The CD spectra were measured on MOS-450/AF-CD-STP-A (Bio-Logic, France) at a protein concentration of 0.1 mg/mL in 50 mM Tris/HCl buffer (pH 8.6) using a 1 cm path-length

quartz cuvette. To minimize the signal baseline drift, the spectropolarimeter and xenon lamp were warmed up at least 30 min prior to each experiment. The enzyme data in the 190–240 nm bands were collected, and which the spectrum obtained for a buffer blank was subtracted from these data. The assay to determine the kinetic parameters were performed using different concentrations of l-phenylalanine (1–20 mM) (Sigma–Aldrich, Germany). The reactions were initiated by the addition of an appropriate quantity of RgPAL to each reaction system. The reaction was conducted at 40 °C and see more stopped by addition of 0.5 mL of methanol. The formation of

trans-cinnamic acid was find more measured by HPLC (Hitachi, Japan) at 290 nm, the mobile phase contained 50% methanol. The obtained experimental dependences of the initial catalytic rates on the substrate concentrations were fitted to Michaelis–Menten equation through nonlinear regression analysis using Origin (7.5 versions). One enzyme activity unit was defined as the amount of enzyme that produced 1 μmol trans-cinnamic acid per minute at 40 °C. The effects of the pH were determined at 40 °C using a series of buffers with various pH values (pH 5.0–7.0, 50 mM sodium acetate buffer; pH 7.0–9.0, 50 mM Tris–HCl buffer; pH 9.0–12.0, 50 mM sodium carbonate buffer). The chiral resolutions of dl-phenylalanine using RgPAL and RgPAL-Q137E were performed at pH 7 and pH 9, respectively. The experiments were carried out in

500 mL batch conical flasks with lid in a rotating shaker and contained 300 mL of dl-phenylalanine (100 mM) and 250 μg of pure enzyme at 40 °C. The conversion rate of l-phenylalanine and the eeD value of d-phenylalanine were calculated by the following equations: conversion rate=[(Lphe,in−Lphe,out)Lphe,in]×100%eeD=[(Dphe−Lphe,out)(Dphe+Lphe,out)]×100%;where the eeD is the enantiomeric excess of d-phenylalanine; the Lphe, in is the initial concentration of l-phenylalanine; the Lphe,out is the residual concentration of l-phenylalanine Nitroxoline after resolution; the Dphe is the concentration of d-phenylalanine. The d-phenylalanine and l-phenylalanine are detected through HPLC (Hitachi, Japan) at 205 nm according to the method described by Fukuhara [7]. The mobile phase contained 20% methanol and a complex of optically active L-Pro-Cu(II) (1.5 mM L-Pro and 0.75 mM CuSO4). The “mutational effect” was determined by dividing the kcat value of the mutant enzyme by that of the wild type, and the free energy (ΔΔG‡) was calculated from the following equation: ΔΔG‡ = −RTln (mutational effect) as described by Olucha (2011, 2012) [17] and [18].

Less frequent stimulation of the network did not have any qualitative effect on its dynamics. In the second approach, the incorporation MK-1775 mw of augmentation, i.e. slow synaptic facilitation (Wang et

al., 2006, see Experimental procedures) added new functional aspects to the dynamics. These simulations correspond to memory processes involved in a memory replay phenomenon, which can be linked to multi-item working memory maintenance in the cortex (Fuentemilla et al., 2010). A specific memory pattern was stimulated at first, as in the previous simulation paradigm, and after the resulting brief initial activation the internal dynamics of the network caused this particular attractor state to periodically reactivate without any successive external stimulation (Mongillo et al., 2008, Lundqvist et al., 2011 and Lundqvist et al., 2012). This occurred since the synaptic augmentation had a longer time constant than the synaptic depression. During periods of activity in the recurrent network these two synaptic mechanisms balanced each other out, but once the memory retrieval terminated synaptic depression started decaying faster. As a result, synaptic conductances of the excitatory recurrent connections of the recently terminated patterns became temporarily boosted. This way 5.0±0.7 (mean±standard deviation, 100 trials) memory items could be encoded by initial ABT-199 solubility dmso sequential activation of the corresponding attractor states

