Nevertheless we have continued to perform annual Al levels on all our dialysis patients. Methods: We retrospectively analysed serum Al from Jan 2010-Dec 2013 using our database (Nephworks 6) as well as RO and water feed levels. Results: 2058 Al tests in 755 patients (62% male, mean age 64 years) were

reviewed showing mean (SD) of 0.41 (0.30) μmol/L. 57 (2.8%) tests from 35 patients had Al levels >1.0 μmol/L and 27 (77%) of these patients were or had been prescribed aluminium hydroxide (AlOH). 7 patients had Al >2.2 μmol/L. In 3 of these patients, no source of Al was identified, at least one patient was dialyzing at home before being transplanted. 182 patients taking AlOH (87% of all patients on AlOH)

had levels ≤ 1.0 μmol/L, but the OR of serum Al >1.0 μmol/L on AlOH see more was 9.98. The cost of CHIR99021 serum Al assay is $30.60, thus costs were $62,974.80 over the study period or over $1300/month. Despite RO feed water Al levels as high as 48 μmol/L (1300 ng/mL), Al output from the RO was almost always undetectable (<0.1 μmol/L). We have detected dialysate Al levels >2.2 μmo/L only 5 times since 2009, and never in last 3 years. Conclusion: Unselected testing of serum Al appears unnecessary and expensive and we will look to more selective testing of dialysis patients. 236 SURVIVAL TRENDS IN ELDERLY DIALYSIS PATIENTS AND THE GENERAL POPULATION AG RITCHIE1,2, PA CLAYTON2,3 1Concord Hospital, Sydney, NSW; 2Sydney Medical School, Sydney,

NSW; 3ANZDATA Registry, Adelaide, South Australia, Australia Aim: To identify survival trends in elderly dialysis patients compared with the general population. Background: Elderly dialysis patients are the most rapidly growing segment in Australia and survival appears to be improving, but the trends and relationship to general population survival have not been recently assessed. Methods: Observed survival of Australian patients commencing dialysis at 60y or older from 1980–2012 extracted from ANZDATA Registry without censoring for transplantation. Exponential parametric survival analysis used to model dialysis patient survival. Matching age-, sex- and era-specific survival data extracted from the GNE-0877 Australian Bureau of Statistics Life Tables. Results: The total number of patients 60y or older commencing dialysis increased from 293 during 1980–82 to 4069 during 2010–2012, and the proportion of patients in this cohort aged 60–64y fell from 60.1 to 21.0%. Over that period the modelled median survival for those commencing dialysis at age 60 improved from 3.5–7.5y (114% increase) in men and women, compared with general population improvements of 17.2–23.3y (35%) in men and 22.0–26.4y (20%) in women. Similar relative survival gains were seen in dialysis cohorts commencing up to 80 years of age however absolute gains were smaller and the life expectancy gap is also increasing.

CKD was defined

as an estimated glomerular filtration rate less than 60 mL/min/1.73 m2 and/or proteinuria greater than 1+ by a dipstick method. Odds ratios for CKD were analyzed in 4 areas. Regional differences in optimal treatment rate in HTN, DM and DL were assessed according to each guideline. Results: CKD prevalence in H, M1, M2 and L areas were 21.4%, 25.5%, 20.9% and 18.5% in male and 18.6%, 15.7%, 16.4% and 11.4% in female, in good agreement with the increasing rate of ESKD. Odds ratios for CKD were significantly high in HTN, DM and OB in all 4 regions. Prevalence Proteasome cleavage of HTN was significantly high in L area, however, the rate of under treatment in HTN and good blood pressure control rate were significantly high in L area. In H area, the rate of no treatment was the highest among 4 areas

in HTN, DM and DL. Conclusion: Association between regional variations in CKD prevalence and those in BMN 673 concentration the increasing rate of ESKD was demonstrated. Although HTN, DM and OB were risk factors for CKD in all 4 areas, the rate of under treatment and good control rate in HTN and DM may affect regional differences. MASSON PHILIP, HUONG MARTIN, TURNER ROBIN, LINDLEY RICHARD, CRAIG JONATHAN, WEBSTER ANGELA University of Sydney Introduction: Reduced glomerular filtration rate (GFR) and proteinuria are associated with increased stroke risk but the consistency and strength of this relationship is unknown. We estimated the independent and combined effects of GFR and proteinuria on stroke risk. Methods: Systematic

