[Post-transfusional graft versus host disease. Apropos of 3 cases].
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Biomedical subjects
Publications and source records attributed to M David.
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High resolution CT examinations with 1.5 mm thick slices were performed on 30 healthy volunteers for the study of normal and accessory pulmonary fissures. In only one case were the three fissures entirely present. The major fissure is incomplete in 87% of the cases on the right side, and in 77% on the left side. When a part of a fissure is absent it is always the internal part. One or more accessory fissures were seen in 59% of the cases. The most frequent accessory fissures are in the inferior lobes (33%). A left minor fissure was seen in 10% of the cases. Some aspects of the top of the minor fissures (opacity, false cavitary lesion) which can be misinterpreted are emphasized.
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We report on a 15-year-old boy suffering from acute morbus moniliformis. To the best of our knowledge, this cutaneous eruption in its acute form has not been described before. We think that morbus moniliformis is a unique dermatosis different from keratosis lichenoides chronica or lichen planus.
The DNA base uracil was derivatized with pentafluorobenzoyl chloride, followed by methylation with methyl iodide in the presence of N,N-dimethylformamide (DMF). In addition to a 3-pentafluorobenzoyl-1-methyl derivative of uracil, GC/MS analysis of the reaction mixture revealed the formation of an unusual product, whose molecular weight was 12 U higher than that of the prior derivative. This unexpected product has been identified as the 3-(para-methoxytetrafluorobenzoyl)-1-methyl derivative of uracil. Isotopic labeling and related experiments have revealed that the DMF solvent contributes the oxygen atom of the methoxy group that replaces the para fluorine atom. This work allowed a single derivative to be obtained for the methylation reaction by changing the solvent to acetonitrile.
We hereby report a case presenting a rare form of secondary syphilis with an unusual nodular eruption accompanied by pruritus and generalized lymphadenopathy, bearing a striking resemblance to lymphoma. The histologic picture was also misleading and was compatible with lymphocytoma cutis. The diagnosis was eventually made after results of serologic tests for syphilis were found to be positive, with an extremely high titer of VDRL, and dark-field microscopy had demonstrated spirochetes in a nodular lesion. Secondary syphilis should thus be considered in the differential diagnosis of nodular lesions resembling lymphoreticular disease. It is also suggested that syphilis be added to the list of diagnoses belonging to the category of pseudolymphoma.
Pigmentary changes in mycosis fungoides usually occur in association with poikiloderma atrophicans vasculare or following therapy and regression of lesions. Several cases of hypopigmented mycosis fungoides have also been reported. We present the case report of a patient who developed pruritic, diffuse macular hyperpigmentation of the skin. Biopsy specimens from hyperpigmented skin revealed histologic and ultrastructural features typical of mycosis fungoides. Giant melanin granules were found in the tumor cells, as well as in keratinocytes and Langerhans cells. As far as we know, this is the first report of cutaneous hyperpigmentation as a single presenting sign of mycosis fungoides.
A patient with Sézary syndrome is reported in whom generalized vitiligo occurred. This is, to our knowledge, the first patient reported with vitiligo following T cell cutaneous lymphoma.
Three patients who received etretinate, two for psoriasis vulgaris and one for exfoliative dermatitis, developed clinical and electromyographic features of muscle damage during treatment. In one patient histological and ultrastructural findings indicated segmental muscle necrosis. Withdrawal of the drug led to clinical recovery and normalization of muscle enzyme levels and electromyogram. To the best of our knowledge, this is the first report to show etretinate-induced reversible skeletal muscle damage.
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A patient suffering from the nevoid basal cell carcinoma syndrome, in whom various surgical and conservative treatment modalities had been tried previously, was placed on oral etretinate therapy. A therapeutic effect of the etretinate on existing basal cell carcinomas and a prophylactic effect in inhibiting new tumor formation were well demonstrated during the 13-month period of treatment.
We examined a 6-year-old boy with seborrheic dermatitis like redness of the face, scaling of the scalp, and palmoplantar keratoderma. Skin biopsy showed hyperkeratosis, parakeratosis, follicular plugging, and mild upper dermal perifollicular mononuclear inflammatory infiltrate, which are compatible with the diagnosis of pityriasis rubra pilaris. Immunologic studies revealed normal values of peripheral B and T lymphocytes. The spontaneous activity of T suppressor cells was activated and the function of T helper cells was impaired, however.
A 290-kilobase (kb) region of the Rhizobium meliloti 2011 pSym megaplasmid, which contains nodulation genes (nod) as well as genes involved in nitrogen fixation (nif and fix), was shown to carry at least six sequences repeated elsewhere in the genome. One of these reiterated sequences, about 5 kb in size, had previously been identified as part of a cluster of fix genes located 220 kb downstream of the nifHDK promoter. Deletion of the reiterated part of this fix cluster does not alter the symbiotic phenotype. Deletion of the second copy of this reiterated sequence, which maps on pSym 40 kb upstream of the nifHDK promoter, also has no effect. Deletion of both of these copies however leads to a Fix- phenotype, indicating that both sequences carry functionally reiterated fix gene(s). The fix copy 40 kb upstream of nifHDK is part of a symbiotic cluster which also carries a nod locus, the deletion of which produces a marked delay in nodulation.
We performed a systematic survey of transcription of a large region of the Rhizobium meliloti symbiotic plasmid pSym. This led to the discovery of two new sequences induced during symbiosis. The first sequence was linked to the known nitrogen fixation (nif-fix) gene cluster, and its expression depended on the nifA gene product. The second sequence was a novel fix locus (M.-H. Renalier, J. Batut, J. Ghai, B. Terzaghi, M. Gherardi, M. David, A.-M. Garnerone, J. Vasse, G. Truchet, T. Huguet, and P. Boistard, J. Bacteriol. 169:2231-2238, 1987) whose expression was independent of the nifA gene product; therefore this fix locus undergoes a novel type of symbiotic regulation.