[Pneumococcal pelvioperitonitis revealing HIV seropositivity].
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AIDS-Related Opportunistic Infections↗
Biomedical subjects
M Roger
Publications and source records attributed to M Roger.
HLA-G and HLA-E polymorphisms in an indigenous African population. The ZVITAMBO Study Group.
Studies of HLA-G and HLA-E polymorphisms in different populations from many industrialized countries have uniformly reported little sequence variation within these genes. To date, the polymorphism of these genes has not been characterized in populations from developing countries where more sequence variation would be anticipated due to greater exposure to microbial pathogens. In order to address this issue, we have recently investigated the polymorphism of these MHC genes in an indigenous African population (Shona ethnic group). HLA-G and HLA-E alleles were determined by PCR-restriction fragment length polymorphism (PCR-RFLP) and amplification refractory mutation system (ARMS) analysis in 108 unrelated women recruited from maternity clinics and hospitals in Harare (Zimbabwe). The genotyping analysis identified six different HLA-G alleles and three HLA-E alleles in this population. Of interest, the null-allele HLA-G*0105N was found with 11.1% of frequency, which is higher than in other populations tested so far. We observed the presence of 15 distinct HLA-G genotypes and 6 HLA-E genotypes. These data indicate that this African population contains low levels of allelic polymorphism similar to ethnic groups from industrialized countries. This is the first report describing HLA-G and HLA-E polymorphisms in an indigenous African population.
Africa↗
Stage of specification of the spinal cord and tectal projections from cortical grafts.
In order to determine the embryonic age at which the hodological phenotype developed by neocortical cells is specified, we have examined the spinal or tectal projections developed by embryonic (E) grafts of presumptive frontal or occipital neocortex placed into the frontal or occipital neocortex of newborn host rats. Grafts of E13, E14 and E16 cells of the frontal cortex transplanted into the occipital cortex of newborns are capable of developing and maintaining in adulthood a spinal cord axon. Grafts of E12 cells do not project to the spinal cord but send fibres to the superficial layers of the tectum. In addition, following transplantation into the frontal cortex, early embryonic (E12) cells from the presumptive occipital cortex are capable of differentiating into neurons with spinal cord projection but are practically incapable of developing a tectal projection. When grafted at E14 into the frontal cortex, occipital cells lose the capacity to project to the spinal cord but become able to send fibres to the tectum. Taken together, these findings indicate that young (E12) embryonic frontal and occipital cortical cells are competent to subsequently differentiate into neurons projecting to the spinal cord or tectum according to instructive signals available in the cortical territory where they complete their development. By E13/E14, some cortical cells are specified and their capacity to contact targets that are not appropriate to their embryonic origin is much reduced. These findings are consistent with the notion that cortical specification involves progressive restriction in cell multipotentiality and fate specification toward region-specific phenotypes.
Animals↗
Early commitment of embryonic neocortical cells to develop area-specific thalamic connections.
In this study we examined the thalamic connectivity developed by grafts of embryonic (E16) parietal or occipital cortex placed homo- or heterotopically into the neocortex of newborn rats. We also examined the cytoarchitectonic organization developed by the grafts. Our findings indicate that E16 parietal cortex grafted into the parietal cortex of newborn recipients develops reciprocal connections with the host thalamic ventrobasal complex (VB) but does not establish connections with the host dorsal lateral geniculate nucleus (DLG). When implanted into the occipital cortex, these grafts are still able to establish connections with the VB. In contrast, E16 occipital cortex grafted into the parietal cortex establishes only a few connections with the VB. These grafts are, however, able to develop a substantial system of connections with the host DLG. At 16 days of embryonic age, graft cells are committed to establish thalamic connections appropriate to their tangential locus of origin. In addition, our results show that E16 parietal or occipital cortical cells do not possess the capacity to differentiate and maintain barrel organization even though they are grafted into the terminal field of developing VB axons.
Animals↗
An important proportion of genital samples submitted for Chlamydia trachomatis detection by PCR contain small amounts of cellular DNA as measured by beta-globin gene amplification.
