Less Is Best in the Convergent Evolution of Typhoidal Salmonella

Publication date: 14 February 2018
Source:Cell Host & Microbe, Volume 23, Issue 2
Author(s): Andrés Vázquez-Torres
Related works in this issue of Cell Host & Microbe (Bronner et al., 2018) and in a recent issue of Cell Reports (Hiyoshi et al., 2018) demonstrate how loss-of-function mutations in butyrate utilization and lipopolysaccharide O-antigen processing contribute to evasion of innate host defenses and the convergent evolution of distinct typhoidal Salmonella lineages.

Teaser

Related works in this issue of Cell Host & Microbe (Bronner et al., 2018) and in a recent issue of Cell Reports (Hiyoshi et al., 2018) demonstrate how loss-of-function mutations in butyrate utilization and lipopolysaccharide O-antigen processing contribute to evasion of innate host defenses and the convergent evolution of distinct typhoidal Salmonella lineages.


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Infectious Scarring: Setting the Trigger for Intestinal Inflammation

Publication date: 14 February 2018
Source:Cell Host & Microbe, Volume 23, Issue 2
Author(s): Andrew M.F. Johnson, R. William DePaolo
The initiating factors that trigger inflammatory bowel disease (IBD) are poorly understood. In a recent paper, Yang et al. (2017) demonstrate that IBD-like syndrome in mice can develop as a consequence of recurrent pathogen infection. Pathogenic triggering of inflammatory disease is a re-emerging concept that has significant therapeutic implications.

Teaser

The initiating factors that trigger inflammatory bowel disease (IBD) are poorly understood. In a recent paper, Yang et al. (2017) demonstrate that IBD-like syndrome in mice can develop as a consequence of recurrent pathogen infection. Pathogenic triggering of inflammatory disease is a re-emerging concept that has significant therapeutic implications.


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BCG Vaccination Protects against Experimental Viral Infection in Humans through the Induction of Cytokines Associated with Trained Immunity

Publication date: 10 January 2018
Source:Cell Host & Microbe, Volume 23, Issue 1
Author(s): Rob J.W. Arts, Simone J.C.F.M. Moorlag, Boris Novakovic, Yang Li, Shuang-Yin Wang, Marije Oosting, Vinod Kumar, Ramnik J. Xavier, Cisca Wijmenga, Leo A.B. Joosten, Chantal B.E.M. Reusken, Christine S. Benn, Peter Aaby, Marion P. Koopmans, Hendrik G. Stunnenberg, Reinout van Crevel, Mihai G. Netea
The tuberculosis vaccine bacillus Calmette-Guérin (BCG) has heterologous beneficial effects against non-related infections. The basis of these effects has been poorly explored in humans. In a randomized placebo-controlled human challenge study, we found that BCG vaccination induced genome-wide epigenetic reprograming of monocytes and protected against experimental infection with an attenuated yellow fever virus vaccine strain. Epigenetic reprogramming was accompanied by functional changes indicative of trained immunity. Reduction of viremia was highly correlated with the upregulation of IL-1β, a heterologous cytokine associated with the induction of trained immunity, but not with the specific IFNγ response. The importance of IL-1β for the induction of trained immunity was validated through genetic, epigenetic, and immunological studies. In conclusion, BCG induces epigenetic reprogramming in human monocytes in vivo, followed by functional reprogramming and protection against non-related viral infections, with a key role for IL-1β as a mediator of trained immunity responses.

Graphical abstract

Teaser

In this paper, Arts et al. describe that BCG vaccination induces genome-wide epigenetic reprogramming of human monocytes that correlates with protection against experimental viral infection. Reduction of viremia correlated with upregulation of non-specific IL-1β production, and genetic polymorphisms in the IL-1 pathway affect the induction of trained immunity by BCG.


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An Additive Sugar Helps the C. diff Go Round

Publication date: 14 February 2018
Source:Cell Host & Microbe, Volume 23, Issue 2
Author(s): Michael C. Abt
Outbreaks of hypervirulent strains of Clostridium difficile began to be reported in healthcare facilities worldwide around 20 years ago. Concurrently, trehalose became a common additive used by the global food industry. A new study provides evidence that these two observations are a linked phenomenon (Collins et al., 2018).

