However, careful examination of the agar plates for pinpoint colo

However, careful examination of the agar plates for pinpoint colonies after 3 days of incubation would help find sVISA. Even stored culture of

VISA strains may contain the original sVISA strain as a minor subpopulation. In fact, we identified a few pinpoint colonies on the drug-free agar plates streaked with the glycerol stocks of 3 of the 33 VISA clinical strains listed in Table 1. The slow-growing strains established from these pinpoint colonies expressed high and unstable vancomycin resistance as well as a colony morphology similar to those observed with Mu3-6R-P (Table 3). All of the strains lost the VISA phenotype and returned to the large colony morphology within a week’s passage. This indicated that generation of sVISA is not infrequent. They are generated during vancomycin therapy but escaped FG-4592 manufacturer recognition since they easily reverted to hVISA or became stabilised as VISA during propagation in the clinical laboratory. Generation of sVISA during vancomycin Paclitaxel therapy may well explain the discrepancy between the frequency of vancomycin therapeutic failure and the frequency of VISA isolation from patient samples. Whole-genome sequencing of Mu3-6R-P revealed only one single nucleotide polymorphism relative to the Mu3 genome.

The mutation was identified in the rpoB gene, changing the arginine-512 to proline. Sequence determination of the rpoB gene identified non-synonymous rpoB mutations in 7 (21%) of 28 sVISA strains; they Sorafenib were rpoB(G744R), rpoB(S746F) (2 strains), rpoB(H929T) (2 strains) and rpoB(G977V). Unlike the rpoB mutations in extant VISA strains, these mutations were all identified outside of the RRDR and, except for rpoB(R512P), were located in the C-terminus half of the RpoB protein ( Fig. 5). Three Mu3-derived sVISA strains Mu3-6R-P, 17–6 d and 21–4 d carrying rpoB(R512P), rpoB(S746F) and rpoB(H929T), respectively, were cultivated in drug-free medium, and large-colony derivative strains were established to determine their rpoB gene sequences. The rpoB(H929T) mutation was back-mutated to wild-type

and the rpoB(R512P) mutation was replaced by alternate mutations such as rpoB(R512L), rpoB(R512H) or rpoB(R512S). Only the rpoB(S746F) mutation was not changed in three independently isolated large-colony strains. All of the large-colony strains reverted to hVISA phenotype with comparable levels of vancomycin resistance and DTs to that of Mu3. Therefore, it is likely that certain rpoB mutation does serve as an on-and-off switch for the sVISA phenotype. A single mutation in the rpoB gene can make the cell survive otherwise growth-inhibitory concentration of vancomycin. After the vancomycin selective pressure is lifted, the bacteria can start to diverge themselves beyond the constraints imposed by the rpoB regulatory mutation.

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1 and 2 Mouth breathing, a pathological condition,3 may be due to

1 and 2 Mouth breathing, a pathological condition,3 may be due to upper airway obstruction, sagging facial muscles, or habit;1 any individual who has exhibited this type of breathing for a minimum of six months should be considered a mouth breather.4 Genetic factors and exposure to obstructive factors, regardless of etiology, can be detrimental to child development. Among the consequences of mouth breathing

are alterations in cranio-orofacial growth, speech, nutrition, GDC-0449 mouse body posture, sleep quality, and school performance.1 Overall, the mouth breather presents alterations in posture, tone, and mobility of lips, tongue and cheeks, resulting in less efficiency in stomatognathic functions: chewing, swallowing and speech, flaccid jaw elevator muscles, anterior head posture, maxillary atresia, and speech disorders.5 and 6 Speech can be altered due to flaccid facial muscles, incorrect positioning of the tongue,7 or structural problems of the oral cavity caused by malocclusion and/or deficiencies in facial growth and development.2 and 8 The most commonly described speech disorders in mouth breathers are: anterior position of tongue during production of lingual dental phonemes,9 imprecision in bilabial (/p/,/b/,/m/) and fricative (/f/,/v/,/s/,/z/,/ʒ/,/∫/) phonemes in Portuguese, frontal lisp (FL), and lateral (LL) lisp.10, 11 and 12 Children

