IL-6, along with IL-8, has been shown to promote Treg migration to certain tumours [45] and may therefore play a crucial role in Treg signalling. A recent study in type II diabetes has also shown that the percentage of CD4(+)CD25(hi)CD127(–) Tregs are correlated positively BYL719 solubility dmso with plasma IL-6 [46]. Mesenchymal stem cells from mice were shown to promote the differentiation

of uncommitted naive T cells to FoxP3+ regulatory T cells [47]. This study has shown that the major cytokines involved in these processes were transforming growth factor (TGF)-β and IL-6 and that immunomodulation could be blocked by administration of anti-TGF-β or anti-IL-6, suggesting paracrine mechanisms. In another study in mice, excessive GW-572016 research buy IL-6 production caused an increase in natural Tregs, which maintained their immunosuppressive capacities both in vitro and in vivo [48]. This suggests that IL-6 may be a key mediator in effector/regulatory T cell balance. However, there are also data that are in contrast to our findings. In another study, using Tregs derived from the rheumatic synovium, blocking IL-6

or TNF increased the suppressive immunomodulatory capacities of these cells [49]. This study suggests that Treg function varies importantly with the inflammatory milieu in the joint. These findings are not in accordance with our experiments, in which IL-6 maintained the percentage of Tregs. This discrepancy may be due to differences in the underlying pathologies, but also reflect the dual role of IL-6. However, the functional consequences remain to be identified in upcoming experiments. We have chosen to carry out our study on Tregs taken from healthy donors in order to provide information Buspirone HCl on the immunomodulatory

capacities of MSCs and ruling out possible influences of OA on Tregs and thus on Treg–MSC interaction. An important question is whether or not Tregs taken from OA patients differ in their interaction with MSCs. Our findings therefore raise several questions that need to be verified by future research. Understanding the effects of MSCs in local joint inflammation in OA may pave the way for future cell-based approaches, as MSCs can be supposed to not only exert their regenerative potential when administered, but also intervene in local immunity. This study has several limitations. First, a comparison to MSCs taken from healthy donors would be useful to detect whether the inability to recruit Tregs from a CD4+ population, as has been shown by other groups, should be interpreted as a reduced capacity of immunomodulation in OA. This question has not yet been addressed due to ethical questions, as synovium from healthy individuals is not easily available. Taking synovium from a young population undergoing hip or knee arthroscopy might falsify the results, as it is known that cartilage injuries are found in up to 65% of the patients during arthroscopy, irrespective of the underlying pathology [50].

The technique reduces the dissection time and does not require sophisticated https://www.selleckchem.com/products/Roscovitine.html surgical devices and skill, when compared to endoscopic LD flap harvesting from the literature. © 2012 Wiley Periodicals,

Inc. Microsurgery, 2013. “
“The purpose of this study was to investigate sensory recovery in 33 patients who underwent conventional mastectomy, skin-sparing mastectomy, or nipple-sparing mastectomy with immediate breast reconstruction using abdominal flaps. Reconstructions included a pedicled transverse (28 cases) or vertical (five cases) rectus abdominis musculocutaneous flap. Sensory reconstruction was performed in 15 cases by neurorrhaphy using intercostal nerve. Patients were classified into six groups according to H 89 cost type of mastectomy and use of neurorrhaphy. Sensory recovery was estimated by touch, pain, and hot and cold sensation at the nipple,

areola, and 4 points at a distance of 2 cm from the areolar circumference. For touch sensation, conventional mastectomy with innervated flap provided greater sensitivity than the other groups (P < 0.05). For pain sensation, conventional mastectomy with innervated flap provided greater sensitivity than the other groups (P< 0.05). In terms of short-term postoperative sensitivity, skin- and nipple-sparing mastectomies with abdominal flap appear inferior to conventional mastectomy with innervated abdominal flap. © 2011 Wiley-Liss, Inc. Microsurgery, 2011. "
“The Internal Mammary Artery (IMA) and its perforators play an important role in coronary bypass grafting and reconstructive

