A new nomogram prediction model for pulmonary embolism in older hospitalized patients.

Purpose: Diagnosing pulmonary embolism (PE) in older adults is relatively difficult because of the atypical clinical symptoms of PE in older adults accompanied by multiple complications. This study aimed to establish a nomogram model to better predict the occurrence of PE in older adults. Methods: Data were collected from older patients (≥65 years old) with suspected PE who were hospitalized between January 2012 and July 2021 and received confirmatory tests (computed tomographic pulmonary angiography or ventilation/perfusion scanning). The PE group and non-PE (control) group were compared using univariable and multivariable analyses to identify independent risk factors. A nomogram prediction model was constructed with independent risk factors and verified internally. The effectiveness of the nomogram model, Wells score, and revised Geneva score was assessed using the area under the receiver operating characteristic curve (AUC). Results: In total, 447 eligible older patients (290 PE patients and 157 non-PE patients) were enrolled. Logistic regression analysis revealed nine independent risk factors: smoking, inflammation, dyspnea, syncope, mean corpuscular hemoglobin concentration, indirect bilirubin, uric acid, left atrial diameter, and internal diameter of the pulmonary artery. The AUC, sensitivity, and specificity of the nomogram prediction model were 0.763 (95 % confidence interval, 0.721-0.802), 74.48 %, and 67.52 %, respectively. The nomogram showed superior AUC compared to the Wells score (0.763 vs. 0.539, P < 0.0001) and the revised Geneva score (0.763 vs. 0.605, P < 0.0001). Conclusions: This novel nomogram may be a useful tool to better recognize PE in hospitalized older adults.

Long non­coding RNA HHIP­AS1 inhibits lung cancer epithelial­mesenchymal transition and stemness by regulating PCDHGA9.

The aim of the present study was to investigate the effect of hedgehog­interacting protein antisense RNA 1 (HHIP­AS1) on epithelial­mesenchymal transition (EMT) and cellular stemness of human lung cancer cells by regulating the microRNA (miR)­153­3p/PCDHGA9 axis. Reverse transcription­quantitative PCR was used to compare the expression of HHIP­AS1 in lung cancer and adjacent normal lung tissues. In addition, the correlation of HHIP­AS1 with E­cadherin, Vimentin, N­cadherin and Twist1 was analyzed. HHIP­AS1 overexpression vector was transfected into lung cancer A549 and NCI­H1299 cell lines. Cell Counting Kit­8 and Transwell and clonogenic assays were used to detect the proliferation, invasion and clonogenesis of the lung cancer cells, respectively. The associations among HHIP­AS1, miR­153­3p and PCDHGA9 were predicted by bioinformatics analysis and verified by a dual­luciferase reporter system. The results showed that the expression of HHIP­AS1 in lung cancer tissues was significantly lower than that in normal tissues (P<0.001). HHIP­AS1 was positively correlated with E­cadherin and negatively correlated with Vimentin, N­cadherin and Twist1. HHIP­AS1 overexpression inhibited the proliferation, invasion and clonal formation of the A549 and NCI­H1299 cells. The luciferase reporter system verified that HHIP­AS1 could adsorb miR­153­3p and that PCDHGA9 was the target gene of miR­153­3p. A549 cells were transfected with HHIP­AS1 overexpression vector and miR­153­3p mimic, and the miR­153­3p mimic had a mitigating effect on HHIP­AS1 inhibition (P<0.001). In conclusion, HHIP­AS1 inhibits the EMT and stemness of lung cancer cells by regulating the miR­153­3p/PCDHGA9 axis. Thus, HHIP­AS1 may be a new potential target for lung cancer treatment.

Lapiferin protects against H1N1 virus-induced pulmonary inflammation by negatively regulating NF-kB signaling.

H1N1 virus-induced excessive inflammatory response contributes to severe disease and high mortality rates. There is currently no effective strategy against virus infection in lung. The present study evaluated the protective roles of a natural compound, lapiferin, in H1N1 virus-induced pulmonary inflammation in mice and in cultured human bronchial epithelial cells. Initially, Balb/C mice were grouped as Control, H1N1 infection (intranasally infected with 500 plaque-forming units of H1N1 virus), lapiferin (10 mg/kg), and H1N1+lapiferin (n=10/group). Lung histology, expression of inflammatory factors, and survival rates were assessed after 14 days of exposure. Administration of lapiferin significantly alleviated the virus-induced inflammatory infiltrate in lung tissues. Major pro-inflammatory cytokines, such as interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-α, were decreased at both mRNA and protein levels by lapiferin administration in the lung homogenate. Lapiferin also reduced inflammatory cell numbers in bronchoalveolar fluid. Mechanistically, lapiferin suppressed the transcriptional activity and protein expression of NF-κB p65, causing inhibition on NF-κB signaling. Pre-incubation of human bronchial epithelial cells with an NF-κB signaling specific activator, ceruletide, significantly blunted lapiferin-mediated inhibition of pro-inflammatory cytokines secretion in an air-liquid-interface cell culture experiment. Activation of NF-κB signaling also blunted lapiferin-ameliorated inflammatory infiltrate in lungs. These results suggested that lapiferin was a potent natural compound that served as a therapeutic agent for virus infection in the lung.

