Overall, there is stronger molecular evidence that IL-2 is important for Th2 generation 23 than for Th1 cells. This leaves open the possibility that a direct Th2-skewing effect of IL-2 may also contribute to the protective function of IL-2-antibody complexes in myasthenia gravis. Although recent interest in IL-2 for the treatment of autoimmunity stems from IL-2′s role in the maintenance of Treg, the activities of this growth factor on effector cells must be taken into account when evaluating IL-2′s therapeutic potential. Indeed, in a study using IL-2 to prevent diabetes in Rucaparib the NOD mouse 16, it was found that high doses

of IL-2 complexes expanded effector cells and led to accelerated onset of diabetes. To the contrary, low doses of IL-2 prevented the onset of diabetes by restoring functional Treg in the pancreas. The detrimental outcome see more of IL-2 treatment is likely due to the induction of strong effector and memory responses in the autoimmune-prone mice. Recent studies have demonstrated a prominent role for IL-2 in

the generation of CD4+ and CD8+ memory T cells 24, 25. This function is obviously unwanted when treating autoimmune disease but the current body of evidence suggests that careful determination of IL-2 complex doses and timing to specifically target Treg provides a rationale to circumvent these problems 16. It may be that lower doses of IL-2 complexes favor Treg function, whereas higher doses will boost effector/memory cell formation. The high levels of CD25 on Treg compared with naïve and effector cells may explain this differential sensitivity, allowing Treg to outcompete effector cells for capturing

environmental IL-2. It is likely that assays for IL-2 action, such as phospho-flow analyses 14, will help us better define IL-2′s targets under different conditions of exposure. In addition, combination therapy, such as IL-2 to promote Treg numbers and function and mTOR inhibitors to block the generation of effector T cells, may prove to be beneficial in immunological disorders. IL-2 is one of the first cytokines Etofibrate discovered and it was thought that IL-2′s function is well understood. Studies in the past 10 years have led to new insights into the biology of IL-2 and an astonishing re-evaluation of the dogma. It is especially remarkable that almost two decades ago this cytokine was being tested for its ability to boost immune responses and now it is being considered as a therapy to inhibit immune responses. The development of better assays to define cytokine actions in vivo and rational strategies to optimize the actions of cytokines may help to realize the potential of IL-2 as an immunotherapeutic agent. Supported by NIH grants RO1 AI073656 and P01 AI35297 (to A. K. A.), and JDRF grant 32-2008-354 (to H. D.). Conflict of interest: The authors declare no financial or commercial conflict of interest. See accompanying article: http://dx.doi.org/10.1002/eji.

CRMD endocarditis accounts for about 10% of all device-related infections, and cardiac infection caused by Candida sp. is a rare event. To date, only sporadic reports of this unusual and life-threatening event have been reported. By describing a case learn more of CRMD-related Candida endocarditis and conducting a literature review, we provide a detailed characterisation of this unusual clinical entity with an emphasis on diagnosis, management and treatment. A case of CRMD-related Candida endocarditis is presented and a computer search for confirmed

cases of CRMD-Candida endocarditis was conducted. Current recommendations for management and treatment were documented. From 1969 to 2009, 15 patients with CRMD-Candida endocarditis (12 pacemaker and three implanted cardioverter-defibrillator) were documented. All were males, non-albicans Candida sp. were frequently recovered, a major fungal embolus occurred in 27% of patients and two of 10 patients who received defined antifungal therapy and device explantation expired. CRMD Candida endocarditis is a rare www.selleckchem.com/products/iwr-1-endo.html and serious clinical event; isolates can include Candida albicans and other Candida sp., and treatment involves both targeted antifungal therapy and device removal. In their 2006 publication, Voigt et al. [1] described

an impressive increase in the number of cardiac rhythm management device (CRMD) implants in the US for the period 1996–2003. Coincidentally, during this 7-year oxyclozanide period, there was over a threefold increase in the number of hospitalisations associated with CRMD infections and the increase in infection was greater for implanted cardioverter-defibrillators (ICDs) than for permanent pacemakers (PPMs). Numerous authors have addressed the problem of CRMD infections2–5 and, in one recent study, Uslan et al. [6] evaluated 1524 patients with PPM and/or ICD

implants and found the incidence of pocket infection with bloodstream infection or device related endocarditis to be 1.14/1000 device years. When rhythm device infections do occur, pocket infections are more commonly documented than endocarditis,7 the microbiology usually involves staphylococci (coagulase-negative staphylococci, Staphylococcus aureus)5,8 and management includes both device explantation and appropriate antimicrobial therapy.7 CRMD-associated endocarditis accounts for about 10% of all device-related infection cases,2 and is a life-threatening complication9; several authors have noted the rarity of fungal organisms involved in such infections.2,10–14 There are sporadic case reports that address the problem of CRMD endocarditis caused by Candida species and a single review, published in 199712 included only four well-defined cases and it pre-dated the availability of certain newer anti-fungal agents.

