Uczucie dyskomfortu w jamie brzusznej (nieprzyjemne uczucie nieopisywane jako ból) lub ból spełniający co najmniej 2 z poniżej wymienionych warunków przez minimum 25% czasu: – poprawa po defekacji, W porównaniu z II kryteriami rzymskimi skrócono czas niezbędny do rozpoznania zespołu z 3 do 2 miesięcy, co pozwala na szybsze ustalenie rozpoznania i wcześniejsze włączenie leczenia [1]. Zespół jelita nadwrażliwego jest jednym z najczęstszych zaburzeń czynnościowych przewodu pokarmowego. selleck monoclonal humanized antibody W krajach zachodnich jego

występowanie ocenia się na 15–20% populacji młodocianych i dorosłych [2]. Objawy chorobowe najczęściej pojawiają się w okresie od dojrzewania do 30 roku życia [3]. W populacji wieku rozwojowego zespół jelita nadpobudliwego jest rozpoznawany rzadziej niż u dorosłych. Hyams i wsp. [3] stwierdzili występowanie IBS u 8% uczniów klas szkół średnich (średni wiek 12,6 lat) z nawracającymi bólami brzucha w wywiadzie. Statystycznie częściej chorują kobiety (stosunek kobiet do mężczyzn wynosi 2,5:1) [4]. Etiopatogeneza zespołu jelita drażliwego jest złożona i nie została dotychczas dokładnie wyjaśniona. W piśmiennictwie zwraca się uwagę na nieprawidłową motorykę jelit oraz zaburzenia czucia trzewnego (nadwrażliwość trzewna)

[5]. Osimertinib price Zaburzenia motoryki jelit są spowodowane nieprawidłowym uwalnianiem enterohormonów i neuroprzekaźników oraz wadliwą czynnością mięśni gładkich jelita. U pacjentów z rozpoznanym zespołem jelita wrażliwego skurcze odcinkowe jelit występują częściej i są dłuższe niż u osób zdrowych. Czynnikami predysponującymi do rozwoju choroby są uwarunkowania genetyczne oraz silne przeżycia emocjonalne. Zaostrzenie dolegliwości klinicznych obserwuje się pod wpływem stresu, błędu dietetycznego, infekcji, procesów zapalnych, urazu oraz substancji drażniących śluzówkę jelita (laktozy, fruktozy, kwasów żółciowych, alergenów pokarmowych). Do rozpoznania zespołu jelita drażliwego u dzieci konieczne jest spełnienie 3 warunków: 1. Wywiad kliniczny odpowiadającej III kryteriom rzymskim, Zespół jelita nadpobudliwego

u dzieci charakteryzuje Inositol monophosphatase 1 się występowaniem nawracających czynnościowych bólów brzucha oraz zmianami w częstości i konsystencji oddawanych stolców. Bóle brzucha mają różną lokalizację, ale typowo umiejscowione są w prawym lub lewym podbrzuszu [6]. Wykazują one różne nasilenie i przerywany charakter. Dzieci skarżą się na dolegliwości bólowe brzucha głównie w dzień, często 60–90 minut po posiłku. Oddanie gazów lub stolca znacznie zmniejsza natężenie bólu. Do objawów klinicznych mogących wskazywać na zespół jelita nadwrażliwego u dzieci należą [7]: – nieprawidłowa częstość oddawania stolców (więcej niż 3 wypróżnienia dziennie lub mniej niż 3 wypróżnienia tygodniowo), Ze względu na charakter oddawanych przez pacjenta stolców wyróżnia się 3 postacie choroby (biegunkową, zaparciową i mieszaną). Zespół jelita nadpobudliwego ma charakter przewlekły i przebiega z okresami zaostrzeń i remisji.

g. Fox et al., 2012b). We stress that this can only be

achieved through urgently needed open political and scientific communication and collaboration, in which quantity, proportions and quality of marine environments are considered when proposing MPAs. We thank Mike Beck and James J. Roper for suggestions and corrections to the text. This study was supported by FAPESP (2010/52324-6; 2011/50242-5), CNPq (562143/2010-6, 563106/2010-7, 477156/2011-8) and CAPES, and is a contribution of the Research Center on Marine Biodiversity of the University of São Paulo. “
“Outbreaks of GSK2118436 clinical trial the crown-of-thorns starfish, Acanthaster planci, represent one of the most significant biological BKM120 cell line disturbances on coral reefs ( Kayal et al., 2012). Despite recent increases in the prevalence of climate induced coral bleaching and coral disease ( Yakob and Mumby, 2010), outbreaks of A. planci remain one of the principal causes of coral loss in the Indo-Pacific ( Rivera-Posada et al., 2012). On Australia’s Great Barrier Reef (GBR), for example, it is estimated that 40% of coral loss recorded over the last 27 years is due to reef-wide outbreaks of A. planci ( De’ath et al., 2012). Given widespread declines in coral cover ( Bellwood et al., 2004 and Bruno and Selig, 2007) and associated degradation of coral reef ecosystems ( Pratchett et al.,