review and meta-analysis of observational studies and randomised trials using Meta-analysis Of Observational Studies in Epidemiology and Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. We searched MEDLINE and Embase for studies which prospectively measured GFR, proteinuria or both, and quantified subsequent risk of stroke. Reviewers abstracted risk (RR) of stroke, synthesized data using a random-effects model and explored heterogeneity with meta-regression. We assessed study quality using Tobramycin the Newcastle-Ottawa scale or Cochrane risk of bias tool. Results: We included 71 studies (1,693,306 participants): 53 cohort studies (1,537,097 participants) and 18 trials (156,209 participants). Risk of stroke increased by 39% in people with eGFR <90 ml/min/1.73 m2 (RR1.39, 95%CI1.31 to 1.48) and increased with declining GFR (figure 1). We estimated stroke risk increased by 7% for every 10% decline in GFR (RR1.07, 95%CI 1.04 to 1.10). Larger studies (≥20,000 participants) reported smaller risk (RR0.67, 95%CI 0.52 to 0.87) and studies where participants were undergoing cardiac surgery reported larger risk of stroke (RR1.42, 95%CI1.15 to 1.60). Considering proteinuria, risk of stroke increased by 69% when any proteinuria was detectable (RR1.69, 95%CI1.55 to1.84) and rose further as proteinuria increased (figure 1). We estimated that stroke risk increased by 6% for every 10-fold increase in the quantity of proteinuria (RR1.06, 95%CI1.

In addition we had one case of re-stricture later in the tubularized technique and one urethracutaneous fistula in the onlay technique. We did not have any case of penile curvature (chordee) on the base of surgery in our series. Compared with other studies, this is an acceptable complication. All parameters – including maximum urinary flow rate (Qmax), IPSS, QoL and residual urine were much improved after the operation, which indicates the usefulness of TV pedicle flap for urethroplasty. Moreover, there was no significant difference in the abovementioned parameters between 3 and 12 months after surgery. It means that significant changes have not occurred on the caliber of the urethra during learn more the

interval of 9 months. This result leads us to extrapolate a positive long-term outcome of our study. Tunica vaginalis has several favorable characteristics for use as pedicle flap in urethroplasty including close proximity to the surgical field, easy availability, high vascularity, and good resistance for handling during surgery[4, 11] Also another important characteristic is that the tunica vaginalis form of the pedicle flap does

not need a serum imbibitions phase early after surgery. The ultimate outcome of any grafting including urethroplasty depends on revascularization of the donor graft by abundant vascularity of the recipient site. But initial viability of the graft, especially during first 24–48 h after click here grafting when revascularization is not established is clearly dependent on the serum imbibitions phase. In this phase 02 and other important nutrients are transported to the basal cell of epithelium via lamina propria by diffusion, which is called the serum imbibitions phase.[15] The vascularity of the tunica vaginalis as a pedicle flap will

be intact. Thus there is no need for a serum imbibitions phase for initial viability. Before our study, tunica vaginalis had been used for four main purposes: correction Fluorometholone Acetate of penile chordee, as a second layer for augmentation of neo-urethra during tubularized incised plate (TIP), substitution of urethra for anterior urethroplasty, and surgical treatment of Peyronie’s disease. Regarding its use in urethroplasty, several experimental and a few clinical studies have been carried out. Historically, in 1967 Ariyoshi[9] reported the first use of tunica vaginalis for urethroplasty in an experimental study. After that, in 1987 Talja et al.[10] used it as a ventral onlay graft. In 1988 Khoury et al.[11] used tunica vaginalis as a tubularized flap. In 1998 Theodorescu et al.[12] compared tunica vaginalis ventral onlay with tubularized and found that ventral onlay is better than tubularized for tunica vaginalis urethroplasty. Two studies in 2005 by Calado et al.[16] and also another in 2009 by Leslie et al.[17] reported the use of tunica vaginalis as a dorsal graft.