who are mouth-breathers can Akt inhibitor review also have daytime sleepiness,13 and 14 poor brain oxygenation,15 or immature auditory processing. All of these complications can lead to learning disabilities.16 Thus, the aims of this study were to assess the development of speech, the most frequently observed speech alterations, and to correlate them with the etiology of mouth breathing The knowledge of these aspects can help health professionals to prevent or minimize the consequences of mouth breathing. Mouth-breathing children (n = 439) aged 4 to 12 years, enrolled in and regularly attending the Mouth-breather Gefitinib ic50 Center (Centro do Respirador Bucal – CRB) of the Universidade Federal de São Paulo/Escola Paulista de

Medicina (UNIFESP-EPM) from May of 2000 to May of 2011, were evaluated. Patients with genetic syndromes, orofacial malformations, or mental retardation were excluded. Patients were evaluated according to standards established by the CRB. First, patients were evaluated by the otorhinolaryngology specialist and then, by the other specialists of the CRB: allergist, physical therapis, dentist, orthodontist, and speech therapist, always on the same day. Patients with a history of mouth breathing for at least six months, with nasal obstruction, pallid or hyperemic nasal mucosa, with or without hypertrophy of adenoid (volume occupying less than 70% of airway) and tonsils (grade I or II), and nonobstructive nasal septal deviation/turbinate (Brozek et al.5), conditions observed by the otorhinolaryngology specialist during clinical examination and nasal fibroscopy, were included.

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14 The abovementioned studies barely addressed children and adole

14 The abovementioned studies barely addressed children and adolescents, and Kelishadi et al.15 explored the relationship among VDD, insulin resistance, and related cardiometabolic disease risk factors such as blood glucose, blood pressure, blood lipids, and obesity in obese children with vitamin D supplementation. The authors concluded that vitamin D supplementation was beneficial to cardiometabolic disease control

in obese children and adolescents. This is the evidence regarding the correlation between VDD and cardiometabolic diseases in younger populations. However, there Rucaparib price are some caveats in the research by Kelishadi et al.15 Firstly, a control group of normal-weight children is necessary, since there was no data demonstrating that vitamin D levels in the obese children was lower than that of eutrophic children;

this was assumed by the authors based on a previous result.16 If there were no obvious differences of vitamin D levels between the subjects of the study and the eutrophic population, the rationale of vitamin D interference would be a concern. Secondly, to meet the statistical analysis requirement, the authors carefully designed the experiment to Selleckchem FK228 guarantee that there were at least 20 samples in each group, and that there was positive result in each group. However, the authors didn’t describe in detail the standards applied to decide which samples would be included, especially regarding the differentiation between

Leukotriene-A4 hydrolase simple obesity from secondary obesity that should be excluded. It’s unknown whether vitamin D supplementation would be effective in secondary obesity patients, in whom VDD is probable. It was unclear why the authors chose obese children and adolescents aged 10 to 16 years old, and it is quite possible that the data accuracy and conclusion validity might have be compromised due to the inconsistency of the baseline for different populations included in the study. To define cardiometabolic risk factors and metabolic syndrome, the authors applied the latest cut-off points provided by the National Heart, Lung, and Blood Institute for the pediatric age group and the continuous value of metabolic syndrome (cMetS) score, as recommended by the American Diabetes Association and by the European Association for the Study of Diabetes for children and adolescents, respectively. It is a concern whether these standards are appropriate for the study and whether they reflect the true situation of the population of interest. Analyzing previous research on VDD and cardiometabolic diseases, it’s natural to hypothesize that a small sample pool and improper sample selection are important reasons for the negative results obtained by the authors.

