Deep Neural Network for Slip Detection on Ice Surface.

Slip-induced falls are among the most common causes of major occupational injuries and economic loss in Canada. Identifying the risk factors associated with slip events is key to developing preventive solutions to reduce falls. One factor is the slip-resistance quality of footwear, which is fundamental to reducing the number of falls. Measuring footwear slip resistance with the recently developed Maximum Achievable Angle (MAA) test requires a trained researcher to identify slip events in a simulated winter environment. The human capacity for information processing is limited and human error is natural, especially in a cold environment. Therefore, to remove conflicts associated with human errors, in this paper a deep three-dimensional convolutional neural network is proposed to detect the slips in real-time. The model has been trained by a new dataset that includes data from 18 different participants with various clothing, footwear, walking directions, inclined angles, and surface types. The model was evaluated on three types of slips: Maxi-slip, midi-slip, and mini-slip. This classification is based on the slip perception and recovery of the participants. The model was evaluated based on both 5-fold and Leave-One-Subject-Out (LOSO) cross validation. The best accuracy of 97% was achieved when identifying the maxi-slips. The minimum accuracy of 77% was achieved when classifying the no-slip and mini-slip trials. The overall slip detection accuracy was 86% with sensitivity and specificity of 81% and 91%, respectively. The overall accuracy dropped by about 2% in LOSO cross validation. The proposed slip detection algorithm is not only beneficial for footwear manufactures to improve their footwear slip resistance quality, but it also has other potential applications, such as improving the slip resistance properties of flooring in healthcare facilities, commercial kitchens, and oil drilling platforms.

Transfer and analysis of Salmonella pdu genes in a range of Gram-negative bacteria demonstrate exogenous microcompartment expression across a variety of species.

Bacterial microcompartments (MCPs) are protein organelles that typically house toxic or volatile reaction intermediates involved in metabolic pathways. Engineering bacteria to express exogenous MCPs will allow these cells to gain useful functions involving molecule compartmentalization. We cloned a 38 kb region from the Salmonella enterica serovar Typhimurium genome containing the pdu 1,2 propanediol (1,2 PD) utilization and cob/cbi genes using the FRT-Capture strategy to clone and transfer large genomic segments. We transferred this clone to a range of Gram-negative bacteria and found the clone to be functional for 1,2 PD metabolism in a variety of species including S. Typhimurium Δpdu, Escherichia coli, Salmonella bongori, Klebsiella pneumoniae, Cronobacter sakazakii, Serratia marcescens, and different Pseudomonas species. We successfully isolated MCPs expressed from the clone from several, but not all, of these strains, and we observed this utilizing a range of different media and in the absence of protease inhibitor. We also present a mini-prep protocol that allows rapid, small-scale screening of strains for MCP production. To date, this is the first analysis of cloned, exogenous microcompartment expression across several different Gram-negative backgrounds and provides a foundation for MCP use in a variety of bacterial species using a full, intact clone.

Colonisation dynamics and virulence of two clonal groups of multidrug-resistant Escherichia coli isolated from dogs.

The study established the virulence potential of multidrug-resistant Escherichia coli (MDREC) isolates from nosocomial infections in hospitalised dogs. The isolates were resistant to fluoroquinolones, belonged to two distinct clonal groups (CG1 and CG2) and contained a plasmid-mediated AmpC (CMY-7) beta-lactamase. CG1 isolates (n=14) possessed two of 36 assayed extraintestinal virulence genes (iutA and traT) and belonged to phylogenetic group A, whereas CG2 isolates (n=19) contained four such genes (iutA, ibeA, fimH and kpsMT K5) and belonged to group D. In a mouse gastrointestinal tract colonisation model, colonisation by index CG1 strain C1 was transient, in contrast to the index CG2 strain C2b, which persisted up to 40days post-inoculation. In a mouse subcutaneous challenge model, both strains were less virulent than archetypal group B2 extraintestinal pathogenic E. coli (ExPEC) strain CFT073; strain C1 caused no systemic signs and strain C2b was lethal to only one of six mice. In a mouse urinary tract infection model, strain C2b colonised the mouse bladder over 2 logs higher compared to strain C1. Whilst both groups of canine MDREC appear less virulent than a reference human ExPEC strain, CG2 strains have greater capacity for colonisation and virulence.

Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response.

In innate immune responses, activation of Toll-like receptors (TLRs) triggers direct antimicrobial activity against intracellular bacteria, which in murine, but not human, monocytes and macrophages is mediated principally by nitric oxide. We report here that TLR activation of human macrophages up-regulated expression of the vitamin D receptor and the vitamin D-1-hydroxylase genes, leading to induction of the antimicrobial peptide cathelicidin and killing of intracellular Mycobacterium tuberculosis. We also observed that sera from African-American individuals, known to have increased susceptibility to tuberculosis, had low 25-hydroxyvitamin D and were inefficient in supporting cathelicidin messenger RNA induction. These data support a link between TLRs and vitamin D-mediated innate immunity and suggest that differences in ability of human populations to produce vitamin D may contribute to susceptibility to microbial infection.

Unsymmetrical DNA cross-linking agents: combination of the CBI and PBD pharmacophores.

A set of 10 compounds, each combining the seco-1,2,9,9a-tetrahydrocyclopropa[c]benz[e]indol-4-one (seco-CBI) and pyrrolo[2,1-c][1,4]benzodiazepine (PBD) pharmacophores, was designed and prepared. These compounds were anticipated to cross-link between N3 of adenine and N2 of guanine in the minor groove of DNA. The compounds, which differ in the chain length separating the two alkylation subunits, and the configuration of the CBI portion, showed great variation in cellular toxicity (over 4 orders of magnitude in a cell line panel) with the most potent example exhibiting IC50s in the pM range. Cytotoxicity correlated with the ability of the compounds to cross-link naked DNA. Cross-linking was also observed in living cells, at much lower concentrations than for a related symmetrical PBD dimer. A thermal cleavage assay was used to assess sequence selectivity, demonstrating that the CBI portion controlled the alkylation sites, while the PBD substituent increased the overall efficiency of alkylation. Several compounds were tested for in vivo activity using a tumor growth delay assay against WiDr human colon carcinoma xenografts, with one compound (the most cytotoxic and most efficient cross-linker) showing a statistically significant increase in survival time following a single iv dose.