Seeking the cellular and

molecular targets for Tregs in control of T-lymphocyte activation in the neonatal liver, we identified CD11b+ mDCs expressing the costimulatory molecule CD86 as mediators of intrahepatic CD8 lymphocyte activation. Although hepatic DCs are often tolerogenic and inhibit T-cell responses under physiologic conditions, DCs are critical for effector cell activation during hepatobiliary inflammation. Here we show that during peak inflammatory ductal obstruction at 7 dpi, mDCs constitute the predominant DC subset in regulation of T-lymphocyte activation, which is in keeping with reports by other investigators showing cholestasis induced expansion of hepatic mDCs STA-9090 datasheet in a bile duct ligation model.27 Further, we found that antibody mediated blockade of CD86, more

than Galunisertib ic50 of CD80, decreased DC-mediated proliferation of naïve, neonatal CD8 cells and diminished their production of IFN-γ in an in vitro coculture assay, recapitulating the cellular network in the neonatal liver. We propose that in experimental BA hepatic mDCs are critical for intrahepatic T-lymphocyte activation by way of the B7/CD28 pathway. Importantly, in infants with BA, increased B7 expression in the liver is correlated with poor prognosis.28 Our data in an experimental model suggest that this increase is directly involved in pathogenesis and not just a reflection of immune activation. Finally, we examined how Tregs control this pathogenic DC/T-lymphocyte crosstalk in the neonatal liver. Important findings include: (1) Tregs down-regulated expression of CD86 on neonatal hepatic mDCs in vitro; (2) AT of Treg-containing CD4 cells reduced expression of CD86 on mDCs in vivo; and (3) on the contrary, Treg-depletion in older mice enhanced the stimulatory capacity of hepatic DCs. Based on the association between decreased

CD8 responses RNA Synthesis inhibitor and down-regulated CD86 on mDCs in livers of mice subjected to AT of Treg-containing CD4 cells compared with infected controls without AT, we conclude that modulation of maturation of hepatic DCs is critical for Treg-inhibition of T cell activation in BA. Similar crosstalks between Tregs and tissue specific DC populations have been described in other experimental systems.12, 18 An increased number of hepatic mDCs following AT of CD25−CD4 likely drives aberrant CD8 expansion in these mice, although the mechanisms for this interaction and its effects on bile duct injury require further investigations. Importantly, this study focuses on immune regulation during ductal obstruction at 7 dpi. The cellular targets for Tregs during other stages of bile duct injury and timepoints may be different.

There was no difference in the genotypic resistance rate (complete or partial) in both groups (14.5% vs. 13.6%, P=0.886). 3 patients in the ETV group and 1 in the LAM-ADV group required tenofovir rescue (P=0.332). The HBeAg seroconversion rate was higher in the ETV group (20.3% vs 6.1%, P=0.015). The LAM-ADV group had higher incidence of renal impairment (10.6% vs 0%, P=0.005), which generally resolved with ADV dose reduction. There was no significant difference in the incidence of malignancy (7.2% vs 6.1%, P=0.782)

and the overall mortality (5.8% vs 4.5%, P=0.728) between the 2 groups. CONCLUSION: This study showed that long-term entecavir therapy provided significantly higher virological response rate, higher HBeAg seroconversion rate and lower risk of renal impairment than the adefovir-lamivudine Luminespib mouse combination. However, there was no difference in drug resistance, malignancy or mortality in the 5-year study period. Disclosures: Yock Young Dan – Advisory selleck screening library Committees or Review Panels: Merck Sharp Dome, Gilead, Novartis; Speaking and Teaching: Furui Kieron B. Lim – Advisory Committees or Review Panels: Gilead, Sirtex; Consulting: AstraZeneca, Novartis;

