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N Brousse

Publications and source records attributed to N Brousse.

At least 181 records · Page 10Linked to original sources
PubMed1993

Immunohistochemical detection of granulocyte/macrophage colony-stimulating factor in Langerhans' cell histiocytosis.

Granulocyte/macrophage-colony stimulating factor (GM-CSF) induces in vitro activation of Langerhans' cells. The association of GM-CSF and tumour necrosis factor alpha (TNF alpha) induces the differentiation of Langerhans' cells from CD34 positive haematopoietic progenitors. Intradermal administration of recombinant GM-CSF is associated with local accumulation of Langerhans' cells. We investigated the presence of GM-CSF in tissue samples of 10 patients with Langerhans' cell histiocytosis. Four patients had skin involvement, three had bone and three had diffuse disease. Eight normal skin samples were analysed as controls. Immunohistochemistry was performed on frozen tissue samples with two specific monoclonal antibodies directed against two different epitopes of GM-CSF. We detected GM-CSF in all the histiocytosis tissue samples. The GM-CSF was detected within the cytoplasm of all the tumoral Langerhans' cells. We did not find GM-CSF in any other cell type. These results suggest that GM-CSF may be implicated in the pathogenesis of Langerhans' cell histiocytosis.

Antigens, CD↗
PubMed1993

Numbers of T cell receptor (TCR) alpha beta+ but not of TcR gamma delta+ intraepithelial lymphocytes correlate with the grade of villous atrophy in coeliac patients on a long term normal diet.

Numbers of T cell receptor (TcR) gamma delta+ and alpha beta+ intestinal lymphocytes were studied in 34 coeliac patients in respect of their diet and the grade of villous atrophy. Particular attention was given to a group of 21 patients with coeliac disease according to ESPGAN criteria who were on a well tolerated long term normal diet and in nine of whom the mucosa had returned to normal or nearly normal. A significant increase in TcR gamma delta+ cells was observed in the gut epithelium of coeliac patients compared with age matched controls, and this did not correlate with either the presence of gluten in the diet or with the grade of villous atrophy. Thus, numbers of TcR gamma delta+ intraepithelial lymphocytes (IEL) were considerably above the normal range in four of seven patients on a gluten free diet and in four of nine patients who had recovered a normal or nearly normal mucosa in spite of a normal diet. In contrast, numbers of intestinal TcR alpha beta+ cells varied with the stage of the disease. Their number was high in the epithelium of patients with active coeliac disease (n = 18) but significantly less in patients whose mucosa had returned to normal or nearly normal either after gluten free diet (n = 7) or in spite of a normal diet (n = 9). Immunohistochemical markers of intestinal mononuclear cell activation detected in active coeliac disease were either weakly expressed or absent in the latter patients. It is suggested that TcR alpha beta+ but not TcR gamma delta+ IEL are sensitised to gliadin in coeliac disease, and that only the former cells play a direct part in the pathogenesis of the villous atrophy. The normal counts of TcR alpha beta+ IEL and the absence of detectable mononuclear activation in the biopsy specimens of a few patients who have recovered clinical and histological tolerance to gluten sustains this hypothesis and also suggests that immunological tolerance to gluten may be acquired in a subgroup of coeliac patients. Hte appreciable increase in TcR gamma delta+ IEL observed in some of the latter patients, however, is similar to that observed in latent coeliac disease urging for their careful and prolonged follow up until the role of TcR gamma delta+ IEL in the pathogenesis of coeliac disease is elucidated.

Adolescent↗
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↗
PubMed1993

[Sudden crib death. Experience in a referral center 1986-1991].

BACKGROUND: Sudden infant death syndrome (SIDS) may have several etiologies, all of which must be identified in order to recognize those infants believed to be at risk. One of the best ways to do this is by prospective studies on a large population of infants who died of SIDS. METHODS: A total of 171 infants who died from SIDS between January 1, 1986 and June 30, 1991, were studied. 154 infants were completely investigated, including a post mortem examination. They were assigned to one of 4 groups, according to whether death was due to diseases of poor prognosis (group A), diseases that are occasionally fatal but potentially treatable (group B), minor diseases not normally fatal (group C), or was essentially unexplained (group D). RESULTS: The classical risk factors for SIDS were found in this population: incidence peaked in males (sex-ratio 1.5), during the cold seasons (62%), between 1 and 6 months of age (94%), mainly between 1 and 4 months of age (84%). Symptoms were definitely present during the 2 days before death in 50%. 20% of cases had clinical histories of congenital disease, complicated or recurrent postnatal disease, or fulminant recent disease. Group A included 107 infants (69% of the 154 completely investigated patients). Premature birth (17.5%) and low birth weight for gestational age (10.5%) were more frequent in our series than in the normal population. CONCLUSION: The cause of death was identified in about 75% of cases. This possibility improves management of further siblings of SIDS victims even though the variety of risk factors makes prevention of SIDS difficult.

Autopsy↗
PubMed1993

[Myxoma of the pulmonary infundibulum as the cause of sudden death in an 18-month-old infant].

BACKGROUND: Myxoma, a benign cardiac tumor, develops in intracavitary locations. It is most frequent in the left atrium, but rare in the pulmonary infundibulum. CASE REPORT: An 18 month-old girl suddenly became cyanotic during playing and lost consciousness. Resuscitation was ineffective. Post-mortem examination showed diffuse pulmonary edema and multiple small pulmonary emboli. There was a myxoma of the septal wall of pulmonary infundibulum and histological examination showed that the infundibulum and the pulmonary valve were completely infiltrated by myxoid tissue. CONCLUSION: The death of this girl was probably due to a sudden embolism of blood clots developed in contact with the myxoma. This case emphasizes the need for pathologic investigation in all cases of sudden death.

Female↗
PubMed1992

Multicentric Kaposi's sarcoma in a 5-year-old human immunodeficiency virus-negative renal allograft recipient.

We describe the clinical and pathologic features of a case of pediatric multicentric Kaposi's sarcoma (KS) associated with allograft transplantation in a human immunodeficiency virus (HIV)-negative child. A lethal polyadenopathic and visceral KS occurred in a 5-year-old Caribbean boy who had undergone an allogenic renal transplantation for diffuse mesangial sclerosis with end-stage renal failure 4 months previously. The HIV-1 and HIV-2 serologies were negative. Despite its rarity, KS must be considered as a differential diagnosis in posttransplantation polyadenopathic or multisystemic syndromes in children.

Autopsy↗
PubMed1992

Rejection in lung transplantation--an immunohistochemical study of transbronchial biopsies.

The number, distribution, and phenotype of mononuclear cells infiltrating the allograft lung transplant were determined immunohistochemically with monoclonal antibodies directed against cellular antigens (CD3, CD4, CD8, CD22, CD25, CD16, CD56, CD68, HLA-DR) on frozen sections of transbronchial biopsies. Seventy-two transbronchial biopsies from 21 patients undergoing lung or heart-lung transplantation were evaluated histologically and immunohistologically in a prospective study. Four major results were obtained in the graft lung parenchyma: (1) whatever the histological grading of rejection, T lymphocytes expressing CD3 were present and in a significantly higher number than in control subjects (P < 0.0005); (2) there was a positive correlation between histological rejection and the number of CD3+, CD8+, CD25+, CD16+ cells (P < 0.01); (3) the CD4/CD8 ratio was inverted (0.52 +/- 0.04), with no correlation with the histological rejection; and (4) the number and location of CD3+, CD25+ cells did not correlate with CMV identification in bronchoalveolar lavage. Immunohistochemical criteria could be used for diagnosis of rejection in the management of heart-lung transplantation.

Adolescent↗