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The plate was then stained with orcinol–sulphuric acid–methanol s

The plate was then stained with orcinol–sulphuric acid–methanol solution by a colour reaction after heating at 125 °C. After fixation with 0.02% polyisobutylmethacrylate (PIBM) in hexane solvent (90% hexane with 10% chloroform, v/v) for 1 min, the HPTLC was blocked with 0.5% bovine serum albumin (BSA) in PBS (137 mM NaCl, 10 mM Phosphate buffer, 2.7 mM KCl, and a pH of 7.4) with 0.02% tween-20 for 30 min at room temperature. About 22 nM of LEC-8 in 10 ml of PBS buffer (0.5% BSA, pH 7.4) was overlaid with the plate for two hours at room temperature (about 20 °C).

The plate was washed with PBST for four times and incubated with antibodies against LEC-8 in a ratio of 1:1000 overnight. After washing with PBST for four times, the plate was incubated with antibodies anti-Rabbit IgG conjugated with Trichostatin A ic50 alkaline phosphatase in a ratio of 1:1000 for two hours. After washing with PBST for four times, the HPTLC overlay was detected by a colour reaction in an alkaline buffer with NBT and BCIP as substrates. To further assess whether pre-incubation with LEC-8 can reduce or inhibit the binding of Cry1Ac to glycolipid, after HPTLC resolution the glycolipid was first incubated with 22 nM of LEC-8 for 2 h at 20 °C before incubation with 20 nM Cry1Ac for 2 h. The plate was then incubated with antibodies against Cry1Ac

for overnight and the second antibodies for 2 h and developed by using the same method as above. To test whether binding of LEC-8 to insect glycolipids inhibit the glycolipids binding to Cry1Ac, an in vitro competition experiment was performed based Topoisomerase inhibitor on the method of Refs. [4] and [11] with some modifications. In brief, the Nunc Polysorp 96-well flat microplate was equilibrated with 25 μl of methanol. The plate was dried at room temperature followed by application

of 7.5 μl gut glycolipids. The plate was then left at room temperature for completely drying followed by blocking the wells with 100 μl of 0.5% BSA in PBS buffer for 30′ at RT. Three treatments with three replicates Rucaparib solubility dmso were performed: LEC-8 only (concentration from 0 to 140 nM), active Cry1Ac only (concentration from 0 to 140 nM) and the mixture of 20 nM Cry1Ac and variable LEC-8 (from 0 to 900 nM). The three treatments at various concentrations in 100 μl PBS were incubated with glycolipids for two hours at room temperature. After washing four times with 200 μl of PBS, the plate was incubated with 100 μl of the first antibodies (anti-Cry1Ac for treatments Cry1Ac and mixture of LEC-8 with Cry1Ac, anti-LEC-8 for treatments LEC-8) at 1:1000 for one hour at room temperature. After washing four times with 200 μl of PBS, the plate was incubated with 100 μl of the second antibodies (anti-IgG conjugated with alkaline phosphatase) at 1:1000 for one hour at room temperature.

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She retrospectively reported cooking over open fires

A f

She retrospectively reported cooking over open fires.

A follow-up CT scan at 6-months showed completely stable appearances, with some pulmonary nodules, likely intrapulmonary lymph nodes, and part calcified mediastinal lymphadenopathy. Clinically she remained well having gained 2 kg in weight, with no night sweats, fevers, cough or breathlessness. She is due further follow-up at 18 months. A 74-year-old woman with a 20-year history of non-productive cough underwent a CT scan as part of evaluation of a left lower lobe calcified nodule. She was otherwise healthy and examination was unremarkable. The CT scan identified curvilinear shadowing in the right middle lobe and a second non-calcified nodule Luminespib inferiorly Selleck CDK inhibitor in the left lower lobe. Right middle lobe bronchial washings were culture negative for bacterial or fungal infection and there were no malignant cells.

