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Biomedical subjects

K D Burman

Publications and source records attributed to K D Burman.

At least 73 records · Page 4Linked to original sources
PubMed1990

A comparison of the health risk, health status, self-motivation, psychological symptomatic distress, and physical fitness of overweight and normal-weight soldiers.

The purpose of this study was to analyze the assumptions underlying the Army's Weight Control Program (AWCP) and to determine whether overweight and normal-weight soldiers differed with respect to health risk, health status, self-motivation, psychological symptomatic distress, and physical fitness. The sample consisted of 154 active-duty male and female enlisted Army soldiers assigned to the Maryland and District of Washington area: 77 overweight soldiers and 77 normal-weight soldiers were randomly selected from a gender-stratified, unit-specific list. To test the hypothesis that the two groups would differ, data were analyzed using multivariate analysis of variance (MANOVA). The hypothesis was supported. The overweight and normal-weight soldiers differed, with the former having greater health risk, lower health status, and lower physical fitness; but the two groups did not differ in self-motivation or psychological symptomatic distress. These results support the concept that obesity is associated with increased morbidity. Further studies are necessary to examine the mechanisms by which endogenous physiological factors contribute to the expression of obesity.

Adult↗
PubMed1990

Management of patients with thyroid carcinoma: application of thallium-201 scintigraphy and magnetic resonance imaging.

Thyroid carcinoma has the ability to concentrate radioiodine, an attribute that can be used both for detection of thyroid cells and for treatment. Unfortunately, however, radioiodine uptake is not observed in all patients and a radioiodine scan requires that the patient be rendered hypothyroid for 4-6 wk. In the present study, we analyzed the utility of thallium-201 scanning and the usefulness of magnetic resonance imaging (MRI) in the detection of thyroid cancer. Nineteen patients with thyroid cancer had a total of 24 radioiodine scans, 33 thallium scans, and 10 MRI examinations. Of the 19 patients in the study, 17 had differentiated thyroid carcinoma. In these 17 cases, all paired studies were concordant for the presence (n = 7) or absence (n = 10) of disease. However, in one case (Patient 10), the 201Tl studies showed far more extensive disease than was observed on the 131I scan. Thyroid cancer was also detected on seven MRI studies. In summary, thallium and MRI scans are adjunctive techniques to radioiodine scanning that can either confirm the presence of neck bed activity, residual disease or metastatic cancer and may delineate tumor deposits not detected by radioiodine scanning. Thallium may be capable of detecting tumor deposits even while a patient remains euthyroid.

Adenocarcinoma↗
PubMed1990

Nasal radioiodine activity: a prospective study of frequency, intensity, and pattern.

The nose has been reported as a site of radioiodine accumulation on 131I whole-body scintigraphy. To determine the frequency, intensity, and pattern of nasal radioiodine accumulation, a prospective study was performed on 21 patients referred for 131I whole-body scintigraphy during a 26-mo interval. All patients were dosed with 5 mCi (18.5 MBq) of 131I p.o., and imaged 72 hr later. Ninety-five percent (20/21) of patients had nasal radioactivity greater than background, and in 75% (15/20) of positive patients the pattern of activity was round. Clinical follow-up of these patients has shown no evidence of tumor involvement in the nasal area. We conclude that nasal radioiodine activity is a normal finding. Radioiodine uptake in the nasal area, without clinical suspicion of metastatic disease, should not be considered a criterion for surgical intervention or radioiodine therapy.

Adult↗
PubMed1989

Binding of thyrotropin to selected Mycoplasma species: detection of serum antibodies against a specific Mycoplasma membrane antigen in patients with autoimmune thyroid disease.

Radiolabeled human (hTSH) and bovine (bTSH) thyroid stimulating hormone was shown to bind to five species of Mycoplasma, the wall-less prokaryotes. The maximum binding capacity of 125I-bTSH to these five species was about 7.9 x 10(-13) moles-1.4 x 10(-12) moles for 50-100 micrograms protein with dissociation constants of approximately 1.7 to 2.2 x 10(-7)M. Approximately 50% of the 125I-bTSH binding was displaced by excess, unlabeled bTSH or hTSH, but labeled bTSH was not effectively displaced by growth hormone, LH, FSH, prolactin, or the beta subunit of hTSH, FSH and LH. Antisera prepared against Mycoplasma gallisepticum and Mycoplasma pneumoniae bound to human thyroid membranes and guinea pig fat cells, suggesting that receptors on human thyroid tissues and on Mycoplasma cells may have similarities in antigenicity. These findings were substantiated by the occurrence of TSH binding to Mycoplasma antisera. Further, sera from three of six patients with Graves' disease containing antibodies to thyroid tissues also reacted to a 108 Kd polypeptide of Mycoplasma gallisepticum.

