Alterations of fecal bacterial communities in patients with lung cancer.

Emerging evidence suggests the microbiome may affect a number of diseases, including lung cancer. However, the direct relationship between gut bacteria and lung cancer remains uncharacterized. In this study, we directly sequenced the hypervariable V1-V2 regions of the 16S rRNA gene in fecal samples from patients with lung cancer and healthy volunteers. Unweighted principal coordinate analysis (PCoA) revealed a clear difference in the bacterial community membership between the lung cancer group and the healthy control group. The lung cancer group had remarkably higher levels of Bacteroidetes, Fusobacteria, Cyanobacteria, Spirochaetes, and Lentisphaerae but dramatically lower levels of Firmicutes and Verrucomicrobia than the healthy control group (P < 0.05). Despite significant interindividual variation, eight predominant genera were significantly different between the two groups. The lung cancer group had higher levels of Bacteroides, Veillonella, and Fusobacterium but lower levels of Escherichia-Shigella, Kluyvera, Fecalibacterium, Enterobacter, and Dialister than the healthy control group (P < 0.05). Most notably, correlations between certain specific bacteria and serum inflammatory biomarkers were identified. Our findings demonstrated an altered bacterial community in patients with lung cancer, providing a significant step in understanding the relationship between gut bacteria and lung cancer. To our knowledge, this is the first study to evaluate the correlations between certain specific bacteria and inflammatory indicators. To better understand this relationship, further studies should investigate the underlying mechanisms of gut bacteria in lung cancer animal models.

Two single-nucleotide polymorphisms of the RELN gene and symptom-based and developmental deficits among children and adolescents with autistic spectrum disorders in the Tianjin, China.

Increasing evidence has revealed that genetic variants in Reelin (RELN) gene, especially single-nucleotide polymorphisms (SNPs), correlate with autistic spectrum disorders (ASD) risk; however, no consensus have been reached. This study aimed to provide additional evidence for the association between two SNPs of RELN (i.e., rs736707, rs2229864) and ASD risk, as well as the relationship between RELN gene and symptom-based and developmental deficits of ASD patients in Chinese Han children and adolescents. 157 ASD subjects and 256 typical development (TD) controls were genotyped by TaqMan® genotyping assay. ASD patients were assessed by Childhood Autism Rating Scale (CARS), Autism Behavior Checklist (ABC), and Early Childhood Development Questionnaire (ECDQ). We found that SNP rs2229864 was associated with the genetic predisposition of ASD, whereas a negative association between SNP rs2229864 and symptom-based and developmental features was detected. In contrast, RELN rs736707 correlated with the sensory subscale of the ABC, the relating subscale of the ABC and the total score of ABC, although we did not detect a significant association between SNP rs736707 and ASD risk. Furthermore, a significant rs736707-rs2229864 haplotype was detected. Individuals with a CC haplotype were more likely to have ASD, but individuals with a CT haplotype had more chance be TD controls. Further studies using more samples and including more gene variants in RELN are warranted to confirm our results.

Triptolide reverses the Taxol resistance of lung adenocarcinoma by inhibiting the NF-κB signaling pathway and the expression of NF-κB-regulated drug-resistant genes.

Paclitaxel (or Taxol®) is a first-line chemotherapeutic drug for the treatment of non-small cell lung cancer; however, resistance to the drug is an important factor, which influences the outcome of chemotherapy. The present study aimed to investigate the role of triptolide (TPL) in reversing Taxol­resistant human lung adenocarcinoma and to elucidate the underlying molecular mechanism of resistance reversal mediated by TPL. It was hypothesized that this experimental approach would assist in solving the problem of chemotherapeutic resistance in non­small cell lung cancer, thereby improving the clinical outcomes. The human Taxol­resistant lung adenocarcinoma cell line, A549/Taxol, was established. The resistance index of the cell line was calculated, according to the half maximal inhibitory concentration (IC50) of A549/Taxol IC50 of A549, to be 51.87. The levels of apoptosis and the cell cycle in the A549/Taxol cell line were assessed to confirm the effects of TPL at three different concentrations (0.03, 0.3 and 3 µmol/l) and treatment durations (2, 4, 6 and 12 h) by flow cytometric analysis, and the inhibition of the NF­κB signaling pathway and the expression of NF­κB­regulated drug­resistant proteins were determined by immunofluorescence and western blotting, respectively. The administration of TPL promoted cell apoptosis in the A549/Taxol lung adenocarcinoma Taxol­resistant cell line and also promoted cell cycle regulation. The drug was also able to elicit a reversal of the drug resistance. TPL inhibited the nuclear factor­κB (NF­κB) signaling pathway and the expression of NF­κB­regulated drug­resistant genes, including those for FLICE­like inhibitory protein, X­linked inhibitor of apoptosis protein, Bcl­2, Bcl­xL and cyclo­oxygenase­2. TPL exerted a marked drug­resistance­reversal effect on human lung adenocarcinoma Taxol resistance, and the effect was revealed to be dose­ and time­dependent. In conclusion, TPL exerted its role in the process of resistance reversal by inhibiting the NF­κB signaling pathway, and the transcription and expression of NF-κB-regulated drug-resistant genes.

