Learning Efficient Deep Feature Extraction For Mobile Ocular Biometrics

Title from PDF of title page viewed March 4, 2021Dissertation advisors: Reza Derakhshani and Cory BeardVitaIncludes bibliographical references (page 137-149)Thesis (Ph.D.)--School of Computing and Engineering. University of Missouri--Kansas City, 2020Ocular biometrics uses physical traits from eye regions such as iris, conjunctival vasculature, and periocular for recognizing the person. Ocular biometrics has gained popularity amongst research and industry alike for its identification capabilities, security, and simplicity in the acquisition, even using a mobile phone's selfie camera. With the rapid advancement in hardware and deep learning technologies, better performances have been obtained using Convolutional Neural Networks(CNN) for feature extraction and person recognition. Most of the early works proposed using large CNNs for ocular recognition in subject-dependent evaluation, where the subjects overlap between the training and testing set. This is difficult to scale for the large population as the CNN model needs to be re-trained every time a new subject is enrolled in the database. Also, many of the proposed CNN models are large, which renders them memory intensive and computationally costly to deploy on a mobile device. In this work, we propose CNN based robust subject-independent feature extraction for ocular biometric recognition, which is memory and computation efficient. We evaluated our proposed method on various ocular biometric datasets in the subject-independent, cross-dataset, and cross-illumination protocols.Introduction -- Previous Work -- Calculating CNN Models Computational Efficiency -- Case Study of Deep Learning Models in Ocular Biometrics -- OcularNet Model -- OcularNet-v2: Self-learned ROI detection with deep features -- LOD-V: Large Ocular Biometrics Dataset in Visible Spectrum -- Conclusion and Future Work -- Appendix A. Supplementary Materials for Chapter 4 -- Appendix B. Supplementary Materials for Chapter 5 -- Appendix C.Supplementary Materials for Chapter 6 -- Appendix D. Supplementary Materials for Chapter 7xxii, 150 page

Biometric Systems

Because of the accelerating progress in biometrics research and the latest nation-state threats to security, this book's publication is not only timely but also much needed. This volume contains seventeen peer-reviewed chapters reporting the state of the art in biometrics research: security issues, signature verification, fingerprint identification, wrist vascular biometrics, ear detection, face detection and identification (including a new survey of face recognition), person re-identification, electrocardiogram (ECT) recognition, and several multi-modal systems. This book will be a valuable resource for graduate students, engineers, and researchers interested in understanding and investigating this important field of study

Sox10 regulates enteric neural crest cell migration in the developing gut

Concurrent Sessions 1: 1.3 - Organs to organisms: Models of Human Diseases: abstract no. 1417th ISDB 2013 cum 72nd Annual Meeting of the Society for Developmental Biology, VII Latin American Society of Developmental Biology Meeting and XI Congreso de la Sociedad Mexicana de Biologia del Desarrollo. The Conference's web site is located at http://www.inb.unam.mx/isdb/Sox10 is a HMG-domain containing transcription factor which plays important roles in neural crest cell survival and differentiation. Mutations of Sox10 have been identified in patients with Waardenburg-Hirschsprung syndrome, who suffer from deafness, pigmentation defects and intestinal aganglionosis. Enteric neural crest cells (ENCCs) with Sox10 mutation undergo premature differentiation and fail to colonize the distal hindgut. It is unclear, however, whether Sox10 plays a role in the migration of ENCCs. To visualize the migration behaviour of mutant ENCCs, we generated a Sox10NGFP mouse model where EGFP is fused to the N-terminal domain of Sox10. Using time-lapse imaging, we found that ENCCs in Sox10NGFP/+ mutants displays lower migration speed and altered trajectories compared to normal controls. This behaviour was cell-autonomous, as shown by organotypic grafting of Sox10NGFP/+ gut segments onto control guts and vice versa. ENCCs encounter different extracellular matrix (ECM) molecules along the developing gut. We performed gut explant culture on various ECM and found that Sox10NGFP/+ ENCCs tend to form aggregates, particularly on fibronectin. Time-lapse imaging of single cells in gut explant culture indicated that the tightly-packed Sox10 mutant cells failed to exhibit contact inhibition of locomotion. We determined the expression of adhesion molecule families by qPCR analysis, and found integrin expression unaffected while L1-cam and selected cadherins were altered, suggesting that Sox10 mutation affects cell adhesion properties of ENCCs. Our findings identify a de novo role of Sox10 in regulating the migration behaviour of ENCCs, which has important implications for the treatment of Hirschsprung disease.postprin

