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Biomedical subjects

F Picard

Publications and source records attributed to F Picard.

At least 73 records · Page 4Linked to original sources
PubMed1999

Response of adipose tissue lipoprotein lipase to the cephalic phase of insulin secretion.

Modulation of lipoprotein lipase (LPL) allows a tissue-specific partitioning of triglyceride-derived fatty acids, and insulin is a major modulator of its activity. The present studies were aimed to assess in rats the contribution of insulin to the response of adipose tissue and muscle LPL to food intake. Epididymal and retroperitoneal adipose LPL rose 65% above fasting values as early as 1 h after the onset of a 30-min high-carbohydrate meal, with a second activity peak 1 h later that was maintained for an additional 2 h. Soleus muscle LPL was decreased by 25% between 0.5 and 4 h after meal intake. The essential contribution of insulin to the LPL response to food intake was determined by preventing the full insulin response to meal intake by administration of diazoxide (150 mg/kg body wt, in the meal). The usual postprandial changes in adipose and muscle LPL did not occur in the absence of an increase in insulinemia. However, the early (60 min) increase in adipose tissue LPL was not prevented by the drug, likely because of the maintenance of the early centrally mediated phase of insulin secretion. In a subsequent study, rats chronically implanted with a gastric cannula were used to demonstrate that the postprandial rise in adipose LPL is independent of nutrient absorption and can be elicited by the cephalic (preabsorptive) phase of insulin secretion. Obese Zucker rats were used because of their strong cephalic insulin response. After an 8-h fast, rats were fed a liquid diet ad libitum (orally, cannula closed), sham fed (orally, cannula opened), or fed directly into the stomach via the cannula during 4 h. Insulinemia increased 10-fold over fasting levels in ad libitum- and intragastric-fed rats and threefold in sham-fed rats. Changes in adipose tissue LPL were proportional to the elevation in plasma insulin levels, demonstrating that the cephalic-mediated rise in insulinemia, in the absence of nutrient absorption, stimulates adipose LPL. These results demonstrate the central role of insulin in the postprandial response of tissue LPL, and they show that cephalically mediated insulin secretion is able to stimulate adipose LPL.

Adipose Tissue↗
PubMed1999

[Autosomal dominant nocturnal frontal lobe epilepsy: the syndrome].

The identification of the autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) in 1994 was rapidly followed by that of other familial forms of non lesional partial epilepsies (familial temporal lobe epilepsy, autosomal dominant partial epilepsy with variable foci). Since then around forty families with ADNFLE have been described, most of them having only 3 or 4 affected individuals. The epilepsy usually begins during childhood (mean age at onset: 11 years). The seizures mainly consist of motor elements which can be dystonic, tonic or hyperkinetic (bipedal automatisms, pelvic thrashing movements...), often preceded by a non specific aura. They are brief and frequent, taking place at night, in clusters. Some patients also present some diurnal seizures. One third of the patients report the occurrence of rare secondarily generalized tonic-clonic seizures. There is a large intra-familial variability as to age of onset, intensity of the manifestations and the course of the epilepsy. During the period of highest frequency of seizures, some patients may present moderate neuropsychological disturbances concordant with frontal dysfunctioning, or transitory behavioral disorders. The seizures often subside with age and may even disappear at adulthood. The most effective antiepileptic drug is carbamazepine, however pharmacoresistance is seen in 20 to 30 p. 100 of the cases. Interictal EEG shows non specific epileptiform anomalies with a frontal predominance, often seen solely on sleep recording, in more than half of all patients. Ictal EEG does not always give evidence of definite ictal discharges. The clinical heterogeneity of ADNFLE as it is especially observed in very variable types of auras which are non localizing, aside form the EEG's own limits, makes it difficult to localize the primary epileptic focus with certainty in the frontal lobe in all cases. In all, the clinical and electrical spectrum of ADNFLE is large, and the topographical identification of these familial frontal lobe epilepsies sets the same problems as for sporadic, classical cryptogenic frontal lobe epilepsies.

