Initial HRCT findings of novel influenza A (H1N1) infection.

OBJECTIVES: The aim of our study was to describe the presentation and illustrate the imaging features of chest high-resolution computed tomography (HRCT) of patients with novel influenza A (H1N1) virus infection. METHODS: Data were collected from 163 hospitalized patients between November 2009 and March 2011, who fulfilled the clinical criteria for H1N1 influenza infection and underwent HRCT examinations within 24 hours of admission. RESULTS: Abnormal findings were observed in 40.5% of the patients. The patients with positive imaging findings were significantly older than patients with normal HRCT findings (P=0.02). The most common finding was ground-glass opacity (GGO) (n=35). Interlobular septal thickening (n=31) and centrilobular nodules (n=30) were the second most frequent findings. Other common findings were consolidation, reticulation, and linear shadow. The most common imaging finding for lung involvement was GGO with a patchy pattern. Pulmonary involvement of the disease may be extensive and variable, but the total volume of affected lung was mostly <1 lobe. CONCLUSION: The baseline HRCT may be valuable and suggestive even for non-severe H1N1 infections. When a severe case or a evolution is suspected, chest CT could be essential both for determining the precise extent of parenchymal damage and for monitoring its evolution.

MiRNA synergistic network construction and enrichment analysis for common target genes in small-cell lung cancer.

BACKGROUND: Small-cell lung cancer (also known as SCLC) is an aggressive form and untreated patients generally die within about 3 months. To obtain further insight into mechanism underlying malignancy with this cancer, an miRNA synergistic regulatory network was constructed and analyzed in the present study. METHOD: A miRNA microarray dataset was downloaded from the NCBI GEO database (GSE27435). A total of 546 miRNAs were identified to be expressed in SCLC cells. Then a miRNA synergistic network was constructed, and the included miRNAs mapped to the network. Topology analysis was also performed to analyze the properties of the synergistic network. Consequently, we could identified constitutive modules. Further, common target genes of each module were identified with CFinder. Finally, enrichment analysis was performed for target genes. RESULTS: In this study, a miRNA synergistic network with 464 miRNAs and 2981 edges was constructed. According to the topology analysis, the topological properties between the networks constructed by LC related miRNAs and LC unrelated miRNAs were significantly different. Moreover, a module cilque0 could be identified in our network using CFinder. The module included three miRNAs (hsa-let-7c, hsa-let-7b and hsa-let-7d). In addition, several genes were found which were predicted to be common targets of cilque0. The enrichment analysis demonstrated that these target genes were enriched in MAPK signaling pathways. CONCLUSIONS: Although limitations exist in the current data, the results uncovered here are important for understanding the key roles of miRNAs in SCLC. However, further validation is required since our results were based on microarray data derived from a small sample size.

[Clinical features of ventilator-associated pneumonia caused by acinetobacter].

OBJECTIVE: To investigate the clinical features of ventilator-associated pneumonia (VAP) caused by acinetobacter. METHODS: The clinical manifestations of 45 cases with ventilator-associated pneumonia caused by acinetobacter between 1995 and 2002 were analyzed. Bacterial susceptibility of acinetobacter strains was determined by Kerby-Bauer method. RESULTS: The mean age of the subjects was 58 +/- 13 years with 31 patients older than 60 years. All the patients had underlying diseases, most of which were respiratory diseases (37.8%), nervous system diseases (22.2%), and trauma (22.2%). Thirteen cases (28.9%) were mixed infections with other bacteria. The main manifestations were fever, purulent secretion, and solidification in the lung. X-ray revealed inflammatory infiltration in lower lobes of both sides. The mortality was 37.8%. The in vitro activity tests of 28 antibiotics against the acinetobacter strains showed that they were multiresistant. Polymysin B, imipenem, minocycline, ofloxacin, and amikacin were relatively active. CONCLUSION: The patients with VAP caused by acinetobacter usually had underlying diseases without unique features and high mortality, and the isolated strains were often mutiresistant. It is necessary to make early diagnosis, select the appropriate agents, and improve the disinfection of the breath loop in the ventilator.

[Treatment of spontaneous metastatic lung cancer with interleukin-12 gene-modified dendritic cells vaccine].

BACKGROUND & OBJECTIVE: Although many works have been done in treatment of metastatic lung cancer, effective method is lacked. This study was designed to investigate the treatment of spontaneous metastatic lung cancer by interleukin-12 (IL-12) gene-modified dendritic cells (DC) vaccine. METHODS: The spontaneous metastatic lung cancer model, prepared by injection of the 3LL Lewis lung cancer cells into the footpads of C57BL/6 mice, were treated by subcutaneous vaccination with tumor antigen peptide Mut1-pulsed, IL-12 gene-modified dendritic cells (DC-IL-12/Mut1) derived from the normal bone marrow. After treatment, the lung weight, the number of lung metastatic nodes, the survival time of the tumor-bearing mice were observed, and the NK and CTL activities were respectively determined. RESULTS: Compared with mice treated with Mut1-pulsed, control LacZ gene modified DC and untreated DC, tumor-bearing mice treated with DC-IL-12/Mut1 had the lightest lung weights (P < 0.01), the least lung metastatic node numbers (P < 0.01), the longest survival time (P < 0.01), also with the induction of potent CTL activity (P < 0.01) and NK activity (P < 0.01). CONCLUSION: Tumor antigen-pulsed, IL-12 gene-modified dendritic cells have significant therapeutic effects on the spontaneous metastatic lung cancer, the possible mechanism involved with induction of CTL activity and enhancement of NK activity.