“
“Recently, mutations in IDH1 and IDH2 have been reported as an early and common genetic alteration in diffuse gliomas, being possibly followed by 1p/19q loss in oligodendrogliomas and TP53 mutations in astrocytomas. Lately, IDH1 mutations have also been identified in adult gliomatosis cerebri (GC). The aim of our study was to test the status of IDH1/2, p53 and of chromosomes 1 and 19 in a series of 12 adult and three

pediatric GC. For all tumors, clinico-radiologic characteristics, histopathologic features, status of IDH1/2, p53 and of chromosomes 1 and 19 were evaluated. IDH1 mutations were detected only in GC of adult patients (5/12). They all corresponded to R132H. Additional 1p/19q losses were observed in two of them with histological features of oligodendroglial lineage. Proteasome inhibitor Other copy number alterations of chromosomes 1 and 19 GSK458 supplier were also noticed. The median overall survival in adults was 10.5 months in non-mutated GC and 43.5 months in mutated GC. IDH1 mutations were present in GC of adult patients, but not in those of children. There was a trend toward longer

overall survival in mutated GC when compared to non-mutated ones. Concomitant 1p/19q loss was observed in IDH1-mutated GC with oligodendroglial phenotype. These observations contribute toward establishing a stronger link between GC and diffuse glioma. In addition, these results also emphasize the importance of testing for IDH1/2 mutations and 1p/19q deletions in GC to classify them better and to allow the development of targeted therapy. “
“We report autopsy cases of two siblings who developed muscular atrophy and dementia, clinically considered to be familial motor neuron disease (MND). They presented with motor neuron signs predominantly in the distal limbs without sensory impairment. At autopsy, Astemizole severe neuronal

loss in the anterior horn consistent with MND was found, but histopathological hallmarks like Bunina bodies and skein-like inclusions were absent. Surprisingly, numerous huge axonal swellings (about 30 µm in diameter) and onion-bulb-like structures were found in the spinal ventral roots. These changes were not observed in spinal dorsal roots or peripheral nerves. However, obvious segmental demyelination of the ventral root was not found. In addition, neurofibrillary tangles (NFTs) and neuritic plaques were present in the frontal cortex, temporal cortex and hippocampus, and to a lesser degree, in the amygdala, substantia nigra and thalamus. Our two cases are a hitherto unreported type of MND, which shows focal giant axonopathy and prominent formation of onion-bulb-like structures due to Schwann cell proliferation restricted to the spinal ventral roots. “
“O. Cataltepe, M. C. Arikan, E. Ghelfi, C. Karaaslan, Y. Ozsurekci, K. Dresser, Y. Li, T. W. Smith and S.

Conclusion: 3D CTA with stereotactic fiducials allows surgeons to adequately estimate abdominal flap volume before surgery, potentially giving guidance in the amount of tissue that can be harvested from a patient’s lower abdomen. © 2011 Wiley-Liss, Inc. Microsurgery, 2011 “
“The present study investigates the vascular anatomy of the vastus lateralis motor nerve (VLMN) to be used as a vascularized nerve graft in facial nerve reconstruction. We evaluated the maximum length of the nerve that can be included in the flap and its vascular pedicle. In addition, we discuss its adequacy for use in early reconstruction of the facial GW-572016 order nerve both as ipsilateral facial nerve reconstruction and

as cross-facial nerve graft. Five fresh cadavers were used in this study. In all specimens, the VLMN and its vascular pedicle were dissected, photodocumented and measured using calipers. In addition, two vascularized

VLMN were injected with a radiopaque Selleck Everolimus contrast and underwent CT angiography and three dimensional reconstructions were scanned to illustrate the vascular supply of the nerve using OsiriX Software. The VLMN was divided into two divisions, an oblique proximal and a descending distal, in 70% of the dissections with a mean maximal length of 8.4 ± 4.5 cm for the oblique division and 15.03 ± 3.87 cm for the descending division. The length of the oblique division, when present, was shorter than the length of the descending branch in all specimens. The mean length of the pedicle was 2.93 ± 1.69 cm, and 3.27 ± 1.49 cm until crossing the oblique and the descending division of the nerve respectively.

