397 research outputs found
Bushell, R F, SX10450
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/375113Surname: BUSHELL
Given Name(s) or Initials: R F
Military Service Number or Last Known Location: SX10450
Missing, Wounded and Prisoner of War Enquiry Card Index Number: 24718187294
Item: [2016.0049.07421] "Bushell, R F, SX10450
Bushell, D R (Dante Ronald), VX59697
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/375115Surname: BUSHELL
Given Name(s) or Initials: D R (DANTE RONALD)
Military Service Number or Last Known Location: VX59697
Missing, Wounded and Prisoner of War Enquiry Card Index Number: 17752187310
Item: [2016.0049.07423] "Bushell, D R (Dante Ronald), VX59697
Iteration of order preserving subhomogeneous maps on a cone
No full textWe investigate the iterative behaviour of continuous order preserving subhomogeneous maps , where is a polyhedral cone in a finite dimensional vector space. We show that each bounded orbit of converges to a periodic orbit and, moreover, the period of each periodic point of is bounded by where is the number of facets of the polyhedral cone. By constructing examples on the standard positive cone in , we show that the upper bound is asymptotically sharp
Advances in imaging of new targets for pharmacological intervention in stroke: real-time tracking of T-cells in the ischaemic brain
No full textBackground and purpose: T‐cells may play a role in the evolution of ischaemic damage and repair, but the ability to image these cells in the living brain after a stroke has been limited. We aim to extend the technique of real‐time in situ brain imaging of T‐cells, previously shown in models of immunological diseases, to models of experimental stroke.
Experimental approach: Male C57BL6 mice (6–8 weeks) (n= 3) received a total of 2–5 × 106 carboxyfluorescein diacetate succinimidyl ester (CFSE)‐labelled lymphocytes from donor C57BL6 mice via i.v. injection by adoptive transfer. Twenty‐four hours later, recipient mice underwent permanent left distal middle cerebral artery occlusion (MCAO) by electrocoagulation or by sham surgery under isoflurane anaesthesia. Female hCD2‐green fluorescent protein (GFP) transgenic mice that exhibit GFP‐labelled T‐cells underwent MCAO. At 24 or 48 h post‐MCAO, a sagittal brain slice (1500 µm thick) containing cortical branches of the occluded middle cerebral artery (MCA) was dissected and used for multiphoton laser scanning microscopy (MPLSM).
Key results: Our results provide direct observations for the first time of dynamic T‐cell behaviour in living brain tissue in real time and herein proved the feasibility of MPLSM for ex vivo live imaging of immune response after experimental stroke.
Conclusions and Implications: It is hoped that these advances in the imaging of immune cells will provide information that can be harnessed to a therapeutic advantage
Imaging T-cell movement in the brain during experimental cerebral malaria
No full textT-cells are known to play a role in the pathology associated with experimental cerebral malaria, although it has not previously been possible to examine their behaviour in brain. Using multiphoton laser scanning microscopy, we have examined the migration and movement of these cells in brain tissue. We believe that this approach will help define host-parasite interactions and examine how intervening in these relationships affects the development of cerebral pathology
Regulatory immune cells in transplantation.
No full textImmune regulation is fundamental to any immune response to ensure that it is appropriate for the perceived threat to the host. Following cell and organ transplantation, it is essential to control both the innate immune response triggered by the injured tissue and the adaptive immune response stimulated by mismatched donor and recipient histocompatibility antigens to enable the transplant to survive and function. Here, we discuss the leukocyte populations that can promote immune tolerance after cell or solid-organ transplantation. Such populations include regulatory T cells, B cells and macrophages, as well as myeloid-derived suppressor cells, dendritic cells and mesenchymal stromal cells. We consider the potential of these regulatory immune cells to develop and function in transplant recipients and their potential use as cellular therapies to promote long-term graft function
Altered antibiotic transport in OmpC mutants isolated from a series of clinical strains of multi-drug resistant E. coli
No full textThis work is also partially supported by BBSRC and the Scottish Funding Council (through SULSA)Antibiotic-resistant bacteria, particularly Gram negative species, present significant health care challenges. The permeation of antibiotics through the outer membrane is largely effected by the porin superfamily, changes in which contribute to antibiotic resistance. A series of antibiotic resistant E. coli isolates were obtained from a patient during serial treatment with various antibiotics. The sequence of OmpC changed at three positions during treatment giving rise to a total of four OmpC variants (denoted OmpC20, OmpC26, OmpC28 and OmpC33, in which OmpC20 was derived from the first clinical isolate). We demonstrate that expression of the OmpC K12 porin in the clinical isolates lowers the MIC, consistent with modified porin function contributing to drug resistance. By a range of assays we have established that the three mutations that occur between OmpC20 and OmpC33 modify transport of both small molecules and antibiotics across the outer membrane. This results in the modulation of resistance to antibiotics, particularly cefotaxime. Small ion unitary conductance measurements of the isolated porins do not show significant differences between isolates. Thus, resistance does not appear to arise from major changes in pore size. Crystal structures of all four OmpC clinical mutants and molecular dynamics simulations also show that the pore size is essentially unchanged. Molecular dynamics simulations suggest that perturbation of the transverse electrostatic field at the constriction zone reduces cefotaxime passage through the pore, consistent with laboratory and clinical data. This subtle modification of the transverse electric field is a very different source of resistance than occlusion of the pore or wholesale destruction of the transverse field and points to a new mechanism by which porins may modulate antibiotic passage through the outer membrane.Peer reviewe
Calcium/calmodulin dependent protein kinase II δ modulates intracellular CA2+ release and cell proliferation in adult cardiac fibroblasts
No full textCalcium/calmodulin dependent protein kinase II δ (CaMKIIδ) is a well-recognised mediator of cardiomyocyte function and dysfunction, however little is known of its role in the cardiac fibroblast (CF). [Ca2+]i plays a crucial role in cell proliferation, yet the mechanism by which this is regulated in adult CFs remains elusive. We hypothesised that CaMKIIδ can regulate intracellular Ca2+ release channel activity and proliferation in adult CFs. Using Fura-2 loaded cells, we initially confirmed agonist-mediated intracellular Ca2+ release using Angiotensin II (1 µM). We demonstrated that CaMKIIδ and Inositol 1,4,5-triphosphate receptor type 2 (IP3R2) are both highly expressed in adult rat CFs but the ryanodine receptor (RyR2) is not. This identifies IP3R2 as the main intracellular Ca2+ release channel in these cells. To investigate whether CaMKIIδ modulates IP3R activity in CFs, cells were pre-treated with inhibitors autocamtide inhibitory peptide (AIP) (1 µM) and KN-93 (5 µM) prior to Angiotensin II application. Ca2+ release was significantly inhibited in the presence of both inhibitors (81±6.5% (AIP) vs 123±6% (control), p<0.001, n=4 and 65±4% (KN-93) vs 123±6% (control) respectively, p<0.001, n=4). Both CaMKII inhibition and IP3R inhibition also inhibit CFs proliferation (∼10% and 30% inhibition, AIP and 2-APB treatments respectively). The possibility that Ca MKIIδ may modulate IP3R2 activity directly via protein-protein interaction has also been explored using co-immunoprecipitation. Collectively, this study reveals for the first time that CaMKIIδ modulates intracellular Ca2+ release and proliferation in adult CFs and more specifically, that this may be modulated via physical interaction between CaMKIIδ and IP3R2
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