Therefore, the following monoclonal mouse antibodies were applied: IC16 ([30], raised against Aβ1–16; 1:2000), AT8; Thermofisher, Bonn, Germany; 1:1000), MC-1 ([31]; 1:50), CP13 ([32]; 1:500), β-actin (Sigma; 1:5000) Doxorubicin cost and β3-tubulin (Millipore, Schwalbach, Germany; 1:2000). In addition, we applied rabbit antisera directed against human tau (Dakocytomation, Hamburg; 1:1000), anti-pS199

(BioSource, 1: 500), anti-pS422 ( [33]; 1:500) and anti-glial fibrillary acidic protein (GFAP; Synaptic Systems, Göttingen, Germany; 1:4000). Following overnight incubation, membranes were washed in TBST two times for 10 min. Secondary anti-rabbit or anti-mouse conjugates of horseradish peroxidase (Dianova, Hamburg, Germany) were applied for 2 h. Membranes were check details rinsed two times in TBST, and blots were developed using enhanced chemiluminescence,

followed by scanning of X-ray films (Hyperfilm EC, Amersham Biosciences, Freiburg, Germany). For quantification of relative protein amounts, protein levels were determined via ImageJ software (1.46r, National Institutes of Health, USA) by measuring band intensity in densitometric analyses normalized to β-actin or β3-tubulin levels, respectively. Sections containing hippocampi from several animals of all animal groups were pre-treated for 10 min with concentrated formic acid (98–100%, Merck) and routinely used for sensitive 4G8 staining new (see below). These and all other free-floating sections were extensively rinsed with TBS followed by blocking of non-specific binding sites for subsequently applied immunoreagents with 5% normal donkey serum in TBS containing

0.3% Triton X-100 (NDS-TBS-T). For the analysis of cholinergic markers, forebrain sections were either applied to affinity-purified goat-anti-ChAT (AB144P, Millipore; 1:50 in NDS-TBS-T) or rabbit-anti-p75 (G323A, Promega, Mannheim, Germany; 1:100 in NDS-TBS-T), followed by several rinses with TBS and incubation for 1 h with Cy3-conjugated donkey antibodies recognizing goat or rabbit (both from Dianova, 20 μg/ml TBS containing 2% bovine serum albumin = TBS-BSA), respectively. Markers applied for double labelling of β-amyloidosis and tauopathy in hippocampal sections are summarized in Table 1. For triple fluorescence labelling of Aβ deposits, astrocytes and microglia, sections were first incubated overnight in a mixture of biotinylated mouse antibody 4G8 ([34]; Covance, 1:500 in NDS-TBS-T), Cy3-conjugated-mouse-anti-GFAP IgG (Sigma; 1:250) and rabbit-anti-ionized calcium binding adapter molecule 1 (Iba; Wako, Neuss, Germany; 1:200). Following several rinses with TBS, immunoreactivities were visualized by incubating sections for 1 h in a mixture of Cy3-streptavidin and Cy5-tagged donkey-anti-rabbit IgG (both at 20 μg/ml TBS-BSA and from Dianova).

Ly49Q binds MHCI and is functionally NVP-AUY922 price analogous to human killer Ig-like receptors (KIRs) 83. Intriguingly, it was recently demonstrated that in addition to binding HLA, KIR3DL2 can directly bind CpG DNA, which leads to enhanced cytokine production 84. It would be interesting to examine whether Ly49Q has similar binding capacities. The importance of cellular localization of inhibitory receptors is also evident from the studies in NK cells. Inhibitory receptor-mediated inhibition of NK-cell activity is known to act locally, as NK cells

contacting both resistant and susceptible target cells are capable of selective killing of susceptible target cells 85, 86. Inhibitory receptors present in the immunological synapse between MLN0128 manufacturer target cell and effector cell mediate the localized inhibition of activating receptor cytotoxicity 85. Thus, SHP-1 and SHP-2 play an important role in ITIM-mediated inhibition of various activation pathways (Fig. 2). As described by the study of Kong 14 and Sasawatari et al. 23,

the mode of action of SHP-1 and SHP-2 may involve the mechanisms other than dephosphorylation of upstream molecules; controlled cellular localization of the receptor itself or associated molecules may lead to inhibition of cell activation by sequestration or, conversely, be essential in cellular activity. Possibly, the capacity to colocalize with activating receptors may determine whether the inhibitory receptor is selective in its action or has broad capacity. Adenosine Few

