[5] Optimizing the management of lupus nephritis is therefore important, both to reduce the healthcare burden to society and to improve the outcome of patients. In view of the greater propensity of severe renal disease, Asian patients with SLE should be closely monitored for renal manifestations, since early diagnosis and treatment are prerequisite to secure optimal clinical outcome. The management of lupus nephritis (LN) has evolved considerably, and the outcome of

treatment learn more has improved, over the past three decades. Treatment is guided by disease severity, based on histopathological (Table 1) and/or clinical manifestations.[4] Results reported by the National Institute of Health (NIH)

in U.S.A. since the 1980s showed that cyclophosphamide (CYC) combined with corticosteroids was superior to corticosteroids alone in the treatment of proliferative LN,[6-8] maintenance immunosuppression was necessary to maintain sustained remission, and monthly intravenous pulse CYC for ��-catenin signaling approximately six months led to fewer adverse effects compared with prolonged oral CYC when given to induce disease remission, and this ‘NIH regimen’ is commonly adopted as standard therapy for severe LN.[8, 9] However, CYC was associated with significant adverse effects such as amenorrhea, hemorrhagic cystitis and malignancies, and the long-term survival of patients remained suboptimal despite improved renal response initially.[6, 8, 9] Since the mid-1990s mycophenolic acid, given as mycophenolate mofetil

(MMF) or mycophenolic sodium, Cell Cycle inhibitor has emerged as a useful alternative to CYC during the induction phase or to azathioprine (AZA) during the maintenance phase of treatment.[4] Novel immunomodulatory therapies with a potential role in LN, such as calcineurin inhibitors and biologic agent(s), continue to emerge.[10-12] There is evidence that treatment outcomes following CYC or MMF therapy vary according to race and ethnicity.[13] Part of the differences could be due to socioeconomic factors such as education level, treatment compliance, and healthcare setup, though it is conceivable that there would be genetic variations in disease processes and/or response to drugs. Data from the Collaborative Study Group showed more severe LN and worse treatment outcome in Blacks compared with Caucasians,[14] while data from the Aspreva Lupus Management Study (ALMS) showed a lower response rate to CYC treatment in Blacks and Hispanics, compared with Caucasian or Asian patients.[13, 15] The Asian Lupus Nephritis Network (ALNN) Steering Group comprises a group of rheumatologists and nephrologists in Asia with special interest in LN research. The ALNN, an independent group unaffiliated to any institution or industry, aims to serve as a platform for exchange and collaboration.

[1, 2] Moreover, the allergen-specific CD4+ T cells of non-allergic subjects were mostly either unpolarized or produced low levels of interferon-γ (IFN-γ) and interleukin-10 (IL-10).[1, 2] In the current study, we sought to confirm these findings by examining the CD4+ T-cell response to the major horse allergen Equ c 1, an important lipocalin allergen[8] with the prevalence of IgE reactivity close to 80% among horse

dust-allergic subjects.[9, 10] For this purpose, we analysed the CD4+ T-cell responses of horse dust-exposed Equ c 1-sensitized and healthy subjects focusing on the dominant epitope region of the allergen. This region is strongly recognized by the T cells of almost all Equ c 1-sensitized subjects examined.[11] As with the major allergen Hydroxychloroquine of dog, Can f 1[1], and the major allergen of cow, Bos d 2[2], the frequency of Equ c 1-specific CD4+ T cells in the peripheral blood is very low. In allergic subjects, it is mostly higher than in non-allergic ones. Moreover, the function and phenotype of Equ c 1-specific CD4+ T cells differ between these two subject groups. p143–160 (GIVKENIIDLTKIDRCFQ), an 18-mer peptide containing the immunodominant

epitope Palbociclib region of Equ c 1, was synthesized and purified by GL Biochem (Shanghai, China). Recombinant (r) Equ c 1 was produced in Pichia pastoris, as described previously.[11] Fourteen clinically diagnosed horse-allergic subjects (subjects A–N) with positive (≥ 3 mm) skin prick tests with rEqu c 1 and nine horse dust-exposed non-atopic control Cediranib (AZD2171) subjects (subjects O–W) with negative skin prick tests were recruited to the study. The subjects were characterized

