Our data cannot distinguish these possibilities and further studies will be required

to resolve find more these issues. Yet, the transfer of pre-activated Treg cells resulted in a demonstrable effect on the trafficking capabilities of Teff cells. Understanding the dynamics of this interaction is important as transferred, pre-activated polyclonal Treg cells are the most likely to be used in clinical situations. The mechanisms by which Treg cells inhibit Teff cell trafficking remain to be fully elucidated. The decrease in S1P1 expression at the mRNA level in Teff cells that had been primed in the presence of Treg cells is an attractive mechanism for the retention of the Teff cells in the LN, but other effects of Treg cells on chemokine expression 6 or on adhesion molecule expression 9 must also be considered. Although our studies were performed in a model system using TCR transgenic Teff cells, recent studies have shown

that polyclonal Treg cells may also regulate trafficking of CD8+ Teff cells in vivo during acute infection with respiratory syncytial virus 21. It is clear from these studies that polyclonal Treg cells do not influence the immune response by selleckchem simply “shutting down” immunity. In fact, it has recently been shown that polyclonal Treg cells enhance antibody responses when mice are immunized intranasally in the presence of the cholera toxin potentially by promoting Teff cell retention in the LN and promoting T-dependent B-cell responses 22. It would therefore be expected that the therapeutic administration of polyclonal Treg cells would not necessarily lead to global immunosuppression or the inhibition of responses to all antigens or pathogens. Rather, they influence the Teff-cell responses by specifically targeting trafficking pathways, thus allowing immunity to develop in lymphoid organs, but limiting the number of potentially auto-aggressive cells that are allowed to enter tissues. C57BL/6 and B10.A mice were obtained

from DCT, NIH. C57BL/6 CD45.1+ and CD45.1+ 5CC7 TCR-Tg mice Flavopiridol (Alvocidib) on RAG−/− background were obtained from Taconic Farms. 2D2 TCR-Tg and B6 Thy1.1 (B6.PL) mice were obtained from The Jackson Laboratory. 2D2-Thy1.1 mice were generated in house by crossing 2D2 TCR-Tg mice with Thy1.1 (B6.PL) mice and screening the progeny by flow cytometry with anti-Vβ11 and Thy1.1 antibodies. EAE was induced in C57BL/6 mice by subcutaneous immunization in the hind flank with 200 μL of an emulsion containing 400 μg of MOG35–55 peptide and 400 μg of Mycobacterium tuberculosis strain H37Ra in CFA (Difco). On days 0 and 2, the mice received an i.p. injection of 200 ng pertussis toxin (CalBiochem) dissolved in 100 L PBS.

Anticoagulation can be considered in cases of small vessels, significant size mismatch, vein graft, or vessels of poor quality. Monitoring should be done hourly during the first 24 hours and then every 4 hours for the next 2 postoperative days. © 2010 Wiley-Liss, Inc. Microsurgery, 2010. “
“Several microsurgical techniques have been described for the treatment of osteonecrosis of the talus (ONT). Recently reported in children, vascularized periosteal grafts showed promising

revascularizing properties. We report a novel technique using a pedicled periosteal graft from the first metatarsal bone to treat steroid-induced early Ficat-Arlet stage III ONT in an 11-year-old boy. The patient presented initial favorable clinical and radiological results which were maintained at 34 months during the last follow-up. Through this original technique, and basing on the powerful osteogenic and vasculogenic propreties of periosteal flaps, we could high throughput screening assay selleck products effectively induce bone revascularization and prevent further collapse of the talar dome. © 2012 Wiley Periodicals,

Inc. Microsurgery, 2013 “
“In microvascular transfer of fibular osteocutaneous flap for mandible reconstruction after cancer ablation, good bone union is necessary to allow timely radiation therapy after surgery. As the area of bone contact between fibula and the original mandible at the edge of the mandibular defect is small, a periosteal excess at both ends of the fibula covering the bone junction can be used to increase the chance of bone union. The purpose of this study is to investigate whether a periosteal excess surrounding both ends of the fibula flap can provide better blood supply and, therefore, ensure bone union and wound healing at 6 weeks after surgery and before radiation therapy initiation. Sitaxentan The transfer of fibular osteocutaneous flap with periosteal excess was only applied to reconstruct segmental mandibular defects. As a consequence, only

