It can be excluded that surface opsonisation represents a major reason for the elimination of C3 and C1q from CSF since such a mechanism would not explain the generation of fragments of C1q, which is not cleaved during complement activation. Although the complement protein C3 is cleaved during complement activation, this mechanism cannot be responsible for the appearance of large fragments in the supernatant as visible by Western blotting, since but

only very small C3-derived peptides are soluble, all larger parts of the molecule remain attached to the pathogen surface. Second, the hypothesis of proteolytic complement degradation C59 wnt cell line is strongly supported by an additional experiment: after growth, the culture supernatants of various Pseudallescheria

and Scedosporium isolates were separated from the fungal hyphae by filtration; these supernatants were supplemented with purified C1q or C3 proteins. Carfilzomib Again, a time-dependent elimination of the purified complement proteins could be observed for the fast-degrading isolates with appearance of larger fragments after incubation of up to 2 days, which are then progressively disappear over time (data not shown). Third, Pseudallescheria and Scedosporium isolates were grown in nutrient-rich Sabouraud medium that makes the secretion of proteolytic enzymes for nutrient gaining dispensable, as shown for Aspergillus species.27,30 These fungal Sabouraud supernatants did not induce any decrease in the concentration of supplemented complement proteins. In summary, we hypothesise that the ability to deal with the possible effects

of complement proteins has a phylogenetic background and is largely species-specific. The predilection of infecting the CNS could have favoured the evolution of enzyme systems for degrading C3 and C1q. Furthermore, our results support the theory that – depending on the taxonomy – different species can be supposed to develop and exploit various mechanisms that facilitate growth and survival in the host and in specific organs. To identify these additional mechanisms in the different Pseudallescheria/Scedosporium species and to further examine the regulation of protease secretion remains an interesting topic for further investigations. All contributing authors declare that there are no conflicts of interest. “
“Candidemia is an important cause of morbidity and mortality SPTLC1 in the healthcare setting. However, there is limited information about risk factors for such infection among elderly patients. A case–control study was conducted during the period 2008–2011. For each case, two controls were selected among patients admitted to the same hospital, and individually matched by sex, age, time of admission, hospital ward and hospitalisation duration. The adjusted odds ratio (OR) was calculated using multiple conditional logistic regression. We identified 145 episodes of candidemia occurring in 140 patients with a median age of 80 years.

It will be necessary to examine by autopsy whether the type (artery or vein) and size of the involved vessels and the pathological subtype of angiitis is related to the etiopathogenesis and prognosis. It is also pointed out that the entity of lymphocytic angiitis is problematic. “
“K. Masui, T. F. Cloughesy and P. S. Mischel (2012) Neuropathology and Applied Neurobiology38, 271–291 Molecular pathology in adult high-grade gliomas: from molecular diagnostics to target therapies The classification

Birinapant mw of malignant gliomas is moving from a morphology-based guide to a system built on molecular criteria. The development of a genomic landscape for gliomas and a better understanding of its functional consequences have led to the development of internally consistent molecular classifiers. However, development of a biologically insightful classification to guide therapy Dasatinib is still a work in progress. Response to targeted treatments is based not only on the presence of drugable targets, but rather on the molecular circuitry of the cells. Further, tumours are heterogeneous and change and adapt in response to drugs. Therefore, the challenge of developing molecular classifiers that provide meaningful ways to stratify patients for therapy remains a major challenge for the field. In this

review, we examine the potential role of MGMT methylation, IDH1/2 mutations, 1p/19q deletions, aberrant epidermal growth factor receptor and PI3K pathways, abnormal p53/Rb pathways,