Age of Onset↗
PubMed1999

De novo highly complex chromosome rearrangement (CCR) involving five breakpoints with congenital anomalies analyzed by FISH.

We report on a child with ptosis, epicanthal folds, depressed nasal bridge, carp-shaped mouth, low set ears, hirsutism, pectus excavatum, and developmental and language delay presenting with a balanced complex chromosomal rearrangement (CCR). R- and G-banding methods and fluorescence in situ hybridization were used to document that this is a complex translocation with five breakpoints involving chromosomes 1, 7, 10 and 21.

Abnormalities, Multiple↗
PubMed1999

Efficacy of lamotrigine in idiopathic generalized epilepsy syndromes: a video-EEG-controlled, open study.

PURPOSE: This prospective, open, video-EEG-controlled study examined the efficacy of lamotrigine (LTG) as add-on and monotherapy in idiopathic generalized epilepsy (IGE). METHODS: 47 patients received LTG either because of insufficient seizure control (n = 35) or serious side effects of prior antiepileptic drugs (AED). Long-term video-EEG recordings were performed before and after the introduction of LTG. The mean follow-up time was 25.5 months. RESULTS: Of 12 patients with refractory childhood absence epilepsy, 9 became seizure free; in one child with absences with eyelid myoclonia, absence frequency was reduced > 50%; in 2 children with absences with a mild atonic component, seizure reduction was only transient. Of 12 patients with juvenile absence epilepsy, 10 became seizure-free and, in 2, a > 50% reduction was obtained. In 15 patients with juvenile myoclonic epilepsy, complete seizure control was achieved in 7 patients, in 6 patients myoclonia persisted. In one patient generalized tonic-clonic seizures also persisted and another patient developed a rash, LTG was therefore stopped. Of 5 patients with grand-mal on awakening, 3 became seizure-free, and a reduction of > 50% was obtained in one patient; LTG was stopped in one patient because of poor compliance. Three patients with pure photosensitive epilepsy became seizure-free. At the end of the study, 11 patients were seizure-free on LTG monotherapy, and in most other patients concomitant AED dosage could be substantially reduced. CONCLUSIONS: Lamotrigine was effective and well tolerated in patients with various IGE syndromes, although differences were observed between individual syndromes and seizure types.

Adolescent↗
PubMed1998

Measurement of the lateral diffusion of dipalmitoylphosphatidylcholine adsorbed on silica beads in the absence and presence of melittin: a 31P two-dimensional exchange solid-state NMR study.

31P two-dimensional exchange solid-state NMR spectroscopy was used to measure the lateral diffusion, D(L), in the fluid phase of dipalmitoylphosphatidylcholine (DPPC) in the presence and absence of melittin. The use of a spherical solid support with a radius of 320 +/- 20 nm, on which lipids and peptides are adsorbed together, and a novel way of analyzing the two-dimensional exchange patterns afforded a narrow distribution of D(L) centered at a value of (8.8 +/- 0.5) x 10(-8) cm2/s for the pure lipid system and a large distribution of D(L) spanning 1 x 10(-8) to 10 x 10(-8) cm2/s for the lipids in the presence of melittin. In addition, the determination of D(L) for nonsupported DPPC multilamellar vesicles (MLVs) suggests that the support does not slow down the lipid diffusion and that the radii of the bilayers vary from 300 to 800 nm. Finally, the DPPC-melittin complex is stabilized at the surface of the silica beads in the gel phase, opening the way to further study of the interaction between melittin and DPPC.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1998

Analysis of megakaryocyte growth and development factor (thrombopoietin) effects on blast cell and megakaryocyte growth in myelodysplasia.