2009), there is an urgent need to identify immediate and practical interventions that will reduce or reverse sustained declines in coral cover. Outbreaks of A. planci, rank alongside climate change, severe tropical storms and increasing prevalence of coral disease, as one of most significant threats to coral reefs ( De’ath et al., 2012), but of these threats, outbreaks of A. planci are probably the only threat that is amenable to direct intervention. In the last few decades, it is estimated that >17 million starfishes have been killed or removed from coral reefs in the Indo-Pacific ( Pratchett et al., 2013). Control measures have been costly, largely ineffective, and often involved dangerous side effects. Currently

the most efficient technique to kill A. planci is to inject individual sea stars with lethal doses of chemicals. A variety of chemicals have been used since 1960s to control A. PLEK2 planci but are noxious to the marine environment. For example, formaldehyde (CH2O) is well known for his flammable, explosive, and carcinogenic properties; copper sulfate (CuSO4) is highly toxic to fish and aquatic invertebrates, such as crabs, shrimps, and oysters ( Yanong, 2010). Sodium hypochlorite (NaClO), ammonia (NH3), ammonium hydroxide (NH4OH) and many other toxic organic solvents have been also used in past control efforts ( Birkeland and Lucas, 1990 and Harriott et al., 2003). Sodium bisulfate is currently considered the best option to kill COTS in situ.

The initial workshop to generate the ideas for this paper took place in Brisbane, Australia, July 2012, with joint financial support from Institute for Water, Environment & Health, United Nations University (UNU-INWEH) and the Global Change Institute, University of Queensland. PFS thanks Lisa Benedetti, UNU-INWEH for help in planning and running the workshop, and helping with

the subsequent flow of communication among selleck products authors. “
“The continuing degradation of coral reefs around the world (Bruno and Selig, 2007, De’ath et al., 2012 and Gardner et al., 2003) has serious consequences for the provision of ecosystem goods and services to local and regional communities. While climate change is considered the most serious risk to coral reefs around the world, agricultural pollution threatens approximately 25% of the total global reef area (Burke, 2011) (Fig. 1). To ensure the future of coral reefs, the 2012 Consensus Statement on Climate Change and Coral Reefs has called for the immediate management of local anthropogenic pressures including reducing land-based pollution (12th International Coral Reef Symposium, 9–13 July 2012). Attempts are being made to reduce land-based pollution to coral reefs (Brodie et al., 2012 and Richmond

et al., 2007), however, these efforts are impeded by a current Alectinib datasheet paucity of studies demonstrating whether improvements check details to coral reef health are realized following watershed management. For the next 50 years, riverine fluxes of sediment, nitrogen (N) and phosphorus (P) to tropical coastal areas are projected to increase (Mackenzie et al., 2002). It is therefore timely to inform coral reef policy using insights gained from global cases that were successful in reducing agricultural pollution to coastal ecosystems. Here, we synthesize successful examples of reduced agricultural pollution that could be used as a model to improve coral reef

water quality, with the assumption that improved water quality will result in a concomitant improvement in ecological health of coral reefs. Previous reviews of the problem of coastal eutrophication (Boesch, 2002 and Cloern, 2001) do not include recent reports on reduced fluxes of sediment and nutrients at end-of-river (Chu et al., 2009, Duarte et al., 2009, GEF-UNDP, 2006, Pastuszak et al., 2012, Stålnacke et al., 2003 and Windolf et al., 2012), and associated declines in nutrient concentrations and algal biomass in receiving coastal waters (Carstensen et al., 2006, Duarte et al., 2009, Jurgensone et al., 2011 and Oguz and Velikova, 2010). Our review focuses on restoration of diffuse fluxes of freshwater, suspended sediment, and nutrients, while acknowledging the presence of other pollutants (e.g. pesticides, herbicides and heavy metals) and their potential impact on coral reef resilience (Van Dam et al., 2011).