The mean caliber of the nerve was 2.4 ± 0.62 mm. Three-dimensional computed tomography angiography demonstrated perfusion throughout the entire VLMN by branches from the descending branch of the lateral femoral circumflex artery which ran parallel to the descending division of the VLMN. Additionally, we observed that technically it was possible to preserve the Megestrol Acetate oblique branch of the VLMN. This study confirms that VLMN presents adequate anatomic features to be used as a vascularized nerve graft for facial nerve reconstruction in terms of length, pedicle, and caliber. © 2014 Wiley Periodicals, Inc. Microsurgery, 2014. “
“Introduction: Although, the success of free flaps has increased in the last years, more details about its characteristics might improve the clinical outcome of the flaps. This study examined the thermoregulatory ability as a sign of neural re-innervation of two different types of microsurgical free flaps in the postoperative course. Methods: A total of 22 patients were examined after grafting two different flap types: The latissimus dorsi myocutaneous (LDM) flap (n = 11) and the anterolateral thigh (ALT) flap (n = 11).

This is evident in all vowels; our example compares the first formant (F1) location at .75 of the duration of the vowel/ae/ in hamlet and candle. Although there is no effect of word (hamlet,

candle) on F1 for the native speakers (both p > .19), the Spanish-accented speaker produces different F1s depending on the word, F(1, 38) = 8.9, p < .005, either because these sounds are coarticulated more in Spanish or because the slower RG7204 cell line movements involved in the production of nonnative sounds affects coarticulation. In addition, findings from a listening experiment provided perceptual evidence that stimuli produced by Can and MidW are more similar as compared with MidW-Span.3 A repeated-measures ANOVA with average looking time as dependent measure, age group (younger, older), condition (kingdom/hamlet, candle/raptor), and order (American test, Canadian test) as factors, and familiarity (familiar,

unfamiliar) as repeated measures revealed a main effect of familiarity, F(1, 44) = 10.88, p = .002, main effect of order, F(1, 44) = 8.41, p = .005, significant interaction between age group and familiarity, F(1, 44) = 4.55, p = .04, and no other significant interactions, F(1, 44) < .18. Follow-up paired, ABT-263 mouse two-tailed comparisons of looking time averaged across blocks revealed that familiar and unfamiliar trials differed significantly in the older age group, t(1, 23) = 3.77,

p = .001, but not in the younger group, t(1, 23) = 0.88, p = .39, as shown in Figure 3. The main effect of order emerges because both groups showed higher looking times when tested with the American speaker. As evidenced by the lack of interaction with order and familiarity, the pattern of looking remained the same in both the novel and familiar test trials, and only 12-month-olds showed a significant difference in looking time between passages containing familiar and novel Molecular motor words. These findings suggest that 12-month-olds successfully recognized words in the face of variation in dialectal accent, as evidenced by the significant preference for test passages containing familiar words. In contrast, 9-month-olds showed no preference, suggesting that dialectal differences were large enough to impede word recognition. This work extends the finding that infants are sensitive to dialect differences by showing the functional relevance of this sensitivity for word recognition in 9-month-olds. The 9-month-olds’ poor performance could be attributed to their lack of familiarity with dialectal accents, perhaps complicating the representation of words in unfamiliar speech streams.

E5K020. Study subjects (n=999) were evaluated by ultrasound (SSD 500 echo camera and 3.5-MHz convex probe; Aloka, Amsterdam, the Netherlands) before treatment in May 1999. Three hundred and seventy-seven subjects were evaluated again in August 2002 by the same ultrasonographer (Q.M.-A.). Only 177 subjects were included in the study because they had completed the planned ultrasound investigations. The degree Selleck Fulvestrant of PPF was graded as F0, FI, FII

and FIII according to the standardized Cairo classification (Cairo Working Group, 1992) and as reported by many authors (Dittrich et al., 1983; Homeida et al., 1991; Mohamed-Ali et al., 1999). In brief, liver size, peripheral portal branches (PPBs), the degree of PPF, the thickness of the PPB wall, spleen size and splenic vein diameter (SVD) were assessed. Livers and spleens were measured as described previously

this website (Abdel-Wahab et al., 1989; Homeida et al., 1996). The portal vein diameter (PVD) was measured at its entrance to the porta hepatis at the lower end of the caudate lobe in subjects who had fasted ∼8–10 h. The thickness of secondary PPB was observed for all subjects with FI–FIII grade of fibrosis. PPF was graded as 0–III. Grade 0 (F0) corresponds to a normal liver, with no thickening of the PPB wall and PPB diameters (outer to outer) ∼2–3 mm. Grade I (FI) corresponds to a pattern of small stretches of fibrosis around secondary portal branches and PPB diameters ∼4 mm. Grade II (FII) still shows the patchy fibrosis observed in FI, but a continuous fibrosis affects most second-order branches, and PPBs appear as long segments of fibrosis. Grade III (FIII) shows a thickening of the walls of most PPBs. A medical history, personal data (name, sex, age and number of pregnancies for married women), current symptoms, number of malaria attacks per year and physical Resminostat examination for each subject were performed. Informed consent was obtained from each patient or parents in the case of children. spss software was used for statistical analysis. The χ2-test was used to compare the two phenotypes

