Hopf quasigroups and the algebraic 7-sphere

We introduce the notions of Hopf quasigroup and Hopf coquasigroup $H$ generalising the classical notion of an inverse property quasigroup $G$ expressed respectively as a quasigroup algebra $k G$ and an algebraic quasigroup $k[G]$. We prove basic results as for Hopf algebras, such as anti(co)multiplicativity of the antipode $S:H\to H$, that S^2=\id if $H$ is commutative or cocommutative, and a theory of crossed (co)products. We also introduce the notion of a Moufang Hopf (co)quasigroup and show that the coordinate algebras $k[S^{2^n-1}]$ of the parallelizable spheres are algebraic quasigroups (commutative Hopf coquasigroups in our formulation) and Moufang. We make use of the description of composition algebras such as the octonions via a cochain $F$ introduced in \cite{Ma99}. We construct an example $k[S^7]\rtimes\Z_2^3$ of a Hopf coquasigroup which is noncommutative and non-trivially Moufang. We use Hopf coquasigroup methods to study differential geometry on $k[S^7]$ including a short algebraic proof that $S^7$ is parallelizable. Looking at combinations of left and right invariant vector fields on $k[S^7]$ we provide a new description of the structure constants of the Lie algebra $g_2$ in terms of the structure constants $F$ of the octonions. In the concluding section we give a new description of the $q$-deformation quantum group \C_q[S^3] regarded trivially as a Moufang Hopf coquasigroup (trivially since it is in fact a Hopf algebra) but now in terms of $F$ built up via the Cayley-Dickson process.Comment: 43 pages latex; added Maurer-Cartan equation (Prop 6.5) and computation of it for S^7 (lemma 6.8). No other change aside typo

A review of potential contaminants in Australian livestock feeds and proposed guidance levels for feed

Contaminants of man-made and natural origin need to be managed in livestock feeds to protect the health of livestock and that of human consumers of livestock products. This requires access to information on the transfer from feed to food to inform risk profiles and assessments, and to guide management interventions such as regulation or Hazard Analysis Critical Control Point approaches. This paper reviews contaminants of known and potential concern in the production of livestock feeds in Australia and compares existing but differing state and national regulatory standards with international standards. The contaminants considered include man-made organic chemical contaminants (e.g. legacy pesticides), elemental contaminants (e.g. arsenic, cadmium, lead), phytotoxins (e.g. gossypol) and mycotoxins (e.g. aflatoxins). Reference is made to scientific literature and evaluations by regulators to propose maximum levels that can be used for guidance by those involved in managing contamination incidents or developing feed safety programs. © 2013 CSIRO

Fibrinolytic-deficiencies predispose hosts to septicemia from a catheter-associated UTI

Catheter-associated urinary tract infections (CAUTIs) are amongst the most common nosocomial infections worldwide and are difficult to treat partly due to development of multidrug-resistance from CAUTI-related pathogens. Importantly, CAUTI often leads to secondary bloodstream infections and death. A major challenge is to predict when patients will develop CAUTIs and which populations are at-risk for bloodstream infections. Catheter-induced inflammation promotes fibrinogen (Fg) and fibrin accumulation in the bladder which are exploited as a biofilm formation platform by CAUTI pathogens. Using our established mouse model of CAUTI, here we identified that host populations exhibiting either genetic or acquired fibrinolytic-deficiencies, inducing fibrin deposition in the catheterized bladder, are predisposed to severe CAUTI and septicemia by diverse uropathogens in mono- and poly-microbial infections. Furthermore, here we found that Enterococcus faecalis, a prevalent CAUTI pathogen, uses the secreted protease, SprE, to induce fibrin accumulation and create a niche ideal for growth, biofilm formation, and persistence during CAUTI

Quantifying human-animal contact rates in Malaysian Borneo: Influence of agricultural landscapes on contact with potential zoonotic disease reservoirs

Changing landscapes across the globe, but particularly in Southeast Asia, are pushing humans and animals closer together and may increase the likelihood of zoonotic spillover events. Malaysian Borneo is hypothesized to be at high risk of spillover events due to proximity between reservoir species and humans caused by recent deforestation in the region. However, the relationship between landscape and human-animal contact rates has yet to be quantified. An environmentally stratified cross-sectional survey was conducted in Sabah, Malaysia in 2015, collecting geolocated questionnaire data on potential risk factors for contact with animals for 10,100 individuals. 51% of individuals reported contact with poultry, 46% with NHPs, 30% with bats, and 2% with swine. Generalised linear mixed models identified occupational and demographic factors associated with increased contact with these species, which varied when comparing wildlife to domesticated animals. Reported contact rates with each animal group were integrated with remote sensing-derived environmental data within a Bayesian framework to identify regions with high probabilities of contact with animal reservoirs. We have identified high spatial heterogeneity of contact with animals and clear associations between agricultural practices and high animal rates. This approach will help inform public health campaigns in at-risk populations and can improve pathogen surveillance efforts on Malaysian Borneo. This method can additionally serve as a framework for researchers looking to identify targets for future pathogen detection in a chosen region of study

Quantifying human-animal contact rates in Malaysian Borneo: influence of agricultural landscapes on contact with potential zoonotic disease reservoirs

Changing landscapes across the globe, but particularly in Southeast Asia, are pushing humans and animals closer together and may increase the likelihood of zoonotic spillover events. Malaysian Borneo is hypothesized to be at high risk of spillover events due to proximity between reservoir species and humans caused by recent deforestation in the region. However, the relationship between landscape and human-animal contact rates has yet to be quantified. An environmentally stratified cross-sectional survey was conducted in Sabah, Malaysia in 2015, collecting geolocated questionnaire data on potential risk factors for contact with animals for 10,100 individuals. 51% of individuals reported contact with poultry, 46% with NHPs, 30% with bats, and 2% with swine. Generalised linear mixed models identified occupational and demographic factors associated with increased contact with these species, which varied when comparing wildlife to domesticated animals. Reported contact rates with each animal group were integrated with remote sensing-derived environmental data within a Bayesian framework to identify regions with high probabilities of contact with animal reservoirs. We have identified high spatial heterogeneity of contact with animals and clear associations between agricultural practices and high animal rates. This approach will help inform public health campaigns in at-risk populations and can improve pathogen surveillance efforts on Malaysian Borneo. This method can additionally serve as a framework for researchers looking to identify targets for future pathogen detection in a chosen region of study

Loss of mouse Stmn2 function causes motor neuropathy

Amyotrophic lateral sclerosis (ALS) is characterized by motor neuron degeneration accompanied by aberrant accumulation and loss of function of the RNA-binding protein TDP43. Thus far, it remains unresolved to what extent TDP43 loss of function directly contributes to motor system dysfunction. Here, we employed gene editing to find whether the mouse ortholog of the TDP43-regulated gene STMN2 has an important function in maintaining the motor system. Both mosaic founders and homozygous loss-of-function Stmn2 mice exhibited neuromuscular junction denervation and fragmentation, resulting in muscle atrophy and impaired motor behavior, accompanied by an imbalance in neuronal microtubule dynamics in the spinal cord. The introduction of human STMN2 through BAC transgenesis was sufficient to rescue the motor phenotypes observed in Stmn2 mutant mice. Collectively, our results demonstrate that disrupting the ortholog of a single TDP43-regulated RNA is sufficient to cause substantial motor dysfunction, indicating that disruption of TDP43 function is likely a contributor to ALS