At peak, the mean parasitemia percentages in IL-15−/− and control mice were similar, 10.43 ± 2.66% and 9.81 ± 5.44% respectively. Differences in the results published 5-Fluoracil in vivo by Ing et al. (14) and our findings may be attributed to the differences in virulence of the subspecies of P. chabaudi used in the different studies. Our results indicate that the IL-2R complex has an essential protective

role in immunity to blood-stage malaria. Protection is achieved by γc cytokine family members signalling through the IL-2Rγc signifying the importance of a single gene in immunity to malaria but leaves unanswered two important questions. (1) Which members of the γc cytokine family are responsible for stimulating protective immunity to blood-stage parasites and (2) what are the protective mechanisms activated through IL-2Rγc signalling? IL-2Rγc−/y mice are also deficient in NK cells, NKT cells and CD8+ T cells (24). However, our recent findings do not suggest a protective role for any of these cells in immunity to blood-stage

malaria (25). Although the roles of IL-7, IL-21 and IL-9 are unknown in blood-stage infections caused by P. c. adami, no single member of the γc cytokine family has been identified as having such a protective role. Furthermore, our data indicate that neither IL-2 nor IL-15 signalling separately through the IL-2R has an essential role in protective immunity. Whether they or other γc cytokine family members can function together sequentially, additively or synergistically Opaganib cost to activate protective immunity to blood-stage DCLK1 malarial parasites remains to be determined. As a model, the IL- 2Rγc−/y

mouse provides a unique opportunity to analyse down-stream gene activation and its contribution to immunity. This work was supported by grants AI12710 (WPW) and AI49585 (JMB) from the National Institutes of Health. “
“Human genetics research has had a great impact on the genesis of the inflammasome field and the treatment of certain inflammasomopathies. The identification of mutations causing rare autoinflammatory syndromes, reproductive wastage disorders and of single nucleotide polymorphisms influencing susceptibility to complex diseases such as vitiligo, sepsis, and Crohn’s disease has not only led to the characterization of novel proteins involved in NOD-like receptor-coupled inflammatory signaling pathways but also to greater insights into pathogenic mechanisms. It is widely recognized that diseases that exert considerable burden on human health worldwide, including cancer, infectious diseases, sepsis, and inflammatory disorders, have both an intrinsic genetic susceptibility component and an extrinsic environmental component (chemical factors, physical factors, infectious agents, etc.). The complex interaction between these two interfaces determines the time of disease onset, progression, and pathogenic outcome.

Strains used for this study have been verified by rDNA internal transcribed spacer (ITS) and partial β-tubulin (BT2) sequencing and compared with ex-type isolates in the reference collection of the CBS-KNAW Fungal Biodiversity Centre, Utrecht, the Netherlands. We analysed 32 strains of Pseudallescheria, Petriellopsis and Scedosporium (Table 1). Methods of DNA extraction, alignment and phylogenetic analysis were those of Badali et al. [18] Species attribution was verified by sequencing ITS rDNA and partial β-tubulin (BT2) according to Gilgado et al. [10] and by comparing them with ex-type isolates from the reference collection of CBS (Utrecht, the

Netherlands). Pseudallescheria angusta and P. ellipsoidea this website are listed as part of P. boydii. Three different microtitre plates were used with the Taxa Profile Micronaut system (Merlin Diagnostika GmbH): Taxa Profiles A, C and E. On each microtitre plate, two strains were analysed synchronously for 191 reactions in the case of Taxa Profiles A and C (one growth control) and 188 reactions for Taxa Profile E (three negative controls and one growth control). Taxa Profile A contains amines, amides, amino acids, other organic acids, and includes heterocyclic aromatic compounds. Taxa Profile C contains mono-, di-, tri- and polysaccharides, and sugar derivatives.

