Association between serum adropin levels and isolated coronary artery ectasia in patients with stable angina pectoris.

OBJECTIVE: Dilation of one or more coronary artery segments to a diameter at least 1.5 times that of a normal adjacent segment is referred to as coronary artery ectasia (CAE). Adropin is a protein involved in endothelial function and is shown to have a protective effect on the regulation of cardiac functions. Atherosclerosis and endothelial dysfunction play an important role in the development of CAE. The aim of this study was to investigate the association between serum adropin levels and isolated CAE. METHODS: Patients with stable angina pectoris who underwent coronary angiography (CAG) between August 2017 and July 2018 were evaluated prospectively. A total of 92 subjects were included in the study-40 patients over 18 years old and diagnosed with isolated CAE based on CAG findings and a control group of 52 patients. RESULTS: Serum adropin level was found to be significantly lower in the isolated CAE group compared to the control group (1019.57 pg/mL and 1151.10 pg/mL, respectively, p=0.010). The isolated CAE group also exhibited a significantly higher mean platelet volume than that in the control group (10.75 fL and 10.17 fL, respectively, p=0.011). CONCLUSION: Our results show that there is an association between low serum adropin level and isolated CAE.

The role of Syk/IĸB-α/NF-ĸB pathway activation in the reversal effect of BAY 61-3606, a selective Syk inhibitor, on hypotension and inflammation in a rat model of zymosan-induced non-septic shock.

Spleen tyrosine kinase (Syk), a non-receptor tyrosine kinase, plays an important role in allergic diseases and inflammation. Syk triggers several intracellular signalling cascades including Toll-like receptor signalling to activate inflammatory responses following fungal infection but the role of this enzyme in zymosan (ZYM)-induced non-septic shock and its impacts on hypotension and inflammation in rats is not well understood. This study was conducted to determine the effects of Syk inhibition on ZYM-induced alterations in the expression and/or activities of Syk, inhibitor ĸB (IĸB)-α, and nuclear factor-ĸB (NF-ĸB) p65. We also examined the effect of Syk inhibition on inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and tumour necrosis factor (TNF)-α, and activity of myeloperoxidase (MPO) that contribute to hypotension and inflammation. Administration of ZYM (500 mg/kg, ip) to male Wistar rats decreased blood pressure and increased heart rate. These changes were associated with increased expression and/or activities of Syk, NF-κB p65, iNOS and COX-2 and decreased expression of IκB-α with enhanced levels of nitrite, nitrotyrosine, 6-keto-PGF1α , and TNF-α and activity of MPO in renal, cardiac and vascular tissues. ZYM administration also elevated serum and tissue nitrite levels. The selective Syk inhibitor BAY 61-3606 (3 mg/kg, ip) given 1 hour after ZYM injection reversed all of these changes induced by ZYM. These results suggest that Syk/IĸB-α/NF-ĸB pathway activation contributes to hypotension and inflammation caused by the production of vasodilator and proinflammatory mediators in the zymosan-induced non-septic shock model.

The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multiple traumas.

BACKGROUND: Blunt chest trauma and its complications are commonly encountered in emergency medicine. Herein, we used a rat model to investigate the role of thoracic trauma in inflammation, apoptosis and bacterial translocation following multiple traumas. METHODS: Ninety Wistar rats were divided equally into nine groups. Rats underwent a standardized blunt thoracic and/or head trauma and were sacrificed 24 or 48 hours after the trauma. Specimens from various organs and blood samples were collected and quantitatively cultured for aerobic organisms. Interleukins, TNF-α, and MCP-1 levels were assessed in the sera and markers of apoptosis were detected in the lungs. RESULTS: Levels of interleukins, TNF-α and MCP-1 in all of the groups undergoing trauma were significantly higher than those of the control group (p=0.001). Levels of apoptotic cells in the groups undergoing head and thoracic trauma (HTT) were significantly higher than those of the control group (p=0.009). Light microscopic evaluation indicated that damage in the HTT groups was significantly higher than that in the control group. The incidence of bacterial translocation was also significantly higher in the HTT groups (p=0.003). CONCLUSION: Multiple inflammatory mediators are activated in multiple traumas (including blunt thoracic trauma), which allow bacterial translocation and apoptotic processes to occur. Our results indicate that thoracic trauma plays a major role in post-traumatic bacterial translocation, inflammation, and apoptosis following multiple traumas.

Determination of plasma microRNA for early detection of gastric cancer.

Gastric cancer is the fourth most prevalent malignancy worldwide and remains the second most common cause of cancer-related death globally. Understanding the molecular structure of gastric carcinogenesis might identify new diagnostic and therapeutic strategies for this disease. Thus, early detection of gastric cancer is a key measure to reduce the mortality and improve the prognosis of gastric cancer. There have recently been several reports that microRNAs (miRNAs) circulate in highly stable, cell-free forms in blood. Because serum and plasma miRNAs are relatively easy to access, circulating miRNAs also have great potential to serve as non-invasive biomarkers. Although a number of miRNAs associated with gastric cancer have been identified, the underlying mechanism of these miRNAs in tumorigenesis and tumor progression remains to be investigated. The purpose of this study is to identify the potential of serum miRNAs as biomarkers for early detection of gastric cancer patients. RNA was isolated using the High Pure miRNA Isolation Kit (Roche) following the manufacturer's protocol. cDNA and preamplification protocols were obtained from the isolated plasma miRNAs. The BioMark™ 96.96 Dynamic Array (Fluidigm Corporation) for real-time qPCR was used to simultaneously quantite the expression of 740 miRNAs. All statistical analyses were performed using the Biogazelle's qbase PLUS 2.0 software. In this study, among 740 miRNAs that we analyzed only miR-195-5p was significantly (p < 0.05, fold changes = 13, 3) down-regulated in gastric cancer patients compared with control. We demonstrated that miR-195-5p is a novel tumor suppressor miRNA and may contribute to gastric carcinogenesis. The miRNA expression profile described in this study should contribute to future studies on the role of miRNAs in gastric cancer.

CYP2C19 gene polymorphism may be a risk factor for bronchial asthma.

OBJECTIVE: The aim of the present study was to investigate whether the genetic polymorphism of CYP2C19 plays a role in susceptibility to bronchial asthma. SUBJECTS AND METHODS: 104 healthy individuals who visited our hospital, including hospital staff, and 97 patients with bronchial asthma (62 atopic and 35 nonatopic) participated in this study. CYPC19*2 and CYP21C9*3 alleles were detected by using LightCycler and CYP2C19 mutation detection kits by real-time PCR with LightCycler. RESULTS: The CYP2C19*3 genotype was found to be the wild type in all cases, and in the control group, the CYP2C19*2 heterozygous genotype had a 2.46-fold increased risk of bronchial asthmacompared with the CYPC19*2 homozygous wild genotype in the control group(p = 0.01, OR = 2.46, 95% CI 1.24-4.88). CONCLUSION: Our data suggest that the CYP2C19*2 heterozygous genotype may be involved in the development of bronchial asthma.