Teaser

Outbreaks of hypervirulent strains of Clostridium difficile began to be reported in healthcare facilities worldwide around 20 years ago. Concurrently, trehalose became a common additive used by the global food industry. A new study provides evidence that these two observations are a linked phenomenon (Collins et al., 2018).


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Identification of a Botulinum Neurotoxin-like Toxin in a Commensal Strain of Enterococcus faecium

Publication date: 14 February 2018
Source:Cell Host & Microbe, Volume 23, Issue 2
Author(s): Sicai Zhang, Francois Lebreton, Michael J. Mansfield, Shin-Ichiro Miyashita, Jie Zhang, Julia A. Schwartzman, Liang Tao, Geoffrey Masuyer, Markel Martínez-Carranza, Pål Stenmark, Michael S. Gilmore, Andrew C. Doxey, Min Dong
Botulinum neurotoxins (BoNTs), produced by various Clostridium strains, are a family of potent bacterial toxins and potential bioterrorism agents. Here we report that an Enterococcus faecium strain isolated from cow feces carries a BoNT-like toxin, designated BoNT/En. It cleaves both VAMP2 and SNAP-25, proteins that mediate synaptic vesicle exocytosis in neurons, at sites distinct from known BoNT cleavage sites on these two proteins. Comparative genomic analysis determines that the E. faecium strain carrying BoNT/En is a commensal type and that the BoNT/En gene is located within a typical BoNT gene cluster on a 206 kb putatively conjugative plasmid. Although the host species targeted by BoNT/En remains to be determined, these findings establish an extended member of BoNTs and demonstrate the capability of E. faecium, a commensal organism ubiquitous in humans and animals and a leading cause of hospital-acquired multi-drug-resistant (MDR) infections, to horizontally acquire, and possibly disseminate, a unique BoNT gene cluster.

Graphical abstract

Teaser

Botulinum neurotoxins (BoNTs) are potent toxins produced by diverse bacteria in the Clostridium genus. Zhang et al. report that a commensal strain of Enterococcus faecium carries a conjugative plasmid encoding a BoNT-like toxin gene. Thus, a commensal organism can acquire and possibly disseminate BoNT genes.


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Loss of Paneth Cell Autophagy Causes Acute Susceptibility to Toxoplasma gondii-Mediated Inflammation

Publication date: 14 February 2018
Source:Cell Host & Microbe, Volume 23, Issue 2
Author(s): Elise Burger, Alessandra Araujo, Américo López-Yglesias, Michael W. Rajala, Linda Geng, Beth Levine, Lora V. Hooper, Ezra Burstein, Felix Yarovinsky
The protozoan parasite Toxoplasma gondii triggers severe small intestinal immunopathology characterized by IFN-γ- and intestinal microbiota-mediated inflammation, Paneth cell loss, and bacterial dysbiosis. Paneth cells are a prominent secretory epithelial cell type that resides at the base of intestinal crypts and releases antimicrobial peptides. We demonstrate that the microbiota triggers basal Paneth cell-specific autophagy via induction of IFN-γ, a known trigger of autophagy, to maintain intestinal homeostasis. Deletion of the autophagy protein Atg5 specifically in Paneth cells results in exaggerated intestinal inflammation characterized by complete destruction of the intestinal crypts resembling that seen in pan-epithelial Atg5-deficient mice. Additionally, lack of functional autophagy in Paneth cells within intestinal organoids and T. gondii-infected mice causes increased sensitivity to the proinflammatory cytokine TNF along with increased intestinal permeability, leading to exaggerated microbiota- and IFN-γ-dependent intestinal immunopathology. Thus, Atg5 expression in Paneth cells is essential for tissue protection against cytokine-mediated immunopathology during acute gastrointestinal infection.

