Increasing evidence indicates that inflammation plays a vital role in tumorigenesis and progression. However, the prognostic value of inflammatory biomarkers in colorectal cancer (CRC) has not been established. In this study, a retrospective analysis was conducted in patients with CRC in Fudan University Shanghai Cancer Center (FUSCC) between April 1, 2007 and April 30, 2014, and 5,336 patients were identified eligible. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), and albumin/globulin ratio (AGR) were analyzed. Kaplan-Meier analysis was used to calculate the 5-year overall survival (OS) and disease-free survival (DFS). Cox regression analysis was performed to assess the prognostic factors. Nomograms were established to predict OS and DFS, and Harrell's concordance index (c-index) was adopted to evaluate prediction accuracy. As results, the 5-year OS was 79.2% and the 5-year DFS was 56.0% in the cohort. Patients were stratified into 2 groups by NLR (2.72 and >2.72), PLR (219.00 and >219.00), LMR (2.83 and >2.83) and AGR (<1.50 and 1.50). Patients with NLR > 2.72, PLR > 219.00, LMR 2.83 and AGR < 1.50 were significantly associated with decreased OS and DFS (p < 0.001). Multivariate analysis indicated that NLR, LMR and AGR were independent factors of OS (p 5 0.047, p 5 0.008 and p < 0.001, respectively) and DFS (p 5 0.009, p < 0.001 and p 5 0.008, respectively). In addition, nomograms on OS and DFS were established according to all significant factors, and c-indexes were 0.765 (95% CI: 0.744-0.785) and 0.735 (95% CI: 0.721-0.749), respectively. Nomograms based on OS and DFS can be recommended as practical models to evaluate prognosis for CRC patients.Colorectal cancer (CRC) is the third most commonly diagnosed cancer in males and the second in females.1 The estimated global 5-year prevalence rate of CRC was 68.2/100,000, and cancer death rate caused by CRC was about 8.5%. 2 Compared with developed countries, the 5-year prevalence rate of CRC is significantly lower in China (52.7/100,000), but the mortality-to-prevalence ratio (MPR) of CRC in China (14%) is a lot higher, 2 which indicates that the overall survival outcome of CRC is apparently worse in China. Surgical resection remains the only curative treatment option for colorectal cancer. However, a considerable proportion of CRC patients develop recurrence or metastasis within 5 years after surgical treatment. Thus, a better model to predict the prognosis of CRC patients after radical resection is urgently needed.

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The metastatic site was an independent prognostic factor in stage IV colorectal cancer. Also, carefully chosen patients may benefit from surgery.

Abstract. Receptor for advanced glycation end products (RAGE) is associated with the pathogenesis of cancer progression. The pathological effects mediated through RAGE are physiologically inhibited by soluble RAGE (sRAGE). The aim of the present study was to identify the expression of the sRAGE, RAGE and RAGE ligands in serum samples and lung cancer tissue obtained from lung cancer patients. Using ELISA and immunohistochemistry, it was observed that the sRAGE levels were downregulated in the serum, the expression of RAGE was decreased in the lung cancer tissue and the RAGE ligands HMGB1 and S100 were upregulated in cancer tissue. Furthermore, the presence of several selected types of RAGE polymorphism that occur in lung cancers were measured in the tissue samples. An association between the -429T/C and 2184A/G polymorphisms of RAGE and the genesis and progression of lung cancer was identified. The comparison between various histological subtypes and stages of lung cancer was performed with the aim to clarify the biological role of the RAGE gene, and identify a biomarker to aid diagnosis and predict the prognosis for lung cancer patients.

Background: Long non-coding RNAs (lncRNAs) have been consistently reported to be involved in the progression of non-small cell lung cancer (NSCLC). In this study, we aimed to identify aberrantly expressed lncRNAs in NSCLC, in order to explore new therapeutic targets for NSCLC.Methods: Two pairs of NSCLC and adjacent normal tissues were first analyzed by RNA sequencing. The expressions of LINC00702 in 40 pairs patient samples and in 4 NSCLC cell lines was measured by quantitative real-time PCR. Putative target miRNAs of LINC00702 were predicted by the bioinformatics tools. The effect of LINC00702 on tumor growth in vivo was evaluated.Results: LINC00702 was significantly down-regulated in patients with NSCLC, which was correlated with tumor size and metastasis. In addition, overexpression of LINC00702 markedly suppressed proliferation and metastasis in NSCLC cells via inducing apoptosis in vitro and in vivo. Moreover, bioinformatics and luciferase reporter assays demonstrated that LINC00702 functioned as a competing endogenous RNA (ceRNA) for miR-510 in NSCLC, and upregulated its target gene PTEN.Conclusion: Our results indicated that LINC00702 modulated the expression of PTEN gene by acting as a ceRNA for miR-510 in NSCLC. Therefore, LINC00702 may serve as a potential target for the diagnosis and treatment of patients with NSCLC.

