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F Rousseau

Publications and source records attributed to F Rousseau.

At least 109 records · Page 6Linked to original sources

[A computerized method for optimization of radioimmunoassays].

The authors have developed a one step quantitative method for radioimmunoassay optimization. The method is rapid and necessitates only to perform a series of saturation curves with different titres of the antiserum. After calculating the saturation point at several antiserum titres using the Scatchard plot, the authors have produced a table that predicts the main characteristics of the standard curve (Bo/T, Bo and T) that will prevail for any combination of antiserum titre and percentage of sites saturation. The authors have developed a microcomputer program able to interpolate all the data needed to produce such a table from the results of the saturation curves. This computer program permits also to predict the sensitivity of the assay at any experimental conditions if the antibody does not discriminate between the labeled and the non labeled antigen. The authors have tested the accuracy of this optimization table with two in house RIA systems: 17-beta-estradiol, and hLH. The results obtained experimentally, including sensitivity determinations, were concordant with those predicted from the optimization table. This method accelerates and improves greatly the process of optimization of radioimmunoassays.

Humans↗

Bacterial prostatitis in patients infected with the human immunodeficiency virus.

Bacterial prostatitis was diagnosed in 17 of 209 human immunodeficiency virus-infected men hospitalized from October 1985 to October 1987. A history of urogenital disease was found in 13 of 17 patients. Clinical signs of prostatitis were present in 16 of 17 patients, including fever in 13, urinary symptoms in 11 and tender prostate on rectal palpation in 7. Bacteriuria was found in 14 of the 17 patients. Prostatic ultrasound examination showed an abscess in 11 of 16 patients studied. Prostatitis was diagnosed at autopsy in 1 patient. Within 6 weeks after onset of antimicrobial therapy 9 of 13 patients were cured and 4 of 13 did not respond to therapy. Among the 7 patients followed for more than 2 months after the end of antimicrobial therapy 5 had relapse. The prevalence of bacterial prostatitis among human immunodeficiency virus-infected patients increased from 3 per cent in asymptomatic human immunodeficiency virus-infected patients to 14 per cent in patients with the acquired immunodeficiency syndrome.

Acquired Immunodeficiency Syndrome↗

Immunologically mediated hypothyroidism.

In this article, new avenues in the understanding of immunologic processes involved in hypothyroidism have been explored. The discovery of a family of TSH-R directed antibodies, including TSI-block, TGI, and TGI-block, has afforded perspectives on the etiology of autoimmune thyroid disorders. Thus, whereas TSI and TSI-block influence thyroid function, TGI and TGI-block are involved in thyroid cell proliferation and maturation. We have focused on three clinical entities that have been elucidated relatively recently--namely, silent thyroiditis, postpartum thyroiditis, and congenital hypothyroidism. Silent thyroiditis, a common form of transient thyroiditis, yields very few clinical symptoms or signs but significant alterations in biological tests, including a thyroid 131I uptake compatible with silent thyroid destruction. Although an autoimmune etiology is really not certain at this moment, it is not completely excluded. Silent thyroiditis does not usually require therapy, except in the rare cases in which symptoms are very severe. Postpartum thyroiditis, probably a special form of silent lymphocytic thyroiditis, differs from silent thyroiditis only by its relation to pregnancy and its higher rate of persistent thyroid disease. It has a high prevalence in pregnant women (5.5 to 10.2 per cent) in all populations studied, and may be responsible for a substantial proportion of cases of postpartum depression. Although the etiology is not clear, an autoimmune process seems to be involved. Although prediction of this state is difficult, a previous episode or high titers of microsomal antibodies in the first trimester show good correlations with the disease. Thyroid hormone replacement therapy is recommended for persistent disease. Congenital hypothyroidism appears to be mediated by passively transferred maternal blocking antibodies. TSI-block is likely responsible for the transient form of congenital hypothyroidism in the same way that TSI may cause transient congenital thyrotoxicosis. Passive transfer of maternal TGI-block appears to be causal in the majority of newborns with the sporadic form of congenital hypothyroidism. Early (in utero) onset of the disease could explain why 15 per cent of adequately treated infants subsequently demonstrate subtle neurologic sequelae. Because screening procedures for TGI-blocking antibodies are being made available, it should be possible to detect those potentially severe in utero cases and commence thyroid hormone replacement therapy before birth.

