Search PubMed⌕ Search

Biomedical subjects

A Picard

Publications and source records attributed to A Picard.

At least 109 records · Page 6Linked to original sources
PubMed1983

Activity of the maturation-promoting factor and the extent of protein phosphorylation oscillate simultaneously during meiotic maturation of starfish oocytes.

Maturation-promoting factor (MPF) activity and the protein phosphorylation pattern were monitored throughout the time course of meiotic maturation following hormonal stimulation of prophase-arrested starfish oocytes. MFP activity disappeared or decreased dramatically during the first and second meiotic cleavages. MPF activity came back to a very high level after the first but not the second meiotic cleavage. The state of protein phosphorylation was monitored using both tracer experiments and direct measurements of the absolute amount of phosphate in phosphoproteins. High and low levels of MPF activities were, respectively, associated with high and low levels of protein phosphorylation. It is suggested that the turn over of phosphate already bound to proteins in prophase-blocked oocytes does not change following hormone addition.

Adenine↗
PubMed1983

Hormone-induced parthenogenetic activation of mature starfish oocytes.

1-Methyladenine, which has been previously shown to be the hormone responsible for meiosis reinitiation in starfish oocytes, triggers parthenogenetic activation when applied to matured starfish oocytes after emission of the second polar body and formation of the pronucleus. In Marthasterias glacialis and Asterias rubens oocytes parthenogenetic activation includes elevation of a fertilization membrane, cleavage and the formation of normal bipinnaria larvae. Activation is likely to result from 1-methyladenine interaction with the category of stereospecific membrane receptors involved in meiosis reinitiation, since structural requirements of this compound are identical for both biological responses. Appearance of oocyte responsiveness to 1-MeAde after, but not before emission of the second polar body cannot be accounted for by their increased sensitivity to intracellular Ca2+ at that time, although it is shown that Ca2+ mediates hormone effect in inducing parthenogenetic activation. Pretreatment of immature oocytes with the free hormone in excess strongly inhibits the 1-methyladenine-induced parthenogenetic activation of the oocytes when they have completed maturation. It is suggested that reappearance of 1-MeAde sensitivity when oocytes form a pronucleus depends either upon recruitment or new receptor units or on the reactivation of pre-existing inactivated receptors at this stage of oocyte maturation.

Adenine↗
PubMed1983

Is calcium the second messenger of 1-methyladenine in meiosis reinitiation of starfish oocytes?

Microinjection of EGTA into prophase-blocked oocytes does not inhibit hormone-induced meiosis reinitiation, although it prevents oocyte activation by fertilization, by ionophore A23187, or by subsequent microinjection of otherwise efficient Ca2+ buffers. In contrast microinjection of Ca2+ buffers inhibits 1-methyladenine-induced meiosis reinitiation. Oocytes can be released from Ca2+ inhibition by raising hormone concentration or by the subsequent transfer of cytoplasm taken from maturing oocytes. Ca2+-microinjected oocytes remain inhibited up to 1 h after microinjection, although free Ca2+ concentration comes back to its resting value less than 30 sec after microinjection. Cyanide, which decreases ATP content and depresses Ca2+-pumping activity, reversibly inhibits 1-methyladenine-induced meiosis reinitiation. These results do not support the hypothesis that Ca2+ is the second messenger of the hormone in meiosis reinitiation of starfish oocytes, although they support the view that elimination of Ca2+ from some component of the oocyte cortex (perhaps the plasma membrane) might be a compulsory event for transduction of the hormonal message.

Adenine↗
PubMed1983

Lithium inhibits amplification or action of the maturation-promoting factor (MPF) in meiotic maturation of starfish oocytes.

Microinjection of LiCl reversibly inhibits hormone-induced meiotic maturation of starfish oocytes. Microinjection of NaCl (even in ouabain-treated oocytes) or KCl, or external application of LiCl have no such effect. Blockade of meiotic maturation by Li+ occurs even when microinjection is performed after the hormone dependent period has ended, that is the period during which the hormone must be present in the medium in order that meiosis can take place. Li+ microinjection prevents oocytes from meiosis reinitiation following transfer of cytoplasm taken from maturing oocytes, which contain a maturation-promoting factor (MPF). Cytoplasm taken from Li+-injected and hormone-treated oocytes does not trigger meiosis reinitiation when transferred in control immature oocytes. Intracellular pH does not change following LiCl microinjection. Simultaneous microinjection of either K+, Na+, or EGTA does not prevent Li+-dependent inhibition in oocytes.

Animals↗
PubMed1982

[Long-term results of urinary rehabilitation in acquired infantile paraplegia (author's transl)].

The urinary rehabilitation of children suffering from acquired paraplegia is here the subject of a retrospective study of 29 patients observed over a long period. The study shows that the detrusor-sphincter balance cannot be exploited on a personal level before the age of 10 ; bacteriuria and persistent residue after the initial period may ultimately disappear under discontinuous bacteriostatic treatment and thanks to the acquisition of autonomy in relation to the residue ; out of the total of 29 patients, the authors only noted 3 morphological and functional deteriorations requiring cutaneous diversion by Bricker's method. Today, the number would have been even smaller thanks to better knowledge of the striated sphincter syndrome, which accounted for 2 of the 3 cases noted. At last in the case of 16 of the 20 initial results considered as favourable, in other words in a little over 3 out of 4 patients, the social and uro-nephrological situation is holding steady, and even improving.

Adolescent↗
PubMed1980

[Cranial osteitis: a report on four cases, including a Gradenigo-Lannois syndrome (author's transl)].

