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In response to myocardial infarction (MI), extracellular vesicles (EVs), including large (lEVs) and small (sEVs), are released within and from the heart to facilitate intercellular communication and maintain cardiac homeostasis by transporting cargo to recipient cells. We investigated how glucose intolerance influences the intracardiac EV release post-MI and their content. B6J mice were fed chow (CD) or high-fat diet (HFD) for 3 months. MI was induced by permanent coronary artery ligation. EVs were isolated from left ventricles and quantified by tunable resistive pulse sensing. EVs were characterised by flow cytometry. EV miRNA content was determined by RNAseq and qPCR. Using cardiomyocyte specific GFP+ mice, plasma lEVs were analysed by flow cytometry to determine if cardiomyocyte EVs (CMEVs) are circulating. Labelled hypoxic cardiomyocyte cell line (HL-1) lEVs were injected in HFD/CD mice post-MI to determine target cells. In CD mice, EV release was significantly increased 24 h post-MI compared to sham. HFD lEV levels were significantly higher compared to sham and CD mice post-MI with no difference in sEV release between sham and MI HFD mice. Intracardiac lEVs originate from cardiomyocyte and endothelial cells in response to MI and MI + HFD respectively. qPCR analyses identified miRNA candidates that were modulated by MI and HFD. Intracardiac GFP + lEV levels were lower in HFD than in CD mice whereas levels of circulating GFP + lEVs were higher. In vivo biodistribution studies revealed a preferential uptake of hypoxic HL-1 lEVs by splenic myeloid cells in HFD spleens versus CD post-MI. Our results show that glucose intolerance modulates intracardiac EV release post-MI and their miRNA cargo. Circulating CMEV levels as well as their uptake by splenic myeloid cells are increased. Further investigations will aim to decipher the impact of the intracardiac EV miRNA mediated transfer in the diabetic heart post-MI. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is the main cause of death in non-communicable diseases. In response to myocardial infarction (MI), extracellular vesicles (EVs), large (lEVs) and small (sEVs), are released within and from the heart to facilitate intercellular communication and maintain cardiac homeostasis, transferring their content such as miRNA, to recipient cells. As diabetes increases the risk of CVD, the objective was to investigate how diabetes influences the release of cardiac EVs post-MI and to determine EV miRNA content. B6J mice were fed chow diet or high-fat diet (HFD) for 3 months and subjected to MI by permanent ligation of the left anterior descending artery. Left ventricles were harvested at different timepoints post-MI and processed for EV extraction by differential centrifugation. EVs were analysed by Tunable Resistive Pulse Sensing (TRPS), flow cytometry and Western blot (WB). RNA sequencing of cardiac EVs was performed to reveal miRNAs of interest that were upregulated in cardiac EVs of MI mice and validated in HFD mice. In control mice, release of both lEVs and sEVs was increased at 24 h and 7 d post-MI. Similarly, in HFD mice, lEVs peaked at 24 h and 7 d post-MI and this increase was greater than in chow diet mice but there were no differences in sEV release between sham and MI HFD mice. TRPS analysis revealed that diabetes does not change EV size and flow cytometry showed that they are mainly of cardiomyocyte origin. Furthermore, EVs harboured cardiomyocyte marker (Troponin T) and sEVs carried tetraspanin markers as revealed by WB. Different miRNAs were also found to be upregulated in lEVs and sEVs in MI mice. Our results show that diabetes modulates the release of both cardiac lEVs and sEVs post-MI. Furthermore, there is a difference in miRNA content between the 2 types of EVs post-MI. Further work is needed to investigate the functional impact of cardiac EVs in the diabetic heart post-MI. [ABSTRACT FROM AUTHOR]

Introduction Cardiovascular disease (CVD) is the main cause of death in non-communicable diseases. In response to myocardial infarction (MI), extracellular vesicles (EVs) including large (lEVs) and small (sEVs), are released within and from the heart to facilitate intercellular communication and maintaining cardiac homeostasis. Objective As diabetes increases the risk of CVD, the purpose of the study was to investigate how diabetes influences the release of intracardiac EVs after MI. Method C57BL/6 J male mice were fed normal chow diet or high-fat diet (HFD) for 3 months. HFD fed mice were glucose intolerant as attested by the measure of GTT above 200 mg/mL. Mice were subjected to MI by permanent ligation of the left anterior descending artery and sham animals underwent similar surgical procedure without ligation. Left ventricles from sham or MI mice were then harvested at either 15, 24, 48 or 72 hours after surgery (N = 5 per group at each time point) and processed for EV extraction by differential centrifugation. EVs were quantified and analyzed via Tunable Resistive Pulse Sensing Technology (TRPS), flow cytometry and Western blot. Results In chow diet fed mice, release of both lEVs and sEVs was increased at 24 h post-MI when compared to shams. These findings were in agreement with previous data obtained in younger control animals. In diabetic mice, lEVs peaked at 24 h post-MI and this increase was slightly greater than that observed in chow diet fed mice. However, there were no differences in sEV release between sham and MI diabetic mice. TRPS analysis revealed that diabetes does not change EV size and population. Furthermore, both control and diabetic derived EVs harboured cardiomyocyte marker (Troponin T) as revealed by Western blot. Conclusion Our results show that diabetes modulates the release of both intracardiac sEVs and lEVs after MI. Further work will be needed to fully investigate the functional impact of cardiac EVs in the diabetic heart after MI. [ABSTRACT FROM AUTHOR]

