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Biomedical subjects

J Lord

Publications and source records attributed to J Lord.

At least 73 records · Page 4Linked to original sources
PubMed1981

The femoral hypoplasia-unusual facies syndrome: a genetic entity?

Nine patients with bilateral femoral hypoplasia have been investigated in an attempt to elucidate the syndromic identity and pathogenesis of the femoral hypoplasia-unusual facies syndrome (FH-UFS). We believe that the FH-UFS represents the end of the spectrum of a malformation complex and that it does not exist as a specific syndromic entity. Available evidence indicates that the pathogenesis is multifactorial rather than the result of any simple genetic mechanism.

Abnormalities, Multiple↗
PubMed1979

Alteration of specific binding of prostaglandin F2 alpha by hyperproliferative skin membrane fractions from essential fatty acid-deficient rats.

Specific binding of [3H] PGE2 and [3H] PGF2 alpha to smooth endoplasmic reticulum (SER) membranes prepared from rat skin at various stages of the development of essential fatty acid (EFA)-deficiency syndrome was demonstrated in these studies. The normal SER-binding capacity for [3H] PGE2 per mg of membrane protein was approximately two-fold that for [3H] PGF2 alpha in control rats fed a diet rich in essential fatty acids (EFA). Two weeks following the feeding of the animals with the EFA-deficient diet: histological evaluation revealed hyperplasia and acanthosis of the epidermal layer; a two-fold increase in labeling index (a marker for DNA synthesis) and no alteration in the SER-binding capacity for [3H] PGE2 or [3H] PGF2 alpha. By the 12th week however, labeling index had increased six-fold, accompanied by a five-fold increase in SER-binding capacity for [3H] PGF2 alpha. SER-binding for [3H] PGE2 was relatively unaltered. These results have demonstrated a relationship between marked alteration of skin SER-binding capacity for PGF2 alpha and the increase in epidermal hyperplasia and proliferation characteristic of the skin of the EFA-deficient rat. Refeeding of the animals with EFA-rich diet restored the epidermal proliferation and the SER-binding capacity to PGF2 alpha to normal conditions.

Animals↗
PubMed1976

Pathogenesis of Woronoff ring in psoriasis.

As a result of ultraviolet light and coal tar therapy, a white ring (Woronoff) may develop in the normal skin adjacent to psoriatic plaques. Injection of prostaglandin E2 (PGE2) 1 cm outside of Woronoff ring produced redness in the ring, demonstrating that vessels within the ring were not unresponsive to PGE2. Whole skin homogenates from Woronoff ring contained an inhibitor of prostaglandin synthesis that was not found in uninvolved skin that was obtained from either psoriatics or normal controls. Prostaglandin E2 levels in the ring were one third of those in uninvolved skin from either psoriatics or normal controls. These findings suggest that the white ring that surrounds ultraviolet-light-treated psoriatic plaques is produced by a local inability to synthesize PGE2 in response to an ultraviolet light stimulus, resulting from the presence of an inhibitor of prostaglandin synthesis.

Coal Tar↗