Sulforaphane is a common antioxidant selectively abundant in cruciferous plants, which exhibits effective anti-cancer actions in control of tumorigenesis or progression of various cancers. A recent study has shown that sulforaphane attenuates the EGFR signaling pathway in non-small cell lung cancer (NSCLC), suggesting its potential anti-metastatic effects. In this study we assessed the involvement of sulforaphane and miR-616-5p in epithelial-mesenchymal transition (EMT) and NSCLC metastasis. Sulforaphane suppressed the cell proliferation in human NSCLC cell lines H1299, 95C and 95D with IC 50 values of 9.52±1.23, 9.04±1.90 and 17.35±2.03 μmol/L, respectively. At low concentrations (1-5 μmol/L), sulforaphane dose-dependently inhibited the migration and invasion of 95D and H1299 cells with relatively high metastatic potential. The anti-metastatic action of sulforaphane was confirmed in 95D and H1299 cell xenografts in vivo. In fresh NSCLC tissue samples from 179 patients, miR-616-5p levels were upregulated in late-stage NSCLCs, and strongly correlated with risk of NSCLC recurrence and metastasis. Consistent with the clinic observation, miR-616-5p levels in the 3 NSCLC cell lines were correlated with their metastatic ability, and were decreased by sulforaphane treatment. Silencing miR-616-5p markedly suppressed the migration and invasion of 95D cells in vitro and NSCLC metastasis in vivo. Further studies revealed that miR-616-5p directly targeted GSK3β and decreased its expression, whereas sulforaphane decreased miR-616-5p levels by histone modification, and followed by inactivation of the GSK3β/β-catenin signaling pathway and inhibition of EMT, which was characterized by loss of epithelial markers and acquisition of a mesenchymal phenotype in NSCLC cells. Our findings suggest that sulforaphane is a potential adjuvant chemotherapeutic agent for the prevention of NSCLC recurrence and metastasis, and miR-616-5p can be clinically utilized as a biomarker or therapeutic target to inhibit metastasis.

Background Although oncogenic driver mutations were thought to be mutually exclusive in non‐small cell lung cancer (NSCLC), certain tumors harbor co‐occurring mutations and represent a rare molecular subtype. The evaluation of the clinical features and therapeutic response associated with this NSCLC subtype will be vital for understanding the heterogeneity of treatment response and improving the management of these patients. Methods This retrospective study included 3774 samples from patients diagnosed with NSCLC. All samples were screened for EGFR, ALK, ROS1, KRAS, and BRAF mutation using the amplification‐refractory mutation system. The relationship between concomitant driver mutations and clinicopathologic characteristics, and patient clinical outcomes were evaluated. Results Sixty‐three (1.7%) samples had more than one driver gene mutation. Among these, 43 were coalterations with an EGFR mutation, 20 with an ALK rearrangement, and eight with an ROS1 rearrangement. Except for ROS1 concomitant mutations that were more frequent in male patients (87.5%, P = 0.020), the clinicopathological features of the concomitant mutation patients were not significantly different from those harboring a single EGFR, ALK, or ROS1 mutation. Furthermore, first‐line EGFR‐TKI treatment did not significantly improve the progression‐free survival (PFS) of patients harboring EGFR concomitant mutation, compared to patients harboring a single EGFR mutation. However, for EGFR concomitant mutation patients, TKI therapy was more effective than chemotherapy (median PFS of 10.8 vs 5.2 months, P = 0.023). Lastly, KRAS mutations did not influence the EGFR‐TKI therapy treatment effect. Conclusion In this study, concomitant mutations were found in 1.7% of the NSCLC. EGFR‐TKI therapy was more effective than chemotherapy for patients harboring EGFR concomitant mutation, and ROS1 concomitant mutations were more frequent in male patients. For patients harboring coalterations with an ALK or ROS1 rearrangement, we should be cautious when considering the therapeutic options.

