Objective: To explore and analyze the risk factors of depression and anxiety in diabetics during perioperative period and study the nursing intervention.Methods: 101 patients with type-2 diabetes in perioperative period in our hospital were assessed by self-rating depression scale (SDS, n=61) and self-rating anxiety scale (SAS, n=40). The psychological factors and metabolic indexes were compared and analyzed. The patients with depression or anxiety were divided into special nursing group (n=30) and control group (n=30). Special nursing mainly included psychological comfort intervention, dietary nursing intervention and exercise guidance intervention. The effects of special nursing intervention on the improvement of depression or anxiety, metabolic indexes and quality of life were studied.Results: The psychological factors of patients with depression or anxiety were compared with those of patients without depression or anxiety during perioperative period of type-2 diabetes, including therapeutic effect, fear of disease and operation, medical atmosphere, worrying about carelessness of curing and nursing, pain degree, sleep quality, disease knowledge, marital relationship, family economic status, worrying about the influence of career, and metabolic indexes, including fasting blood glucose detection, 2-hour postprandial blood glucose and glycosylated hemoglobin, had significant differences (p<0.01). The Logistic multivariate analysis found that the above indicators were independent risk factors (p<0.05). After special nursing, the condition of depression and anxiety, metabolic indicators and qualityConclusion: The important factors of depression and anxiety in the perioperative period of type-2 diabetes included the above psychological factors and metabolic indicators. The use of special nursing intervention had a great assistant therapeutic effect on the condition of depression and anxiety of patients with type-2 diabetes mellitus in perioperative period.

Method: COPD has been proposed to represent “accelerated lung aging” , but the precise role of ageing in COPD is unclear. BMI1 is a cell cycle-associated protein that regulates cell senescence, proliferation and regeneration. Objective: To study expression and mechanism of action of BMI1 in COPD. Methods: BMI1 expression in lungs of COPD patients was quantified using IHC. BMI1 knockout and wild-type (wt) mice were exposed to ozone as a model of COPD/emphysema. b-Gal staining was measured as a marker senescence in murine lung tissue. BMI1 function was investigated in murine pulmonary alveolar epithelial cells (MLE12) using siRNA and exposure to cigarette smoke extract (CSE). Results: BMI1 was mainly expressed in the nucleus of airway epithelial cells in human lungs. BMI1 protein levels decreased in lungs of healthy smokers and COPD patients compared with healthy controls. The lung levels of BMI1 protein and mRNA were reduced in ozone-exposed mice compared to controls. Ozone-exposed BMI1 knockout mice were more likely to form emphysema and had a greater level of inflammation than wt mice. This was accompanied by increased expression of the cell aging markers p16/INK4a and b-Gal, enhanced TUNEL staining and reduced Ki67 staining in knockout compared to wt mouse lung indicating that BMI1 deletion decreased cell proliferation and increased apoptosis. In MLE12 cells, CSE exposure reduced BMI1 expression whilst BMI1 knockdown decreased cell proliferation via the p16/INK4a and ROS pathways since BMI1 knockdown upregulated p16/INK4a and promoted oxidative stress. Conclusion: Our results suggest that the absence of BMI1 accelerates senescence in alveolar epithelial cells and promotes COPD formation.

Given rapid economic developments and urbanization over the last few decades, China has experienced frequent haze episodes, which have adverse effects on public health. Children and elderly individuals are more susceptible than the general population to air pollution. In this study, we introduce interventions to reduce the exposure of elderly individuals and children to air pollution during hazy weather. These interventions include avoiding outdoor activities, wearing a dust mask, reducing burning biomass fuels, reducing frying and smoking at home, using an air filtration unit and taking supplemental antioxidants. However, the actual benefits of these measures remain unproven and are unlikely to be adequate. Sustained clean air policies remain the most important and efficient solution to reduce air pollution-related health effects.

The primary function of the bronchial epithelium is to act as a defensive barrier aiding the maintenance of normal airway function. Bronchial epithelial cells (BEC) form the interface between the external environment and the internal milieu, making it a major target of inhaled insults. However, BEC can also serve as effectors to initiate and orchestrate immune and inflammatory responses by releasing chemokines and cytokines, which recruit and activate inflammatory cells. They also produce excess reactive oxygen species as a result of an oxidant/antioxidant imbalance that contributes to chronic pulmonary inflammation and lung tissue damage. Accumulated mucus from hyperplastic BEC obstructs the lumen of small airways, whereas impaired cell repair, squamous metaplasia and increased extracellular matrix deposition underlying the epithelium is associated with airway remodelling particularly fibrosis and thickening of the airway wall. These alterations in small airway structure lead to airflow limitation, which is critical in the clinical diagnosis of chronic obstructive pulmonary disease (COPD). In this review, we discuss the abnormal function of BEC within a disturbed immune homeostatic environment consisting of ongoing inflammation, oxidative stress and small airway obstruction. We provide an overview of recent insights into the function of the bronchial epithelium in the pathogenesis of COPD and how this may provide novel therapeutic approaches for a number of chronic lung diseases.

Alpha B-crystallin (CRYAB) is one of the principal members of the small heat-shock protein family, and several studies described the CRYAB expression in human cancers. However, the association between CRYAB expression and the clinical features of non-small cell lung cancer (NSCLC) is rarely elucidated. In this present study, one-step quantitative reverse transcription-polymerase chain reaction with 12 fresh-frozen NSCLC samples and Western blotting as well as immunohistochemistry (IHC) analyses in 101 NSCLC cases were conducted to investigate the relationship between CRYAB expression and the clinicopathological attributes of NSCLC. The results showed that CRYAB mRNA and protein expression levels were significantly higher in NSCLC than in matched non-cancerous tissues (p < 0.05). The IHC data indicated that the CRYAB protein expression in NSCLC was significantly correlated with TNM stage (p = 0.043), and overall survival (p = 0.029). Kaplan-Meier method and Cox multifactor analysis suggested that higher CRYAB protein level (p = 0.032) and TNM stage (p = 0.048) were statistically associated with the poor survival of patients with NSCLC. The data suggested that CRYAB may be identified as a novel prognostic marker and targeting CRYAB may provide a promising strategy for NSCLC treatment.