Grant/Research Support: Astellas, Bayer Seng Gee Lim – Advisory Committees or Review Panels: Bristol-Myers Squibb, Achillon Pharmaceuticals, Pfizer Pharmaceuticals, Janssen Pharmaceuticals, Novartis Pharmaceuticals, Merck Sharp and Dohme Pharmaceuticals, Vertex Pharmaceuticals, Boehringer-Ingelheim, Gilead Pharmaceuticals, Roche Pharmaceuticals, Tobira Pharmaceuticals; Speaking and Teaching: GlaxoSmithKline, Bristol-Myers

Squibb, Merck Sharp and Dohme Pharmaceuticals, Boehring-er-Ingelheim, Gilead Pharmaceuticals, Novartis Pharmaceuticals The following people have nothing to disclose: Guan Huei Lee, Wah Wah Phyo, Yin-Mei Lee, How Cheng Low, Maung Aye Thwin, Poh Seng Tan Background: Patients with CHB are at risk for development of cirrhosis and liver cancer, especially if left untreated, and it is important for these patients to start treatment soon after they meet treatment criteria. Our goal is to study treatment rates and time to treatment initiation on long-term follow-up in a cohort of treatment-eligible patients. Methods: We performed a retrospective cohort study of consecutive treatment-eligible CHB patients (by US Panel 2008 and AASLD criteria MycoClean Mycoplasma Removal Kit 2009) at 2 U.S. centers between 2007 and 2011. Patients were observed until they started treatment or until their last follow-up if untreated. Results: Median age was 42 years and almost all were Asian (96%). A total of 62% started treatment after median follow-up of 2 months (range = 1-77 months), and 38% remained untreated after median follow-up of 17 months (range = 1-81 months). Most treated patients started therapy within the first year. Treatment rate within the first year was significantly higher at the university clinic (Figure 1), but community patients were younger. In multivariate analysis, older age (HR 1.02, p < 0.

Results:  The mean diameter of type 2a nodules was significantly smaller than that of other Ku0059436 HCC types (P < 0.05). Overall, moderately differentiated HCC was the predominant histological type, except for type 2a, all of which were well-differentiated HCC. The percentage of poorly differentiated HCC was significantly higher

in type 2c nodules (19%) than in other HCC types (P < 0.01). The percentage of Lens culinaris agglutinin-reactive α-fetoprotein (AFP-L3) positivity was significantly higher in type 2c nodules (55%) than in other HCC types (P < 0.01). Classification on B-mode ultrasonography was correlated with the histological differentiation and serum level, an indicator of a poor prognosis. Conclusion:  The malignant potential of type 2a is the lowest and that of type 2c is the highest, both histologically and serologically. Assessment of buy ABT-263 the malignant potential of small, hypervascular HCC is possible by B-mode ultrasonography. “
“Divalent metal-ion transporter-1 (DMT1)

is required for iron uptake by the intestine and developing erythroid cells. DMT1 is also present in the liver, where it has been implicated in the uptake of transferrin-bound iron (TBI) and non-transferrin-bound iron (NTBI), which appears in the plasma during iron overload. To test the hypothesis that DMT1 is required for hepatic iron uptake, we examined mice with the Dmt1 gene selectively inactivated in hepatocytes (Dmt1liv/liv). We found that Dmt1liv/liv mice and controls (Dmt1flox/flox) did not differ in terms of hepatic iron concentrations or other parameters of iron status. To determine whether hepatocyte DMT1 is required for hepatic iron accumulation,

we crossed Dmt1liv/liv mice with Hfe−/− and hypotransferrinemic (Trfhpx/hpx) mice that develop hepatic iron overload. Double-mutant Hfe−/−Dmt1liv/liv and Trfhpx/hpx;Dmt1liv/liv mice were found to accumulate similar amounts of hepatic iron as did their respective controls. To directly assess the role of DMT1 in NTBI and TBI uptake, we injected 59Fe-labeled ferric citrate (for NTBI) or 59Fe-transferrin into plasma of Dmt1liv/liv and Dmt1flox/flox mice and measured uptake of 59Fe by the liver. Dmt1liv/liv mice displayed no impairment of hepatic NTBI uptake, but TBI uptake was 40% lower. Hepatic levels of transferrin receptors 1 and 2 and ZRT/IRT-like protein 14, which may Ponatinib concentration also participate in iron uptake, were unaffected in Dmt1liv/liv mice. Additionally, liver iron levels were unaffected in Dmt1liv/liv mice fed an iron-deficient diet. Conclusion: Hepatocyte DMT1 is dispensable for hepatic iron accumulation and NTBI uptake. Although hepatocyte DMT1 is partially required for hepatic TBI uptake, hepatic iron levels were unaffected in Dmt1liv/liv mice, suggesting that this pathway is a minor contributor to the iron economy of the liver. (Hepatology 2013;58:788–798) A typical adult male has roughly 4 g of total body iron, including approximately 1 g of iron stores.

