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Biomedical subjects

P Marie

Publications and source records attributed to P Marie.

At least 19 recordsLinked to original sources

Mechanically responsive films of variable hydrophobicity made of polyelectrolyte multilayers.

Mechanically responsive surfaces that allow to switch reversibly from a hydrophobic to a hydrophilic substrate are reported. The surfaces are constituted of polyelectrolyte multilayers deposited on modified charged silicone sheets. n bilayers of poly(allylamine)-Nafion (PAH-Naf) and m bilayers of poly(allylamine)-poly(acrylic acid) (PAH-PAA) composed the multilayers. A (PAH-Naf)(n) film possesses a water contact angle of around 105 degrees, whereas the contact angle of a (PAH-Naf)(4)-(PAH-PAA)(m) multilayer is around 50 degrees. When such a film with m < 5 and terminated by PAA is stretched out, its water contact angle increases up to around 100 degrees. Successive elongation/retraction cycles allow the water contact angle to alternate reversibly between 100 and 57 degrees indicating the reversible mechanical responsive nature of the film.

Letter↗

Small-angle neutron scattering study of particle coalescence and SDS desorption during film formation from carboxylated acrylic latices.

Four monodisperse core-shell latices were synthesized for small-angle neutron scattering (SANS) studies, differing by the acrylic acid content in the particle shell (1 or 4 wt%) and the T(g) of the acrylic core (around -40 or 10 degrees C). In a first part, the coalescence kinetics of the surfactant-free latices were studied. It was shown that coalescence was hindered by an increase in the acrylic acid content of the shell, pH of the latex, and Tg of the core. These results could be interpreted in terms of chain mobility in the shell and in the core. Upon coalescence, the hydrophilic phase was segregated in spherical, polydisperse domains with an average diameter of 110 nm. In a second part, labeled SDS was used to follow desorption of the surfactant during film formation. It was shown that desorption occurred early in the film formation process when the latex still contained around 20% of water. A small fraction of the surfactant remained irreversibly adsorbed at the particle surface.

Journal Article↗

Distribution of water-soluble and surface-active low-molecular-weight species in acrylic latex films.

Monodisperse core-shell latices were synthesized, differing in the acrylic acid (AA) content in the particle shell (1 or 4 wt%) and the Tg of the acrylic core (around -40 or 10 degrees C). In a first step, the drying mechanisms of the dialyzed latices were studied by confocal Raman spectroscopy. It was shown that, besides some unexpected features (briefly described in the article), drying occurred in a rather classical way, i.e., simultaneously from top to bottom and from edge to center. Then, the distributions of sulfate ion (SO4) (from sodium sulfate) and sodium dodecyl sulfate (SDS) in the dry latex films were established by confocal Raman spectroscopy and attenuated total reflectance (ATR). The two techniques were complementary. SO4 and SDS distributions were quite different, although presenting some common characteristics. In both cases, repartition of the low-molecular-weight species in the film was even less homogeneous when the AA content was lower and the particle core softer. However, SO4 showed enrichment at the film-substrate interface and depletion at the air side, whereas SDS showed concentration maxima at both interfaces. Interpretations stress the importance of desorption from the particle-water interface, transport by water, size effects, and diffusion.

Journal Article↗

[Cellular and molecular biology of fibrous dysplasia].

Several recent studies reflect major progress on the molecular biology and on the mechanisms of the lesions of fibrous dysplasia (monostotic and polyostotic forms) as well as the McCune-Albright syndrome. This review includes a detailed histological description of fibrous dysplasia: disorganized collagen fibers, woven bone formation, immature cytology of the osteoblasts and preosteoblastic cells. Histological lesions are also associated with an alteration of bone proteins: such as an increase in the expression of osteonectin, decrease of osteopontin and bone sialoprotein. Cell cultures of dysplasic osteoblastic cells have shown that the bone lesions are the result of abnormalities of the proliferation and differentiation of bone forming cells with a rise in CAMP levels. Poorly differentiated cells are associated with the formation of disorganized collagen fibers and with a trouble of synthesis of bone proteins. All these findings are linked to mutations of the Gs alpha (sub-unit alpha) protein. Various activating mutations are described as well as the molecular mechanisms of different forms of fibrous dysplasia, involving specially the c-fos proto-oncogene. Therapeutic implications are quoted, specially calcitonin and bisphosphonates.