Animals↗
PubMed1989

Persistence of low serum thyroid hormone levels in a Graves' disease patient receiving supraphysiologic L-thyroxine replacement therapy.

A patient with Graves' disease was treated with radioactive iodine. For several years following treatment, the patient displayed clinical hypothyroidism and persistently low serum thyroxine (T4) and triiodothyronine (T3) levels despite large T4 replacement dosage (0.3-0.4 mg L-thyroxine daily). A defect in T4 absorption was considered unlikely since absorption of fat soluble materials (vitamins A and E) was essentially normal as reflected by their serum concentrations. Abnormalities in serum protein binding of T4 especially by immunoglobulins were suspected; however, thyroid hormone binding antibodies were absent. Thyroxine binding prealbumin (TBPA) levels were either frankly elevated or in the upper normal range and such variations were mirrored by retinol binding protein (RBP) concentrations. Thyroxine binding globulin (TBG) concentration was normal. A surprising finding was an elevated percent dialyzable thyroxine (.041%; normal range, .018-.034%) in spite of a normal concentration of TBG. Serum free fatty acid levels were also elevated. The marked increase in percent free T4 (FT4) fraction together with a low serum total T4 concentration resulted in normal or marginally elevated FT4 levels. An increase in T4 metabolic clearance as suggested by the elevated percent FT4 fraction was corroborated by steady state serum T4 values observed following changes in T4 dosage.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1989

Thyrotropin modulates receptors for atrial natriuretic peptide on intact human thyroid cells.

Interest in the mechanism of impaired salt and water metabolism in hypothyroidism has led to growing evidence of an interaction between atrial natriuretic peptide (ANP) and the thyroid, which includes reports of direct effects of thyroid hormone on ANP synthesis and circulating ANP levels, and of the presence of specific ANP receptors in human thyroid tissue, which may act to inhibit thyroglobulin (Tg) secretion. The authors questioned whether or not thyrotropin (TSH) has a role in this interaction. They used 125I-ANP to study the effect of TSH on ANP binding to human thyroid cells in primary culture. Binding competition by increasing concentrations of unlabeled ANP in the presence or absence of TSH was assessed by Scatchard analysis. At lower temperatures of 4 degrees C or 23 degrees C, TSH had no effect either on the ANP receptor equilibrium dissociation constant (Kd) or number of binding sites. However, at 37 degrees C, bovine TSH at 1 mU/ml reduced measurable binding sites by about 50% without affecting receptor affinity (Kd = 0.2 nM). Prolonged (6 days) coincubation of TSH with thyroid cells decreased the assayable ANP receptor. The effects of TSH appear to be specific because human luteinizing hormone, follicle-stimulatory hormone, growth hormone, human chorionic gonadotropin and iodide had no effect on ANP binding. Thus, human thyroid cells possess a single class of high-affinity, specific receptors for ANP with binding activity that is temperature dependent and modulated by TSH at physiologic temperature. TSH-mediated reduction of binding at 37 degrees C but not at 4 degrees C suggests an energy-dependent process that acts possibly by activating an ANP degradative enzyme or by changing the rate of receptor internalization and subsequent degradation.

Atrial Natriuretic Factor↗
PubMed1989

Effects of epidermal growth factor on thyroglobulin and adenosine 3',5'-monophosphate production by cultured human thyrocytes.

While several workers have identified epidermal growth factor (EGF) receptors on human thyroid membranes, very few reports have described EGF effects on intact human thyroid cells in primary culture, and these were short term studies indicating that EGF effects were primarily inhibitory [reduced iodide uptake and thyroglobulin (Tg), T4, and T3 release]. Paradoxically, in vivo EGF stimulates thyroid growth and increases colloid stores. In this study we examined the effects of EGF on cultured thyroid cells in regard to thymidine incorporation, Tg secretion, and cAMP production during a 12-day period. Addition of EGF (0-30 ng/mL) to medium for 6 or 12 days stimulated thymidine incorporation and enhanced Tg synthesis by thyroid cells. However, the profile of Tg release into medium was biphasic. Tg release was inhibited by EGF (0.1-10 ng/mL) during the first 3 days of culture, but the inhibitory effect disappeared by the sixth day, and EGF stimulated Tg release by day 12 and thereafter. EGF enhanced endogenous cAMP levels in thyroid cells, but did not augment TSH-stimulated increases in cAMP production. Our observations of EGF-stimulated growth and inhibited Tg secretion during short term culture are consistent with the findings of earlier studies with nonhuman thyrocytes. However, the later phase of enhanced cAMP levels with stimulation of Tg secretion indicates that EGF may have trophic effects on thyrocytes previously unrecognized because of the short term nature of the studies. These observations suggest an important role for EGF in maintenance of normal thyroid physiology.

