Results of the tofacitinib-AS study are still pending. In this issue, a meta-analysis of adalimumab in AS by Wang et al. has reported higher efficacy as well as better quality of life without any major infection or serious adverse events[34]. GSK126 Prince et al. reported similar results with infliximab in a small Australian cohort[35]. Overall there are some excellent leads from pathogenic, genetic and functional studies in AS. The future

is bright and we can hope for newer and more effective drugs leaving behind the concept of ‘bamboo spine’ in oblivion. “
“To compare the prevalence of diverse histopathologic features among patients with Sjögren’s syndrome (SS) and controls, and to evaluate their relationship with age, a focus score (FS) ≥ 1 and some clinical and serological SS features. A blinded pathologist examined 63 SS and 11 control minor salivary gland biopsies. Focal lymphocytic sialadenitis (FLS) was defined as a focus score (FS) ≥ 1. We also evaluated lymphoepithelial lesions, germinal centers (GCs), epithelial metaplasia, dilatation

and hyperplasia in the main secretory duct, perivascular APO866 in vitro cell infiltrate, adipose infiltration, acinar atrophy, interstitial fibrosis and lymphocytes/plasma cells remote from the FLS. We registered demographics, anti-Ro/La status and clinical features. We used Kendall’s tau coefficients and logistic regression RVX-208 analysis. Sjögren’s syndrome patients had a higher frequency of FS ≥ 1 (92% vs. 27%), acinar atrophy (78% vs. 18%), lymphocytes and plasma cells external to the FSL (92% vs. 64%) and stromal fibrosis (68% vs. 36%). A FS ≥ 1 correlated

with the presence of GCs and acinar atrophy; whereas age correlated with duct dilation, duct epithelial hyperplasia, adipose infiltration and fibrosis. SS patients with hepatic involvement exhibited more frequent duct dilatation. After adjusting by age, anti-Ro/SSA (odds ratio [OR] 30.8, 95% CI 2.2–423.5, P = 0.01), a FS ≥ 1 (OR 54.3, 95% CI 4.8–612, P = 0.001) and fibrosis (OR 15.2, 95% CI 1.2–186.2, P = 0.03) were associated with SS. Other histologic findings coexist with FLS, but only GC formation and acinar atrophy correlated with a FS ≥ 1. Age is mostly correlated with the remaining histological features. However, the clinical relevance of these findings is unknown. “
“To describe Filipino patients with rheumatoid arthritis (RA) entered in the Rheumatoid arthritis database and registry (RADAR) of the Philippine General Hospital. Cases entered to RADAR from 2010–2012 were included. All fulfilled the 1987 American College of Rheumatology criteria for classification of RA. Included cases gave written infomed consent. Data extracted were demographics, clinical presentation, laboratory tests, treatment and disease course.

French recommendations are updated each year in the Bulletin Epidémiologique find protocol Hebdomadaire (BEH).7,8 Briefly, in French recommendations, three zones of malaria chemoprophylaxis are defined. Chloroquine (Nivaquine®) is recommended in area 1 without chloroquino-resistance. Area 2 corresponds to an intermediate level of resistance to chloroquine, and chloroquine/proguanil (Savarine©) is recommended as well as atovaquone/proguanil (Malarone®) especially for India, Sri Lanka, and Madagascar. Area 3 is a chloroquino-resistance

area, where atovaquone/proguanil, mefloquine, or doxycycline is recommended. These recommendations are summarized in Table 1. For vaccines, recommendations are similar to those from the Center of Diseases Control,9 especially for yellow fever vaccination. Yellow fever vaccine is recommended for all trips to African or American endemic areas,9 even if there is no administrative obligation. SB431542 Yellow fever vaccine is contra-indicated in case of immune suppression and is not recommended during pregnancy, but may be performed if the trip cannot be cancelled. For this study we considered that hepatitis A vaccine was needed for all travelers to Africa, Asia, or South America, except for people likely to be already immunized (born before 1945 or who grew up in a high