6, top left and middle left). Tactile and erogenous sensitivity was also rated as excellent. Urethrography carried out by the urologists showed a stricture at the urethral anastomosis 4 months postoperatively which required an open urethroplasty. Two months later, another urethroplasty was necessary due to recurrent stricture. Twelve months postoperatively, the patient was able to urinate while standing (Fig. 6, bottom left). No donor-site complications were recorded. The patient regained full range of motion of the wrist with unimpaired

strength. No nerve-related complications were encountered. The patient was a 48-year-old female-to-male transsexual with an osteogenesis imperfecta, arterial hypertension, and a heavy smoking selleck products history with chronic obstructive pulmonary disease. In this case, vaginectomy had been performed in a previous procedure combined with adnexectomy and hysterectomy. We performed the free sensate RFF-phalloplasty

from the right side using the Chang-design. The microsurgical anastomoses were performed in the right groin: the radial artery onto the common femoral artery in an end-to-side fashion, Ruxolitinib and three venous end-to-end anastomoses of the flap onto branches of the greater saphenous vein. Both antebrachial nerves were coapted to the ilioinguinal and to one of the dorsal clitoral nerves respectively. The same pharmacological and flap monitoring protocol was followed as for case 1. Starting from POD 11, a partial flap necrosis appeared, Osimertinib manufacturer affecting the areas of the lateral flap borders. The debridement resulted in a complete loss of the neo-urethra. We decided to apply an identical approach to reconstruct the neo-phallus and the neo-urethra. The same modified, shortened Chang-designed RFF was harvested on the contralateral left forearm. The flap dimensions were identical to the ones described in case 1 (Fig. 2). The anastomoses were carried out in the intact left groin: an end-to-side anastomosis of the radial artery onto the common femoral artery,

one of the comitant veins and a total of three subcutaneous veins of the flap onto branches of the great saphenous vein in an end-to-end fashion. No nerve reconstruction was performed. The postoperative course was uneventful. No flap-related complications occurred. Due to a filiform stricture at the urethral anastomosis, the patient underwent open urethroplasty 10 months postoperatively. Twelve months postoperatively, the patient was able to urinate while standing. The appearance of the neo-phallus was subjectively rated as good, and the patient reported on an excellent tactile and erogenous sensitivity (Fig. 6, right column). No donor-site complications were recorded. Partial flap necrosis is reported to occur in 7–11% of phalloplasty cases.[1-3] The largest series published by Doornaert et al. showed a rate of 7.2% (23 out of 316 cases) with a higher incidence in smokers, patients who insisted on large-sized neo-phalluses, and after anastomotic revision.

In line with this, several recent publications demonstrated a surprisingly high plasticity of differentiated CD4+ T-cell subpopulations generated either in vitro or in LEE011 mw vivo. First, a number of studies showed that Foxp3+ Treg

in both mouse and human can be redirected to express IL-17 16–20. Similarly, a recent report showed that transferred natural Treg develop to follicular B-helper T cells in the Peyer’s patches of T-cell-deficient hosts 21. Second, several groups demonstrated that Th17 cells generated in vitro are plastic upon exposure to Th1 cytokines and start to express IFN-γ (22–24). Finally, studies with purified in vitro generated Th17 cells transferred to NOD mice showed infiltrating cells changing their phenotype to become Th1 cells 22, 23. Very importantly, human Th17 T-cell clones were shown to be highly flexible and to co-express IFN-γ and IL-17A when stimulated in the presence of IL-12 24. Similarly a specific CD161+ subpopulation derived from human umbilical cord blood,

which is prone to contain and differentiate to Th17 cells, develops strongly toward Th1 cells under the influence of IL-12 in vitro25. Since these groups demonstrated IFN-γ production by Th17 cells following adoptive transfer, we aimed to define whether indeed trans-differentiation of IL-17 expressing cells is the cause of this finding. To address this question, we used our recently generated IL-17F fate mapping mouse line 26. When these IL-17F-Cre BAC-transgenic mice are crossed to ROSA26-EYFP Selleck Talazoparib reporter mice 27, IL-17F-expressing cells are irreversibly genetically tagged by Cre-mediated excision of a loxP flanked stop cassette, resulting in ubiquitous expression of EYFP in all recombined cells. We analyzed the behavior of transferred, sorted Th17 reporter