Biochemistry and Molecular Biology. Universitat de Barcelona. Barcelona, Spain Levels or the cyclic nucleotides cGMP or cAMP that play Selleck PS-341 important roles

in memory processes are not characterized in Alzheimer′s disease (AD). The aim of this study was to analyze the levels of these nucleotides in cerebrospinal fluid (CSF) samples from patients diagnosed with clinical and prodromal stages of AD and study the expression level of the enzymes that hydrolized them (phosphodiesterases: PDEs) in the brain of AD patients vs controls. For cGMP and cAMP CSF analysis the cohort (n=79) included cognitively normal participants (SCI), individuals with mild cognitive impairment stable or AD converters (sMCI and cMCI) and mild AD patients.

A high throughput liquid chromatography–mass spectrometry method (LC-MS/MS) was used. Interactions between CSF cGMP or cAMP with MMSE score, CSF Aβ(1-42), and CSF p-tau were analyzed. For PDE4, 5, 9 and 10 expression analysis, brains of AD patients vs controls (n=7 and n=8) were used. cGMP, and not cAMP levels, were significantly lower in the CSF of patients diagnosed with mild-AD when compared to non-demented controls. CSF levels of cGMP showed a significant association with MMSE-diagnosed clinical dementia and with CSF biomarker Aβ42 in AD patients. Significant increase in PDE5 expression was detected Selleck Crizotinib in temporal cortex of AD patients compared to that of age-matched healthy control subjects. No changes in the expression of others PDEs were detected. These results support the potential involvement of cGMP in the pathological and clinical development of AD. The cGMP reduction in early stages

of AD might participate in the aggravation of amyloid pathology and cognitive decline. “
“Edited by Arie Perry and Daniel J. Brat . Practical Surgical Neuropathology: A Diagnostic Approach . Churchill Livingstone Elsevier , Philadelphia, PA , 2010 . 656 Pages. Price £183.35 ( hardback) (http://www.amazon.co.uk ). ISBN 10 : 0-443-06982-4 ; ISBN Adenosine triphosphate 13 : 978-0-443-06982-6 I will be honest. I had not expected to like this book. At approximately 570 pages of text, it sits between small books such as Escourolle and Poirier[1], Adams and Graham’s[2] and of course the WHO Tumour Classification[3], and reference texts such as Ellison and Love[4], and Greenfield[5]. Neuropathology is a small discipline with a reasonable number of well-written specialist texts, and sections in books with wider remit. I was not sure that there was a need for an ‘in-betweener’. I was quickly proved wrong.

IL-17 is a newly described member of a cytokine family and has several members, including IL-17A-E. IL-17A (IL-17 in brief), and enhances T cell priming and stimulates fibroblasts, endothelial cells, neutrophils, macrophages

and epithelial cells to drive these cells to produce multiple proinflammatory mediators, including IL-1, IL-6, tumour necrosis factor (TNF)-α, nitric oxide synthase 2, metalloproteinases and chemokines [8]. Based on these properties, IL-17 may protect against bacterial, fungal and protozoal infection. However, IL-17 is also proposed as being involved predominantly in an array of inflammatory disorders such as systemic rheumatic diseases, multiple sclerosis, inflammatory bowel disease and asthma selleck compound [9,10]. Published studies have noted that staphylococcal enterotoxin B (SEB) has a relation with allergic disorders [11,12]. SEB can induce IL-6 expression in the nasal mucosa [13]. Because the synergistic effect of IL-6 and transforming growth factor (TGF)-β induces IL-17 expression in CD4+ T cells, we speculate that SEB-induced IL-6 may be in synergy with TGF-β to initiate the expression of IL-17

in CD4+ FoxP3+ Treg to drive these cells to become CD4+ FoxP3+ IL-17+ T cells. To test the hypothesis, we analysed surgically removed nasal mucosa from patients with AR or AR/NP. Indeed, CD4+ FoxP3+ IL-17+ T cells were localized in the nasal mucosa SB431542 nmr of patients with AR/NP. Cell culture-related reagents and Western blotting reagents were purchased from (Invitrogen, Shanghai, China). Enzyme-linked immunosorbent assay (ELISA) kits of immunoglobulin (Ig)E, IL-17, IL-6 and SEB were purchased from R&D Systems (Shanghai, China). Magnetic cell sorting reagents were purchased from (Miltenyi Biotec, Suntec City, Singapore). IL-6 siRNA and scrambled siRNA, antibodies of FoxP3, TGF-β, β-arresting