On panels A and C, each well contains 1.6 g L−1 of the respective chemical compound. Results were read https://www.selleckchem.com/products/sotrastaurin-aeb071.html visually and photometrically at 620 nm (single scan). Taxa Profile E contains 95 aminopeptidase and protease reactions, 76 glycosidases, phosphatidases and esterases (each for testing at the different pH values of 8.2, 7.5, 5.5 and 4.0), desaminases and decarboxylases (arginine-dihydrolase, glutamate-, lysine-, ornithine-decarboxylases and relevant control reactions), and 17 classical reactions (such as urease, indol, nitrate and nitride). A full

list of the reactions is provided in Supporting Information. Strains were cultured on potato dextrose agar (PDA; Oxoid, Wesel, Germany), Sabouraud’s 4% glucose agar, water agar, Müller Hinton’s agar and Columbia sheep blood agar. The incubation period was up to 7 days at 35 ± 1 °C to Fluorometholone Acetate obtain optimal conidiation. The plates were covered with 5–6 ml sterilised 0.9% NaCl solution. Conidia were scraped off carefully and transferred into a sterile glass tube using a sterile pipette. The suspensions were vortexed and centrifuged for 5 min at 21 °C at 3000 rpm; sediments were washed three times in 5 ml sterile 0.9% NaCl solution. Suspensions were adjusted with a UV 160 spectrophotometer for Taxa Profiles A and C panels to 0.150–0.170 at 530 nm (1–5 × 104 colony forming units ml−1),19 and to 0.20–0.28 at 560 nm for Taxa Profile E.

,

2006), while Chawla et al. (2009) have suggested preserving those tissue samples in normal saline and not in the formalin as the latter is known to cause alterations in DNA for PCR assays. The combined use of nested PCR targeting IS6110 and mycobacterial culture (both automated and conventional) for the diagnosis of osteoarticular TB has also been documented (Agashe et al., 2009). Recently, Sharma et al. (2011b) introduced a highly sensitive and specific multiplex PCR targeting IS6110 and MPB-64 protein genes in the prospective evaluation of synovial fluid and pus samples from 80 cases of osteoarticular TB. The rpoB PCR-plasmid TA cloning-sequencing method to detect M. tuberculosis in the joint tissue, synovial fluid and pus samples from osteoarticular TB has been developed by Yun et al. GS-1101 order (2005) and their method could simultaneously determine rifampin (RIF)

susceptibility of tubercle bacilli. Fujimoto et al. (2010) also confirmed a case of TB pleuritis with knee-joint involvement by PCR analysis of the synovial fluid. Interestingly, Colmenero et al. (2010) developed a reliable and sensitive multiplex real-time PCR based on conserved region of the gene coding for an immunogenic membrane protein of 31 kDa of Brucella abortus (BCSP31) and SenX3-RegX3 (intergenic region of M. tuberculosis) gene for the rapid differential diagnosis of TB vertebral osteomyelitis and brucellar vertebral osteomyelitis. Ensartinib concentration Genitourinary TB comprising of genital and renal TB is the second most common EPTB and contributes up to 46% cases of EPTB (Jacob et al., 2008). Renal TB occurs up to 20 times more frequently in kidney transplant recipients than in the general population (Wise, 2009). The early diagnosis of renal TB is very important in preventing progressive destruction of the kidney (Wise, Amobarbital 2009). Recently, Sun et al. (2010) described an early and rapid diagnosis of renal TB from renal biopsy specimens by real-time PCR using 35-

and 40-cycle threshold (CT) cut-off values. It was found that the real-time PCR (CT 40) showed better sensitivity than the real-time PCR (CT 35). Genital TB has been involved in the infertility of both men and women, and majority of such cases remain undiagnosed owing to asymptomatic presentation of the disease (Rana et al., 2011). Hence, a high index of suspicion is necessary for the diagnosis of genitourinary TB. To confirm genitourinary TB (both in men and women) in urine samples, PCR targeting MPT-64 protein gene has earlier been demonstrated to be the most sensitive indicator as compared to intravenous urography, bladder biopsy or urine culture (Hemal et al., 2000). The utility of PCR targeting IS6110 or 16S rRNA gene has also been evaluated in urine samples for the diagnosis of genitourinary TB (Moussa et al., 2000; Abbara & Davidson, 2011). High sensitivity up to 100% has been claimed by nested PCR based on MTP-40 protein gene of M. tuberculosis (Garcia-Elorriaga et al., 2009).