groups have thoroughly addressed this issue; expansion of these studies would further improve our understanding on the mechanism behind inhibitory receptor function. In addition to ITIM-mediated inhibition of TLR responses, ITAM-mediated signaling may also inhibit TLR signaling. For example, DAP12-deficient macrophages show increased cytokine production after stimulation with TLR ligands such as LPS and CpG 70. As with the FcαR, it has been hypothesized that clustering of DAP12 by high-avidity interactions will result in activating effects, whereas DAP12 recruitment following low-avidity interactions will lead to inhibitory effects 87. Low-avidity receptor ligation would result in a weak phosphorylation of the ITAMs and basal Syk phosphorylation, which leads to inhibition of TLR signaling. The nature of the DAP12 recruiting receptor may determine whether TLR signaling is impaired. Supportive of this concept is that TREM-2-DAP12 chimeras lead to inhibitory effects on TLR signaling, whereas TREM-1 chimeras do not 71. Also integrin signaling may reduce TLR activation. DAP12 and FcRγ are required to relay integrin signals in neutrophils and macrophages, thus coupling integrin ligation to Syk activation and downstream signaling events 69, 88.

m. did induce Gag-specific gut-homing T cells [20]. Thus, in the BALB/c mice, triple regimens of DCM and selleckchem DMC elicited robust CD8+ TEM cells early after vaccination, which converted into TCM and in the spleen maintained the markers for GALT homing. In the first part of this work, we rederived ChAdV-68 by inserting its whole genome into a BAC in a single step, which simultaneously generated a deletion at the E1 locus, for easy further manipulation using recombineering. This simplified cloning strategy paves a way for future derivation and exploration of other human and animal adenoviruses so far untested

for vaccine delivery [40]. The application of BAC recombineering also facilitates modulation of adenovirus immunogenic properties by rational activation of various innate pathways, which will in turn lead to functionally distinct properties of vaccine-elicited

adaptive responses. Clearly, not all the HIV-1-host interactions and workings of the immune system are yet completely understood to, on one hand, identify desired protective properties of vaccine-elicited T cells and, on the other hand, manipulate the intra- and intercellular signaling so as to bias the actively induced responses toward a desired type. Nevertheless, BAC-facilitated selleck chemical genetic manipulation prepares the grounds for such future molecular manipulations. The AMQ epitope-mediated protection of BALB/c mice against EcoHIV/NDK infection [35] best approximates the clearance of HIV-1-infected cells during primary HIV-1 infection. For human vaccines, Gag is a suitable first-generation immunogen, to which broad and robust T-cell responses correlate with good control of chronic HIV-1 infection

[43]. For more efficient early protection particularly in humans, responses to conserved regions of HIV-1 [44, 45] that the virus cannot easily change without Fenbendazole a likely significant fitness cost and/or mosaic protein design [46] might be even more beneficial due to the increase coverage of HIV-1 variants and escape mutants. However, these are theoretical arguments: which vaccine design will induce the most effective T-cell responses can be only determined by protection of humans against acquisition of HIV-1 and/or decrease of virus load at set point, which in turn delays development of AIDS possibly without the need of antiretroviral drugs. While the HIV-1-derived Tg determines specificity of the vaccine-elicited T cells, route of immunization and choice of vaccine vector(s) determine the T-cell quality, tissue localization and longevity [47, 48]. In this respect, ChAdVs are gaining center stage as vectors for subunit vaccines against a number of challenging infections such are malaria, HCV, pandemic influenza virus, and HIV-1 [7].

By real-time polymerase chain reaction (RT-PCR), the PTEN gene expression in the tumor was lower than in the five non-neoplastic brain tissues used as control.

Mutation analysis did not show any variation in INI-1 and PTEN sequence while P53 analysis showed the presence of homozygote P72R variation. Fluorescent in situ hybridization analysis showed polysomy of chromosome 2 while amplification of N-MYC was not detected. Owing to the rarity of embryonal tumor with abundant neuropil and true rosettes, each new case should be recorded to produce a better clinical, pathological and molecular see more characterization of this lesion. “
“Neurofibromatosis type 2 (NF2) is a hereditary tumor syndrome. The hallmark of NF2 is bilateral vestibular schwannoma. In addition, glioma is one of the diagnostic criteria of NF2. In this retrospective study the clinical presentation and histopathological features of 12 spinal gliomas from NF2 patients were assessed. Ten tumors were previously diagnosed as ependymomas and two as astrocytomas. However, upon re-evaluation Navitoclax cell line both astrocytomas expressed epithelial membrane antigen in a dot-like fashion and in one case it was possible to perform electron microscopy revealing junctional complexes and cilia typical for ependymoma. The findings suggest that NF2-associated spinal gliomas are ependymomas. Based on the fact that NF2-associated gliomas are

