Seven preoperative factors have strong predictive value for postoperative pneumonia in patients undergoing thoracoscopic lung cancer surgery.

Background: Postoperative pneumonia (POP) is a hospital acquired pneumonia that occurs >48 hours after tracheal intubation. The diagnosis of POP should be based on clinical and radiological findings within 30 days after surgery. It is a common complication after thoracoscopic surgery for lung cancer patients. However, the specific impact of preoperative comorbidities on the incidence of POP remains unclear. This study aimed to analyze the preoperative data of patients with lung cancer to help surgeons predict the risk of incidence of POP after thoracoscopic lung resection. Methods: This study is a prospective study that included patients with lung cancer who were scheduled for thoracoscopic surgery in 1 year. All cases came from two medical centers. Preoperative demographic information, tumor information, preoperative comorbidities, quality of life scores, and incidence of POP were collected. Variables were screened by univariate analysis and multivariate regression. Finally, a prediction model was constructed. A total of 53 preoperative factors were included as candidate predictors. The binary outcome variable was defined as the presence or absence of POP. The incidence of POP was the primary outcome variable. The predictive performance of the model was verified internally through 1,000 iterations of bootstrap resampling. Results: A total of 1,229 patients with lung cancer who underwent thoracoscopic surgery were enrolled. In addition, 196 cases (15.95%) had POP; 1,025 (83.40%) patients had comorbid conditions. The total number of comorbidity diagnosed in all samples was 2,929. The prediction model suggested that patients with advanced age, high body mass index (BMI), smoking, poor physical condition, respiratory diseases, diabetes, and neurological diseases were more likely to develop POP. The area under the curve (AUC) and Brier scores were 0.851 and 0.091, respectively. The expected and observed results were in strong agreement, according to the likelihood of POP calibration curve. Conclusions: The constructed model is capable of evaluating the probability of POP occurrence in patients with lung cancer. Seven preoperative factors in patients with lung cancer were found to be associated with increased probability of having pneumonia after thoracoscopic lung resection. This model can help predict the incidence of POP after surgery.

ß-Amyrin ameliorates pulmonary fibrosis by inhibiting inflammatory response and oxidative stress in mice.

The study aimed to determine efficacy and mechanisms of ß-Amyrin on pulmonary fibrosis. Use bleomycin (BLM) to induce the marine model of pulmonary fibrosis. ß-Amyrin (20, 40, 80 mg/kg) was once treated via intragastrical administration for five consecutive days when after BLM stimulation. HE/Masson staining, hydroxyproline (HYP) content, Arterial blood gas analysis (BGA), inflammatory cytokines and oxidative stress factors were performed in this study. The lung gas-exchange function was significantly improved after being treated ß-Amyrin with different concentrations, while IL-6, IL-1ß, TNF-α and MCP-1 levels were decreased. And the increased fibrotic lesion in lung was also determined after treatment of ß-Amyrin. Additionally, reduced MDA level and increase levels of GPX, SOD and GSH were also demonstrated using ß-Amyrin in BLM-induced mice in a dose-dependent manner. In conclusions, our study determined that ß-Amyrin has a potent efficacy in protecting against BLM-induced pulmonary fibrosis via suppressing inflammatory response and oxidative stress.

Utilities and placement skills of the incision protective sleeve in video-assisted thoracoscopic surgery (VATS).

BACKGROUND: The incision protective sleeve can protect incisions and help to establish an operating port and thus has been widely applied in thoracic surgeries. However, its other utilities are often neglected. This article explores the additional functions and placement techniques of incision protective sleeves in video-assisted transthoracic surgery (VATS). METHODS: Operators with different surgical experience were divided into three groups: resident group, attending surgeon group, and professor group. Each group independently chose one of the four surgical maneuvers, and the incision protective sleeve was placed during the operation. Up to 200 operations were randomly selected in each group, and the patients' gender, age, incision site, incision length, the operator's experience, and the time and technique of incision protective sleeve placement were recorded. CT was performed to measure the thickness of chest wall and the width of intercostal spaces. Data were analyzed using SPSS 21.0 software package. Multivariate linear regression analysis was performed was performed for the time required for incision protective sleeve placement. RESULTS: The operator's experience was inversely related to the time required for incision protective sleeve placement, width of intercostal spaces was negatively correlated with operative time, chest wall thickness and incision length were positively correlated with operative time. Among the maneuvers, incision protective sleeve placement skills were significant different. CONCLUSIONS: The placement of the incision protective sleeve for VATS is affected by multiple factors, which are not only related to the patient's condition, chest wall thickness and intercostal space, but also closely related to the operator's experience and the manipulation adopted.