breast, head, and neck surgery. This study aimed to obtain anatomic data pertaining to these vessels using Multi Detector Computed Tomography Angiography (MDCTA) and to demonstrate that the MDCTA could be a considerable assessment tool prior to surgery. In 50 outpatients (27 males and 23 females), the above-mentioned arteries were bilaterally evaluated with a 16-detector spiral computed tomography scanner. Based on the obtained images, diameters of the bilateral IMAs were separately measured in each intercostal spaces from 1 to 5 through their traces. IMAPs mafosfamide greater than 0.5 mm in diameter were bilaterally evaluated in terms of distance from the sternal border to the ramification point under the muscular layer, maximal external diameter at ramification from the IMA, and the length between the ramification point from the IMA and enter point to the subcutaneous fat tissue. Mean diameters of the left and right IMAs were 2.05 ± 0.50 mm and 2.20 ± 0.57 mm, respectively. Mean diameters, distances, and lengths of the perforators were 1.30 ± 0.30 mm, 6.80 ± 3.40 mm, 17.05 ± 6.07 mm on the left side and 1.32 ± 0.25 mm, 6.71 ± 3.43 mm, 17.35 ± 3.48 mm on the right side, respectively. No statistically difference was found between the sides (P > 0.05).

, 2003). However, recent reports contend that the contribution of homologous

recombination to core diversity in S. aureus may be underestimated (Chan et al., 2011). Nevertheless, mutation is a significant driving force selleck products in S. aureus diversification allowing for evolutionary classification of strains into ST types (see above) (Enright et al., 2000). Most SNPs are within coding regions reflecting the fact that ~ 80% of the core genome encodes protein (Highlander et al., 2007). Synonymous SNPs, those that do not result in amino acid changes, by far outweigh amino acid substituting nonsynonymous SNPs in S. aureus (Herron et al., 2002; Gill et al., 2005; Herron-Olson et al., 2007; Sivaraman & Cole, 2009). This is likely selleck chemicals because nonsynonymous mutations are more often detrimental and are therefore subject to evolutionary loss via purifying selection. Consequently, the relative

ratio of nonsynonymous to synonymous substitution rate (dN/dS) among staphylococci is generally less than 1. In contrast, a recent report comparing the complete genome sequences of 10 newly isolated USA300 clones with the published FPRF3757 USA300 sequence revealed an unusually high ratio of nonsynonymous : synonymous SNPs (as high as 2.6 : 1, much higher than reported in comparisons of non-USA300 S. aureus lineages) (Kennedy et al., 2008). This discrepancy can be rationalized by assuming a recent clonal expansion of the USA300 lineage such that new isolates still harbor nonsynonymous SNPs that have not yet undergone purifying selection (Holden et al., 2004). To be sure, the unusually high dN/dS ratio of USA300 3-mercaptopyruvate sulfurtransferase clones is inconsistent with evolutionary convergence among distantly related clones, an event that would only be consistent with normal to low dN/dS ratios if the converging progenitors were of sufficiently diverse origins (Kennedy et al., 2008). It is important to note that overall low dN/dS ratios are not necessarily constant across all functional gene families. For instance, while housekeeping and metabolic genes generally exhibit low dN/dS ratios, genes encoding surface associated or secreted proteins can often

have elevated dN/dS ratios (Jordan et al., 2002; Rocha & Danchin, 2004). This is indicative of forward selective pressures driving variability in these genes either to promote functional differences (e.g. an adhesin adapting to a host receptor molecule) or immune avoidance through changes in antigenicity. Indeed, comparisons among divergent S. aureus clones reveal higher dN/dS ratios for genes encoding components of the cell envelope and secreted proteins than genes encoding housekeeping or metabolic enzymes (Herron et al., 2002; Herron-Olson et al., 2007; Highlander et al., 2007). USA300 clones, however, seem to be an exception to this rule. A recent comparison of genome sequences from USA200, USA300, and a distantly related S.

fumigatus and Aspergillus terreus, eight sputum samples were collected between 22 November 2007 to 16 February 2010, and no Scedosporium was detected by culture. Likewise, for patient 14 (sample 26), 37 samples were collected between 4 July 2007 and 29 May 2009. Mycological analysis gave strictly the same results for almost all these samples,

with an exclusive growth of Candida albicans. Mycological analysis of 21 sputum samples and three broncho-alveolar fluids collected between 3 January 2007 and 29 May 2009 from patient 10 (sample 21 in this study) revealed a chronic colonisation of the airways by C. albicans, sometimes associated with Candida dubliniensis or A. fumigatus, but Scedosporium species were never detected. In addition, Maraviroc in vivo two consecutive samples from seven CF patients were analysed. For one of these patients (patient 24), PCR-RLB yielded identical results for the two samples, with a positive signal with