followed by spontaneous periodic reactivations

of these specific patterns. Fig. 2B illustrates a spike raster obtained during part of a trial with periodic reactivations. Trials were typically run for 20 s to obtain reliable statistics. We analyzed both the spiking activity and the synthesized LFP signals collected during simulated memory processes implicated in memory pattern completion or sequential memory replay phenomena. During periods of interleaved idling in the non-coding ground state and memory activation we found in both types of memory simulations distinct frequency components in the power spectrum corresponding to the upper alpha/lower beta oscillations and the coupled (Chrobak and Buzsaki, 1998; Palva et al., 2005 and Canolty et al., 2006) theta- (2–5 Hz) and gamma- (25–35 Hz) band activity (Fig. 2C and D). The nested theta and gamma oscillations accompanied the coding attractor states (Fig. 3). In cued trials, an additional ~10 Hz Silibinin alpha rhythm coupled to the gamma and theta emerged in the synthesized LFPs (Fig. 2C). Finally, the aforementioned upper-alpha-/lower-beta-band activity (15−20 Hz) was manifested as an attribute of the idling non-coding ground state. Here however we only focused on the nested oscillations during memory retrieval in the coding attractor states. The coherence analysis performed on the LFPs within as well as between hypercolumns revealed a generally decreasing trend with both distance and frequency. Spiking, although highly irregular for single cells (Lundqvist et al.

6b). Modeled station-specific FIB decay – driven only by advection and diffusion – was exponential for all alongshore stations ( SI Fig. 6), and exhibited a spatial pattern similar to HB06 FIB data, with significantly faster decay observed at northern stations than southern stations (Fig. 5a). Although the spatial patterns of decay estimated by the AD model matched those of HB06 FIB well, the actual magnitudes of the this website decay rates were lower than observed (Fig. 5). The only station where the AD model captured FIB decay rates accurately (p < 0.05) was SAR, for E. coli (Fig. 5a). At all other stations, AD modeled FIB decay accounted for ⩽50% of observed decay (Fig. 5). This underestimation of FIB

decay rates suggests that an additional source of decay must be included in the model to accurately reproduce FIB dynamics during HB06. This additional decay is likely to be intrinsic to the FIB taxa, as the amount of unexplained FIB decay during HB06 was group-specific (Fig. 5). In the cross-shore, the AD model successfully reproduced FIB patterns for surfzone stations (F1, F3) and the offshore mooring (Enterococcus only), where FIB concentrations were consistently

near zero. It failed, however, to reproduce FIB patterns for offshore stations exhibiting FIB contamination (F5, F7) (Fig. 6b). find more Poor model-data fits at these stations likely reflect over-retention of offshore FIB (Figs. 4 and 6a). Modeled FIB decay at these stations was significantly slower

than decay at F1 and F3, while observed FIB decay rates were constant across-shore (Fig. 5b). Together, the relatively poor model-data fits and decay-rate estimates for offshore stations suggest that, although the AD model performs well in the surfzone, it is missing a dominant process structuring offshore FIB concentrations during HB06. Through a synthesis of field observations and models, we have shown that a model including only horizontal advection and diffusion can explain a significant portion of the variability in FIB concentrations at Huntington Beach, why especially in the alongshore (Skill of 0.45–0.90 at alongshore stations and −0.23 to 0.74 at cross-shore stations, Fig. 6b). To our knowledge, HB06 is the first study to perform high-resolution monitoring of FIB, waves, and currents both in the surfzone and offshore, providing an opportunity to directly quantify the importance of these physical processes in structuring nearshore FIB pollution. The strong role of advection and diffusion in structuring patterns of FIB during HB06 was somewhat surprising given the temporal decays observed at each sampling station often attributed to solar insolation (e.g., Ki et al., 2007). Our analyses suggest, however, that a significant portion of this decay (mean of 38% for E. coli, and 14% for Enterococcus) was due to southward advection and diffusion of FIB patches through the study area (Fig. 5).

, 1992, Kajiwara et al., 1996, Simmons-Willis et al., Dasatinib supplier 2002, Adachi, 2006 and Yin et al., 2008). Corroborating this hypothesis, our group recently reported that mice chronically treated with the MeHg–Cys complex show enhanced Hg uptake, especially in the liver, when compared

to other organs, such as the brain and kidney (Roos et al., 2010). These results are most likely due to the fact that the liver is a central organ of protein metabolism and receives amino acids absorbed at the intestinal levels as well as those derived from other organs and systems (Duarte, 2003). Although hepatic cells contain some of the same carriers that have been implicated in the transport of Hg in other organs, the precise mechanisms underlying the MeHg uptake across the membrane into normal hepatocytes as well as the influence of the MeHg–Cys complex on Hg uptake and hepatoxicity have not previously been well defined. Consequently, our study was primarily designed to investigate the Hg content in hepatic cells, at both cytosolic and mitochondrial levels after exposure to MeHg or the MeHg–Cys complex. Several previous studies have investigated and reported on the toxicology of MeHg, but, to date, only chelating agents have been employed to facilitate