cancer stem-cell markers and microRNAs as prognostic and predictive molecular markers in the setting of adult high-grade gliomas and we outline the clinically relevant subtypes of glioblastoma with genomic, transcriptomic and proteomic integrated analyses. Furthermore, we describe how these advances, especially in epidermal growth factor receptor/PI3K/mTOR GBA3 signalling pathway, affect our approaches towards targeted therapy, raising new challenges and identifying new leads. “
“Cryptococcal meningitis is rarely complicated by immune-mediated leukoencephalopathy, but the precise pathomechanism is uncertain. A 72-year-old Japanese man treated with prednisolone for Sweet disease developed a subacute progression of meningitis, which was considered as neuro-Sweet disease. A treatment by methylprednisolone rapidly improved CSF findings with a remarkable decrease in lymphocyte numbers in the blood, but the patient’s consciousness still worsened after the cessation of the treatment. The patient developed cryptococcal meningitis and MRI showed abnormal intensities predominantly in the cerebral deep white matter along with the recovery of lymphocyte numbers in the blood, which resulted in death. A postmortem examination of the brain revealed degenerative lesions, especially at the cerebral white matter and cortex adjacent to the leptomeninges abundantly infiltrated by Cryptococcus neoformans.

3). The ability of Mϕ to reduce T-cell responses has been documented for many years.32 In tumour models, this is thought to contribute to tumour escape from immunosurveillance, but it is unlikely that this represents a normal physiological expression of this process. In inflammation stimulated by infection, restricting T-cell proliferation within the tissue could have a role simply by sparing finite metabolic resources for other effector cells that are present. Rapid T-cell division is highly dependent on local glucose33 and activated Mϕ also consume glucose and other sources of metabolic Dabrafenib ic50 energy at a high rate.34,35 Therefore, limiting proliferation may be a form of immune system triage at the site of

inflammation. Another possibility is that restricting T-cell activation prevents the differentiation of antigen-specific T cells within tissues. Segregating the environment in which T cells differentiate, from that in which they exercise effector function, could reduce the generation of T-cell effector cells that can be activated by autoantigens. At a site of acute inflammation, Mϕ will be processing large amounts of damaged normal tissue that might lead to an increased risk of local autoimmunity. It is not, however, the case that T-cell immunity is entirely shut down in this inflammatory microenvironment.

Our demonstration that T cells removed from the presence of Mϕ can resume proliferation (Fig. 2) shows that T cells that traffic away from the inflammatory environment will still be able to contribute selleck screening library to the pool of circulating activated antigen-specific cells. This local immune response could still serve to amplify T-cell responses and support the production of immunological memory. In terms of Mϕ function, our data suggest that a lack of TNFR1 signalling impedes the development of Mϕ with the capacity to inhibit T cells. This critical role for TNFR1 in the generation of these cells also suggests TNFR1 may be important to the generation of MDSC in tumours. Therefore, our study throws light on other previously unexplained findings: that in a model of metastasizing

lung carcinoma, although tumours initially expand at normal rates, in TNFR1−/− mice, metastases regress after 21 days.36 Also in TNFR1−/− mice and mice treated with TNFR1−/− bone marrow,37 there Guanylate cyclase 2C is a reduced tumour burden in a model of colorectal carcinoma. We suggest that this may relate to a failure to generate functional MDSC. However, other factors also remain important, because the efficacy of TNF-α blockade, which has been used as a therapy in late-stage ovarian carcinoma, maps at least partially to a defect in TNFR1 signalling to T cells.38 The lack of TNFR1 was also associated with a lack of PGE2 production. It has been previously demonstrated that PGE2 is required for MDSC maturation in vivo.30,39 PGE2 can also modulate the function of dendritic cells as APCs, and this effect depends on expression of EP2 or EP4 by the dendritic cell.