Cells, Cultured↗
PubMed1989

[Molecular genetic detection of polyclonal immune response in autoimmune thyroiditis and inflammatory bowel diseases].

Southern blot hybridization techniques were used to analyze the arrangements of the immunoglobulin and the T cell antigen receptor genes in lymphocytes of patients with Graves disease and Hashimoto's thyroiditis as well as in patients with Crohn's disease, chronic ulcerative colitis, and with other gastrointestinal disease. The results indicate that the immune response of autoimmune thyroid disease and inflammatory bowel disease is of polyclonal origin.

Adolescent↗
PubMed1988

Development of a human monoclonal antibody from a Graves' disease patient that identifies a novel thyroid membrane antigen.

To investigate the interaction between antibodies and the thyroid gland in Graves' disease, PBL were harvested from seven Graves' disease patients and transformed into lymphoblasts by the addition of EBV in the presence of cyclosporine A. These lymphoblasts were cloned by limiting dilution and then assayed for binding activity to human thyroglobulin, thyroid-stimulating hormone, thyroid microsome, and thyroid as well as guinea pig fat cell membranes. Four patients' cells produced antibody that bound to at least one of the Ag; a single clone from one patient that bound equally well to both thyroid and guinea pig fat cell membranes (but not to other thyroid Ag) was selected for further evaluation. Fusion of these cells with SHM-D33 heteromyeloma cells yielded three cell lines that produced genetically identical mAb. Immunostaining of human thyrocytes with this mAb demonstrated an Ag present on both nuclear and cell membranes. This Ag was identified as an 18,000 m.w. protein band on Western blots of both human thyroid and guinea pig fat cell membranes. The mAb was also able to alter thyrocyte physiology as the short term incubation of this mAb with FRTL-5 cells in vitro inhibited thyroid-stimulating hormone-mediated production of cAMP. Thus, this mAb and the Ag it identifies may be relevant to Graves' disease.

Animals↗
PubMed1988

Alterations in magnesium and zinc metabolism in thyroid disease.

Magnesium (Mg) and zinc (Zn) status was assessed in subjects to evaluate the effects of thyroid diseases on Mg and Zn metabolism. Plasma and red blood cell (RBC) concentration and peripheral blood mononuclear cell (MNC) content of Mg and Zn, and 24-hour urinary excretion of Mg, Zn, creatinine (Cr), calcium (Ca), sodium (Na), and potassium (K) were measured in 11 thyrotoxic, 29 hypothyroid, and 25 euthyroid control subjects. Serum albumin, alpha 2-macroglobulin, and the binding of Zn to albumin were also determined. Plasma and RBC Mg concentrations were low in half of the hyperthyroid subjects, but mean values were not significantly different from controls. Urinary excretion and clearance of Mg were lower in hypothyroid subjects, but differences were removed when expressed relative to Cr excretion and clearance. Similar patterns were noted for urinary Ca, Na, and K, suggesting that their reduced excretion reflects alterations in renal hemodynamics. Plasma Zn was lower in hypothyroid subjects and correlated with serum albumin; MNC Zn and urinary Zn were also low. Plasma Zn concentration was normal and serum albumin significantly lower in the hyperthyroid group than in the control group. Further, RBC Zn content was significantly lower in hyperthyroid subjects, and inversely related to plasma thyroxine concentration. The hyperthyroid group also excreted significantly greater amounts of Zn than controls, indicative of a catabolic process. This increased urinary loss may reflect a shift in the distribution of plasma Zn between ultrafilterable and Zn-albumin complexes. In summary, this study provides evidence for marked alterations in Zn homeostasis in persons with thyroid disease. Whether the observations indicate deficiency states and have clinical implications will require further investigation.

Adolescent↗
PubMed1988

Immunohistochemical analysis of intrathyroidal lymphocytes in Graves' disease: evidence of activated T cells and production of interferon-gamma.