cells generated either in vitro or in vivo and found that a considerable amount of these triclocarban cells ceased IL-17A expression entirely, and expressed purely IFN-γ. Additionally, we found a number of previously highly pure Th1 cells co-expressing IL-17A together with IFN-γ in the mesenteric LN (mLN). In a first attempt to define whether in vitro generated Th17 cells maintain their cytokine phenotype upon EAE induction, we performed transfer EAE using in vitro polarized Th17 cells generated from MOG35–55-specific CD4+ cells isolated from 2D2 TCR-transgenic mice 28. After 5 days of stimulation in Th17-polarizing conditions, about 50% of cells expressed IL-17A, whereas only negligible numbers produced IFN-γ (Supporting Information Fig. S1A). We adoptively transferred 5×106 of these cells per mouse to RAG1-deficient mice (of the C57BL/6 background), resulting in severe EAE symptoms (Supporting Information Fig. S1B). In line with the findings by O’Connor et al.

2A, right panel). Then, microglia was pulsed with OVA and incubated

with OT-1 cells. Results showed that microglia from irradiated and, as expected [10], from non-irradiated mice induced similar levels of IL-2 (46.40 ± 2.40 and 42.00 ± 2.83 pg/mL, respectively; mean ± SD, n = 5) and IFN-γ secretion (133.60 ± 16.13 and 132.40 ± 5.80 pg/mL, respectively) by OT-1 cells (Fig. 2D). These results demonstrate that 16 Gy body irradiation does not alter the in vitro cross-presentation activity of microglia. Finally, in order to support our above results showing that irradiation eliminate CNS-associated APCs (Fig. 2C), we compared the cross-presentation activity of CNS-CD11b+ cells isolated from irradiated and non-irradiated mice DMXAA supplier in the absence of perfusion and meninges removal. CNS-CD11b+ GDC-0068 research buy cells were pulsed in vitro with OVA and then incubated with OT-1 cells. CNS-CD11b+ cells

from non-irradiated mice (that include microglia and CNS-associated APCs) were more efficient than CNS-CD11b+ cells from irradiated mice (microglia only) in inducing IFN-γ secretion (165.60 ± 12.64 pg/mL) by OT-1 cells while as potent in inducing IL-2 secretion (47.20 ± 2.13 pg/mL; Fig. 2D). Moreover, in irradiated mice, perfusion and meninges removal did not modulate the capacity of CNS-CD11b+ cells to stimulate OT-1 cells, again supporting the absence of CNS-associated APCs in irradiated mice (Fig. 2D). No significant production of IL-2 and IFN-γ were detected when CNS-cells were incubated with BSA (Fig. 2D). Collectively, these results demonstrate that 16 Gy body irradiation eliminates CNS-associated APCs while preserving the quiescent status and the activity of microglia. To evaluate the ex

vivo cross-presentation activity of microglial cells, OVA and BSA (used as a negative control) were injected into the brain of body-irradiated mice as previously described [10]. Then, these in vivo-pulsed microglia were used to stimulate in vitro OT-1 cells. Results showed that microglia isolated from OVA-injected irradiated mice induced IL-2 (28.83 ± 1.27 pg/mL; mean ± SD, n = 3; Fig. 3A) Abiraterone and IFN-γ production (99.23 ± 20.30 pg/mL) by OT1 CD8+ T cells (Fig. 3B). No significant production of IL-2 and IFN-γ was observed with microglia from BSA-injected mice. As expected [10], CNS-CD11b+ cells isolated from non-irradiated mice (that include microglia, CNS-associated and peripheral APCs which infiltrate brain) also induced IL-2 (50.87 ± 6.56 pg/mL) and IFN-γ (356.63 ± 18.48 pg/mL) production by OT-1 cells with a higher efficiency than microglia from irradiated mice. We thus investigated whether stimuli of microglia may enhance their cross-presentation. Irradiated mice were intracerebrally injected with OVA plus CpG-ODN, GM-CSF and sCD40L. Interestingly, these adjuvants greatly enhanced the capacity of microglia to trigger IL-2 (56.25 ± 2.62; **p < 0.005; Fig. 3A) and IFN-γ (369.75 ± 25.95 pg/mL) production by OT-1 cells (Fig. 3B).

