[MRI and drug-resistant partial epilepsy. What protocol and why? Experiences of the Department of Neuroradiology of the Pité-Salpêtrière Group Practice Hospital].
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Anticonvulsants↗
Biomedical subjects
D Dormont
Publications and source records attributed to D Dormont.
HIV predominantly induces IL-1 receptor antagonist over IL-1 synthesis in human primary monocytes.
Interaction of HIV with cultured human monocytes triggers not only cytokine production but also the release of natural cytokine inhibitors such as the soluble TNF receptors, levels of which are increased in the circulation of HIV-infected patients. We found that HIV-1 LAI induced the production by human monocytes from HIV-seronegative donors of another type cytokine inhibitor, the IL-1Ra receptor antagonist (IL-1Ra). HIV mainly induced the secreted form (83%) of IL-1Ra through de novo mRNA synthesis. IL-1Ra production was triggered at an early step of the infection process and involved the HIV envelope protein and the CD4 receptor. HIV-triggered IL-1Ra production occurred after a lag time, suggesting an indirect mechanism. Neutralizing Abs to IL-1 beta and IL-10 had no effect, while simultaneous treatment with anti-TNF-alpha, anti-granulocyte-macrophage CSF, and anti-TGF-beta nearly abrogated IL-1Ra release, supporting an indirect induction through the concerted action of the co-produced cytokines. IL-1Ra was induced by HIV in a mean 1,000-fold increase over IL-1 alpha beta, a ratio 20-fold higher than that obtained with LPS. This production masked 80% of IL-1 bioactivity in HIV-induced monocyte supernatants. These results suggest that the net balance between pro-inflammatory cytokines and their natural inhibitors could be critical in the control of the inflammatory process associated with HIV infection.
Cells, Cultured↗
Specificity and neutralizing capacity of three monoclonal antibodies produced against the envelope glycoprotein of simian immunodeficiency virus isolate 251.
Three mouse monoclonal antibodies (mAb) were produced against soluble recombinant vaccinia virus gp140 from SIV-mac251. Two mAbs (1B9 and 6C11) were mapped at the aa 411-430 sequence within the V4 domain, and the third mAb (3C8) recognizes a conformation-dependent epitope on the external envelope glycoprotein. This was shown by its loss of reactivity in Western blot and ELISA with dithiothreitol-reduced gp140. mAb 3C8, but not 1B9 and 6C11, cross-reacts well with gp140 and gp125 from HIV-2ROD, indicating that this discontinuous epitope includes conserved regions localized within the external envelope glycoprotein. Analysis of the neutralizing activities of the mAbs showed that only mAb 1B9 is able to inhibit both syncytium formation and SIVmac251 infection of human peripheral blood lymphocytes.
Animals↗
Human growth hormone-related iatrogenic Creutzfeldt-Jakob disease: search for a genetic susceptibility by analysis of the PRNP coding region.
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Creutzfeldt-Jakob Syndrome↗
Registration in neurosurgery and neuroradiotherapy applications.
Because of the high level of accuracy needed in neurosurgery, many computer-assisted surgery (CAS) and augmented reality techniques have been developed in this field. A common issue with all of these techniques is registration between preoperative three-dimensional images (computed tomography and magnetic resonance imaging) and the patient in the operating room. We present, in the first part of this paper, a survey of the latest CAS technologies, using fully automatic registration without fiducial landmarks. All of the registration algorithms described are based on minimization of a cost function. We then describe our approach. Our cost function is simply the mean square error (MSE), minimized by the iterative closest point algorithm (ICP). Because the weak point of the ICP algorithm is the closest point computational cost, we precalculate it by a "closest point map," inspired from classical distance map. We finally perturb the found solution to eliminate local minima close to the global minimum. This paper summarizes the various methods presented. We study the shape of the different cost functions and show that there is no need for a complex cost function. MSE has sufficiently good convergence properties to reach a position very close to the global minimum. We also demonstrate the influence of a final perturbation of the found solution to improve registration. Finally, we test the registration on different regions of the patient's head.