the P. apiosperma-specific probe, and mycological analysis of the second sample (sample 93 collected on 15/12/2008) permitted the recovery of this fungus. This suggests a lack of sensitivity of culturing for the first sample (sample 150 collected on 16/10/2007). Discrepant results between the two successive samples were obtained for the six other patients, with a PCR-negative signal for one of the samples in three patients (patients 2, 21 and patient 29) or with positive signals with different species-specific probes between the two samples in the other three cases (patients 19, 22 and 25). Several molecular methods CHIR99021 targeting the internal transcribed spacer (ITS) region have been described, but with insufficient resolution to differentiate all clinical species of the P. apiosperma/P. boydii complex. The fragment BT2 of the β-tubulin gene provided more information than

ITS as a target for the identification of Scedosporium species.17,22 We chose the RLB format, given the advantages of low cost and the simultaneous analysis of multiple specimens against multiple probes. The assay analyses up to 43 specimens in a single run and the membrane can be reused up to 20 times without loss of signal. The PCR-RLB assay was able to identify GPCR & G Protein inhibitor five species except S. dehoogii. The latter species has not been proven to have clinical relevance, and thus PCR-RLB is sufficient for use in clinical diagnostics. Although a single amplification PCR round was sufficient for DNA extracted from cultures, a second PCR format maximises detection limits. Two PCR reactions might carry a higher risk of cross contamination due to the amplification of contamination from e.g., Scedosporium DNA contaminated tubes, sampling equipment (bronchoscope), PCR water or reagents; however, it made it possible to detect DNA extracted directly from clinical specimens. Fifty-nine sputum samples were analysed using methods dedicated to the selective isolation of Scedosporium species; five samples (8.5%) proved to be positive.

The bacterial agents causing the urinary infections are Escheria coli, followed by other gram negative germs such as Klebsiella pneumonia, Proteus species and gram positive germs such as Staphylococcus species. Methods: The aim of study was to identify the bacterial agents of urinary tract infections in

children and to study their sensitivity and resistence to antibiotics. In this retrospective study the bacterial agents of urinary tract infections were studied in 203 children under 5 year of age, between January till December 2012. Results: The aim of study was to identify the bacterial agents of urinary tract B-Raf inhibitor drug infections in children and to study their sensitivity and resistence to antibiotics. In this retrospective study the bacterial agents of urinary tract infections were studied in 203 children under 5 year of age, between January till December 2012. Conclusion: A highly resistance of uropathogens to co-trimoxazole in children, suggest caution before giving a empiric treatment HM781-36B in vivo with cotrimoxazole, and recommanded use of nitrofurantoin as empiric treatment of children’s urinary tract infections. Key words: Uropathogen, co-trimoxazole, nitrofuranoin GHEISSARI ALALEH1, KELISHADI ROYA2, BAZOOKAR NEDA3 1Isfahan University of Medical sciences; 2Isfahan University of Medical sciences; 3Isfahan University of Medical Sciences Introduction: Obesity in accordance with metabolic

syndrome (MetS) confronts populations at the higher risk of morbidity and mortality of chronic diseases including, chronic kidney diseases (CKD). The renal complication of obesity and MetS

has been less debated in young adolescents. The objective of this study was to assess the kidney function in obese adolescents Non-specific serine/threonine protein kinase with or without MetS. Methods: The data used in this study were collected as part of a national study entitled Childhood and Adolescence Surveillance and Prevention of Adult Non-communicable disease Study. The present study was conducted on a sub-sample of 113 obese adolescents (body mass index > 95th percentile) aged between 10 years and 16 years selected by convenient sampling from the whole population studied. Anthropometric indexes and blood pressure were examined. A 12-h fasting serum was obtained for each participant to measure blood glucose, lipid profile, quantitative C-reactive protein (hs-CRP), Cystatin-c, urea, and creatinine. Fasting spot urine was collected to determine microalbumin and creatinine. Based on the study findings, participants were assigned into two groups with and without MetS. Results: The mean of microalbuminuria was in similar ranges in two groups and while the mean glomerular filtration rate (GFR) calculated by Bokenkamp’s, updated and combined Schwartz’s formulas were significantly lower in MetS + obese group in comparison with obese group.

