Topology estimation for thousand-camera surveillance networks

Copyright © 2007 IEEESurveillance camera technologies have reached the point whereby networks of a thousand cameras are not uncommon. Systems for collecting and storing the video generated by such networks have been deployed operationally, and sophisticated methods have been developed for interrogating individual video streams. The principal contribution of this paper is a scalable method for processing video streams collectively, rather than on a per camera basis, which enables a coordinated approach to large-scale video surveillance. To realise our ambition of thousand camera automated surveillance networks, we use distributed processing on a dedicated cluster. Our focus is on determining activity topology - the paths objects may take between cameras' fields of view. An accurate estimate of activity topology is critical to many surveillance functions, including tracking targets through the network, and may also provide a means for partitioning of distributed surveillance processing. We present several implementations using the exclusion algorithm to determine activity topology. Measurements reported for the key system component demonstrate scalability to networks with a thousand cameras. Whole-system measurements are reported for actual operation on over a hundred camera streams (this limit is based on the number of cameras and computers presently available to us, not scalability). Finally, we explore how to scale our approach to support multi-thousand camera networks. ©2007 IEEE

Neurofibromatosis 2011: a report of the Children's Tumor Foundation annual meeting.

The 2011 annual meeting of the Children's Tumor Foundation, the annual gathering of the neurofibromatosis (NF) research and clinical communities, was attended by 330 participants who discussed integration of new signaling pathways into NF research, the appreciation for NF mutations in sporadic cancers, and an expanding pre-clinical and clinical agenda. NF1, NF2, and schwannomatosis collectively affect approximately 100,000 persons in US, and result from mutations in different genes. Benign tumors of NF1 (neurofibroma and optic pathway glioma) and NF2 (schwannoma, ependymoma, and meningioma) and schwannomatosis (schwannoma) can cause significant morbidity, and there are no proven drug treatments for any form of NF. Each disorder is associated with additional manifestations causing morbidity. The research presentations described in this review covered basic science, preclinical testing, and results from clinical trials, and demonstrate the remarkable strides being taken toward understanding of and progress toward treatments for these disorders based on the close interaction among scientists and clinicians

The Grizzly, November 12, 2009

Picasso at the Lapin Agile Draws in Audiences • Ursinus Awarded Teagle Grant • H1N1: How Ursinus is Battling the Swine Flu • Health Stats on the Ursinus Campus • Guest Speaker Addresses Urban (Dis)order • Four Students Hope to Pursue their Dreams with Watson Fellowship • Philly\u27s Practically Single Proves Pop-Punk Prevails; Set to Play Ursinus Friday • Veterans: The Brave Who Allow Us to be Free • Ghost Hunter Gives Presentation on Campus • Opinion: Hamid Karzai: Further Complicating Issues in Afghanistan; Ursinus\u27 Need for an Intro to Writing Class • Field Hockey Hoists C.C. Trophy for Sixth Consecutive Yearhttps://digitalcommons.ursinus.edu/grizzlynews/1799/thumbnail.jp

The Grizzly, September 24, 2009

CIE Celebrates 10 Year Anniversary, Makes Changes • Introducing Ursinus\u27 New Graduate Assistant • Tenth Annual Fringe Festival Kicks Off This Week • Visiting Professor Taije Silverman Shares Poetry • Is American Idol Rigged? An Investigatory Review • How Far Will You Go to Stretch Your Dollar in This Economy? • Restaurant Review: Molly Maguire\u27s Irish Restaurant and Pub • Opinions: Freshmen Parking on Campus; Glenn Beck and Rush Limbaugh • Ursinus Women\u27s Gymnastics Spends Weekend Volunteering • Coach Thomas Announces Baseball Captains for 2010 Seasonhttps://digitalcommons.ursinus.edu/grizzlynews/1792/thumbnail.jp

Transcriptome-Wide Assessment of Human Brain and Lymphocyte Senescence

Identifying biological pathways that vary across the age spectrum can provide insight into fundamental mechanisms that impact disease and frailty in the elderly. Few methodological approaches offer the means to explore this question on as broad a scale as gene expression profiling. Here, we have evaluated mRNA expression profiles as a function of age in two populations; one consisting of 191 individuals with ages-at-death ranging from 65-100 years and with post-mortem brain mRNA measurements of 13,216 genes and a second with 1240 individuals ages 15-94 and lymphocyte mRNA estimates for 18,519 genes.Among negatively correlated transcripts, an enrichment of mitochondrial genes was evident in both populations, providing a replication of previous studies indicating this as a common signature of aging. Sample differences were prominent, the most significant being a decrease in expression of genes involved in translation in lymphocytes and an increase in genes involved in transcription in brain, suggesting that apart from energy metabolism other basic cell processes are affected by age but in a tissue-specific manner. In assessing genomic architecture, intron/exon sequence length ratios were larger among negatively regulated genes in both samples, suggesting that a decrease in the expression of non-compact genes may also be a general effect of aging. Variance in gene expression itself has been theorized to change with age due to accumulation of somatic mutations and/or increasingly heterogeneous environmental exposures, but we found no evidence for such a trend here.Results affirm that deteriorating mitochondrial gene expression is a common theme in senescence, but also highlight novel pathways and features of gene architecture that may be important for understanding the molecular consequences of aging

The 4q12 Amplicon in Malignant Peripheral Nerve Sheath Tumors: Consequences on Gene Expression and Implications for Sunitinib Treatment

Malignant peripheral nerve sheath tumors (MPNST) are highly aggressive tumors which originate from Schwann cells and develop in about 10% of neurofibromatosis type 1 (NF1) patients. The five year survival rate is poor and more effective therapies are needed. Sunitinib is a drug targeting receptor tyrosine kinases (RTK) like PDGFRα, c-Kit and VEGFR-2. These genes are structurally related and cluster on chromosomal segment 4q12.) was present in MPNST cell lines suggesting an autocrine loop. We show that VEGF triggered signal transduction via the MAPK pathway, which could be blocked by sunitinib. might serve as predictive markers for efficacy of sunitinib