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Biomedical subjects

C A Elmets

Publications and source records attributed to C A Elmets.

At least 73 records · Page 4Linked to original sources
PubMed1987

Molluscum contagiosum and the acquired immunodeficiency syndrome: clinical and immunological details of two cases.

We report here the clinical and immunological findings in two patients with molluscum contagiosum poxvirus infection and the acquired immunodeficiency syndrome (AIDS). These cases support earlier evidence that the molluscum contagiosum virus may act as cases support earlier evidence that the molluscum contagiosum virus may act as an opportunistic pathogen. There is now evidence that members of all five families of double stranded DNA-containing human viruses have been associated with unusual clinical manifestations in AIDS patients, and the significance of DNA virus infections in patients with AIDS is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Deleterious effect of ultraviolet-B radiation on accessory function of human blood adherent mononuclear cells.

The effects of ultraviolet-B radiation (UV-B) on accessory function of human blood adherent mononuclear cells (ADH) for antigen and mitogen-induced responses, and production by ADH of the amplifying cytokine interleukin 1 (IL-1) were examined. Responder lymphocytes were rendered accessory cell dependent by treatment of nonadherent cells with OKIal+complement. UV-B depressed accessory function of ADH in a dose-dependent manner. UV-B at 5 mJ/cm2 decreased accessory function of 2 x 10(4) ADH for tetanus toxoid-induced responses (measured as incorporation of 3H-thymidine) by 84% (P less than 0.001, n = 6) and phytohaemagglutinin-induced responses 91% (P less than 0.001, n = 4). UV-B also decreased accessory activity of peripheral blood mononuclear cells but not Epstein-Barr virus-transformed B cells for a PPD-reactive T cell line. Viability was approximately 90% 0-72 h after exposure of ADH to 5 mJ/cm2 of UV-B. Interleukin 1 (IL-1) activity of supernatants of ADH was assayed on C3H/HeJ mouse thymocytes. Pretreatment of ADH with 5 mJ/cm2 UV-B decreased lipopolysaccharide-stimulated IL-1 activity from 169 +/- 34 (mean U/ml +/- s.e.) to 4 +/- 1 (P less than 0.01, n = 4). Lysates of UV-B irradiated. LPS-stimulated ADH had no discernible IL-1 activity. Addition of IL-1 partially restored accessory activity of UV-B irradiated ADH for lymphocyte responses to TT. Exposure of ADH to TT or PHA for 30 min before irradiation blocked the inhibitory effect of UV-B on accessory activity. Thus, low doses of UV-B are deleterious to accessory function and to production of IL-1 by ADH. Interference with production of cytokines and with initial interactions of accessory cells with antigen and mitogen may be critical to the effects of UV-B on immunoregulatory function of ADH.

Antigen-Presenting Cells↗
PubMed1986

Relation between complications of type I diabetes mellitus and collagen-linked fluorescence.

Nonenzymatically glycosylated proteins gradually form fluorescent cross-linked protein adducts--a process termed "browning." The rate of this reaction increases with the glucose concentration. Assaying for the presence of browning products in long-lived proteins should therefore provide information on long-term metabolic control. We measured collagen-linked fluorescence typical for nonenzymatic browning in skin-biopsy specimens from 41 subjects with longstanding Type I diabetes and from 25 controls. Fluorescence correlated with age and (weakly) with the duration of diabetes. Mean age-adjusted fluorescence values were twice as high in diabetic subjects as in control subjects (P less than 0.0001) and increased with the severity of retinopathy, nephropathy, and arterial and joint stiffness. The correlation was significant for retinopathy (r = 0.42; P less than 0.01), arterial stiffness (r = 0.41; P less than 0.01), joint stiffness (r = 0.34; P less than 0.05), and the sum of all complications (r = 0.47; P less than 0.01). Fluorescence also correlated with systolic (r = 0.42; P less than 0.01) and diastolic (r = 0.36; P less than 0.05) blood pressures. If one can assume that the fluorescence results from a browning product of glucose, our data suggest that there is an overall correlation between the severity of diabetic complications and cumulative glycemia over many years.

Adult↗
PubMed1986

Immunohistologic identification of antigen-presenting cells in cutaneous sarcoidosis.