Our results indicate that this signalling shift in T cells is triggered due to ligation of low-affinity FcRs by ICs in the presence of TCC. Phosphorylation of ITAM in FcRγ chain is responsible for Syk activation, which then subsequently participate in downstream activation of mitogen-activated protein kinases (MAPKs), PI3K and PLCγ activation in lymphocytes. In order to establish a role for Syk in IC-mediated T cell

activation via low-affinity FcRs, we probed for phosphorylated Syk in the activation loop at Tyr525/526 in cells treated with ICs and TCC. The immunoprecipitates prepared using monoclonal anti-FcγRIIIA/B antibody from cells treated with TCC and ICs, when probed with anti-pSyk, showed phosphorylation of a protein band that migrated at 72 kD. This suggested Syk activation check details in T cells, in response to ICs and TCC (Fig. 2c). These

findings are also supported by our previous observation of Syk phosphorylation in Jurkat cells treated with TCC and in vitro formed ovalbumin–anti-ovalbumin ICs and ICs purified from plasma of SLE patients [26]. These results are also supported by the previous observation that www.selleckchem.com/products/gsk1120212-jtp-74057.html Syk is activated in SLE T cells [28]. Syk activation is mediated via FcRγ chain [17]. We observed that in CD4+ T cells treated with ICs or ICs and TCC, the FcRγ chain was recruited to the site of membrane receptors (Fig. 3a). The co-localization analysis of all the Z-series sections (Fig. 3biii) confirmed this finding. The presence of TCC during the IC treatment enhanced the recruitment of the FcRγ chain with membrane FcγRIIIA (Fig. 3biii). Although the observed scatter-pattern for the co-localization of FcRγ chain was different from the pSyk and FcγRIIIA/B staining, we presume that this was due to wider distribution of the staining intensity of the FcγRIIIA and FcγRIIIB receptors, both of which were recognized by the monoclonal antibody that was used for the staining (Fig. 3a). The scattergram obtained in both co-localization GBA3 experiments demonstrated data where a line of best fit could be

drawn confirming the association among these proteins. An antibody that recognizes both receptors was used in this study due to the unavailability of an antibody that recognizes only FcγRIIIA. TCC alone was insufficient to trigger these events. The cells stained using anti-FcγIIIA/B antibody demonstrated localized peripheral membrane staining (Fig. 1b). A similar staining pattern was also observed with an affinity-purified anti-FcγRIIIB antibody. Both FcγRIIIA and FcγRIIIB co-localized with labelled AHG on cell membrane (Fig. 1b). Co-staining of expanded naive CD4+ T cells using anti-FcγRIIIA/B and anti-FcγRIIIB demonstrated that those CD4+ T cells that expressed FcγRIIIA always expressed FcγRIIIB.

Another important consideration Bortezomib in vivo in translating the in vitro murine data to the bedside is the dosing regimen. Serum concentrations of atorvastatin, for lipid lowering, are in the nanomolar range [42], while inhibition of T cell activation and MMP-9 production occurs only at micromolar concentrations in tissue culture. Direct comparisons of human serum concentrations to in vitro experiments are not appropriate, especially for a lipophilic drug such as atorvastatin. Additionally, previous

work has shown that statin treatment inhibits MMP-9 production indirectly in the vessel wall of abdominal aortic aneurysms [43,44], thus serum levels may not reflect accurately local tissue concentrations at work, similar to the disconnect between serum and tissue levels of MMP-9 in KD [45]. An altered lipid profile has been reported in children with KD. During the acute phase of disease a pro-atherogenic lipid profile [46,47], with a decrease selleck kinase inhibitor in total cholesterol, high-density lipoprotein-cholesterol (HDL-C), apoA1 and apoA2 and an increase in triglycerides and apoB, is observed [46,48,49]. Total cholesterol returns quickly to normal, but HDL-C recovery is slow and remains

significantly lower than expected up to years later [46]. In addition to the observed mild dyslipidaemia in patients with KD, arterial function may be abnormal with abnormal measures

