1(a), LTC4 increased in a dose-dependent manner, the expression of MHC class II on immature DCs was more significant at 10−8 m, so the trials were conducted using this concentration. Then, considering that LTC4 is released during inflammatory responses,17,30 we studied the effect of LTC4 (10−8 m) on the phenotype of immature DCs and LPS-stimulated DCs. Interestingly, after MAPK inhibitor 18 hr of culture, LTC4 strongly inhibited the expression of CD86 and CD40 molecules (Fig. 1b,c,f) when DCs were activated with 1 μg/ml LPS, whereas the lipid mediator

had no effect on immature DCs. However, in the case of the class II molecules, LTC4 had antagonistic effects depending on the activation status of DCs, increasing its expression in immature DCs and inhibiting in LPS-treated DCs (Fig. 1d,f). As shown in Fig. 1(g), although MHC class II decreased its expression in LPS-activated DCs, LTC4 had the ability to prime T lymphocytes, because it induced a low but significant increase Seliciclib in the allostimulatory response mediated by activated DCs. This effect was also observed in immature DCs, which correlates with the increased expression of class II molecules by LTC4. Immature DCs are specialized to

sense the microenvironment and when stress or infection are detected they incorporate the antigen through phagocytosis or endocytosis.28,29,31,32 We aimed to determine whether LTC4 was able to affect the antigen uptake of immature and activated DCs. To this end, cells were treated or not with LPS (1 μg/ml) for 30 min at 37°, then DCs were incubated without or with 10−8 m LTC4 for 30 min at 37°. Finally, cells were washed and incubated in the presence of Zy (10 particles/DC) coupled to FITC for 30 min at room temperature or DX-FITC (100 μg/ml) for 40 min at 37°. The phagocytosis controls were supplied by DCs treated with cytochalasin B, a disruptor of actin microfilaments, 33 previous to their incubation with Zy-FITC. For DX endocytosis, the control of reaction was provided by DCs incubated with the antigen at 4°, because this is a temperature-dependent phenomenon. In

addition, we analysed the uptake of HRP. For this, after treatment with LTC4 (0·01 μm) of both DCs and LPS-stimulated DCs, these were cultured with 150 μg/ml HRP for 40 min at 37°. Subsequently, cells were washed Tangeritin several times with cold PBS and permeabilized by addition of 0·5% Triton X-100 in PBS for 30 min at room temperature. The control was provided by DCs treated with HRP but not permeabilized. Finally, the enzymatic activity was measured in supernatants of reaction by addition of the substrate [alpha-phenylendiamine (OPD)] and read at 492 nm. In Fig. 2(a), we demonstrated that LTC4 increased the phagocytosis of Zy-FITC by immature DCs but had no effect in LPS-activated DCs. In contrast, as shown in Fig. 2(b,c), uptake of DX and HRP was increased by LTC4 in both immature and LPS-stimulated DCs.

“
“This study evaluated the potential of plasma treatments to modify the surface chemistry and hydrophobicity of a denture base acrylic resin to reduce the Candida glabrata adhesion. Specimens (n = 54) with smooth surfaces were made and divided into three groups (n = 18): control – non-treated;

experimental groups – submitted to plasma treatment (Ar/50 W; AAt/130 W). The effects of these treatments on chemical composition and surface topography of the acrylic resin were evaluated. Surface free energy measurements (SFE) were performed after the treatments and after 48 h of immersion in water. For each group, half (n = 9) of the specimens were preconditionated with saliva before the adhesion assay. The number of adhered C. glabrata was evaluated

Cobimetinib datasheet by cell counting after crystal violet staining. The Ar/50 W and AAt/130 W treatments altered the chemistry composition, hydrophobicity and topography of acrylic surface. The Ar/50 W group showed significantly lower C. glabrata Selleck INCB024360 adherence than the control group, in the absence of saliva. After preconditioning with saliva, C. glabrata adherence in experimental and control groups did not differ significantly. There were significant changes in the SFE after immersion in water. The results demonstrated that Ar/50 W treated surfaces have potential for reducing C. glabrata adhesion to denture base resins and deserve Florfenicol further investigation, especially to tailor the parameters to prolong the increased wettability. “
“The respiratory tract of cystic fibrosis patients is colonised by bacteria and fungi. Although colonisation by slow growing fungi such as Pseudallescheria, Scedosporium and Exophiala species has been studied previously, the colonisation rate differs from study to study. Infections caused by these fungi have been recognised,

