MBL has been shown to be involved in the control of many microorganisms, including bacteria, fungi, parasites and viruses [6–9], and MBL deficiency has been associated with an increased frequency of various infections, including sepsis, aspergillosis,

meningococcal disease and invasive pneumococcal infections [8,10–13]. Intracellular pathogens, including Mycobacterium tuberculosis, co-opt macrophage phagocytosis to assist with establishing and disseminating infection [14]. Therefore, it has been proposed that high MBL GSK126 mw serum levels may lead to increased tuberculosis infections (TB) through promotion of M. tuberculosis opsonization [15]. This has been strengthened by studies demonstrating that MBL enhances phagocytic activity against other mycobacteria and demonstration of a protective effect of MBL deficiency against at least some forms of M. leprae infection [15–18]. A number of clinical and genetic studies have been performed to consider the impact of MBL levels or MBL polymorphisms on the development of TB. Results from these studies have been conflicting or contradictory, and it has been unclear whether MBL deficiency states result in increased susceptibility to tuberculosis infection. To attempt to clarify this APO866 concentration situation, therefore, we carried out a meta-analysis of studies

considering the association between MBL deficiency and tuberculosis infection. For the meta-analysis, we included all published studies that considered the association between tuberculosis and MBL2 polymorphisms. A literature search for the MeSH terms ‘tuberculosis OR TB OR mycobacteria’ and ‘MBL OR mannose-binding lectin OR mannose-binding protein’ was performed using Medline and PubMed and abstracts were reviewed for relevance. No language restrictions were applied to the search strategy. References of articles were also reviewed for additional relevant citations not included in the original search

protocol. Two of the authors (J.T.D. selleck chemical and D.P.E.) independently reviewed the full text of all articles to ensure that they met preset criteria for inclusion. The primary outcome considered in the meta-analysis was the association between pulmonary tuberculosis infection and the presence of MBL2 polymorphisms in patients without human immunodeficiency virus (HIV). For the primary analysis, and to allow appropriate comparison of all studies, cases and controls were classified as AA (wild-type MBL2 genotype), AO (structural gene polymorphism heterozygous MBL2 genotype) or OO (compound heterozygote MBL2 genotype). Subsequent analyses were also performed for the association between pulmonary tuberculosis and MBL2 polymorphisms in HIV-positive patients, and of the association between tuberculosis and serum MBL levels.

HUVEC were incubated with mixtures of 50 μg/mL WT FI or mutants and C3b/125I-C3b see more at 37°C. As positive control 20 μg/mL FH was added and in the negative control FI was omitted. The presence of cleavage products of C3b degradation was assessed by gradient SDS-PAGE (Fig. 7A). The intensity of the 68-kDa-cleavage product was calculated and presented as mean value from three independent experiments (Fig. 7B). The results demonstrate that endogenous membrane-bound MCP acts

as cofactor for FI-mediated cleavage of C3b. D501N mutant did not cleave C3b α′-chain, while P32A and A222G cleaved C3b as efficiently as the WT FI. In the presence of membrane-bound MCP as cofactor M120V, H165R and R299W degraded C3b α′-chain significantly more KU-60019 datasheet efficiently than WT FI (Fig. 7B). We next tried to rationalize the functional consequences of several of the point mutations examined above in the context of the predicted three-dimensional (3D) structures of each domain of FI (Fig. 8). The homology modeling approach is described in detail in 34, although further details regarding the modeling of the FIMAC domain are given below. The models of the domains, FIMAC, CD5, LDLr1 and SP (Fig. are presented separately because at present there are no reliable experimental data to suggest

how the domains are oriented in the full-length protein. The structural and functional consequences of the mutations are listed in Table 2. The residue Cys25 is located in the FIMAC domain and forms a disulfide bond with the adjacent Cys36 (Fig. 8). A mutation to