almost FAD exclusively spinal and that no NF2 mutations have been found in sporadic cerebral gliomas, we suggest that “glioma” in the current diagnostic criteria for NF2 should be specified as “spinal ependymoma”. “
“Rhabdoid meningioma is an uncommon meningioma variant categorized as WHO grade III. The majority of cases occur in adulthood. Herein, we describe a right fronto-temporal rhabdoid meningioma affecting a 3-year-old boy. The lesion measured approximately

4 cm in diameter and incorporated the ipsilateral middle cerebral artery. Sub-total surgical excision of the mass was performed. Histologically, the tumor was mainly composed of globoid plump cells with inclusion-like eosinophilic cytoplasm, peripheral nuclei, prominent nucleoli and occasional intra-nuclear cytoplasmic pseudo-inclusion. The cells appeared in many areas loosely arranged and focally disclosed a papillary architecture. At immunohistochemistry, the tumor cells were EMA, vimentin, HHF35, PgR, INI-1 and p53 positive. The proliferative index (Mib-1) was 15% in the most positive areas. Ultrastructurally, tumoral cells showed an abundant cytoplasm, which was filled with numerous intermediate filaments. Desmosomal junctions were seen. RT-PCR revealed the presence of NF2 gene expression. Molecular study did not indicate alterations of the INI-1 gene, whereas it showed the presence of Pro72Arg in exon 4 at heterozygous state in the TP53 gene.

Here, we discuss the multi-layered regulation of inducible gene expression in the immune system, focusing on the interplay between transcription factors, and the T-cell epigenome, including the role played by chromatin remodellers and epigenetic enzymes. We will also use IL2, a key inducible cytokine gene in T cells, as an example of how the different layers of epigenetic

mechanisms regulate immune responsive genes during T-cell activation. It is now well established that the chromatin landscape Rapamycin supplier plays an important role in the regulation of inducible genes. The mature cells of the immune system represent an exquisitely poised system for rapid response to pathogens and have proved to be a valuable model for investigating the contribution of chromatin to the regulation

of genes that respond rapidly to environmental signals. For example, activation of naive CD4+ T cells in the immunological response to infection leads to a concerted programme of proliferation and slow differentiation that results in the acquisition and regulated expression of multiple effector genes. The stimulation of T cells involves activation of protein kinase and calcium signalling pathways, including tyrosine and serine/threonine kinases and phosphatases, protein kinase LY2606368 concentration C (PKC) and calcineurin, respectively; following which, numerous transcription factor families, including nuclear factor-κB and nuclear factor of activated T cells are activated and translocated into the nucleus to bind to target genes. Individual genes respond to immune stimulation in distinct temporal and cell-type-specific patterns, and this is governed by the nature Elongation factor 2 kinase of the antigenic stimulus and the interactions between the inducible

transcription factors and the gene-specific chromatin environment. Chromatin can act as a barrier to the binding of transcription factors and the transcription machinery and it must therefore be modified or reorganized to facilitate changes in gene transcription. These changes may occur at a localized level or at a higher-order chromatin level. The gene expression changes that occur during T-cell activation and differentiation therefore require a co-ordinated effort from inducible transcription factors, chromatin-remodelling complexes, histone-modifying enzymes and the more recently discovered chromatin-associated signalling kinases. Herein we will focus our efforts on the chromatin events that are required to facilitate changes in gene expression programmes during T-cell activation. The broadest definition of epigenetics refers to gene expression that is governed by mechanisms other than the DNA sequence.

These findings altogether suggested that TGF-β-expressing immature AE-pe-DCs might play a significant role in the generation of a regulatory immune response within the peritoneal cavity of AE-infected mice. Alveolar echinococcosis (AE) is a severe chronic helminthic disease accidentally affecting humans. Following infection by peroral uptake of Echinococcus multilocularis eggs, AE develops as a consequence of intrahepatic establishment of the larval stage (= metacestode) of the tapeworm. From the liver, the metacestode spreads to other organs by

infiltration or metastasis formation, thus clinically AE rather resembles a tumour-like disease. The natural intermediate hosts involved in the life cycle of the parasite are predominantly small rodents. Therefore, the laboratory mouse is an excellent model to study the host–parasite interplay. this website Experimentally, intraperitoneal inoculation of metacestode vesicles is referred to as secondary infection. In the peritoneal cavity of metacestode-infected mice [AE-mice], inter-visceral tumour-like growth of the metacestode overcomes the immune system such as to establish a chronic