prevalence area such as Africa, Asia, or South America, or who have already received two vaccines in less than 5 y). A Microsoft Access database was developed to capture the data from the questionnaires. These data were then exported to Microsoft Excel where Amino acid they were cleaned and imported to STATA version 8.0 (Stata Corp., College Station, TX, USA) for analysis. During the 3-month period of the study, 730 patients were seen at our travel

clinic and all were included in the analysis. The travelers were predominantly females (57%: 414/730), with a median age of 28 years (range 15–75). Median time between the visit and the date of departure was 22 days (range 1–150), and 252 (34.5%) travelers came less than 15 days before departure, with 106 patients (14.6%) less than a week. Only three patients were immunocompromised and one woman was pregnant. The principal destinations were sub-Saharan Africa (n = 421, 57.7%), Asia (n = 150, 20.5%), and South America (n = 129, 17.7%). Eleven patients planned to travel around the world (1.5%). Median duration of travel was 4 weeks (range 1–150), with 20 trips of more than 50 weeks. Most trips were both urban and rural (n = 523, 72%) and 207 (28%) were exclusively urban, with a lower exposure to malaria. The main purposes of the trip were tourism for 521 persons (71.4%), visiting friends or relatives for 120 patients (16.4%), professional for 32 persons (4.4%), and various other reasons for 57 persons (7.8%). Among the 730 patients, 608 (83%) traveled to malaria-endemic area, including 565 to a chloroquino-resistance area (zone 3). Of 608 persons, 590 (97%) received a prescription for malaria chemoprophylaxis.

Finally the big one: global health. Increasingly global issues are on all our minds as we come http://www.selleckchem.com/products/AZD8055.html to terms with, and seek to address

issues of, health inequality not just within our own communities and nations but on a global level. Should we be spending money on expensive third-generation products, leading to ever-increasing marginal improvements in the life of perhaps only relatively small numbers of our own population, when the same expenditure on first-generation treatments could improve the lives of millions of people elsewhere? I am suggesting neither that we no longer develop new treatments or allow patients to experience their benefit, nor that there is an easy answer, but I do not think we can continually neglect this moral question. For too long we have looked at these population- versus individual-level judgements on a national level but we need to think more globally. www.selleckchem.com/products/BKM-120.html Furthermore, should we throw away unused medicines here because of a technicality, when they could save lives elsewhere? How transferable are our standards of care to other contexts and needs and should these standards be flexible and proportionate to the context and scope of the problems we are addressing? These issues I can almost certainly predict will not be answered in the next decade but hopefully our colleagues’ research efforts can

help shed light on some of these by more accurately quantifying benefit and risk and allowing informed judgements to be made. I hope the International Journal of Pharmacy Practice will contribute to the debate by publishing quality research in these as well as other areas. “
“Prison healthcare has undergone a significant transformation over recent times. The main aim of these changes was to ensure prisoners

received the same level L-gulonolactone oxidase of care as patients in the community. Prisons are a unique environment to provide healthcare within. Both the environment and the patient group provide a challenge to healthcare delivery. One of the biggest challenges currently being faced by healthcare providers is the misuse and abuse of prescription medication. It seems that the changes that have been made in prison healthcare, to ensure that prisoners receive the same level of care as patients in the community over recent times, have led to an increase in this problem. Prison pharmacy is ideally placed to help reduce the misuse and abuse of prescription medication. This can be achieved by using the skills and knowledge of the pharmacy department to ensure appropriate prescribing of medication liable to misuse and abuse. “
“Good warfarin knowledge is important for optimal patient outcomes, but barriers exist to effective education and warfarin knowledge is often poor. This study aimed to explore the educational outcomes of home-based warfarin education provided by trained pharmacists.

