2,759 research outputs found
Acidification effects on biofouling communities: winners and losers
How ocean acidification affects marine life is a major concern for science and society. However, its impacts on encrusting biofouling communities, that are both the initial colonizers of hard substrata and of great economic importance, are almost unknown. We showed that community composition changed significantly, from 92% spirorbids, 3% ascidians and 4% sponges initially to 47% spirorbids, 23% ascidians and 29% sponges after 100days in acidified conditions (pH 7.7). In low pH, numbers of the spirorbid Neodexiospira pseudocorrugata were reduced x5 compared to controls. The two ascidians present behaved differently with Aplidium sp. decreasing x10 in pH 7.7, whereas Molgula sp. numbers were x4 higher in low pH than controls. Calcareous sponge (Leucosolenia sp.) numbers increased x2.5 in pH 7.7 over controls. The diatom and filamentous algal community was also more poorly developed in the low pH treatments compared to controls. Colonization of new surfaces likewise showed large decreases in spirorbid numbers, but numbers of sponges and Molgula sp. increased. Spirorbid losses appeared due to both recruitment failure and loss of existing tubes. Spirorbid tubes are comprised of a loose prismatic fabric of calcite crystals. Loss of tube materials appeared due to changes in the binding matrix and not crystal dissolution, as SEM analyses showed crystal surfaces were not pitted or dissolved in low pH conditions. Biofouling communities face dramatic future changes with reductions in groups with hard exposed exoskeletons and domination by soft-bodied ascidians and sponges.EU [227799, 00415/2010]; Natural Environment Research Council [bas0100036, bas0100025
Discourse or gimmick? Digital marginalia in online scholarship
Marginalia has been studied as discourse, as historical documentation and as evidence of reader response. As many academic texts are now available electronically, it seems a natural step to incorporate the interactive, social functions of the Web 2.0. Digital marginalia in an academic publishing context has been a largely unsuccessful venture to this date, yet there are several promising developments. Tools have emerged that enable readers annotate online texts in an approximation of paper-based marginalia, with the additional affordances of two- (or many-) way discourse, digital archiving, and the ability to hide the annotations. This article reviews the contemporary practices of digital marginalia, narrowing in to focus on digital marginalia as a form of academic discourse and peer review. I analyse several case studies of digital marginalia and discourse within this context, including Natureâs trial of open peer review, Wellcome Open Research, PLOS ONE and PubPeerâs systems, as well as my own experience using open peer review with Hypothes.is in a special âdisruptedâ issue of the Journal of Media Practice. The article examines the relative success of these initiatives, attitudes toward open peer review and concludes with some promising developments for the future of digital marginalia and discourse in academic publishing
How CrossâExamination on Subjectivity and Bias Affects Jurorsâ Evaluations of Forensic Science Evidence
Contextual bias has been widely discussed as a possible problem in forensic science. The trial simulation experiment reported here examined reactions of jurors at a county courthouse to crossâexamination and arguments about contextual bias in a hypothetical case. We varied whether the key prosecution witness (a forensic odontologist) was crossâexamined about the subjectivity of his interpretations and about his exposure to potentially biasing taskâirrelevant information. Jurors found the expert less credible and were less likely to convict when the expert admitted that his interpretation rested on subjective judgment, and when he admitted having been exposed to potentially biasing taskâirrelevant contextual information (relative to when these issues were not raised by the lawyers). The findings suggest, however, that forensic scientists can immunize themselves against such challenges and maximize the weight jurors give their evidence by adopting context management procedures that blind them to taskâirrelevant information
The Off-Shell Electromagnetic T-matrix: momentum-dependent scattering from spherical inclusions with both dielectric and magnetic contrast
The momentum- and frequency-dependent T-matrix operator for the scattering of
electromagnetic waves by a dielectric/conducting and para- or diamagnetic
sphere is derived as a Mie-type series, and presented in a compact form
emphasizing various symmetry properties, notably the unitarity identity. This