Phe destroys this stabilizing bond and further destabilizes by introducing steric clashes with the side chain of Cys36. It is likely that the Cys25 mutation imposes structural changes within the N-terminal region of this domain, possibly explaining why a decreased secretion of this mutant is observed experimentally. The Pro32 residue is fully Oxymatrine solvent exposed in a surface loop, at least in the isolated FIMAC domain (Fig. 8). Proline usually imposes greater conformational constraints on the polypeptide backbone than other amino acids and, in places where it can be tolerated, such as in loops and turns, proline makes a positive contribution to protein stability through entropic effects. In the present situation, while this mutation could slightly destabilize the domain, it could be structurally tolerated at this position. We found that the P32A mutant expressed as well as WT FI, and showed only slightly reduced function in degrading C4b and C3b in solution and only when C4BP and FH were used as cofactors. However, the P32A mutant showed substantially impaired ability to degrade C3b deposited on cell surfaces. A proline at position 32 could perturb interdomain contacts or form new interactions with a FI ligand when C3b is part of a deposited C3-convertase. The residue Met120 is located in the CD5 domain (Fig.

On multivariate logistic regression analysis, the association of fusion transcript status and age was confirmed adjusting KU-60019 price for tumour location (P = 0.006). Conclusions: The frequency of BRAF-KIAA1549 fusion transcripts is significantly lower in adult patients with pilocytic astrocytoma, weakening the sensitivity of this specific diagnostic marker in that age group. “
“This chapter contains sections titled: Introduction Number of Animals Tissue Sampling Tissue Preparation Control Groups Qualitative Examination: Detection of Treatment-Related Effects Dose Dependence of Treatment-Related Effects References Note Added in Proof “
“This chapter contains sections titled: Introduction Retraction

Spaces Around Neurons, Vessels, and Glial Cells Dark (Basophilic) Neurons Artifacts Involving Myelin, Axons, and Sensory Ganglion Neurons Miscellaneous Artifacts References “
“Richard Prayson, Bette Kleinschmidt-DeMasters, Mark Cohen and David Elder Brain SCH 900776 concentration Tumors Demos Medical Publishing , New York , 2010 . 318 + xv Pages. Price $140 (hardback). ISBN 978-1933864693 Brain Tumors is one of a series of pathology texts by Demos Medical Publishing which aim to cover the full spectrum of surgical pathology in a case-based series format. In addition to a volume on brain tumours the Consultant Pathology Series currently includes volumes on head and neck pathology

and tumorigenic melanocytic proliferations with forthcoming volumes in the series covering pathology of the liver, bladder and thyroid papillary lesions. The authors are all experienced pathologists who have accumulated large collections of difficult cases. The cases presented in Brain Tumors are based on actual consultations with no less than 101 individual chapters over 318 pages. The text covers a full range of histopathological diagnoses, ranging from normal and reactive conditions to the rarer tumours which have only recently been included in the most up to date World Health Organization (WHO) classification. Each Fossariinae chapter follows an identical format.

A short introductory paragraph provides background clinical information including age, clinical presentation and imaging findings. Next is a summary of the reporting pathologist’s opinion with a description of the histological findings. This opinion is then expanded upon in a section of comment and discussion with further details of the diagnostic histological features, a review of relevant differential diagnoses and some clinicopathological correlation. A discussion of the immunohistochemical findings and, where relevant, the molecular pathology, is also included. Each case is accompanied by a series of illustrations to highlight the relevant diagnostic features and two or three references for those wishing to do some further reading.

These cytoplasmic eosinophilic granules and bundles were negative on PAS staining. Intracytoplasmic eosinophilic granules of tumor cells were strongly positive for αB-crystallin, HSP 27 and GFAP, respectively. These findings suggest that the clinicopathological characteristics of the present case should be consistent with the criterion of ependymosarcoma by Rodriguez et al. “
“A. Vihola, M. Sirito, L. L. Bachinski, O. Raheem, M. Screen, T. CP 690550 Suominen, R. Krahe and B. Udd (2013) Neuropathology and Applied Neurobiology39, 390–405 Altered expression and splicing of Ca2+ metabolism genes in myotonic dystrophies

