Miracle-dz/UniFAR-FTUs huggingface dataset:
Court Reconstruction for Camera Calibration in Broadcast Basketball Videos

We introduce a technique of calibrating camera motions in basketball videos. Our method particularly transforms player positions to standard basketball court coordinates and enables applications such as tactical analysis and semantic basketball video retrieval. To achieve a robust calibration, we reconstruct the panoramic basketball court from a video, followed by warping the panoramic court to a standard one. As opposed to previous approaches, which individually detect the court lines and corners of each video frame, our technique considers all video frames simultaneously to achieve calibration; hence, it is robust to illumination changes and player occlusions. To demonstrate the feasibility of our technique, we present a stroke-based system that allows users to retrieve basketball videos. Our system tracks player trajectories from broadcast basketball videos. It then rectifies the trajectories to a standard basketball court by using our camera calibration method. Consequently, users can apply stroke queries to indicate how the players move in gameplay during retrieval. The main advantage of this interface is an explicit query of basketball videos so that unwanted outcomes can be prevented. We show the results in Figs. 1, 7, 9, 10 and our accompanying video to exhibit the feasibility of our technique.
Epstein-Barr Virus-Encoded Bcl-2 Homologue Functions as a Survival Factor in Wp-Restricted Burkitt Lymphoma Cell Line P3HR-1

ABSTRACT Burkitt lymphoma (BL) is etiologically associated with Epstein-Barr virus (EBV). EBV-positive BL tumors display two latent forms of infection. One is referred to as latency I infection, in which EBV expresses the virus genome maintenance protein EBNA1 as the only viral protein. The other is referred to as Wp-restricted latency and was recently identified in a subset of BL tumors. In these tumors, EBV expresses EBNA1, EBNA3A, EBNA3B, EBNA3C, a truncated form of EBNA-LP, and the viral Bcl-2 homologue BHRF1, all of which are driven by the BamHI W promoter (Wp). To investigate the role of EBV in Wp-restricted BL, we conditionally expressed a dominant-negative EBNA1 (dnEBNA1) mutant which interrupts the virus genome maintenance function of EBNA1 in the P3HR-1 BL cell line. Induction of dnEBNA1 expression caused loss of the EBV genome and resulted in apoptosis of P3HR-1 cells in the absence of exogenous apoptosis inducers, indicating that P3HR-1 cells cannot survive without EBV. Stable transfection of the BHRF1 gene into P3HR-1 cells rescued the cells from the apoptosis induced by dnEBNA1 expression, whereas stable transfection of truncated EBNA-LP, EBNA3A, or EBNA3C did not. Moreover, knockdown of BHRF1 expression in P3HR-1 cells resulted in increased cell death. These results indicate that EBV is essential for the survival of P3HR-1 cells and that BHRF1 functions as a survival factor. Our finding implies a critical contribution of BHRF1 to the pathogenesis of Wp-restricted BLs.
Visual Analysis of Multi-Run Spatio-Temporal Simulations Using Isocontour Similarity for Projected Views

Multi-run simulations are widely used to investigate how simulated processes evolve depending on varying initial conditions. Frequently, such simulations model the change of spatial phenomena over time. Isocontours have proven to be effective for the visual representation and analysis of 2D and 3D spatial scalar fields. We propose a novel visualization approach for multi-run simulation data based on isocontours. By introducing a distance function for isocontours, we generate a distance matrix used for a multidimensional scaling projection. Multiple simulation runs are represented by polylines in the projected view displaying change over time. We propose a fast calculation of isocontour differences based on a quasi-Monte Carlo approach. For interactive visual analysis, we support filtering and selection mechanisms on the multi-run plot and on linked views to physical space visualizations. Our approach can be effectively used for the visual representation of ensembles, for pattern and outlier detection, for the investigation of the influence of simulation parameters, and for a detailed analysis of the features detected. The proposed method is applicable to data of any spatial dimensionality and any spatial representation (gridded or unstructured). We validate our approach by performing a user study on synthetic data and applying it to different types of multi-run spatio-temporal simulation data.
Complete Genome of Pseudomonas aeruginosa Phage PA26

ABSTRACT PA26, a novel lytic bacteriophage infecting Pseudomonas aeruginosa, was isolated, and the whole genome was sequenced. It was found to belong to the myoviridae by an electron microscopic observation. It had a linear double-stranded DNA genome of 72,321 bp. Genomic analysis showed that it resembled another Pseudomonas phage, LIT1.
Association of the pr Peptides with Dengue Virus at Acidic pH Blocks Membrane Fusion