Our results demonstrate the neuroprotective effects of –Cu, −Cu+Mn and +Mn diets in a murine model of scrapie. However, neuronal death induced by infection with prions seems to be independent of apoptosis marker signalling. Moreover, copper-modified diets were neuroprotective against the possible toxicity of the prion transgene in Tga20 control and infected mice even though manganese supplementation could not counteract this toxicity. “
“We report a clinical case report JQ1 cell line of the MV2K+C subtype of sporadic Creutzfeldt-Jakob disease (sCJD). The patient was a 72-year-old woman who exhibited progressive dementia over the course of 22 months. Diffusion-weighted

MRI during this period showed abnormal hyperintensity in the cerebral cortex in the early stage. The clinical course was similar to that of previously reported patients with the MV2K or MV2K+C subtype of sCJD. However, histopathological examination revealed unique features: severe extensive spongiform changes with perivacuolar deposits in the cerebrum and basal ganglia, plaque-like PrP deposits in the cerebrum, and only mild changes in the cerebellum with small amyloid plaques (∼20 μm in diameter), smaller than those in the MV2K subtype or variant CJD (40–50 μm in diameter). Molecular analysis showed a methionine/valine heterozygosity GDC-0068 cell line at codon 129 and no pathogenic mutation in

the PrP gene (PRNP). Western blot analysis of the protease-resistant PrP (PrPSc) in the right temporal pole revealed the type 2 pattern, which is characterized by a single unglycosylated band, in contrast to the doublet described for the typical MV2 subtype of sCJD. The other intermediate band might exist in the cerebellum with kuru plaques. Therefore, small amyloid plaques in the cerebellum can be crucial for MV2K+C subtype. “
“Frequencies of typical myohistological changes such as ragged red fibers (RRF) and cytochrome c oxidase (COX)-deficient fibers have been suggested

to be dependent on underlying mitochondrial DNA (mtDNA) defect. However, there are no systematic studies comparing frequencies of myohistological changes and underlying genotypes. Phosphatidylethanolamine N-methyltransferase The histopathological changes were analysed in 29 patients with genetically confirmed mitochondrial myopathies. Genotypes included multiple mtDNA deletions due to POLG1 mutations (n = 11), single mtDNA deletion (n = 10) and mtDNA point mutation m.3243A>G (n = 8). Histochemical reactions, including Gomori-trichome, COX/SDH (succinate dehydrogenase) and SDH as well as immunohistological reaction with COX-antibody against subunit I (COI) were carried out in muscle biopsy sections of all patients. The COX-deficient fibers were observed most frequently in all three patient groups. The frequencies of myopathological changes were not significantly different in the different genotypes in all three histochemical stains.

Method of study  The MIF-173G/C single-nucleotide polymorphism (SNP) was detected in 529 PCOS

patients and 585 healthy female controls of Chinese Han ancestry. The association of the gene variants with clinical and metabolic parameters and hormone levels was investigated. Results  The frequencies of genotypes and allelotypes of the MIF-173G/C SNP did significantly differ between women with PCOS and healthy controls (P = 0.017 and P = 0.003, respectively). They did significantly differ between obese PCOS patients and obese controls (P = 0.029 and P = 0.039, respectively). The MIF-173 CC and CG genotypes were associated with higher body mass index (BMI) and waist-to-hip Src inhibitor ratio (WHR) in both PCOS patients (P < 0.001, P = 0.001) and normal controls (P < 0.001, P = 0.002). The PCOS patients with CC and CG genotypes had higher fasting plasma glucose levels (P < 0.001), higher fasting insulin levels (P < 0.001), and higher HOMA-IR (P < 0.001) compared with patients with the GG genotype. Selleckchem Staurosporine Conclusion  The MIF-173G/C polymorphism is associated with PCOS in Chinese Han women and may contribute to the phenotypic

expression of PCOS. “
“Intestinal microflora play a critical role in the initiation and perpetuation of chronic inflammatory bowel diseases. In genetically susceptible hosts, bacterial colonization results in rapid-onset chronic intestinal inflammation. Nevertheless, the intestinal and systemic immune response to faecal bacteria and antigen exposure into a sterile intestinal lumen of a post-weaned animal with a mature immune system are not understood clearly. This study examined the effects of faecal bacteria and antigen exposure on the intestinal mucosal and systemic immune system in healthy axenic mice. Axenic wild-type mice were inoculated orally with a crude faecal slurry