(regression and progression) in the study subjects. Ethical approval for the study was obtained from the ethical committee of the University of Gezira, and from the State Ministry of Health, Wad Medani. The study was conducted in Um-Zukra, a Sudanese village highly endemic for S. mansoni. Fibrosis grades in 177 study subjects [82 (46%) males and 95 (54%) females] were reported before and 39 months after treatment (Table 1). The proportions of patients with FI and F0 before therapy were 128 (72.3%) and 0 (0%), respectively, and 74 (41.8%) and 49 (27.7%), respectively, 39 months after treatment. The difference was statistically significant (P=0.0001, P=0.000) for FI and F0 before and after treatment. As shown in Table 2 (49, 27.7%), PPF in patients with FI and FII was regressed to F0 39 months after treatment, while in the other patients (14, 7.9%), PPF regressed either from FII to FI (8, 4.5%) or from FIII to FII (6, 3.

In the in vivo model too, AQP4 expression was markedly increased

in the microvessels of the cerebral cortex and hippocampus after water intoxication but was reduced in the LIUS-stimulated rats. These data show that LIUS has an inhibitory effect on cytotoxic brain edema and suggest its therapeutic potential to treat brain edema. We propose that LIUS reduces the AQP4 localization around the astrocytic foot processes thereby decreasing water permeability into the brain tissue. “
“Craniopharyngiomas are histopathologically classified as adamantinomatous type (AD) and squamous-papillary type (SP). However coexistence of a mixed type seen on histopathologic specimens has not been reported. In this report, GDC-0449 supplier a patient diagnosed with mixed type craniopharyngioma is presented and the etiology and pathologic features are discussed. “
“Recently, Nishihira et al. demonstrated the presence

of two types of TDP-43 pathology in sporadic amyotrophic lateral sclerosis (ALS) (Acta Neuropathol 2008; 116: 169–182). Type 1 represents INK 128 research buy the TDP-43 distribution pattern observed in classic ALS, whereas type 2 shows the presence of TDP-43 inclusions in the frontotemporal cortex, hippocampal formation, neostriatum and substantia nigra and is significantly associated with dementia. However, ALS with however pallido-nigro-luysian degeneration (PNLD) is very rare. We recently encountered a case of ALS with PNLD of 9 years duration, in which the patient received artificial respiratory support for 6 years. In our case, neuronal loss and TDP-43-positive neuronal cytoplasmic inclusions were found in the globus pallidus, substantia nigra and subthalamic nucleus. Neither neuronal loss nor TDP-43-immunoreactive inclusions were found in the frontotemporal cortex and hippocampus. These findings suggest that the pallido-nigro-luysian system is also involved in the disease process of ALS and that ALS with PNLD is different from ALS with dementia based on the distribution pattern of neuronal loss

and TDP-43 accumulation. “
“Frontotemporal lobar degeneration (FTLD) is clinically and pathologically heterogeneous. Although associated with variations in MAPT, GRN and C9ORF72, the pathogenesis of these, and of other non-genetic, forms of FTLD, remains unknown. Epigenetic factors such as histone regulation by histone deacetylases (HDAC) may play a role in the dysregulation of transcriptional activity, thought to underpin the neurodegenerative process. The distribution and intensity of HDACs 4, 5 and 6 was assessed semi-quantitatively in immunostained sections of temporal cortex with hippocampus, and cerebellum, from 33 pathologically confirmed cases of FTLD and 27 controls.