2, retinoic acid-related orphan receptor (ROR)γt and β-actin were purchased from (Santa Cruz Biotech, Santa Cruz, CA, USA). Fifty patients were recruited into this study, comprising 20 NP/AR, 20 AR and 10 CR (chronic rhinitis). The diagnosis of AR followed the established criteria in our department, which has also selleck chemicals llc been published elsewhere [14]. All patients were treated with conventional medical intervention that did not respond well and asked for inferior turbinectomy, NP resection and some with endoscopic sinus surgery if the patient complicated with chronic sinusitis. Another five nasal or sinus cancer patients were recruited into this study. Marginal non-cancer nasal mucosa was collected and used as control (Con). Informed consent was obtained from each patient. The study protocol was approved by the Human Research Ethic Committee at Shanxi Medical University. No subjects had used any medicines during the past 2 weeks.

It appeared clearly from these models that the abnormal metabolic control, as assessed by hyperglycaemia and glycosuria, the hallmarks of T1D clinical diagnosis, was preceded by a long phase defined as ‘prediabetes’ during which the β cell autoantigen-specific inflammatory response developed silently, yet progressively. Thus, in NOD mice

progressive infiltration of the islets of Langerhans by mononuclear cells, also termed insulitis, evolves in two distinct phases [1]. Insulitis appears by 3–4 weeks of age and up to 8–10 weeks is confined to the periphery of the islets (peri-insulitis) without any sign of active destruction of insulin-secreting β cells. As disease progresses, by 10–14 learn more weeks of age the infiltrating cells invade the islets quite abruptly, i.e. aggressive insulitis, and

rapid β cell destruction occurs causing overt hyperglycaemia. The orchestrated mechanisms leading to β cell destruction all represent potential targets for therapeutic intervention. These mechanisms involve a central triad constituted by β cells, autoantigen-presenting cells and T lymphocytes. Autoantigen-presenting cells are heterogeneous and include dendritic cells (DCs), BYL719 in vitro macrophages and B lymphocytes. The observation that B cell-deficient NOD mice are disease free indicates that disease development is B cell-dependent [2]. In addition to their antigen-presenting role, macrophages and DCs are also key inflammatory effector cells. T lymphocytes involved in T1D are functionally heterogeneous, comprising pathogenic T cells and specialized subsets of regulatory T cells. β cell destruction involves

pathogenic T cells, as demonstrated by the capacity of ‘diabetogenic’ CD4+ and CD8+ lymphocytes from the spleen of diabetic NOD mice to transfer disease into syngeneic immune-compromised recipients [NOD neonates, irradiated adult NOD mice, NOD severe combined immunodeficiency (SCID) mice][3]. In parallel, there is evidence to show that Branched chain aminotransferase disease progression is controlled by T cell-mediated immune regulatory circuits involving distinct subsets of regulatory T cells [4,5]. It is also important to stress that β cells must not be viewed simply as ‘passive’ targets that are killed immediately by the immune-mediated insult. In a first step they ‘suffer’ from the inflammatory environment created by the insulitis that, in a partially reversible fashion, inhibits their capacity to secrete insulin but also provides all the premises for establishing ‘cross-talk’ between the β cell and the immune cells and cytokines from the environment [6]. It is only in a second step that the β cell is eventually destroyed through apoptosis. During recent years the epidemiology of T1D has become alarming.

Identification of a triggering mechanism will represent a major step forward towards disruption of the differentiation process and effective control of Toxoplasma infections. The process of reactivation (bradyzoite-to-tachyzoite differentiation) is critical to pathogeneses but one that is highly understudied. It is tempting to assume that reactivation may be a direct reversal of the tachyzoite-to-bradyzoite differentiation selleck compound process. This could provide the premise for comparing gene expression patterns during differentiation

in both directions. Perhaps more challenging is the question of why some differentiation processes are reversible (e.g. tachyzoite-bradyzoite), while others are not (e.g. sporozoite–tachyzoite). A better understanding of the molecular mechanisms driving these processes could provide the tools required to arrest parasites growth and prevent the fatal effects of reactivation. While the sequencing selleck screening library of the Toxoplasma genome has been a significant step forward, transcript expression data and proteomic studies are important to better understand the functional significance that