It has also been demonstrated that the premotor–motor interactions are very sensitive to ISIs and stimulus intensity (Civardi et al., 2001; Davare et al., 2008, 2009). It is thus possible that the PMv–M1 interactions might be shifted towards different components (latencies, activation threshold) in patients with FHD. As our study focused on investigating the role of the premotor–motor

interactions in SI at various phases of movement, the experiment even with one ISI took about 2 h. Hence, we could not test more ISIs. We decided to test the ISI that exerted the most efficient premotor–motor influence (6 ms), as shown by Davare et al. Ganetespib (2008). In order to fully define the importance of the impairment of the premotor–motor interactions in patients with FHD, more ISIs should be tested in future studies. Looking at the synergistic muscle, the current study shows that MEP amplitudes in the FDI are not modulated by stimulation of the PMv. This is probably due to the fact that PMv–M1 interactions are muscle specific (Davare et al., 2009) and are extremely sensitive DAPT cell line to the parameters of stimulation. Indeed, small variations of the conditioning stimulus intensity greatly influence the outcome (Civardi et al., 2001). As the stimulation intensities used in the current study were adjusted to RMTAPB, we cannot make clear conclusions about the effects of the paired

stimulations over the FDI. Indeed, although the FDI and APB hotspots and RMT are very close to each other, we showed that, at rest, MEPFDI was higher than MEPAPB in both groups. This difference is probably explained by a Montelukast Sodium difference in the input–output curve. Thus, a stimulation set at 80% RMTAPB might correspond to approximately 90% RMTFDI. It is then reasonable to expect significant differences in results between the FDI and APB, as it has been demonstrated that a stimulation at 90% AMTFDI over the dorsal premotor cortex could inhibit M1, whereas a stimulation set at 80 or 100% AMTFDI had no effect on the M1 (Civardi et al., 2001). As a consequence, we can only make conclusions about significant premotor–motor interactions regarding the APB muscle, a surrounding muscle, not involved in the task. Although the APB is not recruited

during this task, it is probable that this latter muscle might be under the influence of the PMv. Indeed, it has been shown that the PMv exerts an important role in hand posture and fingertip position, and elaborates the appropriate pattern of activation of intrinsic hand muscles (Ceballos-Baumann et al., 1997; Ibanez et al., 1999; Davare et al., 2006). It has also been described that the PMv plays a relevant role in visually-cued finger movements (Pollok et al., 2009; Ruspantini et al., 2011). PMv might thus play a key role in finger positioning in our task. Patients with FHD suffer from an abnormal activation pattern of the hand muscles during writing or music playing, with abnormal overflow of agonist and antagonist muscles (van der Kamp et al., 1989).

PCR was performed using Biomix (Bioline, London, UK) polymerase or HotStar HiFidelity polymerase kit (Qiagen, Crawley, UK) according to the manufacturer’s instructions with the addition of 5% DMSO. Generation of a GlnR deletion mutant and the GlnR D48A point mutation strain were performed using the recombineering method (van Kessel & Hatfull, 2007, 2008a, b). For generation of the GlnR deletion mutant, upstream and downstream sequences flanking glnR (msmeg_5784) were amplified from M. smegmatis genomic DNA by PCR as stated; primer sequences are listed in Table 2. The flanking regions were designed so as not to disrupt any neighbouring

Volasertib cost genes or introduce any downstream effects. Vector pYUB854 was used to subclone the homologous flanking sequences either side of

a hygromycin resistance (HygR) cassette (Bardarov et al., 2002). Allelic exchange sequence (AES) DNA was prepared by digesting the pYUB854_glnR construct with AflII and SpeI. Linear AES DNA (200 ng) was used to transform M. smegmatis cells containing the pJV126 recombineering plasmid (a gift from Graham Hatfull). Putative null mutants were selected on 7H11 Fluorouracil mouse agar containing hygromycin (50 μg mL−1) and kanamycin (50 μg mL−1). The GlnR_D48A point mutation was generated using M. smegmatis containing the pJV128 recombineering plasmid (a gift from Graham Hatfull). Cells were cotransformed with 100 ng of two ssDNA oligonucleotides: GlnR_Point_mut containing the base pair changes for the required glnR D48A point mutation and HygS_Repair containing the required base pair changes to convert the hygromycin resistance cassette from nonfunctional to functional (Table 2). Rebamipide This hygromycin resistance repair method was used to select colonies that had undergone recombination. A mismatch amplification