Auramine stain and TB cultures were negative. An FDG-PET scan demonstrated normal metabolic activity in the nodules but identified increased activity in enlarged right paratracheal, para-oesophageal and bilateral hilar lymph nodes (SUV 5-7) and an incidental right adrenal adenoma. EBUS-TBNA of the right paratracheal lymph node macroscopically showed lightly bloodstained material that contained small black flecks up to two millimetres in diameter. Microscopically there were striking amounts of anthracotic macrophages, arranged in aggregates and as singly dispersed cells. No multinucleated giant cells, necrosis or malignant cells were seen and was auramine and culture negative for TB. A follow-up CT scan at 12 months showed no significant change in the appearance of the lung with no new nodules or significant change in the existing nodules. She was asymptomatic and due further follow-up at 18 months. A 68-year old Pakistani

woman presented with persistent cough and wheeze. Past Ergoloid medical history included atrial fibrillation, hypertension, hypothyroidism, asthma and IgA nephropathy. Examination was unremarkable. CT chest demonstrated mediastinal and hilar lymphadenopathy, and a small, non-specific left-sided pulmonary nodule. An EBUS-TBNA was performed on the mediastinal and hilar lymph nodes. No black pigment was seen macroscopically. Microscopically large numbers of anthracotic macrophages were seen, singly distributed and in dense clusters. There was no multinucleated giant cell reaction, necrosis or malignant cells and was culture, smear and PCR negative for TB. A follow-up CT scan at 9 months revealed unchanged appearances of the pulmonary nodule and mediastinal lymphadenopathy. She remained clinically well and is due a further follow-up CT imaging at 24 months. A 65-year old Punjabi woman with a 3-year history of cough was referred for investigation. She denied any associated symptoms. Ten months prior to presentation she had been treated for presumed TB, on the basis of enlarged mediastinal lymph nodes on CT imaging and a strongly positive mantoux test.

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Besides TLR2 and TLR4, in vitro-differentiated

Besides TLR2 and TLR4, in vitro-differentiated Venetoclax molecular weight odontoblasts constitutively express TLR1, 3, 5, 6 and 9 genes [53]. A recent study has reported that TLR9 is expressed in the mouse odontoblast-like cell line MDPC-23, a spontaneously immortalized cell line derived from fetal

mouse molar dental papillae, and that CpG DNA induces potent pro-inflammatory cytokine expression via the activation of TLR9 [56]. Additionally, an immunohistochemical report revealed that the NOD2 protein expression was localized in odontoblasts and some vascular endothelial cells in normal human dental pulp 57]. However, more detailed studies on the functional role of these PRRs in the odontoblasts to recognize intradentinal irritation of caries-related bacteria are required in future. Dental pulp cells, especially dental pulp fibroblasts, are known to

produce various inflammatory mediators, LY294002 manufacturer such as IL-8, IL-6 and vascular endothelial growth factor (VEGF), in response to the components of caries-related bacteria, prior to the discovery and establishment of the innate immune system feature that PRRs including TLRs recognize various PAMPs [29], [31], [32] and [58]. TLR2, TLR3, TLR4 and TLR5 expressions have been determined in dental pulp fibroblasts and their specific agonists can induce TLR-mediated inflammatory signals [54], [55], [59] and [60], although immunohistological detection of TLRs was not clear in the fibroblasts of dental pulp tissues [49] and [52]. A recent study has shown that the dental pulp stem cells as well as the dental pulp fibroblasts express TLR4, and that LPS-induced VEGF is dependent upon mitogen-activated protein kinase (MAPK) activation [61]. In our study, flow cytometric analysis showed that the expression level of TLR2 was higher than that of TLR4 in human dental pulp fibroblasts [59]. In accordance with this analysis, the levels of pro-inflammatory mediators, such as CXCL10, IL-8 and PGE2, Phosphatidylethanolamine N-methyltransferase induced by LPS stimulation were much lower than those