phase of infection, which persists approximately between 2 and 6 months p.i. By the end of this time period, infection/disease reaches a terminal stage where mice have to be sacrificed because of severity of symptoms. In the host–parasite interplay, metacestode surface molecules as well as excretory/secretory (E/S) products are considered as important key players (1). The intraperitoneal murine model ACP-196 of AE offers the opportunity to study the direct effect of metacestodes on periparasitic peritoneal cells, including especially dendritic cells (DCs), the most important antigen-presenting cells (APC) in the initiation of a Th1- or Th2-oriented immune response. Several studies so far suggested that distinct subsets

of DCs differentially modulate T-helper responses, but other studies pointed to a dominant role for microbial stimuli and the local microenvironment in this process (2). In the frame of a Th1 immune orientation, it is largely accepted that DCs are activated mostly by bacterial or viral pathogens via toll-like receptor (TLR) ligation to produce IL-12 and TNF-α, both pro-inflammatory cytokines inducing a Th1-oriented response (3,4). Th1-associated DC activation by microbial products evokes C1GALT1 rapid phenotypic changes, including up-regulation of surface markers for DC maturation such as MHC class II, CD80, CD86 and CD40 molecules (5,6). How DCs elicit a Th2 response is more controversial. There is no mirror image signature of cytokine and surface ligands that DCs express to stimulate Th2 differentiation. Some examples of helminth antigens, including the products of filarial Acanthocheilonema viteae (ES-62) (7), Schistosoma mansoni soluble egg antigen (SEA) (8) and the schistosome-associated glycan lacto-N-ficopentaose III (LNFPIII) (9), do not appear to induce IL-12 production by DCs (8,10).

The Th1 cells secrete high levels of interferon-γ (IFN-γ) and IL-2, and

drive immunity against intracellular pathogens but also promote autoimmunity. Interleukin-12, in synergy with IL-18, drives Th1 differentiation, in large part via induction of T-bet (T-Box expressed in T cells), a master regulator transcription PD-1/PD-L1 inhibitor cancer factor that controls the expression of IFN-γ.14 Interleukin-12 signals through JAK2 and Tyk2, and activates mainly STAT4, also a key transcription factor for Th1 commitment4 (Fig. 2). Indeed, STAT4-deficient CD4+ T cells do not produce IFN-γ following IL-12 or Listeria monocytogenes stimulation,15,16 and STAT4-deficient mice fail to secrete IFN-γ in response to Toxoplasma gondii and therefore die as the result of an uncontrolled parasite burden.17 It later emerged that STAT4 controls T-bet expression,18,19 with which it then collaborates for efficient binding to the Ifng promoter1 and to induce both IL-18Rα

and IL-12Rβ2.3 The STAT4 also induces tumour progression locus 2 (Tpl-2), a serine threonine kinase essential for T-bet and STAT4 up-regulation and so essential for optimal IFN-γ secretion.20 Therefore Sunitinib research buy STAT4 not only promotes the expression of IFN-γ and T-bet, but also of other genes that consolidate the Th1 phenotype (Fig. 2), as summarized in Table 1. Importantly, IFN-γ also facilitates the development of Th1 cells in a positive autocrine feedback loop,21 and STAT1-deficient T cells have reduced T-bet levels following infection,22 although IFN-γ secretion does not seem to be affected. Moreover, several studies Niclosamide have shown that JAK3 and STAT5 activation by IL-2 enables optimal IFN-γ secretion.23,24 Indeed, JAK3-deficient T cells fail to secrete IFN-γ,23 whereas

IL-2-mediated STAT5 activation is required for optimal IFN-γ secretion.23,24 STAT5 binds the first conserved non-coding sequence upstream of the Ifng promoter, which suggests that it might permit T-bet access.23,25 Therefore, STAT1 and STAT5 contribute to Th1 differentiation by enhancing T-bet and IFN-γ expression, respectively (Fig. 2). SOCS1 is a key inhibitor of IFN-γ signalling26,27 and blocks IFN-γ-mediated STAT1 activation by targeting JAK2 and IFN-γRα chain28 (Fig. 2). The SOCS1-deficient mice also have enhanced type 1 IFN responses, which render them more resistant to viral infection.27 Importantly, SOCS1 is up-regulated during Th1 commitment29 and not surprisingly, SOCS1-deficient T cells proliferate strongly in response to IL-12,30 which enhances their polarization towards the Th1 lineage.31 However, these cells also secrete elevated levels of IL-4, and exhibit heightened IL-4-mediated STAT6 phosphorylation, suggesting that SOCS1 could also be an important regulator of Th2 differentiation.