DM1 and DM2 Aims: Myotonic dystrophy types 1 and 2 (DM1 and DM2) are multisystem disorders caused by similar repeat expansion mutations, with similar yet distinct clinical features. Aberrant splicing of multiple effector genes, as well as dysregulation of transcription and translation, has been suggested to underlie different aspects of the complex phenotypes in DM1 and DM2. Ca2+ plays a central role in both muscle contraction and control of gene expression, and recent expression profiling studies have

indicated major perturbations of the Ca2+ signalling pathways in DM. Here we have further investigated the expression of genes and proteins involved in Ca2+ metabolism in DM patients, including Ca2+ channels and Ca2+ binding proteins. Methods: We used patient muscle biopsies BGB324 supplier to analyse mRNA expression and splicing of genes by microarray expression profiling and RT-PCR. We studied protein expression by immunohistochemistry and immunoblotting. Results: Most of the genes studied showed mRNA up-regulation in expression profiling. When analysed by immunohistochemistry the Ca2+ release channel ryanodine receptor was reduced in DM1 and DM2, as was calsequestrin 2, a sarcoplasmic MYO10 reticulum lumen Ca2+ storage protein. Abnormal splicing of ATP2A1 was more pronounced in DM2 than DM1. Conclusions: We observed abnormal mRNA and protein

expression in DM affecting several proteins involved in Ca2+ metabolism, with some differences between DM1 and DM2. Our protein expression studies are suggestive of a post-transcriptional defect(s) in the myotonic dystrophies. “
“Multiple system atrophy (MSA) is a sporadic neurodegenerative disease that is pathologically characterized by the filamentous aggregation of α-synuclein. We report a case of MSA showing unusual neuropathological findings and review six autopsied cases of MSA. The patient progressively developed parkinsonism and ataxia for the 9 years prior to her death at the age of 72 years. Neuropathological examinations revealed neuronal loss restricted to the olivopontocerebellar and striatonigral region, which was more severe in the putamen.

It remains to be investigated whether these disturbances in the thymus compartment can have consequences for the immune response against this protozoan. We sincerely thank Ana Leda Longhini from Centro Integrado de Pesquisas Onco-hematológicas na Infância (CIPOI/UNICAMP). This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP), grant number #04/03599-1. P.R.A.N. was a recipient of a doctoral fellowship from Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq #14229/2005-1) and State University of Campinas (UNICAMP). F.T.M.C. and W.S. are recipients of a research scholarship from CNPq.

The authors declare no competing interests. “
“Citation Koga K, Mor G. Toll-like receptors at the maternal–fetal interface in normal pregnancy find more and pregnancy disorders. Am J Reprod Dorsomorphin Immunol 2010 Toll-like receptors (TLR) form the major family of pattern recognition receptors (PRR) that are involved in innate immunity. Innate immune responses against microorganisms at the maternal–fetal interface may have a significant impact on the success of pregnancy, as intrauterine infections have been shown to be strongly associated with certain disorders of pregnancy.

At the maternal–fetal interface, TLRs are expressed not only in the immune cells but also in non-immune cells such as trophoblasts and decidual cells; moreover, their expression patterns vary according to the stage of pregnancy. Here, we will describe potential functions of TLRs in these cells, their recognition and response to microorganisms, and their involvement in the innate immunity. The impact of TLR-mediated innate immune response will be discussed Resveratrol via animal

model studies, as well as clinical observations. The maternal–fetal interface is an immunologically unique site that must promote tolerance to the allogeneic fetus, while maintaining host defense against possible pathogens. Clinical studies have shown a strong association between intrauterine bacterial or viral infections and pregnancy disorders such as abortion, preterm labor, intrauterine growth retardation (IUGR) and pre-eclampsia.1–3 Therefore, immediate immune responses against microorganisms at the maternal–fetal interface may have a significant impact on the success of pregnancy. The innate immune system is the immunological first line of defense that provides an immediate response against invading pathogens through its ability to distinguish between ‘infectious non-self’ and ‘non-infectious self’.4 Furthermore, activation of innate immunity is a critical step to the development of antigen-specific acquired immunity. Therefore, innate immunity at the maternal–fetal interface has fundamental significance for establishing an adequate microenvironment during pregnancy, elimination of ‘infectious non-self’ (bacteria, virus, etc.

