146 research outputs found

    Ertragsstabilität und Qualität von Weizensortenmischungen im Ökologischen Anbau

    Get PDF
    Disease development, yield and baking quality were assessed on the winter wheat cultivars Arina and Capo and their 1:1 mixture in a total of 12 sites on-farm in 2002/2003. Due to a severe drought disease severities were very low and probably had little effect on the plants. The more drought tolerant variety Capo over-yielded in mixtures on average by 21% while Arina yielded in mixtures as expected. Protein and gluten contents and baking volume in pure stands of Arina were usually higher than for Capo. Both varieties changed their quality parameters in mixtures. However, the parameters of the mixtures were not equal to the mean of the pure stands indicating some unknown interactions. The quality parameters of each variety or mixture were compared to the mean of all treatments in a given site allowing for regression analysis across sites. Capo was least able to improve its quality in reaction to improved site potential (expressed as mean baking volume) (slope: 0.64) while the mixtures reacted strongest (slope: 1.47). This indicates that mixtures might be better able to profit from good growing conditions than pure stands

    Time evolution of in vivo articular cartilage repair induced by bone marrow stimulation and scaffold implantation in rabbits

    Full text link
    Purpose: Tissue engineering techniques were used to study cartilage repair over a 12-month period in a rabbit model. Methods: A full-depth chondral defect along with subchondral bone injury were originated in the knee joint, where a biostable porous scaffold was implanted, synthesized of poly(ethyl acrylate-co-hydroxyethyl acrylate) copolymer. Morphological evolution of cartilage repair was studied 1 and 2 weeks, and 1, 3, and 12 months after implantation by histological techniques. The 3-month group was chosen to compare cartilage repair to an additional group where scaffolds were preseeded with allogeneic chondrocytes before implantation, and also to controls, who underwent the same surgery procedure, with no scaffold implantation. Results: Neotissue growth was first observed in the deepest scaffold pores 1 week after implantation, which spread thereafter; 3 months later scaffold pores were filled mostly with cartilaginous tissue in superficial and middle zones, and with bone tissue adjacent to subchondral bone. Simultaneously, native chondrocytes at the edges of the defect started to proliferate 1 week after implantation; within a month those edges had grown centripetally and seemed to embed the scaffold, and after 3 months, hyaline-like cartilage was observed on the condylar surface. Preseeded scaffolds slightly improved tissue growth, although the quality of repair tissue was similar to non-preseeded scaffolds. Controls showed that fibrous cartilage was mainly filling the repair area 3 months after surgery. In the 12-month group, articular cartilage resembled the untreated surface. Conclusions: Scaffolds guided cartilaginous tissue growth in vivo, suggesting their importance in stress transmission to the cells for cartilage repair.This study was supported by the Spanish Ministry of Science and Innovation through MAT2010-21611-C03-00 project (including the FEDER financial support), by Conselleria de Educacion (Generalitat Valenciana, Spain) PROMETEO/2011/084 grant, and by CIBER-BBN en Bioingenieria, Biomateriales y Nanomedicina. The work of JLGR was partially supported by funds from the Generalitat Valenciana, ACOMP/2012/075 project. CIBER-BBN is an initiative funded by the VI National R&D&i Plan 2008-2011, Iniciativa Ingenio 2010, Consolider Program, CIBER Actions and financed by the - Instituto de Salud Carlos III with assistance from the European Regional Development Fund.Sancho-Tello Valls, M.; Forriol, F.; Gastaldi, P.; Ruiz Sauri, A.; Martín De Llano, JJ.; Novella-Maestre, E.; Antolinos Turpín, CM.... (2015). Time evolution of in vivo articular cartilage repair induced by bone marrow stimulation and scaffold implantation in rabbits. International Journal of Artificial Organs. 