especially after lung transplants. Monitoring of respiratory tract colonisation in cystic fibrosis patients includes the use of several semi-selective culture media to detect bacteria such as Pseudomonas aeruginosa and Burkholderia cepacia as well as Candida albicans. It is relevant to study whether conventional methods are sufficient for the detection of slow growing hyphomycetes or if additional semi-selective culture media should be used. In total, 589 respiratory specimens from cystic fibrosis patients were examined for the presence of slow growing hyphomycetes. For 439 samples from 81 patients, in addition to conventional methods, erythritol–chloramphenicol agar was used for the selective isolation of Exophiala dermatitidis and paraffin-covered liquid Sabouraud media for the detection of phaeohyphomycetes. For 150 subsequent samples from 42 patients, SceSel+ agar was used for selective isolation of Pseudallescheria and Scedosporium species,and brain–heart infusion bouillon containing a wooden stick for hyphomycete detection.

CD4+CD25− and CD8+ T cells

were isolated from pooled spleen and lymph node using negative selection of B cells by panning followed by positive selection using FACS Aria. Collagenase treated BALB/c splenocytes were enriched for CD11c+ cells by CD11c-labeled beads and MACS sorting. These CD11c enriched populations were FDA-approved Drug Library screening further sorted for CD11c+CD8− DC using FACS Aria flow cytometer. For proliferation, T cells (20 000 cells/well) were cultured in anti-CD3 coated 96-well plate (flat bottomed) in RPMI 1640 (Mediatech) supplemented with 50 μM 2-ME (Fisher Scientific), 5% FBS (Biowhitaker), 10 mM HEPES (Invitrogen), penicillin and streptomycin (Cellgro) and 2 mM glutamine (Cellgro). Cells were pulsed after 72 h with 0.5 mCi of 3H-thymidine (GE healthcare) for the next 12 h and 3H-thymidine see more incorporation was determined using beta scintillation counter (Perkin Elmer). For stimulation of T cells with

allogenic APC, CD4+CD25− T cells (15 000/well) or CD8+ T cells (30 000 cells/well) were cultured with a graded dosage of CD4−CD8− spleen cells from F1 (CBAxC57BL/6) or CD11c+CD8− DC (4000/well). Four to five days later, proliferation of cells was determined by 3H-thymidine incorporation as above. For cell cycle and apoptosis determination, T-cells (0.25×106/well) were cultured on anti-CD3 coated (1 μg/mL) 24-well plates in 2 mL complete medium. At indicated time cells were harvested and analyzed for apoptosis using annexin-V and 7-AAD staining or cell cycle. Teicoplanin For cell cycle, cells were fixed with ice cold 70% methanol and stored at −20°C for at least 1 day. Methanol fixed cells from all the time points were collected and

stained with 50 μg/mL of PI (Sigma) in the presence of 100 μg/mL of RNase followed by Flow cytometric analysis. For EdU incorporation, cells were pulsed with 10 mM of EdU (Invitrogen) for 3.5 h. Cells were harvested and incorporation of EdU and cell cycle was determined using the CLICK–iT EdU kit (Invitrogen) according to manufacturer’s recommendations. EG.7 (EL-4 transfected with OVA) were injected subcutaneously in left flanks of mice (106/mouse). At indicated time growth of tumor was monitored, and measured as perpendicular and vertical diameters. For determination of in vivo CTL activity, syngeneic spleen cells were labeled with two concentrations of CFSEhigh and CFSElow. CFSEhigh cells were further pulsed with 100 μg/mL of OVA-peptide SIINFEKL for 45 min. CFSEhigh and CFSElow cells were mixed at equal ratio (50:50) and injected intravenously into EG.7 transplanted mice and naive B6 mice as control. Four hours later spleen cells from recipient mice were harvested and ratio of CFSEhigh and CFSElow cells were determined using flow cytometry. The ratio of CFSEhigh and CFSElow cells obtained from naive B6 recipient was taken as no killing of CFSEhigh cells. We thank Dr. Andrew Mellor, Dr. Phillip Chandler, Dr. David H. Munn, Dr. G. Zhou, Dr. Yukai He and Dr.

