Experimental Study of Preheated Secondary Air on the Performance of an Updraft Coal Heating Stove.

Although the Chinese government encourages using clean fuels for heating, many households in remote areas still rely on coal as their energy, especially in the Qinghai Tibet Plateau. An updraft coal heating stove was modified to preheat secondary air. The performance of the modified stove was studied compared with a baseline stove. The temperatures in the combustion chamber and near the chimney exit are measured, and the undiluted exhaust concentrations of CO, NO x , and SO2 are obtained. The results indicated that the temperatures and exhaust gas concentrations varied periodically with the coal addition. The oxygen concentration in the flue gas for the modified stove is higher than that for the baseline stove, and the O2 concentration was decreased with the increase in fuel feed rate. The CO concentration peaked 5-15 min after fuel addition and descended quickly toward a baseline with the higher fuel feed rates. It remained almost unchanged at the beginning and then slightly increased when the combustion began to fade with a lower fuel feed rate for the modified stove. The NO x emission for the modified stove is generally lower than that for the baseline stove. The NO x formation during coal combustion mainly comes from prompt NO and fuel NO, while the SO2 emission is mainly related to the sulfur element in the raw coal in the present work. The modified stove is effective in reducing NO x and SO2 emissions. However, the CO emission of the modified stove is higher than that of the baseline stove, especially at the end of the batch.

The efficacy and safety of anti-PD-1/PD-L1 antibody therapy versus docetaxel for pretreated advanced NSCLC: a meta-analysis.

Antibodies against the immune checkpoint proteins PD-1 and PD-L1 are novel therapeutic drugs for the treatment of advanced non-small cell lung cancer (NSCLC). Many clinical trials involving these drugs achieved breakthroughs in patients previously treated for advanced NSCLC. However, the results of these clinical studies are not consistent. In this report, we performed a meta-analysis to assess the efficacy and safety of anti-PD-1/PD-L1 antibodies compared with docetaxel treatment for advanced NSCLC patients from 5 randomized clinical trials. We demonstrated that the patients in anti-PD-1/PD-L1 antibody therapy groups had significantly longer overall survival (OS) (HR = 0.69, 95% CI 0.63-0.75, P < 0.05) and progression-free survival (PFS) (HR = 0.76, 95% CI 0.63-0.92, P < 0.05) than those in chemotherapy groups, especially PD-L1 positive patients. Anti-PD-1/PD-L1 antibodies improved the objective response rate (ORR) compared with docetaxel (OR = 1.64, 95% CI 1.19-2.26, p < 0.05). In addition, the anti-PD-1/PD-L1 antibody therapy had fewer treatment-related adverse events (AEs) (OR = 0.33, 95% CI 0.28-0.39, P < 0.05) than docetaxel, especially the grade ≥3 AEs (OR = 0.18, 95% CI 0.12-0.28, P < 0.001). In conclusion, our study revealed that, compared with docetaxel, anti-PD-1/PD-L1 antibody therapy improved clinical efficacy and safety in previously treated advanced NSCLC patients. This therapy may be a promising treatment for advanced NSCLC patients.

miR-367 promotes tumor growth by inhibiting FBXW7 in NSCLC.

miR-367 is one of the most abundant miRNAs in human embryonic stem cells (hESCs) and is mainly involved in maintaining the pluripotency of stem cells. However, its role in cancer development remains poorly understood. In the present study, we explored the function and mechanism of the endogenous miR-367 in non-small cell lung cancer (NSCLC). In the present study, we demonstrated that the level of miR-367 in NSCLC was significantly higher than that in adjacent normal tissues, and its upregulation was positively correlated with tumor size, tumor differentiation and tumor-node-metastasis (TNM) stage. miR-367 was an indicator of a poorer prognosis in NSCLC patients. Furthermore, overexpression of miR-367 significantly inhibited apoptosis and enhanced proliferation by promoting cell cycle transition from G1 to S phase. In contrast, knockdown of miR-367 markedly reversed the cellular events observed with miR-367 overexpression. Moreover, we identified that F-box and WD repeat domain-containing 7 (FBXW7) is a novel target of miR-367. It reverses the oncogenic effects of miR-367 by downregulating its substrates, c-Myc and c-Jun, in NSCLC cells. Finally, studies in vivo revealed that knockdown of miR-367 inhibited the growth of xenografts in the nude mice by increasing the expression of FBXW7. In summary, our findings indicate that miR-367 exerts tumor-promoting effect by negatively regulating FBXW7 in NSCLC, and it could become a potential therapeutic target for NSCLC intervention.