enterica serovar Typhimurium harboring the empty pYA3560 vector. Furthermore, PrV-specific IgG levels induced by oral administration of S. enterica serovar Typhimurium expressing either swIL-18 or swIFN-α were comparable to levels of those that received Alum-absorbed inactivated PrV vaccine, and were significantly enhanced by co-administration of S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α (Fig. 1a). These results indicate that oral co-administration of S. enterica serovar Typhimurium

expressing swIL-18 and swIFN-α could induce enhancement of PrV-specific IgG SB525334 nmr levels raised by single administration of S. enterica serovar Typhimurium expressing either swIL-18 or swIFN-α. When the modulatory effect of the co-administered S. enterica serovar Typhimurium

expressing swIL-18 and swIFN-α on the production of PrV-specific IgG isotypes (IgG1 and IgG2) was evaluated, piglets that received Alum-absorbed inactivated PrV vaccine produced a higher amount of PrV-specific IgG1 isotype compared to the other groups (Fig. 1b). In contrast, the oral co-administration of S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α induced the production of a higher amount of PrV-specific IgG2 isotype (Fig. 1c). Therefore, the enhancement of IgG2 isotype production through the co-administration of S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α resulted in a higher IgG2 to IgG1 ratio in the sera (Fig.

1d). The modulatory effect Vemurafenib datasheet of co-administration of S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α on the generation of cellular MRIP immune responses was also examined. To accomplish this, PBMCs (responder) isolated from piglets immunized with the indicated protocols were stimulated with autologous PBMCs (stimulator) that had been previously pulsed with inactivated PrV antigen. This stimulation using inactivated PrV-pulsed PBMCs is known to induce a predominant expansion of immune CD4 + T cells (8). As shown in Figure 2a, PBMCs isolated from PrV-vaccinated piglets were significantly proliferated by stimulation with PrV-pulsed PBMCs, when compared to PBMCs isolated from the control group. Notably, PBMCs obtained from piglets co-administered S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α proliferated more upon stimulation with PrV-pulsed PBMCs but did not show the apparently enhanced proliferation, when compared to piglets that received S. enterica serovar Typhimurium expressing either swIL-18 or swIFN-α. Also, PBMCs isolated from Alum-absorbed PrV-vaccinated piglets showed comparable proliferation to those from piglets co-administered S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α.

78–0.96, I2 = 71.6%). When combining the nine studies[30, 36, 37, 41-43, 45-47] with adjustment of confounders by propensity score method, the protective effect was still significant (pooled OR, 0.83; Selleck INK-128 95% CI 0.75–0.92, I2 = 67.1%). However, when the five studies[24-28] with a RCT design were combined, a non-significant trend for protective effect was shown (pooled OR, 0.49; 95% CI 0.22–1.09, I2 = 0.0%). In patients undergoing isolated cardiac operation in 18 studies,[24-30, 32, 34-38, 40-42, 44, 47] use of statins was associated with a borderline reduced risk of postoperative AKI (pooled OR, 0.93; 95% CI 0.86–1.00, I2 = 49.4%). When the surgery type is restricted to isolated coronary artery bypass grafting (CABG),[24-27,

