Effects of climate and environment on migratory old people with allergic diseases in China: Protocol for a Sanya cohort study.

Background: Several studies have reported that the mountain climate can alleviate asthma, however, the effect of tropical climate on migratory elderly, especially in people with respiratory or allergic diseases is unknown. Objectives: This cohort study aims to explore impact of climate and environmental changes on allergic diseases in migratory old people. Methods: In this prospective cohort study, we recruited 750 older migratory people, the majority of whom were homeowners to minimize the risk of loss to follow up. The study's inclusion criteria were elderly individuals had moved from northern China to Sanya and suffered from either asthma or allergic diseases. Prior to participation, these individuals provided informed consent and underwent baseline assessment. Subsequently, they will be followed for three years. A face-to-face interview was conducted to gather information regarding their living environment and habits. Trained investigators administered the questionnaires and performed physical examinations including height, weight, and blood pressure, while a professional respiratory doctor conducted pulmonary function tests. Blood samples were promptly tested routine blood test, liver function, kidney function, glucose, triglyceride, allergens, and inflammatory factors. Climate and environmental data were obtained from Sanya Meteorological Bureau and Ecological Environment Bureau, respectively. We primarily compared the differences of participants with asthma or allergic diseases between northern China and Sanya in southern China by Chi-square test, t-test or Wilcoxon rank-sum test. Findings: A total of 750 participants were recruited in this cohort from fourteen communities. All participants were surveyed questionnaires about health and family environment, underwent physical examinations, and collected biological samples for laboratory examinations. Novelty: This is the first study to evaluate the effects of tropical climate and environment on elderly migrants from cold regions. This study has important implication for the health tourism and aging health, especially for the elderly migrants who suffered the respiratory and allergic diseases. Furthermore, this cohort study establishes a solid foundation for investigating the influence of environmental changes on elderly migrants with allergic diseases.

Sanya climatic-treatment cohort profile: objectives, design, and baseline characteristics.

Background: The prevalence of allergic diseases has increased globally, climate and environment also have important effects on respiratory or allergic diseases. However, population-based studies investigating the impact of tropical climates and environments on migratory-bird old people (MBOP) are lacking. Methods/Design: For this prospective cohort study, we recruited 756 participants from the community in Sanya City, Hainan Province, China. In addition to the completed baseline survey, a follow-up survey will be conducted during the periods of October-December and March-April for the next 3 years of MBEPs from northern China who spend the winter in Sanya. We will continue to record the height, weight, and blood pressure of all participants, as well as lung function for those with asthma and chronic obstructive pulmonary disease (COPD). Venous blood at baseline and urine samples will be collected during follow-up. Results: A total of 756 volunteers were recruited. Their average age is 66.1 years; 32.1% of them have high-school educations, while 37.3% have graduated from college or done undergraduate studies. The top five diseases in this cohort are allergic rhinitis (57.9%); eczema, urticaria, or dermatitis (35.6%); bronchitis and bronchiectasis (35.6%); asthma (14.7%); and emphysema (11.7%). Compared with their symptoms while at their summer places of residence, rates of remission reported by participants while living in Sanya were 80.4% for allergic rhinitis, 82.3% for bronchitis and emphysema, 85.2% for asthma, 96.0% for COPD (P < 0.001). Conclusions: The baseline survey has been completed. The preliminary findings support that a tropical climate may relieve the symptoms of allergic diseases in migratory-bird old people.

Igf2bp2 knockdown improves CCl4-induced liver fibrosis and TGF-ß-activated mouse hepatic stellate cells by regulating Tgfbr1.

Progressive liver fibrosis is a dynamic process characterized by the net accumulation of extracellular matrix (ECM), which could eventually develop into cirrhosis, leading to malignant transformation. In this study, insulin-like growth factor 2 mRNA binding protein 2 (Igf2bp2) was found to be up-regulated in carbon tetrachloride (CCl4)-induced liver fibrosis and transforming growth factor-beta 1 (TGF-ß)-activated hepatic stellate cells (HSCs). Igf2bp2 knockdown in the CCl4-induced hepatic fibrosis mice model significantly improved CCl4-induced liver damage by decreasing necrosis and fibrotic septa, reducing hydroxyproline levels, and down-regulating fibrotic markers levels. In TGF-ß-activated HSCs, Igf2bp2 knockdown partially attenuated TGF-ß-induced cellular effects by suppressing HSCs viability and DNA synthesis and reducing the ECM-associated factors such as α-SMA, COLLAGEN I, and COLLAGEN III. Integrative network and signaling analysis revealed that the Igf2bp2 could bind to Tgfbr1. Transforming growth factor-beta receptor 1 (Tgfbr1) was found to be significantly up-regulated in the fibrotic liver and activated HSCs, and positively correlated with Igf2bp2. Tgfbr1 knockdown partially eliminated TGF-ß-induced fibrotic changes and Igf2bp2 overexpression effects on TGF-ß-activated HSCs in vitro. Moreover, Igf2bp2 overexpression promoted the phosphorylation of SMAD2/SMAD3, AKT, and PI3K, whereas Tgfbr1 knockdown exhibited the opposite effect; Tgfbr1 knockdown also partially attenuated the effects of Igf2bp2 overexpression on the phosphorylation of SMAD2/SMAD3, AKT, and PI3K. In closing, Igf2bp2 and Tgfbr1 are up-regulated in CCl4-induced liver fibrosis and TGF-ß-activated mHSCs. Igf2bp2 knockdown improved CCl4-induced liver fibrosis and TGF-ß-activated HSCs by targeting Tgfbr1, possibly through the PI3K/Akt pathway.