Recently, further evidence was provided for the involvement of APOBEC3B in human cancers, as its expression was elevated in tumours compared to their matched normal samples [ 88 and 89]. By comparing the substitution patterns

of all signatures with experimental data, one of the mutational signatures was associated with exposure to ultraviolet light while another with benzo[a]pyrene, a known tobacco carcinogen. The signature associated with UV-light exhibited a higher presence of CC > TT dinucleotide substitutions as well as a strand bias indicative of the formation of photodimers, which further confirmed the association. In contrast, a mutational signature associated in lung cancer exhibited predominantly C > A LGK-974 ic50 mutations with a transcriptional strand bias suggesting the formation of bulky adducts on guanine. Interestingly, this mutational signature was also associated with CC > AA dinucleotide substitutions with a strong strand

bias. Statistical tests comparing smokers with non-smokers in two cancer types (viz. lung adenocarcinoma and tumours of the head and neck) confirmed a highly significant elevation of this ‘tobacco smoking signature’ in smokers indicating that it was due to tobacco mutagens. Further statistical analysis was performed to associate mutations in genes with the presence of mutational signatures. Distinct mutational signatures 5-Fluoracil order were associated with: mutations in BRCA1/2 in breast and pancreatic cancers; failure of the DNA mismatch repair pathway (e.g. due to methylation of the MLH1 promoter) in colorectal cancers; hypermutation of the immunoglobulin gene in CLL; recurring polymerase ɛ mutations in uterine and colorectal cancers. Interestingly, the mutational signature associated with failure of DNA mismatch repair was observed in nine different cancer types. While this process was operative in ∼20% of colorectal cancers and ∼15% of uterine cancers, it was also found in at least 1% of cancer samples in another seven cancer types. Another interesting

observation was that while almost all BRCA1/2 mutants exhibit a specific mutational signature, there were also BRCA1/2 wild-type samples with high number of mutations due to this mutational process. Thus, it is possible that some BRCA1/2 wild-type samples might harbour somatic mutations or other abnormalities ifoxetine that result in a failure of homologous repair and activation of this mutational process. Chemotherapy treatment could cause its own set of somatic mutations [24]. Examining the pre-treatment history of all 7 042 cancer samples revealed that melanomas and glioblastomas pre-treated with an alkylating agent exhibit a distinct mutational signature. The performed global analysis was able to propose an association for 11 of the 22 validated mutation signatures, while the origins and aetiology of the other 11 mutational signatures remains unknown.

The reasons for participation articulated here appear prima facie to have clear implications for how participants respond to their allocated study condition. SRT1720 datasheet The lack of fit between reasons for participation (to access to new forms of help) and the content of the control condition (usual care) explains the thwarted preference and disappointment in this trial, but not participants’ reactions to their

disappointment. This is important in relation to possible performance bias, which is concerned with unintended aspects of the conduct of the study. The origins of the reactions captured here lie implicitly within the design of the trial itself, where there is potential for conflict between reasons for participation which involve preferences and the outcome of randomization. It is find more a moot point whether performance bias is the most appropriate conceptualization of this problem, yet these reactions do deserve to be recognized as a distinct source of bias. This is because they lead the randomized groups to differ in ways other than the intended experimental contrast. It may be that a conceptualization is needed that distinguishes

unintended differences between groups in how participants are treated in the conduct of the trial (performance bias) from systematically different reactions between randomized groups to identical trial procedures. A different definition of performance bias that is

not restricted to how participants are treated by the study may be useful, and more fine grained attention to how participants react to what they are asked to do in research, and how this may impact on study outcomes, is needed. The possible direction and magnitude of bias is important to consider. In this trial, there was some evidence of small differences in outcomes, though not in the primary outcome of weight loss Abiraterone in vivo [21]. Inferences about effectiveness in studies which find differences between groups must take account of the possibility that the types of reactions described here may be responsible for some of these differences if it seems possible or likely that disappointment may be involved. Compensatory rivalry responses to the outcome of randomization may attenuate differences between groups and resentful demoralization may exaggerate them, so the former are particularly worth considering where there are null findings. In this study, we saw evidence of both, and there is thus no strong evidence that trial findings are systematically biased in this instance. Usual care or standard practice is a very common control condition. Indeed, it is the standard against which innovations should be assessed for ethical as well as methodological reasons, hence its incorporation into the Helsinki Declaration [29].

