Expression of PCT, BNP and Inflammatory Factors in Children with Kawasaki Disease and Their Correlation with Coronary Artery Lesions.

Background: Kawasaki disease (KD), as one of the most common vascular diseases in children, will cause the risk of coronary artery lesions (CAL) without treatment. This study is to explore the expression of procalcitonin (PCT), brain natriuretic peptide (BNP), tumor necrosis factor-α (TNF-α), C-reactive protein (CRP) and interleukin-6 (IL-6) in children with KD and their correlation with CAL. Methods: 86 KD children in Baoding Hospital of Beijing Children's Hospital were selected as the study subjects from January 2020 to June 2021. According to whether CAL occurred, they were divided into the CAL group (n=30) and NCAL group (n=56). The clinical data of the two groups were collected from the medical record system. The levels of PCT and BNP were detected by chemiluminescence microparticle assay, the CRP level was detected by immunoturbidimetry, and the levels of TNF-α and IL-6 were detected by flow immunofluorescence method. The relationship of PCT, BNP, and inflammatory factors with CAL in KD children was explored by Pearson correlation analysis. Results: The comparative result of clinical data showed no overt difference in gender, disease types, age and blood routine indexes between the two groups, except for coronary artery diameter (P >.05). The levels of PCT, BNP, CRP, TNF-α and IL-6 in CAL group were (1.70±0.39) µg/L, (289.21±29.78) ng/L, (83.16±17.35) mg/L, (9.38±1.23) pg/mL and (59.97±0.97) ng/mL, respectively. The levels of PCT, BNP, CRP, TNF-α and IL-6 in NCAL group were (1.04±0.18) µg/L, (170.85±23.58) ng/L, (69.70±16.64) mg/L, (6.32±0.73) pg/mL and (44.16±11.97) ng/mL, respectively. The levels of each index in the CAL group were notably higher than in the NCAL group (P < .001). Pearson correlation analysis revealed that PCT, BNP, CRP, TNF-α and IL-6 were positively correlated with CAL in KD children (r=0.829, 0.865, 0.823, 0.894, 0.784, P < .001). Conclusion: The increase of PCT, BNP, and inflammatory factors has a certain warning effect on CAL in KD children. In clinical practice, health care professionals should strengthen the detection of PCT, BNP and inflammatory factors in KD children, carry out early monitoring of CAL in children with high expression of biomarkers, and formulate personalized preventive intervention based on the disease progress, so as to reduce the risk of cardiovascular disease. However, due to the limitations of research conditions and methods, the sample size of this study is small, which may affect the reliability and representativeness of the conclusion. In order to provide a new direction for the clinical prevention and treatment of the disease, future work will improve the research design, expand the sample size, and carry out more in-depth exploration on the prediction of CAL in KD children.

MicroRNA-320a is downregulated in non-small cell lung cancer and suppresses tumor cell growth and invasion by directly targeting insulin-like growth factor 1 receptor.

Accumulating evidence has demonstrated that microRNAs (miRs/miRNAs) are implicated in carcinogenesis and cancer progression, and can function as oncogenes or tumor suppressor genes in human cancer types. Previous profile studies of miRNA expression levels have revealed that miR-320a was downregulated in breast cancer, colon cancer, bladder cancer, glioblastoma and salivary adenoid cystic carcinoma. However, its expression level, potential functions and the mechanisms underlying its functions in non-small cell lung cancer (NSCLC) require further investigation. The present study investigated the expression level, biological roles and underlying molecular mechanisms of miR-320a in NSCLC. The expression levels of miR-320a in NSCLC tissue and cell lines were detected using the reverse transcription-quantitative polymerase chain reaction. Cell proliferation and Transwell invasion assays were performed to examine the effects of miR-320a on NSCLC cells. In addition, bioinformatic analysis, western blot analysis and luciferase reporter assays were performed to identify the direct gene target of miR-320a in NSCLC. In the present study it was demonstrated that miR-320a was significantly downregulated in NSCLC tissues and cell lines. Ectopic overexpression of miR-320a suppressed the proliferation and invasion of NSCLC cells. Further studies indicated that miR-320a directly targeted the 3'-untranslated region of insulin-like growth factor 1 receptor (IGF-1R) and suppressed its expression at the mRNA and protein levels. As well as restoring the miR-320a expression level, the knockdown of IGF-1R also decreased the growth and invasion of the NSCLC cells. These results suggested that miR-320a served as a tumor suppressor in the NSCLC cells by directly targeting IGF-1R. Therefore, miR-320a should be investigated as a therapeutic target for the treatment of NSCLC.

Chemical constituents of tobacco smoke induce the production of interleukin-8 in human bronchial epithelium, 16HBE cells.

BACKGROUND: Interleukin-8 (IL-8) functions as a major chemoattractant and plays pivotal roles in the initiation and development of chronic obstructive pulmonary disease (COPD), and tobacco smoke is a most risk factor contributing to the development of COPD. Hence, we have screened some of the tobacco smoke-derived chemical compounds that potentially induce the production of IL-8 in human bronchial epithelium, 16HBE cells. METHODS: Twenty-eight hazardous smoke components belonging to 9 classes including nicotine, ammonia, aromatic amines, polycyclic aromatic hydrocarbons, phenols, carbonyls, hydrocyanic acid, nitrosamines and other volatile organics were used in the experiments. Proliferation of 16HBE cells was determined by cell counting kit-8 kit, luciferase activity was measured in IL-8 reporter gene-expressing 16HBE cells, and IL-8 levels in culture supernatants were quantified by enzyme-linked immunosorbent assay. RESULTS: At the non-toxic dosages, chemical compounds belonging to nicotine, aromatic amines, benzopyrene, phenols, aldehydes, and some other volatile organics dose-dependently increased IL-8 reporter gene expression. Consistently, the representative compounds belonging to nicotine, aromatic amines, benzopyrene, phenols, aldehydes, and some other volatile organics significantly and dose-dependently increased IL-8 levels in the culture supernatants of 16HBE cells, among these compounds, benzopyrene is a most potent stimulator for inducing IL-8 production. CONCLUSIONS: The present study has identified particular tobacco smoke constituents responsible for inducing the IL-8 production in human bronchial epithelium, which might help shed light on the pathogenesis of tobacco smoke-induced COPD.