Endostar combined with cisplatin inhibits tumor growth and lymphatic metastasis of lewis lung carcinoma xenografts in mice.

OBJECTIVE: To investigate the effects of endostar, a recombined humanized endostatin, plus cisplatin on the growth, lymphangiogenesis and lymphatic metastasis of the Lewis lung carcinoma (LLC) in mice. METHODS: A tumor model were established in C57BL/6 mice by intravenious transplantation of LLC cells. Then the mice were randomized to receive administration with NS, endostar, cisplatin, or endostar plus cisplatin. After the mice were sacrificed, tumor multiplicity, tumor size and lymph node metastasis were assessed. Then the expression of vascular endothelial growth factor-c (VEGF-C) and podoplanin were determined by immunohistochemical staining. RESULTS: Endostar plus cisplatin significantly suppressed tumor growth. lymphatic metastasis and prolonged survival time of the mice without obvious toxicity. The inhibition of lymphatic metastasis was associated with decreased microlymphatic vessel density (MLVD) and expression of VEGF-C. CONCLUSIONS: Endostar combined with cisplatin was more effective to suppress tumor growth and lymphatic metastasis than either agent alone. Thus this may provide a rational alternative for lung carcinoma treatment.

[Effects of endostatin on the growth and lymphangiogenesis of Lewis lung carcinoma xenograft in mice].

OBJECTIVE: to investigate the effects of endostar, a recombined humanized endostatin, on the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenograft in mice. METHODS: lewis lung carcinoma (LLC) xenograft were established in C57 mice by intravenous transplantation of 1 × 10(6) cells. Then tumor-bearing mice were assigned into two groups: control group received caudal vein injections of 0.2 ml of 0.9% sodium chloride for 15 days, and treatment group received 500 µg endostar daily. Six weeks after LLC cell injection mice were sacrificed, and then tumor numbers and size were recorded. The expression of vascular endothelial growth factor-c (VEGF-C) and microlymphatic vessel density (MLVD) were observed by immunohistochemical staining. RESULTS: tumor number and size of control group were significantly higher than those of treatment group. The microlymphatic vessel density (MLVD) was 5.7 ± 1.6 in the treatment group, which was markedly lower than in the control mice (7.8 ± 1.6). Two lymph node metastases were observed in treatment group, and eight in control group. Lymphatic metastases were more frequent in control group than in treatment group. Expression of VEGF-C in control group was significantly higher than that in treatment group. CONCLUSION: endostar significantly inhibits the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenografts, and the inhibitory effect is due to its ability to regulate the expression of VEGF-C of tumors in part.

[Relation of vascular endothelial growth factor-D expression to microvessel density, microlymphatic vessel density, and lymph-node metastasis of lung adenocarcinoma].

OBJECTIVE: To investigate the relationship of expression of vascular endothelial growth factor (VEGF)-D to microvessel density (MVD), microlymphatic vessel density (MLVD), and lymph node metastasis in lung adenocarcinoma. METHODS: Fresh specimens of lung adenocarcinoma were collected form 48 patients with lung adenocarcinoma, 28 males and 20 females, aged 35 - 78, during operation. Semi-quantitative RT-PCR was used to detect the mRNA expression of VEGF-D, and immunohistochemistry was used to detect the protein expression of VEGF-D, CD34 (marker of MVD), and VEGF receptor (VEGFR)-3 (marker of MLV). RESULTS: The expression of VEGF-D mRNA in the lung cancer was significantly higher than that in the normal lung tissue, and the expression of VEGF-D protein in the cancerous invasive edge was significantly higher than that in the center of cancerous tissues. Twenty-one of the 29 lung adenocarcinoma patients at stages III - IV were VEGF-D positive, a proportion significantly higher than that of the patients at stages I - II (7/19, P = 0.015). The MLVD of the VEGF-D positive group was 10.25 +/- 2.50, significantly higher than that of the VEGF-D negative group (6.8 +/- 2.2, P < 0.01). Twenty-three of the 28 VEGF-D positive patients showed lymph node metastasis, a proportion significantly higher than that of the VEGF-D negative group (9/20, P = 0.012). CONCLUSION: VEGF-D is related with the lymphangiogenesis and lymph node metastasis in lung adenocarcinoma, but not with angiogenesis.

[Application of correlation spectroscopy method to fiber gas sensor].

In this paper, we employ correlation spectroscopy method to detect gases and gas mixtures which have multi-line absorption in near infrared. The theories of correlation spectroscopy are discussed and a new modulation measure is proposed, which inherits the excellence of the correlation spectroscopy and makes the modulation easy. Then we compare this method with the traditional correlation spectroscopy method. Experimental results for the selective detection of methane by this method are also presented. The change in signal from interference gas is only equal to 7.4% of that from methane absorption. It has been proven that the proposed method is practicable for both theory and experiment. This method can reach a high accuracy for mixed gas detection.