is one of the most common causes of death in modern society. The concept of “no reflow” (NR) refers to a state of myocardial tissue hypoperfusion in the presence of a patent epicardial coronary artery. The main mechanisms of this phenomenon are thought to be high platelet activity and much thrombus burden. So, we researched the role of SCUBE1 in the pathogenesis of NR.Methods:A total of 142 patients with ST elevation myocardial infarction (STEMI) (n=42 with NR and n=100 without NR) and 50 healthy individuals were prospectively case-control recruited between March 2015 and October 2016 from our outpatient clinics of cardiology department. Patients with STEMI were diagnosed according to American Heart Association (AHA) guideline for the management of STEMI.Results:The mean SCUBE1 levels of the control subjects were 34±8.4 ng/mL, the mean SCUBE1 levels of patients with STEMI who were treated successfully with primary percutaneous coronary intervention (PCI) were 51±6.2, and the mean SCUBE1 levels of patients with STEMI who had NR phenomenon after primary PCI procedure were 97.2±8.9 ng/mL.Conclusion:In our opinion, SCUBE1 might contribute to NR phenomenon via thrombus activation and aggregation. The pathophysiology of NR phenomenon is unclear. The present study is the first clinical study that demonstrated that serum SCUBE1 level was significantly higher in patients with NR and that serum SCUBE1 was an independent predictor for the presence of NR in our study population.
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