Some aspects of this issue have been previously studied in the British literature. Attanoos et al., studied phraseology in surgical reports and communication of uncertainty between surgeons and pathologists at the University Hospital Wales [3]. Galloway and Taiyeb examined the interpretation of phrases used to describe uncertainty amongst pathologists, other doctors, and medical students click here online and at the University College London Medical School

[4]. In both of these studies, akin to our findings, there was wide variance in the interpretation of phrases between the groups studied. They similarly concluded adoption of a limited number of descriptive phrases that are mutually understood and accepted by both pathologists and clinicians is needed to avoid ambiguity in surgical pathology reports. An additional study addressed the need for uniformity in reporting cancer for the British National Cancer Registry [5]. In his 2000 commentary on individuality in surgical pathology,

Dr. Foucar aptly concluded, “…There is no place for the pathologist who expresses individuality by subjecting unsuspecting patients to uncontrolled diagnostic self-expression” [6]. Although a clear consensus solution, either at our institution or among our colleagues elsewhere remains elusive; we have reached several important conclusions. Like the British studies, communication PD0325901 cost of uncertainty indeed is a common practice and an unexamined source of possible medical error in the United States. We plan to study this possible relationship more fully. Our own anecdotal experience in tumor boards and an array of practice settings have provided several “near miss” examples,

and more than a few needless repeat biopsies or other procedures due to cautiously worded reports with these phrases. Further study is needed to further refine the specimens and diagnostic settings in G protein-coupled receptor kinase which diagnostic uncertainty is most commonly expressed in order to encourage improved diagnostic criteria and provide better follow-up guidance when such are not fully present and an uncertainty phrase mandated. Additionally, it would be helpful to be able to calculate the possible cost to the health care system due to repeat biopsies in specific cases. Secondly, action needs to be taken to address the issue of the gap between uncertainty intention and perception at least locally and preferably at a national level. An interesting trend appears to be emerging from both our discussion at our institution and those at the national meeting: more recently trained pathologists more fully support national guidelines on terminology while more senior pathologists tend to resist this loss of individuality in reporting. In this and so many other aspects, it will be fascinating to see where the new generations of pathologists take our field.

According to the data obtained, the inhibition of 506 siRNA was 39.2%, while those of 859 siRNA and 891 siRNA were 89.4% and 54.1%, respectively (Fig. 6). The best interference effect was observed on 859 siRNA, up to 89.4% of inhibition rate. Ishii et al. [10] reported that MeWo fibroblast cell (BCRC 60540), a kinds of human melanoma cells, can express spontaneously the endogenous

AZD2281 solubility dmso MMP1 protein, and the expression quantity could be enhanced by exposure to nitric oxide (NO) or S-nitroso-N-acetyl-dl-penicillamine (SNAP) in a dose-dependent manner. Therefore, the MeWo cells were employed as target cells in quantitative PCR and western blot analysis to investigate whether the evaluation of effective designed siRNAs by the GFP reporter systems was able to interfere with the expression of MMP1 mRNA or protein. According to the results of preliminary experiments, Fig. 7 and Fig. 8, , the expression quantity and the siRNA interfering efficiency of endogenous mRNA or protein of MMP1 in MeWo cells without induction by NO or SNAP was visible in the blanks (without siRNA treatment). Accordingly, the MeWo cells used in this study were not treated with NO or SNAP to

avoid influence by other factors. selleck chemicals llc To confirm the interference efficacy of siRNAs against endogenous MMP1 gene expression in MeWo cells, the quantitative PCR (real-time PCR) was prepared. The MeWo cells were transfected with various concentrations (10, 30, 50, 70 or 90 nM) of 506 siRNA, 859 siRNA and 891 siRNA, separately. The total RNA was extracted and cDNA were synthesized as described in the methodology. The remained MMP1 mRNA was analyzed by real-time quantitative polymerase chain reaction (RT-PCR) and agarose gel electrophoresis analysis. According to the results of preliminary experiments, when the concentration of any one of the three

designed siRNAs was higher than 100 pmol, the interference efficacy was not consistent and had high standard deviation between repetitive experiments (data not shown). This might be attributed to short half-life and instability of siRNAs. The phenomenon was similar to [11], they had suggested that when the concentration of siRNA was higher than 100 nM, it could cause off-target http://www.selleck.co.jp/products/BafilomycinA1.html effect, resulting in the error judgments of the experimental results, so in this study, all the concentration of siRNA used in different tests was ranged from 10 to 90 nM. As shown in Fig. 7, the endogenous MMP1 mRNA could be interfered with 506 siRNA and 859 siRNA, but the interference efficacy of various concentrations of siRNAs on endogenous MMP1 gene expression were not dose-dependent. The inhibition rates of 506 siRNA and 859 siRNA against endogenous MMP1 gene expression were 55% and 85%, respectively (Fig. 7).

