Urinary felinine excretion in intact male cats is increased by dietary cystine

Felinine is a branched-chain sulfur amino acid present in the urine of certain Felidae, including domestic cats. The objective of the present study was to determine if additional cystine and/or dietary N would increase felinine and N-acetylfelinine excretion by intact male cats fed a low-protein (LP) diet. Feeding five adult intact male cats an LP diet (18·8% of metabolisable energy (ME) as protein) v. a high-protein diet (38·6% of ME as protein) resulted in a trend (P¼0·08) for decreased urinary felinine and no change in N-acetylfelinine excretion. In a 23 d study, when the LP diet was supplemented with L-cystine at 9·3 g/kg DM, urinary felinine:creatinine ratio showed a linear two-fold (121 %) increase (P,0·01) from 0·24 (SEM 0·05) to 0·53 (SEM 0·13) after 10 d. Subsequent feeding of the LP diet resulted in a decrease in felinine excretion to base levels. Plasma gglutamylfelinylglycine concentrations were consistent with the excretion of felinine. Supplementation of the LP diet with L-cystine (9·3 g/kg DM), dispensable amino acids and arginine to a second group (n 5) also resulted in a significant (P,0·01) but smaller (þ72 %) increase in the daily felinine:creatinine ratio (0·25 (SEM 0·04) to 0·43 (SEM 0·05)). The degree of felinine N-acetylation within groups was unaffected by dietary addition and withdrawal of amino acids. The results indicate that felinine synthesis is regulated by cystine availability, and that arginine may be physiologically important in decreasing felinine biosynthesis in intact male cats

A paradigm-shift in water treatment: in-reservoir UV-LED-driven TiO2 photocatalysis for the removal of cyanobacteria: a mesocosm study.

Potentially harmful cyanobacteria challenge potable water treatment globally, with high biomass events, and dissolved toxic and nuisance metabolites. Retrofitting existing water treatment infrastructure is often impractical (if not impossible) and often prohibitively expensive. In a paradigm-shifting move, we propose in-reservoir pre-treatment of cyanobacteria-contaminated raw waters to ease the burden on existing water treatment infrastructure. In an iterative design approach over three years, treatment modules have been designed, refined and optimised, in bench and pilot-scale studies for in-reservoir deployment. TiO2-coated beads made from recycled glass are employed in conjunction with UV-light emitting diodes (LEDs), to create highly reactive hydroxyl radicals that preferably remove cyanobacteria and subsequently released cyanotoxins from raw water. In a mesocosm study using a drinking water reservoir in Brazil, water quality parameters were markedly improved within 72h of deployment and cyanobacterial presence was decreased by over 90% without affecting other phytoplankton communities. The treatment system is virtually plastic-free, low cost, utilises recycled materials and could ultimately be powered by renewable energies, thus providing a true green treatment option. We have conclusively demonstrated that a paradigm-shift towards in-reservoir treatment is not only possible but feasible and can provide a valuable addition to conventional water treatment methods

Percolation model for structural phase transitions in Li1−x_{1-x}Hx_xIO3_3 mixed crystals

A percolation model is proposed to explain the structural phase transitions found in Li$_{1-x}$H$_x$IO$_3$ mixed crystals as a function of the concentration parameter $x$. The percolation thresholds are obtained from Monte Carlo simulations on the specific lattices occupied by lithium atoms and hydrogen bonds. The theoretical results strongly suggest that percolating lithium vacancies and hydrogen bonds are indeed responsible for the solid solution observed in the experimental range $0.22 < x < 0.36$.Comment: 4 pages, 2 figure

Suppressing cyanobacterial dominance by UV-LED TiO2-photocatalysis in a drinking water reservoir: a mesocosm study.

Cyanobacteria and their toxic secondary metabolites present challenges for water treatment globally. In this study we have assessed TiO2 immobilized onto recycled foamed glass beads by a facile calcination method, combined in treatment units with 365 nm UV-LEDs. The treatment system was deployed in mesocosms within a eutrophic Brazilian drinking water reservoir. The treatment units were deployed for 7 days and suppressed cyanobacterial abundance by 85%, while at the same time enhancing other water quality parameters; turbidity and transparency improved by 40 and 81% respectively. Genomic analysis of the microbiota in the treated mesocosms revealed that the composition of the cyanobacterial community was affected and the abundance of Bacteroidetes and Proteobacteria increased during cyanobacterial suppression. The effect of the treatment on zooplankton and other eukaryotes was also monitored. The abundance of zooplankton decreased while Chrysophyte and Alveolata loadings increased. The results of this proof-of-concept study demonstrate the potential for full-scale, in-reservoir application of advanced oxidation processes as complementary water treatment processes

Lung disease phenotypes caused by overexpression of combinations of α-, β-, and γ-subunits of the epithelial sodium channel in mouse airways