29, selleck products 30, 35, 36, 40, 44, 47] the pooled effect estimate was still significant (pooled OR, 0.78; 95% CI 0.62–0.98, I2 = 56.8%). We also analyzed the seven studies[28, 37, 38, 41, 44-46] using standard RIFLE or AKIN criteria to define AKI. The summary estimate showed a null effect though a trend in favour of statin treatment was seen (pooled OR, 0.88; 95% CI 0.76–1.01, I2 = 55.4%). There were 14 studies[28, 31-35, 37, 39-41, 43-46] reporting the association between use of statins and risk of postoperative AKI defined by a more stringent criterion: need for RRT. Galbraith plots for these studies (Appendix Fig. App1) showed that studies by Borger et al.[39] and Huffmyer et al.[35] were potential sources

of heterogeneity. After excluding

the two studies, a total of 94 439 cases and 850 817 controls were included (Table 1). Again, the effect size of the highest methodological quality in each study was included in the analysis. When these 12 studies were combined, the use of statins was associated with a significantly reduced risk on perioperative AKI requiring RRT (pooled OR, 0.80; 95% CI 0.72–0.90, I2 = 00.0%) (Fig. 2B). After excluding RCTs from analysis, the same pooled summary effect estimate was shown (pooled OR, 0.80; 95% CI 0.72–0.90, I2 = 00.0%). In the contrary, pooled results from crude OR reported in seven[31, 32, 37, 41, 43, 44, 46] studies showed a non-significant harmful effect of statin ZD1839 research buy therapy on postoperative AKI requiring RRT (pooled OR, 1.26; 95% CI 0.90.–1.76, I2 = 53.1%). However, when the seven studies[33, 34, 37, 40, 43, 45, 46] with effect sizes adjusted by PSM or multivariate analysis were included, use of statins was associated with a significant protective effect (pooled OR, 0.81; 95% CI 0.72–0.91, I2 = 0.0%). When the five studies[33, 37, 43, 45, 46] reporting effect sizes adjusted specifically by PSM analysis were included, the result still showed a protective effect (pooled OR, 0.81; 95% CI 0.72–0.92, I2 = 00.0%). Consistent with our previous finding, in patients undergoing isolated cardiac operation in the nine studies,[28, 31-34, 37, 40, 41, 44] we also observed a borderline protective effect (pooled OR, 0.77; 95% CI 0.59–1.00, I2 = 67.5%).

They were examined at 0, 1, 3, 6 and 12 months. The factors influencing the prognosis were investigated. The stone discharge was monitored by ultrasonography. Overt renal and liver damage and underlying renal injury markers were analyzed. Results:  The stone discharge rates 1, 3, 6 and 12 months after the diagnoses were 52.5%, 67.2%, 88.3% and 95.5%, respectively. Stone size was a stable influencing factor for the stone discharge rate.

Additionally, the values of the potential renal injury markers in children with stones already discharged is Selleck R428 equivalent to normal children. Conclusion:  This 12 month follow up of early renal injury markers indicated that the damage to the kidney is temporary with no persistent negative outcomes being found till now. Additionally, the gross development of the children seemed not yet jeopardized by melamine. Longer-term follow up will be conducted. “
“To investigate the potential effects of berberine on renal interstitial fibrosis (RIF) of obstructed kidneys in a unilateral ureteral obstruction (UUO) rat model. Forty-eight rats were randomly divided into three groups: sham-operated, vehicle-treated UUO, and berberine-treated UUO. Rats were gavaged with berberine (200 mg/kg per day) or vehicle. Eight randomly chosen rats in each group were kiled and specimens were collected at day 14 after UUO. Physiological

parameters Rapamycin clinical trial and histological changes were assessed, RIF was evaluated using Masson’s trichrome and Sirius red staining, oxidative stress and inflammation markers were determined, transforming growth factor β1 (TGF-β1), phosphorylated Smad3 (pSmad3) and α-smooth muscle actin (α-SMA)