Levels of spontaneous apoptosis in HUVEC control cultures varied between 10·00 and 12·50%. The mean percentage of EC apoptosis induced by cell starvation and staurosporine was 55·46 and 66·80%, respectively. As demonstrated by the enumeration of hypoploid Gefitinib chemical structure cells, purified IgG from the AECA-positive SLE patients induced a significantly higher percentage of apoptosis of HUVECs in comparison to AECA-negative SLE patients (P = 0·001) and healthy controls (P < 0·0001) (Fig. 2). Purified

IgG from the AECA-positive PAH patients did not induce a higher percentage of apoptosis of HUVECs compared to the AECA-negative PAH patients (P = 0·92) and healthy controls (P = 0·08), as assessed by the enumeration of hypoploid cells (Fig. 2). Also in the SSc cohort, no induction of apoptosis was observed (Fig. 2). Further analysis of the PAH cohort demonstrated that IgG from the AECA-positive IPAH patients did not induce a significantly higher percentage of apoptosis of HUVECs compared to the AECA-negative PAH patients (P = 0·94) and healthy controls (P = 0·09), as assessed by the enumeration of hypoploid cells. Incubation with IgG from AECA-positive SLE (n = 3) patients induced a significant decrease in the CI value compared to IgG from AECA-negative SLE (n = 3) patients (P = 0·050) and healthy controls (P = 0·020) (Fig. 3). In fact,

IgG from AECA-positive SLE patients induced a decrease in CI value of 79%, which was comparable with the decrease in CI values induced by cell starvation YAP-TEAD Inhibitor 1 mw (82%) and incubation with 5 nmol/ml staurosporine (93%). Incubation of HUVECs with IgG from the AECA-positive PAH (n = 8) and SSc (n = 6) patients, however, did not alter the CI value significantly compared to IgG from the

AECA-negative PAH (n = 8) and SSc (n = 6) patients (P = 0·248 and P = 0·749, respectively) and healthy controls (P = 0·121 and P = 0·337, respectively). The aetiology of PAH is still poorly understood, and it is postulated that dysfunction of pulmonary ECs plays next an important role in the pathophysiology of PAH [5]. EC dysfunction may lead to pulmonary vascular remodelling and ultimately to the development of PAH [4, 5]. Mounting evidence suggests an important role for EC apoptosis in this process. Taraseviciene-Stewart et al. demonstrated that selective blockade of the vascular endothelial growth factor receptor 2 (VEGFR-2) resulted in severe irreversible pulmonary hypertension associated with precapillary arterial endothelial cell proliferation in chronically hypoxic rats [7]. EC apoptosis following VEGFR-2 blockade was a prerequisite for endothelial proliferation, because caspase inhibition throughout the course of chronic hypoxia and VEGFR-2 blockade prevented EC proliferation and the development of severe pulmonary hypertension [7].

In line with this, several recent publications demonstrated a surprisingly high plasticity of differentiated CD4+ T-cell subpopulations generated either in vitro or in JQ1 order 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 find more 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 DNA Synthesis inhibitor 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.

