Objective To observe the clinical effect of treating Alzheimer's disease (AD) using transcranial magnetic stimulation.Methods One hundred and ninety-six patients with Alzheimer's disease were randomly divided into an observation group and a control group,each of 98.The observation group was given transcranial magnetic stimulation of the left and right dorsolateral frontal lobes of the brain and simultaneously given "8-shaped" coil stimulation.The stimulation intensity was 80％ of the motor threshold with a sequence of 2 s of stimulation at 5 Hz and 30 s rest for 30 min in each session.There were two sessions a day for 28 days.The control group was treated with identical pseudo-stimulation.Moreover,both groups were treated with intravenous injections of 20 ml of Ginkgo biloba extract dissolved in 250 ml of sodium chloride,or in the control group a glucose injection,one daily for two weeks.Before and after the treatment,the cognition,behavior and neuropsychological symptoms of both groups were evaluated using the mini mental state examination scale (MMSE),the AD rating scale (ADAS-cog),the activity of daily living (ADL) scale,a neuropsychiatric questionnaire (NPI) and an AD behavioral pathology rating scale (BEHAVE-AD) to compare the clinical effects.Results There were no significant differences in the groups' average scores on any of the evaluations before the treatment.After the treatment,the average MMSE and ADAS-cog scores in both groups had improved significantly,but with significantly greater improvement in the observation group.After the treatment,the average ADL,NPI and BEHAVE-AD scores of the observation group and the average ADL score of the control group were significantly lower than before the treatment.No significant differences were observed in the average NPI and BEHAVE-AD scores of the control group.After the intervention,the average ADL,NPI and BEHAVE-AD scores in the observation group were significantly lower than those of the control group.The total effectiveness rate of the observation group (90.8％) was significantly higher than that of the control group (62.2％).Conclusion Transcranial magnetic stimulation can significantly improve the cognitive,behavioral and neuropsychological status of patients with Alzheimer's disease.

High-risk human papillomavirus (HPV) persistent infection is the most common cause of cervical cancer and precancerous lesions. As a primary prevention measure, especially in developing countries, HPV vaccine can greatly reduce the incidence of cervical cancer.However, researches on the safety, efficacy, and coverage of the HPV vaccine still remain insufficient. Therefore, in this review, we outlined the recent research progress of the HPV vaccine in terms of immunogenicity, safety, efficacy, latest vaccination concepts and strategies. It may provide a theoretical basis for further research on the use of the HPV vaccine.

Valid animal models are useful for studying the pathophysiology of specific disorders, such as neural disease, diabetes and cancer. Previous molecular phylogeny studies indicate that the tree shrew is in the same order as (or a close sister to) primates, and thus may be an ideal model in which to study human disease. In this study, the proteome of liver and muscle tissue in tree the shrew was identified by combining peptide fractionation and LC-MS/MS identification. In total, 2146 proteins were detected, including 1759 proteins in liver samples and 885 proteins in skeletal muscle samples from the tree shrew. Further sub-source analysis revealed that nearly half of the identified proteins (846 proteins and 418 proteins) were derived from human database. In this study, we are the first to describe the characteristics of the proteome from the liver and skeletal muscle of the tree shrew. Phylogenetic tree analysis based on these proteomic data showed that the tree shrew is closer to primates (human) than to glires (the mouse and rat).
Animals ; China ; Chromatography, High Pressure Liquid ; Databases, Protein ; Liver ; metabolism ; Muscle, Skeletal ; metabolism ; Phylogeny ; Proteome ; analysis ; Proteomics ; Tandem Mass Spectrometry ; Tupaia ; classification ; metabolism

Objective:To explore the protective effect and underlying mechanism of hyperbaric oxygen (HBO) on delayed encephalopathy after carbon monoxide poisoning (DEACMP) in mice.Methods:Totally 225 adult male Kunming mice were selected to establish CO poisoning model via intraperitoneal injection carbon monoxide (CO), and were randomly divided into the air control group, CO poisoning group, and HBO group. Each group was further divided into five time points group, that was 1, 3, 7, 14 and 21 d. The mice in the air control group were injected intraperitoneally with the same amount of air, and the HBO group received HBO treatment at the same time every day. DEACMP mice model was screened by behaviors using the open field test, new object recognition test and nesting test, and the content of myelin basic protein (MBP) were assayed. The mouse brain tissue and mitochondrial were prepared and malonialdehyde (MDA) and adenosine triphosphate (ATP) content were measured with ultraviolet spectrophotometer. MBP content in brain tissue and cytochrome C (CytC) content in the mitochondrial were measured by ELISA. The mitochondria membrane potential (MMP) was measured by flow cytometry.Results:Compared with the air control group, the content of carboxyhemoglobin (COHB) in blood increased significantly and the content of MBP in brain tissue decreased significantly in CO poisoning mice. CO poisoning mice showed motor ability and cognitive dysfunction. Compared with the air control group, the contents of MMP, CytC and ATP were significantly decreased ( P<0.01) in the CO poisoning group; while the MDA content was significantly increased ( P<0.01). Compared with the CO poisoning group, mice behaviors were improved significantly ( P<0.05), the content of MBP, MMP, CytC and ATP were increased ( P<0.05), while the MDA content decreased significantly ( P<0.01) in the HBO group. Conclusions:The abnormal mitochondrial function might be closely related to the occurrence and development of DEACMP, and HBO therapy plays an effective role in preventing and treating the DEACMP mice model via the mitochondrial pathway.