Background: The global COVID-19 epidemic remains severe, with the cumulative global death toll reaching more than 207,170 as of May 2, 2020 (1). Purpose: Our research objective is to establish a reliable nomogram to predict mortality in COVID-19 patients. The nomogram can help us distinguish between patients who are at high risk of death and need close attention. Patients and Methods: For the single-center retrospective study, we collected 21 cases of patients who died in the critical illness area of the Optical Valley Branch of Tongji Hospital, Huazhong University of Science and Technology, from February 9 to March 10. Additionally, we selected 99 patients discharged during this period for analysis. The nomogram was constructed to predict the mortality for COVID-19 patients using the primary group of 120 patients and was validated using an independent cohort of 84 patients. We used multivariable logistic regression analysis to construct the prediction model. The nomogram was evaluated for calibration, differentiation, and clinical usefulness. Results: The predictors included in the nomogram were c-reactive protein, PaO 2 /FiO 2 , and cTnI. The areas under the curves of the nomogram were 0.988 (95% CI: 0.972-1.000) and 0.956 (95% CI, 0.874-1.000) in the primary and validation groups, respectively. Decision curve analysis suggests that the nomogram may have clinical usefulness. Conclusion: This study provides a nomogram containing c-reactive protein, PaO 2 /FiO 2 , and cTnI that can be conveniently used to predict individual mortality in COVID-19 patients. Next, we will collect as many cases as possible from multiple centers to build a more reliable nomogram to predict mortality for COVID-19 patients.

Context: Previous studies have reported that caveolin-1 (Cav-1) is associated with lung fibrosis. However, the role of Cav-1 expression in pirfenidone-treated idiopathic pulmonary fibrosis (IPF) is unknown.Objective: This study investigated Cav-1 expression in pirfenidone-treated IPF, and compared the effects of pirfenidone with acetylcysteine and prednisone on IPF.Materials and methods: Rat IPF model was established by endotracheal injection of 5 mg/kg bleomycin A5 into the specific pathogen-free Wistar male rats. Pirfenidone (P, 100 mg/kg once daily), prednisone (H, 5 mg/kg once daily) and acetylcysteine (N, 4 mg/kg 3 times per day) were used to treat the rat model by intragastric administration for 45 consecutive days, respectively. The normal rats without IPF were used as the controls. After 15, 30 and 45 days of drug treatment, lung histopathology was assessed. The expression of Cav-1 was determined using real-time quantitative PCR and Western blot; the expression of tumour necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1) and platelet-derived growth factor (PDGF) was determined by enzyme-linked immunosorbent assay.Results: After 15, 30 and 45 days of drug treatment, comparison of the three drug-treated groups with the model group showed significantly lower (p < 0.05) significance of airsacculitis and fibrosis scores of lung tissues, as well as expression of TGF-β1, TNF-α and PDGF, but the expression of Cav-1 was higher (p < 0.05). Compared with the N group, the fibrosis score was significantly lower and the protein expression of Cav-1 was significantly higher in the P group (p < 0.05). Additionally, the expression of Cav-1 was negatively correlated with the airsacculitis and fibrosis scores (r = −0.506, p < 0.01; r = -0.676, p < 0.01) as well as expression of TGF-β1, TNF-α and PDGF (r = −0.590, p < 0.01; r = −0.530, p < 0.01; r = −0.553, p < 0.01).Discussion and conclusion: Pirfenidone, prednisone and acetylcysteine can inhibit airsacculitis and pulmonary fibrosis in rat IPF models, which may be related with enhanced caveolin-1, reduced TNF-α, TGF-β1, PDGF.

BackgroundCystic fibrosis (CF) is a disease characterized by chronic airway infection with a high incidence and poor prognosis. Pseudomonas aeruginosa and Aspergillus fumigatus are pathogens commonly found in CF patients. Clinically, these two microorganisms often coexist in the airway of CF patients. Combined infection with P. aeruginosa and A. fumigatus results in worsening lung function and clinical condition.MethodsIn this review, we focus on the mutual inhibition and promotion mechanisms of P. aeruginosa and A. fumigatus in CF patients. We also summarized the mechanisms of the interaction between these pathogenic microorganisms.ResultsP. aeruginosa inhibits A. fumigatus growth through the effects of phenazines, the quorum sensing system, iron competition, bacteriophages, and small colony variants. P. aeruginosa induces A. fumigatus growth through volatile organic compounds and subbacteriostatic concentrations of phenazines. A. fumigatus interferes with P. aeruginosa, affecting its metabolic growth via phenazine metabolic transformation, gliotoxin production, and reduced antibiotic sensitivity.DiscussionCoexistence of P. aeruginosa and A. fumigatus can lead to both mutual inhibition and promotion. In different stages of CF disease, the interaction between these two pathogenic microorganisms may shift between promotion and inhibition. A discussion of the mechanisms of P. aeruginosa and A. fumigatus interaction can be beneficial for further treatment of CF patients and for improving the prognosis of the disease.