Whether type I IFNs also regulate

IL-10 through the FcγR pathway is not yet known and should be investigated, as depletion of CD25+ T cells did not change any of the important immunological parameters, parasite burdens, or lesion progression in our previous studies of L. mexicana infection in B6 mice (22). IgG plays an important role in chronic disease in L. mexicana infection. IgG1, which Ceritinib mouse appears earlier than IgG2a/c, has a high affinity for FcγRIII, and immune complexes of L. mexicana amastigotes can induce IL-10 through this receptor (22). Mice lacking either IL-10 or FcγRIII heal their lesions and have many orders of magnitude fewer parasites with an associated enhanced

IFN-γ response (4,22). In the current studies, we found that IFN-α/βR KO mice had stronger Leishmania-specific IgG1 and IgG2a/c responses at 12 weeks of infection than WT mice, indicating that IFN-α/β directly or indirectly partially suppresses the IgG response, possibly by decreasing or slowing B cell proliferation or IgG secretion. The stronger effect is on IgG1, which is Z-VAD-FMK clinical trial increased by >10-fold, with a 7-fold increase in IgG2a/c. Later, in infection, the increased IgG1 response could dampen the IFN-γ response by induction of IL-10 through FcγRIII, with suppression of Th1 development. In fact, we do see that the decrease in IFN-γ in IFN-α/βR KO mice resolves by 17 weeks of infection. Although IFN-γ is known to drive IgG2a/c and IL-4 to drive IgG1 class switching, the KO mice had no measurable change in IL-4 levels (which are very low) and actually had diminished IFN-γ production. Thus, IFN-α/β must be acting on IgG isotype selection through other undescribed pathways. Later, in infection, this enhancement of IgG in the KO mice was no longer evident, similar to the effects on IFN-γ.

At 4 weeks of infection, there is a weaker IFN-γ response in IFN-α/βR KO mice, and yet parasite loads are not different. This is consistent with several other studies in which early parasite loads (4–8 weeks) did not correlate with defects in various immunological factors such as IL-10 and FcγRIII despite early increases on IFN-γ (4,22), CYTH4 but parasite loads then dropped by 12 weeks of infection. This may be because of delays in T cell development and migration to the lesion. Later in infection, the T cell IFN-γ levels and IgG levels are comparable in IFN-α/βR KO and WT mice, consistent with the similar lesion sizes and parasite loads. As mentioned above, the IL-10 in lesions from IgG-FcγR pathways correlates better with parasite loads and lesion size than does LN T cell IL-10, and the lower IL-10 seen in IFN-α/βR KO at 17 weeks agrees with this assessment.

2%, n = 3). Rejection of donor BM-derived cells was greatly inhibited in the positive control group (killing rate mean ± SD = 31.3 ± 3.3%, n = 3, p < 0.05) in which NK cells were depleted by anti-Asialo LBH589 order GM1, indicating that the killing was mainly mediated by recipient NK cells in absence of T cells. Interestingly, adoptive transfer of DN Treg cells significantly inhibited the killing of donor-derived cells (Fig. 4C, mean ± SD = 58.1 ± 1.1% versus 95.4 ± 6.2% in PBS-control group, n

= 3, p < 0.05), suggesting that the transfer of DN Treg cells can effectively suppress NK cells-mediated BM rejection. Next, we further studied the mechanism of DN Treg cell-mediated NK cells suppression. DN Treg cells were purified from gld lpr, and peforin−/− mice and were used for adoptive transfer before BM transplantation. As showed in Fig. 4D and E, perforin−/− DN Treg cells have significantly crippled inhibition capability compare with DN Treg cells purified from gld or lpr mice, indicating a perforin-dependent mechanism for DN Treg cell-mediated NK-cell suppression. The dilemma that limits

the success of organ transplantation is the difficulty Nutlin-3a ic50 with suppressing the host immune response to the foreign graft without excessively compromising the host normal immune system. Mixed chimerism, which denotes a state of the coexistence of recipient and donor hematopoietic cells following donor BM into conditioned recipients, holds the key to solve this problem [[12, 13]]. In this study, we tried to establish mixed chimerism in an irradiation-free protocol by adoptive transfer of C57BL/6 DN Treg cells prior to C57BL/6 to BALB/c BM transplantation in combination of CY treatment (Fig. 1). The recipient TCR Vβs clones deletion (Fig. 3) and NK-cell suppression (Fig. 4) could be achieved after DN Treg-cell transfer. The results that adoptive transfer of DN Treg cells can control both adoptive and innate immunity, promote a stable-mixed chimerism, and donor-specific tolerance in the irradiation-free regimen

