Biomedical subjects

K A Fritz

Publications and source records attributed to K A Fritz.

12 recordsLinked to original sources

PubMed1998

18-Methoxycoronardine attenuates nicotine-induced dopamine release and nicotine preferences in rats.

Two studies were conducted to assess, in vivo, potential anti-nicotinic effects of the iboga alkaloid ibogaine and its synthetic congener 18-methoxycoronaridine (18-MC). As previously demonstrated for ibogaine, using microdialysis, pretreatment (19h beforehand) with 18-MC (40 mg/kg, i.p.) significantly attenuated nicotine-induced dopamine release in the nucleus accumbens of awake and freely moving rats. In an oral model of nicotine self-administration, both ibogaine and 18-MC decreased rats' preferences for nicotine for at least 24 h. Acutely, during the first hour after administration, ibogaine depressed responding for water as well as for nicotine; however, during this same time, 18-MC reduced nicotine intake without affecting responding for water. The results suggest that 18-MC might be the prototype of a new treatment for smoking.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1987

The particulate (speckled-like thread) nuclear staining pattern: species and cellular distribution of Ro/SSA antigen.

Anti-Ro/SSA antibodies are associated with a particulate (speckled-like thread) nuclear immunofluorescence (IF) staining pattern when human spleen imprints are employed as substrate. The present study was undertaken to determine if these antibodies would yield a similar IF pattern with splenic imprints from other species, and with other human cell lines. All splenic imprints (mammalian, avian, amphibian and fish origin) demonstrated a particulate nuclear pattern when treated with anti-Ro/SSA antibody positive serum samples. Cytospin preparations of a variety of peripheral blood cells also demonstrated this particulate pattern when treated with anti-Ro/SSA antibodies. Similar findings were noted when cytospin preparations of cultured keratinocyte cell lines were used as substrate. The antigen, associated with the particulate IF staining pattern when treated with anti-Ro/SSA antibody positive serum samples, is expressed in a variety of tissues and species.

Animals↗

PubMed1985

Immunopathologic mechanisms in pemphigus and bullous pemphigoid.

Pemphigus and bullous pemphigoid are autoimmune bullous diseases of the skin. Pemphigus, an intraepidermal blistering disease, is characterized by autoantibodies reactive with antigens located in the intercellular spaces or on the surfaces of epidermal cells. These antibodies, which have recently been shown to activate complement, appear to be the cause of the basic pathologic process of pemphigus, acantholysis. The complement system and the plasminogen-plasmin system may be important mediators in the detachment of epidermal cells. Bullous pemphigoid, a subepidermal blistering disease, is characterized by autoantibodies reactive with an antigen located in the lamina lucida region of the basement membrane zone. These autoantibodies, which will avidly fix complement, appear to mediate subepidermal separation by attraction of a variety of inflammatory cells. Anaphylatoxins, released by activation of C4 and C3, or specific IgE antibodies, may activate mast cells with release of ECF-A attracting eosinophils. With activation of C5, C5a is released which could attract polymorphonuclear leukocytes. Antigen-specific lymphocytes, which can also contribute histamine releasing substances, may also be involved. The exact mechanism by which the epidermis separates from the dermis in bullous pemphigoid, however, remains unresolved.

Adolescent↗

PubMed1985

Systematic comparison of antibody-mediated mechanisms of keratinocyte lysis in vitro.

We have conducted a systematic comparison of lysis of TNP-coated keratinocyte targets by TNP-specific antibody, by antibody plus complement, by antibody-dependent cellular cytotoxicity (ADCC), and by natural killing with the use of monocyte, lymphocyte, and neutrophil effectors. With chromium-release assays, human keratinocytes, HEp-2 cells (transformed human keratinocytes), PAM 212 cells (transformed mouse keratinocytes), and RSC (transformed rabbit keratinocytes) were all susceptible to monocyte- and lymphocyte-mediated ADCC (p less than 0.01 to p less than 0.02). All trypsinized keratinocyte targets were also susceptible to natural killing by monocyte or lymphocyte effectors (p = 0.05 to p less than 0.001). Antibody and antibody plus complement were poor mediators of keratinocyte lysis. If protein and complex lipid synthesis of keratinocytes were inhibited by 16-hr cycloheximide preincubation, then keratinocytes were susceptible to complement-mediated lysis, implying that the resistance of these cells to complement may be due to repair of transmembrane pores. Comparison of chromium-release assays with fluorescein diacetate dye uptake viability assays showed that human keratinocytes were still susceptible to monocyte and lymphocyte ADCC but not to antibody, antibody plus complement, or natural killing. The reproducible and uniform susceptibility of normal and transformed keratinocyte targets from three different species to monocyte and lymphocyte ADCC supports the hypothesis that this mechanism of cellular lysis may be important in antibody-associated diseases of epidermal cytotoxicity.

Animals↗

PubMed1985

Oral lesions in pityriasis rosea.