Introduction The chemokine CXCL12 is essential for cardiovascular system development and plays a major role in physio-pathological processes such as inflammation, angiogenesis but also tissue remodeling after an ischemic insult. In addition to the binding to its receptors, CXCR4 and CXCR7, CXCL12 interaction with heparan-sulfates (HS) commands its biological activity. Studies in experimental models of myocardial infarction (MI) revealed a protective role for CXCL12α. However, in mice, three CXCL12 isoforms (α, β and γ) have been identified and the CXCL12γ isoform shows an unchallenged ability to cooperate with HS, suggesting a pivotal role in tissue repair. Objective The aim of the study is to analyze the role of CXCL12γ isoform and the importance of CXCL12/HS interactions in post-ischemic cardiac remodeling in an acute model of MI. Method MI are induced in mice carrying a Cxcl12 gene mutation that precludes interactions with HS (Cxcl12Gagtm) and in Cxcl12γ knock-in animals (Cxcl12γ-KI), harboring CXCL12γ deficiency. Alternatively, the impact of CXCL12γ overexpression is also evaluated in wild-type (WT) mice receiving transcutaneous echo-guided injections of adenovirus encoding Cxcl12γ in cardiac tissue. Cardiac function and remodeling have been assessed through echocardiography analysis and evaluation of infarct size, interstitial fibrosis, capillary and arteriole densities and as well as inflammatory cell infiltration. Results After MI, Cxcl12Gagtm and Cxcl12γ-KI animals exhibit reduction in cardiac function and adverse left ventricular remodeling when compared to their respective WT littermates. Interestingly, overexpression of CXCL12γ in WT mice normalizes cardiac function by reducing the size of the infarcted area, interstitial fibrosis and promoting vascular growth. Conclusion We show that CXCL12γ isoform plays an important role in the regulation of cardiac function after MI and that its interactions with HS seems essential for adequate cardiac repair. [ABSTRACT FROM AUTHOR]

Abstract: Here we report a case of sustentorial brain abscess due to Listeria monocytogenes. Blood culture and procalcitonine blood measurement were negative. L. monocytogenes was isolated from CSF after inoculation in Castañeda medium. [Copyright &y& Elsevier]

• Hydrolysis of PBT grades differing by initial molar mass and / or presence of pigments. • Kinetic modeling of PBT hydrolysis auto accelerated by chain ends. • Embrittlement criteria common for all PBT's marterials. This paper reports the hydrolysis of several PBT materials (pigmented or not). Degradation was monitored by gel permeation chromatography (chain scission), DSC (crystalline morphology), tensile test (residual mechanical properties) and DVS (polymer-water interaction). The embrittlement comes from chain scission associated with a small chemicrystallization effect. Results lead to the proposal of a kinetic model for the chain scission rate aimed to describe the auto-acceleration effect induced by carboxylic acids (chain ends) and successfully compared to results both from this work or literature. The mixed "average molar mass – crystallinity" criterion proposed in a previous paper was specified. At last, the effect of pigments is illustrated and shows that carbon black (present in particular in one masterbatch) plays an aggravating role on hydrolysis. [ABSTRACT FROM AUTHOR]

• Study of PBT thermal and hydrolytic ageinginducing plasticity loss. • Study of molar mass decrease induced by chain scissions. • Study of crystalline changes (annealing and chemicrystallization). • Proposal of a mixed (Mw,xC) failure criterion separating ductile and brittle behavior. This paper reports the study of embrittlement of PBT submitted either to thermal or hydrolytic ageing. All changes were followed up by tensile tests, rheometry in molten state and gel permeation chromatography for molar mass changes, SAXS and DSC experiments for crystallinity changes. Both kind of ageing were shown to induce predominant chain scissions with moderate crystallinity increase, in great part due to annealing. The combination of all results were used to establish a M w - χ c embrittlement window helping for a determination of an end of life criterion. [ABSTRACT FROM AUTHOR]