Autoantibodies↗

Quality-control scheme for blood glucose measured outside the laboratory.

We propose a quality-control (QC) scheme to evaluate the performance of blood glucose estimates made with a reflectometer in hospital wards or at home. We constructed a chart illustrating the comparison by regression analysis of the results of 254 reflectometer readings (y) and simultaneous capillary blood glucose analyses in the laboratory (x). Arbitrary acceptance limits around the regression line (y = 0.5 + 0.87x; r = 0.97, Sy/x = 0.8 mmol/L) were established, based on the mean +/- 2 SD of the reflectometer readings of a series of classes of 1.1 mmol/L interval, made with the results from the laboratory analyzer. Each ward using a reflectometer is provided with the QC chart, and the first blood glucose estimation with the reflectometer on each working shift is controlled by re-assay in the laboratory. If the reflectometer reading is outside the limits, the next glucose estimation is also re-assayed. If two consecutive readings are outside the limits, the reflectometer procedure is considered to be failing, the instrument's readings are not used for medical decisions, and remedial action is taken. The chart can also be used as a teaching tool for training the patients or the nurses and to evaluate individual performance.

Blood Glucose↗

Digitization of electrophysiological documents.

The mechanism presented in this paper is devoted to the transfer of paper documents as electrophysiological records into 'electronic documents' for direct storage and analysis by a computer.

Computers↗

Gas-chromatographic determination of levamisole in human plasma-normalization and reliability of the method.

Levamisole has been used by many authors as an immunostimulant agent but the relationship between oral doses, plasma level and the therapeutic effects were not known. For such a study it was necessary to establish an accurate and reproducible method of measurement. We describe a modification of the gas chromatographic method of Wynants et al. (1975). The normalization of the extraction of the extraction process leads to greater reliability and accuracy (4 ng +/- 7.6%). Reproducibility was established using a series of 30 determinations from standard solutions and plasmas supplemented with Levamisole. The relative standard deviation in K evaluation was varied between 0.9 and 1.8%, 3.7 and 6.1% for standard solutions and plasmas respectively. Consequently this method was adopted for this pharmacokinetic study which was carried out on healthy and cancer patients.

Chromatography, Gas↗

[Not Available].

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Canada↗

New polymorphism and a new chromosome breakpoint establish the physical and genetic mapping of DXS369 in the DXS98-FRAXA interval.

Recently some of us cloned a new probe RN1 (DXS369), which appears a close marker for the fragile X locus (FRAXA) [Oostra et al.: Genomics 1990]. We present here new evidence for its physical and genetic mapping in the DXS98--FRAXA interval. We used 2 different somatic cell hybrid lines with breakpoints in the Xq27-q28 region: L10B Rea and PeCHN, and we established the order: (DXS105, DXS98)-L10B Rea-DXS369-PeCHN- (DXS304, DXS52). We detected an additional TaqI RFLP at the DXS369 locus which increases its informativeness up to 57%. Two point linkage analysis in a large set of families gave high lod scores for the FRAXA-DXS369 linkage (z(theta) = 10.1 at theta = 0.044) and for DXS369-DXS304, a marker distal to FRAXA (z = 19.2 at theta = 0.070). By multipoint analyses we established the localization of DXS369 in the DXS98-FRAXA interval. DXS369 is a much closer proximal marker for FRAXA than DXS105 or DXS98 and any new probe mapping between the breakpoints in L10B Rea and PeCHN will be of potential interest as a marker for FRAXA.

Adult↗

Mode of inheritance influences behavioral expression and molecular control of cognitive deficits in female carriers of the fragile X syndrome.