were measured using immunohistochemistry or western blotting analysis. The obstruction was relieved at day 14 by percutaneous nephrostomy in the remaining UUO rats. The resistive index of left kidneys was undertaken by coloured Doppler flow imaging at day 14 before nephrostomy and day 7 after the Myosin relief. Berberine treatment significantly attenuated RIF induced by UUO. The UUO-induced reduction in kidney superoxide dismutase and catalase activities increased, whereas elevated kidney malondialdehyde level markedly decreased. Berberine treatment significantly ameliorated UUO-induced inflammation, and decreased TGF-β1, pSmad3 and α-SMA expression of UUO kidneys. Moreover, berberine treatment significantly suppressed the increase of resistive index compared with UUO group at day 14 after UUO as well as day 7 after the relief of obstruction. Berberine treatment ameliorates RIF in a UUO rat model by inhibition of oxidative stress, inflammatory responses, and TGF-β1/pSmad3 signalling. “
“Observational reports suggest extended dialysis hours are associated with improved outcomes. These findings are confounded by better prognostic characteristics among people practising extended hours.

They also produce several cytokines in response to stimulation signals www.selleckchem.com/products/gdc-0068.html from pathogen-associated molecular patterns or whole bacteria. Hence, DCs contribute to immunological homeostasis by promoting inflammatory responses to pathogens, inducing tolerance to self antigen, and suppressing excessive immune responses.1,2 Dendritic cells play a critical role in the maintenance of immunological homeostasis and DC dysregulation can lead to autoimmune diseases and chronic inflammatory disorders. Abnormally excessive immune responses to commensal bacteria, food antigens and self antigens have been reported in the pathogenesis

of these diseases. Therefore, conditioning DCs to display desirable selleck products properties, such as inducing an immunosuppressive DC phenotype, might represent a novel therapeutic strategy for these diseases. Recent studies have indicated that signalling through nuclear receptors, such as the retinoic acid receptor, the farnesoid X receptor (FXR) and the peroxisome proliferator-activated receptor-α, plays an important role in modulating the transcription of cytokine genes in innate immune cells.3 Interleukin-1 (IL-12) produced by DCs has been implicated in promoting a type 1 helper T cell immune response

and contributing to the pathogenesis of several chronic inflammatory disorders.4–6 We previously demonstrated that Am80, a retinoic acid receptor agonist, promotes

DC differentiation towards an IL-12 hypo-producing phenotype and that this molecule potentially represents a novel therapeutic molecule for inflammatory bowel disease.7 The identification of similar molecules that induce an IL-12 hypo-producing DC phenotype might allow the development of novel therapeutic molecules for chronic inflammatory disorders. We hypothesized that bile acids (BAs), which are ligands for FXR and TGR5, might regulate DC differentiation and so we examined whether a BA can induce an IL-12 hypo-producing DC phenotype. Bile acids are a family Oxymatrine of steroid molecules generated in the liver by cholesterol oxidation. They accumulate in the blood, intestine and liver via enterohepatic circulation. In addition to their role in nutrient absorption, BAs are signalling molecules that can regulate immune cell responses via FXR and TGR5.8 FXR is a member of the nuclear receptor superfamily of ligand-activated transcription factors8–12 and is primarily expressed in enterohepatic tissues. FXR is known to regulate genes involved in BA synthesis, detoxification and excretion, and an increase in intracellular BA concentrations promotes transcriptional activation of FXR.13–15 In addition, it has been reported that the FXR signalling pathway influences immunological responses such as cytokine production by immune cells.

T cell receptor signalling upon antigen presentation results in T cell activation or inhibition when accompanied by CD28 or CTLA-4 co-stimulation, respectively [11, 12]. CTLA-4–immunoglobulin (Ig) is a fusion molecule of the extracellular domain of CTLA-4 and the heavy chain of human or mouse IgG [13, 14]. This molecule has been shown to exhibit tolerogenic properties towards Enzalutamide chemical structure self- and allograft antigens in human patients and in animal models [15-17]. CTLA-4–Ig is a US Food and Drug Administration (FDA)-approved compound that has been used in the treatment of rheumatoid arthritis and prevention of allograft rejection