Thrombocytopenia is a frequent feature of myelodysplastic syndromes (MDS) that could be improved by the use of recombinant human megakaryocyte growth and development factor (rHuMGDF). Using short-term liquid cultures and progenitor assays, we have found that rHuMGDF stimulated DNA synthesis and potentiated leukemic cluster growth of bone marrow mononuclear cells in 10/38 MDS cases (26%). Cytogenetically malignant colonies were detectable in rHuMGDF-stimulated cultures (n=3) by fluorescence in situ hybridization. rHuMGDF was able to stimulate CFU-MK formation in 45% of the samples tested. Finally, rHuMGDF-induced blast cell proliferation correlated with elevated expression of c-MPL, previously identified as a bad prognosis factor in MDS.

Blast Crisis↗
PubMed1998

Effects of leptin adipose tissue lipoprotein lipase in the obese ob/ob mouse.

OBJECTIVE: To characterize the adaptations of lipid metabolism, with special emphasis on tissue lipoprotein lipase, to negative energy balance brought by chronic treatment of obese ob/ob mice with leptin. DESIGN: According to a 2 x 2 factorial analysis, lean and obese C57BL/6J mice were subcutaneously infused with leptin (100 micrograms.kg-1.day-1) or vehicle (phosphate-buffered saline) during seven days. RESULTS: Cumulative food intake and final body weight of vehicle-infused obese mice were twofold higher than in lean controls. Leptin decreased cumulative food intake and body weight of obese, but not lean mice. Lipoprotein lipase (LPL) activity in white inguinal and epididymal and brown interscapular adipose tissues of control obese mice was at least twofold higher than in lean mice, but comparable in the vastus lateralis muscle. Leptin treatment of obese mice significantly lowered LPL activity to that of lean mice in all tissues examined. Vehicle-infused obese mice had higher liver triglyceride content and were hypertriglyceridemic compared to lean mice, and triglyceride concentrations in plasma and liver were decreased proportionally after leptin treatment. Leptin lowered glycemia and insulinemia of obese mice to lean levels and decreased plasma corticosterone. Leptin infusion had no notable effect on tissue lipoprotein lipase nor plasma variables of lean mice. CONCLUSIONS: Leptin infusion abolished hyperinsulinemia in the ob/ob mouse, an effect that was probably responsible for the concomitant normalization of adipose LPL activity. This study shows that decreased LPL activity, plasma triglyceride concentrations and hepatic triglyceride production constitute some of the adaptive peripheral adaptations of lipid metabolism, which accompany the reduction in fat mass accretion brought by leptin treatment of the obese ob/ob mouse.

Adipose Tissue↗
PubMed1998

Computer assisted knee replacement.

Accurate alignment of knee implants is essential for the success of total knee replacement. Although mechanical alignment guides have been designed to improve alignment accuracy, there are several fundamental limitations of this technology that will inhibit additional improvements. Various computer assisted techniques have been developed to examine the potential to install knee implants more accurately and consistently than can be done with mechanical guides. For example, computer integrated instrumentation incorporates highly accurate measurement devices to locate joint centers, track surgical tools, and align prosthetic components. Image guided knee replacement provides a three-dimensional preoperative plan that guides the placement of the cutting blocks and prosthetic components. Robot assisted knee replacement allows one to machine bones accurately without the use of standard cutting blocks. The rationale for the development of computer assisted knee replacement systems is presented, the operation of several different systems is described, the advantages and disadvantages of different approaches are discussed, and areas for future research are suggested.

Arthroplasty, Replacement, Knee↗
PubMed1998

[Autosomal dominant nocturnal frontal lobe epilepsy].

Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is a recently identified seizure disorder. The disease maps to the long arm of chromosome 20 and may be related in some families to a missense mutation in the neuronal nicotinic acetylcholine receptor alpha 4 subunit. We describe one of the first European family with ADNFLE, including five affected individuals spanning four generations. In the most severely affected subject, the onset was during the second month of life and persisted through adult life. Seizures were very frequent during infancy, although long-term evolution was relatively benign. Ictal video-EEG studies showed that attacks occurred in clusters during sleep and were partial seizures that were consistent with a frontal origin. Neuro-imaging was normal. Carbamazepine had a dramatic effectiveness. Although recognition of this syndrome is important for appropriate therapy and genetic counselling, underestimation of cases is likely: the disease was in our family perceived like a hereditary curse, and subsequently concealed, including to medical attention. Relationships with other partial familial epilepsies and with idiopathic benign partial epilepsies of childhood are discussed.