at the Pulmonary Clinic of Kuopio University Hospital, as described in detail previously.[11] In brief, the allergic subjects exhibited a positive horse UniCAP result (FEIA; Pharmacia, Uppsala, Sweden; > 0·7 kU/l) and a positive skin prick test (≥ 3 mm) with a commercial horse epithelial extract (ALK Abellò, Hørsholm, Denmark), whereas the control subjects were negative in these tests. The non-atopic control subjects had horse riding as a hobby, and were therefore constantly exposed to horse allergens. Human leucocyte antigen (HLA) class II genotyping for the DQ and DR alleles of the subjects was performed in the Clinical Laboratory of the Finnish Red Cross Blood Service (Helsinki, Finland[12]) or in the Immunogenetics Laboratory of the University of Turku (Turku, Finland[13]) with PCR-based lanthanide-labelled sequence-specific oligonucleotide hybridization (Supplementary material, Table S1). Signed informed consent was provided by all subjects participating in the study and the study was approved by the Ethics Committee of Kuopio University Hospital, permission # 182/99.

The authors do not have any conflict of interest related to the topic of this study. “
“Photodynamic therapy (PDT) is a minimally invasive approach, in which a photosensitiser compound is activated by exposure to visible light. The activation of the sensitiser drug results in several chemical reactions, such as the production of oxygen reactive species and other reactive molecules, whose presence

in the biological site leads to the damage of target cells. Although PDT has been primarily developed to combat cancerous lesions, this therapy can be employed for the treatment of several conditions, including infectious diseases. www.selleckchem.com/products/Trichostatin-A.html A wide range of microorganisms, including Gram positive and Gram negative bacteria, viruses, protozoa and fungi have demonstrated susceptibility to antimicrobial photodynamic therapy. This treatment might consist of an alternative to the management of fungal infections. Antifungal photodynamic therapy has been successfully employed against Candida albicans and other Candida species and also against dermatophytes. The strain-dependent antifungal effect Lumacaftor supplier and the influence of the biological medium are important issues to be considered. Besides, the choice of photosensitiser to be employed in PDT should consider the characteristics of the fungi and the medium to be treated, as

well as the depth of penetration of light into the skin. In the present review, the state-of-the-art of antifungal PDT is discussed and the photosensitiser characteristics are analysed. “
“Fifty-three soil samples were collected from various

sites click here in the vicinity of Vedanthangal Water Bird Sanctuary and screened for the presence of keratinophilic fungi using the hair baiting techniques for isolation. Twenty-eight isolates were recovered and identified by recognition of their macro- and micromorphological features. Seven species related to five genera were recorded viz. Auxarthron conjugatum (1.89%), Chrysosporium fluviale (3.77%), Chrysosporium indicum (20.75%), Chrysosporium tropicum (7.55%), Chrysosporium state of Ctenomyces serratus (5.66%), Gymnoascus petalosporus (1.89%) and Microsporum gypseum complex (11.32%). The study shows that migratory birds harbour a variety of keratinophiles and may be a potential source of transfer of these fungi from one location to another. “
“Candida albicans is the predominant causal agent of candidiasis. Its ability to form hyphae and biofilm has been suggested to be key virulence factors. In this study, we investigated the effect of major licorice compounds licochalcone A, glabridin and glycyrrhizic acid on growth, biofilm formation and yeast-hyphal transition of C. albicans. The synergistic effect of licorice compounds with the antifungal drug nystatin was also evaluated. Minimal inhibitory concentrations (MICs) for C.

JNK activation by ER stress was dependent on the IRE1 kinase domain [60]. In mouse embryonic fibroblasts, ER stress caused by thapsigargin, activated p38

MAPK and JNK in a PERK-dependent manner [64]. NF-κB lies inactive in the cytoplasm due to direct interaction with its inhibitor IκB. Once phosphorylated by IκB kinase (IKK), IκB is degraded and releases active Autophagy inhibitor datasheet NF-κB, which then translocates to the nucleus and induces transcription of several genes, including pro-inflammatory cytokines (reviewed by [65]). Activation of NF-κB by the UPR pathway occurs by at least two distinct mechanisms. Once activated by ER stress, the kinase domain of IRE1 interacts with TRAF2 and IKK, leading to degradation of IκB, activation of NF-κB, and TNF-α synthesis by several cell types [63]. Alternatively, PERK phosphorylates eIF2α, inhibiting IκB translation. As the half-life of IκB is much shorter than the one of NF-κB, an accumulation of free NF-κB occurs, followed by nuclear translocation and transcription activation [61, 62] (Fig. 2). The production of type I interferons (IFNs) also seems