of endothelial dysfunction even in those without aneurysms [50–53]. Carotid artery intima-media thickness among KD patients is greater, and endothelial dysfunction has been reported both in children with persistent coronary lesions as well as in those without detectable early coronary artery involvement, Dolichyl-phosphate-mannose-protein mannosyltransferase indicated by decreased brachial artery flow-mediated dilatation [40,48,49,53]. Thus, all patients with KD, even in the absence of echocardiographic evidence of coronary artery involvement, may be at risk for premature atherosclerosis even if managed appropriately during the acute phase of the illness. The potential benefits of statin therapy are recognized outside the acute phase of illness. Recognizing the limitations of the in-vitro results reported, confirmation of the immunomodulatory effects of atorvastatin are needed in vivo using the LCWE-induced coronary arteritis animal model of KD. This model, which mimics accurately the histopathological changes seen in the coronary arteries of KD patients [19,20,54], provides a unique opportunity to study treatment protocols and potential side effects of statin therapy in young animals, providing important insight prior to human studies.

Immunohistochemistry, TD and TI-II Z-VAD-FMK supplier immunizations, TNP-specific and total Ig subclass ELISA assays were performed as described 28, 41. Levels of anti-nucleosome antibodies were measured by ELISA (using coated oligonucleosomes and peroxidase-coupled anti-mouse Ig isotype-specific antibodies for subsequent detection). For ELISPOT assays, 96-well Multiscreen plates (MAHAN4550; Millipore) were coated overnight at 4°C with 1 μg/mL anti-Ig subclass antibodies (BD Pharmingen) and subsequently blocked in PBS/1% BSA at r.t. for 1 h. Serial dilutions of splenic cell suspensions were incubated at 37°C for 3 h. Production was detected with corresponding biotin-labeled anti-Ig isotype-specific

antibodies, streptavidin-peroxidase (BD Pharmingen) and 3-amino-9-ethylcarbazole. Antibody secreting cells were counted under the microscope. Statistical significance was calculated using the Mann–Whitney U test. The authors thank the people from the Erasmus MC Animal Care facility for their assistance. This work was supported by the Netherlands Organization for Scientific Research, the Dutch Cancer Society and the

Dutch Arthritis Association. Conflict of interest: The authors declare no financial or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. “
“Bronchiolitis

obliterans syndrome (BOS) is associated with lack Maraviroc order of immunosuppression of T cell proinflammatory cytokines and increased T cell granzyme B. Repeated antigen-driven proliferation down-regulates T cell CD28. We hypothesized that down-regulation of CD28 and up-regulation of alternate co-stimulatory molecules (CD134, CD137, CD152 and CD154) on T cells may be associated with BOS. Co-stimulatory molecules, granzyme B, perforin and intracellular cytokines were measured by flow cytometry on T cells from stable lung transplant patients (n = 38), patients with BOS (n = 20) and healthy controls (n = 10). There was a significant increase in the percentage of CD4/28null and CD8/28null T cells producing Clomifene granzyme B, interferon (IFN)-γ and tumour necrosis factor (TNF)-α in BOS compared with stable patients. Down-regulation of CD28 was associated with steroid resistance and up-regulation of CD134, CD137, CD152 and CD154 on CD4+ T cells and CD137 and CD152 on CD8+ T cells. There was a significant correlation between increased CD28null/CD137 T cells producing IFN-γ, TNF-α with BOS grade (r = 0·861, P < 0·001 for CD28null/CD137 IFN-γ/CD8) and time post-transplant (r = 0·698, P < 0·001 for CD28null/CD137 IFN-γ/CD8). BOS is associated with down-regulation of CD28 and up-regulation of alternate co-stimulatory molecules on steroid-resistant peripheral blood proinflammatory CD4+ and CD8+ T cells.

Thus, this study was undertaken to further investigate the efficacy of ABT-199 purchase recNcPDI vaccination employing both CT and CTB as adjuvants, and application of corresponding emulsions via the intranasal route. In addition, both antigen formulations were assessed in

the pregnant mouse model to investigate the capacity of recNcPDI to limit foetal Infection. Besides assessing the splenic transcript levels of classical Th1 (IL-12, IFN-γ) and Th2 (IL-4, IL-10) cytokines upon challenge, we also investigated expression levels of the proinflammatory cytokine IL-17 and the transcription factor Foxp3, a marker for T regulatory (Treg) cell activation, both of which are implicated in immune regulation of Inflammatory responses during pregnancy. Unless otherwise stated, all cell culture reagents were supplied ROCK inhibitor by Gibco-BRL (Zurich, Switzerland), and chemicals were purchased from Sigma (St. Louis, MO, USA). Neospora