result extends to magnetic properties one previously obtained for purely
dielectric contrasts by other authors. Several situations useful to
spatially-dispersive effective-medium approximations to one-body order are
examined. Partial summation of the Mie series is achieved in the case of
elastic scattering.Comment: 22 pages. Preprint of a paper to appear in `Waves in Complex And
Random Media' ((c) Taylor and Francis, 2011
Differences between <i>Trypanosoma brucei gambiense</i> groups 1 and 2 in their resistance to killing by Trypanolytic factor 1
<p><b>Background:</b> The three sub-species of <i>Trypanosoma brucei</i> are important pathogens of sub-Saharan Africa. <i>T. b. brucei</i> is unable to infect humans due to sensitivity to trypanosome lytic factors (TLF) 1 and 2 found in human serum. <i>T. b. rhodesiense</i> and <i>T. b. gambiense</i> are able to resist lysis by TLF. There are two distinct sub-groups of <i>T. b. gambiense</i> that differ genetically and by human serum resistance phenotypes. Group 1 <i>T. b. gambiense</i> have an invariant phenotype whereas group 2 show variable resistance. Previous data indicated that group 1 <i>T. b. gambiense</i> are resistant to TLF-1 due in-part to reduced uptake of TLF-1 mediated by reduced expression of the TLF-1 receptor (the haptoglobin-hemoglobin receptor (<i>HpHbR</i>)) gene. Here we investigate if this is also true in group 2 parasites.</p>
<p><b>Methodology:</b> Isogenic resistant and sensitive group 2 <i>T. b. gambiense</i> were derived and compared to other T. brucei parasites. Both resistant and sensitive lines express the <i>HpHbR</i> gene at similar levels and internalized fluorescently labeled TLF-1 similar fashion to <i>T. b. brucei</i>. Both resistant and sensitive group 2, as well as group 1 <i>T. b. gambiense</i>, internalize recombinant APOL1, but only sensitive group 2 parasites are lysed.</p>
<p><b>Conclusions:</b> Our data indicate that, despite group 1 <i>T. b. gambiense</i> avoiding TLF-1, it is resistant to the main lytic component, APOL1. Similarly group 2 <i>T. b. gambiense</i> is innately resistant to APOL1, which could be based on the same mechanism. However, group 2 <i>T. b. gambiense</i> variably displays this phenotype and expression does not appear to correlate with a change in expression site or expression of <i>HpHbR</i>. Thus there are differences in the mechanism of human serum resistance between <i>T. b. gambiense</i> groups 1 and 2.</p>
The genome sequence of <i>Trypanosoma brucei gambiense</i>, causative agent of chronic Human African Trypanosomiasis
<p><b>Background:</b> <i>Trypanosoma brucei gambiense</i> is the causative agent of chronic Human African Trypanosomiasis or sleeping sickness, a disease endemic across often poor and rural areas of Western and Central Africa. We have previously published the genome sequence of a <i>T. b. brucei</i> isolate, and have now employed a comparative genomics approach to understand the scale of genomic variation between <i>T. b. gambiense</i> and the reference genome. We sought to identify features that were uniquely associated with <i>T. b. gambiense</i> and its ability to infect humans.</p>
<p><b>Methods and findings:</b> An improved high-quality draft genome sequence for the group 1 <i>T. b. gambiense</i> DAL 972 isolate was produced using a whole-genome shotgun strategy. Comparison with <i>T. b. brucei</i> showed that sequence identity averages 99.2% in coding regions, and gene order is largely collinear. However, variation associated with segmental duplications and tandem gene arrays suggests some reduction of functional repertoire in <i>T. b. gambiense</i> DAL 972. A comparison of the variant surface glycoproteins (VSG) in <i>T. b. brucei</i> with all <i>T. b. gambiense</i> sequence reads showed that the essential structural repertoire of VSG domains is conserved across <i>T. brucei</i>.</p>
<p><b>Conclusions:</b> This study provides the first estimate of intraspecific genomic variation within <i>T. brucei</i>, and so has important consequences for future population genomics studies. We have shown that the <i>T. b. gambiense</i> genome corresponds closely with the reference, which should therefore be an effective scaffold for any <i>T. brucei</i> genome sequence data. As VSG repertoire is also well conserved, it may be feasible to describe the total diversity of variant antigens. While we describe several as yet uncharacterized gene families with predicted cell surface roles that were expanded in number in <i>T. b. brucei</i>, no <i>T. b. gambiense</i>-specific gene was identified outside of the subtelomeres that could explain the ability to infect humans.</p>