Although the Dat1-cocaine insensitive mice exhibit hyperactivity, their locomotor activity and responses to amphetamine are dependent

on their genetic background [24], suggesting a crucial role of gene–gene interactions for these phenotypes. Other phenotypes relating to attention and impulsivity in these mice have not been documented. Although genes encoding DA receptors are classic candidates for ADHD, experimental evidence from Drd1, Drd2, Drd3, Drd4, and Drd5 KO mice for these genes affecting ADHD-relevant endophenotypes is weak [25•]. Interesting results were reported for Drd4-heterozygous mice [26]. Young et al. applied a 5-choice continuous performance test (5C-CPT), which is a modification of the 5-choice serial reaction time test (5CSRTT) [27] that may more closely correspond to the CPT used in humans [28]. In the 5C-CPT, rodents must continue to respond to signal stimuli (illumination of any 1 of 5 holes), buy Fasudil and must also inhibit their response to non-signal stimuli (simultaneous illumination of all 5 holes). Heterozygous but not homozygous Drd4-KO mice

exhibited attention deficits in the 5C-CPT [26]. High impulsivity was also measured by false alarms but not by premature responses. The mice showed no deficits in Afatinib mw PPI or spontaneous exploratory behavior. It is plausible that the complete lack of D4 receptors leads to a robust compensatory system(s) at the molecular and/or neural circuit levels. Interactions of the gene with

other genetic or environmental factors require further evaluation. Recent works for catechol-O-methyltransferase (COMT)-KO mice support the notion that gene–environment interactions and gene–gene interactions are involved in attention and impulsivity domains 29•• and 30••]. COMT methylates and inactivates DA. In the 5CSRTT, male and female COMT+/+,+/− and COMT−/− mice equally acquire the task. Interestingly, environmental factors induced genotype-sex interactions in the task. For example, a mild stress (15 min exposure in an empty cage at ∼800 lx before test) increased impulsive premature responses in COMT+/− Clomifene and −/− males, but not in females [29••]. In contrast, females, but not males, exhibited genotype differences in perseverative responses. COMT−/− females showed perseverative responses at a lower rate compared to other genotypes [29••]. Differential effects of various stimuli are consistent with the sex difference in ADHD prevalence [1]. DTNBP1 (dysbindin) is a molecule that has a role in homeostasis of excitatory synapses [31]. C57BL6/J congenic COMT+/− and −/− males and C57BL6/J congenic Dtnbp1+/− and −/− males learn the T-maze working memory task, which demands a high level of attention, faster than wild-type mice. In contrast, double mutants (double heterozygotes and homozygotes) learn slower than wild-types [30••]. Although Papaleo et al.

22, 23 and 30 High-threshold splanchnic nociceptors were investigated in intact colonic preparations and in those where the mucosa had been removed. Mice received an enema of either saline or linaclotide (1000 nM). Five minutes TSA HDAC datasheet later, under anesthesia, a 4-cm CRD balloon catheter was inserted transanally into healthy or CVH mice.26 After regaining consciousness, CRD was performed (80 mmHg for 10 seconds, then deflated for 5 seconds and repeated 5 times). After sacrifice via anesthetic overdose, mice underwent fixation by transcardial

perfusion and the thoracolumbar (T10−L1) spinal cord was removed and cryoprotected. Frozen sections were cut and incubated with monoclonal rabbit anti−phosphorylated MAP kinase ERK 1/2 (pERK) with AlexaFluorR488 used for visualization. Quantitative polymerase chain reaction was performed using mouse-specific Gucy2c and glyceraldehyde-3-phosphate dehydrogenase Taqman probes on complementary DNAs synthesized from total RNAs extracted from a panel of mouse tissues. For in situ hybridization, sections were hybridized overnight at 55°C with either 35S-labeled complementary RNA anti-sense or sense probes

to Gucy2c. Cells were grown in monolayers and stimulated for 1 hour with linaclotide (1000 nM) in the presence or absence of the cGMP transporter inhibitor probenecid (0.5 mM or 2 mM). Samples from the basolateral chambers were collected and cGMP concentrations determined by liquid chromatography

