313 research outputs found
Studies on the Magneto-transport properties of perovskite based Colossal Magneto Resistance (CMR)
No full textNot availabl
sj-docx-1-pus-10.1177_09636625221138494 – Supplemental material for Audience segmentation analysis of public intentions to get a COVID-19 vaccine in Australia
No full textSupplemental material, sj-docx-1-pus-10.1177_09636625221138494 for Audience segmentation analysis of public intentions to get a COVID-19 vaccine in Australia by Jagadish Thaker, Lucy M. Richardson and David C. Holmes in Public Understanding of Science</p
Conservation marketing and education for less charismatic biodiversity and conservation businesses for sustainable development
No full textLizards from suburban areas learn faster to stay safe
No full textEnhanced cognitive ability is beneficial in unpredictable and harsh environments, as it enables animals to respond with flexibility. For animals living in urbanized areas, local environments not only are altered but can rapidly change during their lifetime. Urban residents are therefore challenged with identifying novel dangers and safe refuges in dynamic environments. We demonstrate that the tropical agamid lizard Psammophilus dorsalis experiences dramatically different habitats not only across the rural to urban spatial scale but also over the short temporal scale of a few years in suburban areas. Differences in environmental stability are expected to affect rates of learning and reversal learning in resident lizards. In testing arenas, lizards from these populations were required to choose a designated 'safe' refuge instead of an 'unsafe' one after simulated predator attacks. The contingency for safety was switched during the reversal learning task. In general, P. dorsalis showed high rates of learning and reversal learning, but lizards from suburban areas were quicker to learn and unlearn the location of the safe refuge than those from rural areas. This demonstrates for the first time to our knowledge that suburban lizards have faster learning and reversal learning skills for a key survival-related behaviour, finding safety in unpredictable environments. © 2019 The Author(s) Published by the Royal Society. All rights reserved
Sortilin: The Mechanistic Link Between Genes, Cholesterol, and Coronary Artery Disease
No full textHyperlipidemia is an important risk factor for cardiovascular disease globally, but there is still much mystery surrounding the topic of lipid regulation. Many studies have attempted to assess the underlying genetic basis of low-density lipoprotein (LDL) metabolism. Recently, multiple genome-wide association studies identified genes that strongly associate with plasma lipid concentration and cardiovascular disease. Compelling evidence linking the SORT1 gene to both LDL cholesterol (LDL-C) levels and the risk of coronary artery disease emerged from the data, prompting the search for the molecules and mechanisms responsible for this association. Three recent studies explored this relation through sortilin, the gene product of SORT1, and an intracellular trafficking molecule. Careful, hypothesis-driven experimental designs elucidated the potential mechanisms of sortilin\u27s role in LDL-C metabolism. However, each study\u27s conclusions differed in the details of SORT1\u27s association to LDL-C and the subcellular mechanisms at work. Nevertheless, these 3 studies demonstrate how a complex disease such as hyperlipidemia can be evaluated from the scope of the genome down through the level of cellular regulation. Their findings serve as a platform for further study of LDL-C metabolism and hyperlipidemia while also providing lessons on how to better study other complex diseases
Comparative studies on structural properties and antimicrobial potential of spinel ferrite nanoparticles synthesized using various methods
No full textAbsence of xenotropic murine leukaemia virus-related virus in UK patients with chronic fatigue syndrome
No full textBackground: Detection of a retrovirus, xenotropic murine leukaemia virus-related virus (XMRV), has recently been reported in 67% of patients with chronic fatigue syndrome. We have studied a total of 170 samples from chronic fatigue syndrome patients from two UK cohorts and 395 controls for evidence of XMRV infection by looking either for the presence of viral nucleic acids using quantitative PCR (limit of detection <16 viral copies) or for the presence of serological responses using a virus neutralisation assay.
Results: We have not identified XMRV DNA in any samples by PCR (0/299). Some serum samples showed XMRV neutralising activity (26/565) but only one of these positive sera came from a CFS patient. Most of the positive sera were also able to neutralise MLV particles pseudotyped with envelope proteins from other viruses, including vesicular stomatitis virus, indicating significant cross-reactivity in serological responses. Four positive samples were specific for XMRV.