38(4):210-223. https://doi.org/10.5301/ijao.5000404S210223384Becerra, J., Andrades, J. A., Guerado, E., Zamora-Navas, P., López-Puertas, J. M., & Reddi, A. H. (2010). Articular Cartilage: Structure and Regeneration. Tissue Engineering Part B: Reviews, 16(6), 617-627. doi:10.1089/ten.teb.2010.0191Nelson, L., Fairclough, J., & Archer, C. (2009). Use of stem cells in the biological repair of articular cartilage. Expert Opinion on Biological Therapy, 10(1), 43-55. doi:10.1517/14712590903321470MAINIL-VARLET, P., AIGNER, T., BRITTBERG, M., BULLOUGH, P., HOLLANDER, A., HUNZIKER, E., … STAUFFER, E. (2003). HISTOLOGICAL ASSESSMENT OF CARTILAGE REPAIR. The Journal of Bone and Joint Surgery-American Volume, 85, 45-57. doi:10.2106/00004623-200300002-00007Hunziker, E. B., Kapfinger, E., & Geiss, J. (2007). The structural architecture of adult mammalian articular cartilage evolves by a synchronized process of tissue resorption and neoformation during postnatal development. Osteoarthritis and Cartilage, 15(4), 403-413. doi:10.1016/j.joca.2006.09.010Onyekwelu, I., Goldring, M. B., & Hidaka, C. (2009). Chondrogenesis, joint formation, and articular cartilage regeneration. Journal of Cellular Biochemistry, 107(3), 383-392. doi:10.1002/jcb.22149Ahmed, T. A. E., & Hincke, M. T. (2010). Strategies for Articular Cartilage Lesion Repair and Functional Restoration. Tissue Engineering Part B: Reviews, 16(3), 305-329. doi:10.1089/ten.teb.2009.0590Hangody, L., Kish, G., Kárpáti, Z., Udvarhelyi, I., Szigeti, I., & Bély, M. (1998). Mosaicplasty for the Treatment of Articular Cartilage Defects: Application in Clinical Practice. Orthopedics, 21(7), 751-756. doi:10.3928/0147-7447-19980701-04Steinwachs, M. R., Guggi, T., & Kreuz, P. C. (2008). Marrow stimulation techniques. Injury, 39(1), 26-31. doi:10.1016/j.injury.2008.01.042Brittberg, M., Lindahl, A., Nilsson, A., Ohlsson, C., Isaksson, O., & Peterson, L. (1994). Treatment of Deep Cartilage Defects in the Knee with Autologous Chondrocyte Transplantation. New England Journal of Medicine, 331(14), 889-895. doi:10.1056/nejm199410063311401Richter, W. (2009). Mesenchymal stem cells and cartilagein situregeneration. Journal of Internal Medicine, 266(4), 390-405. doi:10.1111/j.1365-2796.2009.02153.xBartlett, W., Skinner, J. A., Gooding, C. R., Carrington, R. W. J., Flanagan, A. M., Briggs, T. W. R., & Bentley, G. (2005). Autologous chondrocyte implantationversusmatrix-induced autologous chondrocyte implantation for osteochondral defects of the knee. The Journal of Bone and Joint Surgery. British volume, 87-B(5), 640-645. doi:10.1302/0301-620x.87b5.15905Little, C. J., Bawolin, N. K., & Chen, X. (2011). Mechanical Properties of Natural Cartilage and Tissue-Engineered Constructs. Tissue Engineering Part B: Reviews, 17(4), 213-227. doi:10.1089/ten.teb.2010.0572Vikingsson, L., Gallego Ferrer, G., Gómez-Tejedor, J. A., & Gómez Ribelles, J. L. (2014). An «in vitro» experimental model to predict the mechanical behavior of macroporous scaffolds implanted in articular cartilage. Journal of the Mechanical Behavior of Biomedical Materials, 32, 125-131. doi:10.1016/j.jmbbm.2013.12.024Weber, J. F., & Waldman, S. D. (2014). Calcium signaling as a novel method to optimize the biosynthetic response of chondrocytes to dynamic mechanical loading. Biomechanics and Modeling in Mechanobiology, 13(6), 1387-1397. doi:10.1007/s10237-014-0580-xMauck, R. L., Soltz, M. A., Wang, C. C. B., Wong, D. D., Chao, P.