Considerable evidence exists to show that activated T lymphocytes preferentially accumulate at sites of disease activity in sarcoidosis. Langerhans cells, which can be recognized by reactivity with an antibody to the T6 antigen are thought to play a primary role in T-lymphocyte activation by the skin, a tissue frequently involved in sarcoidosis. This immunohistologic study examined the distribution of OKT6-positive cells and surface expression of HLA-DR antigen in cutaneous sarcoid lesions. Skin specimens stained with an anti-HLA-DR antibody demonstrated diffuse staining of the granulomas. In addition, keratinocytes, which do not normally express HLA-DR antigens, were found to stain with monoclonal antibody to HLA-DR in an intercellular pattern. Examination of specimens for OKT6-reactive Langerhans cells revealed significantly greater concentrations in the epidermis overlying sarcoidal granulomas (33 +/- 7 cells/mm) than in the epidermis of age-, sex-, and race-matched controls (11 +/- 3 cells/mm, p less than 0.001). Of greater importance was the demonstration that significant numbers of OKT6-positive cells were present within the dermal sarcoid granulomas (19-208/mm2) in a distribution that paralleled that of Leu-3a-positive T lymphocytes. These data suggest that the epidermis may participate in activation of lymphocytes in cutaneous sarcoidosis, and implicate OKT6-positive cells in granuloma formation.

Adult↗
PubMed1986

Cutaneous porphyrin photosensitization: murine ear swelling as a marker of the acute response.

Acute cutaneous photosensitivity is a major manifestation of certain forms of human porphyria and also occurs in patients treated with hematoporphyrin derivative (HpD) photoradiation for the diagnosis and treatment of malignant tumors. In this study a quantitative animal model useful for in vivo studies of acute porphyrin photosensitization in cutaneous tissue was developed. C3H mice injected with HpD and irradiated 6 h later with 405 nm energy developed a 40-90% increase in ear thickness which was present immediately after irradiation and persisted for at least 24 h. No ear swelling occurred in animals receiving 405 nm radiation alone or HpD alone. Histologically, this photosensitivity reaction was manifest as edema, vascular dilatation, and mast cell degranulation immediately after irradiation followed by an influx of polymorphonuclear leukocytes and epidermal necrosis 24 h later. Tissue injury evoked by HpD and light was accompanied by extravasation of intravenously administered 125I-labeled albumin in the irradiated ears, indicating that photosensitization was accompanied by transudation of serum into the site of tissue injury. An in vivo correlation of this approach was verified by detection of measurable increase in ear thickness in irradiated mice rendered porphyric by the ingestion of a griseofulvin-containing diet. The mouse ear swelling model offers a useful system with which to study acute porphyrin photosensitization in the skin, and may lead to important new insights into the pathogenesis and prevention of this form of phototoxicity.

Animals↗
PubMed1986

Age-related normalization of the browning rate of collagen in diabetic subjects without retinopathy.

The age-related changes in collagen-linked fluorescence (browning) were investigated in skin from subjects with long-standing type I diabetes. Overall browning rates were 2.4 times higher in diabetics than in controls (P less than 0.02) and slope intercept accurately reflected the mean age of onset of diabetes (11.6 vs. 11.2 yr), suggesting that the browning process has the attributes of a biological clock. Browning rates were not different in controls and diabetics without retinopathy (P greater than 0.05) but were 2.4 (P less than 0.05) and 2.7 (P less than 0.01) times increased in the presence of background and proliferative retinopathy, respectively. Compared with subjects with retinopathy, individual browning rates since onset of diabetes decreased with advancing age in subjects free of retinopathy (P less than 0.001). Extrapolation revealed that they would become identical to that of nondiabetic subjects by the age of 66.4 yr. These results suggest the presence of a mechanism that controls the browning rate of collagen in diabetics who do not develop retinopathy.

Adult↗
PubMed1986

Glycation of skin collagen in type I diabetes mellitus. Correlation with long-term complications.

Nonenzymatic glycosylation (glycation) of collagen was measured by boronate affinity chromatography in skin biopsies from 41 type I diabetics with mean duration of diabetes of 25 yr (range 20-40 yr) and from 25 age-matched controls. Mean level of Amadori products was significantly increased in diabetic [7.85 +/- 1.78 (SD) nmol/mg collagen] versus control subjects [3.34 +/- 1.06 (SD) nmol/mg collagen, P less than .001] but did not correlate with age, diabetes duration, or severity of retinopathy, nephropathy, arterial stiffness, and joint stiffness. Similarly, mean collagen content per biopsies was 42% increased in diabetic versus control subjects (P less than .001) but did not correlate with age, diabetes duration, or severity of complications. A weak but positive correlation between glycohemoglobin level and glycation of skin collagen was observed. These results indicate that Amadori products cannot explain by themselves the pathogenesis of diabetic complications unless individual tissue response to glycation is different in subjects with and without complication. They do not exclude a role for the late stages of the Maillard reaction, nonenzymatic browning, in the formation of some of these complications.

Adult↗
PubMed1986

Immunological suppression in mice treated with hematoporphyrin derivative photoradiation.