Crizotinib the removal of Hg from the body (Pingree et al., 2001 and Carvalho et al., 2007). However, these drugs are of limited use because of their adverse side effects. In the present study, we have tested the possible use of Met as an efficacious agent capable of protecting against the deleterious effects of MeHg. We observed that the Hg concentration in liver slices and in the mitochondria isolated from liver slices was higher after exposure to the MeHg–Cys complex (Fig. 1). Notably, we observed that Met decreased MeHg uptake by liver slices (Fig. 1). These results are different from those reported by Adachi (2006) after exposure of mice to MeHg. Adachi reported that Met can increase the hepatic deposition of Hg 2 h

after intravenously administration of MeHg and/or methionine. Since we have used only a single time-point of exposure of liver slices to MeHg (30 min) and/or Met (45 min), Protein kinase N1 we cannot disregard the possibility that uptake of MeHg could be increased in the presence of Met. Alternatively, the decrease in Hg uptake in the slices by Met may be, at least in part, related to the relatively high concentration of Met in the medium and, consequently, to direct interaction between MeHg and Met, thus lowering the effective free concentration of MeHg. Accordingly, we can posit that the effect observed in the presence of Met may be related to a direct interaction of the sulfur atom and/or amino end of Met with MeHg (Rabenstein and Fairhurst 1975). Alternatively, Met may be reducing the uptake of MeHg complexed with endogenous cysteine in liver slices. In addition, here we have worked with an in vitro system derived from rats.

At day 8, there were statistically significant decreases in the ratio of villous/crypt areas at 170 and 520 mg/L SDD (Fig. 8). At day 91, the villous/crypt ratio was significantly altered at 520 mg/L (Fig. 8). Functional analyses using DAVID and IPA at day 8, revealed the enrichment of the same molecular and cellular functions between non-overlapping differentially expressed find more genes at ≤ 60 mg/L and ≥ 170 mg/L SDD (1295 and 4176 unique genes, respectively, |fold change| > 1.4, P1(t) > 0.95). Over-represented functions included

RNA processing, cell cycle, cell death, cell morphology, and cytoskeleton (data not shown). Similar functional analysis at day 91 identified a total of 3954 genes at ≤ 170 mg/L and 1110 genes expressed only at 520 mg/L SDD (|fold change| > 1.4, P1(t) > 0.95) with overlapping functions related to cell cycle, cellular function and maintenance and post-translational modifications (not shown). This is the first paper to report the genome-wide gene expression effects of Cr(VI), in the form of SDD, on the mouse small intestine and phenotypically

associate differential gene expression to complementary histopathology, biochemical analyses, and tissue dosimetry. SDD elicited dose-dependent differential gene expression in the duodenum and jejunum. Dose–response analysis indicates most changes occur between 14 mg/L SDD (76 differentially expressed genes at 91 days) and 60 mg/L SDD (1857 differentially expressed genes at 91 days), with little differential Oxymatrine expression below 4 mg/L SDD. Quantitative dose–response modeling of gene expression changes indicated that responses NADPH-oxidase inhibitor to SDD were similar in both intestinal segments at both time points. The median EC50 values at day 8 and day 91 in the duodenum and jejunum ranged from 39 to 55 mg/L SDD, whereas

the BMDL values at day 91 were 56 and 49 mg/L SDD in the duodenum and jejunum, respectively. Dose-dependent gene expression and associated functions are consistent with SDD concentrations that elicited phenotypic effects (e.g. cytoplasmic vacuolization) described in Thompson et al. (2011b). Taken together with no evidence of focal proliferation or neoplastic lesions in two 90-day drinking water studies (NTP, 2007 and Thompson et al., 2011b) despite clear signs of Cr(VI)-induced tissue injury (Fig. 8), it is highly plausible that Cr(VI)-induced tumorigenicity is the result of constant tissue damage and compensatory crypt epithelial cell proliferation. SDD-elicited intestinal differential gene expression may also be partially due to Cr(III) that is likely present at high concentrations following the bolus reduction of Cr(VI) at the high SDD concentrations. Although not as bioavailable due to passive uptake (Dayan and Paine, 2001), Cr(III) may alter carbohydrate/insulin signaling, and lipid metabolism pathways (Vincent, 2004).