mutation assay (MAMA) PCR screen using primer pairs MAMA_PCR_F and MAMA_PCR_R was performed to identify glnR containing the desired point mutation (Cha et al., 1992; Swaminathan et al., 2001). MAMA PCR conditions were: 95 °C for 5 min, 39 cycles of 95 °C for 15 s, 32 °C for 1 min, with final extension time of 72 °C for 7 min. Recombineering plasmids were removed from both mutant strains via negative sacB selection (Pelicic et al., 1996). Confirmation of a GlnR D48A point mutation was carried out by amplifying the entire glnR genomic region using primer pairs GlnR_reg_F and GlnR_reg_R with high fidelity polymerase, and sequencing the glnR gene with GlnR_D48A_SeqF and GlnR_D48A_SeqR (Table 2). Confirmation of GlnR deletion was carried out by PCR using primers outside the upstream and downstream flanking regions in combination with hygromycin cassette–specific primers (Table 2). PCR products would only be obtained with insertion of the hygromycin cassette by recombination onto the chromosome at the correct location. Further confirmation of GlnR deletion phenotype was provided by Western analysis using a custom-made GlnR polyclonal antibody (Eurogentec, Seraing, Belgium).

These anatomical results are exciting because they support functional hypotheses such as the dual stream model, proposing that one circuit (area 6) allows mapping of acoustic speech sounds selleck inhibitor to articulatory acts, whereas a more ventral circuit links lateral temporal areas for speech comprehension with Broca’s area (Hickok & Poeppel, 2004). The mapping of speech sounds to articulatory acts in area 6 may be a human homologue to the mirror neuron network, as mirror neurons responding to both the perception and generation of actions are found in monkey homologues of area 6 (Rizzolatti et al., 1996) and the human anterior supramarginal gyrus (Fogassi

et al., 2005). These data linking human and primate anatomy have an important impact on our understanding of the Selleckchem Linsitinib circuits for language processing. “
“Cholinergic inputs to the auditory cortex can modulate sensory processing and regulate stimulus-specific plasticity according to

the behavioural state of the subject. In order to understand how acetylcholine achieves this, it is essential to elucidate the circuitry by which cholinergic inputs influence the cortex. In this study, we described the distribution of cholinergic neurons in the basal forebrain and their inputs to the auditory cortex of the ferret, a species used increasingly in studies of auditory learning and plasticity. Cholinergic neurons in the basal forebrain, visualized by choline acetyltransferase and p75 neurotrophin receptor immunocytochemistry, were distributed through the medial septum,

diagonal band of Broca, and nucleus basalis magnocellularis. Epipial tracer deposits and injections of the immunotoxin ME20.4-SAP (monoclonal antibody specific for the p75 neurotrophin receptor conjugated to saporin) in the auditory cortex showed that cholinergic inputs originate almost CYTH4 exclusively in the ipsilateral nucleus basalis. Moreover, tracer injections in the nucleus basalis revealed a pattern of labelled fibres and terminal fields that resembled acetylcholinesterase fibre staining in the auditory cortex, with the heaviest labelling in layers II/III and in the infragranular layers. Labelled fibres with small en-passant varicosities and simple terminal swellings were observed throughout all auditory cortical regions. The widespread distribution of cholinergic inputs from the nucleus basalis to both primary and higher level areas of the auditory cortex suggests that acetylcholine is likely to be involved in modulating many aspects of auditory processing. “
“The structure and function of the central nervous system strongly depend on the organization and efficacy of the incoming sensory input. A disruption of somesthetic input severely alters the metabolic activity, electrophysiological properties and even gross anatomical features of the primary somatosensory cortex.

