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61.
1. FXIII was isolated and purified over 4000 fold from human placenta to apparent electrophoretic homogeneity by a new procedure including ethanol precipitation. DEAE-Cellulose, molecular sieving on Sephacryl S-300 and Phenyl-Sepharose chromatography. 2. Its pI was about 5.1. Under appropriate conditions, the incubation of FXIII in the presence of thrombin did not lead to inactivation cut in the polypeptidic chain. 3. FXIII was also activated by CaCl2 and, in a lesser extent, by other divalent cations like SrCl2, BaCl2 or MgCl2. 4. The binding of calcium to FXIII exhibited a negative cooperativity. 5. The activity-pH curve of the calcium-activated enzyme did not appear very different from that of the thrombin-activated enzyme. 相似文献
62.
Alkalinity of the medium was shown to be the chief factor involved in the accumulation of oxalate by T. cinnabarina. Glutamate and aspartate are shown to lead to oxalate with this organism and with L. lepideus by dehydrogenation to α-ketoglutarate and oxaloacetate, respectively. Malate was also shown to be dehydrogenated. It is proposed that oxaloacetate may either undergo β-decarboxylation to yield CO2 and pyruvate, or splitting by coenzyme A to yield oxalate and acetylated coenzyme A. The reversal of this latter reaction is suggested as the explanation of the disappearance of oxalate from culture media. The reduction of resazurin by the dehydrogenase systems of the molds is inhibited by cyanide, indicating the participation of metal systems, such as the cytochromes. 相似文献
63.
J Daigneault G Aubin F Simard M De Braekeleer 《Human biology; an international record of research》1992,64(1):115-119
The incidence of cystic fibrosis (CF) in Saguenay-Lac-St.-Jean, a geographically isolated region of Quebec, was estimated to be 1 in 902 during the period 1975-1988. The carrier rate was calculated to be 1 in 15 inhabitants. The high incidence of CF in Saguenay-Lac-St.-Jean is probably the result of a founder effect and genetic drift for one or more mutations. Historical, demographic, and social factors also may have contributed to the high incidence. 相似文献
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65.
S D Kroll J Chen M De Vivo D J Carty A Buku R T Premont R Iyengar 《The Journal of biological chemistry》1992,267(32):23183-23188
66.
Yi-Shiang Huang Virginie Bertrand Dimitriya Bozukova Christophe Pagnoulle Christine Labrugère Edwin De Pauw Marie-Claire De Pauw-Gillet Marie-Christine Durrieu 《PloS one》2014,9(12)
Posterior Capsular Opacification (PCO) is the capsule fibrosis developed on implanted IntraOcular Lens (IOL) by the de-differentiation of Lens Epithelial Cells (LECs) undergoing Epithelial Mesenchymal Transition (EMT). Literature has shown that the incidence of PCO is multifactorial including the patient''s age or disease, surgical technique, and IOL design and material. Reports comparing hydrophilic and hydrophobic acrylic IOLs have shown that the former has more severe PCO. On the other hand, we have previously demonstrated that the adhesion of LECs is favored on hydrophobic compared to hydrophilic materials. By combining these two facts and contemporary knowledge in PCO development via the EMT pathway, we propose a biomimetically inspired strategy to promote LEC adhesion without de-differentiation to reduce the risk of PCO development. By surface grafting of a cell adhesion molecule (RGD peptide) onto the conventional hydrophilic acrylic IOL material, the surface-functionalized IOL can be used to reconstitute a capsule-LEC-IOL sandwich structure, which has been considered to prevent PCO formation in literature. Our results show that the innovative biomaterial improves LEC adhesion, while also exhibiting similar optical (light transmittance, optical bench) and mechanical (haptic compression force, IOL injection force) properties compared to the starting material. In addition, compared to the hydrophobic IOL material, our bioactive biomaterial exhibits similar abilities in LEC adhesion, morphology maintenance, and EMT biomarker expression, which is the crucial pathway to induce PCO. The in vitro assays suggest that this biomaterial has the potential to reduce the risk factor of PCO development. 相似文献
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68.
Human Dermal Fibroblasts Demonstrate Positive Immunostaining for Neuron- and Glia- Specific Proteins
C. J. Janmaat K. E de Rooij H Locher S. C. de Groot J. C. M. J. de Groot J. H. M. Frijns M. A. Huisman 《PloS one》2015,10(12)
In stem cell cultures from adult human tissue, undesirable contamination with fibroblasts is frequently present. The presence of fibroblasts obscures the actual number of stem cells and may result in extracellular matrix production after transplantation. Identification of fibroblasts is difficult because of the lack of specific fibroblast markers. In our laboratory, we isolate and expand neural-crest-derived stem cells from human hair follicle bulges and investigate their potential to differentiate into neural cells. To establish cellular identities, we perform immunohistochemistry with antibodies specific for glial and neuronal markers, and use fibroblasts as negative control. We frequently observe that human adult dermal fibroblasts also express some glial and neuronal markers. In this study, we have sought to determine whether our observations represent actual expression of these markers or result from cross-reactivity. Immunohistochemistry was performed on human adult dermal fibroblasts using acknowledged glial and neuronal antibodies followed by verification of the data using RT-qPCR. Human adult dermal fibroblasts showed expression of the glia-specific markers SOX9, glial fibrillary acidic protein and EGR2 (KROX20) as well as for the neuron-specific marker class III β-tubulin, both at the protein and mRNA level. Furthermore, human adult dermal fibroblasts showed false-positive immunostaining for S100β and GAP43 and to a lower extent for OCT6. Our results indicate that immunophenotyping as a tool to determine cellular identity is not as reliable as generally assumed, especially since human adult dermal fibroblasts may be mistaken for neural cells, indicating that the ultimate proof of glial or neuronal identity can only be provided by their functionality. 相似文献
69.
Paolo d’Errico Marina Boido Antonio Piras Valeria Valsecchi Elena De Amicis Denise Locatelli Silvia Capra Francesco Vagni Alessandro Vercelli Giorgio Battaglia 《PloS one》2013,8(12)
Loss of the survival motor neuron gene (SMN1) is responsible for spinal muscular atrophy (SMA), the most common inherited cause of infant mortality. Even though the SMA phenotype is traditionally considered as related to spinal motor neuron loss, it remains debated whether the specific targeting of motor neurons could represent the best therapeutic option for the disease. We here investigated, using stereological quantification methods, the spinal cord and cerebral motor cortex of ∆7 SMA mice during development, to verify extent and selectivity of motor neuron loss. We found progressive post-natal loss of spinal motor neurons, already at pre-symptomatic stages, and a higher vulnerability of motor neurons innervating proximal and axial muscles. Larger motor neurons decreased in the course of disease, either for selective loss or specific developmental impairment. We also found a selective reduction of layer V pyramidal neurons associated with layer V gliosis in the cerebral motor cortex. Our data indicate that in the ∆7 SMA model SMN loss is critical for the spinal cord, particularly for specific motor neuron pools. Neuronal loss, however, is not selective for lower motor neurons. These data further suggest that SMA pathogenesis is likely more complex than previously anticipated. The better knowledge of SMA models might be instrumental in shaping better therapeutic options for affected patients. 相似文献
70.