The anova test was used to analyze the results of phagocytosis in the study. The growth of P. aeruginosa PAO1 was monitored for 48 h to determine any effect of ginseng on bacterial growth. Growth of the culture was monitored by OD measurements from inoculation to the stationary phase. The results showed that ginseng does not inhibit PAO1 growth, but if anything,

had a weak stimulating effect (Fig. 1). Similar results were obtained with the mucoid strain of P. aeruginosa PDO300 and the clinical isolate of P. aeruginosa NH57388A (data not shown). Nonmucoid P. aeruginosa wild-type PAO1 and its isogenic mucoid derivative PDO300 were cultured for 3 days in flow chambers in the presence or absence of 0.5% medium-supplemented ginseng extract. In the absence of find more ginseng, both mucoid and nonmucoid strains formed biofilms in the flow chambers, but the morphology of the biofilms of the two stains was different (Fig. 2). PAO1 formed a relatively flat biofilm, whereas PDO300 formed biofilms with distinct microcolonies. In contrast, the development of biofilms in both bacterial strains in the presence of 0.5% of ginseng was significantly inhibited (Fig. 2b and d). Moreover, biofilms formed by PAO1 and EPZ-6438 manufacturer PDO300 without ginseng were tolerant to the treatment of tobramycin

in 20 μg mL−1 for 24 h, whereas biofilms of the two strains developing poorly in the presence of 0.5% ginseng were sensitive to tobramycin, and most of the bacterial cells were eventually killed (Fig. 2b and d). Biofilms of wild-type PAO1, mucoid PDO300 and a mucoid clinical isolate NH57388A were developed

in flow chambers for 7 days, after which the medium was supplemented with 0.5% ginseng extract. Surprisingly, after exposure to Edoxaban the ginseng-supplemented medium, the biofilms of the three stains were gradually removed with few or no live bacteria after 20 h of exposure to ginseng (Fig. 3). The biofilm of nonmucoid wild-type PAO1 showed nearly no living bacterial cells after 10 h of exposure to the ginseng extract (Fig. 3a). The PAO1 biofilm disappeared much faster than the two mucoid biofilms (Fig. 3b and c). Constant observations under CLSM revealed that a rapid movement and dissolution of the cellular mass took place inside the preformed biofilms. This phenomenon was observed for all strains including the clinical isolate of NH57388A. The motility of the P. aeruginosa bacterial cells was in general elevated after exposure to ginseng (data not shown). Swarming motility has been characterized as flagella-dependent movement on viscous surfaces. The effect of 0.25% of ginseng on the swarming motility of P. aeruginosa PAO1, the isogenic fliM mutant and the mucoid PDO300 was evaluated. Swarming was only observed in the plate of PAO1 in the absence of ginseng. This result suggests that ginseng reduces the swarming motility of P. aeruginosa PAO1 (Fig. 4a). The swimming motility of P. aeruginosa also depends on flagellar movement.

LI YANHONG1, LI MENGXIA1, LI XIAOZHONG1, FENG XING2 1Department of nephrology, Children’s Hospital of Soochow University; 2Department of neonatology, Children’s Hospital of Soochow University Introduction: Acute kidney injury (AKI) is an independent risk factor for mortality. Since multiple selleck inhibitor factors that influence kidney function and predispose to the development of AKI occur in combination in the neonates, critically ill neonates are at a high risk of having AKI. Cystatin-C is normally filtered freely and completely reabsorbed and catabolized in the proximal tubule. The appearance of increased concentrations of CysC in urine reflects renal tubular injury. In neonates, urinary cystatin-C is demonstrated to be a biomarker

for predicting AKI. This study evaluated the value of urinary cystatin-C level during the first day of life and determined whether urinary cystatin-C can predict mortality in the critically ill neonatal population. Methods: We enrolled 98 critically ill neonates who were admitted to a neonatal intensive care unit this website during the first day of life between July 2010 and April 2011. Urinary samples were collected in the first 24 hours after admission, and the level of cystatin-C was determined. The score for neonatal acute physiology (SNAP) were calculated during the first