ABSTRACT Flavivirus assembles into an inert particle that requires proteolytic activation by furin to enable transmission to other hosts. We previously showed that immature virus undergoes a conformational change at low pH that renders it accessible to furin (I. M. Yu, W. Zhang, H. A. Holdaway, L. Li, V. A. Kostyuchenko, P. R. Chipman, R. J. Kuhn, M. G. Rossmann, and J. Chen, Science 319:1834-1837, 2008). Here we show, using cryoelectron microscopy, that the structure of immature dengue virus at pH 6.0 is essentially the same before and after the cleavage of prM. The structure shows that after cleavage, the proteolytic product pr remains associated with the virion at acidic pH, and that furin cleavage by itself does not induce any major conformational changes. We also show by liposome cofloatation experiments that pr retention prevents membrane insertion, suggesting that pr is present on the virion in the trans-Golgi network to protect the progeny virus from fusion within the host cell.
Identification of the Cellular Prohibitin 1/Prohibitin 2 Heterodimer as an Interaction Partner of the C-Terminal Cytoplasmic Domain of the HIV-1 Glycoprotein

ABSTRACT Our studies aim to elucidate the functions carried out by the very long, and in its length highly conserved, C-terminal cytoplasmic domain (Env-CT) of the HIV-1 glycoprotein. Mass spectrometric analysis of cellular proteins bound to a tagged version of the HIV Env-CT led to the identification of the prohibitin 1 and 2 proteins (Phb1 and Phb2). These ubiquitously expressed proteins, which exist as stable heterodimers, have been shown to have multiple functions within cells and to localize to multiple cellular and extracellular compartments. The specificity of binding of the Phb1/Phb2 complex to the Env-CT was confirmed in various manners, including coimmunoprecipitation with authentic provirally encoded, full-length Env. Strong binding was dependent on Env residues 790 to 800 and could be severely inhibited by the double mutation L799R/L800Q but not by mutation of these amino acids individually. Analysis of the respective mutant virions revealed that their different abilities to bind Phb1/Phb2 correlated with their replicative properties. Thus, mutated virions with single mutations [HIV-Env-(L799R) and HIV-Env-(L800Q)] replicated similarly to wild-type HIV, but HIV-Env-(L799R/L800Q) virions, which cannot bind Phb1/Phb2, exhibited a cell-dependent replicative phenotype similar to that of HIV-Env-Tr712, lacking the entire Env-CT domain. Thus, replicative spread was achieved, although somewhat delayed, in “permissive” MT-4 cells but failed to occur in “nonpermissive” H9 T cells. These results point to binding of the Phb1/Phb2 complex to the Env-CT as being of importance for replicative spread in nonpermissive cells, possibly by modulating critical Phb-dependent cellular process(es).
Preschool Children With Inadequate Communication: Developmental Language Disorder, Autism, Low IQ

1. Introduction to the study - R. Morris, and I. Rapin. 2. Classification of developmental language disorders - N. Hall, and D. M. Aram. 3. Classification of autistic disorders - L. Waterhouse. 4. Methodology R. Morris 5. Historical data I. Rapin. 6. Neurological examination - I. Rapin. 7. Neuropsychologic and language data - D. Fein, and M. Dunn. 8. Behavioural data - L. Waterhouse, and D. A. Allen. 9. Play - L. Wainwright, and D. Fein. 10. Classification issues - I. Rapin. 11. Overview and conclusions - D. Fein.
Leiomyoma Cells in 3-Dimensional Cultures Demonstrate an Attenuated Response to Fasudil, a Rho-Kinase Inhibitor, When Compared to 2-Dimensional Cultures