cases in which osteotomy of fibula was not performed were included in this study. A total of 34 fibular flaps without osteotomies were performed between 2000 and 2008; 17 with and 17 without the periosteal excess. The bone union was evaluated in terms of osseous callus formation using X-rays and CT three-dimensional images at 6 weeks after surgery, and results were assessed by three independent radiologists. There was a significant difference between reconstructions with and without the periosteal excess in terms of bone union (P = 0.022). With reference to postoperative complications, the group reconstructed without periosteal excess presented a higher number of complications, mainly consisting of partial and total flap necrosis, respectively six (35.29%) and two (11.76%) cases. In the group reconstructed with periosteal excess, no loss of the skin island has occurred. A significant difference was observed in terms of partial flap necrosis (P = 0.

28,29 To assess the consequences of miR-155 inhibition, and the resulting decrease in NO production, on CD11b expression, we performed immunocytochemistry to evaluate CD11b labelling in N9 cells. For this purpose, N9 microglia cells were transfected with anti-miR-155 or control oligonucleotides 24 hr before exposure to LPS (0·1 μg/ml). Following 18 hr of incubation with LPS, cells were fixed and labelled with the nuclear dye DAPI, with a specific anti-CD11b antibody and an antibody against the structural protein tubulin (Fig. 7). Results in Fig. 7 clearly show that exposure to LPS Cabozantinib nmr increases CD11b labelling in

N9 cells (Fig. 7e), with respect to control cells (Fig. 7a). In this regard, it was also possible to

observe striking differences in cell morphology, because LPS-treated cells lose the characteristic star Sirolimus cost shape of resting N9 cells and become round and amoeboid, a common feature of activated microglia cells. Similar results were observed in N9 cells transfected with control oligonucleotides followed by LPS exposure (Fig. 7m). These cells present the same intense CD11b labelling and round shape of untransfected, LPS-treated cells. However, cells transfected with the anti-miR-155 oligonucleotides before LPS treatment showed less intense CD11b labelling and a morphology closer to that of control cells (Fig. 7i), indicating

lower levels of CD11b. In view of the pro-inflammatory DOK2 role of miR-155 in activated microglia, as evidenced by our results on N9 cells, we evaluated the potential of miR-155 modulation as an anti-inflammatory and neuroprotective strategy. For this purpose, N9 microglia cells were transfected with anti-miR-155 or control oligonucleotides 24 hr before exposure to LPS (0·1 μg/ml). Following 18 hr of incubation with LPS, the medium of N9 cells was collected and mixed with Neurobasal medium at a ratio of 1 : 1 (v/v). Primary cultures of cortical neurons were incubated with this mixture (conditioned medium) for 24 hr before assessment of cell viability using the Alamar Blue assay (Fig. 8). In parallel, cortical cultures were exposed directly to the same concentration of LPS (0·1 μg/ml). Figure 8 shows that neurons exposed to conditioned medium collected from N9 cells, previously incubated with LPS in the absence of transfection, presented a reduction in viability of 40%. Similar results were observed in neurons incubated with conditioned medium collected from cells transfected with control oligonucleotides. However, neurons treated with medium conditioned by N9 cells, in which miR-155 had been inhibited before LPS treatment, presented only a slight decrease in viability (10%) with respect to control neuronal cells.

[14] As a result of the decrease in recent thymic emigrants, it has been suggested that peripheral T cells in individuals with DS undergo increased homeostatic proliferation in comparison to the general population.[14]

Because of mixed genetic background in Ts65Dn mice, differences in recent thymic emigrants cannot be reliably measured. Nevertheless, the Small molecule library data are consistent with a loss of thymic precursors in the Ts65Dn mice leading to altered peripheral T-cell populations. Defects in Ts65Dn peripheral T-cell function are most evident in the decreased proliferation in response to polyclonal stimulation. This loss of function may be consistent with immune dysfunction in DS, as lymphocytes from individuals with DS have also been shown to exhibit a decreased proliferative response to polyclonal stimuli such as phytohaemagglutinin,[47, 48] in addition to the documented decrease in responses in some individuals with DS to vaccinations.[49, 50] Vaccine studies have shown that IL-7 and TCR signalling can synergize to promote antigen-specific effector cell generation, especially when using subdominant antigens.[51] Therefore decreased IL-7Rα expression as well as the deficient buy Belnacasan proliferation in response to TCR stimulation may