Aim: In this multicenter study, we aimed to compare hepatic and tumor related outcomes of local regional therapy for HCC in patients with chronic HBV or HCV with and without the MetS. Method: Patients with viral hepatitis treated with local regional therapy (transarterial chemoembolization +/− radiofrequency ablation) for HCC between 2007–2013 in two large Sydney hospitals were included in this retrospective study. Medical records for these patients were audited for patient demographics, hepatic and tumor characteristics at diagnosis, number and intervals of local regional therapy as well as episodes of hepatic decompensation (jaundice, ascites, varices, encephalopathy, infections). Patients with viral hepatitis were classified

into 2 groups according to the presence of absence of the MetS, as defined by the Adult Treatment Panel III. Results: A total of 69 patients were included in the study, 32 patients with the MetS GSK126 in vitro and 37 patients without. The mean age of the whole group was 60.9 ± 12.1 and the male to CSF-1R inhibitor female ratio was 4.31. Demographics and clinical data of patients with and without the

MetS are presented in table 1. With respect to tumor response outcomes, there was no statistical difference in the average number of local regional therapy sessions in both groups (2.3 ± 1.62 vs 2.1 ± 1.53, p = 0.5373), and the intervals between therapies. In contrast, with respect to hepatic decompensations; significantly more episodes of hepatic decompensation were seen in those with MetS than those without MetS (34% vs 11%, p = 0.0220). Table 1: Patient demographics and clinical data.   With this website MetS Without MetS p-value Number 32 37 – Age 63.2 ± 10.39 59 ± 13.02 – Male (%) 27 (84%) 29 (78%) 0.5562 %HBV 9 (28%) 23 (62%) 0.0075 %HCV 23 (72%) 14 (38%) 0.0075 Mean Child-Pugh score 6.25 ± 1.83 6.19 ± 1.26 0.8836 Mean max size of lesion (cm) 4.18 ± 2.85 3.84 ± 2.35 0.588 Conclusion: In patients with HCC and viral hepatitis treated with local regional therapy, presence of metabolic syndrome is associated with significantly

higher rates of hepatic decompensation. GS BURNS,1 JA HOLMES,1 R GOLDBERG,1 R TRETHOWAN,1 A WONG,1 O CRONIN,1 NA KURUVILLA,1 T NGUYEN,1 RG SHAW,1 RY CHEN,1 BH DEMEDIUK,1 SJ BELL,1 SA LOCARNINI,2 DS BOWDEN,2 PV DESMOND,1 AJ THOMPSON1 1St Vincent’s Hospital, Melbourne, Australia, 2Victorian Infectious Diseases Laboratory, Melbourne, Australia Introduction: The immune control (IC) phase of chronic hepatitis B (CHB) is defined by HBV DNA < 2000 IU/mL and normal ALT. It has recently been suggested that a single-point HBsAg level <1000 IU/mL is an accurate biomarker for identifying IC patients with a low risk of HBV reactivation at 12 months.(1) The aim of this project was to validate this rule in a cohort of patients with long-term follow-up. Methods: A database search was used to identify treatment naïve patients in the IC phase of CHB for whom an HBsAg level was available, with a minimum of 12 months of follow-up.