Uterine leiomyomata are common benign tumors in women of reproductive age and demonstrate an attenuated response to mechanical signaling that involves Rho and integrins. To further characterize the impairment in Rho signaling, we studied the effect of Rho-kinase inhibitor, fasudil, on extracellular matrix production, in 2-dimensional (2D) and 3-dimensional (3D) cultures of leiomyoma and myometrial cells. Leiomyoma 2D cultures demonstrated a rapid decrease in gene transcripts and protein for fibronectin, procollagen 1A, and versican. In 3D cultures, fibronectin and procollagen 1A proteins demonstrated increased levels at lower concentrations of fasudil, followed by a concentration-dependent decrease. Versican protein increased up to 3-fold, whereas fibromodulin demonstrated a significant decrease of 1.92-fold. Myometrial 2D or 3D cultures demonstrated a decrease in all proteins after 72 hours of treatment. The 3D leiomyoma cultures demonstrated a significant increase in active RhoA, followed by a concentration-dependent decrease at higher concentrations. A concentration-dependent increase in phospho-extracellular regulated signal kinase and proapoptotic protein Bax was observed in 3D leiomyoma cultures. Fasudil relaxed the contraction of the 3D collagen gels caused by myometrium and leiomyoma cell growth. These findings indicate that the altered state of Rho signaling in leiomyoma was more clearly observed in 3D cultures. The results also suggest that fasudil may have clinical applicability for treatment of uterine leiomyoma.
Proteome Differences in the First- and Third-Trimester Human Placentas

Placenta is a transient and unique pregnancy tissue that supports the fetus nutritionally and metabolically. Expression of the unique placental proteins in different stages may influence the development of the fetus as well as the pregnancy outcome. The present study aimed to compare the total placental proteome differences between the normal first- and third-trimester human placentas. In the current study, placental proteome was compared between normal first- and third-trimester placentas using 2-dimensional polyacrylamide gel electrophoresis method for separation and matrix-assisted laser desorption/ionization time-of flight mass spectrometry technique for identification of the proteins. Despite the overall similarities, comparison of the mean intensity of the protein spots between the first- and third-trimester placental proteomes revealed that 22 spots were differentially expressed (P < .05) among which 11 distinct spots were successfully identified. Of the 11 differentially expressed proteins, 4 were increased (protein disulfide isomerase, tropomyosin 4 isoform 2, enolase 1, and 78-kDa glucose-regulated protein), while the remaining 7 (actin γ1 propeptide, heat shock protein gp96, α1-antitrypsin, EF-hand domain family member D1, tubulin α1, glutathione S-transferase, and vitamin D binding protein) showed decreased expression in the placentas from the first-trimester compared to the full-term ones. In summary, the results of the present study as the first research on the comparison of the first- and third-trimester human placental proteomes introduced a group of 11 proteins with altered expression. Interestingly, some of these proteins are reported to be altered in pregnancy-related disorders.
Exosomes Packaging APOBEC3G Confer Human Immunodeficiency Virus Resistance to Recipient Cells

ABSTRACT The human cytidine deaminase APOBEC3G (A3G) is a part of a cellular defense system against human immunodeficiency virus type 1 (HIV-1) and other retroviruses. Antiretroviral activity of A3G can be severely blunted in the presence of the HIV-1 protein Vif. However, in some cells expressing the enzymatically active low-molecular-mass form of A3G, HIV-1 replication is restricted at preintegration steps, before accumulation of Vif. Here, we show that A3G can be secreted by cells in exosomes that confer resistance to both vif-defective and wild-type HIV-1 in exosome recipient cells. Our results also suggest that A3G is the major exosomal component responsible for the anti-HIV-1 activity of exosomes. However, enzymatic activity of encapsidated A3G does not correlate with the observed limited cytidine deamination in HIV-1 DNA, suggesting that A3G-laden exosomes restrict HIV-1 through a nonenzymatic mechanism. Real-time PCR quantitation demonstrated that A3G exosomes reduce accumulation of HIV-1 reverse transcription products and steady-state levels of HIV-1 Gag and Vif proteins. Our findings suggest that A3G exosomes could be developed into a novel class of anti-HIV-1 therapeutics.
Protein Kinase PKR Mediates the Apoptosis Induction and Growth Restriction Phenotypes of C Protein-Deficient Measles Virus