to be mediated by the UPR pathway [66]. A synergic effect was observed when cells where stimulated with ER stressors and pattern recognition receptors (PRRs) agonists. Induction of IFN-β by ER stress was dependent on XBP-1 and the TRIF/IRF3 pathway, downstream to several PRRs such as TLR4 and MDA5 [66]. In accordance to this, a cis-enhancer region that interacts with XBP-1s Opaganib ic50 was found 6.1 kb downstream IFNB1, which codes for IFN-β. One plausible explanation is that after LPS stimulation and consequent ER stress, Enzalutamide supplier XBP-1s binds to this enhancer and recruits IRF3 and CBP. Through a chromatin loop, these factors are brought closer to the IFNB1 promoter region, resulting in more efficient transcription machinery recruitment [67]. ER stress also plays an important role on acute phase responses [68]. CREBH is a liver specific transcription factor

activated upon ER stress. CREBH is found anchored in ER membrane and, once activated, it translocates to the Golgi complex. Proteolytic cleavage by S1P and S2P releases an active N-terminal fragment that translocates to the nucleus, where together with ATF6, regulates transcription of acute phase genes coding for proteins such as C-reactive protein and serum amyloid P component. Although CREBH does not contribute directly to the activation or regulation of the UPR pathway, it is activated by ER stress and is necessary for acute phase response [68]. Recently, it was shown that TLR signalling activates the IRE1/XBP-1 axis and that this loop is crucial for host defense [69]. TLRs are well-conserved receptors that recognize pathogen-associated molecular patterns and danger signals (reviewed by [70]).

Patients received vitamin D therapy were characterized by advanced CKD, low serum calcium level, high serum phosphorus level and high serum intact parathormone level. The Staurosporine cost use of active vitamin D analogs independently decreased the risk of the primary outcome (adjusted hazard ratio, 0.55; 95% confidence interval, 0.31–0.99) by multivariate Cox proportional hazards model adjusted for variables; age, gender, eGFR, product of serum adjusted calcium and phosphate levels, serum intact parathormone level, and other baseline characteristics.

Conclusion: Administration of vitamin D analogs for patients with pre-dialysis chronic kidney disease reduces the risk for progression of CKD. YUVARAJ ANAND1,2, VIJAYAN MADHUSUDAN1,2, NAIR SANJEEV1,2, ABRAHAM GEORGI1,2, T JAYASEELAN1, G PADMA1,2 1Madras Medical Mission; 2Tanker Introduction: In developing countries, anemia is more prevalent in hemodialysis patients and nutritional status plays a major role, we decided to study the profile of anemia and its determinants in hemodialysis patients. Methods: We conducted a cross-sectional study of 81 chronic kidney disease patients (M-56, F-25, Mean age- 50.51 ± 13.27 yrs) on haemodialysis Doxorubicin in two not for profit instituitions in south India. We looked at vintage of dialysis (<1 yr, >1), type of diet-veg/non-veg, haemoglobin (g/dl),

serum iron (mcg/dl), serum TIBC (mcg/dl), TSAT (%), vit B12 (pg/ml), vit D (ng/ml) and their correlations. Results: In our study of 81 patients, 70 non veg, 11 veg, mean HB was 9.81 ± 1.52 g/dl, mean vit B12 645.85 ± 234 pg/ml with normal in 79.01% (>300 pg/ml), Lck mild deficiency in 18.52% (200–300 pg/ml) and severe deficiency only in 2.47% (<200 pg/ml). Mean TSAT was 32.6 ± 21.18%, with <24 in 45.68% and >24% in 54.32%, mean 25 (OH) vitamin D was 27.52+/− 12.49 ng/ml, severe deficiency (<5 ng/ml) in 24.39%, mild deficiency (5.01–15 ng/ml) in 14.63%, Insufficiency (15.01–30 ng/ml) in 31.71%, sufficient (>30 ng/ml) in 29.27%. It was noted that patients on dialysis with vintage >1 year had a higher serum iron (p = 0.01) and higher TSAT

(p = 0.001). Conclusion: Although malnutrition exists widely in Indian dialysis patients, B12 deficiency is not widely prevalent. Vitamin D deficiency is highly prevalent in hemodialysis patients. It was noticed that greater the vintage of dialysis, better was the transferrin saturation and the serum iron levels. SUZUKI HIROYUKI, ARIYASU YUKI, SHINKAWA KANNA, YAMAGUCHI RYOHEI, KANG YOUNG, MIYAKE TAKAFUMI, KAKITA HIROKO, TORIKOSHI KAZUO, ENDO TOMOMI, YONEMOTO SATOMI, MUSO ERI Department of Nephrology and Dialysis, Tazuke Kofukai Foundation, Medical Research Institute, Kitano Hospital Introduction: End stage renal disease due to benign nephroslerosis (BN) is increasing in Japan with elevation of the aged population.