Analysis of craniofacial defects in Six1/Eya1-associated Branchio-Oto-Renal Syndrome

Poster Session I - Morphogenesis: 205/B10117th ISDB 2013 cum 72nd Annual Meeting of the Society for Developmental Biology, 7th Latin American Society of Developmental Biology Meeting and 11th Congreso de la Sociedad Mexicana de Biologia del Desarrollo.Branchio-Oto-Renal (BOR) syndrome patients exhibit craniofacial and renal anomalies as well as deafness. BOR syndrome is caused by mutations in Six1 or Eya1, both of which regulate cell proliferation and differentiation. The molecular mechanism underlying the craniofacial and branchial arch (BA) defects in BOR syndrome is unclear. We have found that Hoxb3 is up-regulated in the second branchial arch (BA2) of Six1-/- mutants. Moreover, Hoxb3 over-expression in transgenic mice leads to BA abnormalities which are similar to the BA defects in Six1-/- or Eya1-/- mutants, suggesting a regulatory relationship among Six1, Eya1 and Hoxb3 genes. The aim of this study is to investigate the molecular mechanism underlying abnormal BA development in BOR syndrome using Six1 and Eya1 mutant mice. Two potential Six1 binding sites were identified on the Hoxb3 gene. In vitro and in vivo Chromatin IP assays showed that Six1 could directly bind to one of the sites specifically. Furthermore, using a chick in ovo luciferase assay we showed that Six1 could suppress gene expression through one of the specific binding sites. On the other hand, in Six1-/- mutants, we found that the Notch ligand Jag1 was up-regulated in BA2. Similarly, in Hoxb3 transgenic mice, ectopic expression of Jag1 could be also detected in BA2. To investigate the activation of Notch signaling pathway, we found that Notch intracellular domain (NICD), a direct indicator of Notch pathway activation, was up-regulated in BAs of Six1-/-; Eya1-/- double mutants. Our results indicate that Hoxb3 and Notch signaling pathway are involved in mediating the craniofacial defects of Six1/Eya1-associated Branchio-Oto-Renal Syndrome.postprin

Handbook of Digital Face Manipulation and Detection

This open access book provides the first comprehensive collection of studies dealing with the hot topic of digital face manipulation such as DeepFakes, Face Morphing, or Reenactment. It combines the research fields of biometrics and media forensics including contributions from academia and industry. Appealing to a broad readership, introductory chapters provide a comprehensive overview of the topic, which address readers wishing to gain a brief overview of the state-of-the-art. Subsequent chapters, which delve deeper into various research challenges, are oriented towards advanced readers. Moreover, the book provides a good starting point for young researchers as well as a reference guide pointing at further literature. Hence, the primary readership is academic institutions and industry currently involved in digital face manipulation and detection. The book could easily be used as a recommended text for courses in image processing, machine learning, media forensics, biometrics, and the general security area

Targeting the sodium iodide symporter (NIS) and apoptotic genes in extrathyroidal tumors.

Sodium Iodide Symporter (NIS), a therapeutic gene, was studied for the first time in retinoblastoma (RB) correlating the expression with clinicopathological invasiveness of the tumor. The specificity of EpCAM based NIS gene therapy was demonstrated in breast cancer cell as a proof of concept model via 1) EpCAM as tissue specific promoter and 2) nanoformulation, both of which showed encouraging outcomes. In addition, for the first time the upregulated expression of splice variants of survivin, Bax and Bcl-2 in RB tumors was explored indicating their possible role in tumor progression through apoptosis dysregulation. Thus, the above study achieved a profound knowledge about NIS and apoptotic genes in extrathyroidal tumors