Around 20 pieces of each section of root were examined for each of the five plants from each ecotype– soil combination (i.e. approximately 60 root pieces per plant). DNA was extracted from approximately 0.5 g freeze-dried and ground root material (one root system for each ecotype–soil combination) as described by Ward et al. (2005). Polymyxa-specific rDNA primers Pxfwd1 (5′-CTG CGG AAG GAT CAT TAG CGT T-3′) and Pxrev7 (5′-GAG GCA TGC TTC CGA GGG CTC T-3′) were used in PCR (Ward & Adams, 1998). Plasmodiophora-specific PCR was performed as

in Cao et al. (2007) using primers TC1F/TC1R. For sequencing drug discovery studies, the Polymyxa-specific forward primer Pxfwd1 and the generic fungal ITS4 reverse primer (5′-TCC TCC GCT TAT TGA TAT GC-3′) (White et al., 1990) were used to amplify rDNA. AZD8055 in vivo Each reaction mix (50 μL) contained 0.2 μM primers, 1 U Taq DNA polymerase (MBI), 0.2 mM dNTPs (Sigma), 1 × PCR buffer NH4 (MBI) and 0.02 mg μL−1 bovine serum albumin. Cycling conditions were 2 min at

95 °C, and then 30 cycles of 94 °C for 30 s, 50 °C for 1 min and 72 °C for 2 min, followed by 72 °C for 10 min. Products were analysed in 1% agarose gels. PCR products were cloned into the pGEM®-T Easy vector (Promega Corporation, Madison, WI). Plasmid DNA was prepared using the QIAprep spin miniprep kit (Qiagen, Crawley, UK) and sequenced using the ABI PRISM™ Big-Dye version 1.1 kit using M13 sequencing primers and run at the Geneservice sequencing facility (http://www.geneservice.co.uk). ITS rDNA sequences were aligned by clustalx and manually adjusted. Phylogenetic analysis was performed using the neighbour-joining method (maximum composite likelihood distances) in mega4 (Tamura et al., 2007) with 10 000 bootstrap replications. Examination by microscopy showed the presence of Polymyxa-like spores in numerous root hairs (but not the main root) of all five Arabidopsis ecotype Ler-0 plants grown in the Woburn soil (Fig. 1). Two of the Col-0 plants grown in the Woburn soil contained structures that resembled Polymyxa zoosporangia (Fig.

2). Three of these structures were seen in total and they were all located in the main root system rather Osimertinib order than the root hairs. No spore clusters were observed. In the root sections examined from Arabidopsis plants grown in the Wiltshire soil, no clusters of Polymyxa-like resting spores or zoosporangia were identified. PCR with the Polymyxa-specific primers Pxfwd1/Pxrev7 demonstrated the presence of Polymyxa spp. in the roots of all four combinations of Arabidopsis ecotypes and soils (Fig. 3). Using a Plasmodiophora-specific PCR assay, we also demonstrated that Plasmodiophora was not present in these samples (Fig. 3). A total of 28 clones were sequenced following the amplification of rDNA products from Arabidopsis roots using primers Pxfwd1/ITS4.