We assessed the quality of genital samples submitted for Chlamydia trachomatis detection by PCR by a second PCR assay for the presence of human beta-globin DNA. Endocervical and urethral samples were first tested by the COBAS AMPLICOR C. trachomatis assay (Roche Diagnostic Systems) with an internal control and were then amplified for the presence of beta-globin DNA with primers PC04 and GH20. Samples that contained inhibitors were retested after dilution 1:10. A total of 407 genital samples (311 endocervical swabs from 311 women and 96 urethral swabs from 95 men and 1 woman) collected over a 1-month period were evaluated. The internal control could not be amplified, despite dilution, from 3 of 23 samples that were retested after dilution because of inhibition, leaving 404 samples that could be analyzed by PCR. Eleven samples tested positive for C. trachomatis. Thirty (7.4%) of the 404 samples were negative for beta-globin. Twelve of the 23 undiluted samples that contained inhibitors tested positive for beta-globin DNA. Amplification of beta-globin DNA in samples submitted for C. trachomatis detection by the COBAS AMPLICOR C. trachomatis assay demonstrated that an important proportion of the samples did not contain cellular DNA. Assessment of the quality of the samples for PCR analysis by beta-globin amplification is feasible but cannot replace use of the internal control.
Cervix Uteri↗
Detection of human papillomavirus type 16 DNA in consecutive genital samples does not always represent persistent infection as determined by molecular variant analysis.
Persistent human papillomavirus (HPV) infection of the uterine cervix is a risk factor for progression to high-grade squamous intraepithelial lesions. Detection in consecutive genital samples of HPV-16 DNA, a frequently encountered HPV type, may represent persistent infection or reinfection. We undertook a study using PCR-single-strand conformation polymorphism (SSCP) analysis and sequencing of PCR products (PCR-sequencing) to determine if consecutive HPV-16-positive samples contained the same HPV-16 variant. Fifty women (36 human immunodeficiency virus [HIV] seropositive, 14 HIV seronegative) had at least two consecutive genital specimens obtained at 6-month intervals that contained HPV-16 DNA as determined by a consensus L1 PCR assay. A total of 144 samples were amplified with two primer pairs for SSCP analysis of the entire long control region. Fifteen different SSCP patterns were identified in our population, while 22 variants were identified by PCR-sequencing. The most frequent SSCP pattern was found in 75 (53%) samples from 27 (54%) women. The SSCP patterns obtained from consecutive specimens were identical for 46 (92%) of 50 women, suggesting persistent infection. Four women exhibited in consecutive specimens different HPV-16 SSCP patterns that were all confirmed by PCR-sequencing. The additional information on the nature of persistent infection provided by molecular variant analysis was useful for 6% of women, since three of the four women who did not have identical consecutive specimens would have been misclassified as having persistent HPV-16 infection on the basis of HPV typing.
Adult↗
Dehydroepiandrosterone replacement administration: pharmacokinetic and pharmacodynamic studies in healthy elderly subjects.
Dehydroepiandrosterone (DHEA; 50 and 25 mg) and placebo tablets were orally administered daily to 24 healthy aging men and women (67.8 +/- 4.3 yr) for 8 days according to a balanced incomplete block design. Nine blood tests on both the first and eighth days allowed the measurement of DHEA, its sulfate DHEAS, and metabolites: testosterone, 5alpha-androstan-3alpha,17beta-diol glucuronide, estradiol, and estrone. Relatively low background levels of DHEA(S) were observed, and with the reestablishment of "young" levels, four important results were obtained. 1) Blood DHEA had an apparent terminal half-life of more than 20 h, the same order of magnitude as that of blood DHEAS, a result explainable by back-hydrolysis of the large amount of DHEAS formed after oral administration of DHEA, a mechanism providing long-lived unconjugated DHEA and metabolites. 2) The metabolic conversion of DHEAS to DHEA was significantly greater in women than in men. 3) No accumulation of steroids was observed. 4) No worrying transformation to androgen and estrogen was recorded; indeed, the limited increased estradiol in aged women could be predicted to be beneficial. These results suggested that daily oral administration of DHEA (25/50 mg) is safe in elderly subjects. The 50-mg dose was chosen for a 1 yr, double blind, placebo-controlled trial of daily oral administration of DHEA in 60- to 80-yr-old individuals (DHEAge).
Aged↗
Pharmacokinetics and pharmacodynamics of GnRH agonists: clinical implications in pediatrics.