Cell Differentiation↗

New factors controlling bone remodeling.

Two factors of crucial importance in bone cell differentiation were discovered within the last two years. One is the transcription factor Osf2/Cbfa1, which allows mesenchymal stem cells to differentiate into osteoblasts. Soluble factors, including bone morphogenetic proteins (BMPs), leptin, and TGF-beta, can modulate differentiation of mesenchymal stem cells to osteoblasts or to other cell types such as chondrocytes or adipocytes. The other recent discovery is osteoclast differentiating factor (ODF), which is specific for and indispensable to osteoclast differentiation. ODF belongs to the TNF family. Its soluble receptor, osteoprotegerin, prevents it from binding to osteoclasts, thus inhibiting its activity. A role of lymphocytes in bone remodeling has long been suspected, and it has now been shown that ODF is produced by activated T lymphocytes, which may therefore be implicated in bone loss accompanying inflammation. Finally, recent evidence supports a role for B lymphocytes in bone loss secondary to estrogen deprivation. In conclusion, these recent data may have important applications. Osteoprotegerin is a potent antiosteoclast agent that may prove useful in the treatment of bone disorders. Osf2/Cbfa1 and ODF are major targets in the treatment of osteoporosis.

Animals↗

Osteopontin is associated with bioprosthetic heart valve calcification in humans.

Calcification of non-osseous tissues such as heart valves or vessels is a major concern in clinical practice. The exact mechanism is still unknown. Numerous studies have shown that mineral deposits of crystalline hydroxyapatite within these tissues were associated with increased non-collagenous protein content. More recently osteopontin was found to be associated with calcification in living tissues such as vessels and native human aortic valves. The aim of this study was to determine whether or not non-collagenous proteins can also be found in non-living tissues such as glutaraldehyde-pretreated porcine valves after implantation in humans. Thirty-eight glutaraldehyde pretreated porcine bioprostheses were studied: 16 not implanted and 22 after 11 years of implantation in the aortic and mitral valve position in humans. In areas of calcification vizualized by Von Kossa staining and microradiography, immunostaining using polyclonal antibodies against calcium-binding proteins showed osteopontin positive staining and no staining for osteocalcin, bone sialoprotein or osteonectin. In uncalcified areas and in non-implanted values, staining for osteopontin or other calcium-binding proteins was negative. Western blot analysis of macroscopically calcified and uncalcified areas showed that several proteins were adsorbed in implanted values and confirmed the presence of osteopontin in the calcified areas, while no immunolabelling was found in non-calcified areas, in uncalcified valves and in non-implanted valves. Thus the presence of osteopontin in the calcified areas of bioprosthetic heart valves implanted in human indicates that this protein is associated with bioprosthetic valvular calcification. Since these values are made of non-living connective tissue, and no cell immunostained for osteopontin was found around the calcified area, this suggests that a non-cellular mediated mechanism involving protein adsorption may play a role in bioprosthetic valvular calcification.

Bioprosthesis↗

Secretory products of breast cancer cells specifically affect human osteoblastic cells: partial characterization of active factors.

