816 research outputs found

    Cellulose hydrolysis-hydrogenolysis to ethyleneglycol and propyleneglycol over Ru and heteropolyacid catalysts

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    Еthylene and propylene glycols (EG and PG) are widely used in industry to produce cooling systems and other valuable chemical products. But PG is non-toxic, therefore it is used in industries where EG can not be used: pharmaceutical, food, etc. This polyols produced by "one-pot" method, which is one of the promising and effective methods for producing alcohols from cellulose under harsh conditions. The purpose of this study was to determine the optimal composition of the solid bifunctional catalyst and the conditions of its preparation for the hydrolysis-hydrogenolysis of cellulose. Catalists are Ru-HPA/ZrO[2], RuHPA/Nb[2]O[5] and Ru/CsHPK. As a result of the study, the most promising catalyst system is 1%Ru/Cs[3.5]H[0.5]SiW[12]O[40]. In the presence of 1%Ru/CsHPA, the yield of 25% EG and 11% PG was detected (EG and PG selectivity is 60 and 27%). The activity of the catalysts was studied in the presence of Ca(OH)[2]

    Hernia fibroblasts lack β-estradiol induced alterations of collagen gene expression

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    BACKGROUND: Estrogens are reported to increase type I and type III collagen deposition and to regulate Metalloproteinase 2 (MMP-2) expression. These proteins are reported to be dysregulated in incisional hernia formation resulting in a significantly decreased type I to III ratio. We aimed to evaluate the β-estradiol mediated regulation of type I and type III collagen genes as well as MMP-2 gene expression in fibroblasts derived from patients with or without history of recurrent incisional hernia disease. We compared primary fibroblast cultures from male/female subjects without/without incisional hernia disease. RESULTS: Incisional hernia fibroblasts (IHFs) revealed a decreased type I/III collagen mRNA ratio. Whereas fibroblasts from healthy female donors responded to β-estradiol, type I and type III gene transcription is not affected in fibroblasts from males or affected females. Furthermore β-estradiol had no influence on the impaired type I to III collagen ratio in fibroblasts from recurrent hernia patients. CONCLUSION: Our results suggest that β-estradiol does not restore the imbaired balance of type I/III collagen in incisional hernia fibroblasts. Furthermore, the individual was identified as an independent factor for the β-estradiol induced alterations of collagen gene expression. The observation of gender specific β-estradiol-dependent changes of collagen gene expression in vitro is of significance for future studies of cellular response

    Biomechanical and morphological study of a new elastic mesh (Ciberlastic) to repair abdominal wall defects

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    The aim of this study was to conduct a preclinical evaluation of the behaviour of a new type of abdominal LW prosthesis (Ciberlastic), which was designed with a non-absorbable elastic polyurethane monofilament (Assuplus, Assut Europe, Italy) to allow greater adaptability to mechanical area requirements and higher bio-mimicking with the newly formed surrounding tissues. Our hypothesis was that an increase in the elasticity of the mesh filament could improve the benefits of LW prostheses. To verify our hypothesis, we compared the short- and long-term behaviour of Ciberlastic and Optilene® elastic commercial meshes by repairing the partially herniated abdomen in New Zealand White rabbits. The implanted meshes were mechanically and histologically assessed at 14 and 180 days post-implant. We mechanically characterized the partially herniated repaired muscle tissue and also determined mesh shrinkage at different post-implant times. This was followed by a histological study in which the tissue incorporation process was analysed over time. The new prosthesis designed by our group achieved good behaviour that was similar to that of Optilene®, one of the most popular LW prostheses on the market, with the added advantage of its elastic property. The mechanical properties are significantly lower than those of the polypropylene Optilene® mesh, and the new elastic mesh meets the basic mechanical requirements for positioning in the abdominal wall, which was also demonstrated by the absence of recurrences after implantation in the experimental model. We found that the growth of a connective tissue rich in collagen over the hernial defect and the proper deposit of the collagen fibres in the regenerated tissue substantially modified the original properties of the mesh, thereby increasing its biomechanical strength and making the whole tissue/mesh stiffer

    Muscle weakness in TPM3-myopathy is due to reduced Ca2+-sensitivity and impaired acto-myosin cross-bridge cycling in slow fibres.

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    Dominant mutations in TPM3, encoding α-tropomyosin(slow), cause a congenital myopathy characterized by generalized muscle weakness. Here, we used a multidisciplinary approach to investigate the mechanism of muscle dysfunction in 12 TPM3-myopathy patients. We confirm that slow myofibre hypotrophy is a diagnostic hallmark of TPM3-myopathy, and is commonly accompanied by skewing of fibre-type ratios (either slow or fast fibre predominance). Patient muscle contained normal ratios of the three tropomyosin isoforms and normal fibre-type expression of myosins and troponins. Using 2D-PAGE, we demonstrate that mutant α-tropomyosin(slow) was expressed, suggesting muscle dysfunction is due to a dominant-negative effect of mutant protein on muscle contraction. Molecular modelling suggested mutant α-tropomyosin(slow) likely impacts actin–tropomyosin interactions and, indeed, co-sedimentation assays showed reduced binding of mutant α-tropomyosin(slow) (R168C) to filamentous actin. Single fibre contractility studies of patient myofibres revealed marked slow myofibre specific abnormalities. At saturating [Ca(2+)] (pCa 4.5), patient slow fibres produced only 63% of the contractile force produced in control slow fibres and had reduced acto-myosin cross-bridge cycling kinetics. Importantly, due to reduced Ca(2+)-sensitivity, at sub-saturating [Ca(2+)] (pCa 6, levels typically released during in vivo contraction) patient slow fibres produced only 26% of the force generated by control slow fibres. Thus, weakness in TPM3-myopathy patients can be directly attributed to reduced slow fibre force at physiological [Ca(2+)], and impaired acto-myosin cross-bridge cycling kinetics. Fast myofibres are spared; however, they appear to be unable to compensate for slow fibre dysfunction. Abnormal Ca(2+)-sensitivity in TPM3-myopathy patients suggests Ca(2+)-sensitizing drugs may represent a useful treatment for this condition

    Long-term recurrence and complication rates after incisional hernia repair with the open onlay technique

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    <p>Abstract</p> <p>Background</p> <p>Incisional hernia after abdominal surgery is a well-known complication. Controversy still exists with respect to the choice of hernia repair technique. The objective of this study was to evaluate the long-term recurrence rate as well as surgical complications in a consecutive group of patients undergoing open repair using an onlay mesh technique.</p> <p>Methods</p> <p>Consecutive patients undergoing open incisional hernia repair with onlay-technique between 01/05/1995 and 01/09/2007 at a single institution were included in the study. For follow-up patients were contacted by telephone, and answered a questionnaire containing questions related to the primary operation, the hernia and general risk factors. Patients were examined by a consultant surgeon in the outpatient clinic or in the patient's home if there was suspicion of an incisional hernia recurrence.</p> <p>Results</p> <p>The study included 56 patients with 100% follow-up. The median follow-up was 35 months (range 4–151). Recurrent incisional hernia was found in 8 of 56 patients (15%, 95% CI: 6–24). The overall complication rate was 13% (95% CI, 4–22). All complications were minor and needed no hospital admission.</p> <p>Conclusion</p> <p>This study with a long follow-up showed low recurrence and complication rates in patients undergoing incisional hernia repair with the open onlay technique.</p
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