Since 1981, GnRH agonist administration has been the treatment of choice for central precocious puberty. Continuous administration of the agonist, instead of permanently stimulating gonadotropin secretion, deeply suppresses LH and FSH levels and induces a marked inhibition of gonadal activity and regression of clinical symptoms. This inhibitory effect is due both to specific kinetic parameters relative to natural GnRH, and to marked alterations of the biosynthetic pathways of gonadotropin subunits. The half disappearance time of infused agonists is 3-10 fold that of natural GnRH. This means that the residence time of GnRH agonists is significantly longer than that of GnRH. The resistance of agonist to enzymatic degradation, mainly due to the substitution of a hydrophobic D-amino acid for glycine 6, is one of the factors involved in the increased availability of GnRH superagonists. The paradoxical effects of GnRH superagonists are still incompletely understood. In children long-term treated with depot formulations of triptorelin or leuprorelin, alpha-subunit secretion is markedly increased, and remains sensitive to exogenous GnRH, which demonstrates that the gonadotrophs are not totally desensitized. Despite the sustained stimulation of a-subunit secretion, no deleterious side effects, either during therapy or during post-therapy follow-up, have been reported in children treated with GnRH agonists. It should be noted that alpha-subunit responsiveness to exogenous GnRH decreases progressively after several years of treatment, although it is never completely abolished. On the other hand, LH beta-subunit secretion is suppressed as evidenced by radioimmunoassay of LH beta-subunit in serum chromatographic fractions from children treated with triptorelin. This differential pattern of secretion parallels that of mRNA levels in rat pituitary after in vivo exposure to triptorelin. Both pharmacodynamic and pharmacokinetic data can help diagnose the situations of resistance or escape. The lack of clinical effect of GnRH in the treatment of precocious puberty can be due to true resistance, or to an inappropriate injection schedule, or to abnormal metabolism. Measurement of serum alpha-subunit level, and, if needed, of serum agonist level, generally provides the answer.
Delayed-Action Preparations↗
Soluble leptin receptor in serum of subjects with complete resistance to leptin: relation to fat mass.
Leptin resistance and obesity have been related to mutations of the leptin receptor gene in rodents and, recently, in a consanguineous family. The latter mutation results in a receptor lacking transmembrane and intracellular domains. Homozygous and heterozygous individuals with this mutation had serum leptin levels higher than expected, given their BMIs: 600, 670, and 526 ng/ml and 145, 362, 294, 240, and 212 ng/ml, respectively. Their serum leptin was fractionated by gel filtration: >80% was present as a high-molecular size complex vs. 7.5% in the nonmutated sister. Western blot analysis showed a band at 146 kDa reacting specifically with an antibody directed against the leptin receptor ectodomain. In 10 obese control subjects, as in the mutated patients, free leptin levels correlated with BMI (r = 0.70, P = 0.0011) and reflected fat mass, regardless of leptin receptor functioning. In the patients, bound leptin levels correlated with BMI (r = 0.99, P = 0.0002) and were related to the number of mutated alleles. These data demonstrate that the truncated receptor is secreted into blood and binds the majority of serum leptin, markedly increasing bound and total leptin. Free serum leptin was similarly correlated with BMI in the mutated and nonmutated obese individuals, providing evidence that the relationship between BMI and circulating free leptin is preserved in this family. This finding suggests that the leptin receptor itself may not be specifically involved in the control of leptin secretion, and it supports the concept of relative resistance to leptin in common obesity.
Adipose Tissue↗
[Linear radiodermatitis following total body electron beam therapy].
BACKGROUND: We describe herein a peculiar clinical presentation of a linear overlapping radiodermatitis, localized on the internal side of the limbs, following a total body electron beam therapy. CASE REPORT: A 68-year-old-man was treated in April 1998 by a total body electron beam therapy, for a stage I mycosis fungoides. Few days after the last irradiation, the patient suffered from a linear eruption localized on the internal side of the limbs and the external side of the abdominal wall. DISCUSSION: Total body electron beam therapy can be proposed in early stage mycosis fungoides with localized or generalized cutaneous lesions. Because penetration depth of electron is well controlled and is limited to the skin, usual side effects of total body electron beam therapy do not concern internal organs (bone marrow,.). We report here a peculiar clinical presentation of a linear radiodermatitis in frontal plane which has not been reported to date, to our knowledge. This radiodermatitis corresponds to overlapping of posterior and anterior fields of irradiation.
Aged↗
[Leiomyosarcoma: unusual presentation].
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Aged↗
Transplants of fetal frontal cortex grafted into the occipital cortex of newborn rats receive a substantial thalamic input from nuclei normally projecting to the frontal cortex.