XIAP inhibits mature Smac-induced apoptosis by degrading it through ubiquitination in NSCLC.

X-linked inhibitor of apoptosis protein (XIAP) and second mitochondrial-derived activator of caspase (Smac) are two important prognostic biomarkers for cancer. They are negatively correlated in many types of cancer. However, their relationship is still unknown in lung cancer. In the present study, we found that there was a negative correlation between Smac and XIAP at the level of protein but not mRNA in NSCLC patients. However, XIAP overexpression had no effect on degrading endogenous Smac in lung cancer cell lines. Therefore, we constructed plasmids with full length of Smac (fSmac) and mature Smac (mSmac) which located in cytoplasm instead of original mitochondrial location, and was confirmed by immunofluorescence. Subsequently, we found that mSmac rather than fSmac was degraded by XIAP and inhibited cell viability. CHX chase assay and ubiquitin assay were performed to illustrate XIAP degraded mSmac through ubiquitin pathway. Overexpression of XIAP partially reverted apoptotic induction and cell viability inhibition by mSmac, which was due to inhibiting caspase-3 activation. In nude mouse xenograft experiments, mSmac inhibited Ki-67 expression and slowed down lung cancer growth, while XIAP partially reversed the effect of mSmac by degrading it. In conclusion, XIAP inhibits mature Smac-induced apoptosis by degrading it through ubiquitination in NSCLC.

OTUD7B and NIK expression in non-small cell lung cancer: Association with clinicopathological features and prognostic implications.

PURPOSE: To investigate the correlation among OTUD7B and NIK expression and the clinicopathological characteristics in NSCLC patients. METHODS: One hundred and twenty patients were involved in this study. We detected OTUD7B and NIK expression by immunohistochemistry and analyzed their correlation with clinicopathological data. RESULTS: The expression of OTUD7B and NIK were negatively correlated in NSCLC tumor samples (rs=-0.421, P<0.001). The higher expression of OTUD7B was associated with smaller tumor size(P=0.018), less lymph node metastasis (P=0.012) and earlier TNM stage(P=0.039), while the higher expression of NIK was only related to more lymph node metastasis(P=0.031) and later TNM stage(P=0.011). MMP-9 was negatively correlated with OTUD7B and positively correlated with NIK. In addition, the high expression of OTUD7B was associated with good prognosis of NSCLC patients (log-rank=6.714, P=0.0096), and a high OTUD7B/low NIK index can predict an even better prognosis (log-rank=11.794, P=0.0006). Moreover, the multivariate Cox regression analysis showed that OTUD7B rather than NIK is an independent marker of overall survival in NSCLC patients(HR=1.602, 95% CI 1.009-2.544, P=0.046). CONCLUSIONS: OTUD7B and NIK may play important roles in the development of lung cancer. The combination of OTUD7B and NIK expression may be a good index for predicting the prognosis of NSCLC.

Fibronectin protects lung cancer cells against docetaxel-induced apoptosis by promoting Src and caspase-8 phosphorylation.

Fibronectin is involved in orchestrating many diverse cellular behaviors, including adhesion, invasion, differentiation, and proliferation and recently has also been shown to participate in the development of chemoresistance. In this study, we found that fibronectin expression was inversely correlated with clinical responses to docetaxel treatment in non-small cell lung cancer patients. Subsequently, we showed that fibronectin pretreatment could enhance cell viability and reduce apoptosis in docetaxel-treated lung cancer cells because fibronectin induced phosphorylated Src and caspase-8, rendering the later inactive, thus inhibiting docetaxel-induced apoptosis. The inhibition of apoptosis by fibronectin was found to be enhanced by Src overexpression and reversed by Src knockdown in lung cancer cells. Further investigation revealed that a downregulation of phospho-Src via treatment with a Src kinase inhibitor could also abolish fibronectin activity and recover docetaxel-induced apoptosis. Molecular studies revealed that this reversion was due to decreased phospho-Src levels rather than a reduction in total Src expression. Inhibition of phospho-Src reduced phospho-caspase-8 and promoted caspase-8 activity, restoring apoptosis following docetaxel and fibronectin co-treatment. Finally, xenografts experiments demonstrated that fibronectin promoted lung cancer cell proliferation during docetaxel treatment in vivo. Our findings indicate that fibronectin promotes Src and caspase-8 phosphorylation in lung cancer cells, which decreases caspase-8 activation and protects tumor cells from docetaxel-induced apoptosis. Therefore, the fibronectin/Src/caspase-8 pathway may play a crucial role in docetaxel resistance in lung cancer.