To explore the effects of mindfulness-based intervention model on the quality of life and psychological status of lung cancer patients during chemotherapy.

A total of 76 patients with lung cancer during chemotherapy were randomly divided into control group and observation group, the control group were given routine nursing. In addition, patients in observation group received mindfulness-based intervention. The EORTC QLQ-30 and SAS scales, SDS scales were used to evaluate the quality of life of the patients before and after the 8-week intervention.

Before intervention, there was no significant difference in quality of life (QOL)between the two groups. After 8 weeks of intervention, the overall health score of observation group was 59.6±5.0, the control group was 59.6±5.0. In fatigue, pain, nausea and vomiting, the score of observation was 43.2±2.7, 26.2±4.3, 30.5±5.6, and the control group was 57.8±4.2, 47.8±3.9, 51.4±5.6, the difference was statistically significant, the QOL of the observation group was better than control group, P<0.05. Two groups of patients with anxiety, depression scores were reduced. The SAS score of observation group was 38.64±5.02, the control group was 44.06±5.24. And the SDS score of observation group was 41.26±5.2, the control group was 46.89±5.34, the psychologic status of observation group was better than the control group, P<0.05.

Mindfulness-based intervention can effectively improve the psychological status and quality of life of lung cancer patients during chemotherapy.

To discuss the value of serum tumor markers in people at high risk of lung cancer and explore the detection methods of lung cancer risk factors.

230 cases were randomly selected in hospitalized patients with lung cancer risk factors from Jan 2013 to Feb 2014.70 cases with benign disease were selected as control group. Serum tumor markers were detected by electrochemiluminescence immunoassay.

160 cases were diagnosed lung cancer by bronchoscope or thoracoscopy. 12 cases were diagnosed lung cancer in following 6-22 months. In the patients hospitalized due to lung nodules, 88 cases were diagnosed lung cancer and 8 cases were diagnosed lung cancer in following period.The increased levels of several serum tumor markers and serum ferritin could distinguish benign and malignant pulmonary nodule(P<0.05). Pulmonary nodule combined with highly serum ferritin detection had significant value in diagnosis lung cancer(P=0.021).

Highly tumor marker and serum ferritin are significant risk factors. Independent Ferritin detection is not statistically significant in benign or malignant tumor. The joint detection of serum ferritin and pulmonary nodules has clinical diagnostic value in lung cancer.

To investigate the mechanism and the relationship between fractalkine and oxidative stress of patients with COPD and pulmonary heart disease.

64 patients with AECOPD were divided into the following 8 groups according to whether merger pulmonary heart disease, whether using NAC, Cardiac function and GOLD classification of COPD disease severity. 8 healthy volunteers were selected as control group. Blood samples before and 10 days after treatment were collected to detect the level of all serum indicators, Color Doppler echocardiography, lung function and CAT score were also examined.

Levels of FKN, NF-κB, OX-LDL and hsCRP in different groups of AECOPD patients were higher than healthy control (P<0.05) and all of them were higher in severe group than mild group (P<0.05). Also, before and after treatment, those in pulmonary heart disease group were higher than COPD group, but decreased significantly in COPD+ NAC group and mild cases of pulmonary heart disease + NAC group (P<0.05). SOD, on the contrary. Administration of NAC resulted in elevated FEV₁ in mild cases of COPD group and pulmonary heart disease group (P<0.05). Pulmonary arterial pressure changed strikingly in the mild cases of pulmonary heart disease + NAC group after treatment (P<0.05), Compared to mild cases of pulmonary heart disease patients, higher pulmonary arterial pressure existed in severe cases. Compared with COPD group, the pulmonary artery pressure of pulmonary heart disease group was significantly higher (P<0.05). Besides, in severe cases of pulmonary heart disease group, CAT score in other groups altered significantly before and after treatment (P<0.05). Also, marked difference was seen between COPD group and pulmonary heart disease group(P<0.05); The level of FKN was positively correlated with CAT score, NF-κB, OX-LDL, hsCRP and pulmonary artery pressure (r=0.417, 0.521, 0.401, 0.456, 0.395, P<0.05), and negatively correlated with SOD(r=-0.387, P<0.05), while had no obvious correlation with FEV₁ (r=0.215, P>0.05).

Oxidative stress in patients with COPD and cor pulmonale is closely related to FKN, Hypoxemia causes an increase in ROS, which activates the NF-κB and promotes FKN to generate and release. NAC could inhibit ROS generation, which prevents the activation of NF-κB and reduces the production of FKN. Our results show that NAC may be helpful for prevention of COPD and pulmonary heart disease in early stage.

To prepare water soluble mangiferin liposome and observe its effect on inhibiting the growth of transplanting Lewis lung carcinoma.

Mangiferin liposome was prepared by film dispersion methodo. The shape, particles size of the liposome was characterized. Anti-proliferation and apoptosis effects induced by mangiferin liposome on the Lewis lung carcinoma cells were determined by MTT method and flow cytometric analysis in vitro. The model of mice carried Lewis lung carcinoma was established. The effect of mangiferin liposome on anti-tumor and apoptosis in vivo was investigated.

The result of electromicrography showed that the liposomes consisted of small spherical or similar to spherical. The average diameter of mangiferin liposome was 207.2±2 nm. Meanwhile, the results of MTT indicated that Mangiferin liposome could more effective inhibit the proliferation of Lewis lung carcinoma than free Mangiferin (P<0.05). The IC₅₀ of Mangiferin liposome is 32.7±4.6 μg/ml on 12 h after Mangiferin treatment and the IC₅₀ of free Mangiferin is 45.2±5.1 μg/ml on the same time point. 24 hours later, the IC₅₀ of Mangiferin liposome is14.8±2.7 μg/ml. In contrast, the IC₅₀ of free Mangiferin is 22.0±3.9 μg/ml. The results in vivo also exhibited the anti-tumor effect of Mangiferin liposmes. Mangiferin liposmes could suppressed tumor growth efficiently and prolong the survival time more than 3days as control group. Furthermore, both flow cytometry of Lewis cell and TUNEL assay indiacated that mangiferin liposomes could induce apoptosis of Lewis lung carcinoma cells both in vitro and in vivo in our studies.