contribute to the T-cell dysfunction observed in DS. It is tempting to speculate that the impaired proliferation in the immature thymocyte subsets as a consequence of decreased IL-7Rα expression Fossariinae may be one of the causes of accelerated thymic involution as well as decreased thymic output in DS. In turn, the increased, possibly excessive, homeostatic cycling of peripheral T

cells in individuals with DS may result in premature senescence and impaired function. The changes in lymphocyte responses were not limited to T cells as B-cell proliferation was also diminished in response to antigen receptor stimulation, but not lipopolysaccharide. This is consistent with an anergic/senescent phenotype in the peripheral lymphocyte pools. However, in contrast to thymic development, B-cell progenitors in the bone marrow and IL-7Rα expression on those cells were not altered in the Ts65Dn mice, suggesting a selective effect on T-lymphocyte precursors. It is interesting, but unclear, why the previously reported decrease in CLP in Ts65Dn bone marrow[6] only results in diminished T-cell progenitors. One postulate is that decreases in Notch signalling, due to BACH1-mediated inhibition of Nrf2 or increased DYRK1a[52] in DS, leads to impaired T-cell specification, but not B-cell development. The resultant changes in mature B-cell function and spleen subsets may be, as has been proposed previously,53 due to altered T-cell help.

Regression analysis confirmed an age-independent association between HCMV infection and the proportions of the NKG2C+ subset (p < 0.001), as well as between the NKG2C LY2157299 datasheet genotype and absolute numbers of NKG2C+ cells (p = 0.003) (Supporting Information Table 2). Stratification for both HCMV infection and NKG2C genotype further supported a relationship of the latter with the absolute numbers of NKG2C+ cells (Fig. 3A). The possibility that these results might be explained by age differences

or a skewed distribution of cases with congenital symptomatic and asymptomatic infection, displaying different levels of NKG2C+ cells (Fig. 1), was ruled out by multivariate analyses. Unexpectedly, NKG2C+/+ children were observed to display as well higher proportions (median 7.2% versus 4.6%; p = 0.003) and absolute numbers (median 359 versus 215 cells/mm3; p = 0.008) of total NK cells than NKG2C+/− children. PD-0332991 price This finding was not

simply explained by the expansion of the NKG2C+ subset, as the numbers of NKG2A+, CD161+, and total NK cells appeared also higher in HCMV-positive NKG2C+/+ children compared to NKG2C+/− individuals (Fig. 3B–D). Multivariate regression analysis confirmed the relation of the NKG2C genotype with both the proportions (p = 0.001) and total numbers (p = 0.014) of NK cells, independently of age as a putative confounding variable [45, 46] (Supporting Information Table 2). In the present study, increased GABA Receptor proportions of NKG2C+ NK cells were detected in children with past congenital HCMV infection; this immunophenotypic feature was particularly marked in symptomatic cases, as further illustrated by studies in twins. The detection in older patients of high proportions of circulating NKG2C+ cells years after symptomatic congenital HCMV infection (Table 2 and Supporting Information Table 1) highlighted the persistence of the NK-cell subset redistribution, consistent with observations in healthy adults (Muntasell and López-Botet, unpublished data). Though the proportions of NKG2C+ NK cells

appeared unrelated to age, the cross-sectional design of this study did not discriminate whether the increase of NKG2C+ cells resulted from a progressive cumulative process, as reported in cord blood transplantation recipients [31, 33]. Prospective longitudinal studies of the NK-cell immunophenotype in congenital and early postnatal HCMV infection are warranted to approach the dynamics of these events. We previously reported that CD94/NKG2C+ cells expanded in vitro in response to HCMV-infected fibroblasts, an effect that was prevented by early treatment with a blocking anti-CD94 mAb [41]. Based on these studies, we hypothesized that a cognate interaction of the activating KLR with HCMV-infected cells might drive a preferential proliferation, differentiation, and/or survival of the NKG2C+ NK-cell subset in response to cytokines (i.e., IL-15).

