145 research outputs found

    Feasibility of the Engager™ aortic transcatheter valve system using a flexible over-the-wire design

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    OBJECTIVES The aim was to investigate the safety and feasibility of the redesigned Engager™ transcatheter aortic valve implantation (TAVI) system. METHODS Transapical aortic valve implantation with the Engager™ valve prosthesis was intended in 11 patients, and performed in 10. Endpoints were defined according to the valve academic research consortium recommendations for reporting outcomes of TAVI in clinical trials. RESULTS All 10 patients were implanted successfully. No devicerelated or delivery system complications like coronary obstruction or aortic dissection emerged. One patient (10%) died from non-device-related reasons at post-operative day 23 of multi-organ failure. The invasively measured peak-to-peak gradient after valve implantation was 7.1±3.5mmHg. In 90%, there was no or only trivial (≤grad I) aortic regurgitation due to paravalvular leakage. In 10% of the patients, aortic regurgitation grade I-II was observed. At 30-day follow up, the mean gradient was 15.6±4.9mmHg, and no more than a mild transvalvular and paravalvular aortic regurgitation was seen as assessed by transthoracic echocardiography. CONCLUSIONS Application of the Engager™ TAVI system is safe and feasible. Prosthesis deployment in an anatomically correct position was facilitated by the design of the valve prosthesis and was successful in all patients. No device or delivery-system-related complications emerged. Safety and feasibility endpoints were met. Good results concerning the aortic valve performance after implantation and at 30-day follow up were ascertained. These results encouraged the start of a European Pivotal trial including patients to dat

    Effect of different concentrations of chitosan coating on storage life and quality characteristics of Papaya (Carica Papaya L.)

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    Mature green stage of papaya fruits were treated with different concentrations of chitosan at 0, 0.5, 0.75 and 1%, and stored at 13±1 °C for 28 days to study the effect of these concentrations on the storage life and maintaining quality of papaya. Chitosan concentrations 0.75 and 1% showed the best control effect on decay compared with 0% (Control) and 0.5%. At 0.75 and 1% of chitosan, flesh firmness maintained resulted in prolonging in storage life of 28 and 26 days compared with 21 and 19 days, respectively for 0.5 and 0%. Furthermore, they were significantly decreased the weight loss of fruit. All of the treatments inhibited increase of soluble solid contents and pH values of pulp fruits after 21 days of storage at 13 ± 1°C. Titratable acidity and ascorbic acid were higher for coated fruits (0.5, 0.75 and 1%) compared with uncoated fruits. Concern treatments of chitosan at 0.75 and 1% improve papaya fruit quality and resistance to decay

    A statistical model that predicts the length from the left subclavian artery to the celiac axis; towards accurate intra aortic balloon sizing

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    <p>Abstract</p> <p>Background</p> <p>Ideally the length of the Intraaortic balloon membrane (22-27.5 cm) should match to the distance from the left subclavian artery (LSA) to the celiac axis (CA), (LSA - CA). By being able to estimate this distance, better guidance regarding IABP sizing could be recommended.</p> <p>Methods</p> <p>Internal aortic lengths and demographic values were collected from a series of 40 cadavers during autopsy. External somatometric measurements were also obtained.</p> <p>There were 23 males and 17 females. The mean age was 73.1+/-13.11 years, weight 56.75+/-12.51 kg and the height 166+/-9.81 cm.</p> <p>Results</p> <p>Multiple regression analysis revealed the following predictor variables (R2 > 0.70) for estimating the length from LSA to CA: height (standardized coefficient (SRC) = 0.37, p = 0.004), age (SRC = 0.35, p < 0.001), sex (SRC = 0.21, p = 0.088) and the distance from the jugular notch to trans-pyloric plane (SRC = 0.61, p < 0.001).</p> <p>Recommendations: If LSA-CA < 21.9 cm use 34 cc IABP & if LSA-CA > 26.3 cm use 50 cc IABP. However if LSA-CA = 21.9- 26.3 cm use 40 cc, but be aware that it could be "aortic length-balloon membrane length" mismatching.</p> <p>Conclusions</p> <p>Routinely, IABP size selection is being dictated by the patient's height. Inevitably, this leads to pitfalls. We reported a mathematical model of accurate intraaortic balloon sizing, which is easy to be applied and has a high predictive value.</p

    Contegra conduit for reconstruction of the right ventricular outflow tract: a review of published early and mid-time results

