Objective To explore the effect of budesonide(BUD) on dendritic cell(DC) and airway inflammation in the asthmatic mice.Methods Forty female Kunming mice were divided into 4 groups:asthmatic model group,therapeutic control group,BUD treated group,and normal control group,with 10 mice in each group.Mice were sensitized by an intraperitoneal injection of 50 ?g ovalbumin(OVA) adsorbed to 1 mg aluminum hydroxide dissolved in 0.2 mL saline.Animals were boosted on the 14th day in the same way.From the 21th to 35th days,and mice were challenged with 10 g/L aerosolized OVA for 30 min a day to establish a murine model of asthma.To evaluate the effect of BUD,60 minutes prior to OVA exposure,the mice were treated with 1 mg aerosolized BUD or placebo(saline).Control animals were sensitized intraperitoneally with saline and challenged with aerosolized saline alone.Eosinophil(EOS) count,degree of mucus secretion and DC count around the airways were measured by haematoxylin and eosin staining,periodic acid schiff's staining,immunochemistry technique and computerized image analysis system.Results In asthmatic model group,EOS count,DC count and the degree of mucus secretion around the airways were increased compared with nomal control group(P_a0.05).In BUD treated group,EOS count,DC count and the degree of mucus secretion around the airways were decreased compared with the asthmatic model group(P_a

Heart Aneurysm ; mortality ; pathology ; surgery ; Humans ; Mitral Valve Insufficiency ; mortality ; physiopathology ; surgery ; Myocardial Infarction ; mortality ; physiopathology ; surgery ; Ventricular Dysfunction, Left ; pathology ; surgery

Adaptive Immunity ; Animals ; Female ; Humans ; Immunity, Innate ; Influenza A Virus, H5N1 Subtype ; chemistry ; immunology ; Influenza A virus ; chemistry ; immunology ; Male

Adolescent ; Adult ; Cat-Scratch Disease ; diagnosis ; therapy ; Child ; Child, Preschool ; Female ; Humans ; Lymphadenitis ; diagnosis ; etiology ; therapy ; Male ; Middle Aged ; Young Adult

Objective To analyze the molecular characteristics of Salmonella paratyphi A ( S. pa-ratyphi A) strains prevailing in Hangzhou area in recent years. Methods Pulse field gel electrophoresis ( PFGE) and multiple-locus variable-number tandem repeat analysis ( MLVA) were performed for molecular typing and epidemiological analysis of 72 S. paratyphi A strains isolated in Hangzhou area during 2002 to 2013. Results The 72 S. paratyphi A strains were divided into 11 PFGE ( by using restriction enzymes of Xba Ⅰ and Bln Ⅰ) and 6 MLVA types. Among the selected 34 variable number tandem repeat ( VNTR) sites, 4 sites (1188K, 2075K, 2201K and 4346K) showed high polymorphism, in which PFGE displayed a higher resolution than MLVA. Except for the 5 PFGE types of X4B5, X7B7, X8B8, X9B9 and X10B10, the other 6 PFGE types belonged to a same clone sharing a similarity of greater than 95%, and the S. Paratyphi A strains in that clone accounted for 93. 1% of the total strains isolated in Hangzhou. Conclu-sion The occurrence of paratyphoid A in Hangzhou area from 2002 to 2013 was mainly caused by S. para-typhi A strains belonging to the same clone. Combination of PFGE with MLVA was conducive to epidemiolog-ical investigation of paratyphoid A.

Objective To identify the key factors triggering medical disputes induced by differences in cognition between doctors and patients in order to control the occurrence and development of medical disputes. Methods From 2002 to 2006,the outpatients,inpatients and medical staff of 3 hospitals in Shanghai(class 3 first level general hospital,n=2;class 3 first level special hospital,n=1) were investigated,and random sampling method was employed for the research analysis. Results There were significant differences between doctors and patients in cognition of influential factors triggering medical disputes such as health law,medical services,rights and obligations. Conclusion The differences in cognition between doctors and patients are important causes for medical disputes,and effective prevention and intervention measures must be taken.

Animals ; Apoptosis ; Female ; Male ; Nasal Mucosa ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Rhinitis, Allergic, Perennial ; metabolism ; pathology

Aged ; Humans ; Male ; Middle Aged ; Mycoses ; complications ; Nasal Septal Perforation ; complications ; microbiology ; Sinusitis ; complications ; microbiology

Animals ; Apoptosis ; physiology ; Carcinoma, Squamous Cell ; drug therapy ; physiopathology ; prevention & control ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors ; therapeutic use ; Head and Neck Neoplasms ; drug therapy ; physiopathology ; prevention & control ; Humans ; Membrane Proteins ; Neoplasm Invasiveness ; Neoplasm Metastasis ; drug therapy ; Neovascularization, Pathologic ; drug therapy ; metabolism ; Prostaglandin-Endoperoxide Synthases ; metabolism

Autophagy is an important homeostatic cellular recycling mechanism responsible for degrading injured or dysfunctional cellular organelles and proteins in all living cells. Aging is a universal phenomenon characterized by progressive deterioration of cells and organs due to accumulation of macromolecular and organelle damage. Growing evidences indicate that the rate of autophagosome formation and maturation and the efficiency of autophagosome/lysosome fusion decline with age. Dysfunctional autophagy has also been observed in age-related diseases. Autophagy disruption resulted accumulation of mutated or misfolded proteins is the essential feature of neurodegenerative disorders. However, in cancers, fibroproliferative diseases or cardiovascular diseases, autophagy can play either a protective or destructive role in different types of disease, and even in different stages of the same disease. The review will discuss the cellular and molecular mechanisms of autophagy and its important role in the pathogenesis of aging and age-related diseases, and the ongoing drug discovery strategies for therapeutic intervention.
Aging ; Autophagy ; Drug Discovery ; Humans ; Lysosomes ; metabolism ; Neurodegenerative Diseases ; Phagosomes ; metabolism ; Protein Folding