Biomedical subjects

F X Lemaire

Publications and source records attributed to F X Lemaire.

4 recordsLinked to original sources

PubMed2001

Speech recognition scores related to age and degree of hearing impairment in DFNA2/KCNQ4 and DFNA9/COCH.

OBJECTIVE: To analyze the relationship between pure-tone hearing threshold and speech recognition performance in DFNA2/KCNQ4 and DFNA9/COCH, 2 types of high-frequency nonsyndromic hearing impairment. DESIGN: Case series with cross-sectional analysis of phoneme recognition scores related to age and hearing level. SETTING: University hospital. PATIENTS: Forty-five members of 4 separate families, all carrying 1 of 3 different mutations in the KCNQ4 gene at the DFNA2 locus (1p34); 42 members of 7 separate families, all carrying the same Pro51Ser mutation in the COCH gene at the DFNA9 locus (14q12-q13). RESULTS: The deterioration of speech recognition dropped to a 90% score at a higher level of hearing impairment (pure-tone-average at 1, 2, and 4 kHz) in DFNA2-affected patients (65 dB) than in DFNA9-affected patients (46 dB). CONCLUSION: At similar levels of hearing impairment, DFNA2/KCNQ4-affected patients showed better speech recognition performance than DFNA9/COCH-affected patients.

Adult↗

PubMed2001

Parathyroid function in the early postoperative period after thyroidectomy.

Serum levels of parathyroid hormone (PTH) and calcium were studied in 132 patients, divided into three groups: unilateral thyroid-lobectomy, (sub)total thyroidectomy for non-toxic goitre and (sub)total thyroidectomy for hyperthyroidism. It was found that all types of thyroidectomy, even unilateral lobectomy, had a temporary influence on the PTH and calcium metabolism in the early postoperative period, albeit to different degrees. The effect was most pronounced after surgery for hyperthyroidism, which carries the greatest risk for postoperative hypocalcemia. The pathogenesis of transient postoperative hypocalcemia as well as the implications for the surgical management are discussed.

Adult↗

PubMed1996

Initiation sites for Ca2+ signals in endothelial cells.

Intracellular Ca2+ signals in response to inositol 1,4,5-trisphosphate-producing agents often present themselves as Ca2+ oscillations and propagating Ca2+ waves originating at discrete initiation sites. We studied the spatial organization of the Ca2+ signal in single CPAE endothelial cells stimulated with adenosine triphosphate. The long, thin processes presented a higher agonist sensitivity and, for the same agonist concentration, a faster rise in cytoplasmic Ca2+ concentration and rate of wave propagation than the cell body. Ca2+ waves originated preferentially in one of these processes and then invaded the cell body. Removal of external Ca2+ induced a progressive inhibition up to blockade of the response in the process but not in the cell body. These findings suggest that CPAE cells contain many individual store units, each of which has the inherent ability to set the stage for Ca2+ release. A diffusing messenger originating from the initiation zone then coordinates the events leading to Ca2+ release in the individual store units to produce a Ca2+ wave.

Animals↗

PubMed1995

Slow kinetics of InsP3-induced Ca2+ release: differences between uni- and bi-directional 45Ca2+ fluxes.

The effects of a long-lasting stimulation with inositol 1,4,5-trisphosphate (InsP3) have been studied in monolayers of permeabilized A7r5 cells. When measured under unidirectional 45Ca2+ efflux conditions, i.e. in the presence of 2 microM thapsigargin, an initial fast release was observed which then progressively slowed down into a slow phase which persisted for up to 20 min. When measured under bidirectional 45Ca2+ flux conditions with functional Ca2+ pumps, a transient phase of re-uptake occurred between the initial fast and the subsequent slow release phase. These kinetics are compatible with intrinsic inactivation of the InsP3 receptor. However, this inactivation did not prevent the slow release component. The slow component was not due to the accumulation of an InsP3 metabolite nor to a GTP-dependent translocation of Ca2+ between stores. The slow release phase was more pronounced when the Ca2+ pumps were active than when they were inhibited. This observation is compatible with other findings indicating that the InsP3 receptor is controlled by luminal Ca2+. The decreasing effectiveness of a 20 min lasting InsP3 challenge in mobilizing Ca2+ from less filled stores is most likely due to a progressive depletion of the store and cannot be considered as an experimental artifact caused by a preferential emptying of InsP3-sensitive Ca2+ stores. We conclude that the InsP3 receptor can intrinsically inactivate but that this inactivation is unable to prevent the slow release, which is especially pronounced when Ca2+ pumps are active.

Animals↗