Mutations in pericentrin cause Seckel syndrome with defective ATR-dependent DNA damage signaling
Large brain size is one of the defining characteristics of modern humans. Seckel syndrome (MIM 210600), a disorder of markedly reduced brain and body size, is associated with defective ATR-dependent DNA damage signaling. Only a single hypomorphic mutation of ATR has been identified in this genetically heterogeneous condition. We now report that mutations in the gene encoding pericentrin (PCNT)--resulting in the loss of pericentrin from the centrosome, where it has key functions anchoring both structural and regulatory proteins--also cause Seckel syndrome. Furthermore, we find that cells of individuals with Seckel syndrome due to mutations in PCNT (PCNT-Seckel) have defects in ATR-dependent checkpoint signaling, providing the first evidence linking a structural centrosomal protein with DNA damage signaling. These findings also suggest that other known microcephaly genes implicated in either DNA repair responses or centrosomal function may act in common developmental pathways determining human brain and body size
A Yersinia Effector with Enhanced Inhibitory Activity on the NF-ÎşB Pathway Activates the NLRP3/ASC/Caspase-1 Inflammasome in Macrophages
A type III secretion system (T3SS) in pathogenic Yersinia
species functions to translocate Yop effectors, which modulate cytokine
production and regulate cell death in macrophages. Distinct pathways of
T3SS-dependent cell death and caspase-1 activation occur in
Yersinia-infected macrophages. One pathway of cell death
and caspase-1 activation in macrophages requires the effector YopJ. YopJ is an
acetyltransferase that inactivates MAPK kinases and IKKβ to cause
TLR4-dependent apoptosis in naĂŻve macrophages. A YopJ isoform in Y.
pestis KIM (YopJKIM) has two amino acid substitutions,
F177L and K206E, not present in YopJ proteins of Y.
pseudotuberculosis and Y. pestis CO92. As compared
to other YopJ isoforms, YopJKIM causes increased apoptosis, caspase-1
activation, and secretion of IL-1β in Yersinia-infected
macrophages. The molecular basis for increased apoptosis and activation of
caspase-1 by YopJKIM in Yersinia-infected
macrophages was studied. Site directed mutagenesis showed that the F177L and
K206E substitutions in YopJKIM were important for enhanced apoptosis,
caspase-1 activation, and IL-1β secretion. As compared to
YopJCO92, YopJKIM displayed an enhanced capacity to
inhibit phosphorylation of IκB-ι in macrophages and to bind IKKβ in
vitro. YopJKIM also showed a moderately increased ability to inhibit
phosphorylation of MAPKs. Increased caspase-1 cleavage and IL-1β secretion
occurred in IKKβ-deficient macrophages infected with Y.
pestis expressing YopJCO92, confirming that the
NF-ÎşB pathway can negatively regulate inflammasome activation.
K+ efflux, NLRP3 and ASC were important for secretion of
IL-1β in response to Y. pestis KIM infection as shown using
macrophages lacking inflammasome components or by the addition of exogenous KCl.
These data show that caspase-1 is activated in naĂŻve macrophages in
response to infection with a pathogen that inhibits IKKβ and MAPK kinases
and induces TLR4-dependent apoptosis. This pro-inflammatory form of apoptosis
may represent an early innate immune response to highly virulent pathogens such
as Y. pestis KIM that have evolved an enhanced ability to
inhibit host signaling pathways
Accuracy and repeatability of wrist joint angles in boxing using an electromagnetic tracking system
Š 2019, The Author(s). The hand-wrist region is reported as the most common injury site in boxing. Boxers are at risk due to the amount of wrist motions when impacting training equipment or their opponents, yet we know relatively little about these motions. This paper describes a new method for quantifying wrist motion in boxing using an electromagnetic tracking system. Surrogate testing procedure utilising a polyamide hand and forearm shape, and in vivo testing procedure utilising 29 elite boxers, were used to assess the accuracy and repeatability of the system. 2D kinematic analysis was used to calculate wrist angles using photogrammetry, whilst the data from the electromagnetic tracking system was processed with visual 3D software. The electromagnetic tracking system agreed with the video-based system (paired t tests) in both the surrogate ( 0.9). In the punch testing, for both repeated jab and hook shots, the electromagnetic tracking system showed good reliability (ICCs > 0.8) and substantial reliability (ICCs > 0.6) for flexionâextension and radial-ulnar deviation angles, respectively. The results indicate that wrist kinematics during punching activities can be measured using an electromagnetic tracking system
- âŚ