RESUMO
Alzheimer's disease (AD) is a neurodegenerative disease, and mild cognitive impairment (MCI) is considered a transitional stage between healthy aging and dementia. Early detection of MCI can help slow down the progression of AD. At present, there are few studies exploring the characteristics of abnormal dynamic brain activity in AD. This article uses a method called leading eigenvector dynamics analysis (LEiDA) to study resting-state functional magnetic resonance imaging (rs-fMRI) data of AD, MCI, and cognitively normal (CN) participants. By identifying repetitive states of phase coherence, intergroup differences in brain dynamic activity indicators are examined, and the neurobehavioral scales were used to assess the relationship between abnormal dynamic activities and cognitive function. The results showed that in the indicators of occurrence probability and lifetime, the globally synchronized state of the patient group decreased. The activity state of the limbic regions significantly detected the difference between AD and the other two groups. Compared to CN, AD and MCI have varying degrees of increase in default and visual region activity states. In addition, in the analysis related to the cognitive scales, it was found that individuals with poorer cognitive abilities were less active in the globally synchronized state and more active in limbic region activity state and visual region activity state. Taken together, these findings reveal abnormal dynamic activity of resting-state networks in patients with AD and MCI, provide new insights into the dynamic analysis of brain networks, and contribute to a deeper understanding of abnormal spatial dynamic patterns in AD patients.NEW & NOTEWORTHY Alzheimer's disease (AD) is a neurodegenerative disease, but few studies have explored the characteristics of abnormal dynamic brain activity in AD patients. Here, our report reveals the abnormal dynamic activity of the patients' resting-state network, providing new insights into the dynamic analysis of brain networks and helping to gain a deeper understanding of the abnormal spatial dynamic patterns in AD patients.
Assuntos
Doença de Alzheimer , Disfunção Cognitiva , Imageamento por Ressonância Magnética , Rede Nervosa , Humanos , Doença de Alzheimer/fisiopatologia , Doença de Alzheimer/diagnóstico por imagem , Feminino , Idoso , Masculino , Disfunção Cognitiva/fisiopatologia , Disfunção Cognitiva/diagnóstico por imagem , Rede Nervosa/fisiopatologia , Rede Nervosa/diagnóstico por imagem , Pessoa de Meia-Idade , Encéfalo/fisiopatologia , Encéfalo/diagnóstico por imagem , Descanso , Idoso de 80 Anos ou maisRESUMO
Effervescent technique, which can accelerate drug disintegration and dissolution, is usually applied in quick release preparations. Along with the development of pharmaceutical technique and theory, effervescent technique is used more and more extensively to adjust the behavior of drug release, such as in sustained and controlled release preparations, pulsatile drug delivery systems, and so on. This review demonstrated the new applying of effervescent technique in effervescent tablets, stomach floating forms, osmotic pump tablets and pulsatile drug delivery systems, adding to the critical common technique of effervescent forms in drug research. This will be benefit for the further research and development of effervescent technique.
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Formas de Dosagem , Preparações Farmacêuticas/administração & dosagem , Sistemas de Liberação de Medicamentos , Humanos , Osmose , ComprimidosRESUMO
<p><b>Background</b>Myocardial ischemia injury is one of the leading causes of death and disability worldwide. Cardiac fibroblasts (CFs) have central roles in modulating cardiac function under pathophysiological conditions. Activating transcription factor 3 (ATF3) plays a self-protective role in counteracting CF dysfunction. However, the precise function of CF-specific ATF3 during myocardial infarction (MI) injury/repair remains incompletely understood. The aim of this study was to determine whether CF-specific ATF3 affected cardiac repair after MI.</p><p><b>Methods</b>Fifteen male C57BL/6 wild-type mice were performed with MI operation to observe the expression of ATF3 at 0, 0.5, 1.0, 3.0, and 7.0 days postoperation. Model for MI was constructed in ATF3TGfl/flCol1a2-Cre+ (CF-specific ATF3 overexpression group, n = 5) and ATF3TGfl/flCol1a2-Cre- male mice (without CF-specific ATF3 overexpression group, n = 5). In addition, five mice of ATF3TGfl/flCol1a2-Cre+ and ATF3TGfl/flCol1a2-Cre- were subjected to sham MI operation. Heart function was detected by ultrasound and left ventricular remodeling was observed by Masson staining (myocardial fibrosis area was detected by blue collagen deposition area) at the 28 day after MI surgery in ATF3TGfl/flCol1a2-Cre+ and ATF3TGfl/flCol1a2-Cre- mice received sham or MI operation. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect cell proliferation/cell cycle-related gene expression in cardiac tissue. BrdU staining was used to detect fibroblast proliferation.