[18, 19]. Interestingly, we have shown previously that CTLA-4–Ig treatment at the time of allergen inhalation in sensitized mice induced long-term tolerance to subsequent allergen-induced airway eosinophilia, but not airway hyperreactivity (AHR), in a mouse model of experimental asthma [20]. CTLA-4–Ig shows tolerogenic properties through two mechanisms: (i) sequestration of B7 and thereby inhibition of CD28 signalling [11, 21] and (ii) reverse signalling into dendritic

cells (DC) through B7 and subsequent activation of the alternative nuclear factor (NF)κB pathway leading to expression of the immunoregulatory enzyme LY294002 in vivo indoleamine 2,3 dioxygenase (IDO) [22]. Interestingly, we have shown previously that IDO contributes to SIT-induced tolerance induction in our model [23]. Recently, an early induction of IDO has been observed after venom SIT, suggesting a role for IDO in SIT-induced allergen tolerance in human patients [24]. In this study, we tested whether CTLA-4–Ig can act as an adjuvant for experimental SIT.

To this aim we administered CTLA-4–Ig with SIT in an ovalbumin (OVA)-driven mouse model of asthma. We show that co-administration of CTLA-4–Ig with SIT highly enhances the SIT-induced suppression of AHR, airway eosinophilia and OVA-specific IgE levels in serum. Furthermore, we show that the effect of CTLA-4–Ig is independent Tolmetin of IDO, indicating that CTLA-4–Ig in our model acts by blocking the CD28-mediated T cell co-stimulatory signal. Specific pathogen-free 6–8-week-old BALB/cByJ mice (Charles River Laboratories, L’Arbresle, France) and IDO-knock-out (IDO-KO; C.129X1(B6)-Ido1tm1Alm) on a BALB/c background (kindly provided by Dr A.L. Mellor, GA, USA), were used according to the guidelines of the institutional animal care and use committee of the University of Groningen. Experimental allergic asthma was induced and SIT was performed according to the previously described protocol [25]. Concisely, as shown in Fig. 1, mice were sensitized by intraperitoneal (i.p.) injection of 10 μg endotoxin-free/low (<5 EU/mg) OVA (Seikagaku Kogyo, Tokyo, Japan) and 2·25 mg alum (Pierce, Rockford, IL, USA) in 100 μl of pyrogen-free saline. Two weeks later, they either received 100 μg OVA in 200 μl saline per injection as OVA-SIT or 200 μl saline as placebo through three subcutaneous (s.c.

The opening chapter is key in attempting to teach the reader, rather than requiring the reader to read and understand. For me, this leads to a deeper level of learning, and therefore I think the book is particularly valuable for neuropathologists in training and histopathologists who are interested in neuropathology. The editors have a self-professed commitment to education and are internationally renowned neuropathologists, and the generosity of knowledge in this book is clear. There are 28 contributors, from the USA, Canada, France, selleck compound Germany and Portugal. The entire book is very well illustrated, with large good-quality colour images of

macroscopic findings, histology, immunohistochemistry and radiology. Images are also included of important molecular tests, for example, dual-colour fluorescence in situ hybridization, and there are a few electron microscopy images. Coloured headers and footers relating to chapter identity are a nice touch. There are several useful tables, again with colour coding that makes interaction with the book very easy. The index, R788 solubility dmso at nearly 50 pages long, is as comprehensive as the book itself. It is printed on good-quality paper, and hard bound. As part of the expert consult

series, the book comes with access through registration at http://www.expertconsult.com to a wealth of images, which may be downloaded and imported into PowerPoint presentations. After the opening ‘pattern’ chapter there is a good description of normal (primarily adult) brain histology, followed by equally useful descriptions of common surgical artefacts and pragmatic intraoperative basics. A fourth chapter explains common and advanced neuroradiological techniques, with well-illustrated examples, and a whole-page table of relevant patterns. Approximately tuclazepam half of the book is dedicated to tumour