Adult↗
PubMed1998

[Anatomo-clinical consequences of the vertical sectioning of the subscapular muscle in Latarjet intervention].

UNLABELLED: The goal of this study was to assess the effects of the vertical section of the subscapularis muscle (internal rotation and muscular degeneration) during Latarjet procedure. MATERIAL AND METHODS: From October 1st, 1990, to June 30th, 1991, 40 patients were operated according to Latarjet for chronic anterior shoulder instability. A vertical section of the subscapular muscle was performed. Except for one female patient, all of them practiced sports. Preoperative delay between first dislocation and surgery averaged 59 months. Postoperative rehabilitation was aimed at external rotation, recovery began 48 hours after surgery, without specific indications as far as internal rotation was concerned. Sports activity was resumed 90 days after surgery. 38 were reviewed after 4 years. Clinical review was made according to Constant's score and by measuring strength, and amplitude of internal rotation. Radiological assessment of the shoulders was made with standard x-rays and CT. RESULTS: For global results, we noted absence of recurrence, a weighted Constant score of 88 per cent, 87 per cent of patients satisfied or very satisfied, 55 per cent of the osteoplastic ridge were on level, 16 per cent were retracted, and 29 per cent overlapped, 19 per cent non union or ridge lysis, 21 per cent glenohumeral osteophytosis. As far as clinical results are concerned, no significant difference was noted associated to osteoplastic ridge position. Internal rotation was assessed by measuring the distance hand to back (lift-off test). On the operated side it averaged 6 cm (0-18 cm), on the other side 13 cm (2-21 cm). The difference between each side was statistically very significant (p = 0.0001). Strength in internal rotation on the operated side averaged 3 kg (0-8 kg), on the other side, 6 kg (2-10 kg). The difference between each side was statistically very significant (p < 0.0001). CT was carried out on thickness and degeneration of the subscapular muscle (n = 29). Thickness of the subscapular muscle (operated side) average 10.5 (5-17 mm) after surgery, and 14.6 mm before surgery. It was thimer than on the contralateral shoulder 21 mm (10-33 mm). In both cases (shoulder before and after surgery, operated and contralateral shoulder), the difference was statistically significant. Degeneration of the subscapular muscle showed 4 stage 0, 13 stage 1, 5 stage 2, 6 stage 3, and 1 stage 4. A non statistical correlation was noted, between muscle degeneration and functional result, strength in internal rotation, distance hand to back. DISCUSSION: This series confirms efficiency and low morbidity of Latarjet procedure. Nevertheless, assessment of the subscapular muscle shows that 50 per cent of its strength and 50 per cent of its thickness were lost, 4 years after surgery. A significant degeneration (stages 2.3.4) was found in 41 per cent of the patients. This limitation is related to the trans-subscapular approach and to the absence of internal rotation postoperative rehabilitation. CONCLUSION: A randomized study comparing the vertical trans-subscapular approach to the horizontal trans-subscapular one would determine the better procedure.

Adolescent↗
PubMed1997

Patterns of allelic loss on chromosome 17 in sporadic breast carcinomas detected by fluorescent-labeled microsatellite analysis.