24 hours after admission. Major outcome measure was 30-days mortality. Results: Of the 98 neonates, 7 (7.1%) died during the first 30 days of life. The median (min-max range) urinary cystatin-C level in critically ill children was 0.6 mg/g urinary Creatinine (0.0–65.5). The urinary cystatin-C level during the first day of life was significantly associated with 30-days mortality (odds ratio [OR] = 1.28; 95% confidence interval [CI], 1.02–1.60; p = 0.030), even after adjustment for gestational age, gender, and the severity of illness assessed by the SNAP score. Multivariate regression analysis showed

that high urinary cystatin-C level, high SNAP score (OR = 1.24; 95% CI, 1.01–1.53; p = 0.041), and mechanical ventilation (OR = 15.79; 95% CI, 1.69–153.10; p = 0.017) were independent risk factors for 30-days mortality in generally critically ill neonates. Urinary cystatin-C achieved an area under-the-receiver-operating-characteristic curve (AUC) of 0.85 (95% CI, 0.74–0.96; p = 0.005) for predicting 30-days mortality, which was Arachidonate 15-lipoxygenase similar to SNAP (AUC = 0.83; 95% CI, 0.71–0.95; p = 0.008). Urinary cystatin-C displayed a sensitivity of 83% and a specificity of 80% to predict 30-days mortality at an optimal cut-off value. Conclusion: A high urinary level of cystatin-C during the first day of life is independently associated with and predictive of 30-days mortality in the general population of critically ill neonates. JEYAKUMAR YOGARANI1, AGUIAR SANDRA2 1Monash Health; 2Monash Health Introduction: Focal Segmental Glomerulosclerosis(FSGS) is a glomerular disease that can affect both children and adults.

[37] However, this

was demonstrated only in vitro in a non-physiological concentration of MnCl2 using X-396 cost isolated RSS substrates and not in the physiological 12RSS and 23RSS pair.[37] The in vivo scenario is still unclear though it is commonly thought that Mg2+ is the physiological divalent metal ion involved in RAG-mediated cleavage. RAG1 and RAG2 are assisted by high mobility group proteins of the HMG-box family (HMGB1 and HMGB2) for bringing two signal ends together. The HMG proteins interact with the nonamer binding domain of RAG1 in the absence of DNA and enhance its intrinsic DNA bending activity.[38] Following resolution of the hairpin structure, the coding ends are joined to create the exon, which forms the antigen-binding region of the antigen receptors (Fig. 2c). The signal ends remain bound to RAGs, which in turn protect the IDO inhibitor ends from further nuclease digestion [36, 39] (Fig. 2c). The blunt-ended signal ends can be directly ligated without any modification, while the coding ends undergo further processing (Fig. 2c).[34,

35] The hairpin at the coding end is opened and joined together by non-homologous end joining (NHEJ), the DNA double-strand break repair pathway.[40, 41] Artemis, in conjunction with DNA-PKcs, acts as an endonuclease and resolves the hairpins formed during V(D)J recombination.[42] Ku heterodimer, consisting of Ku70 and Ku80, binds to the broken DNA ends and forms a complex with DNA-PKcs.[43] Artemis has an inherent 5′-3′ exonuclease activity, whereas in association with DNA-PKcs it acts as a 5′-3′ endonuclease.[42] The ends are filled in by the Pol X family of polymerases namely Pol μ and

PJ34 HCl Pol λ. Mice deficient in Pol μ are shown to have shorter immunoglobulin light chain V to J junctions,[44] while those lacking Pol λ have shorter immunoglobulin heavy-chain D to J and V to DJ junctions.[45] In addition, Pol μ plays a role in the processing of 3′ ends while Pol λ processes the 5′ ends.[45] This would suggest that Pol μ is involved in V(D)J recombination, but not Pol λ.[46] The ligase IV/XRCC4 complex ligates the processed ends[47, 48] with the help of XLF.[49, 50] Ku70, Ku80, XRCC4 and Ligase IV are considered to be the ‘core’ NHEJ factors as these proteins were conserved during evolution and are required for all known NHEJ reactions.[51, 52] These are also inevitable for the joining of both coding and signal ends. On the other hand, DNA-PKcs and Artemis are believed to have evolved more recently and are needed only for the joining of coding ends.[52] At the time of joining of V, D and J subexons, several modifications like insertions and deletions can occur at the junctions resulting in further increase in the antigen receptor diversity. Asymmetric hairpin opening at the coding ends due to nicking a few bases away from the terminus results in one DNA strand longer than the other.

