Biology subjects

Clare, S.

Publications and source records attributed to Clare, S..

4 recordsLinked to original sources

bioRxiv2018

Trace-based correction of breathing-induced field fluctuations in T2*-weighted imaging of the spinal cord

PurposeSpinal cord MRI at ultra-high field is hampered by time-varying magnetic fields associated with the breathing cycle, giving rise to ghosting artifacts in multi-shot acquisitions. Here, we suggest a correction approach based on linking the signal from a respiratory bellows to field changes inside the spinal cord. The information is used to correct the data at the image reconstruction level.\n\nMethodsThe correction was demonstrated in the context of multi-shot T2*-weighted imaging of the cervical spinal cord at 7T. A respiratory trace was acquired during a high-resolution multi-echo gradient-echo sequence, used for structural imaging and quantitative T2* mapping, and a multi-shot EPI time series, as would be suitable for fMRI. The coupling between the trace and the breathing-induced fields was determined by a short calibration scan in each individual. Images were reconstructed with and without trace-based correction.\n\nResultsIn the multi-echo GRE, breathing-induced fields caused severe ghosting in the long echo time images, which led to a systematic underestimation of T2* in the spinal cord. The trace-based correction reduced the ghosting and increased the estimated T2* values. Breathing-related ghosting was also observed in the multi-shot EPI images. The correction largely removed the ghosting, thereby improving the temporal signal-to-noise ratio of the time series.\n\nConclusionsTrace-based retrospective correction of breathing-induced field variations can reduce ghosting and improve quantitative metrics in multi-shot structural and functional T2*-weighted imaging of the spinal cord. The method is straightforward to implement and does not rely on sequence modifications or additional hardware beyond a respiratory bellows.

neuroscience↗

bioRxiv2018

EROS is required for phagocyte NADPH oxidase function in humans and its deficiency causes Chronic Granulomatous Disease.

The phagocyte respiratory burst is mediated by the phagocyte NADPH oxidase, a multi-protein subunit complex that facilitates production of reactive oxygen species and which is essential for host defence. Monogenic deficiency of individual subunits leads to chronic granulomatous disease (CGD), which is characterized by an inability to make reactive oxygen species, leading to severe opportunistic infections and auto-inflammation. However, not all cases of CGD are due to mutations in previously identified subunits. We recently showed that Eros, a novel and highly conserved ER-resident transmembrane protein, is essential for the phagocyte respiratory burst in mice because it is required for expression of gp91phox-p22phox heterodimer, which are the membrane bound components of the phagocyte NADPH oxidase. We now show that the function of EROS is conserved in human cells and describe a case of CGD secondary to a homozygous EROS mutation that abolishes EROS protein expression. This work demonstrates the fundamental importance of EROS in human immunity and describes a novel cause of CGD.\n\nClinical ImplicationsChronic granulomatous disease is caused by an inability to make reactive oxygen species via the phagocyte NADPH oxidase. Mutations in C17ORF62/EROS, which controls gp91phox- p22phox abundance, are a novel cause of chronic granulomatous disease.\n\nKey MessagesO_LIThe murine gene, Eros, is known to regulate abundance of gp91phox-p22phox heterodimer and Eros deficient mice are susceptible to infection\nC_LIO_LIWe show that the function of EROS is conserved in human cells and that a homozygous mutation in EROS causes chronic granulomatous disease\nC_LI

immunology↗

bioRxiv2017

Geospatial statistics of high field functional MRI reveal topographical clustering for binocular stereo depth in early visual cortex

Significance statementFunctional topography is present throughout the cerebral cortex, often in the form of columns or clusters of neurons with similar functional properties within identified cortical regions. Most of the evidence for these structures comes from work with non-human species. Using high-field strength magnetic resonance imaging in living human cortex, the search for this structure is frustrated by the presence of a background of local spatial correlations in the signal across the cortical surface. This structured background, which we term neural dust, is a form of noise that imposes a fundamental limit on the detection of clustering and topography. We apply a novel analysis approach that quantifies the background of spatial correlations, so that we achieve reliable identification of high-signal clusters of activation in the human cortex at a scale previously only visible with invasive optical imaging in animals. We searched specifically in visual cortex for correlates of binocular stereoscopic depth. We show both that signals for stereoscopic depth are clustered into specific zones within the cortex and that these signals occur within spatially extended cortical domains, which have similar preferences for the stereoscopic depth. The revealed structures are reliably identified in all subjects tested and in repeated testing of individual subjects. Our methods provide an objective approach for defining the size and locations of clusters of activation within functional images of neural activity.\n\nAbstractA characteristic principle of the organization of cerebral neocortex is the presence of clusters or columns of neurons with similar functional properties. Animals with forward-facing eyes exploit slight differences between the images in the two eyes to determine binocular depth using stereopsis. Evidence for an organized structure in human visual cortex for the representation of stereoscopic depth has proved elusive. Using 7-tesla functional MRI, with gradient-echo echo-planar imaging at 0.75 mm isotropic resolution and a novel analytical approach based on geospatial mapping methods, we find that clustered responses for disparity-defined depth can be clearly segregated from a background of spatially correlated signals in all subjects tested. High-signal clusters are associated with cortical domains as large as 12-15mm across the cortical surface, in which nearby points in the cortical map tend to respond to the same stereoscopic depth. These domains are found predominantly within visual cortical area V3A.

neuroscience↗

bioRxiv2016

Defining the genetic architecture of stripe rust resistance in the barley accession HOR1428

Puccinia striiformis f. sp. hordei, the causal agent of barley stripe rust, is a destructive fungal pathogen that significantly affects barley cultivation. A major constraint in breeding resistant cultivars is the lack of mapping information of resistance (R) genes and their introgression into adapted germplasm. A considerable number of R genes have been described in barley to P. striiformis f. sp. hordei, but only a few loci have been mapped. Previously, Chen and Line (1999) reported two recessive seedling resistance loci in the Ethiopian landrace HOR 1428. In this study, we map two loci that confer resistance to P. striiformis f. sp. hordei in HOR 1428, which are located on chromosomes 3H and 5H. Both loci act as additive effect QTLs, each explaining approximately 20% of the phenotypic variation. We backcrossed HOR 1428 to the cv. Manchuria and selected based on markers flanking the RpsHOR128-5H locus. Saturation of the RpsHOR1428-5H locus with markers in the region found KASP marker K_1_0292 in complete coupling with resistance to P. striiformis f. sp. hordei and was designated Rps9. Isolation of Rps9 and flanking markers will facilitate the deployment of this genetic resource into existing programs for P. striiformis f. sp. hordei resistance.

plant biology↗