A system for learning statistical motion patterns

Analysis of motion patterns is an effective approach for anomaly detection and behavior prediction. Current approaches for the analysis of motion patterns depend on known scenes, where objects move in predefined ways. It is highly desirable to automatically construct object motion patterns which reflect the knowledge of the scene. In this paper, we present a system for automatically learning motion patterns for anomaly detection and behavior prediction based on a proposed algorithm for robustly tracking multiple objects. In the tracking algorithm, foreground pixels are clustered using a fast accurate fuzzy k-means algorithm. Growing and prediction of the cluster centroids of foreground pixels ensure that each cluster centroid is associated with a moving object in the scene. In the algorithm for learning motion patterns, trajectories are clustered hierarchically using spatial and temporal information and then each motion pattern is represented with a chain of Gaussian distributions. Based on the learned statistical motion patterns, statistical methods are used to detect anomalies and predict behaviors. Our system is tested using image sequences acquired, respectively, from a crowded real traffic scene and a model traffic scene. Experimental results show the robustness of the tracking algorithm, the efficiency of the algorithm for learning motion patterns, and the encouraging performance of algorithms for anomaly detection and behavior prediction

A system for learning statistical motion patterns

Analysis of motion patterns is an effective approach for anomaly detection and behavior prediction. Current approaches for the analysis of motion patterns depend on known scenes, where objects move in predefined ways. It is highly desirable to automatically construct object motion patterns which reflect the knowledge of the scene. In this paper, we present a system for automatically learning motion patterns for anomaly detection and behavior prediction based on a proposed algorithm for robustly tracking multiple objects. In the tracking algorithm, foreground pixels are clustered using a fast accurate fuzzy k-means algorithm. Growing and prediction of the cluster centroids of foreground pixels ensure that each cluster centroid is associated with a moving object in the scene. In the algorithm for learning motion patterns, trajectories are clustered hierarchically using spatial and temporal information and then each motion pattern is represented with a chain of Gaussian distributions. Based on the learned statistical motion patterns, statistical methods are used to detect anomalies and predict behaviors. Our system is tested using image sequences acquired, respectively, from a crowded real traffic scene and a model traffic scene. Experimental results show the robustness of the tracking algorithm, the efficiency of the algorithm for learning motion patterns, and the encouraging performance of algorithms for anomaly detection and behavior prediction

In vitro assessment of the toxicity of lead (Pb2+) to phycocyanin

© 2017 Elsevier Ltd This work reports the influence of lead (Pb2+) on fluorescence characteristics and protein structure of phycocyanin molecules experimentally in vitro. The fluorescence intensity decreases with the increasing concentration of Pb2+ from 0 to 5 × 10−5 mol L−1, showing the fluorescence quenching of phycocyanin by Pb2+. The quenching process is suggested to be static regarding the calculation results and the experimental results of time-resolved fluorescence decay profiles. The synchronous fluorescence spectra show that the effect of Pb2+ on the Tyr residues of phycocyanin is more significant than the Trp residues. The forming of aggregation by the interaction of Pb2+ with phycocyanin molecules is suggested from the results of resonance light scattering spectra. The UV–Vis spectra of the protein skeleton of phycocyanin have a red-shift of about 10 nm with increasing the Pb2+ concentration from 0 to 5 × 10−5 mol L−1, indicating a change in the protein skeleton and its secondary structure. With the increasing Pb2+ concentration, the two negative peaks (209 nm and 218 nm) on circular dichroism spectra become smaller, showing a decrease of the α-helix structure. These results may give people a deeper understanding of that how the heavy metal (Pb2+) can affect the chemo-physical properties of phycocyanin

ZIKV infection activates the IRE1-XBP1 and ATF6 pathways of unfolded protein response in neural cells.

BACKGROUND: Many viruses depend on the extensive membranous network of the endoplasmic reticulum (ER) for their translation, replication, and packaging. Certain membrane modifications of the ER can be a trigger for ER stress, as well as the accumulation of viral protein in the ER by viral infection. Then, unfolded protein response (UPR) is activated to alleviate the stress. Zika virus (ZIKV) is a mosquito-borne flavivirus and its infection causes microcephaly in newborns and serious neurological complications in adults. Here, we investigated ER stress and the regulating model of UPR in ZIKV-infected neural cells in vitro and in vivo. METHODS: Mice deficient in type I and II IFN receptors were infected with ZIKV via intraperitoneal injection and the nervous tissues of the mice were assayed at 5 days post-infection. The expression of phospho-IRE1, XBP1, and ATF6 which were the key markers of ER stress were analyzed by immunohistochemistry assay in vivo. Additionally, the nuclear localization of XBP1s and ATF6n were analyzed by immunohistofluorescence. Furthermore, two representative neural cells, neuroblastoma cell line (SK-N-SH) and astrocytoma cell line (CCF-STTG1), were selected to verify the ER stress in vitro. The expression of BIP, phospho-elF2α, phospho-IRE1, and ATF6 were analyzed through western blot and the nuclear localization of XBP1s was performed by confocal immunofluorescence microscopy. RT-qPCR was also used to quantify the mRNA level of the UPR downstream genes in vitro and in vivo. RESULTS: ZIKV infection significantly upregulated the expression of ER stress markers in vitro and in vivo. Phospho-IRE1 and XBP1 expression significantly increased in the cerebellum and mesocephalon, while ATF6 expression significantly increased in the mesocephalon. ATF6n and XBP1s were translocated into the cell nucleus. The levels of BIP, ATF6, phospho-elf2α, and spliced xbp1 also significantly increased in vitro. Furthermore, the downstream genes of UPR were detected to investigate the regulating model of the UPR during ZIKV infection in vitro and in vivo. The transcriptional levels of atf4, gadd34, chop, and edem-1 in vivo and that of gadd34 and chop in vitro significantly increased. CONCLUSION: Findings in this study demonstrated that ZIKV infection activates ER stress in neural cells. The results offer clues to further study the mechanism of neuropathogenesis caused by ZIKV infection