Algorithms↗
Pregnancy complicated by cerebral venous thrombosis in Behçet's disease.
Pregnancy and Behçet's disease are both disorders with increased risks of cerebral venous thrombosis. However, we describe the first case of central venous thrombosis during the pregnancy of a woman with Behçet's disease, revealed by headaches, visual obscuring, and a slight increase in cerebrospinal fluid opening pressure. Treatment with heparin and corticosteroids led to rapid amelioration.
Adrenal Cortex Hormones↗
Highly attenuated SIVmac142 is immunogenic but does not protect against SIVmac251 challenge.
We report here the use of the highly attenuated SIVmac142 clone, unable to establish permanent infection of rhesus macaques, in a vaccine trial. Four rhesus macaques were immunized over a long time period with HUT-78 cells infected with wild-type SIVmac142 or, in order to reinforce the safety use of the vaccine, a deleted mutant with similar in vitro infectivity. The first two injections were done with living cells and the remaining boosts with cells emulsified in muramyl dipeptide adjuvant. Three control macaques were injected with uninfected HUT-78 cells. Over 3 years, we have been unable except once to detect viral infections by three methods. However, antibodies directed against the viral Gag proteins and envelope glycoproteins were detected by immunoblots and/or in vitro neutralization assays. All macaques were challenged intravenously with a low dose (10 animal infectious doses) of a highly pathogenic biological clone of SIVmac251 grown on macaque PBMCs. All seven animals became persistently viremic following challenge. The cell-associated viral loads of the vaccinated monkeys were not reduced relative to those of unvaccinated controls during the first weeks postchallenge even if vaccinated monkeys did not present a transient CD4 decrease. Thus, our data reinforced the notion that the efficacy of live attenuated SIV requires the establishment of persistent infection.
Animals↗
Functional consequences of macrophage infection by human immunodeficiency virus: bispecific antibody targeting of HIV-1-infected cells to Fc gamma RI expressing effector cells.
Human monocytes/macrophages play a major role in pathogenesis of human immunodeficiency virus (HIV) infection. These cells have been suspected of acting as a reservoir for the virus and are important in viral dissemination and persistence in infected individual. Furthermore, several biologic and clinical features indicate that monocytes/macrophages from HIV-1-seropositive patients have characteristics of an activation status, including the ability to secrete high levels of cytokines. Dysregulation of the cytokine network may influence the level and the consequences of viral replication in infected monocytes/macrophages. Therefore, the development of virus-specific agents that may interfere with viral replication could help to slow down the fatal course of HIV infection. In this article, we try to further quantify the early and late kinetic patterns of the cytokine network during HIV-1 macrophage infection and report the biologic effects of virus-specific bispecific antibody (MDX-240) in HIV-1 macrophage infection.
Antibodies, Bispecific↗
Relationships between humoral factors in HIV-1-infected mothers and the occurrence of HIV infection in their infants.
Based on what is known about the biology of HIV-1 vertical transmission, the HIV burden of the mother, maternal immune factors and the integrity of the placental barrier are likely to play major roles. We therefore sought to determine whether the presence of antibodies in sera from 47 HIV-1-infected mothers, including 30 non-transmitting and 17 transmitting mothers, affected the risk of HIV-1 transmission to infants. Our findings showed no significant correlation between the capacity of antibodies to mediate antibody-dependent cell-mediated cytotoxicity (ADCC) and their capacity to induce protection of the child from HIV-1 infection (P = 0.14). Furthermore, no correlation was found between the capacity of maternal antibodies to neutralize in vitro lymphocyte or macrophage heterologous viral infection and the occurrence of in vivo HIV-1 infection in the infant. Sera recovered from five of 12 transmitting mothers and from five of 11 non-transmitting mothers were compared in their capacity to neutralize the viruses drawn from the same individuals. Four out of five maternal isolates from transmitting mothers and all maternal isolates from non-transmitting mothers were sensitive to enhancement of infection mediated by the maternal serum.
Acquired Immunodeficiency Syndrome↗
Tumor necrosis factor-alpha in serum of macaques during SIVmac251 acute infection.