Hypertension; lumbar radiculopathy; headaches. CRPS04 F/50 Fall; BPTI; cervical plexus traction injury/4 years Positive Tinel sign bilaterally in her brachial plexus; mechano and thermal allodynia; hyperalgesia; weakness; poor initiation of movement; generalized muscle tremor. Pain (NRS) 5 NSAIDs; AED; antidepressants; narcotics. Depression; headaches;

TMJ CRPS05 F/24 Fall; Repetitive strain injury of brachial plexus/7 years Generalized mechano and thermal allodynia; hyperalgesia; poor initiation of movement; weakness; positive Tinel signs. Pain (NRS) 6·5 NSAIDs, AED, antidepressants; spasmolytics; antihistamine; narcotics; intravenous lidocaine; intravenous ketamine. GERD; chronic fatigue; seizure disorder; headaches. CRPS06 F/39 NVP-BEZ235 price BPTI right arm/4 years Mechano and thermal allodynia; hyperalgesia; severe autonomic dysregulation; oedema. Pain (NRS) 8 NSAIDs; AED; narcotics; intravenous ketamine.   CRPS07 F/64 L5-S1 radiculopathy/36 years Dynamic, static and thermal allodynia; deep muscle sensitization; neurogenic oedema; weakness; autonomic dysregulation. Pain (NRS) 7 AED; baclofen; antianxiolytics; intermittent narcotics; NSAIDs; antidepressants Hypertension; hyperlipidaemia;

heart disease; asthma. CRPS08 F/48 Ligament injury of left foot/3·5 years Generalized spread; severe mechano and thermal allodynia; autonomic dysregulation; dystrophy; weakness; spasms, myoclonus. Pain (NRS) 10 selleckchem AED; NSAIDs, antidepressants, narcotics; failed ketamine coma; antianxiolytics; failed intravenous lidocaine. GERD; depression;

Panic attacks/anxiety; headaches. CRPS09 F/55 Left knee injury; surgery/2·5 years Symptoms spread to right leg; generalized; primarily pain; autonomic dysregulation; dystrophy; weakness and decreased initiation of movement. Pain (NRS) 8 AED; antidepressants, NSAIDS; propoxyphene; stellate ganglion blocks. Migraines CRPS10 M/29 Fractured left fibula/3 years Pin prick hyperalgesia; mechano allodynia; swelling; sweating; erythema; difficulty initiating movement; nail atrophy; cold allodynia. Pain (NRS) 10 NSAIDs; spasmolytics; antidepressants; antianxiolytics; intravenous ketamine. GERD; headaches Prostatic acid phosphatase CRPS11 F/30 Motor vehicle accident; Fall BPTI/6 years Autonomic dysregulation; neurogenic oedema; positive Tinel signs; thermal allodynia; weakness; poor initiation of movement; deep muscle pain, joint pain. Pain (NRS) 7 Antidepressants; NSAIDs; narcotics; spasmolytics. Chronic Fatigue; seizure disorder; headaches. CRPS12 F/26 Broke right ankle/8 years Spontaneous burning pain; dynamic and static mechano and thermal allodynia; decreased initiation of movement. Pain (NRS) 6·5 AED; NSAIDs, narcotics; antidepressants; spasmolytics. GERD; Seasonal Allergies; eating disorders CRPS13 F/60 Fell and fractured left wrist 5 years Cold allodynia; pin prick hypoesthesia; weak; difficulty initiating movement; hyperhidrosis. Pain (NRS) 2 AED; NSAIDs; antidepressants. Osteoarthritis; depression.

0 GeneChip (Affymetrix) as described by the manufacturer. Washing and staining steps were performed in a Fluidics Station 400 (Affymetrix) according to the technical manual. Microarrays were scanned with the Affymetrix GeneChip Scanner 3000. Signals, detection calls and corresponding p-values of microarrays were calculated with MAS5.0/GCOS algorithms (default mode). Global normalization was used by scaling

the microarrays to a target intensity value of 100. Signal detection of probe sets and scaling factor for the individual microarrays, also correlation coefficients of signal intensities between duplicate microarrays permitted a comparison of the different data sets obtained for FDC networks (primary, early and late secondary FDC n=6), B cells (naïve, early and late GC B cells n=6) and BP3hi reticular cells (n=2) (Supporting Information Table 1) 44. To determine those genes which are specifically expressed in FDC PD 332991 an in silico subtraction approach was used. Recently, a similar approach was used to analyze the gene expression of the thymic stromal microenvironments https://www.selleckchem.com/products/LBH-589.html 45. Data sets obtained from dissected FDC networks were compared with those of sorted B cells. Parameters (signal log ratios, change calls and change p-values) provided by the algorithm for pair wise array comparison in the GCOS software

were obtained and group comparisons performed between the two groups of arrays using the High Performance Chip Data Analysis 24. In brief, the different parameters derived from signal calculation by the GCOS software were used to calculate mean, median and standard deviation of signal values and the percentage of “present” calls for each group. The mean of the Signal Log Ratio values and the percentage of change calls were used for pair wise comparison information of all possible comparisons. Finally, different Welch t-tests were performed and only p-values<0.05 were considered to be significant. Microarrays of BP3hi Interleukin-2 receptor reticular cells were analyzed as described above for FDC-specific genes (Fig. 1A, subtraction of B-cell transcriptome) and gene expression