Humans can acquire brucellosis by the ingestion of infected food (especially unpasteurized milk), by direct contact with an infected animal (sheep, cattle, or pigs), or by aerosols.1 In humans, brucellosis is a chronic granulomatous infection that is associated with nonspecific, mild clinical symptoms such as fever, fatigue, night sweats, anorexia, and weight loss. It is, therefore,

difficult to diagnose, and screening for Brucella should be performed in the case of fever of unknown origin. Almost every organ and system can be affected, but osteoarticular complications are the most common, with peripheral arthritis, sacroiliitis, and spondylitis occurring.2 Laboratory studies are nonspecific in patients with brucellosis, and white blood cell counts are usually normal GSK-3 inhibitor to low. Although the presence of some degree of hepatitis is frequent, the

click here development of a liver abscess (brucelloma) is rare and occurs in only approximately 1% of patients with brucellosis.3 It most commonly represents a chronic form of the disease that has remained latent. The typical CT scan pattern of liver brucelloma is a rounded or ovoid hypodense area with central calcification5 and is similar to the pattern found in this case. Confirmation of the diagnosis of brucellosis can be achieved by various techniques, including blood cultures, serological tests, and real-time polymerase chain reaction with blood or pus.4 The classic treatment for brucellosis is based on doxycycline and rifampin. In the case of liver abscess, surgery Reverse transcriptase is most often required because the risk of recurrence after conservative management is at least 50%.3 After surgery, which can be performed laparoscopically (as in the present case), a patient’s chance of being cured is extremely good. “
“In a recent report, Choi et al.1 demonstrated that protein arginine methyltransferase-1

(PRMT1)-dependent arginine modification of FoxO1 contributed to the regulation of hepatic glucose production in a mouse model. However, despite presenting the finding of the FoxO1 protein, the investigators failed to discuss another well-defined class of PRMT1 substrates: histones, methylations of which have been identified as key “histone codes” in epigenetic regulation2 and have been shown to regulate hepatic gluconeogenesis under the control of another PRMT in a previous study by Krones-Herzig et al.3 Herein, we compare the two similar studies and suggest that PRMT1-mediated histone arginine methylation should be involved in the network of hepatic glucose metabolism regulation. Both groups found that the PRMTs regulated the same target genes, but methylated different proteins (Table 1). Herzig et al. suggested that PRMT4 contributed to the regulation of hepatic glucose metabolism by methylating histone H3, because methylations of H3 arginines are known to be transcriptional activation markers.

19 T cells

among LMCs were separated using a Pan T cell isolation kit II. Non–T cells (B cells, NK cells, DCs, monocytes, granulocytes, and erythroid cells) were indirectly magnetically labeled using a cocktail of biotin-conjugated antibodies against CD14, CD16, CD19, CD36, CD56, CD123, glycophorin A, and anti-biotin microbeads. find more Isolation of purified T cells was achieved by depletion of magnetically labeled cells by separation over a MACS column, which was placed in the magnetic field of a MACS Separator; a purity of CD3+ T cells of >90% was confirmed by flow cytometry. Monocytes were separated with a monocyte isolation kit. Non-monocytes were indirectly magnetically labeled with a cocktail of biotin-conjugated monoclonal antibodies against CD3, CD7, CD16, CD19, CD56, CD123, and glycophorin A, and anti-biotin microbeads. Isolation of monocytes was achieved by depletion of magnetically labeled cells; a purity of CD14+ monocytes of >90% was confirmed by way of flow cytometry. NK cells were separated with an NK isolation kit. Non-NK cells were indirectly magnetically labeled with a cocktail of biotin-conjugated antibodies against lineage-specific antigens and anti-biotin microbeads. Isolation of NK cells

was achieved through the depletion of magnetically labeled cells; a purity of CD56+ NK cells of >90% was confirmed by way of flow cytometry. mDCs (CD1c+) were separated with an mDC isolation kit performed by two magnetic separation steps. In the first step, CD1c-expressing B cells were magnetically PD184352 (CI-1040) labeled with CD19 microbeads and subsequently depleted magnetically. HM781-36B in vivo In the second step, CD1c+ mDCs in the B cell–depleted flow-through fraction were indirectly magnetically labeled with CD1c-biotin and anti-biotin microbeads. Upon separation, the labeled CD1c+ mDCs were retained within the column and eluted after removing the column from the magnetic field. A purity of CD1c+ CD19− mDCs of >80% was confirmed by way of flow cytometry. NKT cells were separated with an NKT isolation kit. The isolation of NKT cells was performed in two magnetic separation

