Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:031456 (Sep)
 2,027,840 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with atopic dermatitis have abnormal autonomic responses of the arterioles, pilomotor smooth muscle, and sweat glands. Their lesions have been reported to contain increased amounts of the neurohumors, acetylcholine and norepinephrine, as well as increased activity of acetylcholinesterase and catechol-O-methyltransferase. In vitro studies of epidermis show that beta adrenergic agonists fail to evoke the normal inhibition of mitosis of basal cells of patients with atopic dermatitis. Epidermis removed not only from the lesions, but also from normal-appearing skin, responded abnormally. The increase in intracellular levels of cAMP after exposure to catecholamines was similar in normal and atopic epidermis. Lymphocytes and PMN leukocytes isolated from patients with atopic dermatitis show both a decreased physiologic response (glycogenolysis and inhibition of lysosome enzyme release) and a decreased rise in intracellular levels of cAMP upon incubation with beta agonists, but a normal response to PGE1. Cortisol increases the response of lymphocyte adenyl cyclase to both agonists and, in the case of the patients with atopic disease, more than overcomes the depressed response to beta agonists. Because the leukocytes respond normally to PGE1 and because others have reported normal activities of skin and adenyl cyclase, phosphodiesterase, and protein kinases, we conclude that the step responsible for the diminished beta adrenergic response lies antecedent to the catalytic site of adenyl cyclase.
J Invest Dermatol 1976 Sep
PMID:Adrenergic mechanisms and the adenyl cyclase system in atopic dermatitis. 0 56


Vestn Dermatol Venerol 1976 Sep
PMID:[Effect of various stimulants on skin reactivity of guinea pigs]. 1 67

To assess the need for dermatologists in the United States, the potential role of new health practitioners in this specialty is considered. Available data on physician extenders in general and informed opinion on dermatologist extenders in particular suggest that specially trained, nonphysician personnel could substantially augment the supply of dermatological services. At present, however, widespread adoption of new staffing patterns appears unlikely. A long-run trend toward greater use of all categories of ancillary personnel in this specialty is expected, and the profession is urged to play an early and active role in this trend's development.
Arch Dermatol 1977 Sep
PMID:New health practitioners and dermatology manpower planning. 2 62


J Invest Dermatol 1978 Sep
PMID:Lymphocyte traffic, T-cell malignancies and the skin. 2 71


Clin Exp Dermatol 1978 Sep
PMID:The role of bacteria in acne vulgaris: a new approach. 3 79

Isoniazid and hydralazine were covalently crosslinked by epidermal transglutaminase to serum and cell nuclear proteins. Albumin and nucleohistones were excellent acceptors of these drugs in serum and nuclear extracts, respectively. Drug-albumin and drug-histone conjugates were highly antigenic in rabbits within 4 weeks, eliciting drug-specific antibodies in all immunized animals. A radioimmunoassay for antibodies to isoniazid were developed, using a standard drug-albumin conjugate. The methods described here of enzymatic crosslinking of drugs to proteins facilitate studies of drug-induced hypersensitivity in animals and man.
J Invest Dermatol 1979 Sep
PMID:The role of enzymatic coupling of drugs to proteins in induction of drug specific antibodies. 3 85


Arch Dermatol 1979 Sep
PMID:Cutaneous T-cell lymphomas. Summary of the Mycosis Fungoides Cooperative Group-National Cancer Institute Workshop. 3 15


Int J Dermatol 1979 Sep
PMID:Current concepts in lichen planus. 4 Aug 88


Int J Dermatol 1976 Sep
PMID:Keratinization. 6 Nov 81

The mast cell in tissues represents an effector cell capable of elaboration of all the essential mediators of inflammation. The effects of uncontrolled activation may be divided into pharmacologic and inflammatory phases with attendant implications for the initiation of both acute and subacute pathologic processes. The elaboration of chemical mediators by the mast cell makes it possible to recruit blood cells and proteins essential to host defense by a controlled physiologic process that can proceed without significant local tissue damage. When uncontrolled, the same potentiality can be injurious, with the nature of the clinical problem depending upon the location of the cells, the intensity of activation, and the ratio of newly generated and preformed mediators released. The evidence that the mast cell can participate in each form of immunologic reaction--immediate, immune complex, and delayed- as a primary or secondary effector cell and the diversity of its products foretell an evolving recognition of its role in host defense and tissue injury. It is pertinent to develop further methods and criteria to define the nature and extent of mast cell participation in disease processes.
J Invest Dermatol 1976 Sep
PMID:The diversity of mast cell-derived mediators: implications for acute, subacute, and chronic cutaneous inflammatory disorders. 6 Dec 46


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