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Biomedical subjects

P Marie

Publications and source records attributed to P Marie.

At least 19 recordsLinked to original sources
PubMed2000

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↗
PubMed1997

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↗
PubMed1997

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↗
PubMed1997

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↗
PubMed1994

[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↗
PubMed1990

[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↗
PubMed1990

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↗
PubMed1990

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↗
PubMed1989

[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↗
PubMed1989

[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↗
PubMed1989

[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↗
PubMed1986

Lethal osteogenesis imperfecta with amniotic band lesions: collagen studies.

An infant was born with osteogenesis imperfecta (OI) and died after 7 days. In addition, there were amniotic constriction bands and amputations of several digits of the upper and lower limbs. The radiologic picture was suggestive of type III OI. Histomorphometric analysis of the bone showed a trabecular bone volume of 15.1% compared to 26.9% for age-matched controls. This was due to a decreased apposition of matrix by the osteoblasts. Because abnormal collagen synthesis has been suggested as the underlying defect in most forms of OI, collagen studies were undertaken using intact tissues. Bone and skin collagen solubilities were strikingly reduced. Shortened type I collagen molecules, representing 25% of the total type I collagen, were produced by pepsin digestion of the demineralized bone matrix. The molecular weight of the shortened collagen, was 10 kd lower than normal for both the alpha 1 and alpha 2 chains as determined by gel electrophoresis. The bone acetic acid-soluble collagen showed few shortened alpha-chains. Twenty-five percent of the acid-soluble bone collagen was cleaved into shortened molecules by a pepsin digestion. The shortened alpha 1 chain was purified by high-performance liquid chromatography (HPLC) and digested with CNBr. The analysis of the resulting fragments by HPLC and by gel electrophoresis unequivocally demonstrated that the shortened alpha 1 chain was derived from the alpha 1(I) chains and that the pepsin sensitivity extends from the amino terminal end of the chain to the alpha 1(I) CB5 peptide, approximately 120 residues inside the triple helix. These studies show a distinct structural abnormality of type I collagen in the bone matrix of this patient resulting in an increased sensitivity of the collagen to general enzymatic proteolysis. The importance of correlating clinical and biochemical information in OI is emphasized; classification and genetic counseling based only on clinical observations are inaccurate.

Amniotic Band Syndrome↗
PubMed1986

Treatment of post-menopausal osteoporosis with phosphate and intermittent calcitonin.

The progression of osteoporosis depends on an imbalance between the relative rate of bone resorption and formation leading to a decrease in bone mass. The stimulation of bone turnover, also apparently heretical, might be necessary in order to be able to make the skeletons of elderly patients become highly cellular, a prerequisite for significant restoration of bone tissue. Given the usual correlation between bone resorption and bone formation a treatment which only increases bone turnover is unlikely to increase bone mass. For this reason, it is necessary to add sequentially a drug able to block bone destruction and lead to a transient uncoupling. Forty-seven post-menopausal women with vertebral osteopenia, with one or more atraumatic spinal compression fractures were included in a double-blind randomized study in four groups. The control group (PL) (n = 9) received a placebo injection and placebo tablets. The calcitonin group (CT) (n = 15) received CT injection and placebo tablets. The phosphate group (Pi) (n = 10) received a placebo injection and phosphate tablets. The calcitonin and phosphate group (CT + Pi) (n = 13) received calcitonin injection and phosphate tablets. The duration of treatment was six months. Transiliac bone biopsies were taken before and at the end of treatment. No significant changes were noted for the (CT + Pi) group. Trabecular bone volume increased by 31% by the end of treatment. Trabecular osteoblastic surface showed a mean increase of 143% of trabecular surface. Trabecular osteoid surface showed a mean increase of 85%.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1984

Extended treatment of primary osteoporosis by sodium fluoride combined with 25 hydroxycholecalciferol.

Nineteen patients suffering from primary osteoporosis, all having at least one vertebral collapse, initially received 50 mg of sodium fluoride alone per day for 6-18 months. Subsequently fluoride was associated with 25-50 micrograms of 25 OH cholecalciferol (calcifediol) per day for 6-18 months in 12 of these patients and 9 were treated for 31-58 months. As control group, 9 patients were given placebo for 6-18 months. The effect of the treatment was assessed by three methods: 1) the metacarpal index (MI) determined by radiogrammetry, 2) the calcium content of the hand bone (Ca) measured by local neutron activation, 3) the iliac bone histomorphometry. MI and (Ca) did not change significantly at any time in any group. In each group there was a significant increase in trabecular bone volume, osteoid volume, osteoid surfaces and a significant decrease in mineralization fronts. On the other hand, the changes in osteoblastic surfaces, osteoclastic surfaces, number of osteoclasts/mm2 were not significant in any group. No change was observed in the placebo group. These data suggest that the increase in the trabecular volume of fluorided bone is mainly due to the increase in osteoid which itself is due to a bone mineralization defect despite the association of calcifediol. This is probably one of the reasons why (Ca) does not change significantly.

Aged↗
PubMed1984

[Prognostic value of coronary spasm threshold determined by the ergometrine test].

The prognosis of spastic angina is difficult to determine. The object of this study was to try to evaluate the prognosis of coronary spasm on the results of provocative, ergometrine testing. Out of 708 patients with angiographically normal or near-normal coronary arteries undergoing the ergometrine test for assessment of chest pain, 78 patients with positive results were retained for study. The threshold of spasm was established in every case: this was defined as the quantity of ergometrine per kilogramme body weight required to provoke spasm. The values ranged from 1 to 12.5 micrograms/kg (average 7.58 micrograms/kg +/- 3.84). The reproducibility of the ergometrine test appeared to be very satisfactory. In the short term, only 4 out of 32 tests became negative. The test remained positive in 28 cases and the mean value of the threshold of spasm did not change significantly (5.64 +/- 3.27 to 5.52 +/- 3.18 micrograms/kg). In the long term only 2 out of 18 tests became negative. The test remained positive in 16 cases and the mean value of the threshold of spasm did not change significantly (5.68 +/- 2.96 to 6.58 +/- 3.11 micrograms/kg). The ergometrine test with a reference threshold of positivity of 5 micrograms/kg is doubly useful: this threshold value helps predict a good response to calcium inhibitor drugs: the threshold of spasm was less than this value in 6 of the 41 patients whose tests became negative after diltiazem therapy, and in 12 of 14 patients in whom the test remained positive (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Vasospasm↗