Loss of heterozygosity (LOH) on chromosome 17 is a frequent genetic alteration in breast cancer. To assess whether the location of potential tumor suppressor genes is compatible with the LOH pattern in individual tumors, we analyzed allele loss on chromosome 17 in 121 invasive ductal breast carcinomas and 16 benign breast tumors with 14 polymorphic microsatellite markers (4 on 17p and 10 on 17q). Fluorescent polymerase chain reaction (PCR) for typing microsatellites coupled with DNA fragment analysis in an automated DNA sequencer was applied. Frequencies of LOH varied from 29.4% (D17S1322) to 57.4% (TP53-Alu). No LOH could be detected in benign breast tumors. In 54 tumors the deletion patterns were consistent with the complete loss of 17p (n = 28), 17q (n = 9) or the whole chromosome 17 (n = 17). Five smallest regions of overlap (SROs) were identified in tumors with interstial deletion patterns. On 17p, two foci were detected affecting the TP53 locus and the hypermethylated in cancer I (HICI) region (17p13.3). On 17q, SRO1 was localized between markers THRAI and D17S855, centromeric to the breast/ovarian cancer gene BRCAI; SRO2 was flanked by markers AFM234 and NMEI, and SRO3 was centered between markers MPO and GH. Associations between LOH and histopathological characteristics were determined. Significant correlations were found between higher grade and loss of the TP53 gene (marker TP53, P = 0.019), loss of the BRCAI region (P < 0.009), LOH of marker AFM155 (P = 0.003) and marker NMEI (P = 0.026). For positive estrogen receptor status, only LOH of the THRAI marker correlated significantly, whereas highly significant correlations were determined between positive progesterone receptor and markers centromeric to the BRCAI region D17S250 (P = 0.00002), THRAI (P = 0.0006), and the intragenic BRCAI markers [D17S1322 (P = 0.021), D17S855 (P = 0.029)]. Results presented in this study identify five independent regions of chromosome 17 which are likely to contain potential tumor suppressor genes involved in the carcinogenesis of sporadic breast cancer.

Alleles↗
PubMed1997

Multinuclear solid-state NMR spectroscopy of envelopes from virgin and explanted silicone breast prostheses: an exploratory study.

The structure and dynamics of silicone envelopes from virgin and explanted breast prostheses have been studied by 1H, 13C, and 29Si high-resolution solid-state NMR spectroscopy. The results indicate that this combination of techniques can be used to unambiguously identify the presence of methyltrifluoropropylsiloxane units and diphenylsiloxane units at concentrations of about 2.0% and 3.5%, respectively, in some of the envelopes. The presence of about 10% silica also was detected and a trace of lipids was found in the explanted silicone envelopes. We have also measured the proton T2 and T1 relaxation times of the envelopes to characterize the dynamics of the silicone in the envelopes.

Breast Implants↗
PubMed1997

[Pseudotumor manifestation of metallosis in a hip prosthesis].

A pseudo-tumour due to metallosis is described in association with an iso-elastic hip replacement. This is a relatively rare lesion which may be difficult to diagnose. Scintigraphy and radiography may be helpful in distinguishing the lesion from a primary or secondary neoplasm, but the presence of osteolysis adjacent to the prosthesis will suggest the true nature of the lesion.

Aged↗
PubMed1997

Expression of the transcription factor Evi-1 in human erythroleukemia cell lines and in leukemias.

The Evi-1 proto-oncogene is a zinc finger DNA binding protein. Although activation of the Evi-1 gene has been associated with chromosomal rearrangements of the 3q25-q28 region, ectopic expression of Evi-1 could also be observed in acute myelogenous leukemias and myelodysplastic syndromes without cytogenetic abnormalities of the 3q26 locus. In this study, human erythroleukemic cell lines were screened for the expression of Evi-1 mRNA by northern blotting. Evi-1 was expressed in all the erythroid cell lines, whether undifferentiated (K 562, HEL, LAMA 84) or exhibiting spontaneous terminal erythroid differentiation (KU 812, JK-1). Evi-1 mRNA levels were constant or elevated in hemoglobin-synthesizing KU 812 or K 562 cells in response to erythropoietin or hemin treatment, respectively. In human acute myeloblastic leukemias (AML), 11/30 expressed Evi-1 by RT-PCR. Among these cases, 4/6 erythroleukemias without abnormalities of the 3q25-q28 region were found positive. The presence of acidophilic erythroblasts (15-47% of bone marrow cells) accounted for the existence of a terminal erythroid differentiation in all Evi-1-positive AML M6, whereas one negative case was poorly differentiated and referred to as AML M6 variant. These results suggest that Evi-1 mRNA expression can coexist with erythroid differentiation.

