A collaborative VR Murder Mystery using Photorealistic User Representations

The VRTogether project has developed a Social VR platform for remote communication and collaboration. The hyper-realistic representation of users, as volumetric video, allows for natural interaction in a virtual environment with others. This video shows one of the use cases, an escape room style, where remote users need to collaboratively resolve a murder mystery. The experience takes place in the victim’s apartment where the police team (avatars) together with up to four real-time captured users (point clouds), work as a team to find clues and come up with a conclusion about what happened to the victim and who was the criminal. This experience includes a layer of interaction, enabling the users to interact with the environment, by touching objects, and to talk to the characters. It also allows for navigating between the rooms of the apartment. The experience provides immersion and social connectedness, where users are protagonists of the story, sharing the virtual environment and following the narrative. The combination of virtual reality environments (space and characters) with novel technologies for real-time volumetric video conferencing enables unique new experiences in a number of areas such as healthcare, broadcasting, and gaming. The video can be watched here: https://youtu.be/Hsj1YWo55k

BMI1 represses Ink4a/Arf and Hox genes to regulate stem cells in the rodent incisor

The polycomb group gene Bmi1 is required for maintenance of adult stem cells in many organs. Inactivation of Bmi1 leads to impaired stem cell self-renewal due to deregulated gene expression. One critical target of BMI1 is Ink4a/Arf, which encodes the cell-cycle inhibitors p16(Ink4a) and p19(Arf). However, deletion of Ink4a/Arf only partially rescues Bmi1-null phenotypes, indicating that other important targets of BMI1 exist. Here, using the continuously growing mouse incisor as a model system, we report that Bmi1 is expressed by incisor stem cells and that deletion of Bmi1 resulted in fewer stem cells, perturbed gene expression and defective enamel production. Transcriptional profiling revealed that Hox expression is normally repressed by BMI1 in the adult, and functional assays demonstrated that BMI1-mediated repression of Hox genes preserves the undifferentiated state of stem cells. As Hox gene upregulation has also been reported in other systems when Bmi1 is inactivated, our findings point to a general mechanism whereby BMI1-mediated repression of Hox genes is required for the maintenance of adult stem cells and for prevention of inappropriate differentiation

Defective CFTR induces aggresome formation and lung inflammation in cystic fibrosis through ROS-mediated autophagy inhibition

Accumulation of unwanted/misfolded proteins in aggregates has been observed in airways of patients with cystic fibrosis (CF), a life-threatening genetic disorder caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). Here we show how the defective CFTR results in defective autophagy and decreases the clearance of aggresomes. Defective CFTR-induced upregulation of reactive oxygen species (ROS) and tissue transglutaminase (TG2) drive the crosslinking of beclin 1, leading to sequestration of phosphatidylinositol-3-kinase (PI(3)K) complex III and accumulation of p62, which regulates aggresome formation. Both CFTR knockdown and the overexpression of green fluorescent protein (GFP)-tagged-CFTRF508del induce beclin 1 downregulation and defective autophagy in non-CF airway epithelia through the ROS–TG2 pathway. Restoration of beclin 1 and autophagy by either beclin 1 overexpression, cystamine or antioxidants rescues the localization of the beclin 1 interactome to the endoplasmic reticulum and reverts the CF airway phenotype in vitro, in vivo in Scnn1b-transgenic and CftrF508del homozygous mice, and in human CF nasal biopsies. Restoring beclin 1 or knocking down p62 rescued the trafficking of CFTRF508del to the cell surface. These data link the CFTR defect to autophagy deficiency, leading to the accumulation of protein aggregates and to lung inflammation.<br/

Role of Entropy and Autosolvation in Dimerization and Complexation of C 60

The supramolecular chemistry of bowl-shaped heptazinc metallocavitands templated by Schiff base macrocycles has been investigated. Dimerization thermodynamics were probed by 1H NMR spectroscopy in benzene-d6, toluene-d8, and p-xylene-d10 and revealed the process to be entropy-driven and enthalpy-opposed in each solvent. Trends in the experimentally determined enthalpy and entropy values are related to the thermodynamics of solvent autosolvation, solvent molecules being released from the monomeric metallocavitand cavity into the bulk solvent upon dimerization. The relationship established between experimentally measured dimerization thermodynamics and autosolvation data successfully predicts the absence of dimerization in CH2Cl2 and CHCl3 and was used to estimate the number of solvent molecules interacting with the monomeric metallocavitand in solution. Host–guest interactions between heptazinc metallocavitands and fullerene C60 have also been investigated. Interestingly, metallocavitand-C60 interactions are only observed in solvents that facilitate entropy-driven dimerization suggesting entropy and solvent autosolvation may be important in explaining concave-convex interactions