To rule out the possible influence of diabetes on our results, we have analysed differences in fibrinolysis and coagulation parameters between BP patients and normal controls after the exclusion of the three diabetic BP patients and their RAD001 mw sex- and age-matched

controls. In the 17 BP patients with active disease, PAI-1 antigen and active PAI-1 levels were significantly higher (22·13 ± 8·68 ng/ml and 16·76 ± 5·55 ng/ml) than in the 17 sex- and age-matched healthy controls (8·65 ± 6·29 ng/ml and 6·21 ± 4·37 ng/ml) (P = 0·0001 for both). Plasma t-PA levels were also significantly higher in the 17 patients (36·91 ± 32·02 ng/ml versus 6·09 ± 4·45 ng/ml; P = 0·0001). Finally, plasma d-dimer and F1+2 levels were both markedly higher in

the 17 patients with active BP (2774 ± 3817 ng/ml and 631 ± 487 ng/ml) than in the 17 controls (183 ± 107 ng/ml and 106 ± 44 ng/ml) (P = 0·0001 for both). In the patients with active BP, disease severity (expressed as the percentage of involved body surface area) correlated significantly with the number of blood eosinophils (r = 0·705, P = 0·01) and the plasma levels of d-dimer (r = 0·713, P = 0·0001) and F1+2 (r = 0·703, P = 0·001). Plasma CRP levels correlated directly with the levels of PAI-1 antigen (r = 0·722, P = 0·0001), PAI-1 activity (r = 0·514, P = 0·021), t-PA antigen (r = 0·547, P = 0·012) and F1+2 (r = 0·450, P = 0·047) and the number of blood eosinophils MK 1775 correlated with PAI-1 antigen (r = 0·585, P = 0·046), PAI-1 activity (r = 0·680, P = 0·015) and d-dimer (r = 0·710, P = 0·010). Anti-BP180 autoantibody levels only correlated with d-dimer (r = 0·495,

P = 0·026) and F1+2 (r = 0·458, P = 0·042). In the 20 BP patients during remission after treatment, the levels of PAI-1 antigen and active Oxalosuccinic acid PAI-1 decreased significantly from 25·06 ± 8·88 ng/ml to 16·99 ± 7·05 ng/ml and from 15·65 ± 5·75 ng/ml to 11·19 ± 5·14 ng/ml (P = 0·008 and P = 0·006, respectively) (Fig. 1). The mean differences were 5·30 ng/ml [95% confidence interval (CI): 1·65–8·96 ng/ml] for PAI antigen and 4·00 ng/ml (95% CI: 1·66–6·35 ng/ml) for active PAI. There was an albeit not significant decrease in tPA levels (from 34·70 ± 33·22 to 32·74 ± 27·80 ng/ml). Plasma TAFI levels did not change significantly (Fig. 2), but there was a significant decrease in the plasma levels of d-dimer (from 2350 ± 3676 ng/ml to 571 ± 651; P = 0·0001) and F1+2 (from 551 ± 484 ng/ml to 188 ± 216; P = 0·0001). The mean differences were 2804 ng/ml (95% CI: 744–4865 ng/ml) for d-dimer and 414 ng/ml (95% CI: 191–638 ng/ml) for F1+2.

After overnight incubation with polyclonal antibodies against FOXP3 (sc-21072; Santa Cruz Biotechnology, Santa Cruz, CA) and anti-human IL-17 monoclonal antibodies (R&D Systems Inc., Minneapolis, MN), the samples were incubated with the secondary antibodies, biotinylated with anti-IgG for 20 min and then incubated with a streptavidin–peroxidase complex (Vector, Peterborough, UK) for 1 hr. This was followed by incubation with 3,3’-diaminobenzidine (Dako, Glostrup, Denmark). The sections were counterstained with haematoxylin, and samples were photographed with an Olympus photomicroscope (Tokyo, Japan). The LDE225 research buy positivity for each immunohistochemistry stain was examined in a blind fashion relative

to the clinical information. Analysis was performed by counting the total number of infiltrating cells that express FOXP3 or IL-17 in the cortex. The area of cortex was measured with a loupe and the data were expressed as

the number of cells/mm2. The counting of the FOXP3+ and IL-17+ cells was performed by HistoQuest Experiment (TissueQuest Software, TissueGenostics, Vienna, Austria). A pathologist blinded to the results of the HistoQuest Experiment, manually counted the cell number. The FOXP3+ cell and IL-17+ cell numbers counted by pathologist and HistoQuest Experiment were highly correlated (r = 0·901, P = 0·00) AT9283 cell line and the result did not change the classification of the patient. Indirect immunofluorescence staining was Protein kinase N1 performed using monoclonal antibodies against complement protein C4d (Biogenesis, Poole, UK) in 48 (68%) biopsies. In 23 (32%) biopsies where no C4d staining was performed on frozen sections, sections were obtained from paraffin blocks and stained for immunohistochemistry with C4d using a rabbit polyclonal antibody (Biogenesis, Poole, UK). C4d positivity was defined as diffuse (> 50%) and linear staining of peritubular capillaries. Figure 1(a,b) shows representative stains of FOXP3 and IL-17. The cell numbers of the FOXP3+ cell and IL-17+ cell infiltrations were 11·6 ± 12·2 cells/mm2 and 5·6 ±