A meta-analysis of levetiracetam for randomized placebo-controlled trials in patients with refractory epilepsy.

OBJECTIVE: The objective of this study was to investigate the efficacy and safety profile of levetiracetam as add-on therapy in patients with refractory epilepsy. METHODS: Web of Science, MEDLINE (Ovid and PubMed), Cochrane Library, EMBASE, and Google Scholar were systematically searched to identify potential eligible randomized controlled trials by two reviewers independently. Pooled estimates of risk ratios (RRs) for 50%, 75%, and 100% reduction from baseline were calculated using the fixed-effect model or random-effect model. Quality of included studies was assessed with the Cochrane Collaboration's Risk of Bias tool. Serious adverse events and withdrawals induced by interventions and the most common side effects were analyzed. RESULTS: Seventeen trials with a total of 3,205 participants were included in this meta-analysis, including 14 trials for adulthood and three trials for children. Pooled estimates suggested that levetiracetam was an effective anti-epileptic drug at 1,000-3,000 mg/day (RR =2.00 for 1,000 mg/day, RR =2.68 for 2,000 mg/day, RR =2.18 for 3,000 mg/day) for adults and 60 mg/kg/day (RR =2.00) for children compared to placebo in terms of 50% reduction from baseline. Likewise, as for seizure freedom rate, levetiracetam had an advantage over placebo at 1,000-3,000 mg/day (RR =5.84 for 1,000 mg/day, RR =4.55 for 2,000 mg/day, RR =4.57 for 3,000 mg/day, respectively) for adults and 60 mg/kg/day (RR =4.52) for children. Regarding safety profile, patients treated with levetiracetam had significantly higher occurrence than placebo for somnolence, asthenia, dizziness, infection, nasopharyngitis, anxiety, and irritability; however, most studies reported that these adverse events were mild and transient. CONCLUSION: Levetiracetam is an effective anti-epileptic drug for both adults and children with generalized or partial-onset refractory seizures at 1,000-3,000 or 60 mg/kg/day, with a favorable adverse event profile.

Identification of novel lncRNAs involved in the pathogenesis of childhood acute lymphoblastic leukemia.

This study aimed to explore novel long non-coding RNAs (lncRNAs) and the underlying mechanisms involved in childhood acute lymphoblastic leukemia (cALL). The GSE67684 dataset was downloaded from the Gene Expression Omnibus. Differentially expressed genes (DEGs) and lncRNAs (DELs) between Days 0, 8, 15 and 33 were isolated using random variance model corrective analysis of variance. Overlapping DEGs and DELs were clustered using Cluster 3.0. Bio-functional enrichment analysis was performed using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). Interactions between lncRNAs and mRNAs were calculated using dynamic simulations, and interactions among mRNAs were predicted using the STRING database. lncRNA-mRNA and protein-protein interaction (PPI) networks were visualized using Cytoscape. Subsequently, the expression levels of lncRNAs in biological samples from children with or without cALL were validated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). A total of 593 overlapping DEGs and 21 DELs were identified. After clustering, Profile 26 exhibited a continuously increasing temporal trend, whereas Profile 1 exhibited a continuous decreasing trend. Upregulated DEGs were significantly enriched in 1,825 GO terms and 166 KEGG pathways, whereas downregulated DEGs were significantly enriched in 196 GO terms and 90 KEGG pathways. The lncRNAs NONHSAT027612.2 and NONHSAT134556.2 were the top two regulators in the lncRNA-mRNA network. Toll-like receptor 4, cathepsin G, nucleotide-binding oligomerization domain containing 2 and cathepsin S may be considered the hub genes of the PPI network. RT-qPCR results indicated that the expression levels of the lncRNAs NONHSAT027612.2 and NONHSAT134556.2 were significantly elevated in the blood and bone marrow of patients with cALL compared with the controls. In conclusion, the lncRNAs NONHSAT027612.2 and NONHSAT134556.2 may serve important roles in the pathogenesis of cALL via regulating immune response-associated pathways.