Graphical abstract

Teaser

Autophagy is an essential cellular process in all cells. Burger et al. show that the microbiota drives autophagy predominantly in Paneth cells via basal induction of IFN-γ. A Paneth cell-restricted deficiency in autophagy results in the inability to control intestinal inflammation and acute mortality during T. gondii infection.


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Intestinal Epithelial Cell Autophagy Is Required to Protect against TNF-Induced Apoptosis during Chronic Colitis in Mice

Publication date: 14 February 2018
Source:Cell Host & Microbe, Volume 23, Issue 2
Author(s): Johanna Pott, Agnieszka Martyna Kabat, Kevin Joseph Maloy
Genome-wide association studies have linked polymorphisms in the autophagy gene ATG16L1 with susceptibility to inflammatory bowel disease (IBD). However, the cell-type-specific effects of autophagy on the regulation of chronic intestinal inflammation have not been investigated. Here, we assessed the effect of myeloid-specific or intestinal epithelial cell (IEC)-specific deletion of Atg16l1 on chronic colitis triggered by the intestinal opportunistic pathogen Helicobacter hepaticus in mice. Although Atg16l1 deficiency in myeloid cells had little effect on disease, mice selectively lacking Atg16l1 in IECs (Atg16l1^VC) developed severely exacerbated pathology, accompanied by elevated pro-inflammatory cytokine secretion and increased IEC apoptosis. Using ex vivo IEC organoids, we demonstrate that autophagy intrinsically controls TNF-induced apoptosis and in vivo blockade of TNF attenuated the exacerbated pathology in Atg16l1^VC mice. These findings suggest that the IBD susceptibility gene ATG16L1 and the process of autophagy within the epithelium control inflammation-induced apoptosis and barrier integrity to limit chronic intestinal inflammation.

Graphical abstract

Teaser

Autophagy is genetically linked with inflammatory bowel disease. Using tissue-specific Atg16l1 knockout mice, Pott et al. demonstrate that autophagy within the intestinal epithelium maintains barrier integrity and limits inflammation by protecting the cells from TNF-induced apoptosis in a model of chronic colitis.


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Good Bug, Bad Bug: Breaking through Microbial Stereotypes

Publication date: 10 January 2018
Source:Cell Host & Microbe, Volume 23, Issue 1
Author(s): Mihai Cirstea, Nina Radisavljevic, B. Brett Finlay
Our expanding knowledge of microbial mechanisms is challenging the notion of "good" versus "bad" microbes and encouraging a better understanding of their roles in various contexts before their widespread therapeutic and clinical application. The intestinal microbe Akkermansia muciniphila, a promising probiotic with an emerging cautionary tale, best highlights this challenge.

Teaser

Our expanding knowledge of microbial mechanisms is challenging the notion of "good" versus "bad" microbes and encouraging a better understanding of their roles in various contexts before their widespread therapeutic and clinical application. The intestinal microbe Akkermansia muciniphila, a promising probiotic with an emerging cautionary tale, best highlights this challenge.


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Bacteroides fragilis Toxin Coordinates a Pro-carcinogenic Inflammatory Cascade via Targeting of Colonic Epithelial Cells

Publication date: 14 February 2018
Source:Cell Host & Microbe, Volume 23, Issue 2
Author(s): Liam Chung, Erik Thiele Orberg, Abby L. Geis, June L. Chan, Kai Fu, Christina E. DeStefano Shields, Christine M. Dejea, Payam Fathi, Jie Chen, Benjamin B. Finard, Ada J. Tam, Florencia M. McAllister, Hongni Fan, Xinqun Wu, Sudipto Ganguly, Andriana Lebid, Paul Metz, Sara W. Van Meerbeke, David L. Huso, Elizabeth C. Wick, Drew M. Pardoll, Fengyi Wan, Shaoguang Wu, Cynthia L. Sears, Franck Housseau
Pro-carcinogenic bacteria have the potential to initiate and/or promote colon cancer, in part via immune mechanisms that are incompletely understood. Using Apc^Min mice colonized with the human pathobiont enterotoxigenic Bacteroides fragilis (ETBF) as a model of microbe-induced colon tumorigenesis, we show that the Bacteroides fragilis toxin (BFT) triggers a pro-carcinogenic, multi-step inflammatory cascade requiring IL-17R, NF-κB, and Stat3 signaling in colonic epithelial cells (CECs). Although necessary, Stat3 activation in CECs is not sufficient to trigger ETBF colon tumorigenesis. Notably, IL-17-dependent NF-κB activation in CECs induces a proximal to distal mucosal gradient of C-X-C chemokines, including CXCL1, that mediates the recruitment of CXCR2-expressing polymorphonuclear immature myeloid cells with parallel onset of ETBF-mediated distal colon tumorigenesis. Thus, BFT induces a pro-carcinogenic signaling relay from the CEC to a mucosal Th17 response that results in selective NF-κB activation in distal colon CECs, which collectively triggers myeloid-cell-dependent distal colon tumorigenesis.