induced by Pam3CSK4. On the other hand, another group has shown that CXCL10 expression in dental pulp fibroblasts was up-regulated by LPS but not LTA, a TLR2-agonist [54]. These results suggest differences of reactivity between Pam3CSK4 and LTA to elicit chemokine production. In fact, our previous report indicates that the dental pulp fibroblasts can produce CXCL10 in response to peptidoglycan, but not LTA [24]. MAPKs have been implicated in many physiologic processes, including cell proliferation, differentiation and death [62], [63] and [64]. Three major types of MAPKs in mammalian cells are extracellular signal regulated kinase (ERK) 1/2, p38 MAPK and c-Jun NH2-terminal kinases (SAP/JNK). NF-κB is an oxidation-sensitive transcription factor that plays a critical role in the regulation of various genes that are important in cellular responses, including inflammation, innate immunity, growth and cell death [65].

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1 To date, there have been only a few case reports of granulomato

1 To date, there have been only a few case reports of granulomatous

interstitial pneumonitis associated with sirolimus. We describe a patient with polycystic kidney disease with renal transplantation who was switched to sirolimus two months before developing granulomatous interstitial pneumonitis. A 53-year-old woman, a non smoker with a past medical history of hypertension and ESRD secondary to polycystic kidney disease, underwent deceased donor kidney transplantation in 2006. Her medications were changed from mTOR inhibitor tacrolimus and mycophenolic acid to cyclosporine 25 mg twice a day and sirolimus 3 mg daily approximately two months before admission. She presented with fever, malaise, progressive shortness of breath, and cough with minimal sputum for 2 weeks. She did not have any other symptoms. Physical examination showed stable vital signs, O2 saturation 96% on room air, and bilateral basilar fine crackles. Lab tests showed a Hb 8.4 g/dl, Hct 24%, MCV 77 fL, WBC 2.5 kU/l, neutrophils 55%, lymphocytes 32%, eosinophils 0.1%, platelets 141 kU/l, sodium 136 mmol/l, see more potassium 4.2 mmol/l, chloride 102 mmol/l, bicarbonate 22 mmol/l, BUN 15 mg/dl, creatinine 0.9 mg/dl, and normal liver enzyme. Her sirolimus level was high at 28.5 ng/dl. Urinalysis did not show pyuria or hematuria.

Chest radiograph revealed bilateral thickened interstitial markings (Fig. 1). Computed tomography scan of the chest without contrast showed ill-defined patchy ground glass opacities in both lungs (Fig. 2). Cultures were obtained, and antibiotic drugs were started to cover

community-acquired pneumonia. The patient remained tachypneic and desaturated. Broad spectrum antibiotic drugs were continued with Amobarbital an antifungal drug (Mycamine) and trimethoprim and sulfamethoxazole. BAL fluid studies were negative for bacteria, viruses, AFB, and fungi. BAL culture for mycobacteria was also negative at eight weeks. The direct antigen for PCP was negative. She underwent video-assisted thoracoscopic biopsy which showed granulomas, interstitial fibrosis, and focal organizing pneumonia (Fig. 3). She has a normal angiotensin converting enzyme level. The results were highly suspicious for sirolimus induced granulomatous interstitial pneumonitis, and sirolimus was stopped. The patient was started on methylprednisolone 40 mg IV every 12 h. She improved and was discharged on prednisone 30 mg/day, cyclosporine 200 mg/day, and leflunomide 15 mg/day. She was remarkably better two weeks later. Repeat computed tomography scan of the chest one month later showed near complete resolution of the previously seen interstitial lung disease, but some mild interstitial lung disease remained with peripheral interlobular septal thickening (Fig. 4). Sirolimus, initially known as rapamycin, is a macrolide antibiotic derived from the actinomycete “Streptomyces hygroscopicus”.