A number of molecular and hodological experiments have provided evidence that there is an early commitment of neocortical neurons to express features unique to a certain cortical area. However, the findings of several transplantation experiments have indicated that late embryonic cortical tissue heterotopically grafted into the neocortex of newborn rats receives a set of thalamic projections appropriate for the host cortical locus within which it develops. To provide further information on the extent to which neocortical neurons are predetermined to develop area-specific systems of connections, in this study we have compared the pattern of thalamic afferents to grafts of embryonic day 16 occipital or frontal neocortex transplanted into the occipital cortex of newborn rats. Two months after grafting, a retrograde neurotracer (cholera toxin, subunit b) was injected into the grafts to precisely assess the number of cells in the visual- and/or motor-related nuclei of the host thalamus projecting to each category of transplants (occipital-to-occipital or frontal-to-occipital). Transplants of embryonic occipital cortex received significant input from several visual-related thalamic nuclei, i.e. the lateral posterior and lateral dorsal nuclei, and no input from motor-related thalamic nuclei. However, only few labeled cells were found in the dorsal lateral geniculate nucleus, which was systematically affected by a severe atrophy, probably in response to the lesion of the occipital cortex performed prior to the transplantation. By comparison, transplants of frontal origin received a substantial input from the ventrolateral and ventromedial thalamic nuclei, which normally project to the frontal cortex, but received a weak input from the lateral posterior and lateral dorsal nuclei. Neocortical neurons grafted heterotopically into the neocortex of newborn hosts are not only able to contact cortical and subcortical targets appropriate for their embryonic site of origin, but are also susceptible to derive thalamic inputs closely related to their embryonic origin.
Animals↗
The thalamo-fronto-striate system: ultrastructural evidence of appropriate synaptic integration of embryonic neurones grafted within the frontal cortex of newborn rats.
Previous light microscopical studies have indicated that fibres from the ventrolateral thalamic nucleus (VL) establish direct axo-somatic and axo-dendritic presumed contacts with layers III and V neurones of the intact frontal cortex projecting to the striatum. Additional experiments provided evidence that this thalamo-fronto-striate pathway could be partly reconstructed by transplantation of embryonic frontal tissue into the damaged cortex. The present study was undertaken to validate these results at the ultrastructural level. Several months after the transplantation of fetal frontal tissue into the damaged frontal cortex of newborn rats, a retrograde neurotracer (subunit b of the cholera toxin) was used to label the grafted neurones projecting to the striatum whereas an anterograde neurotracer (Phaseolus vulgaris leuco-agglutinin) was used to label within the transplant, axons and terminations arising from the VL. The same injection procedures were applied to intact adult rats (control). The distribution of retrograde and anterograde labellings within the intact cortex and within the graft was examined at light and electron microscopic levels to identify the synaptic contacts. Our findings showed that labelled contacts were less numerous within the transplant than within the intact cortex but their synaptic organization was similar: asymmetrical synaptic axo-dendritic and axo-somatic contacts. This synaptic articulation is probably supplied by a thalamic excitatory input. These results provide ultrastructural evidence of the capacity of a frontal cortical transplant placed in damaged frontal cortex of newborn rats to help reconstruction of appropriate synaptic integration within the thalamo-fronto-striate system.
Animals↗
Main inhibitor of follicle stimulating hormone in the luteal-follicular transition: inhibin A, oestradiol, or inhibin B?
The roles of oestradiol, inhibin A and inhibin B in the luteal-follicular transition were assessed by means of specific assays. Six premenopausal women were studied during a control and then a cycle treated with percutaneous oestradiol 0.1 mg/day from day 10 after the luteinizing hormone (LH) surge until day 4 of the following cycle. Inhibin A concentrations decreased similarly in control and treated cycles from day -5 to day 2, then increased in control cycle to 23.3 +/- 3.4 pg/ml on day 10 (mean +/- SEM). They remained low until day 5 in treated cycles and were lower than controls on day 10 (P < 0.01). Follicle stimulating hormone (FSH) concentrations increased on day 1 in controls and on day 5 in treated cycles when oestradiol concentration fell abruptly. Inhibin B concentrations remained low until day 1 in controls and day 4 in treated cycles. In both, inhibin B concentrations increased 1 day after FSH, peaking at 160 pg/ml. FSH concentrations began to plateau when inhibin B concentrations were >100 pg/ml and oestradiol concentrations below 200 pmol/l. These data suggest that inhibin A is not responsible for FSH suppression in the luteal phase and that the negative control of FSH shifts from oestradiol in the luteal phase to inhibin B in the mid-follicular phase.
Adult↗
Evaluation of a vanA-specific PCR assay for detection of vancomycin-resistant Enterococcus faecium during a hospital outbreak.
We investigated the use of PCR as an alternative to culture of fecal samples for detection of vanA-containing Enterococcus faecium during a recent hospital outbreak. Rectal swabs collected consecutively from 223 patients were analyzed by culture with and without enrichment broth and by vanA-specific PCR of enrichment broth samples. Fifty-five specimens were positive for vanA-containing E. faecium by at least one method. The sensitivities of the vanA-specific PCR assay and agar culture with and without enrichment broth were 94.5, 98, and 89%, respectively. All three methods were 100% specific. Final results were obtained much more rapidly by PCR (within 24 to 30 h of specimen submission) than by the culture methods (4 to 5 days). Thus, PCR is an accurate and rapid alternative to culture for detection of vancomycin-resistant enterococci during hospital outbreaks.
