An improved Gaussian Mixture Model with post-processing for multiple object detection in surveillance video analytics

Gaussian Mixture Model (GMM) is an effective method for extracting foreground objects from video sequences. However, GMM fails to detect the object in challenging scenarios like the presence of shadow, occlusion, complex backgrounds, etc. To handle these challenges, intrinsic and extrinsic enhancement is required in traditional GMM. This paper presents a novel framework that combines improved GMM with postprocessing for multiple object detection. In the proposed system, GMM with parameter initialization is considered an intrinsic improvement. Video preprocessing and postprocessing are considered extrinsic improvements. Integration of morphological operation with GMM helps for better segmentation than traditional GMM, and it also helps to increase detection performance by reducing false positives. Video preprocessing is the process of noise removal that prepares input video ready for further processing. In the final step gradient of morphological operations is used for postprocessing. The proposed approach was tested on challenging surveillance video sequences from benchmark datasets such as PETS 2009 and CD 2014(Change Detection). The experimental results are compared using ground truth and performance evaluation metrics. The results show that the proposed approach performs better than GMM, and the method can detect the object effectively even in illumination variation and partial occlusion

Translocator protein is a marker of activated microglia in rodent models but not human neurodegenerative diseases

Microglial activation plays central roles in neuroinflammatory and neurodegenerative diseases. Positron emission tomography (PET) targeting 18 kDa Translocator Protein (TSPO) is widely used for localising inflammation in vivo, but its quantitative interpretation remains uncertain. We show that TSPO expression increases in activated microglia in mouse brain disease models but does not change in a non-human primate disease model or in common neurodegenerative and neuroinflammatory human diseases. We describe genetic divergence in the TSPO gene promoter, consistent with the hypothesis that the increase in TSPO expression in activated myeloid cells depends on the transcription factor AP1 and is unique to a subset of rodent species within the Muroidea superfamily. Finally, we identify LCP2 and TFEC as potential markers of microglial activation in humans. These data emphasise that TSPO expression in human myeloid cells is related to different phenomena than in mice, and that TSPO-PET signals in humans reflect the density of inflammatory cells rather than activation state.Published versionThe authors thank the UK MS Society for financial support (grant number: C008-16.1). DRO was funded by an MRC Clinician Scientist Award (MR/N008219/1). P.M.M. acknowledges generous support from Edmond J Safra Foundation and Lily Safra, the NIHR Senior Investigator programme and the UK Dementia Research Institute which receives its funding from DRI Ltd., funded by the UK Medical Research Council, Alzheimer’s Society, and Alzheimer’s Research UK. P.M.M. and D.R.O. thank the Imperial College Healthcare Trust-NIHR Biomedical Research Centre for infrastructure support and the Medical Research Council for support of TSPO studies (MR/N016343/1). E.A. was supported by the ALS Stichting (grant “The Dutch ALS Tissue Bank”). P.M. and B.B.T. are funded by the Swiss National Science Foundation (projects 320030_184713 and 310030_212322, respectively). S.T. was supported by an “Early Postdoc.Mobility” scholarship (P2GEP3_191446) from the Swiss National Science Foundation, a “Clinical Medicine Plus” scholarship from the Prof Dr. Max Cloëtta Foundation (Zurich, Switzerland), from the Jean et Madeleine Vachoux Foundation (Geneva, Switzerland) and from the University Hospitals of Geneva. This work was funded by NIH grants U01AG061356 (De Jager/Bennett), RF1AG057473 (De Jager/Bennett), and U01AG046152 (De Jager/Bennett) as part of the AMP-AD consortium, as well as NIH grants R01AG066831 (Menon) and U01AG072572 (De Jager/St George-Hyslop)