Hematoporphyrin derivative (HPD) is a potent photosensitizer which localizes preferentially in malignant tumors. Parenteral administration of this compound followed by irradiation with the appropriate wavelengths of light has been used for the diagnosis and treatment of various epithelial neoplasms. In this study the effects of such treatment on immunological responses were evaluated by examining the capacity of HPD and light to inhibit contact hypersensitivity to dinitrofluorobenzene (DNFB) in C3H mice. Pretreatment of mice with HPD photoradiation resulted in 50% suppression of contact hypersensitivity to DNFB. Inhibition of the response could be produced even when sensitization with DNFB was attempted 2 weeks after a single irradiation procedure, indicating that HPD and light-induced inhibition of contact sensitivity was sustained phenomenon. Prior sensitization with DNFB followed by treatment with HPD and light elicited no immunosuppression. The immunosuppressive response required photoactivation of the porphyrin molecule, since mice treated with HPD alone or light alone developed little or no suppression. In adoptive transfer studies, it was shown that the immunosuppression was associated with the development of suppressor cells. These results indicate that photoradiation therapy with HPD and light can produce systemic suppression of contact hypersensitivity in mice. These data suggest that HPD photoradiation of malignant tumors may inhibit certain types of immune responses in humans.

Animals↗
PubMed1986

Drug-induced photoallergy.

Over the past several years, the exponential growth in the use of topical and systemic medications and drugs has been accompanied by a concomitant increase in the incidence of adverse reactions associated with them. One type of reaction that has been of particular interest to dermatologists has been the development of immunologic photosensitivity to topically applied and orally administered substances. The majority of agents that have been identified as causing photoallergic reactions in a significant percentage of individuals are no longer utilized. However, because new products are introduced with increasing frequency, this type of photosensitivity disease promises to be an ongoing problem for the dermatologic community.

Allergens↗
PubMed1983

Analysis of the mechanism of unresponsiveness produced by haptens painted on skin exposed to low dose ultraviolet radiation.

Acute, low dose ultraviolet B radiation of murine body wall skin followed by local application of DNFB produces a state of antigen-specific unresponsiveness. This state is maintained at least in part by an Lyt-1+ T cell that effects unresponsiveness by impairing the induction phase of contact hypersensitivity. The absence of suppressor cells capable of acting at the effector stage of immunity suggests that tolerogenic signals derived from the skin establish suppressor networks that are incomplete and perhaps different from networks that are induced by systemic administration of tolerogens. It is proposed that ultraviolet radiation produces its effects by impairing the antigen-presenting potential of resident Langerhans cells in whose absence hapten-derivatized keratinocytes (or their products) are able to deliver a tolerogenic signal.

Animals↗
PubMed1982

Differential distribution of Langerhans cells in organ culture of human skin.

Epidermal Langerhans cells (LCs) function as the antigen-presenting cells in such cutaneous cell-mediated immune responses as contact hypersensitivity and in the mixed epidermal cell-lymphocyte reaction. They have also been implicated in the immune response in skin allograft rejection. Since organ culture of thyroid and pancreas has been shown to prolong allograft survival, presumably through the loss of antigen-presenting cells, we examined the effect of skin explant culture on LC survival. Human skin explants were placed in organ culture and examined serially as whole mounts of epidermis for the presence of LCs as judged by ATPase activity, and OKT-6 and HLA-DR antigens. Although we observed morphologic changes and an absolute reduction in the number of positively stained cells, culture for up to 28 days failed to deplete explants of these cells. Langerhans cells were also sought in the epidermal outgrowths that develop peripheral to the original explants. They were never seen in the area beyond 0.3 mm from the explant edge. Organ culture of skin thus provides a means to explore the contribution of LCs to skin allograft rejection by comparing the immunogenicity of epidermal portions of the explant with the epidermal outgrowth.

Adenosine Triphosphatases↗
PubMed1980

Amelanotic melanoma presenting as a pyogenic granuloma.

A sixty-two year old man was diagnosed as having an amelanotic of the right great toe after the lesion had been treated for several months as a pyogenic granuloma. Establishment of the correct diagnosis was aided by the finding of a radiolucent defect on a roentgenogram of the toe. Since amelanotic melanoma usually presents as a vascular or ulcerated nodule, rather than as a pigmented nevus, the lesion may be mistaken for a benign tumor. This case illustrates the necessity of histologic confirmation of all presumed pyogenic granulomas. Furthermore, it also stresses that clinical, histologic, and prognostic distinctions must be made between amelanotic melanoma and its pigmented counterpart.

Diagnosis, Differential↗
PubMed1979

Complications with heparin-lock needles.

The incidence of phlebitis was determined for heparin-lock needles after use of three different methods of skin preparation and follow-up care. Phlebitis was significantly more frequent when iodophor solution and iodophor ointment, respectively, were used than when iodophor solution alone was used for heparin-lock needles in use longer than 48 hours, with more than ten manipulations of the systems, and when only one drug was infused through the systems. Iodophor solution skin preparation followed by daily application of iodophor solution is recommended to minimize the occurrence of associated phlebitis.

1-Propanol↗