China ; Chronic Disease ; prevention & control ; Health Planning ; Humans

Mitochondrial oxidative stress has been recognized as a preliminary and critical factor that aggravates the pathological cascade of Alzheimer's disease, which induces the production of β-amyloid protein, upregulates the expression of phosphorylated tau protein and triggers oxidative damage to lipids, proteins and mitochondrial deoxyribonucleic acid. Central neurons are more vulnerable to oxidative stress than non-neuronal cells due to their high oxygen demand, abundant unsaturated fatty acids and antioxidant enzymes deficiency. On this account, this review introduces the causes of mitochondrial oxidative stress, and analyzes the important role of mitochondrial oxidative stress in the pathogenesis of Alzheimer's disease. Meanwhile, the review focuses on the design and intervention strategies of drug delivery systems targeting mitochondrial oxidative stress in neurons, aiming to provide new ideas for the prevention and treatment of Alzheimer's disease.

Female ; Granulosa Cell Tumor ; Humans ; Ovarian Neoplasms ; Thyroid Neoplasms

Antigens ; immunology ; Child ; Female ; Food Hypersensitivity ; etiology ; Humans ; Infant, Newborn ; Maternal Exposure ; Milk Hypersensitivity ; etiology ; Milk, Human ; immunology ; Pregnancy

Altitude ; Animals ; Blood Glucose ; metabolism ; Cholesterol ; blood ; Hypoxia ; metabolism ; Mice ; Weight Loss

Adult ; Body Mass Index ; Child ; Humans ; Insulin Resistance ; Obesity ; complications ; Sleep Apnea, Obstructive ; etiology ; physiopathology

Adult ; Antithyroid Agents ; therapeutic use ; Autoantibodies ; blood ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Glycosides ; therapeutic use ; Graves Disease ; drug therapy ; immunology ; Humans ; Immunosuppressive Agents ; therapeutic use ; Male ; Methimazole ; therapeutic use ; Middle Aged ; Phytotherapy ; Tripterygium ; chemistry

Adult ; Disease Susceptibility ; complications ; Female ; Hearing Loss, Noise-Induced ; complications ; Humans ; Hypertension ; etiology ; Linear Models ; Logistic Models ; Male ; Middle Aged ; Multivariate Analysis ; Noise, Occupational ; adverse effects ; Occupational Exposure ; adverse effects

Objective To observe neutrophil activation and protease imbalance in airway of children after foreign-body aspiration(FBA).Methods Bronchoalveolar lavage fluid(BALF) was obtained through fiberoptic bronchoscopy.The supernatant was assayed for the concentration of neutrophil elastase(NE) using enzyme-linked immunosorbent assay(ELISA) and elastase inhibition capacity(EIC)/free elastase activity using a colorimetric assay.The cell pellet were smeared for the expression of ?1-antitrypsin(?1-AT) using cellular immunohisto-chemistry and cytologic analysis by Wright-Giemsa stain.Results Percentage of neutrophil,concentration of NE and the expression of ?1-AT in BLAF group,pair group and pneumonia group significantly increased compared with that of control group(Pa0.05).The ratio of Lib NE in FBA,par and peumcria group was 30.3%,27.3% and 22.7%.Conclusions FBA induces similar airway neutrophil activation and protease imbalance to bacterial pneumonia.The contralateral airway showes the same change as the foreign body side.

Objective To observe the correlation between nuclear factor ?B(NF-?B) expression and apoptosis after hypoxia-ischemia brain damage(HIBD).Methods Forty-eight 7-day newborn Sprague-Dawley(SD) rats were randomly divided into 2 groups: control group (n=24) and HI group (n=24).The expression of NF-?B in the hippocampus was detected by immunohistochemical techniques.The apoptosis of the hippocampal cells was detected by terminal deoxynucleotidyltransferase-mediated 2-deoxyuridine 5′-triphosphate-biotin nick end labeling(TUNEL)straining.Results The expression of NF-?B in hippocampal cells increased at 6 h after HIBD,peaked at 48 h,and lasted till 72 h when compared with control group(Pa