Combined analysis of C-reactive protein in pleural fluid and serum is effective in the differential diagnosis of exudative pleural effusions.

BACKGROUND: Exudative pleural effusion (EPE) is one of the common pleural manifestations of various diseases. Differential diagnosis of EPE is imperative clinically as it identifies different causes of EPE, thereby, enabling effective treatments. Thoracoscopy is a useful tool for differential diagnosis of EPE; however, some patients refuse thoracoscopic examination due to its invasive nature. In addition, the specificity and sensitivity of existing routine tests of EPE are unsatisfactory. Therefore, there is a great need to establish an effective method for the differential diagnosis of EPE. METHODS: This study was a single-institution retrospective analysis of diagnostic efficiency of C-reactive protein (CRP) and procalcitonin (PCT) between March 2018 and September 2018. A total of 87 patients diagnosed with EPE were enrolled. All participants underwent diagnostic thoracentesis. The EPE was examined using biochemical, routine, microbiological, and cytological methods. Pathological cytology detection was necessary for those suspected of malignant PE. Benign PE originates in patients with pneumonia, empyema, and tuberculosis. The levels of CRP and PCT in EPE and serum were measured before treatment. Correlation analysis and receiver-operating characteristic (ROC) curve analysis were conducted to determine the underlying relationship between levels of CRP and PCT, and for differential diagnosis. RESULTS: The ROC analysis showed that the sensitivity and specificity for the analysis of pleural fluid CRP (p-CRP) were higher (cut-off: 17.55 pg/mL; sensitivity: 75.00%, specificity: 83.90%) than that of serum CRP (s-CRP, cut-off: 23.90 pg/mL; sensitivity: 71.00%, specificity: 80.4%) in the differential diagnosis for EPE. However, the analysis of pleural fluid PCT (p-PCT) and serum PCT (s-PCT) did not demonstrate correlations with EPE. Combined analysis of p-CRP (cut-off: 17.55 mg/dL) with s-CRP (cut-off: 23.9 pg/mL) showed the highest diagnostic accuracy (88.4%) in diagnosing infectious EPE. CONCLUSIONS: The data support the close relationship between combined analysis of p-CRP with s-CRP and effective and accurate differential diagnosis of EPE, due to its higher sensitivity and specificity. However, as a highly sensitive marker for diagnosing bacterial infections, neither s-PCT nor p-PCT, showed correlations with the differential diagnosis of EPE.

Long non-coding RNA small nucleolar RNA host gene 6 aggravates pancreatic cancer through upregulation of far upstream element binding protein 1 by sponging microRNA-26a-5p.

BACKGROUND: Pancreatic cancer (PC) is a highly deadly malignancy with few effective therapies. We aimed to unmask the role that long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) plays in PC cells by targeting far upstream element binding protein 1 (FUBP1) via microRNA-26a-5p (miR-26a-5p). METHODS: SNHG6 expression was predicted by bioinformatics, followed by verification via reverse transcription quantitative polymerase chain reaction. Then, the interactions among SNHG6, miR-26a-5p, and FUBP1 were detected through online software analysis, dual luciferase reporter assay and RNA pull-down. After that, cells were treated with different small interfering RNAs and/or mimic to determine the interactions among SNHG6, miR-26a-5p, and FUBP1 and their roles in PC cells. Finally, the role of SNHG6 in tumor growth in vivo was evaluated by measuring the growth and weight of transplanted tumors in nude mice. A t-test, one-way and two-way analysis of variance were used for data analysis. RESULTS: Compared with that in normal tissues, SNHG6 was highly expressed in PC tissues (1.00 ±â€Š0.05 vs. 1.56 ±â€Š0.06, t = 16.03, P < 0.001). Compared with that in human pancreatic duct epithelial cells (HPDE6-C7), SNHG6 showed the highest expression in PANC-1 cells (1.00 ±â€Š0.06 vs. 3.87 ±â€Š0.13, t = 34.72, P < 0.001) and the lowest expression in human pancreatic cancer cells (MIAPaCa-2) (1.00 ±â€Š0.06 vs. 1.41 ±â€Š0.07, t = 7.70, P = 0.0015). Compared with the levels in the si-negative control group, SNHG6 (0.97 ±â€Š0.05 vs. 0.21 ±â€Š0.06, t = 16.85, P < 0.001), N-cadherin (0.74 ±â€Š0.05 vs. 0.41 ±â€Š0.04, t = 8.93, P < 0.001), Vimentin (0.55 ±â€Š0.04 vs. 0.25 ±â€Š0.03, t = 10.39, P < 0.001), and ß-catenin (0.62 ±â€Š0.05 vs. 0.32 ±â€Š0.03, t = 8.91, P < 0.001) were decreased, while E-cadherin (0.65 ±â€Š0.06 vs. 1.36 ±â€Š0.07, t = 13.34, P < 0.001) was increased after SNHG6 knockdown or miR-26a-5p overexpression, accompanied by inhibited cell proliferation, migration, and invasion. SNHG6 overexpression exerted the opposite effects. SNHG6 upregulated FUBP1 expression by sponging miR-26a-5p. Silencing SNHG6 blocked the growth of PC in vivo. CONCLUSION: Silencing SNHG6 might ameliorate PC through inhibition of FUBP1 by sponging miR-26a-5p, thus providing further supporting evidence for its use in PC treatment.