TNF secretion was explored in sera during acute SIV-infection of cynomolgus macaques. A peak of TNF was detected in sera of animals in concomitance with SIV replication. Likewise, AZT treatment delayed and reduced peaks of viral replication and TNF production. Thus, SIVmac251-infected monkey could be an excellent model to explore the interdigitation existing between HIV and TNF in acute and chronic infection and to develop new therapeutic strategies that target the production of this cytokine or its inductive effects.
Acquired Immunodeficiency Syndrome↗
MS-8209, a new amphotericin B derivative, provides enhanced efficacy in delaying hamster scrapie.
To test the efficacy of a new amphotericin B derivative, MS-8209, in delaying scrapie, hamsters were infected intracerebrally with the 263K scrapie agent and treated with MS-8209 either early in the course of the disease or continuously. The results show that (i) all treatments lengthened the incubation period of hamster scrapie, (ii) continuous treatment with MS-8209 doubled the length of the incubation period compared with that observed in infected, untreated animals, and (iii) all treatments delayed the accumulation of a proteinase-resistant prion protein and glial fibrillary acidic protein in the brain. These findings suggest that MS-8209 is a powerful tool for investigating the pathogenesis of transmissible subacute spongiform encephalopathies.
Amphotericin B↗
Developmental abnormalities of the medial temporal lobe in patients with temporal lobe epilepsy.
PURPOSE: To evaluate MR temporal lobe malformations and their frequency in patients with temporal lobe epilepsy. METHODS: Two hundred twenty-two consecutive adult patients with temporal lobe epilepsy of varying severity were investigated with 1.0-T or 1.5-T MR units using three-dimensional T1-weighted acquisition protocol. RESULTS: Sixteen patients (7.2%) presented with malformations of the temporal lobe. Four patterns of malformations were encountered: (a) heterotopia (n = 1), lining the temporal horn of the lateral ventricle; (b) focal neocortical dysgenesis (n = 6), which consisted of cortical thickening, poor gray/white matter demarcation, abnormal gyration (n = 5), or limited schizencephaly (n = 1); (c) hippocampal malformations (n = 5), which presented as abnormal hippocampal formation associated with a cyst (n = 2), isolated malformation of the subiculum (n = 1), or bilateral hippocampal malformation (n = 2) consisting of an abnormal shape and a misplaced fimbria; (d) complex malformations of the temporal lobe, combining categories a, b, and c (n = 4). The age at onset, severity of the disease, and occurrence of generalized tonicoclonic seizures were not significantly different between patients with malformations and the entire population of patients with temporal lobe epilepsy. CONCLUSION: MR analysis of temporal lobe malformations allowed a precise determination of the extent of the malformations and the presence or absence of associated hippocampal disease, all of which are of great help in the preoperative evaluation of patients with intractable epilepsy.
Adolescent↗
[Nature and physicochemical and biological properties of non conventional transmissible agents or prions: consequences for public health].
Transmissible spongiform encephalopathies (TSE) are rare lethal diseases induced in humans and animals by unconventional agents (TSA) named also prions or virinos. TSA/prions have unconventional properties; in particular, they resist to almost all the chemical and physical processes which inactivate conventional viruses. Natural history of TSE indicates that organs are infectious a long time before the appearance of the clinical symptoms. The only specific marker of the TSA infections is the post-translational accumulation of the host encoded protein PrP (Prion Protein). Iatrogenic Creutzfeldt-Jakob disease (CJD) cases have been described after neurosurgery, treatment with pituitary derived hormones, and cornea and dura mater grafting. TSA associated infectivity is depending upon the nature of the organ in a given infected individual: central nervous system has the highest infectivity, spleen and lymph nodes a medium infectivity, and organs like bone or skin do not harbor any detectable infectious particle. Therefore, donors with neurologic history must be excluded and treatment with pituitary derived hormones should be considered as potentially infected with TSA, and excluded.
France↗
[Conjugal mycosis fungoides].
