Applications of Face Analysis and Modeling in Media Production

Facial expressions play an important role in day-by-day communication as well as media production. This article surveys automatic facial analysis and modeling methods using computer vision techniques and their applications for media production. The authors give a brief overview of the psychology of face perception and then describe some of the applications of computer vision and pattern recognition applied to face recognition in media production. This article also covers the automatic generation of face models, which are used in movie and TV productions for special effects in order to manipulate people's faces or combine real actors with computer graphics

Developing Fine-Grained Actigraphies for Rheumatoid Arthritis Patients from a Single Accelerometer Using Machine Learning

In addition to routine clinical examination, unobtrusive and physical monitoring of Rheumatoid Arthritis (RA) patients provides an important source of information to enable understanding the impact of the disease on quality of life. Besides an increase in sedentary behaviour, pain in RA can negatively impact simple physical activities such as getting out of bed and standing up from a chair. The objective of this work is to develop a method that can generate fine-grained actigraphies to capture the impact of the disease on the daily activities of patients. A processing methodology is presented to automatically tag activity accelerometer data from a cohort of moderate-to-severe RA patients. A study of procesing methods based on machine learning and deep learning is provided. Thirty subjects, 10 RA patients and 20 healthy control subjects, were recruited in the study. A single tri-axial accelerometer was attached to the position of the fifth lumbar vertebra (L5) of each subject with a tag prediction granularity of 3 s. The proposed method is capable of handling unbalanced datasets from tagged data while accounting for long-duration activities such as sitting and lying, as well as short transitions such as sit-to-stand or lying-to-sit. The methodology also includes a novel mechanism for automatically applying a threshold to predictions by their confidence levels, in addition to a logical filter to correct for infeasible sequences of activities. Performance tests showed that the method was able to achieve around 95% accuracy and 81% F-score. The produced actigraphies can be helpful to generate objective RA disease-specific markers of patient mobility in-between clinical site visits

Proposed Role for COUP-TFII in Regulating Fetal Leydig Cell Steroidogenesis, Perturbation of Which Leads to Masculinization Disorders in Rodents

Reproductive disorders that are common/increasing in prevalence in human males may arise because of deficient androgen production/action during a fetal ‘masculinization programming window’. We identify a potentially important role for Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) in Leydig cell (LC) steroidogenesis that may partly explain this. In rats, fetal LC size and intratesticular testosterone (ITT) increased ∼3-fold between e15.5-e21.5 which associated with a progressive decrease in the percentage of LC expressing COUP-TFII. Exposure of fetuses to dibutyl phthalate (DBP), which induces masculinization disorders, dose-dependently prevented the age-related decrease in LC COUP-TFII expression and the normal increases in LC size and ITT. We show that nuclear COUP-TFII expression in fetal rat LC relates inversely to LC expression of steroidogenic factor-1 (SF-1)-dependent genes (StAR, Cyp11a1, Cyp17a1) with overlapping binding sites for SF-1 and COUP-TFII in their promoter regions, but does not affect an SF-1 dependent LC gene (3β-HSD) without overlapping sites. We also show that once COUP-TFII expression in LC has switched off, it is re-induced by DBP exposure, coincident with suppression of ITT. Furthermore, other treatments that reduce fetal ITT in rats (dexamethasone, diethylstilbestrol (DES)) also maintain/induce LC nuclear expression of COUP-TFII. In contrast to rats, in mice DBP neither causes persistence of fetal LC COUP-TFII nor reduces ITT, whereas DES-exposure of mice maintains COUP-TFII expression in fetal LC and decreases ITT, as in rats. These findings suggest that lifting of repression by COUP-TFII may be an important mechanism that promotes increased testosterone production by fetal LC to drive masculinization. As we also show an age-related decline in expression of COUP-TFII in human fetal LC, this mechanism may also be functional in humans, and its susceptibility to disruption by environmental chemicals, stress and pregnancy hormones could explain the origin of some human male reproductive disorders

Transcriptome analyses based on genetic screens for Pax3 myogenic targets in the mouse embryo

<p>Abstract</p> <p>Background</p> <p>Pax3 is a key upstream regulator of the onset of myogenesis, controlling progenitor cell survival and behaviour as well as entry into the myogenic programme. It functions in the dermomyotome of the somite from which skeletal muscle derives and in progenitor cell populations that migrate from the somite such as those of the limbs. Few Pax3 target genes have been identified. Identifying genes that lie genetically downstream of <it>Pax3 </it>is therefore an important endeavour in elucidating the myogenic gene regulatory network.</p> <p>Results</p> <p>We have undertaken a screen in the mouse embryo which employs a <it>Pax3^GFP</it>allele that permits isolation of Pax3 expressing cells by flow cytometry and a <it>Pax3^PAX3-FKHR</it>allele that encodes PAX3-FKHR in which the DNA binding domain of Pax3 is fused to the strong transcriptional activation domain of FKHR. This constitutes a gain of function allele that rescues the <it>Pax3 </it>mutant phenotype. Microarray comparisons were carried out between <it>Pax3^GFP/+</it>and <it>Pax3^{GFP/PAX3-FKHR}</it>preparations from the hypaxial dermomyotome of somites at E9.5 and forelimb buds at E10.5. A further transcriptome comparison between Pax3-GFP positive and negative cells identified sequences specific to myogenic progenitors in the forelimb buds. Potential Pax3 targets, based on changes in transcript levels on the gain of function genetic background, were validated by analysis on loss or partial loss of function <it>Pax3 </it>mutant backgrounds. Sequences that are up- or down-regulated in the presence of PAX3-FKHR are classified as somite only, somite and limb or limb only. The latter should not contain sequences from Pax3 positive neural crest cells which do not invade the limbs. Verification by whole mount <it>in situ </it>hybridisation distinguishes myogenic markers. Presentation of potential Pax3 target genes focuses on signalling pathways and on transcriptional regulation.</p> <p>Conclusions</p> <p>Pax3 orchestrates many of the signalling pathways implicated in the activation or repression of myogenesis by regulating effectors and also, notably, inhibitors of these pathways. Important transcriptional regulators of myogenesis are candidate Pax3 targets. Myogenic determination genes, such as <it>Myf5 </it>are controlled positively, whereas the effect of <it>Pax3 </it>on genes encoding inhibitors of myogenesis provides a potential brake on differentiation. In the progenitor cell population, <it>Pax7 </it>and also <it>Hdac5 </it>which is a potential repressor of <it>Foxc2</it>, are subject to positive control by <it>Pax3</it>.</p