The pathogenesis of tumor-induced osteolysis (TIO) following breast cancer metastases in bone remains unclear. We postulated that osteoblasts could be target cells for the secretory products of breast cancer cells. We previously showed that serum-free conditioned medium (CM) of the breast cancer cell line MCF-7 inhibits DNA synthesis by 75% of control values in osteoblast-like cells SaOS-2 and that this effect is only in a minor part due to transforming growth factor beta secretion. To establish the specificity of our observations and to look for other biologically active factors, we have tested the effects of medium conditioned by several cancer and noncancer cell lines (breast, colon, placenta, or fibrosarcoma) on the proliferation of osteoblast-like cells (SaOS-2, MG-63), normal human osteoblasts, human fibrosarcoma cells, and normal human fibroblasts. Culture medium (1:2) of the breast cancer cell lines MCF-7, T-47D, MDA-MB-231, and SK-BR-3 inhibited by 25-50% the proliferation of osteoblast-like cells SaOS-2, MG-63, and normal osteoblasts as evaluated by the MTT survival test or [3H]thymidine incorporation. MCF-7 cells completely inhibited the proliferation of normal human osteoblasts in coculture. This inhibitory effect was reversible and not due to cytotoxicity. Moreover, the cyclic adenosine monophosphate (cAMP) response to parathyroid hormone (PTH) of osteoblast-like cells SaOS-2 was also increased by 100-240% by the same CM. Such activities were, however, not detected in medium from the breast noncancer cell line HBL-100 or in the medium conditioned by non-breast cancer cell lines (COLO 320DM, HT-29, JAR, or HT-1080). Medium from the breast cancer cells had no effect on normal human fibroblasts or fibrosarcoma cells (HT-1080), suggesting the specificity of their action on human osteoblasts. After partial purification by ultrafiltration and size-exclusion chromatography, we found that medium of T-47D cells contained at least three nonprostanoid factors of low molecular weights (apparent MW of 700, 1500, and 4000 D) which affected human osteoblast-like cells. These factors were heat stable and could be peptides without disulfide bonds. In summary, our data show that human breast cancer cells release soluble factors that inhibit osteoblast proliferation and increase their cAMP response to PTH, indicating that osteoblasts could be important target cells for breast cancer cells and could be involved in the process of TIO.

Breast Neoplasms↗

Growth factors and bone formation in osteoporosis: roles for IGF-I and TGF-beta.

The cellular mechanisms involved in osteoblast function and bone formation alterations in osteoporosis have been partly elucidated. Recent studies have shown that bone formation abnormalities in various forms of osteopenia result mainly from defective recruitment of osteoblastic cells. These abnormalities in osteoblast function and bone formation are associated with alterations in the expression or production of several growth factors, such as IGFs and TGF-beta, which modulate the proliferation and activity of bone-forming cells. Bone loss related to aging or unloading is characterized by diminished osteoblast proliferation and reduced local concentrations of IGFs and TGF beta. In contrast, estrogen deficiency increases osteoblast proliferation and IGF-I production. These data suggest that alterations in the production of and/or in cell responsiveness to local growth factors may contribute to the bone formation abnormalities seen in these osteopenic disorders. This suggests that preventive or curative treatment with growth factors may be beneficial in osteopenia due predominantly to decreased bone formation. Low doses of IGF-I or TGF-beta have been reported to increase osteoblast recruitment and differentiation, leading to enhanced trabecular bone formation and decreased bone loss in models of osteopenia induced by aging, estrogen deficiency and unloading. A few clinical trials also suggest that low doses of growth factors may stimulate bone formation. Although these findings open up new prospects for the prevention and treatment of osteopenic disorders, progress in this direction awaits the development of factors or analogs that are capable of locally and specifically increasing osteoblast recruitment and differentiation without including side-effects.

Aged↗

[Growth factors and bone tissue. Implications in the formation of bone matrix].

Bone formation is highly dependent on the number of osteoblastic cells. Simulating factors which recruit osteoblastic cells play an essential role in regulating bone formation. Several growth factors produced locally by bone marrow cells and osteoblasts regulate cell growth and differentiation of osteoblastic cells. These growth factors may be systemic or local and can be stocked in the matrix. The factors secreted locally play a dominant role in regulation and are stocked in an active form in the bone matrix. Growth factors act through both autocrine and paracrine effects, or as local mediators of hormones and compression forces. The wide range of effects of the local growth factors and cytokines on bone cells, and the numerous interactions between these factors lead to precise regulation of the osteoblastic function. Thus these factors plan an extremely important role in local regulation and cell growth and osteoblastic differentiation, and are highly implicated in local control of bone formation.