Three cases of hematogenous cranial osteitis are described. The etiology in two cases was a staphylococcus aureus infection from meningeal septicemia. One of these patients died and chronic osteomyelitis developed in the second case. The third case was one of multifocal tuberculous infection, localized in the cranium but asymptomatic. The last case was a Gradenigo-Lannois syndrome, and its etiology, either chronic otitis or sphenoidal sinusitis, is discussed.

Adolescent↗
PubMedDate not supplied

Investigation of the biliary clearances of cefotaxime and desacetylcefotaxime by an original procedure in cholecystectomised patients.

The biliary elimination of cefotaxime (CTX) and its metabolite desacetylcefotaxime (DSCTX) were measured by HPLC in nine recently cholecystectomised patients following the i. v. injection of 15 mg/kg body weight of CTX. All of the bile was collected by an original procedure: the inflated balloon of a Fogarty catheter was introduced into the distal branch of a Kehr drain T-tube. Biliary clearance of CTX and DSCTX was measured for 8 h. Cefotaxime peaked at 90 min after injection at 34.5 +/- 15.3 mg/l; in the 7-8 h sample it was 2.7 +/- 1.7 mg/l. DSCTX peaked at the same time at 49.3 +/- 17.0 mg/l, and was 4.6 +/- 3.2 mg/l at 8 h. The bile/serum ratio of CTX and DSCTX concentrations was above 1 from the first to the eighth hours (range: 1.35 +/- 1.08 to 11.0 +/- 3.1). The biliary clearance of CTX was 0.190 ml/min. The total amounts of CTX and DSCTX eliminated in bile were respectively 1050 +/- 472.8 micrograms and 1902.7 +/- 804.1 micrograms (0.093 +/- 0.041% of the dose and 0.186 +/- 0.077% of the dose). Considering the minimum inhibitory concentration of the pathogens currently encountered in biliary sepsis, CTX should be a suitable antimicrobial agent for the treatment of biliary infections.

Adult↗
PubMedDate not supplied

[Biliary excretion of cefotaxime and desacetylcefotaxime].

The biliary excretion of cefotaxime (CTX) and its metabolite desacetylcefotaxime (DSCTX) was measured by HPLC in 9 recently cholecystectomized-patients following the IV injection of 15 mg/kg body weight of CTX. The totality of bile was collected by an original procedure: the inflated balloon of a Fogarty catheter was introduced into the distal branch of a Kehr drain T-tube. Biliary clearance of CTX and DSCTX was measured for 8 h. Cefotaxime peaked at 90 min. after injection at 34.5 +/- 15.3 micrograms/ml; in the 7-8 h sample it was 2.7 +/- 1.7 micrograms/ml. DSCTX peaked at the same time at 49.3 +/- 17.0 micrograms/ml, and was 4.6 +/- 3.2 micrograms/ml at 8 h. The bile/serum ratio of CTX and DSCTX concentration was 1 from the 1st to the 8th hours (range: 1.35 +/- 1.08 to 11.0 +/- 3.1). The biliary clearance of CTX was 0.190 ml/min. The total amounts of CTX and DSCTX eliminated in bile were respectively 1050 +/- 472.8 micrograms and 1902.7 +/- 804.1 micrograms (0.093 +/- 0.041 p. 100 of the dose and 0.186 +/- 0.077 p. 100 of the dose). Considering the minimum inhibitory concentration of the pathogens currently encountered in the biliary sepsis, CTX should be a suitable antimicrobial agent for the treatment of biliary infections.

Adult↗
PubMedDate not supplied

Short-term memory impairment and unilateral dichotic listening extinction in a child with Landau-Kleffner syndrome: auditory or phonological disorder?

The neuropsychological profile of a child with a Landau-Kleffner syndrome is presented here. The observed cognitive difficulties included verbal short-term memory and seemed partially compensated for when the experimental assessments bypassed the auditory channel. This case study is especially challenging since the child, whose phonological skills were quite efficient and who exhibited a dichotic listening unilateral extinction, had developed average reading and spelling abilities. The fact that B.E.'s performance on memory tasks was quite poor when the stimuli were presented auditorily and more efficient when the stimuli were presented visually, strongly suggests that the observed memory impairment was due to a deficit at the level of cortical auditory processing. B.E.'s phonological skills were efficient, suggesting a neuropsychological dissociation between phonological ability and auditory processing. The fact that B.E. dramatically recovered language and easily acquired reading and spelling accounts for the hypothesis that compensatory strategies allowed him to develop phonological skills from predominantly visual input.

Auditory Perceptual Disorders↗
PubMedDate not supplied

Release of mature starfish oocytes from interphase arrest by microinjection of human centrosomes.

Mature oocytes (unfertilized eggs) are arrested at definite cell-cycle stages which vary from species to species. In frogs and mammals, the oocytes are arrested at the second metaphase of meiosis whereas in echinoderms they are blocked later, at the pronucleus stage. What causes the maturing oocytes to stop at some point in the cell cycle is not entirely clear. In frogs, the metaphase arrest seems to be maintained by a cytostatic factor. In echinoderms, which stop at interphase, no such a factor has so far been found. The fertilization process, beyond the introduction of paternal chromosomes, releases the oocyte from cell-cycle arrest and provides a functional centrosome to replace the endogenous centrosome which is apparently lost during oogenesis in most species. Several lines of evidence suggest that release from cell-cycle arrest is mediated by a Ca2+ burst which is associated with fertilization, and it is known that the functional centrosome provided by the sperm is necessary for mitotic spindle formation and cleavages. We report here that microinjection of purified human centrosomes into mature starfish oocytes is sufficient to release them from arrest at interphase and to support many cleavages leading to the occasional formation of normal embryos. In this species centrosome induced re-entry into the cell cycle does not require a transient calcium burst nor does it require intact microtubules.

Animals↗