is merely hinted at in the genome. In recent years, Toxoplasma has been the subject of a plethora of proteomic studies, the likes of which have been extensively covered in an excellent review by Weiss et al. (58). These proteomic studies have proven to be an invaluable resource for documenting the actively expressed proteins in tachyzoites and for better characterizing significant subproteomes, including the rhoptries and micronemes. The proteomic data from these studies also provide a wealth of information G protein-coupled receptor kinase to validate and improve current gene prediction algorithms. The need for such improvements is highlighted by the global proteomic studies of Dybas et al. (59), which estimate that the currently employed gene prediction

algorithms exhibit false-negative rates ranging from 31 to 42%. Rather than recapitulate what was summarized by Weiss et al. (58), we herein present a summary of more recent developments in the field of Toxoplasma proteomics. The hydrophobic nature of many membrane proteins has been a long-standing hindrance to performing successful proteomic studies on them, as they are largely insoluble in aqueous solution. Detergents are needed to solubilize the proteins, although the inclusion of these detergents has numerous negative effects on subsequent proteomic studies. As an example, ionization products of the detergents can obscure relevant, less abundant peptide products. A common way to surmount the problem of excess detergents in proteomic studies is to resolve the solubilized proteins with one-dimensional gel electrophoresis and couple that with tandem mass spectrometry analysis (1D LC–MS/MS). This was one of the three approaches that Che et al.

To clarify conformational differences between these two isoforms, PrP-deficient mice were immunized with brain homogenates of normal and scrapie-infected

animals. All mice generated anti-PrP antibodies. Peptide array analysis of these serum samples revealed a distinctive epitope of PrPSc consisting of QGSPGGN (PrP41–47) at the N-terminus. This study demonstrated a conformational dissimilarity at the N-terminus between PrPSc and PrPC, a finding that may provide novel information about conformational features of PrPSc. “
“Although NKT cells have been implicated in diverse immunomodulatory responses, the effector mechanisms underlying the NKT cell-mediated regulation of pathogenic T helper cells are not well understood. Here, we show that invariant NKT cells inhibited the

differentiation see more of CD4+ T cells into Th17 cells both in vitro and in vivo. The number of IL-17-producing CD4+ T cells was reduced following co-culture with purified NK1.1+TCR+ cells from WT, but not from CD1d−/− or Jα18−/−, mice. Co-cultured NKT cells from either cytokine-deficient (IL-4−/−, IL-10−/−, or IFN-γ−/−) or WT mice efficiently inhibited Th17 differentiation. The contact-dependent mechanisms of NKT cell-mediated regulation of Th17 differentiation were confirmed using transwell co-culture experiments. On the contrary, the suppression of Th1 differentiation was dependent Selleckchem HDAC inhibitor on IL-4 derived from the NKT cells. The in vivo regulatory capacity of NKT cells on Th17 cells was confirmed using an experimental autoimmune uveitis model induced with human IRBP1–20 (IRBP, interphotoreceptor retinoid-binding protein) peptide. NKT cell-deficient mice (CD1d−/− or Jα18−/−) demonstrated an increased disease severity, which was reversed by the transfer of WT or cytokine-deficient (IL-4−/−, IL-10−/−, or IFN-γ−/−) NKT cells. Our

results indicate that invariant NKT cells inhibited autoimmune uveitis predominantly through during the cytokine-independent inhibition of Th17 differentiation. The long-served Th1/Th2 hypothesis has been updated by the identification of a third subset, IL-17-producing CD4+ Th (Th17 cells) 1. Although Th1 cells mainly provide protection against intracellular microorganisms and Th2 cells protect against helminthes, Th17 cells have been implicated in the host defense against extracellular bacteria and fungi 2. Uncontrolled Th17 responses have been recently reported in autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, psoriasis, and inflammatory bowel diseases in human and mouse models 1–3, which were formerly considered Th1-mediated diseases. In mice, naïve CD4+ T cells differentiate into Th17 cells in the presence of IL-6 and TGF-β 4. TGF-β is a pleiotropic cytokine with potent regulatory capacities that modulates the activation and homeostasis of effector T cells and induces Foxp3+ Tregs 5.