Serum IL-12p40 was measured by ELISA as recommended by the manufacturer (BD Bioscience). Cells from

uninfected mice had no detectable IL-10, IL-4, or IFN-γ production with antigen stimulation in these experiments. Serum from uninfected mice had no detectible IL-12p40. Nitric oxide production was assayed by measuring nitrite in 3-day recall supernatants click here with the Griess reaction (16). Serial dilutions of sera from infected mice were assayed for Leishmania-specific IgG1 and IgG2a/c by ELISA using L. mexicana FTAg for capture, and biotin-conjugated anti-mouse IgG1 and IgG2a/c (BD Biosciences) with peroxidase-conjugated streptavidin (Jackson ImmunoResearch; West Grove, PA, USA) for detection, using 2,2’-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid) (ABTS) as substrate. IgG quantitation shows mean and SEM for ≥5 mice per group. Significant differences were determined by t-test from optical density

(OD) values for the top two dilutions only. Relative amounts of IgG were calculated for the mean WT value by first creating a standard curve from the mean OD values of the KO serum dilution series, plotting OD vs. (1/dilution factor) and fitting the curve using a 6th degree polynomial (KaleidaGraph Mac v.3.6.4). Values of r2 were always very close to 1·0 for this fit (0·9999 for each). The KO dilution, as read from the calculated function, that gave the same OD as the 60-fold dilution of WT serum was designated as the relative amount after the 60-fold dilution Quizartinib datasheet was taken into account. LN cells from infected mice were incubated with or without L. mexicana FTAg for 3 days and

then were stimulated Cytidine deaminase with phorbol myristate acetate (50 ng/mL), ionomycin (0·5 μg/mL), and Brefeldin A (10 μg/mL) for 4 h followed by staining for CD3ε (FITC-145–2C11), CD8α (PerCP-53–6·7), and CD25 (PE-PC61 5·3), fixed with 1% formaldehyde, and stained for intracellular IL-10 (APC-JES5-16E3) after permeabilization with 1% saponin. We used CD3+CD8− staining to determine CD4+ cells because of the relative downregulation of CD4 with antigen stimulation. Antibodies were from BD Biosciences, eBiosciences, or Caltag (CD25) and flow cytometry was acquired and analysed using a FACSCaliber flow cytometer with CellQuest Pro software (BD Biosciences). Isotype controls were used to identify positive vs. negative cell populations. Parasite quantification was performed for three randomly chosen mice per group, by limiting dilution as described previously (17). The limit of detection was 1·4 log = 25 parasites/lesion. Experiments were performed two to four times and representative data are shown. A two-tailed, unequal variance Student’s t-test was used to compare means of lesion sizes, log parasite burdens, cytokine production, IgG levels, mean fluorescence intensity, and FACS distributions from different groups of mice.

There were also no significant changes in terms of cytokine production capacity in the CD4+, CD8+ and CD56+ subsets in check details the patients treated with OK432-stimulated DCs. To assess the effects on T cell responses to tumour antigens, PBMCs were obtained 4 weeks after DC infusion, pulsed with peptides derived from AFP, MRP3, SART2, SART3 and hTERT. IFN-γ production was then quantitated in an ELISPOT

assay. Cells producing IFN-γ in response to stimulation with HLA-A24 [the most common HLA-A antigen (58·1%) in Japanese populations [35]]-restricted peptide epitopes derived from tumour antigens MRP3 and hTERT were induced in three of six HLA-A24-positive patients (numbers 2, 6 and 11) after treatment with TAE and OK432-stimulated DCs (Fig. 4). To understand the immunological and clinical significance of the T lymphocyte responses, PBMCs obtained from the historical control patients who had been treated with TAE without DC administration were also evaluated by ELISPOT. Similarly, positive reactions were observed in four (numbers t8, t19, t20 and t22) of six HLA-A24-positive patients. These data indicate that T lymphocyte this website responses to HLA-A24 restricted peptide epitopes

of tumour antigens were induced following the TAE therapy, but no additional responses were observed aminophylline as a result of OK432-stimulated DC transfer in the current study. To screen for immunobiological responses induced following OK432-stimulated DC transfer, serum levels of cytokines and chemokines were measured simultaneously using the Bio-Plex multiplex suspension array system. The results were compared with the historical control patients treated with TAE without DC administration. Interestingly, serum concentrations of IL-9, IL-15 and TNF-α were greatly increased after OK432-stimulated

DC infusion, in contrast to their reduction following TAE treatment alone (Fig. 5a). Furthermore, the chemokines eotaxin (CCL11) and MIP-1β (CCL4) were induced markedly after DC transfer, although they were also decreased after TAE alone. These data indicate that transfer of OK432-stimulated DC during TAE therapy induced unique immune responses that may be mediated by the cytokines IL-9, IL-15 and TNF-α and the chemokines eotaxin and MIP-1β. In addition, serum arginase activity was reported to reflect numbers of myeloid-derived suppressor cells (MDSCs) that may inhibit T lymphocyte responses in cancer patients [36]. Therefore, serum arginase activity was measured after OK432-stimulated DC infusion, and it was found that it was increased six- or sevenfold in patients treated with TAE. However, this increase was independent of the presence or absence of OK432-stimulated DC transfer (Fig. 5b).

