Use of kidney failure risk equation as a tool to evaluate referrals from primary care to specialist nephrology care.

Background: With rising costs and burden of chronic kidney disease (CKD), timely referral of patients to a kidney specialist is crucial. Currently, Kidney Health Australia (KHA) uses a 'heat map' based on severity and not future risk of kidney failure, whereas the kidney failure risk equation (KFRE) score predicts future risk of progression.

Aims: Evaluate whether a KFRE score assists with timing of CKD referrals.

Maximising access to kidney transplantation: A single-centre audit of people receiving dialysis.

Background: Despite transplantation being well documented as the renal replacement therapy option that gives the best morbidity and mortality outcomes, the best quality of life and the best value for healthcare dollar, not all patients are on a kidney transplant waiting list.

Objectives: The aims of this study were (1) to explore possible reasons for a demonstrated a higher rate of people being listed as suitable for transplant in a non-transplanting unit and (2) to describe a formal process of review and referral as a method for maximising the number of people gaining access to the transplant waiting list.

Methods: We prospectively audited all patients who were undergoing dialysis in our metropolitan, non-transplanting renal unit annually over six years to determine whether not being on the transplant waiting list was in keeping with available eligibility guidelines of medical and behavioural criteria.

The focal adhesion targeting domain of p130Cas confers a mechanosensing function.

Members of the Cas family of focal adhesion proteins contain a highly conserved C-terminal focal adhesion targeting (FAT) domain. To determine the role of the FAT domain in these proteins, we compared wild-type exogenous NEDD9 with a hybrid construct in which the NEDD9 FAT domain had been exchanged for the p130Cas (also known as BCAR1) FAT domain. Fluorescence recovery after photobleaching (FRAP) revealed significantly slowed exchange of the fusion protein at focal adhesions and significantly slower two-dimensional migration.

NURSES' BEREAVEMENT NEEDS AND ATTITUDES TOWARDS PATIENT DEATH: A QUALITATIVE DESCRIPTIVE STUDY OF NURSES IN A DIALYSIS UNIT.

Background: Dialysis nurses have a unique relationship with their patients and often require bereavement support should a patient death occur. This study was conducted in 2014 and aimed to explore the attitudes of dialysis nurses to death and dying and to identify suitable bereavement strategies following a death of a patient.

Methods: A purposeful, convenience sample of all nurses employed in the dialysis service completed a demographic profile and The Death Attitudes Profile Revisited (DAP_R) survey.

PP2A phosphatase suppresses function of the mesenchymal invasion regulator NEDD9.

The mesenchymal mode of cancer cell invasion characterized by active adhesion turnover and a polarized actin cytoskeleton, is critically regulated by the adaptor protein NEDD9/HEF1/Cas-L. While it is known that NEDD9 is subject to extensive phosphorylation modification, the molecules that determine NEDD9 phosphorylation to stimulate adhesion turnover and mesenchymal cell morphologies are currently unknown. Earlier studies have suggested that the serine/threonine phosphatase PP2A regulates interconversion between a low molecular mass NEDD9 phosphoform and higher molecular mass phosphoforms.

Essential biological processes of an emerging pathogen: DNA replication, transcription, and cell division in Acinetobacter spp.

Within the last 15 years, members of the bacterial genus Acinetobacter have risen from relative obscurity to be among the most important sources of hospital-acquired infections. The driving force for this has been the remarkable ability of these organisms to acquire antibiotic resistance determinants, with some strains now showing resistance to every antibiotic in clinical use. There is an urgent need for new antibacterial compounds to combat the threat imposed by Acinetobacter spp.

Role of conserved active site residues in catalysis by phospholipase B1 from Cryptococcus neoformans.

Phospholipase B1 (PLB1), secreted by the pathogenic yeast Cryptococcus neoformans, has an established role in virulence. Although the mechanism of its phospholipase B, lysophospholipase, and lysophospholipase transacylase activities is unknown, it possesses lipase, subtilisin protease aspartate, and phospholipase motifs containing putative catalytic residues S146, D392, and R108, respectively, conserved in fungal PLBs and essential for human cytosolic phospholipase A2 (cPLA2) catalysis. To determine the role of these residues in PLB1 catalysis, each was substituted with alanine, and the mutant cDNAs were expressed in Saccharomyces cerevisiae.

N-linked glycosylation sites affect secretion of cryptococcal phospholipase B1, irrespective of glycosylphosphatidylinositol anchoring.

Secreted phospholipase B enzymes (PLB1) with high levels of N-linked glycosylation are proven fungal virulence determinants. We demonstrated that removal of N-linked glycans from secreted cryptococcal PLB1 leads to loss of enzyme activity. To determine if individual N-glycan attachment sites affect secretion of active enzyme, we altered three along the entire length of the protein, by site-directed mutagenesis, namely Asn56, Asn430 and Asn550 to Ala, in wild-type PLB1 (full length) and a glycosylphosphatidylinositol (GPI) anchorless version (PLB1(GPI-)) that is hypersecreted due to lack of membrane association.

Secretion of cryptococcal phospholipase B1 (PLB1) is regulated by a glycosylphosphatidylinositol (GPI) anchor.

The secreted, multifunctional enzyme PLB1 (phospholipase B1 protein encoded by the PLB1 gene) is a virulence determinant of the pathogenic fungus Cryptococcus neoformans, but the mechanism of its secretion is unknown. The cryptococcal PLB1 gene encodes putative, N-terminal LP (leader peptide) and C-terminal GPI (glycosylphosphatidylinositol) anchor attachment motifs, suggesting that PLB1 is GPI-anchored before secretion. To investigate the role of these motifs in PLB1 secretion, four cDNA constructs were created encoding the full-length construct (PLB1) and three truncated versions without the LP and/or the GPI anchor attachment motifs [(LP-)PLB1 (PLB1 expressed without the LP consensus motif), (LP-)PLB1(GPI-) (PLB1 expressed without the LP and GPI consensus motifs) and PLB1(GPI-) (PLB1 expressed without the GPI anchor attachment motif) respectively].