Oral lesions are not commonly reported with pityriasis rosea (PR). We encountered a patient with clinical and histologic evidence of PR who developed aphthous ulcer-like oral lesions on the buccal mucosa, palate, and tongue. The oral lesions resolved concomitantly with the patient's skin lesions. The previous literature reports a wide variety of oral lesions in association with PR, but few dermatologists, to our knowledge, are aware of such an occurrence.

Adult↗

PubMed1984

The role of RNP, Sm, and SS-A/Ro-specific antisera from patients with lupus erythematosus in inducing antibody-dependent cellular cytotoxicity (ADCC) of targets coated with nonhistone nuclear antigens.

To better understand potential antibody-dependent mechanisms of tissue damage in lupus erythematosus (LE), an examination of whether antibodies to nonhistone nuclear antigens in LE patients' sera can induce ADCC of cellular targets coated with the corresponding antigens was undertaken. With high titer anti-RNP sera, significant ADCC was seen with monocyte (P less than 0.01), T-lymphocyte (P less than 0.001), and low-density lymphocyte (P less than 0.001) effectors. Using monocyte effectors, significant ADCC was seen with anti-RNP (P less than 0.01), anti-Sm (P less than 0.01), and anti-SSA/Ro (P less than 0.01), with the most profound lysis being with the anti-SSA/Ro sera. Neutrophils were ineffective in any nuclear antigen-antibody system tested. The effective mononuclear cell-mediated ADCC seen with anti-RNP, anti-Sm, and anti-SSA antisera may be related to the mononuclear cell-associated tissue change seen in cutaneous lupus lesions.

Antibodies↗

PubMed1984

Systemic glucocorticosteroid therapy of skin disease in children.

The role of systemic glucocorticosteroid therapy in the management of dermatologic disorders in children is limited. Most skin diseases requiring the antiinflammatory or antiproliferative effects of steroids are best managed with topical preparations, because they exert local effects almost exclusively and cause few if any systemic side effects when used properly. There are, however, certain skin diseases, which because of their severity or their intrinsic nature, do not respond adequately to these agents. We propose the indications for pharmacologic doses of systemic glucocorticosteroids in dermatologic disease, the preferred route of administration, the most common as well as the more rare side effects of this therapy. Withdrawal of patients from chronic use of these drugs is also discussed.

Autoimmune Diseases↗

PubMed1984

Bullous dermatoses.

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Bibliographies as Topic↗

PubMed1983

Neonatal lupus syndrome in successive pregnancies.

Two female siblings, born 15 months apart, developed neonatal lupus syndrome. Both had cutaneous lupus erythematosus (LE) lesions resolving with telangiectasis. Their cutaneous lesions were temporally related to transplacental passage of anti-SS-A (Ro) autoantibodies from their asymptomatic mother. Infants with this transient collagen vascular syndrome may have LE skin lesions, congenital heart block, and liver or hematologic abnormalities, and are possibly at risk for developing systemic lupus erythematosus (SLE) later in life. It is important to recognize that this syndrome may occur in successive pregnancies.

Female↗

PubMed1983

Topical glucocorticosteroids.

A review of topical glucocorticosteroids is presented. Included is a discussion of the pharmacology of modern hydrocortisone derivatives and their vehicles, mechanisms of action with respect to skin and host inflammatory response and potential side effects of treatment. Guidelines for therapy and selection of appropriate therapeutic agents are also given.

Administration, Topical↗

PubMed1982

Second cutaneous malignancies in patients with mycosis fungoides treated with topical nitrogen mustard.

Previous reports of skin cancer occurring in mycosis fungoides patients who have been treated with topical nitrogen mustard have been of carcinomas occurring predominantly on sun-exposed skin. Four of twenty-nine mycosis fungoides patients in our clinic treated with topical nitrogen mustard developed six skin cancers on sun-protected skin. Four lesions were squamous cell carcinomas and two were basal cell carcinomas. Few other risk factors for the development of skin cancer were present in our patients. These cases support the hypothesis that topical nitrogen mustard is a carcinogen or tumor promote and emphasize the need for careful examination of the skin of patients treated with topical nitrogen mustard.

Administration, Topical↗

PubMed1980

ADCC effector function in patients with atopic dermatitis. A possible mechanism of susceptibility to severe cutaneous viral infections.

Peripheral blood mononuclear cells from patients with chronic atopic dermatitis were evaluated as effectors of antibody-dependent cellular cytotoxicity (ADCC) to determine if faulty effector function might explain the susceptibility of atopics to severe cutaneous viral infections in spite of adequate specific antibody titers. Eleven atopic patients whose dermatitis was well controlled and who were not infected or on immunosuppressive therapy were studied using sensitized human and chicken erythrocyte targets at three different effector:target ratios. No significant differences in mean ADCC were seen between atopics and controls. However, the function of peripheral blood mononuclear cells from atopic patients who had a previous history of severe cutaneous viral infection was significantly depressed against sensitized chicken, but not human targets. This suggests that atopic patients who develop severe cutaneous viral infections may represent a subset of atopics with an intrinsic or variable defect in K lymphocyte--mediated ADCC which might render them susceptible to persistent, extensive viral infections.

Adult↗