pathology. There are 13 tumour chapters, including one each on peripheral nerve sheath tumours, lymphomas and histiocytic tumours, germ cell tumours, melanocytic neoplasms and pituitary pathology. Following this, there are good chapters on iatrogenic disease, familial tumour syndromes, then inflammatory conditions, white matter disease, epilepsy, vascular disorders and the biopsy in neurodegenerative disorders. If I am to find criticisms, they are minor. With such a useable, practical book, I would have preferred a soft cover to keep the relevant page propped open on my desk. There is no nerve, muscle, bone or ophthalmic section. With the surgical nature of this book, these absences are excusable and understandable, but I cannot help feeling the authors would have benefitted their readers by including their take on broader neuropathological specimens. The preface refers to neuropathology songs used by one of the editors – I have yet to sample these, but will do so quietly, in my office, with the door shut.

5 ± 26.2 ml/min/1.73 m2. Mean proteinuria was 1.19 ± 1.61 g/day, and mean urinary red blood cells were 36.6 ± 35.3 / high powered field. Histologically, mesangial hypercellularity was present in 47.6% of patients, endothelial hypercellularity in 44.3%, segmental sclerosis in 74.6%, and

tubular atrophy/interstitial fibrosis in 28.8% by Oxford classification. Initial treatment consisted of corticosteroids in 26.9% of patients, renin-angiotensin-aldosterone system inhibitor in 28.9%, and tonsillectomy plus steroids in 11.7%. The 10-, 20-, and 30-year renal survival rates were 84.3, 66.6, and 50.3%, respectively. Cox multivariate regression analysis showed that higher proteinuria, lower eGFR, and higher uric acid at the time of renal biopsy

were independent risk factors for the development of end stage renal disease (ESRD). ZD1839 mouse Conclusion: IgAN is not Pexidartinib solubility dmso a benign disease, with about 50% of patients progressing to ESRD within 30 years despite treatment. LAW MAN CHING, FUNG JANNY SF, LAM MAN PING, CHOW KAI MING, POON KA LAI, LI PHILIP KT Prince of Wales Hospital Introduction: Psychosocial support has been identified as one of the important elements in a successful peritoneal dialysis (PD) first program. With an aim to strengthen the psychosocial support for PD patients, our team have developed comprehensive patient and community educational programs. Methods: In order to empower the PD patients and to build up a secure social network for them, we organize varies education programs to our patients, community stakeholders and the general public. The table 1 below lists the educational programs and the interventions. Results: Majority of the kidney patients accept PD as the first-line dialysis modality for them and make an informed choice on PD. Community stakeholders and the general public understand PD is safe and effective for kidney patients. Over 90% of the program participants have positive feedback on the

programs. Conclusion: Educational strategies could facilitate the implementation of PD-first policy by enhancing the society’s overall knowledge and hence the confidence in PD. MATSUBARA CHIEKO1, KASUGA HIROTAKE1, TAKAHASHI RYO1, KIMURA KEIKO1, KAWASHIMA KIYOHITO1, KAWAHARA HIROHISA1, MATSUO Protein tyrosine phosphatase SEIICHI2, ITO YASUHIKO2 1Nephrology, Nagoya Kyoritsu Hospital; 2Nephrology, Nagoya University Graduate School of Medicine Case: A 79-year-old male patient. Chief Complaint: Low grade fever lasting 3 months. Present History: A 79-year-old male patient started peritoneal dialysis in December 2010 and was followed up at the outpatient clinic. He developed fever and his CRP levels were increased. Mediastinal lymphadenopathy was detected by computerized tomography in April 2012, (which was not demonstrated in March, 2011). His QuantiFERON (QFT) was positive and we suspected that his illness and mediastinal lymphadenopathy was due to tuberculosis. It was difficult to biopsy the tissues, and we did not detect other specific findings including laboratory data.