provide a rationale for a potentially novel therapeutic use in transplant HAS1 tolerance induction. Numerous mixed chimerism protocols have been proposed including immunosuppressive drugs, costimulation blockade [[32, 33]], T-cell depletion [[34-36]], Foxp3+ Treg-cell application [[37, 38]]. Despite the success in rodent, large animal [[39, 40]], and nonhuman primate models [[41]], the clinical application of mixed chimerism strategy is still hindered in patients because long-lasting stable-mixed chimerism has not yet been achieved and immunosuppression and irradiation increase risk of cancer, infection, and other side effects. Apparently, more studies are required for the development of mixed chimerism for clinical use. In our previous studies, cotransplantation of BM cells and DN Treg cells, with sublethal irradiation, could suppress NK-cell function and induce stable-mixed chimerism [[24]].

6B). Thus, the cell surface structures sialoadhesin and B7-H1 are involved in the induction of the IL-35+ Treg. We demonstrate

in this study that IL-35 production and release is induced Tipifarnib order in human peripheral blood CD4+ and CD8+ T cells by B7-H1 and sialoadhesin co-stimulation, provided by DC. Such IL-35+ T cells are potent Treg, which, in contrast to IL-10-driven type-1 Treg (Tr1), do not suppress T-cell responses via IL-10 and/or TGF-β 11. Several pieces of evidence support the conclusion that the R-DC-induced Treg act via IL-35. Neutralization with anti-EBI3 and anti-p35 Ab and depletion of IL-35 removed the inhibitory effect of the SN of Treg and naïve T cells from CB, which do not produce IL-35 upon stimulation with R-DC, lack suppressor function. Thus, induction of IL-35 represents a novel activation program in human T cells responding to viral infection. EBI3 is a member of the IL-12 family. It was first identified in B lymphocytes based on its induction following EBV infection. It codes for a 34 kDa-secreted glycoprotein homologous to the p40 subunit of IL-12. Recent studies have shown that EBI3

can dimerize with IL-12 p35 and EBI3/p35 was called IL-35. The in vivo association between EBI3 and p35 was originally evidenced in human placental extracts Cabozantinib ic50 20. Data presented in Fig. 4 and 5 demonstrate that IL-35 and not IL-27 or even IL-12 is responsible for the inhibitory effect of the SN. More recent studies demonstrated that IL-35 is constitutively expressed by mouse CD4+CD25+FOXP3+ Treg 3, 5. Transcripts coding for EBI3 and p35 were observed to be constitutively coexpressed by mouse Treg and EBI3/p35 heterodimer Olopatadine was coprecipitated from the cell culture SN of these cells. In addition, in vitro and in vivo studies suggested that the expression of IL-35 by mouse Treg contributed to their suppressive function 21. However, human CD4+CD25+FOXP3+ Treg do not constitutively express IL-35 and induction of FOXP3 upregulates neither EBI3 nor p35 mRNA in human T cells 6, 7. Yet, recombinant mouse IL-35 was shown to inhibit

the proliferation of mouse effector T cells in vitro. In another recent study, a single chain mouse IL-35-Fc fusion protein was demonstrated to enhance the proliferation of mouse Treg, while inhibiting the development of Th17 cells 5. The data of this study demonstrate for the first time that IL-35 is a potent regulatory cytokine, also in the human immune system, and that a combinatorial signal delivered from DC to T cells via B7-H1 and sialoadhesin is crucial to the induction of human IL-35+ Treg. We observe transient FOXP3 expression in T cells stimulated by R-DC as well as DC. Such temporal activation-induced FOXP3 expression in human T cells has been described before and is not obligatory correlated with a regulatory function, whereas natural CD4+CD25+ Treg show constitutive FOXP3 expression 10, 22.

(iii) Type I predominance or type I fibre uniformity and increased variability in fibre size; and (iv) Nuclear internalization and centralization find protocol in both fibre types, including frequent multiple internalized nuclei. In addition, a discrete increase of endomysial connective tissue was often observed. Noticeably, the muscle biopsies performed at the ages of 4 months for patient 1 and 21 months for patient 2, essentially showed type I fibre predominance, increased endomysial

connective tissue, significant variation in type I or II fibre size and the presence of some small fibres with central nuclei resembling myotubes. No cores were observed. Thereafter, the muscle biopsies performed at the ages of 12 and 14 years for patient 1 and 12 years for patient 2 showed the peculiar morphological pattern observed in all patients.