3a; data shown only for the CD4+ CD25− CD127−/+ effector population from HNSCC patients). At the 1 : 1 ratio, the CD25inter www.selleckchem.com/products/PD-0332991.html Treg cell population consistently induced a greater percentage of suppression compared with CD25high Treg cells regardless of the effector T-cell population being suppressed. This trend was also observed at the different Treg : effector T-cell ratios; however, with increased proportions of effector T cells the level of suppression induced by the two Treg cell populations became less pronounced (Fig. 3a). As all samples were tested at a 1 : 1 ratio of Treg : effector

T cells these data were used for statistical analysis of differences between various cell populations and clinicopathological parameters. Both Treg cell populations (CD25inter and CD25high) from HNSCC patients suppressed the proliferation of CD4+ CD25− CD127−/+ effector T cells to a greater extent than those from healthy controls, but this only reached significance for the CD25high Treg cells (Fig. 3b). The significance Selleckchem Erlotinib observed arose primarily from the oropharyngeal cohort, in particular those with early stage tumours, as both these patient groups induced a significantly greater level of suppression compared with healthy

controls (Table 2). In addition, patients with advanced stage cancer of the larynx and patients with nodal involvement also had CD25high Treg cells with significantly greater suppressive activity than the healthy controls (Table 2). No differences were observed in the suppressive activity between patients with laryngeal and oropharyngeal cancer, early and advanced stage tumours and tumours with and without nodal involvement for both CD25inter and CD25high Treg cells (data not shown). When using the CD4+ CD25+ CD127+ effector T-cell population the only significant difference found was that CD25high Treg cells Farnesyltransferase from patients with tumours that had metastasized to the lymph nodes had a greater suppressive activity than those isolated from patients without

nodal involvement (22·80 ± 2·92% versus 11·21 ± 4·50%; P = 0·04). Both the CD25inter and CD25high Treg cells exerted a greater level of suppression on the proliferation of the CD4+ CD25− CD127−/+ effector T cells compared with the CD4+ CD25+ CD127+ effector T-cell population for all HNSCC patient cohorts; however, this only reached significance for the CD25high Treg cells isolated from patients with cancer of the oropharynx (25·41 ± 4·65% versus 19·33 ± 3·36%; P = 0·03). The percentage of suppression induced by CD25inter Treg cells on the proliferation of CD4+ CD25− CD127−/+ effector T cells at a 1 : 1 ratio was consistently higher compared with CD25high Treg cells, regardless of tumour stage, subsite and nodal status and including healthy controls.

Databases searched: MeSH terms and text words for kidney transplantation were combined with MeSH terms and text words for living donor and combined with MeSH terms and text words for open and laparoscopic nephrectomy. The search was carried out in Medline (1966 – September Week 1, 2006). selleck chemicals The Cochrane Renal Group Trials Register was also searched for trials not indexed in Medline. Date of searches: 15 September 2006. Update search: Databases searched: MeSH terms and text

words for kidney transplantation were combined with MeSH terms and text words for living donor and combined with MeSH terms and text words for open and laparoscopic nephrectomy. The search was carried out in Medline (1966 – March Week 1, 2009). The Cochrane Renal Group Trials Register was also searched for trials not indexed in Medline. Date of searches: 9 March 2009. One meta-analysis has been performed by Nanidis et al., which included 73 studies with a total of 6594 patients, of which 3741 had undergone laparoscopic surgery and 2843 open nephrectomy.18 The authors evaluated operative and warm ischaemia times,

blood loss, donor complications, length of hospital selleckchem stay, time to return to work, and delayed graft function. The open nephrectomy group had shorter operative and warm ischaemia times by 52 min and 102 s (both P < 0.001) but this did not translate into higher delayed graft function or graft loss rates between the two groups. The laparoscopic group had a shorter hospital stay and shorter return to work time. A significantly higher rate of overall donor complications was found in the open nephrectomy group. The authors concluded that laparoscopic nephrectomy GABA Receptor is a safe alternative, and patients may benefit from a shorter hospital stay and return to work time without compromising graft function. By 2007, five randomized controlled trials19–23 had been reported with a total of 754 patients. Several of these series