ABSTRACT The measles virus (MV) accessory proteins V and C play important roles in MV replication and pathogenesis. Infection with recombinant MV lacking either V or C causes more cell death than infection with the parental vaccine-equivalent virus (MVvac), and C-deficient virus grows poorly relative to the parental virus. Here, we show that a major effector of the C phenotype is the RNA-dependent protein kinase PKR. Using human HeLa cells stably deficient in PKR as a result of RNA interference-mediated knockdown (PKRkd cells), we demonstrated that a reduction in PKR partially rescued the growth defect of C knockout (Cko) virus but had no effect on the growth of either wild-type (WT) or V knockout (Vko) virus. Increased growth of the Cko virus in PKRkd cells correlated with increased viral protein expression, while defective growth and decreased protein expression in PKR-sufficient cells correlated with increased phosphorylation of PKR and the α subunit of eukaryotic initiation factor 2. Furthermore, infection with WT, Vko, or especially Cko virus caused significantly less apoptosis in PKRkd cells than in PKR-sufficient cells. Although apoptosis induced by Cko virus infection in PKR-sufficient cells was blocked by a caspase antagonist, the growth of Cko virus was not restored to the WT level by treatment with this pharmacologic inhibitor. Taken together, these results indicate that PKR plays an important antiviral role during MV infection but that the virus growth restriction by PKR is not dependent upon the induction of apoptosis. Furthermore, the results establish that a principal function of the MV C protein is to antagonize the proapoptotic and antiviral activities of PKR.
Possible Role of α1-Antitrypsin in Endometriosis-Like Grafts From a Mouse Model of Endometriosis

Previous study indicated that bleeding into the peritoneum may accelerate inflammatory response in endometriosis-like grafts in mice. To identify changes in protein levels in the grafts from mice that underwent unilateral ovariectomy (uOVX), which causes bleeding from ovarian arteries and vein, the grafts were generated by injecting a suspension of human endometrial cells in BALB/c nude female mice, and protein profile changes were compared with non-uOVX control mice. The level of α1-antitrypsin (α1-AT) decreased in grafts from nude mice that underwent uOVX. The levels of phosphorylated Akt, mammalian target of rapamycin, S6K, regulatory factors for cell survival, and of phosphorylated nuclear factor κB, an inflammatory mediator, were higher in endometriosis-like grafts from the uOVX group than from the control. The grafts were mostly comprised of stromal cells. The bioactivity of α1-AT was assessed by investigating cytokine expression in protease-activated receptor (PAR) 1/2 agonists-stimulated stromal cells. The PARs promoted the expression of interleukin 8 (IL-8), but treatment with α1-AT blocked IL-8 expression dose dependently. Knocking down α1-AT expression increased the constitutive IL-6, IL-8, and cyclooxygenase 2 expression as well as PAR1 agonist-stimulated IL-6 expression. These findings support the notion that decreased α1-AT protein in the grafts constituted with human endometrial cells in mice may have exacerbated inflammation in endometriosis-like grafts, suggesting the possible involvement of α1-AT in the pathophysiology of endometriosis.
Interaction of ICP34.5 with Beclin 1 Modulates Herpes Simplex Virus Type 1 Pathogenesis through Control of CD4+ T-Cell Responses

ABSTRACT Autophagy is an important component of host innate and adaptive immunity to viruses. It is critical for the degradation of intracellular pathogens and for promoting antigen presentation. Herpes simplex virus type 1 (HSV-1) infection induces an autophagy response, but this response is antagonized by the HSV-1 neurovirulence gene product, ICP34.5. This is due, in part, to its interaction with the essential autophagy protein Beclin 1 (Atg6) via the Beclin-binding domain (BBD) of ICP34.5. Using a recombinant virus lacking the BBD, we examined pathogenesis and immune responses using mouse models of infection. The BBD-deficient virus (Δ68H) replicated equivalently to its marker-rescued counterpart (Δ68HR) at early times but was cleared more rapidly than Δ68HR from all tissues at late times following corneal infection. In addition, the infection of the cornea with Δ68H induced less ocular disease than Δ68HR. These results suggested that Δ68H was attenuated due to its failure to control adaptive rather than innate immunity. In support of this idea, Δ68H stimulated a significantly stronger CD4+ T-cell-mediated delayed-type hypersensitivity response and resulted in significantly more production of gamma interferon and interleukin-2 from HSV-specific CD4+ T cells than Δ68HR. Taken together, these data suggest a role for the BBD of ICP34.5 in precluding autophagy-mediated class II antigen presentation, thereby enhancing the virulence and pathogenesis of HSV-1.
Fabricating Diminishable Visual Markers for Geometric Registration in Projection Mapping