INTRODUCTION: The pathophysiology of mycosis fungoides remains uncertain but HTLV I or a similar virus could be involved. We observed a couple who developed mycosis fungoides suggesting the infectious hypothesis might indeed be valid. CASE REPORT: A 70-year-old man who had often travelled in foreign countries developed parapsoriasis en plaques, lymphomatoid papulosis and mycosis fungoides successively over a thirty year period. Several years after the first manifestation of mycosis fungoides, his wife also developed a single plaque of mycosis fungoides. The diagnosis was confirmed on pathology slides and immunohistochemistry tests as well as on the basis of T-receptor gene rearrangement in both patients. Search for HTLV I was negative using serology tests and PCR on circulating lymphocytes. COMMENTS: The epidemiological situation in our observation (several trips in foreign countries and the delayed development of mycosis fungoides in the wife) favours the hypothesis of an infectious mechanism. Search for HTLV I was unsuccessful with classical virology methods. Certain recent work suggests a virus similar but different from the HTLV I virus could be involved in the pathogenesis of mycosis fungoides.
Aged↗
Modulations of 92kDa gelatinase B and its inhibitors are associated with HIV-1 infection in human macrophage cultures.
The macrophage-secreted 92-kDa type IV collagenase and metalloproteinases play a critical role in cell microenvironment regulation and cell movement. HIV infection of macrophages might be capable of deregulating the expression of these gelatinases. Hence, human monocyte-derived-macrophages were infected by lymphotropic HIV-1/Lai and monocytropic HIV-1/DAS isolates. Gelatinase activity and gelatinase and inhibitor (TIMP, alpha 2M) biosyntheses were evaluated in supernatants and cellular extracts. Our data suggest that HIV infection facilitates gelatinase secretion and intracellular inhibitor retention. These argue for the increase of free proteinase that could degrade barriers, which would permit cell movement and viral dissemination into tissues.
Cells, Cultured↗
Selection of specific strains in iatrogenic Creutzfeldt-Jakob disease.
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Animals↗
[Unconventional transmissible agents or prions].
Unconventional transmissible agents, or prions, induce rare, slow, neurodegenerative diseases that are transmissible and always fatal: transmissible subacute spongiform encephalopathies. These diseases are characterised by spongiosis associated with gliosis without inflammation or demyelination. These unconventional transmissible agents have particular biological and physiochemical properties that set them apart from the other micro-organisms. They are resistant to temperatures over 200 degrees C and insensitive to usual disinfectants used in virology; in addition, they are resistant to all the processes that degrade nucleic acids, while being sensitive to those which modify the structure or the composition of proteins. The only specific biological abnormality identified in the brain of affected patients is post-transcriptional accumulation of a normal host protein, PrP, in a form that makes it resistant to proteases; its accumulation is proportional to the titer of infection. The study of animal models in these diseases shows that the nervous system is by far the most infected organ. Infection is present in many organs long before the appearance of histological or clinical signs, explaining the accidental iatrogenic contamination thus far observed.
Humans↗
Induction of soluble tumor necrosis factor receptor (sTNF-R75) release by HIV adsorption on cultured human monocytes.
Soluble tumor necrosis factor (TNF) receptors were recently detected in the circulation of patients with early HIV-induced disease, at significantly higher levels than in control subjects. They were proposed as markers of disease progression and of the degree of immunodeficiency. We report that adsorption of heat-inactivated HIV-1 LAI to isolated human monocytes triggers the release of both TNF-alpha and its natural specific inhibitor, the soluble TNF receptor (sTNF-R)75, but not that of sTNF-R55. Only limited inhibition of sTNF-R release was obtained in the presence of a fully neutralizing anti-TNF-alpha monoclonal antibody, suggesting that stimulation by TNF-alpha was only partially responsible for sTNF-R release. HIV-1 LAI induced a higher sTNF-R/TNF ratio than lipopolysaccharide, a well-known monocyte activator. Monocytes thus represent a cellular source of sTNF-R that can be detected in the circulation of HIV-infected patients from seroconversion onwards. The release of sTNF-R could be of great significance in the control of HIV infection via the cytokine network and especially TNF-alpha.
HIV Infections↗