8·0 cells/mm2, respectively. The average value of the ratio between FOXP3+ cell and IL-17+ cell (FOXP3/IL-17) was 5·6 ± 8·2. We used log transformation to correct data skewness for the FOXP3/IL-17 ratio. When log transformation of the FOXP3/IL-17 ratio (Log FOXP3/IL-17) is 0·45, it conferred the highest sensitivity (0·713) and specificity (0·724) in the prediction of allograft failure by receiver operating characteristic analysis. Therefore, when Log FOXP3/IL-17 was > 0·45, the biopsy was considered as the FOXP3 high group (n = 30) and when it was < 0·45, the biopsy was considered as the IL-17 high group (n = 26). Only the first biopsy tissues were considered in the evaluation of the clinical outcome after ATCMR and the long-term allograft survival. Clinical information was collected by retrospective chart review.

The number of β cells, determined from β cell mass [17–20], is an outcome of developmental turnover and the level of autoimmune destruction [13,16,19,21]. β cell insulin production is regulated by the levels of glucose and inflammatory mediators [22,23]. Autoantigens.  Autoantigens are modelled generically to represent several antigens identified in the literature, including insulin and glutamic acid decarboxylase [24,25]. The autoantigen level is a function of β cell mass, β cell apoptosis and insulin secretion. Autoantigens are acquired and presented on major histocompatibility complex (MHC) class I and II molecules by dendritic cells (DCs), macrophages and B lymphocytes [26–28].

β cells also present autoantigens on MHC class I molecules [29]. Dendritic cells.  DCs are present in each modelled islet, even in the absence of inflammation, and recruitment of DC precursors is amplified by inflammation [30,31]. Both ABT-263 order inflammatory and suppressive (tolerogenic) DC phenotypes are represented [32,33]. Each subset influences the developing adaptive immune response, and each has limited phagocytic capabilities [34]. DCs acquire

and present antigens, produce mediators, interact with other cell types and traffic from the islets to the PLN Cilomilast molecular weight [26,35–37]. Macrophages.  Macrophages are also present in the islets even in the absence of inflammation, and recruitment of macrophage precursors is amplified by inflammation [38,39]. Macrophages perform phagocytic functions, acquire and present antigens, produce mediators, interact with other cell types and traffic to the PLN [27,37,40,41]. CD4+ T lymphocytes.  Two groups of naive CD4+ T lymphocytes are represented: those specific for islet autoantigens and those specific for other antigens. This same distinction is made for all other T lymphocyte and B lymphocyte populations. In the model, thymic output of naive T Buspirone HCl cells is a specified time-dependent

profile representative of what has been observed experimentally [42–44], taking into account the relative proportion of CD4+ and CD8+ T cells [45], but is not regulated dynamically. While the intricate and highly regulated process of thymocyte development has been studied extensively, it was not included in the current model scope based on an initial focus on peripheral mechanisms of autoimmunity and tolerance. The validation protocols used to refine and test virtual mouse behaviours were dependent primarily on peripheral mechanisms. However, the model was designed to accommodate expansion of the represented biology, which could include thymocyte development. During simulations, naive islet-autoantigen-specific (or diabetes-specific) T lymphocytes in the PLN become activated in response to autoantigen presented on MHC class II molecules and differentiate into T helper type 1 (Th1), Th2 or regulatory T cell (adaptive regulatory T cell or aTreg) subsets [46–49].

