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Biomedical subjects

D S Nelson

Publications and source records attributed to D S Nelson.

At least 37 records · Page 2Linked to original sources
PubMed1992

Spectrum and frequency of pediatric illness presenting to a general community hospital emergency department.

Knowledge of the range of pediatric illness presenting to a general emergency department (ED) is needed to optimize the quality of care delivered there. It was hypothesized that the pediatric population treated at a general ED exhibited a broad range of medical complaints, while differing significantly from children seen in a pediatric ED. General ED records from 1 week each season were reviewed, and patient age, chief complaint, diagnosis, time of arrival, season, and disposition were recorded. Data on 874 patients were analyzed and compared with pediatric ED data. General ED patient age affected chief complaint, diagnosis, and admission rate (9.5% less than or equal to 1 year admitted vs 2.6% greater than 1 year, P less than .001). General ED patients were older (7.9 vs 6.0 years, P less than .001) and admitted less frequently (3.8% vs 11%, P less than .001). Admission rates varied by arrival time only at the general ED, where minor trauma was more common (41% vs 22%, P less than .001). It is concluded that a wide range of pediatric illness is treated in a general ED, supporting the decision to have pediatric emergency physicians on staff, and that significant differences exist in the spectrum and frequency of pediatric illness seen in a general ED and pediatric ED.

Adolescent↗
PubMed1990

The effect of gold treatment on monocyte interleukin-1 production in rheumatoid arthritis. A prospective study.

Monocyte interleukin-1 (IL-1) production in vitro was studied in 49 patients with rheumatoid arthritis (RA) and 31 controls. Twenty-six of the RA patients were studied prospectively for up to 12 months after beginning chrysotherapy. About half of the patients (group 1) exhibited pretreatment levels of monocyte IL-1 secretion (as measured by bioassay or B-IL-1) significantly higher than that of the controls. Immunoreactive IL-1 (IR-IL-1) levels, however, were similar to controls. Clinical improvement in this group of patients was modest and transient but could be associated with a fall in the level of IL-1 (B-IL-1 and IR-IL-1) secretion. Other RA patients (group 2) appeared to have normal or reduced pretreatment levels of IL-1 secretion. Chrysotherapy resulted in significant clinical improvement within 3 months, and this was associated with an increase in IL-1 (both B-IL-1 and IR-IL-1) secretion by the patients' blood monocytes to normal or supranormal levels. Thus these two groups of RA patients (which differed only in the average duration of disease) had different prognoses in relation to chrysotherapy and the effect of chrysotherapy-induced remission on monocyte IL-1 secretion was opposite. These results suggest that monocyte IL-1 production in vitro reflects changes secondary to the anti-rheumatic effects of chrysotherapy.

Adult↗
PubMed1990

Seizure disorders in autism.

Several reports have suggested that autistic individuals are at greater risk for developing seizure disorders, particularly in adolescence. In this study the frequency of seizures in a series of 192 autistic individuals was examined; 21% of cases had exhibited a seizure disorder. Seizure disorders were more common among individuals with lower IQ. Age specific incidence revealed a 3- to 22-fold increase in risk for seizure relative to the normal population. In contrast to previous studies, risk for developing seizures was highest during early childhood although it was also elevated during early adolescence.

Adolescent↗
PubMed1990

Cytokine regulation of human monocyte interleukin-1 (IL-1) production in vitro. Enhancement of IL-1 production by interferon (IFN) gamma, tumour necrosis factor-alpha, IL-2 and IL-1, and inhibition by IFN-alpha.