Each experiment was repeated at least three times unless stated otherwise. The statistical significance of the differences between treatments was assessed using t-test and a p value of less than 0.05 was considered significant. We first examined the patterns of AMPK, Akt, mTOR and autophagy activation during 7-day differentiation of hDP-MSC. Osteoblastic differentiation of hDP-MSC was confirmed by a significant increase in alkaline phosphatase activity and the mRNA and/or protein levels of osteogenesis markers osteocalcin, Runx2 and BMP2 (Figs. 1A, B). This was associated with rapid phosphorylation of AMPK and its direct downstream target Raptor, which peaked

at day 1 and then gradually declined (Figs. 1C, D). An inverse activation pattern was observed with mTOR and its substrate S6K, demonstrating an early inhibition at day 1 followed by activation Bioactive Compound Library mouse from

day FDA-approved Drug Library purchase 3 onwards (Figs. 1C, D). The increase in Akt phosphorylation slightly lagged behind that of AMPK, reaching its maximum at day 3 and remaining high during the rest of the differentiation period (Figs. 1C, D). The conversion of LC3-I to autophagosome-associated LC3-II, as a marker of autophagy, was increased at day 1, but then rapidly declined at later stages of differentiation (Figs. 1C, E). The changes in LC3 conversion were correlated with the extent of autophagic proteolysis, which increased early and declined late during differentiation, as reflected in the reduction and increase, respectively, of the intracellular levels of p62 (Figs. 1C, E), a selective autophagy target [22]. In accordance with the early induction of autophagy, the intracellular concentration of the proautophagic protein beclin-1 reached its maximum 24 h after initiation

of differentiation (Figs. 1C, E). These data demonstrate a complex, time-dependent modulation of AMPK/Akt/mTOR signaling and autophagy during osteogenic differentiation of hDP-MSC, involving early activation of AMPK and transient induction of autophagy, followed by the late activation of Akt and PJ34 HCl mTOR. We next investigated the role of an early induction of AMPK and autophagy in osteogenic differentiation of hDP-MSC. Autophagy inhibitors bafilomycin, chloroquine and NH4Cl, which prevent autophagolysosome acidification and/or autophagosome–lysosome fusion [23] and [24], all blocked osteogenic differentiation of hDP-MSC, as confirmed by the reduction in alkaline phosphatase activity and expression of osteocalcin and Runx2 (Fig. 2A). Accordingly, the shRNA-mediated knockdown of the autophagy-essential LC3β blocked the increase of osteoblast differentiation markers in hDP-MSC (Figs. 2B, C). The efficiency of LC3β shRNA silencing was confirmed by reduced levels of both LC3-I and LC3-II in differentiating hDP-MSC at day 1 (Fig. 2D).

The following section attends to how different governance

rationales may be combined in a RBM approach, with a focus on RBM models that involve collective arrangements developed and management by IDH tumor resource users groups. Subsequently, major challenges that can be expected with moving towards RBM in fisheries are discussed. Finally, possibilities for implementing RBM arrangements within the new CFP, which was adopted in 2014, are addressed. The state centric or hierarchical model of fisheries management should be recognized as one among several generic approaches within a broader notion of fisheries governance.f As pointed out by Gray [58], participatory and market based approaches to fisheries governance buy Ku-0059436 are on the advance. Gray relates this tendency to the experience that the state centric model has not met its objectives successfully in different contexts. It may also be related to a change in emphasis regarding the basic values that underpin fisheries governance; i.e. a shift from representative democracy towards participatory democracy, and from administrative rationality towards economic efficiency [58]. However, the fact that the state centred model nevertheless remains dominant within fisheries governance indicates that this approach not only has weaknesses,

but also advantages. It will be suggested here that the recent interest in RBM in Europe as an instrument to deregulate fisheries activities and to delegate responsibility to resource users may be Cyclin-dependent kinase 3 linked to its potential of integrating main rationales from each of these governance modes. The fisheries co-management literature (see e.g. [59]) describes normative and substantive rationales for delegating management and research responsibilities to resource users. Drawing on ideals of direct or participatory democracy, it may be argued that those affected by certain policy decisions should also have an opportunity to voice their opinion or even participate in decision-making regarding such

policies. Participation by affected parties is expected to enhance the legitimacy and compliance to a given policy [60]. A substantive rationale for including resource users in decision-making is to benefit systematically from experience based knowledge in order to secure a broader and potentially more detailed knowledge base for management and implementation. Seen in isolation, these rationales favour a transition from state centric governance to self-governance by resource users. However, there are also important rationales that underpin state centric fisheries governance. As remarked by Gray [58], the hierarchical or top down model fits well with the notion of representative democracy by which policy making regarding public resources is left to elected leaders (supported by relevant scientific expertise).