mass spectrometry. Electrical field stimulation was applied to colonic tissues in the presence and absence of linaclotide Fluorouracil order or membrane permeable 8-bromo-cGMP. Contraction amplitude was compared between each condition. The current results are from a post-hoc efficacy analysis of a phase III, double-blind, parallel-group, placebo-controlled trial that randomized 805 IBS-C patients to placebo or 290 μg oral linaclotide once daily for a 26-week treatment period. The current efficacy Coproporphyrinogen III oxidase analysis are based on a responder end point for abdominal pain, specified as part of a co-primary end point recommended in the May 2012 US Food and Drug Administration final guidance for industry on the clinical evaluation of products for IBS,28 defined as a ≥30% improvement from baseline in average daily worst abdominal pain score.28 We present, for the first time, an evaluation of this abdominal pain responder end point for each week of the 26-week treatment period, comparing treatment and control groups. We hypothesized that linaclotide reduces abdominal pain in IBS-C patients17 via an inhibitory action on colonic nociceptors. In order to test this hypothesis in mice, we performed in vitro single-unit afferent recordings. First, we investigated if linaclotide affected the mechanosensitivity of colonic nociceptors from healthy mice.

Entomological Society of America Annual Meeting 13–16 November Reno, NV, USA ESA, 9301 Annapolis Rd., Lanham, MD 20706-3115, USA Fax: 1-301-731-4538 E-mail: [email protected] Web: http://www.entsoc.org 33rd CONGRESO NACIONAL DE ENTO-MOLOGIA y 1st CONGRESO SUDAMERICANO DE ENTOMOLO-GIA 30 November–02 December La Serena, CHILE Info: http://tinyurl.com/44hhr66. 3rd CONGRESO LATINOAMERICANO DE ARAC-NOLOGIA, Montenegro, Quindio, COLOMBIA 04-09 December www.iiicla.org. 2012 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 Selleckchem Trichostatin A 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 7th INTERNATIONAL IPM SYMPOSIUM 2012 – March USA, in planning phase E. Wolff E-mail: [email protected] VI INTERNATIONAL WEED SCIENCE CONGRESS 17–22 June Dynamic Weeds, Diverse Solutions, Hangzhou, CHINA H.J. Huang, IPP, CAAS, No. 2 West

Yuanmingyuan Rd., Beijing 100193, CHINA Fax/voice: GSK126 clinical trial 86-10-628-15937 E-mail: [email protected] Web: www.iwss.info/coming_events.asp *2nd INTERNATIONAL SYMPOSIUM–TEPHRITID WORKERS OF EUROPE, AFRICA, AND THE MIDDLE EAST 03–06 July Kolymbari, Crete, GREECE. Info: N.

Papadopoulos E-mail: [email protected] Web: www.diptera.info/news.php 2013 INTERNATIONAL HERBICIDE RESISTANCE CONFERENCE 18–22 February Perth, AUSTRALIA S. Powles, AHRI, School of Plant Biol., Univ. of Western Australia, 35 Stirling Hwy., Crawley, mTOR inhibitor Perth 6009, WA, AUSTRALIA Fax: 61-8-6488-7834 Voice: 61-8-6488-7870 E-mail: [email protected] AMERICAN PHYTOPATHOLOGICAL SOCIETY ANNUAL MEETING 10–14 August Providence, RI, USA Info: APS, 3340 Pilot Knob Rd., St. Paul, MN 55121, USAFax: 1-651-454-0755 Voice: 1-651-454-3848 E-mail: [email protected] Web: www.apsnet.org Full-size table Table options View in workspace Download as CSV “
“Bergman JJGHM, Corley DA. Barrett’s esophagus: who should receive ablation and how can we get the best results? Gastroenterology 2012;143:524–526. In the above editorial, a conflict of interest disclosure supplied by Dr Jacques J.G.H.M. Bergman was inadvertently omitted by the Gastroenterology editorial office. The conflict of interest statement should have correctly disclosed that Dr Jacques J.G.H.M. Bergman has received support for IRB-approved clinical studies from BARRX, Olympus Endoscopy, and Cook Medical. He is a consultant for Boston Scientific Endoscopy and for Cook Medical, and has received support for symposia sponsored by BARRX. The online version of the article has been updated to include the correct conflict of interest disclosure.