Such an exchange of information and publicity will promote our missions, collaboration Vadimezan clinical trial and

coordination in this area. The 4th AFCKDI meeting will be held in Seoul on 4 June 2010 to discuss results of these work groups. We need to expand our network of collaborative initiative to broader areas and countries in order to make this initiative truly representative of our region. “
“The Northern Hospital, Epping, Vic., Australia “
“Novartis is delighted to report on the renal cases program held in 2011. The program was initiated with the aim of fostering and sharing innovation, development and the highest standards in the understanding and clinical management of renal transplantation in Australia. This initiative was developed as part of the Novartis commitment to encouraging interest and education in the practice of Transplant Nephrology. Entries for these awards could be made by any RACP Nephrology Advance Trainee currently working in Australia. The case reports submitted for the program were judged

by an independent panel of distinguished Nephrologists who selected the top five case reports according to: Scientific interest We are delighted to sponsor the publication of the top five cases, as chosen by the Panel, to be published in no particular order in this supplement of Nephrology. Novartis Crenolanib mw looks forward to providing more innovative programs as part its commitment to excellence in the practice and research within the field of transplantation. old “
“On behalf of the Asian Pacific Society of Nephrology (APSN) and Japanese Society of Nephrology (JSN), I am pleased to welcome you to the 14th Asian

Pacific Congress of Nephrology (APCN), May 14–17, 2014. The APSN aims to promote and encourage the advancement of scientific knowledge and research in all aspects of nephrology, and to promote the exchange and dissemination of this knowledge in the Asian-Pacific area. We would like to encourage you to join us in discussing the many issues surrounding inflammatory or metabolic renal diseases, acute kidney injury (AKI), and renal replacement therapy (RRT). The three main symposia of APCN 2014 will cover the fields of IgA nephropathy, diabetic nephropathy, and chronic kidney disease (CKD). Moreover, at APCN 2014 we will continue our planned collaboration with the JSN 2013 and APCN 2014 Cooperative Project – the Young Investigators Award for Asian Nephrologists (YIAAN) Session – in order to enhance support for young nephrologists from Asia. This gives opportunities to more researchers than ever before the benefit of learning about various researches from all over Asia. More than 550 abstracts from 24 countries have been accepted for either oral or poster presentations. A wide choice of symposium and CME programs focused on the various fields of basic and clinical nephrology will run throughout the congress.

These recommendations have led to changes in clinical practice, yet they are not based on high level evidence. In fact, most reported studies argue that dialysis should be started early rather than late, many are confounded and a number have reached the opposite conclusion. Probably more important than a prescribed level of renal function at which dialysis is initiated is the widespread

adoption of a structured approach www.selleckchem.com/products/dabrafenib-gsk2118436.html to pre-dialysis care and the recognition of the importance of pre-dialysis patient education. One of the main determinants of optimal initiation of dialysis is the time of referral of the patient to a nephrologist or a renal unit. In particular, early referral of patients with chronic kidney disease allows a planned initiation of dialysis, using from the start permanent vascular or peritoneal dialysis access. There are a number of studies suggesting that early initiation of dialysis for end-stage kidney disease (ESKD) results in improved morbidity, mortality and quality of life. Most of these studies are cohort or case–control, and to date there are no randomized controlled studies examining the question. Bonomini et al.1 reported amongst patients initiated on chronic dialysis

when creatinine clearance (CCr) was between 15 and 20 mL/min, a 4 year survival Deforolimus cell line of 85% at a time when the 4 year survival in the USA was less than 50%. Hakim and Lazarus2 later proposed that the beneficial effect of earlier initiation of dialysis could be attributed to better nutritional status at baseline. Many of the published studies

were not designed to specifically examine this question, or are confounded by factors such as referral and lead-time bias. For example, in the Canada–USA (CANUSA) study,3 which was not designed to examine time of initiation Tolmetin of dialysis, 1 and 2 year survival was higher for those patients starting continuous ambulatory peritoneal dialysis (CAPD) with an initial glomerular filtration rate (GFR) of more rather than less than 38 L/week (∼4 mL/min). A retrospective study from Glasgow4 showed an impaired survival for those patients starting with a CCr greater than the median of 8.3 mL/min; however, when survival was recalculated from the time at which CCr was 20 mL/min, the time of initiation of dialysis had no influence on outcome. The published studies up until mid-2004 are summarized on the website of the Australian clinical guidelines group CARI (Caring for Australasians with Renal Impairment).5 Since the time of the latest CARI review,5 there have been more studies suggesting improved outcome with early initiation of dialysis, but the quality of these studies is no better. Tang et al.6 reported that patients who started chronic dialysis electively when their GFR reached 10 mL/min or lower, had a better 1 year survival than the initial refusers who started dialysis when they developed a uraemic emergency.