18 A STAT-5 phosphorylation assay was used to gauge IL-7 responsiveness in CD4+ and CD8+ cells. The increase of the percentage of P-STAT-5 cells, and an example of constitutive P-STAT-5 and IL-7-induced P-STAT-5, in HD and NHP are shown in Fig. 5(a,b). In NHPs, (n = 15) 84·4 ± 10·8% and 60·6 ± 12% of CD4+ and CD8+ cells showed an increase of P-STAT-5 cells in response to IL-7 stimulation. Similar numbers were obtained in PBMCs from HDs (n = 10): 87·6 ± 7·6% and 62·3 ± 15·4% in CD4+ and selleck chemicals CD8+

cells, respectively. CD4+ and CD8+ subsets showed comparable responses to IL-7 stimulation as measured by STAT-5 phosphorylation in NHPs and HDs. In HDs and NHPs more CD4+ cells than CD8+ cells showed STAT-5 phosphorylation (consistent with higher levels of IL-7Rα expression on CD4+ T cells) but the amplitude (measured by MFI) was not statistically different between CD4+ and CD8+ cells. The presence of regulatory cells was assessed by expression analysis of CD25 and FoxP3 in the CD4+, CD8+ and CD4+ CD8+ T-cell compartments (gating strategy see Supplementary Fig. S2). In NHPs, the

CD4+ T-cell compartment showed the following frequencies: 16·5% (median values) were CD25intermediate (CD25interm.) and 0·5% stained for CD25bright; in CD4+ CD8+ T cells: 19·6% cells were CD25interm. and 1·4% were CD25bright; in CD8+ T cells: 1% were CD25interm. and 0·07% CD25bright (Table 2). Compared with HDs, higher frequencies of CD4+ CD25interm. T cells and CD4+ CD8+ CD25interm./bright,

and CD8+ CD25bright T cells (21%) were detected in PBMCs from NHPs. Analysis Fulvestrant of FoxP3 expression in the different CD25+/− T-cell compartments showed that the majority of CD25bright T cells in NHPs were FoxP3+ (87·5% of CD4+ and 76% of CD4+ CD8+ and CD8+ T cells), whereas Phospholipase D1 only 10–20% of CD25interm. T cells showed FoxP3 expression (Fig. 6a). In contrast, almost no FoxP3 expression could be observed in human CD4+ CD8+ CD8+ T cells that exhibited the CD25interm. phenotype. Analysis of PBMCs from four of eight HDs showed that CD4+ CD8+ and CD8+ T cells, which displayed a CD25bright phenotype, stained also positive for FoxP3. In summary, statistically higher frequencies (P ≤ 0·05) of CD4+/− CD25interm.FoxP3+/−, CD4± CD8± CD25interm./high FoxP3+/− and CD8± CD25interm./high FoxP3+/− were detected in NHPs than in HDs. Expression of the IL-7Rα on NHP CD25bright T cells was inversely correlated with expression of FoxP3, which is similar to the situation described in humans.25 More than 90% of NHP CD4+ CD8+ CD25interm./bright FoxP3+ T-cell subsets did not express the IL-7Rα, whereas the majority of CD4+ CD8+ CD25+/− FoxP3− (33–67%) were positive for IL-7Rα (% of IL-7Rα expression is shown for CD4+ T cells in Fig. 6b). The same trend was observed in HDs. However, 9% of human CD4+ CD25bright FoxP3+ T cells expressed the IL-7Rα (Fig. 6b), this was not true for the same T-cell subset in NHPs (3·8%).

