MWA is an effective, safe and minimally invasive treatment for the patients with lung cancer who cannot be tolerated by surgical resection.

BackgroundCardiovascular diseases (CVDs) are at a badly high-risk of morbidity and mortality in the world.MethodsOur study was attempted to investigate the cardioprotective role of curcumin. Hearts injury was assessed in isolated hearts and the rats of coronary artery ligated.Results and ConclusionsThe inhibition of pro-inflammatory cytokines was observed by curcumin in coronary artery ligated rats. ST segment was also reduced by curcumin. Triphenyltetrazolium chloride staining (TTC) staining and pathological analysis were also showed that curcumin could dramatically alleviate myocardial injury. Besides, the results in vitro also demonstrated that curcumin could improved the function of isolated hearts. Besides, the expressions of inflammation-related pathway in both rats and isolated hearts treated with curcumin were significantly decreased. The present study investigated the protective effects of curcumin on myocardial injury and its mechanism.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related mortality worldwide. However, there is a shortage of suitable diagnostic markers for early stages of NSCLC, and therapeutic targets are limited. Right open reading frame (Rio) kinase 2 (RIOK2) and Nin one binding (NOB1) protein are important accessory factors in ribosome assembly and are highly expressed in malignant tumours; moreover, they interact with each other. However, the RIOK2 expression profile and its clinical significance as well as NOB1’s mechanism in NSCLC remain unknown. In this study, NSCLC cell lines and 15 NSCLC tumour tissues (paired with adjacent normal lung tissues) were collected for a real-time quantitative PCR (RT-qPCR) analysis. In addition, 153 NSCLC cases and 27 normal lung tissues were used in an immunohistochemical analysis to evaluate the RIOK2 and NOB1 expression profiles, their clinicopathological factors in NSCLC and their correlations with prognoses. RIOK2 and NOB1 were highly expressed in NSCLC cells and tissues, and their expression profiles were significantly associated with the Tumour Node Metastasis (TNM) clinical stage, lymph node metastasis, and differentiation. RIOK2 expression was correlated with NOB1. The results suggested that simultaneously determining the expression of RIOK2 and NOB1 will improve the diagnostic rate in early stages of NSCLC. Moreover, RIOK2 and NOB1 might be potential targets for NSCLC therapy.

Aim: Individual differences in chemosensitivity and clinical outcome in non-small cell lung cancer (NSCLC) patients treatment with platinum-based chemotherapy may be due to genetic factors. Our study aimed to investigate the prognostic role of GSTP1, XRCC1 and XRCC3 in NSCLC patients treated with chemotherapy.

Vascular restenosis is a common adverse event following percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). The atypical Ser/Thr protein kinase mammalian target of rapamycin (mTOR) plays an important role in cell differentiation and apoptosis. Vascular restenosis caused by excessive endothelial cell proliferation can be inhibited by local application of the mTOR inhibitor rapamycin (RAPA); however, RAPA can also suppress normal vascular endothelial cell growth by blocking mTOR/VEGF signaling, although the underlying mechanism is still unclear. Here, endogenous mTOR, AP-1, and VEGF were inhibited or overexpressed to investigate the mechanism underlying the effects of RAPA. Inhibition of AP-1 or mTOR with AP-1-siRNA or RAPA treatment respectively, decreased vascular endothelial cell proliferation, upregulation of AP-1 or mTOR increased cell proliferation, and VEGF overexpression increased, while RAPA-induced mTOR inhibition decreased vascular endothelial cell proliferation, the results indicate that combining mTOR downregulation and VEGF upregulation might both inhibit restenosis and maintain normal vascular endothelial cell growth after PCI or CABG, suggest the mTOR/AP-1/VEGF pathway might play a crucial role in regulating vascular endothelial cell growth.

We aim to investigate the relationship between self‐efficacy, cancer‐related fatigue, and quality of life in patients with resected lung cancer. A prospective cohort among 452 patients with resected NSCLC was conducted in 2014 to 2015. The self‐efficacy, cancer‐related fatigue, and quality of life assessments were investigated in the 3‐month follow‐up by General Self‐Efficacy Scale (GSES), Multidimensional Fatigue Symptom Inventory–Short Form (MFSI‐SF), and Short Form Health Survey (SF‐36), respectively. Structural equation modelling was used to evaluate the relationships between the latent variables. Structural equation modelling analysis showed that both GSES (β = 0.69, p < 0.05) and MFSI‐SF (β = −0.46, p < 0.01) had direct effect on SF‐36; GSES also can indirect effect on SF‐36 though MFSI‐SF (β = −0.42, p < 0.01). The model fit indices demonstrated a reasonable fit (χ2 = 27.221, CFI = 0.911, GFI = 0.962, RMSEA = 0.051). The results showed self‐efficacy has direct and indirect effect on quality of life in patients with resected lung cancer. Furthermore, cancer‐related fatigue, as mediated variables, can mediate the relationship between self‐efficacy and quality of life. In the future, self‐efficacy interventions are need for improving quality of life in patients with resected lung cancer.

The protective effects of gastrodin on myocardial ischemia-reperfusion injury in rats and the underlying mechanism were investigated. Sprague Dawley (SD) rats were randomly divided into three groups, of which the gastrodin group was treated with gastrodin, and the other two groups were treated with normal saline. In the myocardial ischemia-reperfusion model group, myocardial ischemia was induced by ligation of the left anterior descending coronary artery, and myocardial reperfusion was performed by ligature removal. Only thread without ligation for the sham operation group was conducted. The rats were euthanized 8 days after surgery. Heart tissues were harvested and used for measurement of apoptotic rate and expression levels of apoptosis-related proteins. Serum levels of cytokines were measured also using blood samples. Compared with the myocardial ischemia-reperfusion model group, significant reduction of cardiomyocyte apoptosis was observed in the gastrodin group (P<0.05). In the gastrodin group, the protein and mRNA expression levels for Bax and activated caspase-3 decreased, while for Bcl-2 increased (P<0.05). Gastrodin can downregulate inflammatory cytokines (P<0.05) and upregulate anti-inflammatory cytokines such as IL-10 (P<0.05) in serum of SD rats. Therefore, gastrodin played a protective role in myocardial ischemia-reperfusion injury by regulating the expression levels of apoptosis-related signaling proteins and inflammatory cytokines.

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