Additionally, it has been theorized that release of nitric oxide by nerves, vessels, or brain tissue may be part of the trigger of for migraine pain [79]. Hyperbaric oxygen causes cerebral vasoconstriction, likely though scavenging of nitric oxide [80] and thus the effect of HBO2T might improve pain directly through decreases in NO as well as through vasoconstriction and anti-inflammatory

mechanisms. There is some evidence that HBO2T is an effective treatment of acute migraine attack. Wilson et al. [81] assigned female subjects selleck chemical with confirmed migraine to either 100% oxygen at normal pressures, or hyperbaric oxygen. They found that subjective pain was significantly reduced in the group receiving hyperbaric oxygen, but not following control treatment. They concluded that Enzalutamide in vivo HBO2T is effective for migraine pain, and the patient’s subjective pain assessment was the best indicator of relief. In a double blind, placebo-controlled

study by Eftedal et al. [82] the prophylactic effect of HBO2T on migraine was investigated. Forty patients were randomly assigned to a treatment group receiving three sessions of hyperbaric oxygen, or a control group receiving three hyperbaric air treatments. Patients kept a standardized migraine diary for eight weeks before and following treatments. Thirty-four patients completed the study. Their primary measure of efficacy was the difference between pre- and post-treatment hours of headache per week. The results showed a non- significant reduction in hours of headache between groups. Levels of endothelin-1 in venous blood pre- and post-treatment showed no difference between the hyperbaric oxygen and control groups. They concluded that the tested protocol does not show a significant prophylactic effect on migraine and does not influence the level of endothelin-1 in venous blood. Bennett et al. [83] conducted a meta-analysis on randomized trials comparing HBO2T or normobaric oxygen with placebo or no treatment in patients with migraine headache or cluster headache. Nine small PRKD3 trials were included

which involved 201 participants. Five trials compared HBO2T vs sham therapy for migraine. Pooling data from three trials suggested that HBO2T was effective in relieving migraine headache compared to sham (relative risk (RR) 5.97, 95% confidence interval (CI) 1.46–24.38, P = 0.01). However, no evidence was found for prophylactic use. No reduction in the incidence of nausea and vomiting was seen. Neither was there a reduction in rescue medication requirements. We are not aware of data looking at HBO2T as a therapy for status migrainosus. Patients arriving to the Emergency Department with a presumed diagnosis of status migrainosus by history will be evaluated by a neurologist. Inclusion in the study requires that the patient, either male or female, be at least 18 years-old and have prior history of migraine consistent with current headache except in duration.

“
“Several studies using trigger high mechanical index (MI) techniques for visualization of cerebral perfusion after ultrasound contrast agent (UCA) injection have been published in the last 13 years [1], [2], [3], [4], [5] and [6]. The studies were mostly performed with triggered harmonic gray scale imaging techniques (conventional, power

modulation or pulse-inversion) analyzing the bolus kinetics in healthy subjects to find out the best way for the detection of UCA in the cerebral microcirculation. Recently low mechanical index gray scale imaging was introduced. With this new real-time technology bolus kinetics as well as refill kinetics could be analyzed. Refill kinetics is based on the reappearance of echo contrast in tissue after complete microbubble destruction using a high MI pulse. After destruction of the contrast agent within the scanning plane new microbubbles enter the volume with a certain velocity, thus allowing calculation of regional