Graphical abstract

Teaser

Chung et al. uncover a complex, microbe-driven carcinogenic mechanism whereby the Bacteroides fragilis toxin targets the colonic epithelium to trigger an IL-17 mucosal immune response that relays back to epithelial cells, inciting pro-tumoral myeloid cell infiltration, principally to the distal colon, corresponding to the region of tumorigenesis in Apc^Min/− mice.


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Cytosolic and Secreted Peptidoglycan-Degrading Enzymes in Drosophila Respectively Control Local and Systemic Immune Responses to Microbiota

Publication date: 14 February 2018
Source:Cell Host & Microbe, Volume 23, Issue 2
Author(s): Bernard Charroux, Florence Capo, C. Léopold Kurz, Sabine Peslier, Delphine Chaduli, Annelise Viallat-lieutaud, Julien Royet
Gut-associated bacteria produce metabolites that both have a local influence on the intestinal tract and act at a distance on remote organs. In Drosophila, bacteria-derived peptidoglycan (PGN) displays such a dual role. PGN triggers local antimicrobial peptide production by enterocytes; it also activates systemic immune responses in fat-body cells and modulates fly behavior by acting on neurons. How these responses to a single microbiota-derived compound are simultaneously coordinated is not understood. We show here that the PGRP-LB locus generates both cytosolic and secreted PGN-cleaving enzymes. Through genetic analysis, we demonstrate that the cytosolic PGRP-LB isoforms cell-autonomously control the intensity of NF-κB activation in enterocytes, whereas the secreted isoform prevents massive and detrimental gut-derived PGN dissemination throughout the organism. This study explains how Drosophila are able to uncouple the modulation of local versus systemic responses to a single gut-bacteria-derived product by using isoform-specific enzymes.

Graphical abstract

Teaser

Since microbiota-derived peptidoglycan activates NF-κB signaling in the gut and remote organs, its levels need to be controlled in vivo. Charroux et al. show how, by generating both secreted and cytosolic peptidoglycan-cleaving enzymes, Drosophila uncouple the modulation of local versus systemic responses to a single gut-bacteria-derived product.


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Ecotoxicity tests with Allium cepa to determine the efficiency of rice husk ash in the treatment of groundwater contaminated with benzene, toluene, ethylbenzene, and xylene

Abstract

The validation of adsorption treatment based on toxicity assays aims to assess the actual environmental impact caused by effluents after treatment. This study describes the use of rice husk ash as adsorbent and evaluates the efficiency of adsorption treatment to remediate groundwater contaminated with benzene, toluene, ethylbenzene, and xylene (BTEX). The synthetic effluent was prepared with standard benzene, toluene, ethylbenzene, and xylene solutions. Adsorption was assessed at treatment times 0, 60, 120, and 240 min. Compounds were quantified by gas chromatography with flame ionization detector. The treatment was validated based on ecotoxicity assays using Allium cepa as indicator organism. For the treatment times stipulated, samples containing 25, 50, and 100% of BTEX were used. The dilutions were carried out with drinking water according to Fiskesjö (1985). The relative growth index (RGI), root inhibition index (Ii), and germination index (GI) confirmed the efficiency of the treatment approach tested. The best adsorption time for an initial BTEX concentration of 3.378 mg/L was 60 min. Critical level (EC50) and critical concentration that induced phytotoxic effect on A. cepa germination was observed only for the undiluted effluent.