solution derived from conventionally acetylcholine raised mice and were analysed prior to and then at days 3, 7, 14 and 28 post-treatment. Ingestion of faecal slurry resulted in a transient, early onset of proinflammatory interferon (IFN)-γ, tumour necrosis factor (TNF)-α and interleukin (IL)-17 response that was maximal at day 3. In contrast, the transient release of the anti-inflammatory cytokines IL-10 and IL-4 occurred later and was maximal at day 7. Both responses subsided by day 14. This early cytokine imbalance was associated with a brief rise in colonic and caecal histopathological injury score at day 7. The bacterial antigen-specific systemic response was found to follow the intestinal immune response with a maximal release of both pro- and anti-inflammatory cytokines at day 7. Thus, first exposure of healthy axenic wild-type mice to normal faecal flora and antigens results in an early proinflammatory cytokine response and transient colonic inflammation that then resolves in conjunction with a subsequent anti-inflammatory cytokine profile. An endogenous intestinal microflora is a natural constituent of all vertebrates [1,2].

However, its judicious use helps in the assessment

of selected patients with PI associated with chronic infective or inflammatory disease. SCIG is becoming well established as a viable alternative to IVIG for patients with primary antibody deficiency. SCIG is as efficacious as IVIG in infection prophylaxis and in achieving satisfactory serum IgG levels as has been demonstrated in several recent key clinical studies of a 16% SCIG versus IVIG formulation. A total of 158 patients with PI were assessed in three different studies and no difference in mean infection scores and in duration of infections was observed for SCIG versus IVIG [3,24,25]. Of particular interest is that for European-based studies, the Vivaglobin® dose given C59 wnt purchase is equivalent when switching patients from IVIG to SCIG, whereas in North American studies the United States

Food and Drug Administration (US FDA) requires the initial SCIG dose at switching to be 1·37 times the previous IVIG dose, in order to achieve a similar area under the IgG concentration–time curve. Despite this, no difference between the rate of SBIs was observed in these European versus North American studies. Carfilzomib There were, however, differences in the overall infection rate, an observation which should generate further evaluation. The European Hizentra trial showed that an increase in IgG dose upon switching from IVIG to SCIG is not necessary

to maintain a low frequency of SBIs, but is beneficial in reduction of the rate of non-serious infections and the associated rates of hospitalization and antibiotic use [7]. As SCIG is given more frequently in smaller doses compared with IVIG, it allows increasing the total monthly dose more easily without risk of compromising tolerability. Additionally, SCIG has a very favourable AE profile. In contrast to IVIG, there have been no reports of associated renal impairment, aseptic meningitis or anaphylaxis. Moreover, SCIG has been used successfully in cases of IVIG-induced anaphylaxis associated with anti-IgA antibodies. In a recent US study, 49 patients previously on IVIG were switched to IgPro20, a 20% liquid SCIG stabilized SPTLC1 with l-proline [2]. No SBIs (defined as per US FDA criteria) were observed and the rate of non-serious infections was low (2·76 infections/patient/year). Subcutaneous administration allows infusion of up to 1·2 g/kg/month and a 20% SCIG formulation enables administration of even higher doses [2]. Furthermore, SCIG therapy results in more stable serum IgG levels over time, as smaller doses are given more frequently compared to the larger IVIG boluses given every 3–4 weeks [26]. A maintenance of serum IgG levels can be achieved with SCIG even with a reduction in total monthly dose compared to the previously IVIG administered dose [27].

