Publications by authors named "Hoyaux D"

Purpose: To increase human bone graft regeneration and quality by the use of a mixture containing autologous ground calvarial bone, human recombinant tissue factor (rhTF), platelet-rich plasma (PRP), and tetracycline.

Materials And Methods: Maxillary sinus floor augmentation was performed on 18 patients by grafting a "bone paste" made of PRP (1.8 x 10(6) platelets/mm3 plasma), about 1 microg rhTF, calvarial bone chips (2 to 5 mm in size), and tetracycline (10 to 30 microg/mL preparation).

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S100A8 and S100A9, also called myeloid related protein (MRP) 8 and 14, are calcium-binding proteins highly expressed in neutrophils, in which they play a key role in the inflammatory progression. In this study, we looked at the expression of S100A8/A9 within gingiva from normal and Cyclosporin A (CsA)-induced overgrowth gingiva. In gingiva from the CsA group, several positive S100A8/A9 cells were seen within the connective tissue, whereas in normal gingiva very few positive S100A8/A9 cells were detected.

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Astrogliosis is one of the earliest pathological changes observed in neurodegenerative diseases in general and in amyotrophic lateral sclerosis (ALS) in particular. ALS is characterized by selective degeneration of motoneurons. There are 2 forms of the disease: sporadic ALS (SALS), comprising 90%-95% of cases, and familial ALS (FALS), comprising 5%-10% of cases.

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It has been previously shown that S100A2 is downregulated in tumor cells. The level of immunohistochemical S100A2 expression was therefore characterized in 424 normal and tumoral (benign and malignant) tissues of various origins, but mostly epithelial (with either glandular, squamous, respiratory or urothelial differentiation). We also investigated whether S100A2 could be co-localized with cytokeratin K14, an intermediate filament protein expressed in basal proliferative keratinocytes.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterised by selective degeneration of motoneurones. Familial ALS is an age-dependent autosomal dominant disorder in which mutations in the homodimeric enzyme Cu/Zn superoxide dismutase 1 (SOD1) is linked to the disease. An animal model for this disease is a transgenic mouse expressing the mutated human SOD1(G93A) gene.

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