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Wound irrigation and the lack of evidence-based-practice

Dear Editor,

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Circadian Control of DRP1 Activity Regulates Mitochondrial Dynamics and Bioenergetics

Publication date: Available online 22 February 2018
Source:Cell Metabolism
Author(s): Karen Schmitt, Amandine Grimm, Robert Dallmann, Bjoern Oettinghaus, Lisa Michelle Restelli, Melissa Witzig, Naotada Ishihara, Katsuyoshi Mihara, Jürgen A. Ripperger, Urs Albrecht, Stephan Frank, Steven A. Brown, Anne Eckert
Mitochondrial fission-fusion dynamics and mitochondrial bioenergetics, including oxidative phosphorylation and generation of ATP, are strongly clock controlled. Here we show that these circadian oscillations depend on circadian modification of dynamin-related protein 1 (DRP1), a key mediator of mitochondrial fission. We used a combination of in vitro and in vivo models, including human skin fibroblasts and DRP1-deficient or clock-deficient mice, to show that these dynamics are clock controlled via circadian regulation of DRP1. Genetic or pharmacological abrogation of DRP1 activity abolished circadian network dynamics and mitochondrial respiratory activity and eliminated circadian ATP production. Pharmacological silencing of pathways regulating circadian metabolism and mitochondrial function (e.g., sirtuins, AMPK) also altered DRP1 phosphorylation, and abrogation of DRP1 activity impaired circadian function. Our findings provide new insight into the crosstalk between the mitochondrial network and circadian cycles.

Graphical abstract

Teaser

Schmitt et al. demonstrate that the circadian clock globally regulates mitochondrial morphology and energy metabolism. Even in non-dividing tissues, rhythmic control of DRP1 phosphorylation directs circadian mitochondrial morphology. This control is not only essential for circadian ATP production but also feeds back to influence the core circadian clock.


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Structure activity relationship studies on rhodanines and derived enethiol inhibitors of metallo-β-lactamases

Publication date: Available online 23 February 2018
Source:Bioorganic & Medicinal Chemistry
Author(s): Dong Zhang, Marios S. Markoulides, Dmitrijs Stepanovs, Anna M. Rydzik, Ahmed El-Hussein, Corentin A.M. Bon, Jos J.A.G. Kamps, Klaus-Daniel Umland, Patrick M. Collins, Samuel T. Cahill, David Y. Wang, Timothy D.W. Claridge, Jürgen Brem, Michael A. McDonough, Christopher J. Schofield
Metallo-β-lactamases (MBLs) enable bacterial resistance to almost all classes of β-lactam antibiotics. We report studies on enethiol containing MBL inhibitors, which were prepared by rhodanine hydrolysis. The enethiols inhibit MBLs from different subclasses. Crystallographic analyses reveal that the enethiol sulphur displaces the di-Zn(II) ion bridging 'hydrolytic' water. In some, but not all, cases biophysical analyses provide evidence that rhodanine/enethiol inhibition involves formation of a ternary MBL enethiol rhodanine complex. The results demonstrate how low molecular weight active site Zn(II) chelating compounds can inhibit a range of clinically relevant MBLs and provide additional evidence for the potential of rhodanines to be hydrolysed to potent inhibitors of MBL protein fold and, maybe, other metallo-enzymes, perhaps contributing to the complex biological effects of rhodanines. The results imply that any medicinal chemistry studies employing rhodanines (and related scaffolds) as inhibitors should as a matter of course include testing of their hydrolysis products.