Adult↗
PubMed1997

Fas/Apo-1 (CD95) expression and apoptosis in patients with myelodysplastic syndromes.

Apoptosis of hematopoietic progenitor cells is increased in myelodysplastic syndromes (MDS). We have studied Fas (CD95/Apo-1) antigen expression in 27 MDS patients (RARS 4, RA 3, RAEB 13; RAEB-t 3, CMML 4) and three AML secondary to MDS. We found that the Fas antigen was not expressed on normal bone marrow (BM) CD34+, CD14+, or glycophorin+ cells, and only slightly on CD33+ cells. Patients with MDS had upregulation of Fas expression on total bone marrow nuclear cells (BMMC) (t-test, P = 0.04), CD34+ (P = 0.013), CD33+ (P = 0.04), and glycophorin+ (P = 0.032) BM cells compared to controls. Fas expression did not correlate to the FAB subtype, the Bournemouth score, or to peripheral cytopenias. However, Fas expression intensity on CD34+ cells negatively correlated to the BM blasts number (Spearman, P = 0.01) suggesting that leukemic blasts cells lose Fas antigen expression with progression of myelodysplasia. Using both proliferation assays in liquid cultures and clonogenic progenitor assays in the presence of an agonist anti-Fas MoAb (CH11), we showed that the Fas protein was functional in some patients. Dose-dependent inhibition of DNA synthesis was observed in three out of seven patients studied. CFU-GM and BFU-E colonies suppression in some patients suggested that Fas can induce apoptosis in myeloid and erythroid BM progenitors of MDS patients. The TUNEL technique on BM smears gave a mean of 12.6% +/- 2.5 of bone marrow apoptotic cells in five controls. Patients with MDS had increased bone marrow apoptosis (mean 39% +/- 5.7, t-test, P = 0.012). Four out of 15 (26%) patients studied with a sensitive radiolabeled DNA ladder technique had typical DNA ladders indicative of advanced stages of apoptosis. Massive BM suicide was observed in patients with RA (2/2) and RAEB (8/11), whereas apoptosis rates were normal or low in patients with RAEB-t (3/3) or secondary AMLs (3/3). Moreover, high rates of apoptosis correlated to low Bournemouth score (Spearman, P = 0.01). No statistical correlation could be found between Fas expression and apoptosis rates. Our results confirm the importance of programmed cell death in MDS. The Fas antigen is clearly upregulated on BM cells, but its role in the pathophysiology of apoptosis in myelodysplasia is still unclear, indicating that many factors positively or negatively interfere with the Fas-mediated pathway of apoptosis in vivo and in vitro.

Adult↗
PubMed1997

Chorea-acanthocytosis: genetic linkage to chromosome 9q21.

Chorea-acanthocytosis (CHAC) is a rare autosomal recessive disorder characterized by progressive neurodegeneration and unusual red-cell morphology (acanthocytosis), with onset in the third to fifth decade of life. Neurological impairment with acanthocytosis (neuroacanthocytosis) also is seen in abetalipoproteinemia and X-linked McLeod syndrome. Whereas the molecular etiology of McLeod syndrome has been defined (Ho et al. 1994), that of CHAC is still unknown. In the absence of cytogenetic rearrangements, we initiated a genomewide scan for linkage in 11 families, segregating for CHAC, who are of diverse geographical origin. We report here that the disease is linked, in all families, to a 6-cM region of chromosome 9q21 that is flanked by the recombinant markers GATA89a11 and D9S1843. A maximum two-point LOD score of 7.1 (theta = .00) for D9S1867 was achieved, and the linked region has been confirmed by homozygosity-by-descent, in offspring from inbred families. These findings provide strong evidence for the involvement of a single locus for CHAC and are the first step in positional cloning of the disease gene.

Acanthocytes↗