To determine factors associated with delayed discharge of hospitalized patients with coronavirus disease (COVID-19). This retrospective cohort study included 47 patients with COVID-19 admitted to three hospitals in Quanzhou City, Fujian Province, China, between January 21, 2020 and March 6, 2020. Univariate and multivariate logistic regression analyses were conducted to identify factors associated with delayed discharge. The median length of hospital stay was 22 days. Patients in the delayed discharge group (length of hospital stay ≥ 21 days, n = 27) were more likely to have diarrhea, anorexia, decreased white blood cell counts, increased complement C3 and C-reactive protein levels, air bronchograms, undergo thymalfasin treatment, and take significantly longer to convert to a severe acute respiratory syndrome coronavirus (SARS-CoV-2) RNA-negative status than those in the control group (length of hospital stay, < 21 days; n = 20). In multivariate logistic regression analysis, the time to SARS-CoV-2 RNA-negative conversion (odds ratio [OR]: 1.48, 95% confidence interval [CI] 1.09–2.04, P = 0.01) and complement C3 levels (OR 1.14 95% CI 1.02–1.27, P = 0.03) were the only risk factors independently associated with delayed discharge from the hospital. Dynamic monitoring of complement C3 and SARS-CoV-2 RNA levels is useful for predicting delayed discharge of patients.

This study aimed to investigate the clinical features of patients infected with novel coronavirus wild strains, Delta variant strains and Omicron variant strains to provide a reference for early clinical diagnosis and prognostic assessment. The demographic, clinical symptoms and ancillary examination data of 47 patients with novel coronavirus wild type strain infection, 18 with Delta variant infection and 20 with Omicron variant infection admitted to the First Hospital of Quanzhou affiliated with Fujian Medical University were collected and analyzed. The novel coronavirus wild strain and Delta strain were the predominant clinical types; patients infected with the Omicron strain were mainly asymptomatic. Fever and fatigue were the main clinical manifestations in the wild strain and Delta strain groups, whereas dry cough, nasal congestion, sore throat and fever were common clinical manifestations in the Omicron strain group. The Delta strain and Omicron variant groups had fewer comorbidities than the wild-type strain group, but no significant reduction was observed in the negative conversion time of nucleic acids. Significant differences were found in the neutrophil count/lymphocyte count ratio, lymphocyte count, eosinophil count, red blood cell count, hemoglobin level, erythrocyte sedimentation rate, C-reactive protein, prothrombin time, international normalized ratio and plasma D-dimer, PH, PaO 2 , lactic acid and albumin levels among the three groups. Patients infected with the Omicron strain in Quanzhou presented with mild symptoms of the upper respiratory tract as the primary clinical manifestation and had few comorbidities and a good prognosis; however, the negative conversion time of the new coronavirus nucleic acid was still considerably long.

Background: Pulmonary embolism (PE) is the third most common cardiovascular syndrome with an average annual incidence rate of 77 per 100,000 population in the worldwide. The diagnose algorithms for suspected PE are generally include clinical scoring assessment and plasma D-dimer evaluation, patients with high risk of PE require computed tomographic pulmonary angiogram (CTPA) detection for confirmation. Methods: In this retrospective analysis, 1035 patients with suspected PE were recruited. All the patients were clinically received simplified Geneva score (SGS) pre-test, determination of plasma D-dimer level, and CTPA detection. All enrolled patients were grouped according to the CTPA results: PE patients and non-PE patients. Then, receiver operating characteristic (ROC) curve were constructed to determine the optimal D-dimer cutoff point value which is based on Yonden's index (YI). Results: 294 (28.4%) patients were confirmed with PE and 741(71.6%) individuals were regarded as non-PE cases by CTPA detection. Using the SGS pre-test, 829 (80.1%) patients were classified PE-unlikely (SGS ≤ 2) and 206 (19.9%) patients were PE-likely (SGS ≥ 3). Patients with D-dimer levels above 1.96 mg/L had a significant risk to suffer from PE (area under curve (AUC), 0.707; 95% CI, 0.678-0.735; p < 0.05). Meanwhile, in patients with SGS ≥ 3, the D-dimer cutoff point value moved to 2.2 mg/L (AUC, 0.644; 95% CI, 0.574-0.709; p < 0.05). Conclusion: D-dimer test in combination with SGS pre-test could improve the accuracy of PE diagnosis. Patients with D-dimer levels over 1.96 mg/L (4 times of the normal level) have a significant risk for PE. In patients with SGS ≥ 3, the D-dimer cutoff point concentration for PE risk moves to the levels of 2.2 mg/L.