Vision Transformer Based Model for Describing a Set of Images as a Story

Visual Story-Telling is the process of forming a multi-sentence story from a set of images. Appropriately including visual variation and contextual information captured inside the input images is one of the most challenging aspects of visual storytelling. Consequently, stories developed from a set of images often lack cohesiveness, relevance, and semantic relationship. In this paper, we propose a novel Vision Transformer Based Model for describing a set of images as a story. The proposed method extracts the distinct features of the input images using a Vision Transformer (ViT). Firstly, input images are divided into 16X16 patches and bundled into a linear projection of flattened patches. The transformation from a single image to multiple image patches captures the visual variety of the input visual patterns. These features are used as input to a Bidirectional-LSTM which is part of the sequence encoder. This captures the past and future image context of all image patches. Then, an attention mechanism is implemented and used to increase the discriminatory capacity of the data fed into the language model, i.e. a Mogrifier-LSTM. The performance of our proposed model is evaluated using the Visual Story-Telling dataset (VIST), and the results show that our model outperforms the current state of the art models.Comment: This paper has been accepted at the 35th Australasian Joint Conference on Artificial Intelligence 2022 (Camera-ready version is attached

Complexity Matching: Restoring the Complexity of Locomotion in Older People Through Arm-in-Arm Walking

The complexity matching effect refers to a maximization of information exchange, when interacting systems share similar complexities. Additionally, interacting systems tend to attune their complexities in order to enhance their coordination. This effect has been observed in a number of synchronization experiments, and interpreted as a transfer of multifractality between systems. Finally, it has been shown that when two systems of different complexity levels interact, this transfer of multifractality operates from the most complex system to the less complex, yielding an increase of complexity in the latter. This theoretical framework inspired the present experiment that tested the possible restoration of complexity in older people. In young and healthy participants, walking is known to present 1/f fluctuations, reflecting the complexity of the locomotion system, providing walkers with both stability and adaptability. In contrast walking tends to present a more disordered dynamics in older people, and this whitening was shown to correlate with fall propensity. We hypothesized that if an aged participant walked in close synchrony with a young companion, the complexity matching effect should result in the restoration of complexity in the former. Older participants were involved in a prolonged training program of synchronized walking, with a young experimenter. Synchronization within the dyads was dominated by complexity matching. We observed a restoration of complexity in participants after 3 weeks, and this effect was persistent 2 weeks after the end of the training session. This work presents the first demonstration of a restoration of complexity in deficient systems

Potential Use of C

The photosensitizing ability of C60/2-hydroxypropyl-β-cyclodextrin (HP-β-CyD) nanoparticles under visible light irradiation was studied by electron spin resonance (ESR) and phototoxicity on cancer cells. In addition, the photoinduced antitumor effect to the tumor-bearing mice was evaluated. C60 nanoparticles were prepared by grinding a mixture of HP-β-CyD. The resulting C60/HP-β-CyD nanoparticles were highly-sensitive to visible light and generated higher levels of 1O2 than protoporphyrin IX (PpIX). C60/HP-β-CyD reduced the viability of cancer cells (HeLa cells and A549 cells) in response to irradiation by visible light in a dose-dependent manner. The IC50 values of the C60/HP-β-CyD nanoparticles was 10 μM for HeLa cells and 60 μM for A549 cells at an irradiation level of 35 mW/cm2. The photodynamic effect of C60/HP-β-CyD nanoparticles on the in vivo growth of mouse sarcoma S-180 cells was evaluated after intratumor injection. The outcome of PDT by C60/HP-β-CyD was directly dependent on the dose of irradiated light. Treatment with C60/HP-β-CyD nanoparticles at a C60 dose of 2.0 mg/kg under visible light irradiation at 350 mW/cm2 (63 J/cm2) markedly suppressed tumor growth, whereas that at 30 J/cm2 was less effective. These findings suggest that C60/HP-β-CyD nanoparticles represent a promising candidate for use in cancer treatment by PDT