Previous immunohistochemical studies of the thyroid gland in Graves' disease (GD) have demonstrated that (i) lymphoid cells infiltrating the interstitium of the gland predominantly express the CD4+ (T-helper) phenotype; (ii) lymphoid cells infiltrating the epithelial compartment express predominantly the CD8+ antigen; and (iii) thyroid epithelial cells (thyrocytes) express class II histocompatibility antigens, possibly in response to endogenous production of interferon-gamma (IFN-gamma) by the infiltrating lymphocytes. In the present study the infiltrating lymphoid cells and thyrocytes in GD were further characterized by immunocytochemistry. Scattered infiltrating interstitial lymphocytes stained positively with antibodies directed against IFN-gamma and the receptor for interleukin 2. These lymphocytes were most prominent around the periphery of lymphoid nodules. The interstitial lymphocytes predominantly expressed the CD4+ 2H4+ phenotype rather than the complementary CD4+ 4B4+ phenotype, suggesting the presence of the suppressor-inducer rather than helper-inducer T cell subset. The infiltrating lymphocytes were associated with thyrocytes expressing HLA-DR antigens, as previously reported, and also HLA-DQ antigens, but to a lesser extent. The presence of HLA-DQ may also suggest the possibility of an induced suppressor response. The intraepithelial CD8+ cells did not stain with antibodies to CD3, 2H4, 4B4, or Leu 7 and their identity remains unknown.

Epithelium↗
PubMed1988

Pituitary and peripheral hormone responses to T3 administration during Antarctic residence.

Very little is known regarding hormonal adaptation in human subjects who are exposed to the extremes of temperature and light that are found in polar latitudes. We have previously reported a 50% elevation in the serum thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH), a fall in serum total triiodothyronine (T3) and free T3 (fT3), and no change in serum total thyroxine (T4) or free T4 (fT4) after 42 wk of Antarctic cold exposure. To differentiate between central and peripheral mechanisms that may lead to these changes, we report the effect of sequentially increasing oral doses of T3 (Cytomel) on serum T3 and fT3 levels and on the resultant attenuation of the TSH response to TRH in nine men before, during, and after 42 wk residence in Antarctica. Serum T3 values basally and following the administration of 25, 50, and 75 micrograms/day of T3 were lower after 42 wk of cold exposure (151 +/- 4, 160 +/- 8, 189 +/- 10, and 222 +/- 14 ng/dl, respectively, compared with control values of 160 +/- 7, 178 +/- 7, 202 +/- 9, and 251 +/- 19 ng/dl, respectively, P less than 0.05). Likewise, the fT3 values measured after these three increasing T3 doses were also lower after 42 wk of cold exposure. The pituitary response to TRH was attenuated by each T3 regimen (48 +/- 6, 68 +/- 4, and 77 +/- 4% decreases in the control period), and this suppression was not different after 20 and 42 wk of Antarctic residence.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1988

Natural killer cell activity and serum autoantibodies in women with postpartum thyroiditis.

Postpartum thyroiditis (PPT) is a form of painless lymphocytic thyroiditis which is thought to be caused by an exacerbation of underlying subclinical autoimmune thyroid disease during a postpartum period of immune rebound. The purposes of this study were to analyze natural killer cell (NK) functional activity and antibody-dependent cell-mediated cytotoxicity (ADCC) of peripheral blood mononuclear cells in patients with PPT compared to those in normal nonpostpartum and postpartum women. NK activity and ADCC were determined by specific lysis of 51Cr-labeled K562 human erythroleukemia tumor cells at varying effector (mononuclear cell) to target cell ratios. Nineteen PPT patients between 4-9 months [mean, 6.5 +/- 0.4 (+/- SE)] postpartum were compared to 20 nonpostpartum women, 31 healthy women between 4-9 months (6.7 +/- 0.3) postpartum, and 14 women 2 days after delivery. There were significant differences in the NK functional activities of the 4 groups (F = 7.95; P = 0.0002). The mean NK activities, as measured by percent specific lysis at an effector to target cell ratio of 10:1, were 31.1 +/- 3.3%, 20.9 +/- 2.3%, 22.5 +/- 2.8%, and 11.5 +/- 2.0% in the nonpostpartum, PPT, postpartum, and 2-day postpartum groups, respectively. Specific lysis by ADCC was not significantly different from lysis by NK activity in any group. The PPT, postpartum, and 2-day postpartum groups had significantly lower NK activity compared to that in nonpostpartum women (P less than 0.05). Both the PPT and postpartum women had higher NK activities than the 2-day postpartum women (P less than 0.05). However, there were no significant differences in the NK activities of the PPT patients compared to those of the healthy postpartum women. Patients with PPT were also found to have associated autoimmune dysfunction. The PPT group had significantly higher serum antinuclear antibody titers; 8 of 24 patients (33%) had titers of 1:160 or greater compared to only 2 of 29 healthy postpartum women (7.4%; P less than 0.05). Seven of the PPT patients had serum immune complexes, and 3 had TSH receptor antibodies. We conclude that functional NK activity and ADCC in peripheral lymphocytes of PPT patients are not different from those in healthy postpartum women; however, the postpartum women had significantly decreased activity compared to that in nonpostpartum women. These data emphasize the importance of studying healthy postpartum women in investigations of PPT, since the immunological changes in pregnancy and the postpartum period remain largely undefined.