The effect of mode of inheritance on expression of fragile X syndrome [fra(X)] was investigated in nonretarded female carriers. Examination included cognitive and molecular measures. A priori predictions about cognitive impairment and size of an unstable region of DNA containing a CGG repeat on the X chromosome were tested in age and education matched heterozygotes grouped according to parental inheritance. Nine carriers with a maternal fra(X) chromosome, 11 carriers with a paternal fra(X) chromosome and 15 control mothers of children with non X-linked developmental disabilities were tested. Inheritance was established through DNA linkage analysis. Cognitive skills were assessed using the Wechsler Adult Intelligence Scale-Revised and the Benton Visual Retention Test. Molecular status was assessed by Southern blot analysis of genomic DNA digested with Eco RI and Eag I, and probed with StB 12.3. Results supported the inheritance models' predictions. Heterozygotes who inherited the fra(X) from their fathers appeared to be a homogeneous group. They were indistinguishable from controls on cognitive measures and all had genomic insertions of less than 500 base pairs. In contrast, heterozygotes who inherited the fra(X) chromosome from their mothers appeared to be made up of 2 sub-populations. They were as a group deficient in measures of attention and visual memory, but not other measures, with scores of some women consistently below the other subjects. Further, they had some members with greater than 500 base pair inserts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

On some technical aspects of direct DNA diagnosis of the fragile X syndrome.

Direct DNA analysis of fragile X [Fra(X)] mutations has already shown its clear superiority for postnatal and prenatal diagnosis of the disorder and for carrier detection. However, it is of great importance to have conditions which guarantee optimal reliability and sensitivity. Some mutations may be more difficult to detect, especially in female carriers: this is the case for small amplifications of the CGG repeat (premutations) or for smears which can be generated by the instability of the full mutation in somatic tissues. We present the various alternatives (probe/enzymes combinations) for Southern blot based diagnosis, the possible artefacts and our detailed experimental protocol, which has given excellent results on a large number of families. While detection of amplification, using for instance EcoRI, appears sufficient for initial testing of mentally retarded patients, once the fra(X) diagnosis has been established, we favor the use of an EcoRI+EagI digest, which detects both amplification and abnormal methylation, for analysis of the family, including carrier detection and prenatal diagnosis. We discuss the place of proposed PCR based techniques for detection of mutations, or for indirect tracking using polymorphic microsatellites in the immediate vicinity of the fra(X) locus.

DNA Mutational Analysis↗

Analysis of full fragile X mutations in fetal tissues and monozygotic twins indicate that abnormal methylation and somatic heterogeneity are established early in development.

The fragile X syndrome, the most common cause of inherited mental retardation, is characterized by unique genetic mechanisms, which include amplification of a CGG repeat and abnormal DNA methylation. We have proposed that 2 main types of mutations exist. Premutations do not cause mental retardation, and are characterized by an elongation of 70 to 500 bp, with little or no somatic heterogeneity and without abnormal methylation. Full mutations are associated with high risk of mental retardation, and consist of an amplification of 600 bp or more, with often extensive somatic heterogeneity, and with abnormal DNA methylation. To analyze whether the latter pattern is already established during fetal life, we have studied chorionic villi from 10 fetuses with a full mutation. In some cases we have compared them to corresponding fetal tissues. Our results indicate that somatic heterogeneity of the full mutation is established during (and possibly limited to) the very early stages of embryogenesis. This is supported by the extraordinary concordance in mutation patterns found in 2 sets of monozygotic twins (9 and 30 years old). While the methylation pattern specific of the inactive X chromosome appears rarely present on chorionic villi of normal females, the abnormal methylation characteristic of the full mutation was present in 8 of 9 male or female chorionic villi analyzed. This suggests that the methylation mechanisms responsible for establishing the inactive X chromosome pattern and the full mutation pattern are, at least in part, distinct. Our results validate the analysis of chorionic villi for direct prenatal diagnosis of the fragile X syndrome.

Adult↗