IL-1 production (secreted and cell-associated) was measured in monocyte cultures stimulated by a variety of agents in vitro. Monocytes either adherent to conventional plastic culture plates in serum-free conditions, or in suspension in culture medium containing serum were stimulated to produce IL-1 during culture. In non-adherent, serum-free conditions, monocytes produced very low or undetectable amounts of IL-1 during 20 h of culture. Lipopolysaccharide (LPS) induced equivalent amounts of secreted and cell-associated IL-1, although at very low concentrations more cell-associated IL-1 was produced. IL-1 production in response to LPS could be augmented by crude lymphokine, IFN-gamma, or tumour necrosis factor (TNF) alpha. TNF-alpha preferentially augmented the production of cell-associated IL-1 in LPS-stimulated cultures. TNF-alpha induced a significant amount of IL-1 (mainly cell-associated) directly but could also induce IL-1 secretion when combined with IL-2 or IFN-gamma, or when in the presence of serum. IL-2 acted synergistically with low concentrations of IFN-gamma or IL-1 to induce significant levels of IL-1 production. IFN-alpha did not induce any IL-1 production, but was a potent inhibitor of IL-1 production induced by a variety of stimuli. These results suggest that IL-1 production may be enhanced or reduced by different cytokines at concentrations likely to be found in chronic inflammatory lesions.

Biological Factors↗
PubMed1990

The effect of gold sodium thiomalate and auranofin on lipopolysaccharide-induced interleukin-1 production by blood monocytes in vitro: variation in healthy subjects and patients with arthritis.

The anti-rheumatic gold compounds gold sodium thiomalate (GST) and auranofin (AF) have variable and often unpredictable effects in patients treated for arthritis. As inhibition of interleukin-1 (IL-1) production may be an important effect of these drugs, we investigated their effect on IL-1 production by lipopolysaccharide (LPS) stimulated monocytes in a serum-free, non-adherent culture system. A bi-modal effect was observed: low concentrations (GST 10-250 ng/ml and AF 1-100 ng/ml) potentiated IL-1 production, and higher concentrations (GST 200-1000 ng/ml and AF10-500 ng/ml) inhibited it. This bi-modal effect was observed for both secreted and cell-associated IL-1 activity with the exception that GST failed to inhibit cell-associated IL-1 generation. The potentiating effect was dependent on the continuous presence of gold for at least the first few hours after LPS stimulation. The inhibitory effect of GST was dependent on its presence after LPS stimulation while that of AF was evident even if cells were pretreated with AF and washed before exposure to LPS. There was considerable individual variation in IL-1 production in response to LPS as well as in the effects of gold on cells from both healthy individuals and patients with arthritis. There was also some overlap in the range of concentrations of gold that potentiated and inhibited IL-1 production, and there was relative insensitivity to the inhibitory effects of gold in certain individuals. These results may explain some of the variability in the response of patients to chrysotherapy and support further studies to see if these in vitro effects might predict clinical response to gold.

Arthritis↗
PubMed1990

A lack of fluctuation in xanthophyll concentrations in blood in laying hens at night and absence of pigmentation rings in the yolk.

Alternate white and yellow layers in the yolk are described in most textbooks. However, it was impossible to distinguish the presence of these layers when hard-cooked yolks from hens fed commercial type diets were examined. Serum xanthophyll concentrations were measured at different times during a 24-h period. Concentrations did not vary significantly due to time of day.

Animals↗
PubMed1989

Tumor cell heterogeneity in multiple myeloma: antigenic, morphologic, and functional studies of cells from blood and bone marrow.

Tumor cells from six patients with immunoglobulin G (IgG) multiple myeloma were analyzed for surface antigens, cytoplasmic paraprotein, morphology, and response to various culture conditions. The tumor marker was the paraprotein idiotype. Low numbers of tumor cells were found in the blood of most of the patients. In some patients, the circulating tumor cells were solely B lymphocytes, whereas in other patients, they were lymphoid, lymphoplasmacytoid, and plasmacytoid. Dual surface antigen analysis of blood and bone marrow cells confirmed that the tumor may be composed of a spectrum of cell types. Thus, cells may range from surface-idiotype+,CD19+,CD20+, PCA-1-,cytoplasmic-idiotype- lymphocytes, to CD19-,PCA-1+,cytoplasmic-idiotype+ plasma cells that are surface-idiotype- or weakly surface-idiotype+. In one patient, some of the tumor cells co-expressed surface idiotype and CD10. The tumor B lymphocytes were activated in vitro to synthesize paraprotein by pokeweed mitogen (PWM), and by low molecular weight B cell growth factor (BCGF). In contrast, spontaneous synthesis of paraprotein by more mature tumor cells was inhibited by agents that also inhibit nonmyeloma plasma cells. These agents included PWM, gamma interferon, and phorbol ester. The results demonstrate that in multiple myeloma there exist different tumor cell types that are similar, by a variety of criteria, to normal B lineage cells at different stages of differentiation. Thus, further evidence is provided for the hypothesis of myeloma cell differentiation.