Graphical abstract

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Aralkyl selenoglycosides and related selenosugars in acetylated form activate protein phosphatase-1 and -2A

Publication date: Available online 22 February 2018
Source:Bioorganic & Medicinal Chemistry
Author(s): Zoltán Kónya, Bálint Bécsi, Andrea Kiss, István Tamás, Beáta Lontay, László Szilágyi, Katalin E. Kövér, Ferenc Erdődi
Aralkyl and aryl selenoglycosides as well as glycosyl selenocarboxylate derivatives were assayed on the activity of protein phosphatase-1 (PP1) and -2A (PP2A) catalytic subunits (PP1c and PP2Ac) in search of compounds for PP1c and PP2Ac effectors. The majority of tested selenoglycosides activated both PP1c and PP2Ac by ∼2-4-fold in a phosphatase assay with phosphorylated myosin light chain substrate when the hydroxyl groups of the glycosyl moiety were acetylated, but they were without any effects in the non-acetylated forms. A peptide from the myosin phosphatase target subunit-1 (MYPT1^23-38) that included an RVxF PP1c-binding motif attenuated activation of PP1c by 2-Trifluoromethylbenzyl 2,3,4,6-tetra-O-acetyl-1-seleno-β-D-glucopyranoside (TFM-BASG) and 4-Bromobenzyl 2,3,4,6-tetra-O-acetyl-1-seleno-β-D-glucopyranoside (Br-BASG). MYPT1^23-38 stimulated PP2Ac and contributed to PP2Ac activation exerted by either Br-BASG or TFM-BASG. Br-BASG and TFM-BASG suppressed partially binding of PP1c to MYPT1 in surface plasmon resonance based binding experiments. Molecular docking predicted that the hydrophobic binding surfaces in PP1c for interaction with either the RVxF residues of PP1c-interactors or selenoglycosides are partially overlapped. Br-BASG and TFM-BASG caused a moderate increase in the phosphatase activity of HeLa cells in 1 hour, and suppressed cell viability in 24 hour incubations. In conclusion, our present study identified selenoglycosides as novel activators of PP1 and PP2A as well as provided insights into the structural background of their interactions establishing a molecular model for future design of more efficient phosphatase activator molecules.

Graphical abstract

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A novel series of 4-methyl substituted pyrazole derivatives as potent glucagon receptor antagonists: Design, synthesis and evaluation of biological activities

Publication date: Available online 22 February 2018
Source:Bioorganic & Medicinal Chemistry
Author(s): Shuangjie Shu, Antao Dai, Jiang Wang, Bin Wang, Yang Feng, Jia Li, Xiaoqing Cai, Dehua Yang, Dakota Ma, Ming-Wei Wang, Hong Liu
A novel series of 4-methyl substituted pyrazole derivatives were designed, synthesized and biologically evaluated as potent glucagon receptor (GCGR) antagonists. In this study, compounds 9q, 9r, 19d and 19e showed high GCGR binding (IC50 = 0.09 μM, 0.06 μM, 0.07 μM and 0.08 μM, respectively) and cyclic-adenosine monophosphate (cAMP) activities (IC50 = 0.22 μM, 0.26 μM, 0.44 μM and 0.46 μM, respectively) in cell-based assays. Most importantly, the docking experiment demonstrated that compound 9r formed extensive hydrophobic interactions with the receptor binding pocket, making it justifiable to further investigate the potential of becoming a GCGR antagonist.

Graphical abstract

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A combination of 19F NMR and surface plasmon resonance for site-specific hit selection and validation of fragment molecules that bind to the ATP-binding site of a kinase

Publication date: Available online 22 February 2018
Source:Bioorganic & Medicinal Chemistry
Author(s): Satoru Nagatoishi, Sou Yamaguchi, Etsuko Katoh, Keita Kajita, Takane Yokotagawa, Satoru Kanai, Toshio Furuya, Kouhei Tsumoto
¹⁹F NMR has recently emerged as an efficient, sensitive tool for analyzing protein binding to small molecules, and surface plasmon resonance (SPR) is also a popular tool for this purpose. Herein a combination of ¹⁹F NMR and SPR was used to find novel binders to the ATP-binding pocket of MAP kinase extracellular regulated kinase 2 (ERK2) by fragment screening with an original fluorinated-fragment library. The ¹⁹F NMR screening yielded a high primary hit rate of binders to the ERK2 ATP-binding pocket compared with the rate for the SPR screening. Hit compounds were evaluated and categorized according to their ability to bind to different binding sites in the ATP-binding pocket. The binding manner was characterized by using isothermal titration calorimetry and docking simulation. Combining ¹⁹F NMR with other biophysical methods allows the identification of multiple types of hit compounds, thereby increasing opportunities for drug design using preferred fragments.