To permeabilize the bacteria for uptake of the FISH probe, the tissue was treated with 0.5 mg mL−1 lysozyme (Sigma-Aldrich, St Louis, MO) in 0.1 M Tris-HCl (Sigma-Aldrich) at pH 8.0 and 0.05 M Na2EDTA (Sigma-Aldrich) for 3 h at 37 °C and washed with ultrapure water. The samples were dehydrated in a graded series of ethanol washes (50%, 80%, and 100%) for 3 min at each concentration. FISH was performed as described previously (Hogardt et al., 2000; Kempf et al., 2000; Nistico et al., 2009) using the 16S ribosomal probe sequences: Sau 5′-(GAAGCAAGCTTCTCGTCCG)-3′(16S 69–87) (Kempf et al.,

2000) labeled JNK inhibitor in vitro with Cy3 (a green fluorescent fluorophore), which was specific for S. aureus. We used the nucleic acid stain Syto59 (red) as a general stain to stain all bacteria and host nuclei, so

that S. aureus would be dual stained both green and red and appear yellow or orange and non-S. aureus bacteria would only stain with the Syto59 stain and appear red. Bacteria stained with only the Syto59 are readily distinguished from host check details nuclei (which also take up the nucleic acid stain) on the basis of size (bacterial cocci are approximately 1 μm in diameter, whereas the nuclei of host cells are approximately 8 μm) and morphology (Hall-Stoodley et al., 2006; Nistico et al., 2009). For a positive FISH control, we stained MRSA cells grown from a patient with an infected elbow after revision surgery of a total elbow arthroplasty attached to a gelatin-coated slide. The individual cocci were readily discernible (data not shown). To control for nonspecific binding, we stained three pieces of tissue independently

with the NonEub338-Cy3 5′-(ACTCCTACGGGAGGCAGC)-3′ probe, which has no known complementation to any 16S rRNA sequences (Kempf et al., 2000; Manz et al., 1992). Reflected confocal microscopy with the 488-nm laser was used to visualize the tissue over a range of magnifications and a minimum of eight different fields of view in each specimen. The FISH-stained tissue was mounted in a 35-mm Petri dish on 0.5% low-temperature-setting Idelalisib supplier agarose and submerged in HBSS before imaging using CLSM. The Ibis assay positively identified both S. aureus and Staphylococcus epidermidis in the tissue, and also noted the presence of the mecA gene for methicillin resistance. The confidence based on the 16 primer sets was 1.00, 0.92, and 1.00, respectively. There were approximately 10 times more S. aureus than S. epidermidis based on counts of 3889 genomes per well and 452 genomes per well, respectively. The mecA gene returned 8184 genomes per well, suggesting, based on the numbers, that the S. aureus was an MRSA strain. However, from these data alone, we could not draw firm conclusions regarding the mecA status of either staphylococcal species, except that at least one was likely methicillin-resistant. No other bacterial species were detected.

In this study, we demonstrate that FOXO3 interferes with p65/RelA binding to the IFN-β promoter (Fig. 4D) and leads to reduction of its transcription (Fig. 4E). Together, our data and the results of others are in favor of the hypothesis that FOXO3 could sequester the proteins and interfere with their DNA binding to target gene. Further experiments will be needed

to dissect the molecular mechanisms of the FOXO3 suppressor action in detail, but it is likely to be a transcription factor- and gene-specific phenomenon, for example TLR-induced IRF7 mRNA expression, which is under the IRF3 control, is not affected by Palbociclib FOXO3 (data not shown). IKK-ε is an important mediator of the IFN type I response as it phosphorylates and activates IRF3 and IRF7 [[17, 18]] via phosphorylation of an extended sequence motif–SxSxxxS–common to IRF3 and IRF7 [[35]]. The C-terminus of FOXO3 contains three putative IKK-ε-phosphorylation sites (Ser349, Ser476, Ser584) in addition to the close-related phosphorylation site Ser644, previously shown to be important for IKK-β regulation [[16]]. Mutation

of this site was not sufficient to block IKK-ε-induced phosphorylation of FOXO3 (Supporting Information Fig. 2B), suggesting that FOXO3 contains a specific IKK-ε-targeted site. The presence of multiple serine and threonine phosphorylations also suggests that IKK-ε may target more than one of the phosphorylation sites and help to fine-tune the Volasertib ic50 Rutecarpine FOXO3 regulation during the immune response, by acting on different aspects of the protein activity and stability, but more work is needed to dissect their role in FOXO3 transactivation activity, protein localization, or protein–protein interaction. FOXO3 is a well-described tumor suppressor involved in triggering cell-cycle arrest and apoptosis and is inhibited in many cancers including prostate, ovarian, and breast cancer. IKK-ε was recently mapped

