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Biomedical subjects

M Tardieu

Publications and source records attributed to M Tardieu.

At least 109 records · Page 6Linked to original sources
PubMed1994

The neuropathogenesis of HIV-1 infection.

HIV infection in brain revolves around productive viral replication in cells of mononuclear phagocyte lineage, including brain macrophages, microglia, and multinucleated giant cells [1-4]. Together, they are the investigators for cellular and viral neurotoxic activities [5-10]. Several published reports show that viral and/or cellular products produced from HIV-1-infected macrophages injure neurons and induce glial proliferation during advancing central nervous system (CNS) infection [11-18]. These findings are supported by the apparent discrepancy between the distribution and numbers of virus-infected cells and concomitant brain tissue pathology [5, 19]. Whether these soluble factors are indirectly responsible for neuronal damage remains undefined. The identification and regulation of neurotoxins produced from HIV-infected macrophages are central to uncovering how HIV mediates CNS disease. The authors who contributed to this work represent laboratories with overlapping areas of expertise. Broad-based complementary hypotheses regarding HIV neuropathogenesis are now provided.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Submicroscopic deletions of 17p13.3 in type 1 Lissencephaly.

DNA markers YNZ22.1 and YNH37.3 were studied by Southern blotting in 14 patients with typical (11 cases) and atypical (3 cases) type 1 Lissencephaly, all with normal high resolution karyotype. A submicroscopic deletion was found in 2 typical cases: one with Miller-Dieker Syndrome (MDS), the other with Isolated Lissencephaly Sequence (ILS). These results suggest a genetic continuum between MDS and ILS. The low frequency of such deletions, especially in ILS, will necessitate direct testing of the newly identified LIS 1 gene.

Cerebral Cortex↗
PubMed1994

HIV-1 and the developing human nervous system: in vivo and in vitro aspects.

HIV-1 is able to penetrate the developing human central nervous system and induce damage. Clinical and neuropathological observations demonstrate that (a) the virus is transmitted during the late phase of pregnancy or at the time of delivery; (b) the main infected cells within the brain are macrophages, and (c) the mere presence of infected macrophages within CNS tissue is not enough to predict disease. Primary cultures of human embryonic or fetal CNS and derived cultures highly enriched in either astrocytes or microglial cells are useful tools to study the mechanisms of HIV-1-induced neuronotoxicity in which both microglial cells and astrocytes play important roles.

Female↗
PubMed1994

Mitogenic and in vitro angiogenic activity of human recombinant heparin affin regulatory peptide.

We have previously described the purification of a heparin binding growth factor from adult bovine brain named heparin affin regulatory peptide (HARP), which was identical to an uterus derived growth factor named pleiotrophin and to a developmentally regulated neurite promoting factor named heparin-binding growth associated molecule. However, for yet unclear reasons, the mitogenic activity of this purified polypeptide following isolation from animal tissue extracts is a subject of controversy, due to conflicting and irreproducible data when produced by recombinant DNA technologies in E. coli or insect cells. The purified protein was inactive in mitogenic assays but the natural molecule was active in assay of neurite outgrowth. In order to clarify these conflicting results and to obtain a recombinant protein free from other contaminating heparin-binding growth factors, we have cloned human cDNA encoding human HARP, engineered its expression in NIH 3T3 cells and characterised the resulting recombinant polypeptide. Purified recombinant HARP displayed mitogenic activity for capillary endothelial cells with half-maximal stimulation at approximately 1 ng/ml (55 pM) and induced angiogenesis in an in vitro model. Interestingly, while the NH2 terminal sequence of tissue purified HARP was NH2-GKKEKPEKK, the NH2 terminal sequence of the biologically active recombinant protein was NH2-AEAGKKEKPEKK, corresponding to a three amino acid extended form.

3T3 Cells↗
PubMed1994

Mesoglycan and sulodexide act as stabilizers and protectors of fibroblast growth factors (FGFs).

Heparin and heparan sulfate proteoglycans (HSPGs) stabilize FGFs which belong to heparin-binding growth factors (HBGFs) on active conformation. They also strongly potentiate their mitogenic activity on many cell types, and protect them against thermal denaturation and enzymatic degradation. In the present work we have tested two heparin-like substances named mesoglycan and sulodexide obtained from bovine intestinal mucosal extracts. These products are used as heparin, in various of therapeutic fields such as atherosclerosis or antithrombotic therapy. The compositions of mesoglycan and sulodexide are partially known and include chondroitin, dermatan and heparan sulfate. We have shown that mesoglycan and sulodexide potentiated the mitogenic activity of FGF1 and FGF2. The magnitude of this effect was identical with that of heparin used as a control substance but at double concentration. Mesoglycan and sulodexide also exerted stabilizing and protective effects on FGFs for heat denaturation and enzymatic degradation. The suppression of the protective properties after heparinase treatment of mesoglycan and sulodexide indirectly demonstrated the presence of heparan sulfate which was shown to represent about 60% of the commercial products.