The p value

was used to test the null hypothesis that the slope of the linear regression was different from zero; a p value of < 0.05 was deemed statistically significant. Correlation results for activation potency versus individual binding parameters at a representative peptide concentration of 8.0 μM are shown in figures for 3D affinity (Fig. 2A), 3D on-rate (Supporting Information Fig. 1B), tetramer decay rate (Supporting Information Fig. 1F), tetramer staining MFI (Fig. 2D), 2D effective affinity (Fig. 7A), 2D off-rate (Fig. 7B), ACP-196 order 2D effective on-rate (Fig. 7C), and /mpMHC (Fig. 7D). Results obtained at other peptide concentrations analyzed are comparable and summarized in Supporting Information Table 1. We also used an alternative set of statistic–Spearman

coefficients ρ and corresponding p value–to evaluate fitting quality. Results for the representative peptide concentration of 8.0 μM are shown in Supporting Information Table 1. We thank New York University and Georgia Institute of Technology flow cytometry cores for technical assistance. We thank Dr. David Kranz and Dr. Michael Dustin for providing cell lines and plasmids, Katelyn McGary and Kevin Huang for assistance in soluble protein productions, and Dr. Jeffrey Donnell for critical reading of the manuscript. M.K. was a Pew Scholar in INCB018424 the Biomedical Sciences supported by the Pew Trust. This work was supported by the National Institute of Health grants NCI 1U01CA137070 and NIGMS 5R01GM085586 (to M.K.) and R01GM096187 and R56AI038282 (to C.Z.), an American Cancer Society Research Scholar grant RSG-09-070-01-LIB (to M.K), and a Cancer Research Investigator grant (to M.K.). The authors declare no financial or commercial conflict of interest. As a service to our authors and readers,

this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support Dehydratase issues arising from supporting information (other than missing files) should be addressed to the authors. Table S1. Statistical analysis of the correlations between 2D/3D kinetic parameters and IL-2 production of 58-/- cells transduced with gp100- specific TCRs at different gp100–2M concentrations. The numbers represent the R2 values obtained from the linear fitting of the log-log plots between a kinetic parameter and IL-2 secretion at a specific gp100–2M concentration; the numbers in parentheses represent the p values from the fitting. Results of Spearman coefficients and corresponding p values for 8.0 μM peptide concentration are also shown (the most right column). p-values ≤0.05 are considered statistically significant and are shown in bold text in the table. All fittings were done in GraphPad Prism 6. Figure S1. Lack of correlation between 3D kinetics and functional activity of TCRs.

HBZY-1 cultured in UA showed evident morphological changes under transmission electron microscopy. The soluble UA stimulated the upregulation of the α-SMA, TGF-β1 and FN mRNA and proteins in a concentration- and time-dependent Y-27632 datasheet manner. UA-induced endoplasmic reticulum (ER) stress, as evidenced by the upregulation of the mRNA and protein expressions of GRP78 and PDI. However, the upregulation was reverted by 4-PBA,

an inhibitor of ER stress. Uric acid induces phenotypic change in HBZY-1 cells. ER stress plays a central role in UA-induced phenotypic transformation in vitro. 4-PBA may be beneficial in attenuating UA-induced glomerular injury. “
“Aim:  Haemodialysis induces endothelial dysfunction by oxidation and inflammation. Intravenous iron administration during haemodialysis could worsen endothelial dysfunction. The aim of this study was to ascertain if iron produces endothelial dysfunction and the possible neutralizing effect of N-acetylcysteine when infused before iron. The oxidative and inflammatory effects of iron during haemodialysis were also assessed. Methods:  Forty patients undergoing haemodialysis were studied

in a randomized and cross-over design with and without N-acetylcysteine infused before Raf inhibitor drugs iron sucrose (50 or 100 mg). Plasma Von Willebrand factor