Analysis was performed using a FACSAria

flow cytometer and data were analysed using FlowJo software. CD8β-expressing cells could not be measured because the monoclonal antibody anti-CD8β chain did now exhibit sufficient stability in the fixation procedure required for FoxP3 protein analysis. Data are presented as median ± SD, and P-values were derived using a Mann–Whitney U-test. The phenotype ABT-888 datasheet of the T-cell compartment in the peripheral blood of 16 healthy human donors (HDs) and 27 rhesus monkeys was assessed by multicolour flow cytometric analysis. CD3− lymphocytes, which express CD56 and CD16, identify natural killer (NK) cells in humans. CD56 identifies mainly monocytes and CD16+ NK cells in rhesus macaques.22 T lymphocytes were determined by CD3 expression and after exclusion of CD16+ and CD56+ cells (gating strategy see Fig. 1a). The (co)expression of CD4, CD8α and CD8β in the T-cell (CD56 CD16− CD3+) compartment was determined in HDs and NHPs. CD8αβ+ T cells and CD8αα+ T cells represented 23·8% and 1·2% in HDs, and 28% and 5·2% in NHPs. In PBMCs from HDs and NHPs, γδ T-cell receptor (TCR)+/− cells exhibited the CD8αα+/−

phenotype. Yet the majority (> 70%) of CD8αα+/− T cells were present in the TCR-αβ T-cell compartment (data Peptide 17 not shown). CD4+ T cells represented the prevalent T-cell subset: 74·3% and 63·6% of T cells in HDs and NHPs, respectively. Two other less frequent cell subsets could be identified: CD4+ T cells expressing either the CD8αα homodimer or the CD8αβ heterodimer (0·2% and 0·1% in HDs; 1·3% and 1·4% in NHPs) (see Fig. 1b). CD8αα+, CD4+ CD8αα+ and CD4+ CD8αβ+ T cells showed a statistically higher frequency in NHPs than in HDs. Four functional T-cell compartments are defined in humans by the expression of CD45RA and CCR7: precursor (CD45RA+ CCR7+), central memory (CD45RA− CCR7+), effector memory (CD45RA− CCR7−) and differentiated effector (CD45RA+ CCR7−) T-cell subsets.15,23 The distribution of the T-cell

subsets defined by CD45RA and CCR7 expression within the different T-cell populations was statistically different in Fossariinae PBMCs between HDs and NHPs (Table 1). We assessed the CD28 and/or CD27 expression within the CD45RA/CCR7 subsets. The median value of the expression frequency of CD45RA+/− CCR7+/− CD28+/− CD27+/− subsets in the parental T-cell population from the PBMC of HDs and NHPs is displayed as heat-maps (Fig. 2). In PBMCs from HDs, precursor, effector memory and central memory CD8αβ+ T-cells co-expressed CD28 and CD27 (CD28− CD27+ and CD28+ CD27− subsets were also found). In contrast, differentiated effector CD8αβ+ T cells were enriched in cells expressing only CD27. In NHPs, CD45RA+ CCR7+ and CD45RA+ CCR7− cells represented the dominant T-cell subsets in the CD8αβ+ T-cell compartment, and the expression of CD28 and CD27 differed from that by HDs within these T-cell compartments.

Supernatants were harvested and counted on an automated gamma counter. Percent specific lysis was calculated as [(sample 51Cr releasespontaneous

51Cr release)/(maximum 51Cr releasespontaneous 51Cr release)]×100. In vivo cytotoxicity experiments were performed as described with modifications 35. Naïve splenocytes (target cells) were pulsed with 1, 0.1 or 0.01 μg/mL of JEV NS4b S9, WNV NS4b S9 peptide or control influenza NP 366–374 peptide (1 μg/mL) for 45 min at 37°C. Cells were stained with 1 μM Cell Trace Far Red 7-hydroxy-9H- (1,3-dichloro-9,9-dimethylacridin-2-one)-SE (DDAO-SE; Invitrogen, Carlsbad, CA, USA) and serial dilutions of CFSE (5 μM, 1.5 μM, 0.4 μM, 0.1 μM; Invitrogen). Target check details cells in PBS (2×107 cell/mL) were injected i.v. into JEV-immunized or naïve mice 8 days post immunization. Splenocytes were harvested 2 h later