have been the subject of more than one publication.21–26 The features and findings of these studies are summarized in Table 1 (Appendix) with one series including an initial report24 with subsequent updating of numbers.22 In these studies, there was no reported donor mortality and no difference between open and laparoscopic nephrectomy with respect to major complications. The types of complications were different in the two groups. In the laparoscopic group, bleeding from the port site, splenic capsular tear, stapler injury, bowel injury, bladder perforation and wound infection were reported. In the open group, complications included hypoxia, pulmonary embolism, thrombophlebitis, deep vein thrombosis (DVT) and wound infection. Recipient outcomes were comparable with respect to technical complications and functional outcome.

epidermidis

spx mutant strain. We followed the same allelic exchange strategy (Bruckner, 1997) as that used in the construction of an S. epidermidis clpP mutant strain (Wang et al., 2007). More than 2000 clones were screened, but the desired double-crossover strain in which spx is replaced by an erythromycin-resistance cassette was not found, although we indentified single-crossover strains as determined by PCR amplifying the spx bordering regions (data not shown). The attempt to construct an spx mutant stain with a high-efficiency system through pKOR1 (Bae & Schneewind, 2006) also failed (data not shown). We further used a molecular epidemiological approach to examine the existence of spx in a collection of 80 S. epidermidis (Li et al., 2009) clinical isolates. All tested strains harbor the spx gene, indicating Selleckchem Galunisertib the possibility that spx could be an

essential gene (data not shown). Instead, we constructed an spx antisense knockdown plasmid PQG56 coding reversed spx mRNA to downregulate the expression of Spx. In a previous study, Nakano et al. (2003a) overexpressed Spx in B. subtilis to study its regulatory functions. Because the construction of an S. epidermidis spx mutant strain failed, we attempted to overexpress Spx in S. epidermidis to study its regulatory effect on biofilm formation. Attempts to overexpress Spx in B. subtilis were at first unsuccessful due to the rapid degradation of the protein by ClpP protease. selleck compound Successful overexpression of Spx was achieved when an spx mutant allele that codes for a protease-resistant form of Spx (C-terminal mutant) was constructed

and expressed in B. subtilis (Zuber, 2004). Thus, in addition to the expression plasmid pQG54, which carries a WT spx, we constructed another expression vector (PQG55) with an altered spx allele, with a substitution from Ala and Asn codons in the C-terminal to two Asp condons to encode a mutated HSP90 SsrA peptide, in order to avoid the SsrA peptide-tagged proteolysis by ClpXP. These three plasmids were transformed into S. epidermidis. To prevent the resistance from being degraded, we compared the expression level of Spx in strains carrying PQG53, PQG54 and PQG 55 separately. As a result, little Spx protein was detected in the vector control stain harboring PQG53 and the WT expression allele harboring PQG54, whereas Spx accumulated in the strain harboring PQG55 (Fig. 1). Biofilm formations of S. epidermidis strains harboring different plasmids were compared using semi-quantitative assays. Biofilm formation of the strain harboring pQG54 was comparable with that of the vector control strain harboring pQG53, whereas biofilm formation of the strain harboring pQG55 decreased drastically (Fig. 2). The Spx levels in these strains were examined by Western blot. The result that Spx accumulated in the strain harboring pQG55, but not in the strain harboring pQG54, indicates that Spx had a negative effect on the biofilm formation of S. epidermidis.

Results gathered in this study suggest that a status of “immunoprivileged self” in tumors barricades specific Teff cells. This suggestion portends that it might be very difficult, if possible, to circumvent autoimmunity toxicity in a systemic immunotherapy against cancer, unless a substantial antigenic difference is identified between the tumor target and healthy tissue. Therefore, targeting immunoregulatory elements at the tumor site would be desirable. Indeed, local delivery of engineered dendritic cells secreting anti-CTLA4 antibodies promoted immunity against melanoma in

mice without eliciting autoimmunity [44]. A nexus of immunosuppressive elements evolved at the tumor site likely suppress self-antigen-specific T lymphocytes as well as bona fide tumor-specific