-H. G., Valhmu, W. B., … Ateshian, G. A. (2000). Functional Tissue Engineering of Articular Cartilage Through Dynamic Loading of Chondrocyte-Seeded Agarose Gels. Journal of Biomechanical Engineering, 122(3), 252-260. doi:10.1115/1.429656Palmoski, M. J., & Brandt, K. D. (1984). Effects of static and cyclic compressive loading on articular cartilage plugs in vitro. Arthritis & Rheumatism, 27(6), 675-681. doi:10.1002/art.1780270611Khoshgoftar, M., Ito, K., & van Donkelaar, C. C. (2014). The Influence of Cell-Matrix Attachment and Matrix Development on the Micromechanical Environment of the Chondrocyte in Tissue-Engineered Cartilage. Tissue Engineering Part A, 20(23-24), 3112-3121. doi:10.1089/ten.tea.2013.0676Agrawal, C. M., & Ray, R. B. (2001). Biodegradable polymeric scaffolds for musculoskeletal tissue engineering. Journal of Biomedical Materials Research, 55(2), 141-150. doi:10.1002/1097-4636(200105)55:23.0.co;2-jPérez Olmedilla, M., Garcia-Giralt, N., Pradas, M. M., Ruiz, P. B., Gómez Ribelles, J. L., Palou, E. C., & García, J. C. M. (2006). Response of human chondrocytes to a non-uniform distribution of hydrophilic domains on poly (ethyl acrylate-co-hydroxyethyl methacrylate) copolymers. Biomaterials, 27(7), 1003-1012. doi:10.1016/j.biomaterials.2005.07.030Horbett, T. A., & Schway, M. B. (1988). Correlations between mouse 3T3 cell spreading and serum fibronectin adsorption on glass and hydroxyethylmethacrylate-ethylmethacrylate copolymers. Journal of Biomedical Materials Research, 22(9), 763-793. doi:10.1002/jbm.820220903Kiremitçi, M., Peşmen, A., Pulat, M., & Gürhan, I. (1993). Relationship of Surface Characteristics to Cellular Attachment in PU and PHEMA. Journal of Biomaterials Applications, 7(3), 250-264. doi:10.1177/088532829300700304Lydon, M. ., Minett, T. ., & Tighe, B. . (1985). Cellular interactions with synthetic polymer surfaces in culture. Biomaterials, 6(6), 396-402. doi:10.1016/0142-9612(85)90100-0Campillo-Fernandez, A. J., Pastor, S., Abad-Collado, M., Bataille, L., Gomez-Ribelles, J. L., Meseguer-Dueñas, J. M., … Ruiz-Moreno, J. M. (2007). Future Design of a New Keratoprosthesis. Physical and Biological Analysis of Polymeric Substrates for Epithelial Cell Growth. Biomacromolecules, 8(8), 2429-2436. doi:10.1021/bm0703012Funayama, A., Niki, Y., Matsumoto, H., Maeno, S., Yatabe, T., Morioka, H., … Toyama, Y. (2008). Repair of full-thickness articular cartilage defects using injectable type II collagen gel embedded with cultured chondrocytes in a rabbit model. Journal of Orthopaedic Science, 13(3), 225-232. doi:10.1007/s00776-008-1220-zKitahara, S., Nakagawa, K., Sah, R. L., Wada, Y., Ogawa, T., Moriya, H., & Masuda, K. (2008). In Vivo Maturation of Scaffold-free Engineered Articular Cartilage on Hydroxyapatite. Tissue Engineering Part A, 14(11), 1905-1913. doi:10.1089/ten.tea.2006.0419Martinez-Diaz, S., Garcia-Giralt, N., Lebourg, M., Gómez-Tejedor, J.-A., Vila, G., Caceres, E., … Monllau, J. C. (2010). In Vivo Evaluation of 3-Dimensional Polycaprolactone Scaffolds for Cartilage Repair in Rabbits. The American Journal of Sports Medicine, 38(3), 509-519. doi:10.1177/0363546509352448Wang, Y., Bian, Y.-Z., Wu, Q., & Chen, G.-Q. (2008). Evaluation of three-dimensional scaffolds prepared from poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) for growth of allogeneic chondrocytes for cartilage repair in rabbits. Biomaterials, 29(19), 2858-2868. doi:10.1016/j.biomaterials.2008.03.021Alió del Barrio, J. L., Chiesa, M., Gallego Ferrer, G., Garagorri, N., Briz, N., Fernandez-Delgado, J., … De Miguel, M. P. (2014). Biointegration of corneal macroporous membranes based on poly(ethyl acrylate) copolymers in an experimental animal model. Journal of Biomedical Materials Research Part A, 103(3), 1106-1118. doi:10.1002/jbm.a.35249Diego, R. B., Olmedilla, M. P., Aroca, A. S., Ribelles, J. L. G., Pradas, M. M., Ferrer, G. G., & Sánchez, M. S. (2005). Acrylic scaffolds with interconnected spherical pores and controlled hydrophilicity for tissue engineering. Journal of Materials Science: Materials in Medicine, 16(8), 693-698. doi:10.1007/s10856-005-2604-7Serrano Aroca, A., Campillo Fernández, A. J., Gómez Ribelles, J. L., Monleón Pradas, M., Gallego Ferrer, G., & Pissis, P. (2004). Porous