Preliminary comparison of diffusion-weighted MRI and PET/CT in predicting histological type and malignancy of lung cancer.

INTRODUCTION: Emerging evidence shows that diffusion-weighted magnetic resonance imaging (DW MRI) and fluorine 18 fluorodeoxyglucose positron emission tomography/computed tomography (18 F-FDG PET/CT) might be useful in predicting histological type and malignancy of lung cancer, and even in specifically detecting the types of gene mutation. OBJECTIVE: We assessed whether DW MRI is equivalent to PET/CT in lung cancer diagnosis and evaluation. METHODS: The institutional review board approved this study, and written informed consent was obtained from all patients. DW MRI and FDG PET/CT were performed before therapy in 15 lung cancer patients diagnosed by pathological examination. Apparent diffusion coefficient (ADC), ratio of ADC (rADC = ADC in tumor/ADC in spinal cord) and maximal standardized uptake value (SUVmax ) were assessed. RESULTS: ADC, rADC and SUVmax did not reveal significant differences among different types of lung cancer. Sensitivity, specificity and accuracy of ADC, rADC and SUVmax proved to be not significantly different in the detection of adenocarcinoma and squamous cell carcinoma. Difference in the abilities of the sensitivity, specificity and accuracy of ADC, rADC and SUVmax to detect adenocarcinoma and squamous cell carcinoma proved to be insignificant. Although Ki-67 score did not show correlation with ADC, rADC and SUVmax , significant positive correlation was found between ADC and rADC, and ADC and SUVmax . CONCLUSIONS: Both DW MRI and FDG PET/CT had similar limited diagnostic capability of predicting different histological types and malignancy of lung cancer. This study may help provide a novel insight into diagnostic and therapeutic strategies of lung cancer based on DW MRI.

Effect of overexpression of hypoxia-inducible factor-1α induced by hyperoxia in vivo in LNCaP tumors on tumor growth rate.

OBJECTIVE: To study effect of overexpression of hypoxia-inducible factor-1α induced by hyperoxia in vivo in LNCaP tumors on tumor growth rate. METHODS: The prostate cancer LNCaP cells were inoculated in the abdomen of mice. All the mice were randomly placed in the gas chamber with different oxygen content. The groups were divided as follows: twelve mice in hypoxia group, sixteen mice in normoxia group, ten mice in hyperoxia group. After 28 d of treatment, the mice were weighed, the blood samples were taken from the left ventricle, and the tumor was isolated and weighed. Tumor growth, angiogenesis and vascularization, HIF-1α expression and intracellular signal transduction molecules expression in each group of xenografts were detected and analyzed by using Western blotting and immunofluorescence and determination of hemoglobin. RESULTS: Comparison of the growth of xenografts in each group showed that, the xenografts growth of hypoxia group was more quickly than that of normoxia group. The difference was statistically significant (P = 0.004). The difference in xenografts growth between hyperoxia group compared and normoxia group was not statistically significant (P > 0.05). The expressions of HIF-1α, VEGF and VEGF-R of xenografts in hyperoxia group were significantly higher than those of normoxia group (P < 0.05). The expression of HIF-1α of xenografts in hypoxia group and normoxia group were similar. The blood growth rate of xenografts in hypoxia group (170%) was significantly higher than that of normoxia group (40%) (P < 0.05). The expression of Nrf2 of xenografts in hyperoxia group was significantly higher than that of normoxia group (P < 0.05). CONCLUSIONS: When hyperoxia induces the overexpression of HIF-1α in LNCaP tumor, it will not affect tumor growth. It provides a new ideas and theoretical basis for the clinical treatment of prostate cancer.