Animals↗
PubMed1994

[Syndrome of delayed maturation of the sucking-swallowing reflex].

BACKGROUND: Neonates with neurological diseases often have difficulty in sucking or swallowing. This report describes such difficulties in a group of infants with normal development, suggesting late maturation of sucking and swallowing. POPULATION AND METHODS: Seven infants (four girls, three boys) had suffered from aspiration since their first day of life (four cases) with severe asphyxia (two cases), late repeated episodes of airway obstruction by accumulated secretions (two cases), and weak isolated sucking and swallowing (one case). The lack of sucking and swallowing or difficulty with them were the main manifestations in these newborns: the face lacked expression and the tongue movements were abnormal with, in two cases, hyper-extension of the neck. A second phase during the first months of life was marked by episodes of bradycardia and/or drowsiness. A third phase during the first years of life was characterized by repeated episodes of respiratory infections, recurrent stridor and accumulation of saliva. These manifestations required prolonged hospitalization (mean: 2.5 months), nasogastric feeding, and in two cases, surgery. The investigations during the acute phases included a cineradiographic study of swallowing, laryngoscopy, monitoring of the distal esophagus pH, a barium swallow, polygraphic recording during sleep and MR imaging of the brain stem. The difficulties in sucking or swallowing disappeared before the age of 6 months (two cases), between 6 and 12 months (one case), between 1 and 5 years (four cases) without any sequelae or speech disorders. CONCLUSION: These transient sucking or swallowing difficulties suggest late maturation of praxis. They required specialized prolonged education after careful, essentially clinical, investigation.

Deglutition Disorders↗
PubMed1993

In vitro production of IL-6, IL-1 beta, and tumor necrosis factor-alpha by human embryonic microglial and neural cells.

The abilities of the different cells from human central nervous system (CNS) to produce IL-6, IL-1 beta, and TNF-alpha were tested in vitro using either cultures enriched in human embryonic microglial cells or primary cultures of human embryonic CNS cells. High amounts of IL-6, low amounts of IL-1 beta but no TNF-alpha were detected in supernatants of microglial cells, kept either in FCS-free conditions or in FCS-containing medium. Moreover, IL-6 mRNA was also present in 45 to 55% of microglial cells cultured in the presence of FCS as visualized by in situ hybridization, whereas IL-1 beta mRNA remained undetectable. After prestimulation of microglial cells with LPS or IL-1 alpha, the percentage of cells labeled with an antisense IL-6 mRNA probe increased to 70% and hybridization with an antisense IL-1 beta mRNA probe became detectable. In contrast to this dyscoordinate production of cytokines by microglial cells, human monocytes, freshly isolated from blood and kept in the same culture conditions, produced high levels of the three cytokines tested. In primary cultures of human embryonic CNS cells, IL-6, IL-1 beta, and TNF-alpha were produced mostly or only by microglial cells because no IL-1 beta mRNA or IL-6 mRNA were detected in astrocytes, even after prestimulation with LPS or IL-1 alpha. Finally, IL-1 was the main inducer of IL-6 production because IL-1 alpha, but not LPS, induced a significant increase in IL-6 synthesis in cultures kept in FCS-free medium. However, in presence of FCS, LPS appeared to initiate a cascade reaction involving the production of IL-1 by microglial cells, acting as an autocrine loop to trigger IL-6 synthesis.

Astrocytes↗
PubMed1993

Central nervous system lesions in hypomelanosis of Ito: an MRI and pathological study.

A severe form of hypomelanosis of Ito is reported, which presented as fetal macrocephaly and neonatal epileptic encephalopathy. Lymphocyte karyotypes were normal. MRI showed an absence of delineation between cortical grey matter and white matter. The prominent neuropathological finding was an abnormal cortical morphogenesis, with the co-existence of cells migrating normally and cells exhibiting arrêt en route or even the complete absence of migration. Intense astrocytic reaction with moderate dystrophic features was present. Juxtaposition of two migration behaviours in the neural cells paralleled the cutaneous findings and reinforced the hypothesis of a genetic chimerism.

Cell Movement↗
PubMed1993

Genetic restriction of murine hepatitis virus type 3 expression in liver and brain: comparative study in BALB/c and C3H mice by immunochemistry and hybridization in situ.

To study the host-dependent genetic variations in murine hepatitis virus type 3 (MHV 3) induced diseases, we localized the sites of MHV 3 (Mill Hill strain) expression within liver and brain by immunohistochemistry or hybridization in situ. Two strains of mice were studied: BALB/c mice, which develop an acute and lethal hepatitis and C3H mice which develop a chronic brain infection. In BALB/c mice, viral RNA and antigens appeared during the first 24h post infection (p.i.) in liver, whereas viral RNA was barely detectable in brain, up until death at day 3 p.i. In C3H mice, viral RNA and antigens were detected simultaneously in liver and brain only at day 2 p.i. In brain, the virus was detected in meningeal and ependymal cells and in perivascular cortical areas (days 5 and 7 p.i.). After day 49, the virus was no longer detected in brain parenchyma, but persisted in meningeal cells. Two host-dependent genetic differences in viral processing were observed in the liver: (1) the virus was first detected in Kupffer cells in BALB/c mice and mostly in hepatocytes in C3H mice; (2) in BALB/c mice, the 180 kDa S viral glycoprotein appeared more frequently cleaved in 90 kDa form than in C3H mice.