The epithelial Na+ channel (ENaC) regulates airway surface hydration. In mouse airways, ENaC is composed of three subunits, α, β, and γ, which are differentially expressed (α &gt; β &gt; γ). Airway-targeted overexpression of the β subunit results in Na+ hyperabsorption, causing airway surface dehydration, hyperconcentrated mucus with delayed clearance, lung inflammation, and perinatal mortality. Notably, mice overexpressing the α- or γ-subunit do not exhibit airway Na+ hyperabsorption or lung pathology. To test whether overexpression of multiple ENaC subunits produced Na+ transport and disease severity exceeding that of βENaC-Tg mice, we generated double (αβ, αγ, βγ) and triple (αβγ) transgenic mice and characterized their lung phenotypes. Double αγENaC-Tg mice were indistinguishable from WT littermates. In contrast, double βγENaC-Tg mice exhibited airway Na+ absorption greater than that of βENaC-Tg mice, which was paralleled by worse survival, decreased mucociliary clearance, and more severe lung pathology. Double αβENaC-Tg mice exhibited Na+ transport rates comparable to those of βENaC-Tg littermates. However, αβENaC-Tg mice had poorer survival and developed severe parenchymal consolidation. In situ hybridization (RNAscope) analysis revealed both alveolar and airway αENaC-Tg overexpression. Triple αβγENaC-Tg mice were born in Mendelian proportions but died within the first day of life, and the small sample size prevented analyses of cause(s) of death. Cumulatively, these results indicate that overexpression of βENaC is rate limiting for generation of pathological airway surface dehydration. Notably, airway co-overexpression of β- and γENaC had additive effects on Na+ transport and disease severity, suggesting dose dependency of these two variables

Azimuthal asymmetries in lepton-pair production at a fixed-target experiment using the LHC beams (AFTER)

A multi-purpose fixed-target experiment using the proton and lead-ion beams of the LHC was recently proposed by Brodsky, Fleuret, Hadjidakis and Lansberg, and here we concentrate our study on some issues related to the spin physics part of this project (referred to as AFTER). We study the nucleon spin structure through $pp$ and $pd$ processes with a fixed-target experiment using the LHC proton beams, for the kinematical region with 7 TeV proton beams at the energy in center-of-mass frame of two nucleons $\sqrt{s}=115$ GeV. We calculate and estimate the $\cos2\phi$ azimuthal asymmetries of unpolarized $pp$ and $pd$ dilepton production processes in the Drell--Yan continuum region and at the $Z$-pole. We also calculate the $\sin(2\phi-\phi_S)$, $\sin(2\phi+\phi_S)$ and $\sin2\phi$ azimuthal asymmetries of $pp$ and $pd$ dilepton production processes with the target proton and deuteron longitudinally or transversally polarized in the Drell--Yan continuum region and around $Z$ resonances region. We conclude that it is feasible to measure these azimuthal asymmetries, consequently the three-dimensional or transverse momentum dependent parton distribution functions (3dPDFs or TMDs), at this new AFTER facility.Comment: 15 pages, 40 figures. Version accepted for publication in EPJ

Radiotherapy exposure directly damages the uterus and causes pregnancy loss

Female cancer survivors are significantly more likely to experience infertility than the general population. It is well established that chemotherapy and radiotherapy can damage the ovary and compromise fertility, yet the ability of cancer treatments to induce uterine damage, and the underlying mechanisms, have been understudied. Here, we show that in mice total-body γ-irradiation (TBI) induced extensive DNA damage and apoptosis in uterine cells. We then transferred healthy donor embryos into ovariectomized adolescent female mice that were previously exposed to TBI to study the impacts of radiotherapy on the uterus independent from effects to ovarian endocrine function. Following TBI, embryo attachment and implantation were unaffected, but fetal resorption was evident at midgestation in 100% of dams, suggesting failed placental development. Consistent with this hypothesis, TBI impaired the decidual response in mice and primary human endometrial stromal cells. TBI also caused uterine artery endothelial dysfunction, likely preventing adequate blood vessel remodeling in early pregnancy. Notably, when pro-apoptotic protein Puma-deficient (Puma–/–) mice were exposed to TBI, apoptosis within the uterus was prevented, and decidualization, vascular function, and pregnancy were restored, identifying PUMA-mediated apoptosis as a key mechanism. Collectively, these data show that TBI damages the uterus and compromises pregnancy success, suggesting that optimal fertility preservation during radiotherapy may require protection of both the ovaries and uterus. In this regard, inhibition of PUMA may represent a potential fertility preservation strategy.Meaghan J. Griffiths, Sarah A. Marshall, Fiona L. Cousins, Lauren R. Alesi, Jordan Higgins, Saranya Giridharan, Urooza C. Sarma, Ellen Menkhorst, Wei Zhou, Alison S. Care, Jacqueline F. Donoghue, Sarah J. Holdsworth-Carson, Peter A.W. Rogers, Evdokia Dimitriadis, Caroline E. Gargett, Sarah A. Robertson, Amy L. Winship, and Karla J. Hut

Animal models for COVID-19

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the aetiological agent of coronavirus disease 2019 (COVID-19), an emerging respiratory infection caused by the introduction of a novel coronavirus into humans late in 2019 (first detected in Hubei province, China). As of 18 September 2020, SARS-CoV-2 has spread to 215 countries, has infected more than 30 million people and has caused more than 950,000 deaths. As humans do not have pre-existing immunity to SARS-CoV-2, there is an urgent need to develop therapeutic agents and vaccines to mitigate the current pandemic and to prevent the re-emergence of COVID-19. In February 2020, the World Health Organization (WHO) assembled an international panel to develop animal models for COVID-19 to accelerate the testing of vaccines and therapeutic agents. Here we summarize the findings to date and provides relevant information for preclinical testing of vaccine candidates and therapeutic agents for COVID-19