(vWF), soluble intercellular adhesion molecule-1 (sICAM-1) levels, malondialdehyde, total antioxidant capacity, CD11b/CD18 expression in monocytes, interleukin (IL)-8 in monocytes and plasma IL-8 were studied at baseline and during haemodialysis. Results:  Haemodialysis produced significant (P < 0.001) increase in plasma vWF, sICAM-1, malondialdehyde, IL-8 and CD11b/CD18 expression in monocytes, as well as decrease in total antioxidant capacity. Iron induced significant increase in plasma malondialdehyde and IL-8 in monocytes, but had no effect on total antioxidant capacity, CD11b/CD18 expression, plasma IL-8, Acyl CoA dehydrogenase vWF and sICAM-1. The addition of N-acetylcysteine to 50 mg of iron produced a significant (P = 0.040) decrease in malondialdehyde. Conclusion:  Standard (100 mg) and low (50 mg) doses of iron during haemodialysis had no effects on endothelium. Iron only had minor effects on inflammation and produced an increase in oxidative stress, which was neutralized by N-acetylcysteine at low iron dose. Haemodialysis caused a significant increase in oxidative stress, inflammation and endothelial dysfunction markers.

These data suggest that oestrogen contributes to the persistence of autoreactive T cells through the defective control of apoptosis, and may also provide a clue as to how oestrogen triggers SLE

activity. However, it remains unclear as to whether oestrogen affects the survival of peripheral T cells reactive to self-antigens in vivo. In addition, we did not examine the tripartite relationship among oestrogen, T cell apoptosis and disease activity in SLE patients. Further longitudinal study is required to clarify these issues. This research was supported by Basic Science Research Program through LY2835219 ic50 the National Research Foundation funded by the Ministry of Education, Science and Technology (No. 314-2008-1-E00113) and by a grant from the Korea Association of Internal Medicine. None. “
“Increased susceptibility to tuberculosis following

HIV-1 seroconversion contributes significantly to the tuberculosis epidemic in sub-Saharan Africa. Lung-specific mechanisms underlying the interaction between HIV-1 and Mycobacterium tuberculosis infection are incompletely understood. Here we address these questions by examining the effect of HIV-1 and latent M. tuberculosis co-infection on the expression of viral-entry receptors and ligands in bronchoalveolar lavage (BAL) of HIV-1-infected and -uninfected patients with and without latent M. tuberculosis infection. Irrespective of HIV-1 status, T cells from BAL expressed higher levels of the beta-chemokine receptor (CCR)5 than peripheral blood T cells, in particular the CD8+ T cells of HIV-1-infected persons showed elevated CCR5 expression. The concentrations of check details the CCR5 ligands RANTES and MIP-1β were elevated Farnesyltransferase in the BAL of HIV-1-infected persons compared with that in HIV-1-uninfected controls.

CCR5 expression and RANTES concentration correlated strongly with HIV-1 viral load in the BAL. In contrast, these alterations were not associated with M. tuberculosis sensitisation in vivo, nor did M. tuberculosis infection of BAL cells ex vivo change RANTES expression. These data suggest ongoing HIV-1 replication predominantly drives local pulmonary CCR5+ T-cell activation in HIV/latent M. tuberculosis co-infection. “
“Biofilm infections may not simply be the result of colonization by one bacterium, but rather the consequence of pathogenic contributions from several bacteria. Interspecies interactions of different organisms in mixed-species biofilms remain largely unexplained, but knowledge of these is very important for understanding of biofilm physiology and the treatment of biofilm-related infectious diseases. Here, we have investigated interactions of two of the major bacterial species of cystic fibrosis lung microbial communities –Pseudomonas aeruginosa and Staphylococcus aureus– when grown in co-culture biofilms. By growing co-culture biofilms of S. aureus with P.