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Yeast autolysis is a slow process that involves the interaction b

Yeast autolysis is a slow process that involves the interaction between components released by dead yeast cells and the wine and through this study we can conclude that the volume of wine in contact with the lees surface (bottle or tanks) can affect the sequential reactions involved in the whole process, since the compounds

showed different curves to each method, such as the tyrosol and gallic acid ones. Secondly, the grapes are the matrices of the SW profile and we showed that the chardonnay grape has more β-Glucosidase activity than the assemblage used. The metabolism is triggered by enzymes and we proved that this activity not only exists into SW, but also that it remains unchanged while the ageing happens. Therefore, we can conclude that the β-Glucosidase selleck inhibitor activity is stable in the wine conditions. This Capmatinib order is important because the reactions that involve this enzyme, the levels of resveratrol and piceid plus the glucose concentration, may be able to maintain or improve the SW antioxidant capacity. Besides, caffeic and ferulic acids play significant roles in this context and are also affected by the glucose levels in the medium, acting in this way on the overall quality of the SW. Our results showed that the older the SW is, the smaller the antioxidant activity is

too. As white and red wines can act against the oxidative stress in distinct ways, the choice for a short or long ageing on lees will determine the response of the SW, because the sur lie is able to modulate the necessary changes to achieve a specific objective. Therefore, we can conclude that the ageing on lees becomes more important than the production methods of SW due to, mainly, its close relationship with the phenolic profile. The authors are grateful to CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior), UCS (Universidade de Caxias do Sul), ABE (Associação Brasileira de Enologia), Möet Hennessy do Brasil – Vinhos

e Destilados Ltda, Vinícola Geisse Ltda, and Prof. Abel Prezzi Neto for his assistance in the view of English. “
“Arabinoxylans (AX), the principal dietary fibre component in rye and wheat, belong to a group of highly heterogeneous cell wall polysaccharides Dimethyl sulfoxide with high molecular size and specific structural features, which significantly affect the processing of flour and the properties of bread (Biliaderis et al., 1995, Fincher and Stone, 1986, Meuser and Suckow, 1986 and Vinkx and Delcour, 1996). A fundamental trait of cereal AX is their capacity to form highly viscous aqueous solutions at a relatively small concentration. Furthermore, both AX fractions, water-extractable (WE) and water-unextractable (WU), exhibit extremely high hydration capacity (Jelaca and Hlynka, 1971 and Meuser and Suckow, 1986) due to formation of three-dimensional networks by covalent and non-covalent bonds. They may lead to gel formation in aqueous solutions and swelling of WU cell wall materials (Fincher & Stone, 1986).

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The following standards

were applied (the m/z ratios used

The following standards

were applied (the m/z ratios used for quantification are shown in parentheses): cis/trans-linalool oxide (59), linalool (71), hotrienol (71), cis/trans-rose oxide (139), cis-limonene oxide (67), trans-limonene oxide (94), α-terpineol (93), β-terpineol (71) γ-terpineol (121), nerol (69), β-citronellol (69), geraniol (69), nerol oxide (68) and lavandulol (69). Rose oxide was obtained from Moellhausen (Vimercate, Italy), hotrienol from Dabrafenib Treatt (Lakeland, Florida), nerol oxide from Roth (Karlsruhe, Germany). All other standards were obtained from Fluka (Sigma–Aldrich, Vienna, Austria). The limit of quantification (LOQ) was determined as 0.3 μg/L, the relative standard deviation between repeated samples (repeatability) was below 6%. The wines were evaluated in triplicate by a panel of seven trained tasters. The participants are officially approved tasters for the quality assessment of Austrian wines. The tasters are trained according to the Austrian wine law and their performance is evaluated annually. Assessment took place in a standard sensory analysis chamber (EN ISO 8589) equipped with separate booths under yellow light forcing the

tasters to focus only on the aroma and taste of the wines. The tasters were presented with the wines in groups of five wine glasses each. The wines were presented in randomised order in coded standard tasting glasses (ISO 3591). In each group, the tasters were first asked to rank the wines on their aroma intensity using an unstructured MS-275 cost scale ranging from 1 to 5 with 1 the highest and 5 the lowest aroma intensity. The

