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M Faure

Publications and source records attributed to M Faure.

At least 19 recordsLinked to original sources
PubMed2006

[Drug hypersensitivity syndrome associated with a primary HHV6 infection].

INTRODUCTION: Drug hypersensitivity syndrome is a severe life-threatening drug reaction. An association between this syndrome and HHV6 reactivation has been hypothesized. CASE-REPORT: A 45 year-old women was treated with sulfasalazine for polyarthralgia. One month after beginning the treatment, she developed a drug hypersensitivity syndrome with severe acute hepatic failure. HHV6 serology and serum PCR revealed a primary HHV6 infection. DISCUSSION: We report the second case of drug hypersensitivity syndrome associated with a primary HHV6 infection. An immunological disorder may explain such an association by increasing viral replication. Detection and titration of anti-HHV6 antibodies in each case of drug hypersensitivity syndrome should help to confirm this association and possibly modify treatment strategy.

Adrenal Cortex Hormones↗
PubMed2006

[New contraceptives].

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Contraceptive Agents, Female↗
PubMed2006

[Nicorandil-associated anal ulceration].

BACKGROUND: Nicorandil is a potassium-channel activator used in the treatment of angina pectoris. The first cases of anal ulcerations induced by nicorandil were published in 2002. CASE REPORT: A 71-year-old man presented with a 2-year history of anal ulcerations occurring within a few months of initiation of treatment with Nicorandil. Histological tests on a biopsy sample showed granulation tissue with non-specific chronic inflammation. Nicorandil was stopped and this resulted in complete healing of the ulcers after three months. DISCUSSION: Nicorandil can induce chronic and extensive anal ulcerations. The pathogenesis is unknown. Patients are usually treated with high doses of nicorandil. Dermatologists should be aware of this rare side-effect which heals after withdrawal of the drug.

Aged↗
PubMed2004

The chronic colitis developed by HLA-B27 transgenic rats is associated with altered in vivo mucin synthesis.

HLA-B27 transgenic rats spontaneously developing a chronic inflammation mainly involving the colon are recognized as a powerful animal model for IBD. We investigated the mucin production in 6-month-old HLA-B27 rats by measuring in vivo fractional synthesis rate (FSR) and expression of mucins. In the inflamed colon of HLA-B27 rats, the mucin FSR was stimulated by 75% compared to F-344 controls, while MUC2,3 mRNA expression was unchanged. A local depletion in mucus-containing goblet cells was observed, suggesting a rapid mucin production/release and/or a real global decrease in goblet cell number. In the noninflamed jejunum of HLA-B27 rats, the mucin FSR was reduced by 35% compared to controls, while MUC2,3 mRNA expression was unchanged. Different alterations in mucin metabolism and expression are observed between HLA-B27 rats and a model of chemically induced chronic colitis (DSS-treated rats), suggesting that mucin alterations may be dependent on the animal model and colitis underlying mechanism.

Amino Acids↗
PubMed2003

[Acquired zinc deficiency in a breast-fed premature infant].

UNLABELLED: Symptomatic zinc deficiency can occur in exclusively breast-fed infants. We report a case in a preterm infant. CASE REPORT: A 3-months-old exclusively breast-fed premature infant presented with peri-orificial and acral eczematoid lesions. Laboratory investigations revealed lowered zinc levels in the infant's serum and in her mother's milk. A rapid healing occurred after oral zinc supplementation. DISCUSSION: Zinc deficiency in breast-fed infants is a rare disease caused by a low level of zinc in mother's milk. The clinical features resemble those of acrodermatitis enteropathica. Oral zinc supplementation is required until weaning.

Breast Feeding↗
PubMed2003

Mucin production and composition is altered in dextran sulfate sodium-induced colitis in rats.

We evaluated the small and large intestinal mucin production in a rat model of human ulcerative colitis by measuring the in vivo fractional synthesis rate (FSR) and the expression of mucins. A chronic colitis was induced by oral administration of 5% dextran sulfate sodium (DSS) for 9 days followed by 2% DSS for 18 days. DSS-treated rats showed increased colonic MUC2,3 mRNA levels compared pair-fed controls. The mucin FSR was unaffected while mucin-containing goblet cells were depleted in the vicinity of lesions. In the small intestine, no inflammatory lesions were observed but ileal MUC2 mRNA levels and mucin FSR were decreased by 46% and 21%, respectively. Finally, DSS-treated rats showed a marked decrease in mucin's threonine + serine content all along the gut, which may lead to a reduction of potential O-glycosylation sites. Our data indicate that the chronic colitis may impair the mucus layer protective function all along the gut.

Animals↗
PubMed2002

[Acne].

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Acne Vulgaris↗
PubMed2001

Comparative morphology and paleobiology of Middle Pleistocene human remains from the Bau de l'Aubesier, Vaucluse, France.

The discovery of later Middle Pleistocene human remains from the Bau de l'Aubesier, France reinforces an evolutionary model of the gradual accumulation of Neandertal-derived facial and dental features during the Middle Pleistocene of the northwestern Old World. The pronounced maxillary incisor beveling of Aubesier 4 helps to extend the antiquity of nondietary use of the anterior dentition. The interproximal "toothpick" groove on the Aubesier 10 molar increases the sample for these lesions. The pathological loss of the mandibular dentition of Aubesier 11 indicates advanced antemortem masticatory impairment, at a level previously undocumented before the Late Pleistocene. These remains support a view of later Middle Pleistocene humans able to support debilitated individuals despite the considerable use of their bodies to accomplish routine activities.

Animals↗
PubMed2001

Suppression of Ras-mediated tumorigenicity and metastasis through inhibition of the Met receptor tyrosine kinase.

Mutations in the Ras family of GTP binding proteins represent one of the most frequently observed genetic alterations in human cancers. We and others have recently demonstrated that expression of Met, the tyrosine kinase receptor for hepatocyte growth factor/scatter factor (HGF/SF), is significantly up-regulated in Ras-transformed cells. Because HGF/SF-Met signaling is proposed to play a prominent role in tumor development and progression, we assessed the possible requirement for Met during Ras-mediated tumor growth and metastasis. To disrupt endogenous Met signaling, we constructed dominant-negative mutants of both human and murine Met and showed that these can inhibit HGF/SF-mediated Met signaling and cell invasion of ras-transformed cells in vitro. Moreover, ectopic expression of dominant-negative Met mutants reduced the s.c. tumor growth of ras-transformed cells and dramatically suppressed their ability to form lung metastases in vivo. Our data demonstrate that Met plays a prominent role during Ras-mediated tumor growth and metastasis, and further suggest that agents that inhibit HGF/SF-Met signaling may represent an important therapeutic avenue for the treatment of a variety of malignant tumors.

3T3 Cells↗