Liposome delivery system could effectively improve water solubility of mangiferin, and promote the anti-tumor effect.

To investigate the effect and mechanism of SIRT1 on inflammation in acute respiratory distress syndrome (ARDS) mice induced by lipopolysaccharide(LPS) .

The differences of related gene expression of lung tissues in two mice, including the SIRT1^{+ /-} mice with SIRT1 gene is knocked down and the wild-type mice, were detected by qRT-PCR and Western Blot. Then the ARDS model was induced in two kinds of mice by intraperitoneal injection of LPS, and the control group were injected with equal volume of saline. The pathological changes of lung tissue were observed by HE staining and the lung W/D ratio were calculated, the total protein concentration in BALF were detected by BCA, the levels of inflammatory factor tumour necrosis factor-α(TNF-α) and interleukin-6(IL-6) in bronchoalveolar lavage fluid (BALF) and plasma were tested by ELISA, the expression of p38 MAPK, p-p38 MAPK and p-ATF2 in lung tissue were detected by Western Blot.

Compared with wild-type mice, the mRNA and protein expression of SIRT1 in lung tissue in SIRT1^{+ /-} were significantly decreased, The difference was statistically significant(P<0.01). After ARDS induced by LPS, The pathological observation about two kinds of mice both showed infiltration of inflammatory cells in lung tissue, destruction of alveolar structure, edema of interstitial, thickening of alveolar septum, and SIRT1^{+ /-} mice were more severely damaged than wild-type mice. In SIRT1^{+ /-} mice, lung W/D ratio, total protein concentration in BALF, the levels of inflammatory factors TNF-α and IL-6 in BALF and plasma were significantly increased(P<0.05), the expression of p-p38 MAPK/p38 MAPK and p-ATF2 in lung tissues were increased more significantly than in wild-type mice(P<0.05).

The SIRT1 gene plays an important role in the inflammatory process of mice with ARDS induced by LPS, which may be related to the increased activity of p38 MAPK-p-ATF2 signaling pathway.

To explore the recent therapeutic effect and adverse reactions of chemoradiation for epidermal growth factor receptor(EGFR) wild-type LA-non-small cell lung cancer(NSCLC) patients with chronic obstructive pulmonary disease(COPD) and atelectasis.

42 patients receive hypofractionation Intensity-modulated radiotherapy, 5 Gy/ fraction, three times/week, total dose 50-60Gy/10-12fractions, Concurrent chemotherapy with etoposide 50 mg/m² on days1 to 5 and cisplatin on days 1 to 5(total 70 mg/m²)every 4 weeks for two cycles.

After treatment, 42 patients complete remission(CR) 6 cases(14.3%), partial remission(PR) 31 cases(73.8%), stable disease(SD) 5 cases(11.9%), progressive disease(PD) 0 case; Toxic effects mainly for radioactive pneumonia, of which the 0 level 16 cases (38.1%), Ⅰ-Ⅱ level 21 cases (50%), Ⅲ level 5 cases (12%).

hypofractionation Intensity-modulated radiotherapy Concurrent EP chemotherapy is effective and well-tolerated for EGFR wild-type LA-NSCLC patients with COPD and atelectasis.

To explore the differences of efficacy of the chemotherapy and epidermal growth factor receptor-tyrosine kinase inhibitor treatment in advanced lung adenocarcinoma patients harboring exon 21 mutation.

The clinical characteristic of advanced lung adenocarcinoma harboring EGFR 21 L858R mutation receiving first-line chemotherapy and EGFR-TKI treatment in Xinqiao hospital from Jan 2010 to Dec 2015 were studied. The differences between the clinical indicators of the two groups, such as objective response rates (ORR), disease control rates(DCR), progression free survival(PFS), overall survival(OS) were analyzed.

①The data of 68 patients were collected including 40 chemotherapy and 28 EGFR-TKI. Baselines of sex, age, smoking status, ECOG PS between the two groups were consistent (P>0.05) . ②The ORR of the two groups were 45% and 17.9%(P=0.020), the DCR of the two groups were 95% and 71.4%(P=0.012). The PFS of the two groups were 9.901 and 6.746 months (P=0.045), the OS of the two groups were 21.738 and 23.611 months (P=0.378).

Compared with EGFR-TKI, the patients of advanced lung adenocarcinoma treated with chemotherapy had significant advantage of ORR, DCR and PFS, no difference on OS.

The rapid development of modern medical technology leads to the dilution of the basic skills of diagnosis, and challenges the teaching of clinical medicine. A few of preliminary recommendations are given in this paper for deficiencies in diagnostic teaching, promotions of teaching and learning expected. Although the existing teaching in the theory-mutual training-trainee mode has some effect, but there is a long way to go for the teaching of diagnosis. It is proposed to cultivate comprehensive medical talents as the core, by injecting new ideas into the teaching reform, increasing the class hours of practical exercises, rationalizing the construction of teaching team, effectively promoting students′subjective initiative, attaching importance to bilingual teaching, making full use of clinical skills center in diagnosis teaching and adjusting the form of assessment, finally to improve clinical undergraduate comprehensive clinical diagnostic capacity.