Secondly and more importantly, reactivation of bradyzoites to tachyzoites presents profound clinical complications in the immune-compromised host and may lead to potentially fatal neurological diseases as a result of unrestrained tissue destruction (52,53). Understanding the molecular basis of this process, therefore, holds promise for the identification of novel drug targets to effectively eliminate Toxoplasma cysts and/or prevent their reactivation. Stage differentiation is marked by significant morphological and physiological remodelling, which is prompted by extensive alterations in gene expression (35,54). The first unbiased

genome-wide BGB324 mouse query for developmentally regulated genes compared ESTs isolated from tissue cysts with a tachyzoite EST library (55,56). Many genes with unique ESTs in bradyzoites were identified including some previously known bradyzoite-specific genes. The most comprehensive published analysis of developmentally regulated gene expression to date has been performed using serial analysis of gene expression (SAGE) (41). With a 4× coverage of the total mRNA pool of Toxoplasma, transcript abundance was examined progressively through the tachyzoite-to-bradyzoite differentiation process. Almost 700 unique SAGE tags were found to be up-regulated in bradyzoites

relative to tachyzoites. Conversely, genes whose products are involved in high-activity PD0325901 price functions

such as DNA replication and cell division, endocytosis and metabolism were observed to be down-regulated in day 15 in vitro-induced bradyzoites. These findings are consistent with the characteristic decreased growth and activity of bradyzoites and provide an important lead for addressing the regulatory mechanism of this critical stage of the asexual cycle. Analysis of gene expression in stage differentiation mutants has also been explored RVX-208 quite extensively in an attempt to identify gene interactions and pathways that might be required for this process (36,37,57). Using microarrays, global gene expression changes have been compared between differentiation mutants and wild-type strains under different bradyzoite induction conditions. Results from these studies suggest a common pathway for bradyzoite induction, downstream of individual stress response genes, which is able to integrate different induction stimuli to produce bradyzoite phenotypes. Similar expression profiles were observed for a core set of genes under different induction conditions, suggesting that these genes may play a critical role in differentiation (37). All these and other major advances counted, our understanding of stage differentiation still remains incomplete. For instance, a sensory mechanism that detects environmental stress and triggers the differentiation cascade has yet to be identified.

Immunization with 25k-hagA-MBP induced high levels of antigen-specific serum IgG learn more and IgA, as well as salivary IgA. High level titers of serum IgG and IgA were also induced for almost 1 year. In an IgG subclass analysis, sublingual immunization with 25k-hagA-MBP induced both IgG1 and IgG2b antibody responses. Additionally, numerous antigen-specific IgA antibody-forming cells were detected from the salivary gland

7 days after the final immunization. Mononuclear cells isolated from submandibular lymph nodes (SMLs) showed significant levels of proliferation upon restimulation with 25k-hagA-MBP. An analysis of cytokine responses showed that antigen-specific mononuclear cells isolated from SMLs produced significantly high levels of IL-4, IFN-γ, and TGF-β. These results indicate that sublingual immunization with 25k-hagA-MBP induces efficient protective immunity against P. gingivalis infection in the oral cavity via Th1-type and Th2-type cytokine production. Periodontal disease is a chronic inflammatory malady that causes both alveolar bone absorption followed by tooth loss, as well as systemic

diseases such as cardiac disease (Destefano et al., 1993), diabetes mellitus (Roeder & Dennison, 1998), osteoporosis (Krejci, 1996; Reddy, 2002), and premature, low-birth-weight babies (Offenbacher et al., 1996). Therefore, Talazoparib cost prevention or treatment of periodontal disease is very important for maintaining