Albiflorin alleviates ovalbumin (OVA)-induced pulmonary inflammation in asthmatic mice.

In the present study, the effects of albiflorin (ALB) on the pulmonary inflammation induced by ovalbumin (OVA) in an asthmatic mouse model were investigated. Airway hyperreactivity (AHR) in asthmatic mice was detected using the acetylcholine stimulation test. Eosinophilia cells in the serum of asthmatic mice were counted. Hematoxylin and eosin (H&E) staining was used to observe pathological changes in lung tissue. Inflammatory cytokines, including interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-α were detected in bronchoalveolar lavage fluid (BALF) and lung tissue using enzyme-linked immunosorbent assay (ELISA). Western blotting was used to detect the mitogen-activated protein kinase/nuclear factor kappa B (MAPK/NF-κB) signaling pathway in the lungs of asthmatic mice. The results from the present study indicated that ALB dramatically suppressed the expression of inflammatory cytokines including IL-1ß, IL-6, and TNF-α, and inflammatory cells. In addition, ALB significantly decreased malondialdehyde (MDA) content as well as increased superoxide dismutase (SOD) activity. ALB also alleviated AHR in asthmatic mice and improved pathological changes in the lungs. In addition, ALB inhibited the MAPK/NF-κB signaling pathway in the lungs of the asthmatic mice. Thus, ALB appears to inhibit lung inflammation in asthmatic mice via regulation of the MAPK/NF-κB signaling pathway.

Computational design of peptide ligands to target the intermolecular interaction between viral envelope protein and pediatric receptor.

The recognition and binding of viral envelope protein to pediatric receptor subverts the membrane-trafficking apparatus to mediate virion export in young children. Here, we described a successful computational design of peptide ligands to target the intermolecular interaction between the virus large envelope protein (LHB) and adaptin receptor (ADT). Based on the crystal structure of ADT in complex with an oligopeptide segment corresponding to the core binding site of LHB, a sequence-specific amino acid preference profile was determined systematically for the ADT-binding peptides using structural bioinformatics approach. With the information harvested from the profile, a genetic evolution procedure was run to improve the biological potency of a peptide population generated randomly from the LHB. A number of potential hits were obtained from the evolution, and four were measured to interact with ADT at micromolar level. A high-affinity hit peptide was then optimized according to computational structural analysis. It is revealed that a potent peptide can be divided into three regions, i.e. a negatively charged region at N-terminus, a hydrophobic core region in middle, and a small, polar region at C-terminal tail. In addition, the two termini of peptide are partially out of the active pocket of ADT, thus contributing moderately to the peptide binding.

Fluoxetine, an Antidepressant Drug, Inhibited Cigarette Smoke-Induced Pulmonary Inflammation and Apoptosis in Rats.

The present study was designed to evaluate the anti-inflammatory effect of fluoxetine (Flu) against cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD) in rats. Forty male Sprague-Dawley (SD) rats were randomly assigned to five groups: control group, CS group, dexamethasone (2 mg/kg) group, and flu (2 mg/kg). H&E staining demonstrated that Flu inhibited CS-induced pathological injury. In addition, Flu could restore the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in serum. Flu also inhibited the levels of cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1ß (IL-1ß). Furthermore, flu significantly inhibited the protein levels of TLR/NF-κB and apoptosis pathway in CS-induced rats. Our findings suggested that flu might effectively ameliorate the progression of COPD via inflammation and apoptosis pathway in rats.