steps. In the first step, NK cells and monocytes were indirectly magnetically labeled using a cocktail of biotin-conjugated antibodies and anti-biotin microbeads. The labeled cells were subsequently depleted by separation over a MACS Column. In the second step, CD3+CD56+ NKT cells were directly labeled with CD56 microbeads and isolated by positive selection from the pre-enriched NKT cell fraction. Upon separation, the labeled CD56+ cells were retained within the column and eluted after removing the column from the magnetic field. A purity of CD3+ CD56+ NKT cells of >80% was confirmed by flow cytometry. Cell populations (2 × 104/200 μL in 96-well plates) were cultured for 48 hours in the presence of the TLR ligands described above at 10 μg/mL.

The duration of each step was determined experimentally using specific controls (Supporting Fig. 2). The results clearly show that a decrease in HCVcc infection was only observed when EGCG was present during virus infection (Fig. 3A, second, third, fourth, and sixth bars in the bar-graph), and that there was no effect of EGCG if added as a pretreatment of the cells (Fig. 3A, first bar) or postinfection (Fig. 3A, fifth bar). These results suggest that EGCG inhibits an early step of the HCV life cycle, most likely the entry step. To confirm the effect of EGCG on HCV entry, HCVpp harboring E1 and E2 of different genotypes were produced. HCVpp

infectivity was reduced by approximately 10-fold with a concentration of 50 μM, confirming the effect of EGCG on HCV entry, whatever the genotype used (Fig. Palbociclib order 3B). However, Wnt tumor some differences between genotypes could be observed at a lower EGCG concentration (5 μM). In contrast, vesicular stomatitis virus (VSV)pp entry was much less inhibited. These results suggest that the antiviral activity of EGCG is directed against HCV envelope glycoproteins and is genotype independent. Together, these data indicate that

EGCG inhibits HCV entry in a genotype-independent manner. Although the above data indicate that EGCG has a strong effect on HCV entry, we cannot exclude additional effects on other steps of the HCV life cycle. To analyze the effect of EGCG on HCV genome replication, Huh-7 cells were electroporated with in vitro transcribed assembly-defective JFH1-ΔE1/E2-Luc RNA, to bypass the entry step, and avoid any interference with late steps of the HCV life cycle. EGCG had no major effect on HCV replication, even after a longer period of treatment (96 hours postelectroporation) (Fig. 4A). In contrast, IFN-α, at 2 IU/mL, approximately twice the IC50 calculated for HCVcc in Huh-7 cells (1.15 IU/ml), 28 induced 1 log10 decrease of luciferase activity. To determine whether EGCG could have any effect on HCV assembly or secretion, intra- and extracellular core protein was quantified in infected

cells treated postinfection with 50 μM of EGCG for 70 hours. The amount Ribonucleotide reductase of core in the culture supernatant reflects the quantity of secreted viral particles. A slight, but not significant (P = 0.10), decrease in intracellular core was observed in the presence of EGCG (Fig. 4B). This cannot be explained by a decrease in RNA replication, because it has been shown above that EGCG has no effect on HCV replication (Fig. 4A). However, the quantification of extracellular core showed a small, but not significant (P = 0.10), increase of secreted core in the presence of EGCG, as compared to the nontreated control (Fig. 4B), showing that EGCG does not impair viral secretion. Similar experiments were performed with JFH1-ΔE1/E2 to avoid reinfection of the cells and to quantify the levels of extracellular core resulting from cell lysis.