as a new oncogene and was found to be overexpressed in prostate, ovarian, and breast cancer [20, 21, 36]. Interestingly, IKK-ε can replace a PI3K activity to inhibit cell-cycle arrest and apoptosis [[20]] processes associated with FOXO3 activity [[16, 37]]. Thus, it is possible that IKK-ε-mediated inhibition of FOXO3 thwarts cell-cycle arrest and apoptosis in cancer cells. In addition, it would favor the production of normally FOXO3 negatively controlled proinflammatory cytokines IL-6 and IL-8 [10, 21, 29], facilitating tumorigenesis. In summary, we identify FOXO3 as a new IKK-ε-controlled check-point of IRF activation and regulation of IFN-β expression. FOXO3, which antagonizes NF-κB and IRF activities and hampers IFN-β and IFN-λ1 expression, is regulated by IKK-ε. Once the activating signal has been received, IKK-ε provides a positive regulatory signal to IRF3 and at the same time phosphorylates FOXO3, contributing to its inactivation.

Tissues were stained with choline acetyl transferase immunohistochemistry

Y-27632 mouse to label neurones of PPN/LDT and tyrosine hydroxylase for the LC. The burden of tau and α-synuclein pathology was measured in the same regions with immunohistochemistry. Results: Both the LC and PPN/LDT were vulnerable to α-synuclein pathology in LBD and tau pathology in AD, but significant neuronal loss was only detected in these nuclei in LBD. Greater cholinergic depletion was found in both LBD groups, regardless of RBD status, when compared with normals and AD. There were no differences in either degree of neuronal loss or burden of α-synuclein pathology in LBD with and without RBD. Conclusions: Whether decreases in brainstem cholinergic neurones Crizotinib concentration in LBD contribute to RBD is uncertain, but our findings indicate these neurones are highly vulnerable to α-synuclein

pathology in LBD and tau pathology in AD. The mechanism of selective α-synuclein-mediated neuronal loss in these nuclei remains to be determined. “
“Synovial sarcoma is a rare aggressive neoplasm occurring at any site of the body, mainly in young adults. It may also arise in the CNS but has seldom been reported. We report a case of unusual intracranial synovial sarcoma in a young male patient. Neuroimaging revealed a large gadolinium-enhancing mass was located at the right anterior cranial fossa and was associated with multiple cyst formation. The mass was dural-based and was observed to invade the right orbital apex and ethmoidal bulla. Histologically, the tumor was composed of uniform oval and round cells with scant cytoplasm and indistinct borders. The tumor cells were observed to form densely cellular sheets, but in some areas, the tumor showed hemangiopericytomatous vascular pattern consisting of tumor cells arranged around dilated, thin-walled blood vessels. By immunohistochemistry, vimentin, CD99 and Bcl-2

were diffusely positive in most cells, and a focally weak reactivity for S-100 protein was also observed. However, Amino acid the tumor cells were negative for cytokeratin (AE1/AE3), CK7, CK8/18, CK19, epithelial membrane antigen, CD34, synaptophysin, GFAP, desmin, myogenin, and smooth muscle actin. Cytogenetic analysis using fluorescence in situ hybridization (FISH) demonstrated a translocation t(X;18)(p11;q11), an aberration specific for synovial sarcoma. A diagnosis of primary dural-based poorly differentiated synovial sarcoma was made. To our knowledge, this is the first report of a poorly differentiated variant of synovial sarcoma occurring in dura mater and confirmed by cytogenetic analysis. The present case indicates that appropriate immunohistochemical analysis, and in particular molecular analysis, are essential for accurately diagnosing small, round-cell neoplasms in unusual locations. “
“J. C. Palmer, P. G. Kehoe and S.