health. Porphyromonas gingivalis, which is a gram-negative and asaccharolytic anaerobic bacterium with high adherence activity to erythrocytes and epithelial Sitaxentan cells, is one of the major virulent bacteria causing periodontal disease. It exerts virulence through fimbriae, lipopolysaccharides, outer membrane proteins, and outer membrane vesicles (Holt et al., 1999). Hemagglutinin protein, which is expressed on the cell surface of P. gingivalis, regulates bacterial adhesion to the host cells, as well as agglutinates and hemolyzes erythrocytes. Multiple hemagglutinin genes have been cloned from P. gingivalis by functional screening (Lee et al., 1996; Lépine et al., 1996; Song et al., 2005). Among these, hemagglutinin A (hagA) is thought to possess a functional domain and thus to be a potential candidate for periodontal vaccination. Previous studies have demonstrated the efficacy of mucosal immunization for delivering vaccines, which induces mucosal and systemic immune responses via oral (Yamamoto et al., 1997; Liu et al., 2010), nasal (Koizumi et al., 2008; Momoi et al., 2008), and sublingual routes (Cuburu et al., 2007; Song et al., 2008; Zhang et al., 2009). Of the vaccination methods available, sublingual vaccination has recently been reported to induce significant antibody (Ab) production in nasal, bronchial, and oral mucosa (Cuburu et al., 2007; Zhang et al., 2009).

In addition, two out of five mice injected with C2del developed a high level of anti-cardiolipin antibodies (Fig. 4C). These results suggested that C2del could be responsible for the development of SLE in the patient. Approximately 70% of human genes have alternatively spliced transcripts 23. While alternative splicing

generally facilitates the synthesis of click here a greater variety of proteins, mutations disrupting the splice sites or their regulatory elements can cause hereditary disease through the production of aberrant transcripts 24. In this report, we described SLE patients whose MFG-E8 mRNA carry an insertion of 102 nt that resembles a cryptic exon. A splicing assay using a human MFG-E8 minigene carrying intron 6 revealed that the aberrant splicing of the MFG-E8 gene was caused by an A-to-G mutation in the intron. The inclusion of the cryptic exon in the transcript, as a result of this mutation, may be explained by the generation of a GGG motif, an intronic splicing enhancer 25, 26, which activates an exon choice by interacting with trans factors that regulate splicing 27, 28 The cryptic exon incorporated in C2del had a premature termination codon located in the C2 domain of human MFG-E8. In general, mRNA that contain premature termination codons are eliminated by an mRNAs surveillance

mechanism called nonsense-mediated mRNA decay (NMD) 29. In fact, see more in a splicing assay with the MFG-E8 minigene, the transcripts containing the cryptic exon increased when the premature termination was blocked by treating Mannose-binding protein-associated serine protease the cells with cycloheximide or by removing the termination codon with site-directed mutagenesis (data not shown). On the other hand, a significant proportion of the MFG-E8 transcripts from the patient

carried the cryptic exon. There are two possible explanations for this discrepancy: (i) the efficiency of NMD is different between HEp-2 and human peripheral blood mononuclear cells 30, and (ii) the mutant transcript may be more stable in the white blood cells of the patient. In addition, the NMD efficiency is known to differ among individuals. For example, the same mutation that leads to premature termination in the dystrophin gene can cause a mild (Becher muscular dystrophy) or more severe (Duchene muscular dystrophy) phenotype in different individuals 31. Wild-type human MFG-E8 has an apparent Mr of 46 kDa, carries three N-glycosylation sites, and is glycosylated. C2del retained only one of the glycosylation sites, yet its molecular weight increased to 50 kDa, due to higher glycosylation. This aberrant glycosylation was observed in other cell lines, such as HEK293T cells (data not shown), confirming that it was an intrinsic property of C2del, and is not due to the host cell lines.

[79] Dendritic cells and macrophages also

express a combination of surface markers that defines a particular function, for example antigen uptake and presentation. Antigen uptake induces the expression of the costimulatory molecules CD68, CD80 and CD86 on macrophages and DCs in mice and human kidneys.[91, 93, 101-104] Resident renal DCs capture antigens via phagocytosis, pinocytosis and receptor-mediated endocytosis, all functions typically ascribed to macrophages.[104] Ferrostatin-1 price Following antigen uptake, DCs migrate to secondary lymphoid organs where they reduce the expression of costimulatory molecules and gain the ability to activate and prime T cells through increased expression of MHC II. This specialized function of DCs, although potent, is not exclusive. Macrophages also migrate and present antigens,[105, 106] and display an almost complete overlap in MHC II expression with F4/80 mononuclear phagocytes in mucosal sites and kidneys.[102, 107] Macrophages and DCs also occupy overlapping anatomical sites within the normal kidney. During steady state, macrophages identified using F4/80 form an intimate relationship with renal TECs as they are found adjacent to the basement membrane of proximal TECs in the outer medulla.[108] DCs defined by CD11c expression are absent