and analyzed using a FACSAria. Percent specific lysis was calculated by the formula 1(Ratio immune/Ratio naïve)×100, where Ratio=(♯ events of JEV or WNV peptide/♯ events of control influenza peptide). Recombinant H-2Db:Ig fusion protein (4 μg; BD Biosciences) was loaded with variant peptides (>90% purity) at 640 molar excess peptide in PBS (pH=7.2) at 37°C overnight according to manufacturers guidelines. Peptide-loaded dimer was incubated with 2.4 μg APC-anti-mouse IgG (BD Biosciences, mAb A85-1) followed by incubation with purified mouse IgG isotype control (4 μg; BD Biosciences; mAb A111-3). Splenocytes were resuspended in PBS, stained with Live/Dead Aqua and incubated with anti-CD16/32 (2.4G2; BD Bioscience), followed by staining with 4 μg of peptide-loaded dimer. Cells find more were surface stained with anti-CD44, anti-CD62L, anti-KLRG1 and anti-CD127 conjugated with FITC, PE-Cy7 and PerCP-Cy5.5, washed and resuspended in BD stabilizing buffer. Peptide-loaded dimer staining levels in naïve mice were subtracted from experimental Isotretinoin values in infected mice. The gating strategy is shown in Supporting Information Fig. 3A and B. On days 3 and 7 post JEV or WNV infection, spleen, brain and serum were obtained

and flash frozen at −70°C. Tissues were homogenized to give a 10% (spleen) or 20% (brain) homogenate based on tissue weight using a Qiagen mixer mill. Serial dilutions were made in MEM and titers were determined on Vero cells as described 36. Plates were incubated for 2 (WNV) or 4 days (JEV Beijing and SA14-14-2) prior to second agar overlay. The limit of detection was 50 pfu/mL for serum, 250 pfu/g for brain and 500 pfu/g for spleen. Means, medians and standard errors were calculated using GraphPad Prism (GraphPad Software, LaJolla, CA, USA). Comparisons of variables between JEV and WNV infection groups were performed with log transformed data using the Mann–Whitney U test on STATA software (StataCorp, College Station, TX, USA). p<0.05 was considered significant. This work was supported by contract N01-AI25490 and grants U19 AI057319, P30 DK032520 and T32 AI007349 (D.W.

“
“Targeted gene disruption experiments in Trichophyton mentagrophytes are impeded by the dominant of repair of DNA double strand breaks MAPK inhibitor through a nonhomologous end joining pathway (NHEJ). Inactivation of human DNA ligase IV homologs, which is involved in the final step of the NHEJ pathway, has been shown to enhance homologous recombination (HR) frequency in filamentous fungi. To improve the frequency of HR in T. mentagrophytes, the lig4 homolog (TmLIG4) was disrupted. T. mentagrophytes lacking TmLIG4 showed no discernable phenotypic differences when compared to wild-type controls. Both mutant and parent

strains had almost identical growth ability, sporulation rate and sensitivity to DNA damaging agents. When four different loci were disrupted in the TMLIG4-deficient mutant, HR frequencies reached as high

as 93% depending on the locus, whereas they ranged from 0%–40% in the wild-type. These results suggest that studies in strains lacking TmLIG4 would help to improve our understanding of dermatophytosis by facilitating buy Y-27632 the genetic manipulation of dermatophytes. Trichophyton mentagrophytes is a member of a group of closely related superficial fungal pathogens that invade the outermost layer of skin, hair and nails in humans and animals causing superficial mycoses (so-called dermatophytoses) (1, 2). These specialized fungi are characterized by their ability to degrade keratinous tissue through a wide range of secreted endo- and exo-proteases, and are therefore of pathogenic importance (3). Understanding