Antigens, Neoplasm↗
PubMed1989

Effects of CKS-17, a synthetic retroviral envelope peptide, on cell-mediated immunity in vivo: immunosuppression, immunogenicity, and relation to immunosuppressive tumor products.

CKS-17 is a heptadecapeptide corresponding to a region highly conserved in retroviral transmembrane proteins such as p15E. Because a relationship had previously been determined between p15E and immunosuppressive tumor cell products, we examined the effect of CKS-17, control peptides and conjugates thereof on the expression of cell-mediated immunity (delayed-type hypersensitivity, DTH) in mice. Conjugates of CKS-17 inhibited DTH reactions to sheep erythrocytes in the feet of mice. The degree of inhibition was dose-dependent. Unconjugated CKS-17 had almost no effect, and control peptide conjugates had no inhibitory effect. Immunization of mice with CKS-17 conjugates, but not with control conjugates, rendered them resistant to the depression of DTH reactions, not only by CKS-17 conjugates, but also by products of cultured tumor cells. CKS-17 conjugates, but not control conjugates, also depressed the cellular inflammatory reactions induced in mouse footpads by concanavalin A (ConA) and immunized mice against the depression of ConA reactions by products of cultured tumor cells. Injections of globulin from sera of mice immunized with CKS-17 conjugates conferred upon normal recipients resistance to the depression of footpad reactions to ConA by products of cultured tumor cells. Globulin from sera of normal mice or control immunized mice did not confer such resistance. Thus conjugates of a synthetic peptide not only mimic the immunosuppressive effects of tumor products in vivo, but can also immunize mice against those effects.

Animals↗
PubMed1988

Inhibition of cell-mediated immunity by tumour cell products: depression of interleukin-2 production and responses to interleukin-2 by mouse spleen cells.

Supernatants from cultures of mouse and human tumour cells inhibited the production of interleukin-2 (IL-2) by stimulated mouse spleen cells. The tumour cells tested, all of which were active, included a mouse and a human melanoma, three methylcholanthrene-induced fibrosarcomas of mice, and human HeLa cells. Supernatants from normal mouse and human fibroblasts were inactive. Inhibition was dose-dependent. Spleen cells from aged mice were more susceptible to inhibition than spleen cells from young mice. When tumour cell culture supernatants were fractionated on Sephacryl S-300, two peaks of activity were found, with apparent molecular weights of approximately 50 and 18 kD. Supernatants from tumour cell and fibroblast cultures caused variable, but generally weak, inhibition of responses of lymphoblasts to IL-2. It is suggested that inhibition of IL-2 production may be an important mode of action of tumour cell products that inhibit cell-mediated immunity.

Animals↗
PubMed1987

Depression of cell-mediated immunity by tumour cell products: induction of resistance by immunotherapeutically active extracts of bovine ocular squamous cell carcinoma.

Tumours produce substances that inhibit the expression of cell-mediated immunity, in the form of delayed-type hypersensitivity in mice. Phenol-saline extracts of bovine ocular squamous cell carcinoma (BOSCC) which have immunotherapeutic activity in cattle were able to immunize mice against this depressive effect. Such immunization was effective against products of BOSCC, a spontaneous rat tumour, three of four human tumour cell lines and (in other experiments) mouse tumours. Phenol-saline extracts of mouse tumour cell lines were immunogenic (protective against depression of delayed-type hypersensitivity) in mice. Fractions of BOSCC phenol-saline extracts which were immunotherapeutically active in cattle were generally also protective in mice. The protective activity was lost after treatment with proteinase K, and was present in the supernatant after precipitation with 55% ammonium sulphate. It was not affected by treatment with RNase or DNase or by heating to 50 degrees C for 2 h. It was present in gel filtration fractions with an apparent molecular weight of 10,000-37,000 daltons. The immunogenic factor in mice and the immunotherapeutic factor in cattle may be related to each other.