Nuclear internalization increased with age (Table 1; Figure 3). In patients 1 and 3 to 7, ultrastructural analysis of muscle biopsies in longitudinal sections demonstrated large areas of sarcomeric disorganization (Figure 4d). Such areas were present in one or more regions within a fibre, were variable in width and length, frequently covered the entire fibre diameter in cross section (Figures 4a,b) and extended from 2 to 30 sarcomeres in longitudinal sections (Figures 4b,f). Altered fibres often showed one or several misplaced nuclei that were occasionally found at the border of areas of myofibrillar disorganization (Figures 4b,d). Within MG-132 cell line such disorganized areas, accumulation of Z-band proteins, Z-band streaming, enlarged Z-bands and myofibrillar compaction were the most frequent alterations (Figures 4c,e). T-triads-repetitions, honeycomb profiles (corresponding to T-tubules proliferations) and occasional minicore-like Interleukin-2 receptor lesions (Figure 4f)

were also observed amongst other non-specific alterations. Mitochondria were present or not in the disorganized areas. In order to further study the composition of the disorganized intracellular areas, biopsies of patients 2, 3 and 5 were labelled with antibodies to the intermediate filament proteins desmin, αB-crystalline and myotilin. The three markers intensively labelled the disorganized areas, but in serial sections reacting fibres were either labelled with one, two or three of the antibodies used, suggesting a heterogeneous composition of the disorganized zones (Figure 5). Patient 1 and her deceased sister were c.[10348-6C>G; 14524G>A] + c.[8342_8343delTA] compound heterozygous carriers (Table 2). The c.8342_8343delTA frameshift deletion transmitted by the clinically unaffected mother introduced a premature stop codon (p.Ile2781ArgfsX49). The two other variants were inherited from the clinically unaffected father. The c.10348-6C>G change resulted in a loss of splicing of intron 68 and the introduction of a premature stop codon (p.His3449ins33fsX54).

This uncertainty has arisen because trials up until now have primarily focused on haemoglobin targets without considering the roles of ESA dosage per se or other patient-related factors, such as concurrent illness, inflammation and iron therapy. Until such high level clinical U0126 nmr evidence becomes available, it would seem prudent to avoid both high haemoglobin levels (i.e. >120–125 g/L) and high ESA dosages (i.e. erythopoietin dosage ≥200 IU/kg per week or darbepoetin dosage ≥1 µg/kg per week). Future RCTs need to consider

the clinical impacts of therapies purported to reduce ESA resistance, such as oxpenifylline,35 and of different ESA dosages on clinical outcomes within the currently recommended haemoglobin target range of 95–125 g/L. One study, the Clinical Evaluation of the DOSe of Erythropoietins (C.E. DOSE) trial, is currently underway in Italy to evaluate the impacts of two fixed ESA doses (4000 IU/week iv. vs 18 000 IU/week) on a composite primary end-point of all-cause mortality and fatal and non-fatal cardiovascular events in haemodialysis patients.36 We further propose that a trial with a 2 × 2 factorial design will

help better answer the question of whether ESA dose, haemoglobin level or both affect outcomes (See Fig. 1). In this trial proposal, eligible patients would be randomized to high or low dose of ESA and a higher or lower haemoglobin level within the currently recommended AZD2014 mw target range. Considering the sample size required for such a trial, an international collaboration of nephrologists and clinical trialists would be required and

the trial should be developed as a priority. “
“The prevalence of chronic kidney disease (CKD) in children has been on the rise in China and more and more paediatric patients are now relying on chronic renal replacement therapies to sustain their lives. However, there is still a lack of literature in China about Leukocyte receptor tyrosine kinase their outcomes, thus making it difficult, if not impossible for the paediatric nephrology community to develop strategies to guide future developments and to better serve this group of sick children. Our institution has recently conducted a nation-wide survey to obtain data of children with end-stage renal disease (ESRD) between the years 2007 to 2012. Questionnaires were distributed to 39 member hospitals of the Chinese Paediatric Nephrology Association. Only 28 of our member hospitals were actively providing dialysis services to children and their responses were included in this study. There were a total of 1033 children with ESRD and within this cohort, 474 patients (45.9%) received chronic dialysis and 380 patients (80.2%) preferred haemodialysis. Haemodialysis is far more commonly used than peritoneal dialysis in China and the outcomes were similar to the experiences in North America.