compared with that of primary FDC using a modification of the High-Performance Chip Data Analysis. Hereby, duplicate microarrays of primary FDC and BP3hi reticular cells were compared (altogether four comparisons). On average, the signal intensities on FDC microarrays were 2.6-fold lower than on BP3hi microarrays. Only for those genes with >1.5- or<-1.5-fold differences from the mean value of 2.6 (Fig. 3) in at least three of the four comparisons were considered as significantly different. Gene expression profiles of macrophages (GSM106426, GSM106427, GSM106428, GSM117560, GSM117561), T cells (GSM44979, GSM44980, GSM44981, GSM44982), fibroblasts (GSM106139, GSM106141) and myoblasts (GSM126586, GSM126587) were obtained from the NCBI GEO data base.

Data were imported in stata 12.0 (Stata Statistical Software; StataCorp, College Station, TX, USA) and the r statistical software (R Foundation for Statistical Computing, Vienna, Austria) for statistical analysis. Fever

was defined as an observed axillary temperature ≥37·5°C and/or individual-reported fever within the previous 24 h. Patent parasite carriage as any parasite density detected by microscopy; submicroscopic parasitaemia as parasitaemia detected by PCR in the absence of microscopically confirmed parasite carriage. Parasite density was presented as geometric mean Dasatinib molecular weight in patent parasite carriers only, together with the 25th and 75th percentiles (interquartile range, IQR). Duplicate ELISA OD results were averaged and normalized against the positive control sample on each plate. To do this, a titration curve was fitted to the ODs obtained for the standard plasma dilutions by least squares minimisation using a three variable sigmoid model and the solver add-in

in Excel 2007 (Microsoft Corp., Redmond, WA, USA), assuming an arbitrary value of 1000 U/mL of antibody against each antigen in the standard pool [5]. Mean OD values for the spot extracts were converted to units/mL using this fitted curve. Sample, where duplicate optical densities (ODs) differed by more than 50%, results were excluded from the analysis. The binding of antibodies in serum from 44 Europeans never exposed to malaria was used to define a cut-off (mean OD + 3 SD) for positive and negative responses to each antigen. Antibody

titre https://www.selleckchem.com/products/3-deazaneplanocin-a-dznep.html was estimated using the formula dilution/[maximum OD/(OD test serum minimum OD) − 1] where the maximum OD was the maximum value of the standard curve and the minimum OD the lowest value of the negative control. The titre expressed in Arbitrary Units (AU/mL) was used as an indicator of antibody density in the analyses. Only individuals ≥1 year were included in the serological analysis to minimize the effect of maternally derived antibodies in infants. Categorical variables were analysed using chi-square test or chi-square test for trend. Student’s t-test, analysis of variance or nonparametric equivalents were used when comparing continuous variables. Logistic and linear regression models were used to adjust binary and Pyruvate dehydrogenase continuous variables for potential confounding. Titre values were log10 transformed for analyses. To assess the effect of parasite exposure on antibody titres individuals were categorized into one of the following four exposure groups: (i) ‘parasite-free’ (microscopy and PCR-negative at all surveys, no clinical malaria recorded); (ii) ‘always parasitaemic’ (positive at all surveys by either microscopy or PCR); (iii) ‘lost infection’ (initially PCR or microscopy positive, negative at later surveys); and (iv) ‘acquired infection’ (initially PCR and microscopy negative, positive at later surveys).

, 2004a). Recently, Vermoote et al. (2011) reported significant buy Quizartinib differences between H. suis and H. pylori genomes. These studies comparing H. pylori and several H. suis strains can help to elucidate the pathogenesis of gastric disorders induced by H. suis. It was revealed that IL-4 is not essential for the induction of lymphoid follicle formation caused by H. suis infection (Fig. 7), although the mRNA levels of Th2 cytokines were slightly enhanced in the stomachs of the infected C57BL/6J WT mice (Fig. 5). In another study, gastric lymphoid follicles progressed toward a severe MALT lymphoma-like appearance, including