4). When the mice were immunized with SEZ ΔhasB, there was an absence of antibody elicited against capsid protein (0.135 ± 0.007) but a high-level antibody response with the inactive PCV2 vaccine (1.204 ± 0.157). A significant level of antibody (0.629 ± 0.116) could be induced by the recombinant strain compared with the AZD6244 datasheet negative control, indicating that the cap gene was expressed during the course of

immunization. Diseases associated with PCV2 infections are becoming a major problem for the swine industry worldwide. Commercially available and currently developed vaccines focus on the Cap protein, and these include DNA vaccines (Kamstrup et al., 2004; An et al., 2008) and virus-vectored vaccines (Ju et al., 2005; Wang et al., 2007; Fan et al., 2008a). However, producing a sufficient amount of DNA/viral for vaccine development is relatively expensive. To overcome this problem, heterologously expressing Cap protein through attenuated swine pathogenic bacteria is an attractive route: it is cost effective compared with DNA/viral vector-based

vaccines, and the swine bacterial vector benefits selleck inhibitor the recombinant strain against other bacterial infection simultaneously compared with yeast (Bucarey et al., 2009) and Lactococcus lactis (Wang et al., 2008) vectors. Kim et al. (2009) used an aroA mutant of Bordetella bronchiseptica, which efficiently colonized ciliated respiratory mucosa of pigs, as a live vaccine vehicle for Cap protein expression. Results in mice and pigs showed that this bacterial vehicle could elicit an immune response against Cap protein and was effective in preventing PCV2 multiplication in pigs. Unfortunately, the kanamycin-resistant gene used for mutant selection was still present in the B. bronchiseptica

genome, limiting its spread in the field. The SEZ-Cap recombinant stain was a more promising vaccine candidate. Therefore, SEZ rather than B. bronchiseptica coincident with PCV2 plays an important Tacrolimus (FK506) role in respiratory infection development in the swine industry (Metwally et al., 2010), and the recombinant strain was constructed without any resistant marker. In addition, the Cap protein was stably expressed on SEZ at transcriptional and translational level both in vitro and in vivo. Real-time PCR showed that the cap gene could transcript at the same level as the substitutive szp gene, either in TSB culture or during the course of infection in mice. FACS and immunofluorescence microscopy analysis demonstrated that Cap protein could be displayed on the surface of SEZ. Almost all SEZ-Cap immune sera showed a higher S/P value than negative sera assessed by enzyme-linked immunosorbent assay, which indicated that the Cap protein was expressed in vivo and most individuals were able to mount an immune response against this protein. The two conditions above were indispensable to a successful vaccine.

21kPa. Diabetic ketoacidosis was diagnosed and treated

according to hospital guidelines. Over the next six hours, the patient’s symptoms rapidly improved. At the time of diagnosis of DKA, cardiotocograph (CTG) monitoring was pathological with reduced baseline variability which returned to normal within 24 hours of initiation of DKA treatment. Following treatment of DKA, bicarbonate level rose to 17mmol/L and remained at this LGK-974 order level until delivery, two weeks later. The patient went into spontaneous labour; however, in view of the suspected macrosomia, she underwent an uncomplicated lower segment caesarean section resulting in the delivery of a live female weighing 4.34kg with APGAR scores of 8, 9 and 10 at 1, 5 and 10 minutes, although the cord pH was 6.9. The baby had severe neonatal hypoglycaemia, with blood glucose 1.5mmol/L, necessitating admission to the neonatal intensive care unit and treatment with intravenous dextrose for 48 hours. The patient had a six-week postpartum OGTT which showed impaired glucose tolerance with a fasting glucose of 3.9mmol/L and a two-hour glucose of 9.3mmol/L. Both mother and child were well at last contact. This case highlights the fact that Y-27632 datasheet women with GDM are at risk of developing DKA in later pregnancy. Recognised risk factors for DKA in pregnant patients with T1DM include infection, vomiting, treatment non-compliance, new onset diabetes, insulin pump failure,

corticosteroids and beta-adrenergic drugs.1,3 The likely precipitant in this case of GDM was administration of corticosteroids. The use of steroids in patients Farnesyltransferase with DM is associated with a significant worsening of glycaemic