caninum tachyzoites of the Nc-1 isolate [23] were propagated by serial passages in Vero cells. Purified tachyzoites were obtained and counted [24]. Recombinant PDI (recNcPDI) was cloned into the His-tag expression vector pET151 and expressed in Escherichia coli BL21 Star and purified (Invitrogen, Zug, Switzerland) [17]. The protein concentration was measured with the Bio-Rad protein assay. Following dialysis into PBS, recNcPDI was stored at −20°C. Animal procedures were approved by the animal welfare committee of the Canton of Bern and followed the corresponding guidelines. All Balb/c

mice (females, 9 weeks of age) purchased from Charles River Laboratories (Sulzheim, Germany) were checked serologically for the absence of anti-N. caninum IgG by ELISA. Eighty five females were randomly divided into Inositol monophosphatase 1 five groups of 17 animals each (Table 1). The vaccination (three doses at 2-week intervals) was done by intranasal (i.n.) application through the nares under mild isoflurane anaesthesia [17]. Mice in group 1 (PBS) received sterile PBS only, group 2 (CT) received 0·5 μg CT, group 3 (CT-PDI) received 10 μg of recNcPDI emulsified in 0·5 μg CT, group 4 (CTB) received 0·5 μg CTB and group 5 (CTB-PDI) received 10 μg of recNcPDI in 0·5 μg CTB. Mating and gestation were carried out as previously described [25-27]. Females were challenged at day 7 post-mating by i.p. inoculation of 2 × 106 N. caninum tachyzoites. At day 19 post-mating, pregnant and nonpregnant mice were separated, and pregnant mice were housed separately to rear their pups. All mice were inspected daily throughout the experiment for clinical signs of neosporosis (ruffled coat, apathy, hind limb paralysis, rounded back and circular movements) using a standardized score sheet and were killed when clinical signs were evident. Adult mice were weighed at 3-day intervals from 3 days prior to the first vaccination; neonates were weighed from day 14 post-partum until the time of euthanasia.

Median age of patients was

34 years (range 1–73) and 37% had less than 18 years. Acute leukaemia was the most common underlying haematological disease (68/84; 81%). The phase of treatment was as follows: first induction SCH772984 in 21/84 (25%), consolidation phase in 18/84 (21%) and reinduction/salvage in 45/84 (54%). The main site of infection was lung with or without other sites. The principal fungal pathogens were as follows: Aspergillus sp. 68 cases (81%), Candida sp. six cases (8%), Zygomycetes four cases (5%) and Fusarium sp. four cases (5%). The most used combo was caspofungin+voriconazole 35/84 (42%), caspofungin + liposomal amphotericin B (L-AmB) 20/84 (24%) and L-AmB+voriconazole 15/84 (18%). The median duration of combo was 19 days (range 3–180). The overall response rate (ORR) was 73% (61/84 responders) without significant differences between the combo regimens. The most important factor that significantly influenced the response was granulocyte (PMN) recovery (P 0.009). Only one patient discontinued therapy (voriconazole-related neurotoxicity) and 22% experienced mild and reversible adverse

events (hypokalaemia, ALT/AST increase and creatinine increase). The IFDs-attributable mortality was 17%. This study indicates that combo was both well tolerated and effective in haematological patients. The most used combo regimens were caspofungin + voriconazole (ORR Tyrosine Kinase Inhibitor Library in vitro 80%) and caspofungin + L-AmB (ORR 70%). The ORR was 73% and the mortality IFD related was 17%. PMN recovery during combo predicts a favourable outcome. Clinical Trials Registration: Glycogen branching enzyme NCT00906633. “
“Hepatic fungal infection is a frequent complication in patients receiving intensive chemotherapy for acute leukaemia. Hepatic lesions may be detected

using computerised tomographic (CT) scans, but there is no standardised CT protocol for the diagnosis and follow-up of hepatic fungal infection. We therefore retrospectively analysed the number and the volume of hepatic fungal lesions in 24 CT of 20 consecutive patients treated for acute leukaemia during late-arterial and porto-venous phase. The mean number of lesions per patient was 31 (range: 3–105) in the late-arterial and 26 (3–81) in the porto-venous CT (P = 0.026). The mean total volume of all lesions was 6.45 ml in the late-arterial and 4.07 ml in the porto-venous CT representing a 1.6fold difference between the two CT scans (P = 0.008). The total volume of the lesions negatively correlated to the absolute contrast difference between liver parenchyma and liver vein (Pearson correlation, r = −0.62; P = 0.002).