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    <p>Abstract</p> <p>Objective</p> <p>The valved conduit Contegra (bovine jugular vein) has being implanted for more than 7 years in the right ventricular outflow tract and it is noted that the available reports have been mixed. The aim of this study is to review the reported evidence in the literature.</p> <p>Methods</p> <p>Search of the relevant literature for the primary endpoints of operative mortality and morbidity and secondary endpoints of follow-up haemodynamic performance including severe stenosis, regurgitation and need for reintervention are presented.</p> <p>Results</p> <p>We selected and analysed 17 series including 767 patients. Commonest indication was Fallot's tetralogy. Operative mortality was 2.6%. Operative morbidity was 13.9%. In follow-up, the incidence of intraconduit stenosis was 10.9% (incidence of stenosis for the 12 millimetre conduit was 83.3% in one series) and that of at least moderate regurgitation was 6.3%.</p> <p>The aspirin users had a stenosis incidence of 10.5% compared to the non-users had a stenosis incidence of 9.6%.</p> <p>Conclusion</p> <p>A dissent on the performance of the Contegra is discussed, while results are satisfactory in the majority of studies apart for the smallest conduits (12 and 14 millimetre), suggesting an association to compromised run-off. The role of aspirin as antithrombotic modulator remains controversial.</p

    Abnormal X : autosome ratio, but normal X chromosome inactivation in human triploid cultures

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    BACKGROUND: X chromosome inactivation (XCI) is that aspect of mammalian dosage compensation that brings about equivalence of X-linked gene expression between females and males by inactivating one of the two X chromosomes (Xi) in normal female cells, leaving them with a single active X (Xa) as in male cells. In cells with more than two X's, but a diploid autosomal complement, all X's but one, Xa, are inactivated. This phenomenon is commonly thought to suggest 1) that normal development requires a ratio of one Xa per diploid autosomal set, and 2) that an early event in XCI is the marking of one X to be active, with remaining X's becoming inactivated by default. RESULTS: Triploids provide a test of these ideas because the ratio of one Xa per diploid autosomal set cannot be achieved, yet this abnormal ratio should not necessarily affect the one-Xa choice mechanism for XCI. Previous studies of XCI patterns in murine triploids support the single-Xa model, but human triploids mostly have two-Xa cells, whether they are XXX or XXY. The XCI patterns we observe in fibroblast cultures from different XXX human triploids suggest that the two-Xa pattern of XCI is selected for, and may have resulted from rare segregation errors or Xi reactivation. CONCLUSION: The initial X inactivation pattern in human triploids, therefore, is likely to resemble the pattern that predominates in murine triploids, i.e., a single Xa, with the remaining X's inactive. Furthermore, our studies of XIST RNA accumulation and promoter methylation suggest that the basic features of XCI are normal in triploids despite the abnormal X:autosome ratio

    Generating mice with targeted mutations.

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    Journal ArticleMutational analysis is one of the most informative approaches available for the study of complex biological processes. It has been particularly successful in the analysis of the biology of bacteria, yeast, the nematode worm Caenorhabditis elegans and the fruit fly Drosophila melanogaster. Extension of this approach to the mouse, through informative, was far less successful relative to what has been achieved with these simpler model organisms. This is because it is not numerically practical in mice to use random mutagenesis to isolate mutations that affect a specified biological process of interest. Nonetheless, biological phenomena such as a sophisticated immune response, cancer, vascular disease or higher-order cognitive function, to mention just a few, must analyzed in organisms that show such phenomena, and for this reason geneticists and other researchers have turned to the mouse. Gene targeting, the means for creating mice with designed mutations in almost any gene, was developed as an alternative to the impractical use of random mutgenesis for pursing genetic analysis in the mouse. Now gene targeting has advanced the genomic manipulations possible in mice to a level that can be matched only in far simple organisms such as bacteria and yeast

    The X-inactivation trans-activator Rnf12 is negatively regulated by pluripotency factors in embryonic stem cells

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    X-inactivation, the molecular mechanism enabling dosage compensation in mammals, is tightly controlled during mouse early embryogenesis. In the morula, X-inactivation is imprinted with exclusive silencing of the paternally inherited X-chromosome. In contrast, in the post-implantation epiblast, X-inactivation affects randomly either the paternal or the maternal X-chromosome. The transition from imprinted to random X-inactivation takes place in the inner cell mass (ICM) of the blastocyst from which embryonic stem (ES) cells are derived. The trigger of X-inactivation, Xist, is specifically downregulated in the pluripotent cells of the ICM, thereby ensuring the reactivation of the inactive paternal X-chromosome and the transient presence of two active X-chromosomes. Moreover, Tsix, a critical cis-repressor of Xist, is upregulated in the ICM and in ES cells where it imposes a particular chromatin state at the Xist promoter that ensures the establishment of random X-inactivation upon differentiation. Recently, we have shown that key transcription factors supporting pluripotency directly repress Xist and activate Tsix and thus couple Xist/Tsix control to pluripotency. In this manuscript, we report that Rnf12, a third X-linked gene critical for the regulation of X-inactivation, is under the control of Nanog, Oct4 and Sox2, the three factors lying at the heart of the pluripotency network. We conclude that in mouse ES cells the pluripotency-associated machinery exerts an exhaustive control of X-inactivation by taking over the regulation of all three major regulators of X-inactivation: Xist, Tsix, and Rnf12
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