from the glomerulus, but are localized to the tubulointerstitium with overlapping expression with F4/80 in mice.[91] Renal biopsies from normal human kidneys show an abundance of DCs in the tubulointerstitium learn more that are absent in the glomeruli.[101] The localization of DCs strictly within the renal tubulointerstitium is

suggested to be optimal for antigen capture.[109, 110] Soos et al.[93] characterized the anatomy and phenotype of resident DCs Histone demethylase within normal mouse kidneys using the heterozygous CX3CR1GFP/+ mice. Laser scanning microscopy identified CX3CR1+ DCs throughout the entire renal interstitium, including the glomeruli, with dendrite processes extending between the TECs and into the tubular lumen. This DC population was defined by CX3CR1 expression alone. Profiling these cells by flow cytometry revealed that the majority of CX3CR1+ cells exhibited high levels of CD11c and F4/80, and low CD11b expression, thus raising concerns as to whether these cells only represented DCs. The cells expressing CX3CR1 are not fully defined in mice, but are generally homogeneous and indistinguishable from tissue macrophages and infiltrating monocytes, and in some settings cannot migrate to draining lymph nodes or present antigen.[111] In a more recent study using transgenic mice that express GFP and the diphtheria toxin receptor (DTR) driven by the CD11c promoter (CD11c-DTR) revealed CD11c-GFP cells displayed a typical DC morphology that localized to the tubulointerstitium, and not within the glomeruli, as consistent with previous reports.

Excluded were RTR who were not followed at RMH beyond 3 months post operatively, or had SC before transplant. Individual data was included only in those years when that patient

had a functioning graft for at least 3 months. Immunosuppression regimen in nearly all patients was prednisolone, mycophenolate and CNI (cyclosporine pre 2004, then tacrolimus), and all patients were routinely advised to minimise UV exposure. Results: In a total of 1154 RTRs, 410 SCs were diagnosed in 103 patients (73 male): 247 SCCs, 159 BCCs and 4 melanomas. Commonest sites were www.selleckchem.com/products/azd3965.html head n neck, followed by trunk, legs, arms and hands. Average annual incidence of all SC (SCC/BCC) over 15 years was 1.9 ± 0.9% (1.5 ± 0.8%/1.0 ± 0.7%), and no significant trend was seen over time. Conclusions: The annual incidence of SC in RTR followed in our centre has not changed over the past 15 years. 256 ACCESS TO EVALUATION, LISTING AND RENAL TRANSPLANT AMONGST MINORITY RECIPIENTS A HARFORD, O MYERS, P SINGH, E ALAS, M DAVIS, M UNRUH University of New Mexico, Albuquerque, New Mexico, USA Aim: To examine access to renal transplant (RTXP) in minority End Stage Renal Disease

(ESRD) patients. Background: Ethnic and racial minority patients including American Indians (AI) and Hispanics (HSP) have higher rates of ESRD but decreased rates of renal transplant compared to CH5424802 datasheet non-Hispanic whites (NHW). Possible causes for this decreased access to transplant have been proposed including referral bias, distance from the transplant centre, cultural and religious taboos against transplant, as well as financial and insurance barriers to workup. Methods: A retrospective analysis of the UNM database identified 374 potential recipients PtdIns(3,4)P2 referred for RTXP evaluation between 2008 and 2014 who completed workup and considered appropriate candidates for RTXP and placed on the priority list for RTXP. 15 patients were excluded from this analysis because of incomplete data. Of the 359 patients evaluated 331 were listed and 65 patients underwent RTXP. Statistical analysis included univariate tests (Fisher exact and Cochran-Armitage trend tests). Logistic regression was used to assess association

between transplant rate and the distance to the transplant facility (km). Results: Evaluated, Listed, and Transplanted patients were analysed for Race/Ethnicity, Age, and distance in km to Facility. There was a modest effect of Race/Ethnicity: on listing : 81% AI, 90% HSP and 92% NHW progressed from evaluation to listing (P = 0.04). 14%AI, 18%% HSP and 25% NHW were transplanted (P = 0.38). Rates of listing increased with age (P = 0.02). Transplant rate decreased with distance to the transplant facility only for AI, OR = 0.48 per 100 km (CI 0.27,0.87) OR = 1.07 per 100 km (0.78,1.45) for HSP and 0.82 (0.53, 1.27) for NHW. Conclusions: AI experienced decreased listing and decreased transplant rates with increasing distance to the RTXP facility.