The model level significance was α = 0.05. Unless

otherwise stated, values are provided as mean ± se. Colonies (n = 10) comprised 4–17 adult individuals (8.36 ± 1.45) and varied between 2–10 females and 2–7 males. Social interactions aboveground were very rare. In 612 h of observations (summer and winter), only 31 interactions were observed between colony members. Amicable interactions were observed on five occasions, involving two adults (n = 2) and mother and offspring (n = 3) sun basking together; allogrooming was observed in one adult pair. In contrast, agonistic interactions were observed 26 times (3% of the total observation time), significantly more than amicable interactions (z = 3.47, n = SB203580 mouse 10, P < 0.00; sign test), and always (n = 26) consisted of two individuals boxing briefly and one individual chasing the other for up to 12 m. No damaging fights were observed. Individuals of a colony always foraged alone. Season was a significant predictor of the aboveground home-range size (95% MCP), with home range being significantly greater in summer (367.39 ± 30.73 m2) than winter (164.27 ± 24.91 m2; F1, 36 = 20.58, P < 0.001). Sex was a significant predictor of home-range size (F1, 36 = 7.17, P = 0.011), being greater in females (327.01 ± 23.00 m2) than males (210.65 ± 25.88 m2). Season × sex was not a

significant predictor of home-range size (F1, 36 = 2.01, P = 0.165). Colony members exhibited a large degree of spatial overlap (percentage GDC-0199 research buy spatial overlap of 95% MCP; Fig. 1). Season was a significant predictor of home-range overlap (F1, 36 = 8.27, P = 0.001), with overlap being greater in winter (49.144 ± 2.47%) than summer (42.03 ± 2.93%). Sex (F1, 36 = 3.04, P = 0.143) and the interaction between season and sex (F1, 36 = 2.83, P = 0.101) did not predict home-range overlap in summer (females: 43.63 ± 2.46%; males: 42.46 ± 2.38%) and winter (females: 52.43 ± 2.09%; males: 43.31 ± 2.94%). The empty cage was approached in both seasons but cage biting occurred only

once (Fig. 2). Sitting in close proximity to conspecifics (i.e. tolerance) occurred infrequently (36–378 s) and was directed only at female stimulus subjects at Succinyl-CoA their capture site (i.e. non-displaced). Due to low incidences of tolerance, these data were not included in further statistical analyses. In contrast, agonistic behaviour was common (Fig. 2), mainly in the member and stranger treatments. Neither sex (Wald χ21 = 0.01; P = 0.995; GLZ) of the stimulus subject nor season (Wald χ21 = 0.00; P = 0.997) influenced aggression levels in any of the three treatments. However, there was a marked treatment effect (Wald χ21 = 95.99; P < 0.001). Post hoc tests revealed two groupings: low aggression for non-displaced stimulus subjects (β = 8.

DR0101 tetramer staining of T cells from his haemophilic brother, subject IV-2, was quite similar, as a comparable number of T cells recognized the same HLA-DR-FVIII peptide complexes. In addition, the avidities of the T-cell clones isolated from both brothers for DR0101 Tyrosine Kinase Inhibitor Library concentration tetramer loaded with synthetic peptide FVIII2194–2213 were similar, and both sets of clones

showed strong, dose-dependent proliferation when stimulated with FVIII2194–2213. An intriguing difference between the T-cell responses of IV-1 and IV-2 was noted, in that low-level proliferation of T-cell clones from subject IV-2 was elicited by a peptide with the haemophilic missense sequence, FVIII2194–2213 2201P, but this was not seen for any clones isolated from inhibitor subject IV-1. Staining of polyclonal T cells from IV-1 using DR0101 tetramers loaded with the haemophilic peptide was seen only during analysis of the sample obtained 3 days following initial detection of his inhibitor GSK126 cost response. Staining of T cells from this time point was consistent with clinical evidence for an immune response to his self (haemophilic) FVIII protein, as well as against

the wild-type FVIII that he received in infusions to support surgery. At this time point, his peak inhibitor titre of 250 BU mL−1 coincided with a clotting activity (FVIII:C) of 3%, which was well below his preinhibitor baseline FVIII activity of 8–10%. His FVIII activity corrected to his normal baseline level as his inhibitor titre fell to 30 BU mL−1 over the ensuing four weeks. A possible explanation