Adult↗
PubMed1988

Immunoglobulin and T cell antigen receptor gene arrangements indicate that the immune response in autoimmune thyroid disease is polyclonal.

To further define the degree of heterogeneity of the antibody and cellular immune responses in autoimmune thyroid disease, we used Southern blot hybridization techniques to analyze the arrangements of immunoglobulin and T cell antigen receptor genes in circulating lymphocytes and in those infiltrating the thyroid gland in nine patients with thyrotoxicosis due to Graves' disease and five patients with Hashimoto's thyroiditis. The sensitivity of these techniques was sufficient to detect a monoclonal population when there was as little as 1% clonal involvement in a mixed cell population. In the patients studied, DNA from non-T peripheral blood cells and non-T intrathyroid lymphocytes had only a germline gene pattern and no clonal nongermline rearrangements of immunoglobulin genes, as assessed using an immunoglobulin joining heavy chain (IgJH) gene probe. An analysis of the DNA from peripheral blood T cells or intrathyroidal lymphocytes revealed polyclonal gene rearrangement patterns and no clonal nongermline rearrangements of the T cell antigen receptor-beta and -gamma genes, as assessed using T constant-beta and T joining -gamma gene probes. These results indicate that the lymphocytes in peripheral blood and those infiltrating the thyroid gland in patients with autoimmune thyroid disease are of polyclonal origin.

Adult↗
PubMed1988

Autoantibodies to insulin are present in sera of patients with autoimmune thyroid disease.

It has been clinically suspected that patients with autoimmune thyroid disease are at an increased risk of developing other autoimmune diseases later in life. To determine the presence and potential importance of a more generalized deregulation of immune response in patients with Grave's disease and Hashimoto's disease, sera from 33 patients with Graves' disease and 16 patients with Hashimoto's disease were screened for the presence of anti-insulin antibodies and anti-insulin-receptor antibodies. An enzyme-linked immunosorbent assay was used to identify the presence of IgG against human insulin. The optical density indicating the presence of IgG against insulin in sera from patients with Graves' disease averaged .172 +/- .024 (mean +/- SE; range .010-.802), compared to the mean normal value of .098 +/- .0009 (range .012-.238) in 33 control subjects. Ten of 33 patients with Graves' disease had values greater than .200, whereas control sera values were less than .200 in all but one case (P less than .005, Graves' sera vs. controls). The sera from patients with Hashimoto's disease had a mean optical density of .110 +/- .016, with 15 of 16 values between .010 and .200. These values were not significantly different from controls with an insulin-binding inhibition assay. Anti-insulin-receptor antibodies were not detected in any of 33 patients with Graves' disease, and cytoplasmic islet cell antibodies were not detected in sera from seven patients with Graves' disease who had insulin-binding antibodies. These data support the hypothesis that the immunologic response in autoimmune thyroid disease may be more heterogeneous and polyclonal than previously believed.

Autoantibodies↗
PubMed1988

Seronegative Hashimoto thyroiditis with thyroid autoantibody production localized to the thyroid.

A patient without serologic evidence of an autoimmune disorder had a thyroidectomy for neck compression caused by her goiter. Histologic examination of the gland revealed pathologic changes compatible with Hashimoto disease, and lymphocytes isolated from her thyroid gland were transformed into lymphoblastoid cells in vitro by Epstein-Barr virus in the presence of cyclosporine. These cells produced antibodies against thyroglobulin, thyroid microsome, thyrocyte membrane, and thyrotropin, whereas lymphoblastoid cells produced from the patient's peripheral blood lymphocytes showed no antithyroid activity. Several human monoclonal antibodies were produced from the intrathyroidal lymphocytes by fusion with the SHM-D33 heteromyeloma, and the resulting cell lines produced antibodies with high-affinity binding specific for thyroid antigens. These studies show that lymphocytes capable of producing antithyroid antibodies can be present in the thyroid glands of patients with Hashimoto disease without evidence of a peripheral immune response, thus indicating that Hashimoto disease can exist as an organ-restricted autoimmune disorder.

Adipose Tissue↗