Astragaloside IV ameliorates necrotizing enterocolitis by attenuating oxidative stress and suppressing inflammation via the vitamin D3-upregulated protein 1/NF-κB signaling pathway.

Astragaloside IV (AS-IV) is a flavonoid from the plant Astragalus membranaceus (Fisch) Bge that has a wide range of therapeutic effects. The aim of the present study was to examine the effect of AS-IV on rats with necrotizing enterocolitis (NEC) under oxidative stress and inflammation. Newborn Sprague-Dawley rats were induced with NEC by asphyxia and hypothermia applied on 3 consecutive days. The rats were orally administered AS-IV at 25, 50 and 75 mg/kg for 4 days. The results revealed that AS-IV administration prevented NEC-induced decrease in the concentration of malondialdehyde and myeloperoxidase, and increase in the activity of glutathione (GSH) and superoxide dismutase in murine models. AS-IV also inhibited NEC-induced elevation in the levels of interleukin (IL)-6, IL-1ß, tumor necrosis factor-α and nuclear factor (NF)-κB. The effects of AS-IV were achieved under inflammation and oxidative stress. Western blotting demonstrated that AS-IV substantially inhibited the phosphorylated (p)-IκBα, NF-κBp65, p-NF-κBp65 protein levels and increased vitamin D3 upregulated protein 1 (VDUP1) and IκBα protein levels. These data indicate that AS-IV may be effective in the protection of NEC-induced ileum degeneration by inhibiting the levels of inflammatory markers and oxidative stress via the regulation of the VDUP1/NF-κB signaling pathway.

Suppression of P2X7/NF-κB pathways by Schisandrin B contributes to attenuation of lipopolysaccharide-induced inflammatory responses in acute lung injury.

The aim of the present study was to assess the effects and mechanisms of Schisandrin B (SchB) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS (1 mg/kg), and SchB (25, 50, and 75 mg/kg) was injected 1 h before LPS challenge by gavage. After 12 h, bronchoalveolar lavage fluid (BALF) samples and lung tissues were collected. Histological studies demonstrated that SchB attenuated LPS-induced interstitial edema, hemorrhage, and infiltration of neutrophils in the lung tissue. SchB pretreatment at doses of 25, 50, and 75 mg/kg was shown to reduce LPS-induced lung wet-to-dry weight ratio and lung myeloperoxidase activity. In addition, pretreatment with SchB lowered the number of inflammatory cells and pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1ß, and interleukin-6 in BALF. The mRNA and protein expression levels of nuclear factor kappa B (NF-κB) signaling-related molecules activated by P2X7 were investigated to determine the molecular mechanism of SchB. The findings presented here suggest that the protective mechanism of SchB may be attributed partly to the decreased production of pro-inflammatory cytokines through the inhibition of P2X7/NF-κB activation.

MiR-455 enhances adipogenic differentiation of 3T3-L1 cells through targeting uncoupling protein-1.

Accumulating evidence suggests that microRNAs (miRNAs) play an important role in regulating the pathways in adipose tissue that control processes such as adipogenesis, insulin resistance, and inflammation. Adipogenic differentiation of preadipocytes is a complex process regulated by various factors including miRNAs and cytokines. MiR-455 is a well-known miRNA that enhances adipogenesis. Uncoupling protein-1 (UCP-1), a heparinbinding growth factor, plays a negative role in adipogenesis. In this investigation, we demonstrate that UCP-1 is a target gene of miR-455 during adipogenic differentiation in 3T3-L1 preadipocytes. MiR-455 downregulates UCP-1 expression through interaction with a target site of miR-455 in the coding region of mouse UCP-1. The rare codons upstream of the target site regulate miR-455-induced translational knockdown of UCP-1, which provides more insight into the mechanism of adipogenic differentiation. Thus, these results suggest that the acceerative adipogenic effect of miR-455 in 3T3-L1 cells is due, at least in part, to suppression of UCP-1.