poly(2-hydroxyethyl acrylate) hydrogels prepared by radical polymerisation with methanol as diluent. Polymer, 45(26), 8949-8955. doi:10.1016/j.polymer.2004.10.033Diani, J., Fayolle, B., & Gilormini, P. (2009). A review on the Mullins effect. European Polymer Journal, 45(3), 601-612. doi:10.1016/j.eurpolymj.2008.11.017Mullins, L. (1969). Softening of Rubber by Deformation. Rubber Chemistry and Technology, 42(1), 339-362. doi:10.5254/1.3539210Jurvelin, J. S., Buschmann, M. D., & Hunziker, E. B. (2003). Mechanical anisotropy of the human knee articular cartilage in compression. Proceedings of the Institution of Mechanical Engineers, Part H: Journal of Engineering in Medicine, 217(3), 215-219. doi:10.1243/095441103765212712Shapiro, F., Koide, S., & Glimcher, M. J. (1993). Cell origin and differentiation in the repair of full-thickness defects of articular cartilage. The Journal of Bone & Joint Surgery, 75(4), 532-553. doi:10.2106/00004623-199304000-00009SELLERS, R. S., ZHANG, R., GLASSON, S. S., KIM, H. D., PELUSO, D., D’AUGUSTA, D. A., … MORRIS, E. A. (2000). Repair of Articular Cartilage Defects One Year After Treatment with Recombinant Human Bone Morphogenetic Protein-2 (rhBMP-2)*. The Journal of Bone and Joint Surgery-American Volume, 82(2), 151-160. doi:10.2106/00004623-200002000-00001Hunziker, E. B., Michel, M., & Studer, D. (1997). Ultrastructure of adult human articular cartilage matrix after cryotechnical processing. Microscopy Research and Technique, 37(4), 271-284. doi:10.1002/(sici)1097-0029(19970515)37:43.0.co;2-oAppelman, T. P., Mizrahi, J., Elisseeff, J. H., & Seliktar, D. (2009). The differential effect of scaffold composition and architecture on chondrocyte response to mechanical stimulation. Biomaterials, 30(4), 518-525. doi:10.1016/j.biomaterials.2008.09.063Chung, C., & Burdick, J. A. (2008). Engineering cartilage tissue. Advanced Drug Delivery Reviews, 60(2), 243-262. doi:10.1016/j.addr.2007.08.027HUNZIKER, E. B., & ROSENBERG, L. C. (1996). Repair of Partial-Thickness Defects in Articular Cartilage. The Journal of Bone & Joint Surgery, 78(5), 721-33. doi:10.2106/00004623-199605000-00012Schulze-Tanzil, G. (2009). Activation and dedifferentiation of chondrocytes: Implications in cartilage injury and repair. Annals of Anatomy - Anatomischer Anzeiger, 191(4), 325-338. doi:10.1016/j.aanat.2009.05.003Umlauf, D., Frank, S., Pap, T., & Bertrand, J. (2010). Cartilage biology, pathology, and repair. Cellular and Molecular Life Sciences, 67(24), 4197-4211. doi:10.1007/s00018-010-0498-0Karystinou, A., Dell’Accio, F., Kurth, T. B. A., Wackerhage, H., Khan, I. M., Archer, C. W., … De Bari, C. (2009). Distinct mesenchymal progenitor cell subsets in the adult human synovium. Rheumatology, 48(9), 1057-1064. doi:10.1093/rheumatology/kep192Sakaguchi, Y., Sekiya, I., Yagishita, K., & Muneta, T. (2005). Comparison of human stem cells derived from various mesenchymal tissues: Superiority of synovium as a cell source. Arthritis & Rheumatism, 52(8), 2521-2529. doi:10.1002/art.21212Schaefer, D., Martin, I., Jundt, G., Seidel, J., Heberer, M., Grodzinsky, A., … Freed, L. E. (2002). Tissue-engineered composites for the repair of large osteochondral defects. Arthritis & Rheumatism, 46(9), 2524-2534. doi:10.1002/art.1049

    Multi-system neurological disease is common in patients with OPA1 mutations

    Get PDF
    Additional neurological features have recently been described in seven families transmitting pathogenic mutations in OPA1, the most common cause of autosomal dominant optic atrophy. However, the frequency of these syndromal ‘dominant optic atrophy plus’ variants and the extent of neurological involvement have not been established. In this large multi-centre study of 104 patients from 45 independent families, including 60 new cases, we show that extra-ocular neurological complications are common in OPA1 disease, and affect up to 20% of all mutational carriers. Bilateral sensorineural deafness beginning