Adjuvants, Immunologic↗
PubMed1987

Interleukin-1 secretion by peripheral blood monocytes and synovial macrophages from patients with rheumatoid arthritis.

Blood monocytes and synovial fluid and tissue macrophages were examined for their ability to produce interleukin-1 (IL-1) measured in a mouse thymocyte proliferation assay. Spontaneous production of IL-1 by monocytes from patients with rheumatoid arthritis (RA) or ankylosing spondylitis was higher than that by cells from normal subjects, patients with osteoarthritis or patients with RA treated with gold. IL-1 production in response to LPS stimulation was similar in all groups. Spontaneous IL-1 production by synovial fluid macrophages from patients with RA was similar to that of their monocytes, but the response to LPS was smaller. Synovial tissue macrophages produced little IL-1. Similar results were obtained in assays of fibroblast proliferation.

Arthritis, Rheumatoid↗
PubMed1986

Acetylspiramycin and the immune system--II. Effects on lymphocyte proliferation, lymphokine production, delayed-type hypersensitivity and antibody production.

The effects of the antibiotic acetylspiramycin (ASPM) on lymphocyte function were studied in vitro and in vivo. When added to lymphocyte cultures in vitro, ASPM inhibited splenic lymphocyte transformation induced by phytohemagglutinin (PHA), lipopolysaccharide (LPS) and antigen. It also depressed production by spleen cells of the lymphokine inducing procoagulant activity in mouse macrophages. Spleen cells from mice given ASPM orally showed enhanced responses to PHA, but normal responses to LPS. The capacity to produce lymphokine was increased early after oral ASPM and slightly decreased after prolonged administration. Oral ASPM had no effect on the production of antibodies and a very slight enhancing effect on the development of delayed-type hypersensitivity to sheep red blood cells.

Animals↗
PubMed1986

Effects of cyclosporin A on the production of experimental anti-erythrocyte autoantibodies in mice.

Mice were treated with cyclosporin A (CsA) (25-100 mg/kg daily, by mouth) during the induction of autoantibodies to erythrocytes by means of injections of rat erythrocytes. A high dose of CsA inhibited autoantibody production whereas a low dose temporarily potentiated it. Cell transfer and anti-Thy 1.2 treatment indicated the presence of suppressor T cells in the spleens of immunized mice. Their formation was inhibited by treatment with high dose CsA and potentiated by low dose CsA. In the CBA/H mice used, CsA treatment after immunization had no effect on autoantibody titres.

Animals↗
PubMed1986

Mast cell granules cause proliferation of human microvascular endothelial cells.

To investigate the possible role of mast cells in blood vessel formation, rat mast cell granules were studied for their proliferative effect on human microvascular endothelial cells. It was found that granules had a marked proliferative effect and that most of this activity was restricted to a dialyzable fraction. The dialyzable mast cell granule constituent histamine was found to be mitogenic, an effect that was shown with the use of specific agonists and antagonists to be mediated through an H1 receptor. H1 antagonists reduced the proliferation caused by the untreated mast cell granules to the level of proliferation caused by dialyzed granules, suggesting that all the dialyzable mitogenic activity was due to histamine. Histamine was also shown to cause proliferation of cells that were growth arrested by serum deprivation, suggesting that it is an endothelial growth factor. The compound responsible for the undialyzable mitogenic activity could not be identified but was shown not to be mast cell heparin. This demonstration of mast cell granule-induced endothelial proliferation suggests that the mast cell may be of importance in the process of angiogenesis.

Animals↗