Spin Foams and Noncommutative Geometry

We extend the formalism of embedded spin networks and spin foams to include topological data that encode the underlying three-manifold or four-manifold as a branched cover. These data are expressed as monodromies, in a way similar to the encoding of the gravitational field via holonomies. We then describe convolution algebras of spin networks and spin foams, based on the different ways in which the same topology can be realized as a branched covering via covering moves, and on possible composition operations on spin foams. We illustrate the case of the groupoid algebra of the equivalence relation determined by covering moves and a 2-semigroupoid algebra arising from a 2-category of spin foams with composition operations corresponding to a fibered product of the branched coverings and the gluing of cobordisms. The spin foam amplitudes then give rise to dynamical flows on these algebras, and the existence of low temperature equilibrium states of Gibbs form is related to questions on the existence of topological invariants of embedded graphs and embedded two-complexes with given properties. We end by sketching a possible approach to combining the spin network and spin foam formalism with matter within the framework of spectral triples in noncommutative geometry.Comment: 48 pages LaTeX, 30 PDF figure

Mutations in KPTN Cause Macrocephaly, Neurodevelopmental Delay, and Seizures

The proper development of neuronal circuits during neuromorphogenesis and neuronal-network formation is critically dependent on a coordinated and intricate series of molecular and cellular cues and responses. Although the cortical actin cytoskeleton is known to play a key role in neuromorphogenesis, relatively little is known about the specific molecules important for this process. Using linkage analysis and whole-exome sequencing on samples from families from the Amish community of Ohio, we have demonstrated that mutations in KPTN, encoding kaptin, cause a syndrome typified by macrocephaly, neurodevelopmental delay, and seizures. Our immunofluorescence analyses in primary neuronal cell cultures showed that endogenous and GFP-tagged kaptin associates with dynamic actin cytoskeletal structures and that this association is lost upon introduction of the identified mutations. Taken together, our studies have identified kaptin alterations responsible for macrocephaly and neurodevelopmental delay and define kaptin as a molecule crucial for normal human neuromorphogenesis

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care(1) or hospitalization(2-4) after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease. © 2022, The Author(s)

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

The Effect of Some Carbonated Beverages on Enamel of Human Premolars (Scanning and Light Microscopic Study)

In modern societies, the increased consumption of soft drinks is becoming more important because of the concern for dental erosion. The aim of the present study is to reveal and compare the possible effect of some carbonated beverages on occlusal and cervical parts of enamel in the buccal surface of human premolars. Twenty sound (caries- free) human maxillary premolars extracted for orthodontic reasons were used in the present study. The teeth were then divided into: Control group: (before immersion in the beverages), in which the collected teeth were immersed at first in tap water and subdivided into 4 subgroups (5 teeth each) and named; Control Sprite, Control Mirinda Orange, Control Coca- Cola and subgroup R. Experimental group: (after immersion in the beverages) in which the first 3 subgroups which were used as control were then utilized as experimental after immersion in the corresponding beverage. They were named; Subgroup S (Sprite experimental Subgroup), Subgroup M (Mirinda Orange experimental Subgroup) and Subgroup C (Coca-Cola experimental Subgroup). The teeth were examined using SEM and light microscope. Morphometric study was performed, using computerized image analyzer for the assessment of affected band thickness. The SEM results of the experimental subgroups revealed that each beverage cause different pattern of erosion. In Subgroup S, the enamel surface was feather like and pitted. In Subgroup M, the enamel surface presented the honeycomb pattern. In Subgroup C, the enamel surface was nearly smooth with generalized structural loss. It was noticed also that the changes in enamel surface became more accentuated toward the cervical third. The light microscopic examination revealed that in both Subgroups S and C the outer enamel layer exhibited dark band of affection, while in Subgroup M this band was translucent. The affection of subsurface and deep enamel layers was noticed in all the experimental subgroups, in addition the changes in enamel became more accentuated toward the cervical third. The morphometric data revealed that the thickness of the affected band in the outer layer of enamel increased toward the cervical third in all experimental subgroups. This band was minimal in Subgroup S, and increased in Subgroup M, followed by Subgroup C. From the present study we can conclude that acidic beverages had deleterious effect on dental hard tissues. Among the investigated drinks of the present work, the Sprite had the least erosive potential, followed by Mirinda Orange, then Coca-Cola which had the most erosive potential. The erosive potential of a beverage was depended on its pH value, titratable acidity, type and concentration of the acid(s) present. Enamel affection for a given beverage was maximum at the cervical third and minimal in the occlusal