Based on this study, CD137 seems to be involved in priming and might play a role in limiting the early expansion of CD4+ T cells at the initial stage find more of immune response to protein antigen. In line with our observations, this study demonstrates that CD137−/− mice are not compromised in their capacity to elicit CD4+ T cell-mediated immune responses. Similar to our results, Lee et al. could not detect a difference with regard to the IgG1 response, suggesting that even in the absence of CD137 signalling, T cell-dependent humoral antibody responses to protein antigen develop normally [41]. However, in contrast to this study, we did not observe a

strong increase in Th2 cytokine levels in splenocyte cell cultures of CD137−/− OVA group compared with WT OVA. Whereas Lee et al. applied OVA subcutaneously only once to study initial T cell priming, we immunized WT and CD137−/− mice twice i.p. with OVA and aluminium hydroxide as adjuvant,

followed by six i.n. challenge periods. Therefore, the differences seen between these studies might be explained by the prolonged immunization protocol Acalabrutinib manufacturer including OVA challenge periods to induce local recall response in our model. Whether CD137 plays a distinct role in priming versus recall responses in OVA-based models needs to be investigated further. It is possible that experimental models without the powerful effect Exoribonuclease of aluminium hydroxide as adjuvant could reveal minor changes between WT and CD137−/− mice that may be underestimated in our acute model based on OVA/Alum sensitization. Thus, testing of CD137−/− mice in another asthma protocol, i.e. with a weaker immunization protocol or with house dust mite as model allergen, could be a future perspective. Another possible explanation for the missing phenotype of CD137−/− mice with regard to asthma is that the missing CD137/CD137L co-stimulation might be compensated by other co-stimulatory signalling pathways, as we have shown previously for CD30 and CD134 (OX40) in a chronic asthma model [42]. CD30, another co-stimulatory

molecule of the TNFR superfamily, proved to be crucial for the development of asthma in an acute model [29] while, in contrast, we did not see differences between CD30−/− and WT mice in the chronic model [42]. We demonstrated that reduced expression of OX40 on T cells in the acute model and up-regulation in the chronic model indirectly supported a compensatory role of OX40 for CD30 signalling. Similarly, application of agonistic anti-OX40 mAb restored the asthma phenotype in CD30−/− mice in the acute model, whereas chronic airway inflammation was reduced in the presence of an inhibitory anti-OX40 ligand mAb. Therefore, it is possible that in CD137−/− mice the role of CD137 signalling is compensated likewise by other co-stimulatory pathways.

Recurrence is a difficult issue and a major concern in plastic surgery. In this study, we introduce a reusable perforator-preserving gluteal artery-based rotation flap for reconstruction of pressure sores, which can be also elevated from the same incision to accommodate pressure sore recurrence. Methods: The study included 23 men and 13 women with a mean age of 59.3 (range 24–89) years. There were 24 sacral ulcers, 11 ischial ulcers, and one trochanteric ulcer. The defects ranged in size from 4 × 3 to 12 × 10

cm2. Thirty-six consecutive pressure sore patients underwent gluteal artery-based rotation flap reconstruction. An inferior gluteal artery-based rotation fasciocutaneous flap was raised, and the superior gluteal artery perforator was preserved in sacral sores; alternatively, see more Venetoclax a superior gluteal artery-based rotation fasciocutaneous flap was elevated, and the inferior gluteal artery perforator was identified and dissected in ischial ulcers. Results: The mean follow-up was 20.8 (range 0–30) months in this study. Complications included four cases of tip necrosis, three wound dehiscences, two recurrences reusing the same flap for pressure sore reconstruction, one seroma, and one patient who died on the fourth postoperative day. The complication

rate was 20.8% for sacral ulcers, 54.5% for ischial wounds, and none for trochanteric ulcer. After secondary repair and reconstruction of the compromised wounds, all of the wounds healed uneventfully. Conclusions: The perforator-preserving gluteal artery-based rotation fasciocutaneous flap is a reliable, reusable flap that provides rich vascularity facilitating wound healing and accommodating the difficulties of pressure sore reconstruction. © 2012 Wiley Periodicals, Inc. Microsurgery, 2012. “
“A 35-year-old woman, with a 3-week history of an enlarging erythematous, scaly plaque of the scalp vertex associated

with the onset of some painful, subcutaneous nodules on her pretibial regions. Trichophyton mentagrophytes Astemizole was isolated from the scalp lesion and the histological examination of one of the nodular lesions of the legs showed a septal panniculitis. The diagnosis of erythema nodosum (EN) induced by kerion celsi was made and the patient started therapy with oral terbinafine 250 mg per day for 4 weeks associated with naproxene per os 1 g per day for 2 weeks. Erythema nodosum is considered a reaction pattern to a wide variety of microbial and non-microbial stimuli: dermatophytic infections are rarely associated with EN. “
“Pulmonary zygomycosis is a relatively uncommon complication of solid organ or peripheral blood stem cell transplantation and has a high associated mortality. Optimal therapy consists of complete resection of infected tissue and treatment with amphotericin B (AmB).