Lapiferin protects against H1N1 virus-induced pulmonary inflammation by negatively regulating NF-kB signaling

H1N1 virus-induced excessive inflammatory response contributes to severe disease and high mortality rates. There is currently no effective strategy against virus infection in lung. The present study evaluated the protective roles of a natural compound, lapiferin, in H1N1 virus-induced pulmonary inflammation in mice and in cultured human bronchial epithelial cells. Initially, Balb/C mice were grouped as Control, H1N1 infection (intranasally infected with 500 plaque-forming units of H1N1 virus), lapiferin (10 mg/kg), and H1N1+lapiferin (n=10/group). Lung histology, expression of inflammatory factors, and survival rates were assessed after 14 days of exposure. Administration of lapiferin significantly alleviated the virus-induced inflammatory infiltrate in lung tissues. Major pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, were decreased at both mRNA and protein levels by lapiferin administration in the lung homogenate. Lapiferin also reduced inflammatory cell numbers in bronchoalveolar fluid. Mechanistically, lapiferin suppressed the transcriptional activity and protein expression of NF-κB p65, causing inhibition on NF-κB signaling. Pre-incubation of human bronchial epithelial cells with an NF-κB signaling specific activator, ceruletide, significantly blunted lapiferin-mediated inhibition of pro-inflammatory cytokines secretion in an air-liquid-interface cell culture experiment. Activation of NF-κB signaling also blunted lapiferin-ameliorated inflammatory infiltrate in lungs. These results suggested that lapiferin was a potent natural compound that served as a therapeutic agent for virus infection in the lung.

Effect of kaolin on floc properties for reactive orange removal in continuous coagulation process.

Magnesium hydroxide was used as a coagulant for treating reactive orange wastewater in a real continuous process. Effects of kaolin on coagulation performance and floc properties were investigated with controlled experiments through floc size distribution, zeta potential, scanning electron microscopy and Fourier transform infrared spectroscopy. Kaolin had significant influence on magnesium hydroxide-reactive orange floc formation and growth. The results showed that average floc size reached 16.31, 12.88 and 20.50 µm, respectively, in the rapid mixer, flocculation basin and sedimentation tank when kaolin concentration was 10 mg/L and reactive orange initial concentration was 0.25 g/L. The floc size tended to increase with the increase of kaolin suspension to 10 mg/L. All of the flocs under investigation showed that floc breakage led to decreased average floc size and remained stable in the flocculation basin. Reactive orange and kaolin could be removed effectively in the continuous coagulation process. Reactive orange was adsorbed in the surface of magnesium hydroxide through charge neutralization and adsorption.

[Heavy metal concentrations and pollution assessment of edible crops grown on restored manganese mine lands in Guangxi, South China].

A survey on the crops grown on the restored manganese mine lands in Pingle and Lipu of Guangxi was conducted, and the heavy metal concentrations in the edible parts of the crops were analyzed. The results showed that the heavy metal concentrations in the crops were 1.18-20.46 mg x kg(-1) for Zn, 0.52-16.16 mg x kg(-1) for Pb, 0.33-6.62 mg x kg(-1) for Cr, 0.01-6.24 mg x kg(-1) for Cu, and 0.01-2.76 mg x kg(-1) for Cd. Among the crops, beans had the highest concentrations of almost all test metals, followed by potatoes. The assessment of single factor pollution indices indicated that in the main, the crops were not polluted by Zn and Cu, but heavily polluted by Pb, Cr and Cd, with the pollution rate being 100%, 96.9% and 75.0%, respectively. Comprehensive pollution index indicated that all the crops were polluted by heavy metals, with the heavy, medium and light pollution grade being 87.5%, 9.4% and 3.1%, respectively. Planting edible crops directly on manganese mine wastelands might have great risk for human health, and the existing restoration patterns should be reconsidered.