is that under the inflamed conditions at the time of his surgery and FVIII infusions, a subset of his T cells, primed by ‘danger signals’ accompanying this inflammatory response, recognized the lower-avidity self-sequence with P2201 as well as the ‘non-self’ FVIII containing A2201. Signalling from T cells stimulated by wild-type and/or haemophilic FVIII fragments may have contributed to the transient production of antibodies inhibiting the function of the haemophilic FVIII. The presence of T cells recognizing the haemophilic peptide in subject IV-2 is interesting, as he had only very low levels of circulating IgG that inhibited FVIII Lepirudin activity, and this blood sample was not obtained at a time of trauma or major inflammation. Because our sample size is small, it is not yet known how frequently T cells from individuals with mild haemophilia A will recognize their haemophilic ‘self-FVIII’ as well as wild-type ‘non-self’ FVIII. Our documentation of T cells from haemophilia A subjects without a clinically significant inhibitor responding to a specific epitope in FVIII is consistent with several previous reports of T-cell responses in inhibitor-negative haemophilia A subjects or in non-haemophilic subjects. Singer et al.

The aapk1 deletion mutants were identified

from hygromycin-resistant transformants by PCR strategy and confirmed by Southern blot analysis and RT-PCR. The aapk1 deletion mutant exhibited reduced vegetative growth and was less toxic than the wild-type strain sd1. Deletion of aapk1 also delayed disease development on detached tobacco leaves. Thus, we propose that the cAMP signalling pathway is involved in mycelia growth and pathogenic phenotype of Alternaria alternata. “
“In vitro evaluation was carried out on seed selleck kinase inhibitor samples of wild and cultivated rocket cultivars, most frequently grown in Italy, and obtained from farms affected by the leaf spot caused by Alternaria japonica in Piedmont and Lombardy during the fall of 2010. Twelve seed samples were collected and assayed for the presence of A. japonica. The pathogen was isolated only from not disinfected seeds. Among the two seed samples of cultivated rocket (Eruca vesicaria), only one was infected by A. japonica at a level of one infected seed out of 800. Four out of ten samples of wild (Diplotaxis tenuifolia) rocket seeds were contaminated by A. japonica with the highest level of infection detected in a single sample of 3 out of 800. All tested isolates of A. japonica obtained from seeds were pathogenic on both wild and cultivated rocket. “
“Between 2002 and the end of 2009, more

than 4000 samples from hardy ornamental plants, collected in surveys for Phytophthora ramorum, were examined to establish the occurrence and MK-1775 in vivo diversity of Phytophthora species in Scotland. The samples were gathered from more than 77 plant genera in nurseries, gardens and amenity landscapes. Fifteen

different Phytophthora spp. were isolated and identified either by polymerase chain reaction (PCR) or by sequencing of the ITS1, 5.8S subunit and ITS2 region of the ribosomal RNA gene. The most widespread Phytophthora spp. were P. ramorum and P. syringae, followed by P. cactorum, P. kernoviae, P. plurivora, P. cambivora, P. citrophthora, P. taxon ‘Pgchlamydo’, P. pseudosyringae and some single isolates of P. cinnamomi, P. cryptogea, P. gonapodyides, P. nicotianae and P. hibernalis. One isolate did not match any known species. In relation to the number of samples, Phytophthora was found more frequently in trade premises than in gardens or amenity landscapes Histidine ammonia-lyase and the species diversity was higher, highlighting the risks involved in plant trade. “
“Sequence analysis has shown that diseased wheat plants in Northern Germany were infected with the New York strain of soil-borne wheat mosaic virus (SBWMV). This is in contrast to the only other confirmed site of SBWMV occurring in Germany, where a variant closely related to the Nebraska-type strain of SBWMV was found. The results indicate that there have been at least two separate introductions of SBWMV strains to Germany. A survey is required to study the actual distribution of SBWMV in Germany.