the presence of lymphoepithelial lesions (Nakamura et al., 2007). Regarding animal models of the pathogenesis of MALT lymphoma induced by bacterial infection, Fukui et al. (2004) reported that MALT lymphoma like-lesions develop after H. pylori infection in neonatally thymectomized BALB/c mice, which are a Th2-dominant strain, but not in C57BL/6J mice. In patients with gastric see more MALT lymphoma, it is disputed whether the Th1 or the Th2 response is predominant. Notably high levels of Th1 cytokines and relatively low levels of Th2 cytokines were seen in tumor-infiltrating T cells from two patients with MALT lymphoma in vitro (Hauer et al., 1997). On the contrary, Th2 cytokines in combination with costimulatory

molecules are essential for the progression of MALT lymphoma cells (Greiner et al., 1997; Knorr et al., 1999). Therefore, the Th1/2 paradigm alone is supposed to be insufficient to account for the immune response during the development of gastric MALT lymphoma. Further investigation, for example, of Th17 and Treg responses, is required to elucidate the immune response behind the progression of gastric lymphoma. In conclusion, IFN-γ, a Th1 cytokine, is deeply involved in the pathogenesis

of gastric lymphoid follicle formation induced by H. suis infection. The aggregation of B cells was aided 4��8C by CD4-positive T cells and DC. This work was supported, in part, by grants for the Global COE Program, Global Center of Excellence for Education and Research on Signal Transduction Medicine in the Coming Generation (T.A. and M.Y.), Scientific Research in Priority Areas ‘Genome’ (T.A. and M.Y.), and Grant-in-Aid for Scientific Research on Innovative Areas (T.A.) from the Ministry of Education, Culture, Sports, Science, and Technology of Japan, and for the COE research support program from Hyogo prefecture (T.A.). This work was also supported by Grant-in-Aid for Young Scientists (I.M.), Mitsubishi Pharma Research Foundation (M.Y.), and a grant for the Education Program for Specialized Clinicians of the Support Program for Improving Graduate School Education from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (T.M.).

S3). This suggests that modulation of DCs by B10 cells observed in other tissue compartments [17] does not occur in the liver. Having demonstrated that hepatic B cells comprise fewer regulatory subsets than splenic B cells, a question not addressed in this study is why Bregs appear not to contribute to the overall tolerogenic liver environment. One possibility may be to prevent overinhibition of immune responses in the liver. As shown in this report and by others [15-17], the TLR-4 ligand LPS, a normal constituent of portal venous blood, is a potent stimulator of B10 cells. The absence of B10 cells and the presence of B cells with proinflammatory potential in an overall tolerogenic liver environment

could help to balance the hepatic capacities of immune tolerance and immune stimulation. Our data presented here show that the absence of hepatic B cells compromises further the capacity of mDCs to respond to LPS (Fig. 3). To obtain sufficient numbers of liver learn more mDCs for

analysis, Flt3L-treated mice were used in Fig. 3 and Supplementary Figs S2 and S3. We are aware of the caveat that Flt3L might modify the composition of mDC subsets as well as other cells. Extended experiments using animal models are https://www.selleckchem.com/products/apo866-fk866.html needed to confirm the positive regulation of liver mDCs and liver immune responses by hepatic B cells. Future research to understand more clearly the mechanisms underlying hepatic B cell activation and function is merited, and may lead to improved understanding and therapy of different liver-related pathological conditions. The authors thank Dr David Rothstein for the gift of IL-10 reporter mice and Thomson laboratory members for helpful discussion. The work was supported by NIH grant P01AI81678 (A.W.T.), Ketotifen grant (874279717) from the Roche Organ Transplantation Research Foundation (A.W.T.) and by an American Society of Transplantation Basic Science Fellowship awarded to Hong Zhang. Hong Zhang did most of the experiments and wrote the manuscript, Donna

Beer Stoltz performed immunofluorescence, Geetha Chalasani provided direction for B cell subset analysis and Angus W. Thomson provided intellectual input and guided the preparation of the manuscript. The authors declare no financial or commercial conflicts of interest. Fig. S1. Expression of cell surface activation markers on murine B cells following in-vivo poly I:C administration. C57BL/6 (B6) mice were injected intraperitoneally (i.p.) with lipopolysaccharide (LPS). On days 0 and 1 post-injection, the mice were examined for the expression of the indicated surface molecules on spleen versus hepatic B cells; n = 4 mice per group. On day 1, both liver and splenic B cells up-regulated expression of CD39, CD40, CD80 and CD86; *P < 0·05. No significant difference was observed between the liver and spleen. Data are representative of two independent experiments. Fig. S2. Close proximity of B cells (CD19+) and dendritic cells (DCs) (CD11c+) in liver parenchyma.