6). As shown, Listerianeg CD8α+ DCs up- (or down-) regulated the distinct maturation markers with a 1.5- to a 2.5-fold difference between mice that received a protective and a non-protective dose of secA2−Lm. In agreement with our hypothesis, Listeriapos CD8α+ DCs purified from protected animals also exhibited a stronger modulation of their maturation markers (∼two-fold)

than those from non-protected mice. In correlation with this result, cell-surface expression levels of CD86, CD80 and CD40 costimulatory molecules on infected GFP+ CD8α+ cDC this website only but not on the non-infected cDC (CD8α+ or CD8α−) was 2–3 times stronger (Supporting Information Fig. 6). Therefore, in addition to receiving signals from bacteria replicating inside their cytosol, CD8α+ DCs from protected mice integrated additional selleck chemicals llc signals – likely from the stronger inflammatory environment – which accounted for

the observed difference of maturation with non-protected mice. We have investigated the ability of the two splenic cDC subsets to induce antibacterial memory CD8+ T cells that can protect against a recall infection. We found that CD8α+ cDCs from primary immunized hosts are the most efficient cDC subtype for transferring long-term, anti-Lm memory CD8+ T-cell-mediated protection to naïve recipient animals. Since both DCs subsets were loaded with saturating amounts of the same antigenic peptide and expressed equivalent cell-surface levels of MHC class I molecules, such features are independent of their capacity to process MHC class HAS1 I-associated antigens. Interestingly, CD8α+ cDCs become endowed with these functional features as early as 5 h following the primary immunization and this requires cytosolic signals that are potentiated by extracellular inflammatory signals delivered by bacterial infection of the host. Several

seminal studies established that cDCs are key players to prime naïve antigen-specific CD8+ T cells in vivo 3, 4. While these reports support a critical function for splenic CD8α cDCs in initiating primary CD8+ T-cell responses in vivo 3, 4, 9, 11, 12, 14, 27–30, none of them had addressed the question of their ability to set memory development, i.e. whether – and to which extent – they exhibit the functional capacity to induce antibacterial protective CD8 memory. By showing that splenic CD8α cDCs become rapidly conditioned to induce anti-Lm protective memory CD8+ T cells and are best to provide such effect in vivo, we highlight a novel feature of these cells. In addition, we uncouple this functional property of CD8α+ cDCs from their ability to process the antigens from the bacteria.

So far, there are convincing data that preservation of residual renal function (RRF) was associated with better survival and HRQOL in hemodialysis and PD patients. The purpose of our study was to investigate contributing factors including RRF that influence HRQOL in PD patients. Methods: A total 92 prevalent PD patients were consecutively included between March 2001 and May 2012. The Chinese-language

version of KDQOL-SF™ 1.3 was used to evaluate HRQoL, which is an expansion GDC-0068 of the SF-36 that contains 8 dialysis-specific dimensions: burden of kidney disease, cognitive function, symptoms or problems, effects of kidney disease on daily life, quality of social interaction, sexual function, sleep, and work status. Measures of clinical characteristics, PD adequacy indices, and quality of life were recorded at 1 month, 6 months, and 12 months as protocol. Spearman’s rank Olaparib chemical structure correlation coefficient was

used to test for the association between variables. The differences were considered significant with P value <0.05. Results: There was no significant difference between baseline clinical characteristics and the SF-36 dimensions or 8 dialysis-specific dimensions. There were not significant correlation between the given time-point KDQOL-SF “summary scores” and PD adequacy indices. Of note, the change in subscale scores of sexual MRIP function and sleep quality were correlated with baseline renal Kt/V values positively (r = 0.26, p = 0.01; r = 0.23, p = 0.03, respectively).

Baseline nutritional status or dialysis adequacy indices were not closely associated with the change of HRQOL scores. Conclusion: The present study demonstrated the correlations between baseline renal Kt/V values and subscale scores in HRQOL, especially focus on the changes of sexual function and sleep quality. Accordingly, the results implicated RRF contributing to the disturbances in sexual function and sleep in PD patients. MATHUR PIYUSH1, CHAKRAVARTHI RAJASEKARA2, BABU SETU3, REDDY VIKRANTH4, GONDANE SHAILESH5, HEDAU SANTOSH6 1Department of Nephrology, Care Hospital, Hyderabad; 2Department of Nephrology, Care Hospital, Hyderabad; 3Department of Gastrentrology, Care Hospital, Hyderabad; 4Department of Nephrology, Care Hospital, Hyderabad; 5Department of Nephrology, Care Hospital, Hyderabad; 6Department of Nephrology, Care Hospital, Hyderabad Introduction: Refractory ascites accounts for severe morbidity in patients of chronic liver disease. These patients despite on salt restriction and diuretics have poor quality of life and require repeated paracentesis which leads to significant protein loss requiring albumin infusion. Methods: We have done Ascitic Fluid Ultra filtration and Reinfusion Therapy (AURT) in two patients with refractory ascites due to hepatic cirrhosis of varied etiology.