the mechanism of protease secretion and relevant factors at the molecular level is a key approach towards elimination of dermatophytosis. Therefore, establishment of high-throughput molecular genetic approaches is the cornerstone of dermatophyte studies. Targeted gene disruption by homologous recombination is often carried out in fungal molecular genetic studies. However, DSBR in fungi takes place either through HR, requiring homologous sequences, Ceramide glucosyltransferase or NHEJ (4). Unlike some yeasts (5, 6), fungi appear to favor NHEJ over HR, resulting in decreased gene targeting efficiency and making precise genetic manipulation laborious and time-consuming. In yeasts, the role of the RAD52 gene group in HR has been characterized, mainly been based on Saccharomyces cerevisiae, which possesses very efficient HR machinery(7). Accordingly, two approaches can be anticipated to improve fungal gene disruption efficiency: enhancing HR or impairing NHEJ. In several fungi the feasibility of the latter approach has been shown to be advantageous, through production of recipient cells lacking some of the NHEJ-related genes.

Diagnosis is confirmed by low level of ADAMTS-13 activity. This case report describes the occurrence TTP in end stage renal disease (ESRD) patient undergoing continuous ambulatory peritoneal dialysis (CAPD). Methods: A 79 year old Thai female presented with watery diarrhea and alteration of consciousness 1 day before admission. She had history of ESRD due to hypertension and was started on CAPD 3 months ago. Her medications include calcium carbonate,

furosemide, folic acid, metoprolol, GSK2126458 clinical trial amlodipine, simvastatin, elixir KCl and Epoein alfa. Physical examination revealed an old female with drowsiness, no focal neurological deficit. Laboratory examination revealed Hb10.4 g/dL Hct 31% WBC 19,450 PMN 92% lymphocyte 8% platelet 73,000/mm3, >1% of schiztocytosis was noted in peripheral blood smear. LDH level was elevated at 645 U/L (normal 125–220 U/L), her coagulogram was normal, tests for anti-HIV and ANA were negative. Stool examination revealed watery, yellowish stool, no mucous, WBC 0-1, RBC 0-1,

stool culture and hemoculture were negative. CT brain found RG-7388 datasheet no significant abnormality. Serum ADAMTS13 activity was decreased at 15% (normal 58–170%), ADAMTS13 inhibitor was negative. She was treated by plasma infusion 30 ml/kg/day (1) for 2 consecutive days and then started on daily plasma exchange with 1 plasma volume(2) for 3 sessions. Results: After plasma exchange, her platelet count increased and LDH return to normal and regains better consciousness. Two weeks after discharge, she had good consciousness and normal platelet count. Conclusion: We report

the first case of idiopathic TTP confirmed by low ADAMTS13 activity in ESRD patient, successfully treated by plasma infusion and plasma exchange. TAKAHASHI KEIKO1, KOBAYASHI TAKASHI1, SUZUKI YUSUKE1, MEIZI LIU2, SUGAYA TAKESHI1,3, HORIKOSHI SATOSHI1, URABE TAKAO2, TOMINO YASUHIKO1 1Nephrology, Juntendo University Faculty of Medicine; 2Neurology, Juntendo Univetsity Faculty of Medicine; 3CMIC Co., Ltd Introduction: Renal lipid metabolism has been discussed Dynein in many renal diseases. Recent studies revealed the renal metabolism after lipid-overloading in glomerular failure or in acute renal vascular injury such as renal ischemic reperfusion. In addition, it is recently known that such lipid-metabolism may importantly contribute to the progression of renal injury. L-type fatty acid binding protein (L-FABP) is known as a sensitive biomarker for many renal diseases. L-FABP is expressed in human proximal tubules and may play an important role in fatty acid homeostasis in kidneys. L-FABP has high affinity and function to bind free fatty acid. Therefore, L-FABP may has the potential function as an endogenous antioxidant.