Graphical abstract

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Design and synthesis of a fragment set based on twisted bicyclic lactams

Publication date: Available online 22 February 2018
Source:Bioorganic & Medicinal Chemistry
Author(s): Haitham Hassan, Stephen P. Marsden, Adam Nelson
Current fragment sets tend to be dominated by flatter molecules, and their shape diversity does not reflect that of the fragments that are theoretically possible. The design and synthesis of a set of bridged fragments containing a bridgehead nitrogen is described. Many of these fragments contain twisted lactams whose modulated electronic properties may present unusual opportunities for interaction with target proteins. The demonstrated novelty, three-dimensionality and molecular properties of the set of 22 fragments may provide valuable, and highly distinctive, starting points for fragment-based drug discovery.

Graphical abstract

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Use of Optical Motion Capture for the Analysis of Normative Upper Body Kinematics during Functional Upper Limb Tasks: A Systematic Review

Publication date: Available online 23 February 2018
Source:Journal of Electromyography and Kinesiology
Author(s): Aïda M. Valevicius, Peter Y. Jun, Jacqueline S. Hebert, Albert H. Vette
Quantifying three-dimensional upper body kinematics can be a valuable method for assessing upper limb function. Considering that kinematic model characteristics, performed tasks, and reported outcomes are not consistently standardized and exhibit significant variability across studies, the purpose of this review was to evaluate the literature investigating upper body kinematics in non-disabled individuals via optical motion capture. Specific objectives were to report on the kinematic model characteristics, performed functional tasks, and kinematic outcomes, and to assess whether kinematic protocols were assessed for validity and reliability. Five databases were searched. Studies using anatomical and/or cluster marker sets, along with optical motion capture, and presenting normative data on upper body kinematics were eligible for review. Information extracted included model characteristics, performed functional tasks, kinematic outcomes, and validity or reliability testing. 804 publication records were screened and 20 reviewed based on the selection criteria. Thirteen studies described their kinematic protocols adequately for reproducibility, and 8 studies followed International Society of Biomechanics standards for quantifying upper body kinematics. Six studies assessed their protocols for validity or reliability. While a substantial number of studies have adequately reported their protocols, more systematic work is needed to evaluate the validity and reliability of existing protocols.



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Impacts of using a head-worn display on gait performance during level walking and obstacle crossing

Publication date: Available online 23 February 2018
Source:Journal of Electromyography and Kinesiology
Author(s): Sunwook Kim, Maury A. Nussbaum, Sophia Ulman
Use of a head-worn display (HWD) may affect gait performance and increase slip and trip risks, though there is a lack of information on such effects. This study investigated how different display technologies (monocular and binocular HWDs, and a paper list) and visual information presentation modes affect gait performance. Twelve gender-balanced participants completed walking and obstacle crossing trials on a linear walking track under all experimental conditions and a baseline control (without using a technology). During these trials, information relevant to a simulated light assembly task was provided, as representative of a potential occupational application. Gait performance was assessed based on minimum foot clearance (MFC), required coefficient of friction, foot placement locations around the obstacle, and/or walking/obstacle crossing speed. Use of a HWD had no substantial effects on level walking performance. A more conservative/cautious obstacle crossing strategy was, however, observed with HWD use, including a decrease (∼3%) in obstacle crossing speed (compared to the baseline). Gender-specific foot control strategies (lead foot MFC) were also observed that depended on the specific display technology and information modes. Foot placements around the obstacle were not influenced by use of the binocular HWD, yet a conservative strategy was observed with the monocular HWD.



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