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Biomedical subjects

L Hoffman-Goetz

Publications and source records attributed to L Hoffman-Goetz.

At least 37 records · Page 2Linked to original sources

Neutrophil response to prolonged exercise in immune-competent and RAG2/gamma c null mice.

The two aims of this study were (i) to compare the effects of prolonged exercise on circulating neutrophil number and muscle myeloperoxidase (MPO) activity between RAG2/gamma c null and immune-competent mice, and (ii) to evaluate the general suitability of the lymphocyte-deficient RAG2/gamma c null strain for use in exercise models of immune regulation. RAG2/gamma c null (male and female) and C57BL/6 (congenic immune-competent, male) mice were assigned to either control (C) or treadmill exercise (EX, 22 m/min, 90 min, 6% grade) groups. EX mice were killed immediately (EX0) or 24 h (EX24) after exercise. RAG2/gamma c null males had significantly (P < 0.05) fewer circulating CD45+ cells and higher %CD45+ neutrophils than did C57BL/6 males, independent of exercise. A significant interaction was observed for the effects of exercise and gender on %CD45+ neutrophils in the blood. At EX24, gastrocnemius (Gastroc) MPO significantly increased in EX mice. Gastroc MPO activity was 44% and 35% higher in RAG2/gamma c null vs. C57BL/6 males, and in female vs. male RAG2/gamma c null mice, respectively. Heart MPO activity did not differ between strains or among treatments. We concluded that the Rag2/gamma c null strain is a suitable model for future investigations on immune regulation following acute exercise stress.

Animals↗

Thymic stress in artificially reared and maternally reared rat pups.

It is well documented that the hypothalamic-pituitary-adrenal (HPA) axis influences immunological responses to stress. Maternal factors have been shown to be necessary for appropriate modulation of the HPA axis in the developing rat. The purpose of this study was to determine whether artificially reared (AR) infant rat pups (a procedure whereby infant rats are gastrostomized and reared independently of maternal factors) have an altered function of the HPA axis in terms of thymocyte apoptosis (programmed cell death) and other indices of thymic stress. AR and maternally reared (MR) Long-Evans rat pups were randomized to control, fasted, stressed, and fasted+stressed treatment groups, as well as an unhandled, MR naive group that served as a baseline control. AR rat pups were significantly heavier than MR (p<0.001). AR rat pups had significantly lighter thymuses than did the MR pups (p<0.001) and fasted pups had significantly lighter thymuses than unfasted pups, regardless of whether they were in the AR or MR condition (p<0.005). AR pups had significantly lower thymic cell numbers and a greater percent of necrotic cells than did MR pups. There were no significant effects of rearing condition on the percent of apoptotic thymocytes. The thymocyte alterations observed in this study between the two rearing conditions suggest that AR reduces thymic weight and cell numbers, which may have consequences for the development of adult cellular immunity.

Animals↗

Supraphysiological level of estrogen exposure in vivo increases lymphoid cell death in mice.

Estrogen can enhance or reduce lymphocyte functions in vitro depending on dose and exposure duration. The purpose of this study was to determine the effect of in vivo 17 beta-estradiol (E2) on apoptosis and necrosis in lymphoid tissue of female C567BL/6 mice. Animals were ovariectomized (OVX), ovariectomized and 17 beta-estradiol supplemented (OVX + E2; 71 micrograms E2 per day for 14 days), sham ovariectomized (SHAM), or unhandled controls (CONTROL). Thymus and spleen were removed aseptically, cells dispersed into single cell suspensions in RPMI-1640, and measures of cell damage performed: an annexin V flow cytometric assay for markers of apoptosis and an enzyme-linked immunoassay for measures of DNA fragmentation and necrosis. OVX + E2 mice had 620 +/- 72 pg/ml 17 beta-estradiol in serum in contrast to OVX mice which had 7.6 +/- 5 pg/ml, the SHAM mice which had 2.8 +/- 1 pg/ml of serum E2, and the CONTROL mice which had 3.9 +/- 0.8 pg/ml of serum E2 (p < 0.001). There was a significantly lower percentage of viable thymocytes in OVX + E2 mice compared to the other treatment conditions (p < 0.001, respectively). There was also a significantly higher percentage of annexin V positive thymocytes in OVX + E2 mice (p < 0.005). Measures of DNA fragmentation by ELISA were higher in splenocytes from OVX + E2 mice than in the OVX, SHAM or CONTROL mice (p < 0.005). These results suggest that supraphysiological levels of estrogen in vivo induce damage in lymphoid cells; however, the impact of estrogen associated lymphoid tissue damage on specific immune functions remains to be determined.