Conclusions: No association between XMRV infection and CFS was observed in the samples tested, either by PCR or serological methodologies. The non-specific neutralisation observed in multiple serum samples suggests that it is unlikely that these responses were elicited by XMRV and highlights the danger of over-estimating XMRV frequency based on serological assays. In spite of this, we believe that the detection of neutralising activity that did not inhibit VSV-G pseudotyped MLV in at least four human serum samples indicates that XMRV infection may occur in the general population, although with currently uncertain outcomes
Structural model of a2-subunit N-terminus and its binding interface for Arf-GEF CTH2: Implication for regulation of V-ATPase, CTH2 function and rational drug design
No full textWe have previously identified the interaction between mammalian V-ATPase a2-subunit isoform and cytohesin-2 (CTH2) and studied molecular details of binding between these proteins. In particular, we found that six peptides derived from the N-terminal cytosolic domain of a2 subunit (a2N1–402) are involved in interaction with CTH2 (Merkulova, Bakulina, Thaker, Grüber, & Marshansky, 2010). However, the actual 3D binding interface was not determined in that study due to the lack of high-resolution structural information about a-subunits of V-ATPase. Here, using a combination of homology modeling and NMR analysis, we generated the structural model of complete a2N1–402 and uncovered the CTH2-binding interface. First, using the crystal-structure of the bacterial M. rubber Icyt-subunit of A-ATPase as a template (Srinivasan, Vyas, Baker, & Quiocho, 2011), we built a homology model of mammalian a2N1–352 fragment. Next, we combined it with the determined NMR structures of peptides a2N368–395 and a2N386–402 of the C-terminal section of a2N1–402. The complete molecular model of a2N1–402 revealed that six CTH2 interacting peptides are clustered in the distal and proximal lobe sub-domains of a2N1–402. Our data indicate that the proximal lobe sub-domain is the major interacting site with the Sec7 domain of first CTH2 protein, while the distal lobe sub-domain of a2N1–402 interacts with the PH-domain of second CTH2. Indeed, using Sec7/Arf-GEF activity assay we experimentally confirmed our model. The interface formed by peptides a2N1–17 and a2N35–49 is involved in specific interaction with Sec7 domain and regulation of GEF activity. These data are critical for understanding of the cross-talk between V-ATPase and CTH2 as well as for the rational drug design to regulate their function
Soluble Ig-like transcript 3 inhibits tumor allograft rejection in humanized SCID mice and T cell responses in cancer patients
No full textAttempts to enhance patients' immune responses to malignancies have been largely unsuccessful. We now describe an immune-escape mechanism mediated by the inhibitory receptor Ig-like transcript 3 (ILT3) that may be responsible for such failures. Using a humanized SCID mouse model, we demonstrate that soluble and membrane ILT3 induce CD8+ T suppressor cells and prevent rejection of allogeneic tumor transplants. Furthermore, we found that patients with melanoma, and carcinomas of the colon, rectum, and pancreas produce the soluble ILT3 protein, which induces the differentiation of CD8+ T suppressor cells and impairs T cell responses in MLC. These responses are restored by anti-ILT3 mAb or by depletion of soluble ILT3 from the serum. Immunohistochemical staining of biopsies from the tumors and metastatic lymph nodes suggests that CD68+ tumor-associated macrophages represent the major source of soluble ILT3. Alternative splicing, resulting in the loss of the ILT3 transmembrane domain, may contribute to the release of ILT3 in the circulation. These data suggest that ILT3 depletion or blockade is crucial to the success of immunotherapy in cancer. In contrast, the inhibitory activity of soluble ILT3 on T cell alloreactivity in vitro and in vivo suggests the potential usefulness of rILT3 for immunosuppressive treatment of allograft recipients or patients with autoimmune diseases. Copyright © 2007 by The American Association of Immunologists, Inc
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