Anti-Bacterial Agents↗
Final height after long-term treatment with triptorelin slow release for central precocious puberty: importance of statural growth after interruption of treatment. French study group of Decapeptyl in Precocious Puberty.
The impact of treatment of central precocious puberty (CPP) with GnRH agonists on final statural height (FH) remains controversial, and guidelines on the optimal time point for interruption of these treatments have not been established. We analyzed the long term results of 58 girls and 8 boys uniformly treated with triptorelin slow release formulation (Decapeptyl, triptorelin-SR) for CPP and compared their FH with predicted height before treatment and with the FH of a historical group of patients not treated with GnRH agonist. The FH SD score was close to 0 and was not different from the genetic target height. In girls, FH was improved by 4.8 +/- 5.8 cm compared with predicted height before treatment and by 8.3 cm by comparison with a historical group. In boys, comparison with a historical group revealed a 13.7-cm improvement, whereas predicted height before treatment was similar to FH. Three variables were independently associated with FH in girls: the bone age/statural age ratio at the onset of treatment (negatively), the height SD score at the end of treatment, and the posttreatment growth spurt (delta FH - height at the end of treatment). The influence of the posttreatment growth spurt, itself dependent on age and bone age at the interruption of treatment, suggests that continuing treatment beyond the age of 11 yr in girls does not improve and could actually decrease FH. This point should be evaluated in a formal controlled trial.
Age of Onset↗
[Eyelid edema revealing Kikuchi's disease].
INTRODUCTION: In 30 p. 100 of Kikuchi's disease (or necrotizing histiocytic lymphadenitis), polymorphous and non specific cutaneous manifestations are present. We report herein an original case of Kikuchi's disease in which eyelid edema was the first sign. CASE REPORT: An 18-year-old girl was referred to our department for fever, arthralgia, cervical lymphadenitis and an important eyelid edema which had begun 4 days before. The rest of physical examination was normal. Laboratory tests revealed pancytopenia, elevated sedimentation rate, increased transaminases and normal muscular and thyroid tests. Various serologic studies were also negative. Thoracic CT scan, abdominal ultrasound and bone marrow biopsy showed no sign of lymphoma. Cervical lymph node biopsy revealed necrotizing histiocytic lymphadenitis, without neutrophils, suggesting the diagnosis of Kikuchi's disease. Eyelid edema due to lacrimal gland inflammation was resolved after local injections of cortisone. Our patient recovered without therapy within 3 weeks. No recurrence was observed after 4 months. DISCUSSION: Kikuchi's disease is rare and benign. It is clinically manifested by cervical or generalized lymphadenopathy, with fever. Diagnosis is made by lymph node biopsy showing necrotizing histiocytic lymphadenitis. The etiology is not yet well known, although a viral cause is often suspected. The main differential diagnoses of Kikuchi's disease are lupus erythematosus and lymphoma. Skin lesions are not well described. To our knowledge, we report herein the first case of eyelid edema revealing Kikuchi's disease. Therefore, Kikuchi's disease should now be considered as a new cause of eyelid edema.
Adolescent↗
Specific invasion of occipital-to-frontal neocortical grafts by axons from the lateral posterior thalamic nucleus consecutive to neonatal lesion of the rat occipital cortex.
Previous work found that transplants of embryonic (E) day 16 occipital cortex placed into the frontal cortex of newborn hosts failed to receive input from visual-related nuclei of the host thalamus. The present study is aimed at determining the possible causes of the lack of visual-related thalamic input to these transplants. For that purpose, a retrograde neurotracer was injected into transplants of embryonic (E16) occipital origin which were placed into the frontal cortex of newborn rats with either intact or damaged occipital cortex. In rats with intact occipital cortex, occipital-to-frontal transplants were indeed not contacted by axons from the dorsal lateral geniculate (DLG) nucleus and received only sparse to negligible input from, respectively, the lateral posterior (LP) and laterodorsal (LD) thalamic nuclei. Yet, following neonatal lesion of the host occipital cortex, the occipital-to-frontal transplants received a significant input from the LP and to a much lesser degree from the LD but practically none from the DLG. Additional control cases with frontal-to-frontal transplants and prior lesion of the occipital cortex did not receive significant input from any of these thalamic nuclei. Thus, following neonatal deprivation of cortical target cells in their main terminal field, LP and to a lesser extent LD axons have the capacity to recognize and significantly innervate appropriate targets even those at some distance from their normal terminal site. DLG neurons degenerate or are not able to contact and invade available terminal space that is provided at some distance from the occipital cortex.
Animals↗