control for up to 48 hours after steroid administration.6 In pregnant women with DM who receive antenatal steroids, blood glucose control can be achieved with additional insulin, either calculated according to prior insulin requirements or via an insulin sliding scale.6,7 Venous glucose at diagnosis of DKA may be considerably lower in pregnant than in non-pregnant women. In one case-control study the blood glucose levels were compared in 90 pregnant and 286 non-pregnant females at diagnosis of DKA, and were found to be significantly lower in pregnant women with DKA: 16.3±4.6 and 27.5±4.8mmol/L (mean±SD), respectively.8 The reduced glucose level at presentation of DKA in pregnant women with DM, as in this case, may present diagnostic difficulties. All patients with DM, including those with GDM, who are unwell or present with any combination of nausea, vomiting or reduced calorific intake, should be assessed for the possibility of DKA9 with serum urea and electrolytes, venous blood gases and testing of blood or urine for ketones regardless of blood glucose readings. Acid-base balance in pregnancy is characterised by a physiological hyperventilatory response leading to a primary respiratory alkalosis.

Such counseling should theoretically include explanations about the complications of severe malaria, the importance of bite avoidance behavior, and the safety of the regimens approved for long-term chemoprophylaxis. The association between not using chemoprophylaxis

and an elevated risk of acquiring malaria did not reach statistical significance, probably due to the Panobinostat purchase small sample size. Similarly the lack of association between complying with strict bite avoidance behavior and the risk of acquiring malaria is explained by the generally poor compliance with such measures. This study has several important limitations. By and large, the study sample was too small to detect a protective effect of chemoprophylaxis and mosquito avoidance behavior. In addition, the results of the study apply only to long-term travelers with low compliance to malaria prevention

guidelines. Despite these limitations, a new risk factor for contracting malaria has been detected. A large prospective observational study of malaria incidence in modern apartment buildings in sub-Saharan Africa seems warranted. The authors would like to thank Professor Peleg Levi for his valuable remarks. The authors state they have no conflicts of interest to declare. “
“Both the Editorial Office and the entire Editorial Board are most grateful to all of you for having devoted time and energy to our Journal. Your thorough and timely reviews are the cornerstone of JTM. We hope to be able to benefit from your continued support also in future. Eric

Caumes, Editor-in-Chief; Gaby Bossard, Editorial Assistant Abaya PLX-4720 cost Antonio R. Aerssens Annelies Airault Regis Alexander James L. Alves Jesse R. Anderson Susan Andremont Antoine Antinori Spinello Apelt N. Arguin Paul M. Arya Subhash C. Backer Howard Bailey Sarah Lou Barnett Elizabeth D. Bartoloni Alessandro Basnyat why Buddha Bauer Irmgard L. Beadsworth Mike Behrens Ronald H. Bellanger Anne-Pauline Benabdelmoumen Ghania Bishai Daniel M. Bisoffi Zeno Blacksell Stuart D. Boggild Andrea Bottieau Emmanuel Bouchaud Olivier Boulware David R. Boussinesq Michel Braks Marieta Bridger Natalie Brunetti E. Bruschi Fabrizio Brouqui Philippe Buhl Mads Bui Yen-Giang Burchard Gerd-Dieter Burnett Joan C.D. Burtscher Martin Carabello Laura Cartwright Rodney Castelli Francesco Charrel Remi Chatterjee Santanu Chen Lin H. Chlibek Roman Chowell Gerardo Chunge Ruth Clerinx Jan Connor Bradley A. Corkeron Michael Corti Giampaolo Coskun Omer Cottle Lucy E. Croughs Mieke Czerwinski Steven E. Da Rocha Felipe F. Dance David D’Ardenne Patricia De Paula Vanessa De Valliere Serge Debes Jose Delaunay Pascal Derancourt Christian Dobler Gerhard Domingo Cristina Dowdall Nigel DuPont Herbert L. Durham Melissa J. Edelson Paul Enander Richard Epelboin Loic Ericsson Charles Esposito Doug Ezzedine Khaled Feldmeier Hermann Fenner Peter J. Field Vanessa Fielding James E.