We propose a visual marker embedding method for the pose estimation of a projection surface to correctly map projected images onto the surface. Assuming that the surface is fabricated by a full-color or multi-material three-dimensional (3D) printer, we propose to automatically embed visual markers on the surface with mechanical accuracy. The appearance of the marker is designed such that the marker is detected by infrared cameras even when printed on a non-planar surface while its appearance can be diminished by the projection to be as imperceptible as possible to human observers. The marker placement is optimized using a genetic algorithm to maximize the number of valid viewpoints from which the pose of the object can be estimated correctly using a stereo camera system. We also propose a radiometric compensation technique to quickly diminish the marker appearance. Experimental results confirm that the pose of projection objects are correctly estimated while the appearance of the markers was diminished to an imperceptible level. At the same time, we confirmed the limitations of the current method; only one object can be handled, and pose estimation is not performed at interactive frame rates. Finally, we demonstrate the proposed technique to show that it works successfully for various surface shapes and target textures.
Genome-Wide Analyses of Zta Binding to the Epstein-Barr Virus Genome Reveals Interactions in both Early and Late Lytic Cycles and an Epigenetic Switch Leading to an Altered Binding Profile

ABSTRACT The Epstein-Barr virus (EBV) genome sustains substantial epigenetic modification involving chromatin remodelling and DNA methylation during lytic replication. Zta (ZEBRA, BZLF1), a key regulator of the EBV lytic cycle, is a transcription and replication factor, binding to Zta response elements (ZREs) in target promoters and EBV lytic origins of replication. In vitro, Zta binding is modulated by DNA methylation; a subset of CpG-containing Zta binding sites (CpG ZREs) is bound only in a DNA methylation-dependent manner. The question of how the dynamic epigenetic environment impacts Zta interaction during the EBV lytic cycle is unknown. To address this, we used chromatin immunoprecipitation coupled with next-generation sequencing (ChIP-Seq) to identify Zta binding sites across the EBV genome before and after viral DNA replication. Replication did not alter the association of Zta across many regions of the EBV genome, but a striking reduction in Zta binding occurred at some loci that contain CpG ZREs. Separating Zta-bound DNA into methylated and nonmethylated fractions, we found that promoters that contain CpG ZREs were enriched in the methylated fraction but that Zta binding to promoters lacking CpG ZREs was not reduced. We hypothesize that the loss of DNA methylation on the EBV genome during the lytic cycle causes the reduced binding to CpG ZREs; this may act as a lytic cycle epigenetic switch. However, the epigenetic changes associated with the replicated EBV genome do not affect the interaction of Zta with many loci that are rich in non-CpG ZREs; this leads to sustained binding at these regions.
Bovine Herpesvirus 4 Modulates Its β-1,6-N-Acetylglucosaminyltransferase Activity through Alternative Splicing

ABSTRACT Carbohydrates play major roles in host-virus interactions. It is therefore not surprising that, during coevolution with their hosts, viruses have developed sophisticated mechanisms to hijack for their profit different pathways of glycan synthesis. Thus, the Bo17 gene of Bovine herpesvirus 4 (BoHV-4) encodes a homologue of the cellular core 2 protein β-1,6-N-acetylglucosaminyltransferase-mucin type (C2GnT-M), which is a key player for the synthesis of complex O-glycans. Surprisingly, we show in this study that, as opposed to what is observed for the cellular enzyme, two different mRNAs are encoded by the Bo17 gene of all available BoHV-4 strains. While the first one corresponds to the entire coding sequence of the Bo17 gene, the second results from the splicing of a 138-bp intron encoding critical residues of the enzyme. Antibodies generated against the Bo17 C terminus showed that the two forms of Bo17 are expressed in BoHV-4 infected cells, but enzymatic assays revealed that the spliced form is not active. In order to reveal the function of these two forms, we then generated recombinant strains expressing only the long or the short form of Bo17. Although we did not highlight replication differences between these strains, glycomic analyses and lectin neutralization assays confirmed that the splicing of the Bo17 gene gives the potential to BoHV-4 to fine-tune the global level of core 2 branching activity in the infected cell. Altogether, these results suggest the existence of new mechanisms to regulate the activity of glycosyltransferases from the Golgi apparatus. IMPORTANCE Viruses are masters of adaptation that hijack cellular pathways to allow their growth. Glycans play a central role in many biological processes, and several studies have highlighted mechanisms by which viruses can affect glycosylation. Glycan synthesis is a nontemplate process regulated by the availability of key glycosyltransferases. Interestingly, bovine herpesvirus 4 encodes one such enzyme which is a key enzyme for the synthesis of complex O-glycans. In this study, we show that, in contrast to cellular homologues, this virus has evolved to alternatively express two proteins from this gene. While the first one is enzymatically active, the second results from the alternative splicing of the region encoding the catalytic site of the enzyme. We postulate that this regulatory mechanism could allow the virus to modulate the synthesis of some particular glycans for function at the location and/or the moment of infection.