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One of the most challenging milestones for preterm infants is the acquisition of safe and efficient feeding skills. The majority of healthy full term infants are born with skills to coordinate their suck, swallow and respiration. However, this is not the case for preterm infants who develop these skills gradually as they transition from tube feeding to suck feeds. For preterm infants the ability to engage in oral feeding behaviour is dependent on many factors. The complexity of factors influencing feeding readiness has led some researchers to investigate the use of an individualised assessment of an infant's abilities. A limited number of instruments that aim to indicate an individual infant's readiness to commence either breast or bottle feeding have been developed. To determine the effects of using a feeding readiness instrument when compared to no instrument or another instrument on the outcomes of time to establish full oral feeding and duration of hospitalisation. We used the standard methods of the Cochrane Neonatal Review Group, including a search of the Cochrane Central Register of Controlled Trials (The Cochrane Library 2010, Issue 2), MEDLINE via EBSCO (1966 to July 2010), EMBASE (1980 to July 2010), CINAHL via EBSCO (1982 to July 2010), Web of Science via EBSCO (1980 to July 2010) and Health Source (1980 to July 2010). Other sources such as cited references from retrieved articles and databases of clinical trials were also searched. We did not apply any language restriction. We updated this search in March 2012. Randomised and quasi-randomised trials comparing a formal instrument to assess a preterm infant's readiness to commence suck feeds with either no instrument (usual practice) or another feeding readiness instrument. The standard methods of the Cochrane Neonatal Review Group were used. Two authors independently screened potential studies for inclusion. No studies were found that met our inclusion criteria. No studies met the inclusion criteria. There is currently no evidence to inform clinical practice, with no studies meeting the inclusion criteria for this review. Research is needed in this area to establish an evidence base for the clinical utility of implementing the use of an instrument to assess feeding readiness in the preterm infant population. Source

Current immunosuppressive/anti-inflammatory agents target the responding effector arm of the immune response and their nonspecific action increases the risk of infection and malignancy. These effects impact on their use in allogeneic haematopoietic cell transplantation and other forms of transplantation. Interventions that target activated dendritic cells (DCs) have the potential to suppress the induction of undesired immune responses (for example, graft versus host disease (GVHD) or transplant rejection) and to leave protective T-cell immune responses intact (for example, cytomegalovirus (CMV) immunity). We developed a human IgG1 monoclonal antibody (mAb), 3C12, specific for CD83, which is expressed on activated but not resting DC. The 3C12 mAb and an affinity improved version, 3C12C, depleted CD83+ cells by CD16+ NK cell-mediated antibody-dependent cellular cytotoxicity, and inhibited allogeneic T-cell proliferation in vitro. A single dose of 3C12C prevented human peripheral blood mononuclear cell-induced acute GVHD in SCID mouse recipients. The mAb 3C12C depleted CMRF-44+CD83bright activated DC but spared CD83dim/- DC in vivo. It reduced human T-cell activation in vivo and maintained the proportion of CD4+ FoxP3+ CD25+ Treg cells and also viral-specific CD8+ T cells. The anti-CD83 mAb, 3C12C, merits further evaluation as a new immunosuppressive agent in transplantation.Leukemia advance online publication, 2 October 2015; doi:10.1038/leu.2015.231. © 2015 Macmillan Publishers Limited Source

Lott W.B.,Queensland University of Technology | Doran M.R.,Queensland University of Technology | Doran M.R.,Materials Medical Research Institute
Trends in Biochemical Sciences

Complementary sequences at the 5' and 3' ends of the dengue virus RNA genome are essential for viral replication, and are believed to cyclise the genome through long-range base pairing in cis. Although consistent with evidence in the literature, this view neglects possible biologically active multimeric forms that are equally consistent with the data. Here, we propose alternative multimeric structures, and suggest that multigenome noncovalent concatemers are more likely to exist under cellular conditions than single cyclised monomers. Concatemers provide a plausible mechanism for the dengue virus to overcome the single-stranded (+)-sense RNA virus dilemma, and can potentially assist genome transport from the virus-induced vesicles into the cytosol. © 2013 Elsevier Ltd. Source

Barbier V.,Materials Medical Research Institute
Methods in molecular biology (Clifton, N.J.)

An important factor contributing to hematopoietic stem cell (HSC) mobilization is the ability of mobilizing cytokines and chemotherapy to disturb the cellular components of HSC niches, particularly osteoblasts and their progenitors, and to inhibit the production of HSC supportive cytokines and chemokines. Although the mechanisms by which niche cells are inhibited by mobilizing treatments is still incompletely understood, it has recently emerged that bone marrow macrophages play a critical role in maintaining osteoblasts, bone formation, and the expression of CXCL12, KIT ligand, and angiopoietin-1 necessary to HSC maintenance. In this chapter, we describe how to mobilize HSC into the blood in mice by depleting macrophages with clodronate-loaded liposomes and compare this mode of mobilization to mobilization induced by granulocyte colony-stimulating factor and cyclophosphamide. Detailed methods to analyze mobilization of phenotypic and functional reconstituting HSC are described with examples. Source

Coward J.,Materials Medical Research Institute | Harding A.,University of Queensland
Frontiers in Oncology

Tumor evolution presents a formidable obstacle that currently prevents the development of truly curative treatments for cancer. In this perspective, we advocate for the hypothesis that tumor cells with significantly elevated genomic content (polyploid tumor cells) facilitate rapid tumor evolution and the acquisition of therapy resistance in multiple incurable cancers. We appeal to studies conducted in yeast, cancer models, and cancer patients, which all converge on the hypothesis that polyploidy enables large phenotypic leaps, providing access to many different therapy-resistant phenotypes. We develop a flow-cytometry based method for quantifying the prevalence of polyploid tumor cells, and show the frequency of these cells in patient tumors may be higher than is generally appreciated. We then present recent studies identifying promising new therapeutic strategies that could be used to specifically target polyploid tumor cells in cancer patients. We argue that these therapeutic approaches should be incorporated into new treatment strategies aimed at blocking tumor evolution by killing the highly evolvable, therapy-resistant polyploid cell subpopulations, thus helping to maintain patient tumors in a drug sensitive state. © 2014 Coward and Harding. Source

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