Animals↗
PubMed1993

The gene encoding the nucleocapsid protein: sequence analysis in murine hepatitis virus type 3 and evolution in Coronaviridae.

The nucleoprotein-encoding gene (N) of murine hepatitis virus type 3 (MHV 3), from the Mill Hill strain, was cloned and sequenced. It was compared to gene N from other murine coronaviruses and was found to share more similarities with N sequences from MHV 1 and MHV JHM strains than with the published MHV 3 N sequence which is almost identical to MHV A59. We suggest that the evolution of some MHV N sequences resulted from a double recombination phenomenon between two ancestors. Furthermore, comparison of protein N from avian and mammalian coronaviruses leads to the hypothesis that horizontal transfer events of the virus from one host species to another have occurred.

Amino Acid Sequence↗
PubMed1993

[Laurence-Moon (Bardet-Biedl) syndrome with growth hormone deficiency].

BACKGROUND: The features of Laurence-Moon syndrome vary widely from mental retardation, hypogenitalism to retinopathy; the dominant one is progressive neurological involvement, ataxia and spastic paraplegia. Like Bardet-Biedl syndrome, its inheritance is autosomal recessive. This paper describes the endocrine investigation of a new family of Laurence-Moon syndrome subjects. CASE REPORT: The 5 patients (3 girls, 2 boys) in this family of 12 sibs, all suffered from retinopathy, mental retardation and first metacarpal hypoplasia with proximal placement of thumb. All five had had spastic paraplegia since the age of 5-6 years, growth retardation and hypogonadism. Two had had seizures; only one was obese. RESULTS: Four patients (2 girls, 2 boys, aged 19, 15, 18 and 19 years) had low basal plasma FSH and LH levels. They had no FSH-LH response to gonadotropin-releasing hormone; their plasma testosterone and oestradiol concentrations were very low. The growth hormone peak in response to arginine-insulin were low in these 4 patients (1.5 ng/ml; 3.8 ng/ml; 5 ng/ml; 4.8 ng/ml). One boy and one girl were given sex steroids for a few months, with good effect on their sexual characters. Their growth hormone levels remained low (2.9 ng/ml, 6.5 ng/ml). One boy was given FSH and LH analogues with good effects on sexual characters and testicle growth. He was also given growth hormone, and had a growth spurt of 5.5 cm after 9 months treatment. CONCLUSION: The hypogonadism of Laurence-Moon patients seems to be of central origin. It is associated with growth hormone deficiency.

Adolescent↗
PubMed1993

[Epidermoid cyst of the 4th ventricle. Apropos of a case in a child and review of the literature].

A 6 year-old child was admitted for a recurrent bacterial meningitis at Proteus Morganii. She was treated with antibiotics. The C.T. Scanner showed a midline low-density lesion, with a mild annular contrast uptake in the posterior fossa. M.R.I. showed the lesion and revealed a skin-bone-dura fistula. The surgical resection was complete. It was an epidermoid tumor. Intracranial epidermoid tumors constitute about 1% of brain tumors and are considered to be congenital. Epidermoid tumors of the 4th ventricle are exceedingly rare in childhood. The authors reviewed the literature and discuss the pathogeny, the radiographic diagnosis and the treatment of these tumors.

Brain Diseases↗
PubMed1993

[A neuropathological study of 10 HIV-infected children].

In 10 children infected by HIV at birth, who presented early and severe immunodeficiency encephalopathy, the lesions observed in the central nervous system were different from those found in adults. Using standard neuropathological techniques, the main abnormalities were white matter palor and atrophy, pyramidal tract demyelination, moderate perivascular inflammation, numerous calcifications of blood vessels in basal ganglia, white matter and occasional in the cortex, few opportunistic infections including cytomegalovirus ventriculitis, polymorphonuclear microabcessses and aspergillus abscesses; no toxoplasma was detected. An 18-month-old girl presented with an angiocentric lymphoproliferative disorder in central and peripheral nervous system and muscle, with predominance of B cells. In most cases, low levels of HIV replication were detected in brain tissue, as demonstrated by the presence of only few microglial nodules and giant cells, feeble detection of HIV p24 and p17 antigens by immunocytochemistry, in situ hybridization of HIV DNA and RNA and polymerase chain reaction, despite severe clinical encephalopathy. Zidovudine did not improve any patient. In children with severe AIDS encephalopathy, HIV might not be directly implicated in the central nervous system lesions: an intermediate factor such as cytokines or another toxic substance secreted by activated macrophages and/or lymphocytes, could induce severe lesions in the central nervous system and minor pathology of the peripheral nervous system and muscles.

AIDS-Related Opportunistic Infections↗