Comparative Study of Structural Anomaly Diagnosis Based on ANN Model Using Random Displacement and Acceleration Responses with Incomplete Measurements.

Structural anomaly diagnosis, such as damage identification, is a continuously interesting issue. Artificial neural networks have an excellent ability to model complex structure dynamics. In this paper, an artificial neural network model is used to describe the relationship between structural responses and anomalies such as stiffness reduction due to damages. Random acceleration and displacement responses as generally measured data are used as the input to the artificial neural network, and the output of the artificial neural network is the anomaly severity. The artificial neural network model is set up by training and then validated using random vibration responses with different structural anomalies. The structural anomaly diagnosis method based on the artificial neural network model using random acceleration and displacement responses is applied to a five-story building structure under random base excitations (seismic loading). Anomalies in the structure are denoted by stiffness reduction. Structural anomaly diagnosis using random acceleration responses is compared with that using random displacement responses. The numerical results show the effects of different random vibration responses used on the accuracy of predicting stiffness reduction. The actual incomplete measurements include intensive noise, finite sampling time length, and limited measurement points. The effects of the incomplete measurements on the accuracy of predicting results are also discussed.

Protective effects of components of the Chinese herb grassleaf sweetflag rhizome on PC12 cells incubated with amyloid-beta42.

The major ingredients of grassleaf sweetflag rhizome are ß-asarone and eugenol, which can cross the blood-brain barrier and protect neurons. This study aimed to observe the neuroprotective effects and mechanisms of ß-asarone and eugenol, components of the Chinese herb grassleaf sweetflag rhizome, on PC12 cells. First, PC12 cells were cultured with different concentrations (between 1 × 10(-10) M and 1 × 10(-5) M) of ß-asarone and eugenol. Survival rates of PC12 cells were not significantly affected. Second, PC12 cells incubated with amyloid-beta42, which reduced cell survival, were cultured under the same conditions (1 × 10(-6) M ß-asarone and eugenol). The survival rates of PC12 cells significantly increased, while expression levels of the mRNAs for the pro-apoptotic protein Bax decreased, and those for the anti-apoptotic protein Bcl mRNA increased. In addition, the combination of ß-asarone with eugenol achieved better results than either component alone. Our experimental findings indicate that both ß-asarone and eugenol protect PC12 cells through inhibiting apoptosis, and that the combination of the two is better than either alone.

Intrahippocampal injection of Aß1-42 inhibits neurogenesis and down-regulates IFN-γ and NF-κB expression in hippocampus of adult mouse brain.

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by accumulation of amyloid plaques and neurofibrillary tangles. Amyloid-ß (Aß) is widely recognized as a key factor in the pathogenesis of AD. Aß1-42 a major component of amyloid plaques, has shown synaptotoxicity associated with impaired long-term potentiation and cognitive deficits. Alteration of neurogenesis in AD patients has been reported, while little is known about how Aß1-42 affects hippocampal neurogenesis in the adult brain. In this study, we injected human Aß1-42 peptide into hippocampal CA1 area of adult mouse brain bilaterally and evaluated histological change and neurogenesis in the hippocampus. Hematoxylin and eosin (HE) stain showed that Aß1-42-injection resulted in an extensive neurodegeneration in the Aß-accumulated area and CA3 in hippocampus. Immunostaining showed that intrahippocampal Aß1-42-injection dramatically decreased the number of bromodeoxyuridine (BrdU)-positive cells in the dentate gyrus (DG) compared to the vehicle injection. Moreover, a significant decrease in the number of BrdU/double-cortin double-positive cells in Aß1-42-injected hippocampus was observed, suggesting that Aß1-42-injection inhibited progenitor cell proliferation and neurogenesis in subgranular zone of the DG in the adult brain. We also found that the Aß1-42-mediated decline of neurogenesis was associated with decreased protein levels of cytokines interferon-γ (IFN-γ) and transcription factor nuclear factor-kappa B (NF-κB) in the hippocampus. These results suggest that Aß1-42 inhibits hippocampal neurogenesis in the adult brain possibly through down-regulation of INF-γ and NF-κB signaling pathway. This study provides a new insight into Aß1-42-mediated decrease in hippocampal neurogenesis in the adult central nervous system.

Effect of sub-acute exposure to acrylamide on GABAergic neurons and astrocytes in weaning rat cerebellum.

Occupational exposure and experimental intoxication of acrylamide (ACR) can produce skeletal muscle weakness and ataxia. In this study, we tested whether ACR would affect cerebellar function through the regulation of gamma-aminobutyric acid (GABA) and glial fibrillary acidic protein (GFAP) expression in cerebellum. Weaning male Sprague-Dawley rats were gavaged with ACR (5, 15, 30 mg/kg, 5 days per week) or saline for 4 weeks. Effects of ACR on the cerebellum were observed. For the 5 mg/kg group, no obvious change was observed, whereas moderate and severe ataxia were observed in the 15 mg/kg and 30 mg/kg groups, respectively. For the 15 mg/kg and 30 mg/kg groups, cerebellum concentrations of glutamate and GABA were dose-dependently decreased and increased, respectively. Moreover, the expression of GABA, the GABAergic presynaptic marker glutamate acid decarboxylase-65 (GAD65) and GFAP were significantly increased in those 2 groups. The results suggested that weaning rats were sensitive to ACR and that the toxic effects of ACR on the cerebellum may be associated with the increased expression of GABA and reactive astrocytes hypertrophy.

Screening for anti-lipase properties of 37 traditional Chinese medicinal herbs.

BACKGROUND: To find new, crude anti-obesity drugs from natural sources through the inhibition of adsorption of dietary lipids, in vitro porcine pancreatic lipase (PPL; triacylglycerol lipase, EC 3.1.1.3) inhibitory tests were carried out on selected plants with weight-reducing or related potential, used in Chinese traditional medicine. METHODS: The methanolic extracts of 37 traditional Chinese herbal medicines of different families were assayed for their in vitro activity against PPL by using spectrophotometry with 2,4-dinitrophenyl butyrate as a synthetic substrate. Coexistent phytochemicals, or those present in high levels, in the 3 most promising Chinese herbs were tested for their anti-lipase activity. RESULTS: Extracts from 2 herbs, Prunella vulgaris L. (Labiatae) and Rheum palmatum L. (Polygonaceae), at a concentration of 200 mg/mL, significantly inhibited PPL-by 74.7% and 53.8%, respectively. Quercetin exhibited better activity (27.4%) than all the other phytochemicals at a final concentration of 25 mg/mL in the assay system, followed by luteolin, with an activity of 17.3%. CONCLUSION: The results support the view that herbs represent a rich source of anti-lipase compounds. The screening of the methanolic extracts of 37 Chinese medicinal plants in vitro led to the identification of several extracts with potential activity against PPL, in particular, P. vulgaris and R. palmatum. We also found that several monomeric chemicals in these herbs exhibited good or moderate activity against PPL. To the best of our knowledge, these traditional Chinese herbal medicines or phytochemicals have not been previously screened for their lipase inhibitory activity.