</p><p><b>Results</b>After establishment of an MI model, we found that ATF3 proteins were increased in the heart of mice after MI surgery and dominantly expressed in CFs. Genetic overexpression of ATF3 in CFs (ATF3TGfl/flCol1a2-Cre+ group) resulted in an improvement in the heart function as indicated by increased cardiac ejection fraction (41.0% vs. 30.5%, t = 8.610, P = 0.001) and increased fractional shortening (26.8% vs. 18.1%, t = 7.173, P = 0.002), which was accompanied by a decrease in cardiac scar area (23.1% vs. 11.0%, t = 8.610, P = 0.001). qRT-PCR analysis of CFs isolated from ATF3TGfl/flCol1a2-Cre+ and ATF3TGfl/flCol1a2-Cre- ischemic hearts revealed a distinct transcriptional profile in ATF3-overexpressing CFs, displaying pro-proliferation properties. BrdU-positive cells significantly increased in ATF3-overexpressing CFs than control CFs under angiotensin II stimuli (11.5% vs. 6.8%, t = 31.599, P = 0.001) or serum stimuli (31.6% vs. 20.1%, t = 31.599, P = 0.001). The 5(6)-carboxyfluorescein N-hydroxysuccinimidyl ester assay showed that the cell numbers of the P2 and P3 generations were higher in the ATF3-overexpressing CFs at 24 h (P2: 91.6% vs. 71.8%, t = 8.465, P = 0.015) and 48 h (P3: 81.6% vs. 51.1%, t = 9.029, P = 0.012) after serum stimulation. Notably, ATF3 overexpression-induced CF proliferation was clearly increased in the heart after MI injury.</p><p><b>Conclusions</b>We identify that CF-specific ATF3 might contribute to be MI repair through upregulating the expression of cell cycle/proliferation-related genes and enhancing cell proliferation.</p>
Assuntos
Animais , Masculino , Camundongos , Fator 3 Ativador da Transcrição , Fisiologia , Modelos Animais de Doenças , Fibroblastos , Fisiologia , Fibrose , Camundongos Endogâmicos C57BL , Infarto do Miocárdio , Miocárdio , Remodelação VentricularRESUMO
<p><b>OBJECTIVE</b>To evaluate the impact of cerebrovascular disease mortality on life expectancy (LE) in China in 2010 compared with 2005, and to identify the high-risk population (age, sex, and region) where cerebrovascular disease mortality has had a major impact on LE.</p><p><b>METHODS</b>LE and cause-eliminated LE were calculated by using standard life tables which used adjusted mortality data from the Death Surveillance Data Sets in 2005 and 2010 from the National Disease Surveillance System. Decomposition was used to quantitate the impact of cerebrovascular disease in different age groups.</p><p><b>RESULTS</b>LE in China was 73.24 years in 2010, which was higher in women and urban residents compared with men and rural residents. The loss of LE caused by cerebrovascular disease mortality was 2.26 years, which was higher in men and rural residents compared with women and urban residents. More than 30% of the loss of LE were attributed to premature death from cerebrovascular disease in people aged <65 years. Compared with 2005, LE in 2010 increased by 0.92 years. The reduction of cerebrovascular disease mortality in urban residents contributed 0.45 years to the increase of LE, but the increase of cerebrovascular disease mortality caused a 0.12-year loss of LE in rural residents.</p><p><b>CONCLUSION</b>Cerebrovascular disease mortality had a major impact on LE in China, with a significant difference between urban and rural residents. LE is likely to be further increased by reducing cerebrovascular disease mortality, and special attention should be paid to reducing premature deaths in people aged <65 years.</p>
Assuntos
Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Pré-Escolar , Feminino , Humanos , Lactente , Masculino , Pessoa de Meia-Idade , Adulto Jovem , Transtornos Cerebrovasculares , Mortalidade , China , Epidemiologia , Expectativa de Vida , Saúde da População Rural , População Rural , População UrbanaRESUMO
<p><b>OBJECTIVE</b>We aimed to analyze the impact of cardiovascular disease (CVD) deaths on life expectancy (LE) in Chinese population and estimate the percentage reduction in CVD mortality needed to increase LE by 1 year from the current level, a national target of health improvement.</p><p><b>METHODS</b>We used life tables, cause-elimination life tables, and age decomposition of LE with corrected mortality data from the National Disease Surveillance System in 2010.</p><p><b>RESULTS</b>LE at birth of Chinese people was 73.24 years in 2010. Women had a longer LE than men, and urban population had a longer LE than rural population. CVD deaths resulted in a 4.79-year LE loss and premature deaths in people aged 25 to 64 years were responsible for a substantial part of LE loss from CVD. Death from ischemic heart disease and cerebrovascular diseases accounted for 69.2% of LE loss from CVD deaths and death from cerebrovascular diseases was the largest contributor. In rural men, 51.1% LE loss from CVD deaths was caused by cerebrovascular diseases. If there were no changes in mortality rates for all other diseases, a 27.4% reduction in CVD mortality would increase LE by 1 year in Chinese population.</p><p><b>CONCLUSION</b>There is a considerable impact of CVD deaths on LE. A 1-year LE increase in the future requires at least a 27.4% reduction in CVD mortality from the current level. Targeting the rural population and tackling cerebrovascular diseases are important for reaching the national goal of health improvement.</p>