Modelling Light Transmission Through Aperture Arrays

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Altered COUP-TFII expression in fetal rat Leydig cells after <i>in utero</i> exposure to vehicle (control) or to 500 mg/kg/day dibutyl phthalate (DBP) from e19.5-e20.5 (late treatment window) and the relationship to intratesticular testosterone levels at e21.5.

<p>(A–D) Triple immunofluorescence for SMA (blue), 3β-HSD (red) and COUP-TFII (green) on testis sections from representative vehicle (control) and DBP-exposed animals on high resolution tiled images (A and C) and at higher power (B and D). Asterisks in panel D indicate Leydig cell aggregates that are predominantly immunopositive for COUP-TFII. SC = seminiferous cords. Scale bars in A and C = 200 µm, in B and D = 20 µm. (E) Quantification of the percentage of COUP-TFII positive fetal Leydig cells in animals from the treatment groups shown in panels A–D. Values are Means ± SEM for 8–10 animals per treatment group (minimum of 3 litters per group). ***p<0.001, in comparison with respective control. (F) Corresponding intratesticular testosterone levels for the treatment groups in panels A–D. Values are Means ± SEM for 18–20 animals per group (minimum of 3 litters per group). ***p<0.001, in comparison with respective control.</p

Effect of <i>in utero</i> exposure of rats to vehicle (control) or dibutyl phthalate (DBP: 500 mg/kg/day) on age-dependent changes in intratesticular testosterone levels per 10⁶ fetal fetal Leydig cells (A), Leydig cell number per testis (B), Leydig cell nuclear volume (C) and Leydig cell cytoplasmic volume (D).

<p>Values in A are Means ± SEM for 5–12 animals at each age (minimum of 3 litters per group). Values in B–D are Means ± SEM for 4–8 animals in each group (minimum of 3 litters per group). *p<0.05, **p<0.01, ***p<0.001, in comparison with respective controls; other comparisons are indicated by capped lines.</p

An overview of SF-1, COUP-TFII and SF-1/COUP-TFII binding sites in the promoters of <i>StAR</i>, <i>Cyp11a1</i>, <i>Cyp17a1</i>, <i>Hsd3b1</i> and <i>Amh</i>.

*<p>: “weak” COUP-TFII binding site.</p><p>StAR = steroidogenic acute regulatory protein; Cyp11a1 = cytochrome P450, family 11, subfamily a, polypeptide 1; Cyp17a1 = cytochrome P450, family 17, subfamily a, polypeptide 1; Hsd3b1 = hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1; Amh = anti-Müllerian hormone; SF-1 = steroidogenic factor-1; COUP-TFII = chicken ovalbumin upstream promoter transcription factor II; bp = basepair.</p

Effect of <i>in utero</i> exposure of rats to vehicle (control) or to diethylstilbestrol (DES 100 µg/kg on e13.5, e15.5, e17.5, e19.5 and e20.5) on COUP-TFII immunoexpression in fetal Leydig cells at e21.5.

<p>(A) Triple immunofluorescence for SMA (blue), 3β-HSD (red) and COUP-TFII (green) on testis sections from representative vehicle (control) and DES-exposed animals. Note that in controls occasional fetal Leydig cells are COUP-TFII-immunopositive (arrow) whereas exposure to DES resulted in a 3-fold increase in the % of COUP-TFII-immunopositive Leydig cells (asterisks). SC = seminiferous cords. Scale bar = 20 µm. (B) Quantification of the percentage of COUP-TFII positive fetal Leydig cells in animals from the treatment group shown in panel A. Values are Means ± SEM for 3–13 animals per treatment group (minimum of 3 litters per group). ***p<0.001, in comparison with respective control. (C) Corresponding intratesticular testosterone levels for the treatment groups in panel A. Values are Means ± SEM for 13–25 animals per group (minimum of 3 litters per group). ***p<0.001, in comparison with respective control. (E) cytochrome P450, family 11, subfamily a, polypeptide 1 (<i>Cyp11a1</i>), (F) Steroidogenic acute regulatory protein <i>(StAR</i>), (G) cytochrome P450, family 17, subfamily a, polypeptide 1 (<i>Cyp17a1</i>), (H) Anti-Müllerian hormone (<i>Amh</i>) gene expression in testes from control and DES-exposed males at e21.5. Values are Means ± SEM for 11–24 animals per group (minimum of 3 litters per group). ***p<0.001, in comparison with respective control. NS = not significant.</p