Green hair discoloration due to selenium sulfide.
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Biomedical subjects
Publications and source records attributed to H M Goldman.
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A 47-year-old woman presented with a long-standing history of an erythema multiforme-like eruption in association with lupus erythematosus. Unusual laboratory and immunologic findings were consistent with a diagnosis of Rowell's syndrome, which includes lupus erythematosus in association with erythema multiforme-like skin lesions, a speckled antinuclear antibody pattern, and a positive rheumatoid factor. We believe that our patient meets the criteria for this rarely reported entity.
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The cutaneous manifestations of human immunodeficiency virus infection include papulosquamous diseases, viral and fungal infections, and neoplastic disorders. Eczematous photosensitivity disorders have been reported in patients infected with the human immunodeficiency virus. We describe a patient with advanced acquired immunodeficiency syndrome who developed photodistributed hypertrophic lichen planus. We believe this is a distinct cutaneous manifestation of human immunodeficiency virus infection.
Osseous defects may be due to endodontic or to periodontic involvement or a combination of the two. Careful diagnosis is required to determine the correct form of treatment.
A 60-year-old man presented with erythematous papules and plaques on his body as well as a violaceous indurated nodule on his face. A cutaneous drug reaction secondary to allopurinol was considered. Examination of biopsy specimens revealed a dense lymphocytic infiltrate of the skin as is seen in lymphocytoma cutis. The lesions cleared promptly after use of allopurinol was discontinued. A literature review showed that an eruption of this kind, including a nodule on the face that histologically simulated a lymphocytic infiltrate of the skin, has not yet been reported secondary to allopurinol.
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This descriptive study compared the healing of mucoperiosteal and "stimulated" osteoperiosteal flaps for the treatment of surgically created periodontal recessions in dogs. Surgically created defects on the canine teeth of 10 healthy mongrel dogs were covered by specially designed, cemented copper bands for 4 weeks (Several maxillary premolar teeth were managed in the same way). A plaque and calculus-promoting diet was fed to the animals during this period. When the bands were removed the diet was altered and an intensive oral hygiene program was instituted. The contralateral tooth, chosen randomly, was utilized for placement of the mucoperiosteal lateral sliding flap and acted as the control. The experimental side was surgically stimulated 21 days prior to elevation of a "stimulated" osteoperiosteal flap for repositioning over the denuded roots. The animals were sacrificed with an overdose of Nembutal and block sections for histologic study were taken at periods ranging from 14 to 50 days. Histologic findings indicate that healing of the stimulated flaps was accompanied by the formation of a relatively short dentogingival epithelium, cementogenesis which varied in amount and type, and new connective fiber insertion into cementum. By contrast, the mucoperiosteal flaps healed with a long dentogingival epithelial relationship and no cementogenesis or connective tissue reattachment.
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Female guinea pigs were fed a scorbutigenic diet supplemented with either L-ascorbic acid or D-isoascorbic acid or combinations of these. Their responses were judged by changes in body weight, serum alkaline phosphatase levels, wound healing, and tooth structure. Large additions (100 mg daily) of D-isoascorbic acid to the scorbutigenic diet resulted in normal growth over a 7-wk period and normal serum alkaline phosphatase levels, tooth structure development, and collagen formation after wounding. The addition of 0.5 or 5.0 mg of L-ascorbic acid to this high D-isoascorbic diet improved neither growth rate nor collagen deposition during wound healing. On the basis of changes in tooth structure, D-isoascorbic acid has 1/20 the potency of L-ascorbic acid. Its effect is additive to subminimal maintenance levels of L-ascorbic acid implying that there is no competitive inhibition in the utilization of the two compounds. The relatively weak activity of D-isoascorbic acid is probably due to poor transport to the tissues and ineffective binding to functional sites. This explains why the onset of scurvy is much more rapid after withdrawal of D-isoascorbic acid from the diet when it had been the sole antiscorbutic dietary constituent. It is concluded that D-isoascorbic acid is a "weakly" antiscorbutic agent on the basis that it is both poorly absorbed and retained by the tissue; that in fact it may, to the degree that it is taken up by the tissues and retained, be equal in antiscorbutic potency to L-ascorbic acid.