Abstract: Aim of the study: To develop a fast and reliable real time PCR technique for detecting plasmid-mediated quinolone resistance genes qnrA, qnrB and qnrS. Methods: A real-time PCR assay using SYBR Green I and Roche LightCycler® was developed to detect qnr genes. Detection of qnr genes was based on comparison of melting temperature differences with a positive control of each qnr genes. This assay was performed to study 138 isolates collected from diagnostic and screening samples in the Champagne-Ardenne region in 2004 (France). Results: In optimized conditions, the three positive controls tested alone and with isolates confirmed the specificity of the PCR primers. Each PCR assay was able to test 30 strains in 60min for 1 qnr gene. Out of 138 isolates screened, 3.6 % isolates were positive for a qnrA1, 1.5 % for qnrS1 and no qnrB-like gene. Prevalence of qnr determinants was 5 % and reached 9.5 % in clinical isolates. Conclusion: Real-time PCR is a fast and reliable technique for screening of qnr-positive strains. This study shows a relatively high prevalence of qnr determinants (5 %) among ESBL-producing Enterobacteriaceae. [ABSTRACT FROM AUTHOR]

• Injection moulding of PBT parts with various processing conditions (barrel temperature, residence time). • Embrittlement induced by the process, in link with average molar mass decrease. • Embrittlement map common for all PBT's materials was established in line with previous works. • Thermolysis seems here the main cause of thermal degradation. • Kinetic modeling of PBT thermolysis. Embrittlement caused by injection molding was investigated on a commercial grade of Polybutylene terephthalate (PBT). The effect of temperature and residence time in the barrel on mechanical properties was studied. Results were discussed from macromolecular analysis by Gel Permeation Chromatography and crystallinity measurements by differential scanning calorimetry. It was shown that embrittlement exclusively occurs by a chain scission process in those conditions. Oxygen is shown to play a negligible role in degradation while thermolysis seems to be the main source of degradation. It was here described by a first simple kinetic model based on the beta abstraction of hydrogen at the vicinity of ester groups. A processing window was thus determined using this model and might help practitioners for processing PBT parts. [ABSTRACT FROM AUTHOR]

Results Cumulative bleeding events, cumulative joint bleeding events, and cumulative major bleeding events were estimated to be 186.6, 155.9 and 0.4 for octocog alfa and 235.3, 174.4 and 0.5 for antihemophilic factor (recombinant). Hospitalizations and hospitalization days were reduced by 20% for octocog alfa compared to antihemophilic factor (recombinant) (with a total of 0.4 hospitalizations for octocog alfa versus 0.5 for antihemophilic factor (recombinant)), with a mean of 1.3 days (versus 1.7 for antihemophilic factor (recombinant)). [Extracted from the article]

Introduction: L’importance pronostique sur la mortalité et sur l’incidence des complications d’un traitement précoce et adapté des pneumonies à pneumocoque est connue. Streptococcus pneumoniae constitue l’étiologie la plus fréquente et la plus grave. Le but de cette étude était d’évaluer le test BINAX NOW S. pneumoniae dans le diagnostic précoce des pneumonies chez les patients ventilés en réanimation. Matériel et méthodes: Étude prospective de 2003 à 2006, incluant les pneumopathies communautaires hypoxémiantes (score de FINE V). Le diagnostic de pneumonie reposait sur les critères d’ANDREW. Recueil : âge, sexe, IGS II, antibiothérapie préalable. Un lavage broncho-alvéolaire (LBA), des hémocultures (HC), une antigénurie S. pneumoniae étaient effectués dès l’admission. Deux groupes étaient individualisés. Groupe I : patients infectés àS. pneumoniae, Groupe II : patients non infectés àS. pneumoniae. Résultats: Inclusion de 333 patients. Âge moyen : 59 ans, sex ratio de 3, IGS II à 41, 65 % avaient reçu une antibiothérapie avant les prélèvements. 52 patients (groupe I) présentaient une pneumonie àS. pneumoniae dont 11 associés à une bactériémie. Le groupe II comprenait 281 patients. 60 patients avaient une antigénurie positive, 21 patients du groupe I et 39 patients du groupe II. La sensibilité (Se) est égale à 40,4 % [24 %-62,8 %] IC 95 % et la spécificité (Sp) à 86,1 % [64,4 %-85,6 %] IC 95 %. La VPP n’était que de 35 % alors que la VPN était de 88,6 %. En prenant comme test de référence l’HC seule, la Se était de 45,5 % [22,1 %-59,3 %] IC 95 % et la Sp de 82,9 % [57,7 %-85,6 %] IC 95 %. Conclusions: L’intérêt du test réside dans la rapidité du résultat et du caractère non invasif de cette technique, mais la sensibilité médiocre de ce test incite à ne plus pratiquer cet examen en réanimation. [Copyright &y& Elsevier]