GSK-3 beta pathway http://www.selleckchem.com/products/ink128.html blood flow (Fig. 1). Refill kinetics to measure regional cerebral blood flow was first studied in dogs after craniectomy [7]. Recent technological advances in ultrasound equipment with improved sensitivity for detection of microbubbles in the cerebral microcirculation through the acoustic bone window in humans now enable real-time ultrasound perfusion imaging [8] and [9]. This new real-time refill technology has several advantages over the triggered high MI techniques. First refill kinetics could be recorded and analyzed within seconds (Fig. 2); therefore, several insonation planes could be evaluated with one contrast bolus injection. Second software tools like microvascular imaging (display of the amount

of contrast signals over time [8]) help in visualization and documentation of perfusion deficits. On the other hand there are some disadvantages like the limited maximal insonation depth and the high rate of insonation artifacts. As of yet, it is not evident which method is superior for the analysis of brain perfusion, because studies with a direct comparison are missing. The commercially available ultrasound contrast agents Levovist™ (Schering), Optison™ (Amersham Health), and SonoVue™ (Bracco) proved to have contrast enhancing properties in ADAMTS5 human brain perfusion imaging. No severe adverse events were documented in numerous volunteer studies published on brain perfusion analysis using these contrast agents including more than 200 subjects. Various curve parameters have been described for the analysis of the different contrast kinetics (bolus and refill). To date (12/2011), it is not evident which kinetics or which parameter is the most valuable for the analysis of brain perfusion in healthy subjects. Theoretically, time-dependent parameters like time to peak intensity (bolus kinetics) or the β-value (refill kinetics) should be more useful than amplitude-dependent parameters, because the latter depend also on insonation depth.

However, we could not detect any gross changes in the stromal immune cell component http://www.selleckchem.com/products/Sunitinib-Malate-(Sutent).html or blood vessel density of fascin knockout tumors, and we recently reported that fascin loss is dispensable for growth of transplanted tumors.38 Fascin has been implicated in migration and invasion in vitro,

so it was surprising that fascin loss had no effect on invasion in vivo. We previously observed that only melanoma cell lines displaying elongated mesenchymal mechanisms of invasion were dependent on fascin.14 Collective invasion into bowel or peritoneal wall is not limited by loss of fascin and might also not be limited by matrix remodeling or invadopodia formation. Collective PDAC invasion could occur in physiological clefts between tightly packed collagen bundles or muscle strands,39 and fascin-mediated protrusions might not be crucial. We show that fascin null cells are less able to colonize the mesentery. Rho-associated colied-coil-containing protein kinase and myosin-mediated contractility are required for transmesothelial migration of human multiple myeloma and ovarian cancer cells.40 and 41 selleck inhibitor We

provide mechanistic evidence that fascin drives long filopodia that cross between the mesothelial cells and make initial contact with the substratum to aid transmigration. Our study suggests that, at least for PDAC, it is not invasion of the primary tumor, but rather colonization of the new site that is most affected

by fascin loss. The authors thank Joel Habener and Violeta Stanojevic of the Mass General Hospital, Boston, MA for their generous gift of slug antiserum. We also thank Colin Nixon of Beatson Histology Services, Matthew Neilson of Beatson Bioinformatics, and all staff of Biological Services Unit and the Beatson Advanced Imaging Resource imaging facility. Ang Li’s current affiliation is Laboratory of Mammalian Celastrol Cell Biology and Development, The Rockefeller University, New York, NY. “
“Event Date and Venue Details from 2012 NORTHEASTERN WEED SCIENCE SOCIETY ANNUAL MEETING 03-06 JanuaryPhiladelphia, PA, USA Info: http://tinyurl.com/3rfqmnv. INTERNATIONAL ADVANCES IN PESTICIDE APPLI-CATION, WAGENINGEN, THE NETHERLANDS 10-12 January Info: www.aab.org.uk. [email protected]. 3rd GLOBAL CONFERENCE ON PLANT PATHOLOGY FOR FOOD SECURITY AT THE MAHARANA PRATAP UNIVERSITY OF AGRICULTURE AND TECHNOLOGY 10–13 Jan 2012 Udaipur, INDIA Voice: 0294-2470980, +919928369280 E-mail: [email protected] SOUTHERN WEED SCIENCE SOCIETY (U.S.) ANNUAL MEETING 23–25 January Charleston, SC, USA SWSS, 205 W. Boutz, Bldg. 4, Ste. 5, Las Cruces, NM 88005, USA Voice: 1-575-527-1888 E-mail: [email protected] Web: www.swss.ws 1st INTERNATIONAL WORKSHOP ON BAC-TERIAL DISEASES OF STONE FRUITS AND NUTS 14–17 FebruaryZurich, SWITZERLAND B. Duffy, Agroscope FAW, Schloss, Postfach 185, 8820 Waedenswil, SWITZERLANDE-mail: [email protected].