BACKGROUND: Insomnia may affect vascular factors and promote arteriosclerosis. Microparticles (MPs) are a heterogeneous group of bioactive small vesicles that can be found in blood and body fluids following activation, necrosis or apoptosis of virtually any eukaryotic cells. MPs are believed to participate in the pathogenesis of atherosclerosis. Few studies have been concerned with the microparticle level in patients with sleep disorder. The purpose of the present study is to measure the levels of endothelial microparticles (EMPs), platelet microparticles (PMPs) and leukocyte-derived microparticles (LMPs) in middle-aged and elderly patients with or without insomnia.METHODS: Patients with insomnia (N.=30) and without insomnia (N.=18) were enrolled. The insomnia group covered patients with chronic insomnia (N.=16) and acute insomnia (N.=14). Levels of EMPs (CD31 +, CD62E +) and PMPs (CD41a +, CD42a +) and granulocyte-derived (CD11a +) MPs were measured. Flow cytometry was performed on the Beckman Coulter analyzer. Reference gate was defined for the level of MPs using 0.22-0.45-0.88μm microspheres, and the size gate for MPs was 0.5-1.0μm.RESULTS: Of all types of MPs detected, the levels of CD31 +MPs, CD62E +MPs and CD11a +MPs were significantly higher in the insomnia group than in the non-insomnia group (P<0.05). Besides, compared with acute insomnia, the levels of CD31 + MPs and CD11a +MPs were significantly higher in chronic insomnia (P<0.001).CONCLUSIONS: In insomnia patients, atherosclerosis progression may be increased by the CD31+ EMPs-mediated apoptosis and endothelial injury. The level of CD11a+ LMPs kept increasing as insomnia persisted, which may indicate atherosclerosis progression.

BACKGROUND:Recently, evidence indicated that the rapamycin-eluting stent which was used worldwide may contribute to an increased risk for thrombosis. On the contrary, other researchers found it was safe. Thus, it is necessary to clarify the effect of rapamycin on thrombosis and the corresponding mechanisms.RESULTS:The effects of rapamycin in vivo were evaluated by modified deep vein thrombosis animal model. The platelets were from healthy volunteers and the platelet-endothelium (purchased from ATCC) adhesion in cultured endothelial cells was assessed. Membrane rufflings in endothelial cells were examined by confocal and electron microscope. Thrombus formation increased in rats that were injected with rapamycin. Electron microscope analysis exhibited microvilli on the rapamycin-treated endothelium in rats. Rapamycin enhanced membrane ruffling in human umbilical vein endothelial cells (HUVECs) and adhesion of platelets to HUVECs. The platelet-HUVECs adhesion was attenuated when cells were treated with cytochalacin B. Inhibition of autophagy by 3-methyladenine led to suppression of membrane ruffles in HUVECs and augmentation of platelet-endothelial adhesion.CONCLUSIONS:In conclusion, we found that endothelial membrane remodeling induced by rapamycin is crucial for the adhesion of platelets to endothelial cells and thereby for thrombosis in vivo, and that the endothelial membrane remodeling is autophagy dependent.

BACKGROUND:Pneumonia is the most common cause of morbidity and mortality in lung transplant (LT) recipients. The aim of the present study was to evaluate the incidence, etiology, risk factors and prognosis of pneumonia in LT recipients.METHODS:The LT cohort consisted of 28 recipients receiving LT in Beijing Chao-Yang Hospital from August 2005 to April 2011. Data collected included demographic data, underlying disorders, time and type of transplant, follow-up information, date of last follow-up, and patient status. A retrospective analysis was made of observational data that were prospectively collected.RESULTS:Twenty-two patients of 28 LT recipients had 47 episodes of pneumonia throughout the study period. Thirtyeight episodes of pneumonia in 19 recipients occurred post-LT with a median follow-up of 257.5 days (1-2104 days), the incidence of pneumonia was 192.4 episodes per 100 LT/year and its median time of onset was 100.5 days (0-946 days) post-transplantation. Bacteria, virus and fungi accounted for 62%, 16% and 15% of the microbial pathogens, respectively. The most frequent were Pseudomonas aeruginosa (20%), cytomegalovirus (CMV) (15%), and Aspergillus fumigatus (10%). A total of 29% (11/38) of pneumonias occurred in the first month post-LT, and then the incidence decreased gradually. The incidence of CMV pneumonia was 25% (7/28) with a median time of 97 days (10-971 days). More than one bacterial infection and CMV infection were independent risk factors for aspergillus infection. The incidence of pulmonary tuberculosis (TB) was 18% (5/28), and the history of TB was a risk factor for TB relapse. There were 58% (7/12) of recipients who died of infection, and 71% (5/7) of these died in the first year after LT.CONCLUSIONS:Pneumonia is still a major cause of morbidity and mortality in LT recipients. The most frequent microorganisms were Pseudomonas aeruginosa, CMV, and Aspergillus fumigates. The incidence of CMV pneumonia decreases with a delayed median time of onset. More than one incidence of bacterial infection and CMV infection are independent risk factors for aspergillus infection. LT recipients are at high risk for TB, and the history of TB is a risk factor for TB relapse.

Objective: Idiopathic pulmonary fibrosis (IPF) is predominantly a lung fibrotic disease of older adults, and the process underlying aging might significantly influence the development of pulmonary fibrosis. Bleomycin-induced lung injury was investigated in murine models of accelerated senescence (SAMP8) and of normal aging (SAMR1). The levels of Th1/Th2 related cytokine were also measured. Methods: Bleomycin or PBS was injected into the tracheal lumen of 12-month-old SAMP8, 4 and 12-month-old SAMR1 mice. Seven, 14 and 28 days after the injection, the mice were killed and the lungs were harvested for pathological examination, hydroxyproline assay and protein detect. Lung TGF-β1 expression was determined by western blot, and the levels of IL-4 and IFN-γ were detected by ELISA. Results: The aggravated bleomycin induced lung injury was observed in 12-month-old SAMP8 compared with 4 and 12-month-old SAMR1. Twenty eight days after injection of bleomycin, Ashcroft score was significant higher in 12-month-old SAMP8 than in 4 and 12-month-old SAMR1 ( P Conclusions: Bleomycin-induced pulmonary fibrosis in SAM was aggravated by aging. The old SAM with bleomycin-induced pulmonary fibrosis might be inclined to Th2-biased immune responses. (This work was funded by National Natural Science Foundation of China Grants 81070046).

Lungs are located in the chest and lie on both sides of mediastinum.The major function of lung is to balance the external and internal 'gas' environment and to maintain homeostatic equilibrium.Because lung is closely interacted with outside surroundings as well as general circulation,it is fair to say that lung is a delicate organ which may be attacked by so many noxious stimuli,such as bacterial or viral infections,chemical insults (smoke,dust,etc),radiation,autoimmune and allergic responses.Damage to lung tissue can result from these various acute or chronic stimuli,which in tum disrupt lung homeostasis and a dysregulated healing response will eventually occur, such as inflammation,anti-fibrinolytic coagulation cascade and accumulation of pro-angiogenic,and fibrogenic cytokines,growth factors and enzymes.Uncontrolled healing response could gradually evolve into a pathogenic fibrotic response when important checkpoints are missed and inflammation becomes unrelenting.