Patients who would benefit from higher doses are not identifiable a priori, titration for maximal anti-proteinuric effect would be a logical step during the treatment. Higher doses of ACEI and ARB seem well tolerated. Thus, this approach should be considered in patients who have not achieved optimal response for proteinuria reduction with their conventional doses of ACEI or ARB. This work was supported by a National Nature & Science Grant (no. 30830056) and a National 973 Program (no. 2006CB503904) to Dr Fan Fan Hou. All authors are in agreement with the content of the manuscript. The Authors state that there is no conflict of interest regarding

the material

discussed in the manuscript. “
“Date written: June 2008 Final submission: June 2009 SRT1720 No recommendations possible based on Level I or II evidence. (Suggestions are based on Level III and IV evidence) Pre-transplant weight and pre-transplant weight gain increase the risk of the development of diabetes therefore weight management strategies should be a priority for patients awaiting a kidney transplant. (Level III evidence) New-onset Ferroptosis activation diabetes mellitus after organ transplantation (NODAT) has emerged as an increasingly important determinant of outcome and survival in transplant recipients. Its reported prevalence among renal transplant recipients varies widely because of the use of inconsistent definitions of diabetes. However, an International Consensus Expert Panel2 convened in 2003 agreed that the definition of NODAT should be in accordance with the American Diabetes Association (ADA)’s criteria for the diagnosis of diabetes mellitus,3 which specifies: 1 symptoms of diabetes mellitus plus casual plasma glucose ≥200 mg/dL. Casual is defined as any time of day. Classic symptoms include polyuria, polydipsia and unexplained weight loss, OR The

prevalence of NODAT has been Oxalosuccinic acid reported at around 20% at 1 year4 and best available data suggest that the disorder is a life-long problem for the majority of those diagnosed, not a temporary aberration driven by high-dose steroid exposure in the early post-transplant phase.5 NODAT is caused by the combination of insulin resistance and deficient insulin production.3 Non-modifiable risk factors for the development of NODAT include: age, ethnicity, family history of type 2 diabetes and HCV infection. Key modifiable risk factors the choice of immunosuppressive regimen, particularly steroid exposure and use of tacrolimus, and obesity.6–10 Diabetes mellitus has a major impact on graft and patient outcomes. It places patients at increased risk of the key causes of premature graft failure – death with function and chronic allograft dysfunction.

In cases with diffuse traumatic axonal injury the microglial reaction is particularly pronounced in the white matter. These results demonstrate that prolonged microglial activation is a feature of traumatic brain injury, but that the neuroinflammatory response returns to control levels after several years. “
“Cerebral GSI-IX amyloid angiopathy (CAA) predisposes to symptomatic intracerebral hemorrhage (sICH) after combined thrombolytic and anticoagulant treatment of acute myocardial infarction. However, the role

of CAA in stroke thrombolysis has not been established. Here, we describe a confirmed case of CAA-related hemorrhage in a patient receiving thrombolysis for acute ischemic stroke. On autopsy, immunohistochemistry revealed amyloid-β positive staining in thickened cortical and meningeal arteries at sites of hemorrhage. Further research is urgently needed to determine

the hemorrhage risk related to CAA in stroke thrombolysis and develop better diagnostic tools to identify CAA in the emergency room. “
“Sphingosine-1-phosphate receptor (S1PR) modulating therapies are currently in the clinic or undergoing investigation for multiple sclerosis (MS) BAY 80-6946 order treatment. However, the expression of S1PRs is still unclear in the central nervous system under normal conditions and during neuroinflammation. Using immunohistochemistry we examined tissues from both grey and white matter MS lesions for sphingosine-1-phosphate receptor 1 (S1P1) and 5 (S1P5) expression. Tissues from Alzheimer’s disease (AD) cases were also examined. S1P1 expression was restricted to astrocytes and endothelial cells in control tissues and a decrease in endothelial cell expression was found in white matter MS lesions. In grey matter MS lesions, astrocyte expression was lost in active lesions, while in quiescent lesions it was restored to normal expression levels. CNPase PRKACG colocalization studies demonstrated S1P5

expression on myelin and both were reduced in demyelinated lesions. In AD tissues we found no difference in S1P1 expression. These data demonstrate a differential modulation of S1PRs in MS lesions, which may have an impact on S1PR-directed therapies. “
“C. Billingham, M. R. Powell, K. A. Jenner, D. A. Johnston, M. Gatherer, J. A. R. Nicoll and D. Boche (2013) Neuropathology and Applied Neurobiology39, 243–255 Rat astrocytic tumour cells are associated with an anti-inflammatory microglial phenotype in an organotypic model Aim: Microglia form a high proportion of cells in glial tumours but their role in supporting or inhibiting tumour growth is unclear. Here we describe the establishment of an in vitro model to investigate their role in astrocytomas. Methods: Rat hippocampal slices were prepared and, after 7 days to allow microglia to become quiescent, rat C6 astrocytic tumour cells were added.