Bone Matrix↗

[Detection and treatment of deafness in children].

Deafness must be systematically looked for in children during the first year of life, since the behaviour of a child with impaired hearing may closely resemble that of a child with normal hearing. Severe or deep deafness can be detected at birth by means of a babymeter. Between the ages of 6 and 18 months, sound-emitting toy tests enable deafness to be detected. It is only at the age of 2-3 years that testing can be performed separately on each ear to detect unilateral deafness. Treatment varies according to the degree and type of deafness. Conduction deafness is usually due to otitis media serosa and is treated with transtympanic aerators. Perceptive deafness requires acoustic prosthesis associated with orthophony and parental guidance.

Auditory Perceptual Disorders↗

Clinical significance of otoacoustic emissions: a perspective.

The aim of this paper is to review the properties of otoacoustic emissions from a clinical point of view and to discuss the perspective interest of this test. In adults, the clinical significance of evoked otoacoustic emissions seems to be limited either in endocochlear hearing losses or for detecting retrocochlear diseases. In infants, evoked otoacoustic emissions seem to be a reliable, simple, non-invasive, and precise method for estimating auditory sensitivity for midfrequencies (1-4 kHz). Then, EOEs could be considered as an interesting way for screening auditory dysfunction in infants.

Adult↗

Evoked otoacoustic emissions in newborn hearing screening.

Evoked otoacoustic emissions (EOEs) were recorded in a group of normally hearing neonates (n = 100 ears) to study the basic properties of EOEs and the parameters influencing them. The results obtained with EOE recordings were compared with those of behavioral screening investigations. The main properties of EOEs in neonates are: 1. EOEs can be recorded in 98% of the tested ears or neonates; 2. there were no statistically significant variations in EOE detection thresholds of neonates between the ages of 1 and 4 days; 3. no statistical difference in the EOE threshold was found between males and females; 4. all EOEs exhibited a broadband spectrum with high-component frequencies; 5. EOEs demonstrating narrowband frequency peaks super-imposed on the broadband component had detection thresholds lower than EOEs without narrowband frequency peaks. EOEs can be used as a screening test. The main clinical interest of this test is to detect the presence (i.e., normal auditory peripheral function) or the absence (i.e., pathological peripheral auditory function) of EOEs in response to a 30-dBHL click stimulation. The results of this study have important applications concerning the possible clinical use of EOEs for screening peripheral auditory dysfunction in neonates.

Audiometry, Evoked Response↗

[Congenital perilymphatic fistula in children].

We report twenty case of perilymphatic fistulae in children. A fistula was discovered in every case where the cochlear aqueduct is larger than normal on high resolution CT scan of the temporal bone. The surgical treatment of these fistulae allowed only a significant improvement of hearing in the cases were an asymmetry or a dilatation of the cochlear aqueducts and a fluctuating deafness coexisted. Unfortunately these improvements do not look permanent.

Adolescent↗

[The cochlear aqueduct and congenital perilymphatic fistula. An initial report].

The authors present 3 preliminary case reports of congenital perilymphatic fistula and describe their approach, which in the presence of clinical symptoms composed of progressive or fluctuating deafness, should suggest the diagnosis of congenital perilymphatic fistula leading to examination of the cochlear aqueduct by high resolution computed tomography. An anomaly detected on the CT scan, particularly on the intermediate and internal segments, is a decisive argument in the decision to operate on these congenital perilymphatic fistulae.

Adolescent↗

[What should be expected of oto-acoustic emissions? A critical analysis of clinical applications of oto-acoustic emissions].

The aim of this article is to carry out a critical analysis of the clinical applications of acoustic oto-emissions based on analysis of more than 1,000 adult and pediatric audiometric records. The principal technical and clinical properties of acoustic oto-emissions are described. The clinical value would seem to be very limited in adult audiology, whereas this examination would appear to be a reliable and non invasive method for screening in children at risk of cochlear deafness. In this respect, the investigation is principally limited by middle ear pathology and involvement of the central auditory pathways.

Acoustic Stimulation↗