T cells. A subtle reduction of CTLA4 in Teff cells by RNAi silencing could substantially overcome the tumor barrier, suggesting PF-2341066 a practical approach to enhance the efficacies of antigen-specific T cells for cancer therapies. Transgenic and knockout mouse models constructed for auto-immunity studies RO4929097 were transitioned to study autoimmune mechanisms in antitumor immunity. A detailed description of the use of these models in the current study is provided in a supplementary table (Supporting information Table 1). BDC2.5/NOD, Foxp3-deficient C57BL/6 (B6) and NOD, NOD.Foxp3DTR, Rag-deficient-BDC2.5/NOD, and CTLA4 shRNA (CTLA4KD7) and PL4 transgenic mice were described previously [24, 29, 34, 35, 45, 46]. CTLA4KD7 and PL4 mice were backcrossed onto B6 background for more than ten generations, and then crossed with BALB-neuT [36], FIR (Foxp3-IRIS-RFP “knockin”) mice [47], or OT1 transgenic line [33]. All animals were maintained in a specific pathogen-free barrier facility and the studies are approved by the Institutional Animal Care and Use Committee at the University of Miami. The NIT-1 insulinoma, EL4 lymphoma, and E.G7-OVA lymphoma cell Selleckchem ZD1839 lines were obtained from ATCC (Manassas, VA, USA) and implanted subcutaneously

at 5 × 106/mouse for insulinoma and 5 × 105 for lymphoma. For the NIT-1 model, tumor burden was quantified by measuring blood glucose levels and tumor mass. The tumor and pancreas samples were fixed in formalin solution. Paraffin-embedded sections were stained with hematoxylin and eosin (H-E) and examined by microscopy. Scoring for pancreas pathology was determined as follows: 0, intact islet with no lymphocytes in the islet area; 1, lymphocytes within the vicinity of the islet, but no infiltration; 2, peripheral insulitic lesion; 3, near or complete destruction of the islet. Flow cytometry analyses were conducted with a standard procedure [29]. The cells were stained with fluorescent-antibody conjugates to determine cells phenotype.

The FGF-23 holds some promise as a novel marker of CKD-MBD, particularly in early CKD, and as a potential tool to monitor the efficacy for therapies used to treat this disorder. The significance and potential role of FGF-23 in clinical practice needs to be established, with large, prospective, clinical trials. These will determine whether FGF-23 is a more useful biomarker

of CKD-MBD when compared with phosphate or PTH. MD would like to acknowledge BGB324 the support of the Royal Australasian College of Physicians Research Foundation and the Jacquot Awards. “
“Aim:  There is limited data concerning the impact of recipient body mass index (BMI) on graft outcome in Asian renal transplant recipients. The aim of this study is to identify whether obesity (BMI ≥25 kg/m2) and overweight (BMI ≥23 kg/m2) can predict graft outcome. Methods:  This is a single-centre retrospective study. All patients who received kidney transplantation between 1997 and 2005 were recruited. Patients were categorized according to two different designated BMI cut-off values. Results:  One hundred and thirty-one patients were recruited with a median follow-up duration of 73 months. If a BMI cut-off see more value of 25 kg/m2 was used, 86.3%

patients were classified as non-obese and 13.7% as obese. Obesity was significantly RVX-208 associated with poor renal graft function and decreased patient and graft survival. On the other hand, 34.3% patients were classified as overweight and 65.7% patients as normal if a BMI cut-off value of 23 kg/m2 was used. Overweight was significantly associated with a lower glomerular filtration rate only. Cox regression analysis showed that obesity (odds ratio (OR) = 3.09), acute rejection (OR = 5.68), pre-transplant diabetes mellitus (OR = 3.21) and age of recipient (OR = 1.06) were all significant independent risk factors associated

with graft failure. Conclusion:  Recipient BMI ≥25 kg/m2 is a significant predictive factor for long-term renal graft outcome in the Asian population. With the introduction of new immunosuppressive agents, the risk of acute rejection in renal transplantation has been significantly reduced. Much of the focus nowadays has shifted to prolong graft survival. Obesity had been linked with an increased incidence of proteinuria, hypertension, hyperlipidaemia, diabetes mellitus (DM) and focal segmental glomerulosclerosis (FSGS) in the general population.1 On the other hand, the impact of recipient obesity on patient and renal allograft survival is controversial. Higher body mass index (BMI) has been shown to be associated with increased risk for graft failure and patient death among white patients with end-stage renal disease who undergo renal transplantation.