in late childhood and early adulthood was a prominent manifestation, followed by a combination of ataxia, myopathy, peripheral neuropathy and progressive external ophthalmoplegia from the third decade of life onwards. We also identified novel clinical presentations with spastic paraparesis mimicking hereditary spastic paraplegia, and a multiple sclerosis-like illness. In contrast to initial reports, multi-system neurological disease was associated with all mutational subtypes, although there was an increased risk with missense mutations [odds ratio = 3.06, 95% confidence interval = 1.44–6.49; P = 0.0027], and mutations located within the guanosine triphosphate-ase region (odds ratio = 2.29, 95% confidence interval = 1.08–4.82; P = 0.0271). Histochemical and molecular characterization of skeletal muscle biopsies revealed the presence of cytochrome c oxidase-deficient fibres and multiple mitochondrial DNA deletions in the majority of patients harbouring OPA1 mutations, even in those with isolated optic nerve involvement. However, the cytochrome c oxidase-deficient load was over four times higher in the dominant optic atrophy + group compared to the pure optic neuropathy group, implicating a causal role for these secondary mitochondrial DNA defects in disease pathophysiology. Individuals with dominant optic atrophy plus phenotypes also had significantly worse visual outcomes, and careful surveillance is therefore mandatory to optimize the detection and management of neurological disability in a group of patients who already have significant visual impairment

    Risk profiles and one-year outcomes of patients with newly diagnosed atrial fibrillation in India: Insights from the GARFIELD-AF Registry.

    Get PDF
    BACKGROUND: The Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) is an ongoing prospective noninterventional registry, which is providing important information on the baseline characteristics, treatment patterns, and 1-year outcomes in patients with newly diagnosed non-valvular atrial fibrillation (NVAF). This report describes data from Indian patients recruited in this registry. METHODS AND RESULTS: A total of 52,014 patients with newly diagnosed AF were enrolled globally; of these, 1388 patients were recruited from 26 sites within India (2012-2016). In India, the mean age was 65.8 years at diagnosis of NVAF. Hypertension was the most prevalent risk factor for AF, present in 68.5% of patients from India and in 76.3% of patients globally (P < 0.001). Diabetes and coronary artery disease (CAD) were prevalent in 36.2% and 28.1% of patients as compared with global prevalence of 22.2% and 21.6%, respectively (P < 0.001 for both). Antiplatelet therapy was the most common antithrombotic treatment in India. With increasing stroke risk, however, patients were more likely to receive oral anticoagulant therapy [mainly vitamin K antagonist (VKA)], but average international normalized ratio (INR) was lower among Indian patients [median INR value 1.6 (interquartile range {IQR}: 1.3-2.3) versus 2.3 (IQR 1.8-2.8) (P < 0.001)]. Compared with other countries, patients from India had markedly higher rates of all-cause mortality [7.68 per 100 person-years (95% confidence interval 6.32-9.35) vs 4.34 (4.16-4.53), P < 0.0001], while rates of stroke/systemic embolism and major bleeding were lower after 1 year of follow-up. CONCLUSION: Compared to previously published registries from India, the GARFIELD-AF registry describes clinical profiles and outcomes in Indian patients with AF of a different etiology. The registry data show that compared to the rest of the world, Indian AF patients are younger in age and have more diabetes and CAD. Patients with a higher stroke risk are more likely to receive anticoagulation therapy with VKA but are underdosed compared with the global average in the GARFIELD-AF. CLINICAL TRIAL REGISTRATION-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01090362
    corecore