wines where then sorted according to the perceived aroma intensity, following the method of Cartier et al. (2006). Second, the tasters had to assess each wine based on their olfactory and taste sensations on an unstructured scale from 0 to 10, with 10 reflecting the highest intensity of each attribute. The attributes involved were typical Riesling descriptors (stone fruit, citric, pomaceous fruit), attributes usually associated with white wines but not with Riesling (freshness, spice, tropical, candy). Further attributes were “floral” (corresponding to terpenoid aroma compounds) and “typicality” Abiraterone concentration (Riesling). The data from terpene analysis (Section 2.4) were statistically analysed with the software package SPSS 18. One-way analysis of variance (ANOVA) was applied to test for significant differences between the individual treatments. The results were analysed by Student’s t-test (Student–Newman–Keuls) at a significance level of 95% (α = 0.05). The results from the sensory evaluation (Section 2.5) were analysed for significant differences (α = 0.05) by ANOVA (Statgraphics). The first enzyme assays were performed under optimal enzyme conditions (pH 5.5, ethanol removed) using an extract from a white wine (Traminer, Austria). According to Mateo and Jiménez (2000), Traminer is classified as a non-Muscat, but aromatic variety, that depends on monoterpenes as major flavour components.

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This research was supported by funding from the Canadian

This research was supported by funding from the Canadian Tofacitinib mw Breast Cancer Research Alliance

and the Canadian Breast Cancer Foundation (grant # 020659), and an Investigator Award from the Canadian Institutes of Health Research to Dr. Richardson. “
“M. Matar, O. Picone, C. Dalmon, J.-M. Ayoubi, auteurs de l’article « Évaluation des connaissances des échographistes sur les clichés d’échographie de dépistage du deuxième trimestre recommandés par le Comité technique national de l’échographie » (DOI: 10.1016/j.jgyn.2013.04.004), paru dans le Journal de Gynécologie-Obstétrique et PFI-2 in vivo Biologie de la Reproduction 2013;42:473–478, désirent

ajouter à leur texte, à titre de Remerciements, la mention suivante : Les auteurs remercient le Collège français d’échographie fœtale, et particulièrement le Dr Nicolas Fries, pour la diffusion du questionnaire qui a permis de réaliser cette étude. “
“Lors de la publication de l’article « Étude randomisée comparant la promontofixation cœlioscopique à la chirurgie prothétique par voie vaginale pour le traitement des cystocèles : PROSPERE (PROSthetic PElvic organ prolapse REpair » (Journal de Gynécologie-Obstétrique ADAMTS5 et Biologie de la Reproduction, volume 42, no 4–juin 2013, p. 334-341), des erreurs

d’attribution d’affiliations ont été commises, en première page, pour les auteurs suivants : • A. Wattiez, O. Garbin, C. Youssef Azer Akladios, V. Thoma, E. Baulon-Thaveau, C. Saussine, qui exercent au CHU de Strasbourg ; Il fallait donc lire : J.-P. Lucot a,*, X. Fritel j, P. Debodinance g, G. Bader b, M. Cosson a, G. Giraudet a, P. Collinet a, C. Rubod a, H. Fernandez c, S. Fournet c, M. Lesavre c, X. Deffieux d, E. Faivre d, C. Trichot d, G. Demoulin d, B. Jacquetin e, D. Savary e, R. Botchorichvili e, S. Campagne-Loiseau e, D. Salet-Lizee f, R. Villet f, P. Gadonneix f, P. Delporte g, P. Ferry h, J.-S. Aucouturier h, Y. Thirouard h, R. de Tayrac i, B. Fatton i, L. Wagner i, C. Nadeau j, A. Wattiez k, O. Garbin k, C. Youssef Azer Akladios k, V. Thoma k, E. Baulon-Thaveau k, C. Saussine k, J.-F. Hermieu l, V. Delmas l, S. Blanc m, D. Tardif m, A.

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