7 Kidney Disease Outcomes Quality

Initiative: No recommendation. UK Renal Association: No recommendation. Canadian Society of Nephrology: No recommendation. European Best Practice Guidelines: No recommendation. International Guidelines: No recommendation. No recommendations. Long-term, prospective and retrospective studies on food safety practices and incidence of food-borne infections among kidney transplant recipients may help determine the most appropriate methods of prevention of such infections. Maria Chan, Karen Fry, Aditi Patwardhan, Catherine Ryan PARP phosphorylation and Fidye Westgarth have no relevant financial affiliations that would cause a conflict of interest according to the conflict of interest statement set down by CARI. These guidelines were developed under a project funded by the Greater Metropolitan Clinical Taskforce, New South Wales. “
“It remains unclear whether

long-term daily icodextrin use can decrease technique failure and improve survival in PD patients. The aim of the present study was to Proteases inhibitor investigate whether icodextrin use, once daily, can decrease technique failure and prolong patient survival in incident PD patients. Incident PD patients who survived more than 90 days were recruited from the China Medical University Hospital, Taiwan, between January 1, 2007 and December 31, 2011. All patients were followed Ribonucleotide reductase until transfer to hemodialysis (HD), renal transplantation, transfer to another center, death, or December 31, 2011. A total of 306 incident PD patients (89 icodextrin users, 217 icodextrin non-users) were recruited during the study period. Icodextrin users were more likely to have hypertension, diabetes and high or high-average peritoneal transport compared with non-users. During the follow-up

period, 43 patients were transferred to HD: 7 (7.87%) of the icodextrin group, and 36 (16.59%) of the non-icodextrin group. Thirty-two patients died during the follow-up period: 5 (5.62%) of the icodextrin group, and 27 (12.44%) of the non-icodextrin group. Icodextrin use was significantly associated with a better prognosis, in terms of technique failure (adjusted HR= 0.32; 95% CI = 0.14-0.72). With regard to patient survival, icodextrin use (adjusted HR= 0.33; 95% CI = 0.12-0.87) was associated with a significantly lower risk of death. The use of icodextrin once daily may decrease technique failure and improve survival in incident PD patients.

We confirm and extend these previous observations H 89 using another marker

for regulatory T cells, namely the CD4+ cell population with low CD127 expression [38]. Kekaleinen et al. revealed in their study that Tregs in patients with APS I do not function properly and that they have alterations in their TCR repertoire. All these data point towards a role of Tregs in the pathogenesis of APS I. We speculate that AIRE is involved in the development of Tregs, either in the thymus or in the lymph nodes where AIRE is also expressed [7, 8]. Thymic abnormalities could potentially also interfere with the proper development of iNKT cells – another type of cells with immunoregulatory properties. However, we could not confirm the previous reported decreases in iNKT [9] in Norwegian patients with APS I. Changes in the peripherally induced effector or memory cells could also reflect the autoimmune Rucaparib ic50 attack on endocrine organs. The percentage of the CCR4+CCR6+

Th-cell population which includes IL-17A producing Th17 cells was unaltered in patients with APS I in our study. This is in line with a previously published study on isolated CMC [39] and our recent report of unchanged IL-17A responses in spite of severely decreased IL-17F and IL-22 responses in APS 1 patients’ PBMC [1]. IL17-producing cells have been reported to be involved in protection against Candida albicans (reviewed in [40]). These cells are also involved in the pathogenesis of many autoimmune diseases, including psoriasis, rheumatoid arthritis and Crohn’s disease [41–43]. Hence, patho-logical autoimmunity can be associated with an increased Th17-cell

response whereas a decreased function or number of these cells is correlated to CMC. The fact that patients with APS I are both susceptible for autoimmune diseases and for CMC might complicate the cellular analysis. Interestingly, we observed a significant decrease in CCR6+CXCR3+ Th-cell proportion medroxyprogesterone in patients with APS I. The mechanism underlying this phenomenon could be an increased homing of these cells to inflammatory tissues by binding to interferon-induced chemokines CXCL9 and 10; hence, these cells will be found in a decreased level in the circulation. Indeed, we have previously shown increased levels of CXCL10, a CXCR3 ligand, in APS I patient’s sera that is probably secreted by endothelial cells in inflamed tissues in response to IFNγ [44]. The level of different DC subpopulations did not vary between the groups. This is in agreement of what we and others have published earlier [19, 38]. The monocyte level of patients with APS I has been shown by Hong et al. and Perniola et al. [19, 45] to be increased in patients compared to controls. The monocyte frequencies of patients varied a lot in our study, and some of the patients had indeed elevated numbers of these cells. However, when comparing the group as a unifying cohort, the results did not reach significance.