The Fermi level effect in III-V intermixing: The final nail in the coffin?

Copyright 1997 American Institute of Physics. This article may be downloaded for personal use only. Any other use requires prior permission of the author and the American Institute of Physics. This article appeared in Journal of Applied Physics 81, 2179 (1997) and may be found at

Electric field-induced phase transitions in (111)-, (110)-, and (100)-oriented Pb(Mg1∕3Nb2∕3)O3 single crystals

Electric field-induced phase transitions were investigated in (111), (110), and (100) thin platelets of relaxor ferroelectric Pb(Mg1∕3Nb2∕3)O3 single crystals with electric fields applied along the ⟨111⟩, ⟨110⟩, and ⟨100⟩ directions, respectively. Temperature dependences of complex dielectric permittivity, pyroelectric current and dielectric hysteresis loops were investigated. Electric field-temperature (E-T) phase diagrams were proposed for the different directions of the field. Alongside with the high-temperature ergodic relaxor phase and the low-temperature glassy nonergodic relaxor phase existing at E=0, the ferroelectric phase may appear in the diagram at the fields higher than the threshold field (Eth). The temperature of the first-order transition between ergodic relaxor and ferroelectric phases (TC) was located in field cooling and field heating after field-cooling regimes. For the ⟨111⟩ field direction, TC is higher and Eth is lower than for the other directions. For the ⟨100⟩ direction, TC is the lowest and Eth is the highest. The critical point bounding the TC(E) line when the field is applied in ⟨111⟩ direction [ Z. Kutnjak, J. Petzelt and R. Blinc Nature 441 956 (2006)] is not observed in the ⟨110⟩ and ⟨100⟩ directions up to the highest applied field of 7.5 kV∕cm. Extrapolation of experimental data suggests that the critical point for the ⟨110⟩ and ⟨100⟩ directions (if any) can be expected only at much higher fields. In the hysteresis loops experiments performed after zero-field cooling, the lower temperature limit is determined above which a ferroelectric phase can be induced from the frozen glassy state at a given field strength or the polarization of the induced ferroelectric phase can be reversed. This limit is located at much lower temperatures in the (100) platelet than in the (110) or (111) platelets. An additional ferroelectric rhombohedral to ferroelectric orthorhombic phase transition occurs in the (110) platelet at high electric fields (∼20 kV∕cm). The mechanisms of the field-induced transformation from the glassy nonergodic relaxor phase or the ergodic relaxor phase to the ferroelectric phase are discussed

Zika virus promotes CCN1 expression via the CaMKIIα-CREB pathway in astrocytes.

Zika virus (ZIKV) infection in the human central nervous system (CNS) causes Guillain-Barre syndrome, cerebellum deformity, and other diseases. Astrocytes are immune response cells in the CNS and an important component of the blood-brain barrier. Consequently, any damage to astrocytes facilitates the spread of ZIKV in the CNS. Connective tissue growth factor/Nephroblastoma overexpressed gene family 1 (CCN1), an important inflammatory factor secreted by astrocytes, is reported to regulate innate immunity and viral infection. However, the mechanism by which astrocyte viral infection affects CCN1 expression remains undefined. In this study, we demonstrate that ZIKV infection up-regulates CCN1 expression in astrocytes, thus promoting intracellular viral replication. Other studies revealed that the cAMP response element (CRE) in the CCN1 promoter is activated by the ZIKV NS3 protein. The cAMP-responsive element-binding protein (CREB), a transacting factor of the CRE, is also activated by NS3 or ZIKV. Furthermore,a specific inhibitor of CREB, i.e. SGC-CBP30, reduced ZIKV-induced CCN1 up-regulation and ZIKV replication. Moreover, co-immunoprecipitation, overexpression, and knockdown studies confirmed that the interaction between NS3 and the regulatory domain of CaMKIIα could activate the CREB pathway, thus resulting in the up-regulation of CCN1 expression and enhancement of virus replication. In conclusion, the findings of our investigations on the NS3-CaMKIIα-CREB-CCN1 pathway provide a foundation for understanding the infection mechanism of ZIKV in the CNS