Object Manipulation in Virtual Reality Under Increasing Levels of Translational Gain

Room-scale Virtual Reality (VR) has become an affordable consumer reality, with applications ranging from entertainment to productivity. However, the limited physical space available for room-scale VR in the typical home or office environment poses a significant problem. To solve this, physical spaces can be extended by amplifying the mapping of physical to virtual movement (translational gain). Although amplified movement has been used since the earliest days of VR, little is known about how it influences reach-based interactions with virtual objects, now a standard feature of consumer VR. Consequently, this paper explores the picking and placing of virtual objects in VR for the first time, with translational gains of between 1x (a one-to-one mapping of a 3.5m*3.5m virtual space to the same sized physical space) and 3x (10.5m*10.5m virtual mapped to 3.5m*3.5m physical). Results show that reaching accuracy is maintained for up to 2x gain, however going beyond this diminishes accuracy and increases simulator sickness and perceived workload. We suggest gain levels of 1.5x to 1.75x can be utilized without compromising the usability of a VR task, significantly expanding the bounds of interactive room-scale VR

Comparative Chromosome Maps of Neotropical Rodents Necromys lasiurus and Thaptomys nigrita (Cricetidae) Established by ZOO-FISH

This work presents chromosome homology maps between Mus musculus (MMU) and 2 South American rodent species from the Cricetidae group: Necromys lasiurus (NLA, 2n = 34) and Thaptomys nigrita (TNI, 2n = 52), established by ZOO-FISH using mouse chromosome-specific painting probes. Extending previous molecular cytogenetic studies in Neotropical rodents, the purpose of this work was to delineate evolutionary chromosomal rearrangements in Cricetidae rodents and to reconstruct the phylogenetic relationships among the Akodontini species. Our phylogenetic reconstruction by maximum parsimony analysis of chromosomal characters confirmed one consistent clade of all Neotropical rodents studied so far. In both species analyzed here, we observed the syntenic association of chromosome segments homologous to MMU 8/13, suggesting that this chromosome form is a synapomorphic trait exclusive to Neotropical rodents. Further, the previously described Akodontini-specific syntenic associations MMU 3/18 and MMU 6/12 were observed in N. lasiurus but not in T. nigrita, although the latter species is considered a member of the Akodontini tribe by some authors. Finally, and in agreement with this finding, N. lasiurus and Akodon serrensis share the derived fission of MMU 13, which places them as basal sister clades within Akodontini. Copyright (C) 2011 S. Karger AG, Base

Determination of the absolute configuration of bioactive indole-containing pyrazino[2,1-b]quinazoline-3,6-diones and study of their in vitro metabolic profile

In recent decades, fungi-derived naturally occurring quinazolines have emerged as potential drug candidates. Nevertheless, most studies are conducted for bioactivity assays, and little is known about their absorption, distribution, metabolism, and elimination (ADME) properties. To perform metabolic studies, the synthesis of the naturally occurring quinazolinone, fiscalin B (1), and its chloro derivative, 4-((1H-indol-3-yl)methyl)-8,10-dichloro-1-isobutyl-1,2-dihydro-6H-pyra-zino[2,1-b]quinazoline-3,6(4H)-dione (2), disclosed as an antibacterial agent, was performed in a gram scale using a microwave-assisted polycondensation reaction with 22% and 17% yields, respec-tively. The structure of the non-natural (+)-fiscalin B was established, for the first time, by X-ray crystallography as (1R,4S)-1, and the absolute configuration of the naturally occurring fiscalin B (- )-1 was confirmed by comparison of its calculated and experimental electronic circular dichroism (ECD) spectra as (1S,4R)-1. In vitro metabolic studies were monitored for this class of natural products for the first time by ultra-high-performance liquid chromatography (UHPLC) coupled with high-resolution mass spectrometry (HRMS). The metabolic characteristics of 1 and 2 in human liver microsomes indicated hydration and hydroxylation mass changes introduced to the parent drugs.This research was supported by national funds provided by FCT—Foundation for Science and Technology and European Regional Development Fund (ERDF) and COMPETE under the Strategic Funding of CIIMAR UIDB/04423/2020 (Group of Natural Products and Medicinal Chemistry-CIIMAR) and LAQV-REQUIMTE (UIDB/50006/2020) and the project PTDC/SAU-PUB/28736/2017 (Reference: POCI-01–0145-FEDER-028736), as well as CHIRALBIOACTIVE-PI-3RL-IINFACTS-2019. This work is also a result of the project ATLANTIDA (Reference: NORTE-01-0145-FEDER-000040), supported by the Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement and through the European Regional Development Fund (ERDF). Additionally, this research was supported by the Agency for the Improvement of Higher Education Personnel (CAPES) (Finance Code 001), National Council for Scientific and Technological Development (CNPq) (Grant Number 406064/2018-05), São Paulo Research Foundation (FAPESP) (Grant Number: 2020/05965-8 and Ph.D. scholarships 2018/03035-3 and 2019/15040-4)

Placenta-specific Slc38a2/SNAT2 knockdown causes fetal growth restriction in mice

Fetal growth restriction (FGR) is a complication of pregnancy that reduces birth weight, markedly increases infant mortality and morbidity and is associated with later-life cardiometabolic disease. No specific treatment is available for FGR. Placentas of human FGR infants have low abundance of sodium-coupled neutral amino acid transporter 2 (Slc38a2/SNAT2), which supplies the fetus with amino acids required for growth. We determined the mechanistic role of placental Slc38a2/SNAT2 deficiency in the development of restricted fetal growth, hypothesizing that placenta-specific Slc38a2 knockdown causes FGR in mice. Using lentiviral transduction of blastocysts with a small hairpin RNA (shRNA), we achieved 59% knockdown of placental Slc38a2, without altering fetal Slc38a2 expression. Placenta-specific Slc38a2 knockdown reduced near-term fetal and placental weight, fetal viability, trophoblast plasma membrane (TPM) SNAT2 protein abundance, and both absolute and weight-specific placental uptake of the amino acid transport System A tracer, 14C-methylaminoisobutyric acid (MeAIB). We also measured human placental SLC38A2 gene expression in a well-defined term clinical cohort and found that SLC38A2 expression was decreased in late-onset, but not early-onset FGR, compared with appropriate for gestational age (AGA) control placentas. The results demonstrate that low placental Slc38a2/SNAT2 causes FGR and could be a target for clinical therapies for late-onset FGR