Animals↗

Effect of exhaustive exercise on membrane estradiol concentration, intracellular calcium, and oxidative damage in mouse thymic lymphocytes.

Early Ca2+ signaling events in cells of the immune system after exhaustive exercise challenge (8% slope, 32 m/min(-1) speed) of female C57BL/6 mice, and their effects on oxidative reactions in thymus were studied. Intracellular Ca2+ and the oscillation of free extracellular Ca2+ were imaged with cell permeant cell and cell impermeant Fluo 3 calcium indicator in thymocytes. The role of estradiol was assessed by RIA for levels of membrane bound estradiol. Oxidative product release and membrane lipid peroxide were also evaluated. Intracellular Ca2+ levels were significantly higher in thymocytes of exercised compared with control mice (p < .001). There was a continuous flux of Ca2+ after exercise when cells were monitored in Ca2+ rich medium, with a significant influx between 160 and 200 sec (p < .001). Membrane bound estradiol was elevated in thymocytes of exercised compared to control mice (p < .05). Immediately after exercise there was a greater release of oxidative products by thymocytes in exhaustively exercised compared with control animals. There was also significant generation of lipid peroxide in thymus of exercised mice (p < .001). The findings suggest that exhaustive exercise may stimulate estradiol uptake by receptors on thymocytes, with a possible opening up of estradiol-receptor operated channels for Ca2+ entry into cells. This may have damaging effects on thymic lymphocytes by the triggering of oxidative reactions as determined by higher oxidative product release and greater generation of lipid peroxide.

Animals↗

Exercise and the immune system: regulation, integration, and adaptation.

Stress-induced immunological reactions to exercise have stimulated much research into stress immunology and neuroimmunology. It is suggested that exercise can be employed as a model of temporary immunosuppression that occurs after severe physical stress. The exercise-stress model can be easily manipulated experimentally and allows for the study of interactions between the nervous, the endocrine, and the immune systems. This review focuses on mechanisms underlying exercise-induced immune changes such as neuroendocrinological factors including catecholamines, growth hormone, cortisol, beta-endorphin, and sex steroids. The contribution of a metabolic link between skeletal muscles and the lymphoid system is also reviewed. The mechanisms of exercise-associated muscle damage and the initiation of the inflammatory cytokine cascade are discussed. Given that exercise modulates the immune system in healthy individuals, considerations of the clinical ramifications of exercise in the prevention of diseases for which the immune system has a role is of importance. Accordingly, drawing on the experimental, clinical, and epidemiological literature, we address the interactions between exercise and infectious diseases as well as exercise and neoplasia within the context of both aging and nutrition.

Acute-Phase Reaction↗

Impact of treadmill exercise on early apoptotic cells in mouse thymus and spleen.

Lymphocyte apoptosis occurs in response to stressors such as thermal injury, trauma, sepsis, and surgery. This study evaluated the effect of a single bout of physical exercise stress on the induction of apoptosis in murine thymocytes and splenic lymphocytes. Female C57BL/6 mice, treadmill exercised at a submaximal intensity (35 m/min, 6% grade) for 90 min or serving as controls (walking on treadmill at 12 m/min, 6% grade, 5 min), were sacrificed 5 min or 120 min after completion of exercise. The percent of apoptotic, necrotic, and viable thymocytes and splenocytes were determined by flow cytometry using annexin V FITC and propidium iodide. There was a significantly higher percent of viable splenocytes in the mice sampled 120 min after cessation of exercise than treadmill control animals (p<0.05). In the thymus, there was a significantly lower percent of apoptotic (p<0.5) and a significantly higher percent of viable (p<0.05) cells in exercised mice sampled at 120 min after exercise relative to controls. Absolute numbers of thymocytes and splenocytes did not differ by exercise treatment condition. Plasma corticosterone levels were elevated immediately after exercise and were negatively correlated with the percent of viable lymphocytes in the spleen. During the time frame sampled, submaximal exercise is associated with a lower % of thymocytes expressing early markers of apoptosis, despite elevated plasma corticosterone levels. Retention of self-reactive, viable thymocytes which would normally be deleted or selective trafficking of apoptotic thymocytes out of the thymus may be involved in the exercise effect. Additional studies are necessary to identify the mechanisms for this shift in proportions of apoptotic and viable cells in lymphoid compartments with exercise.

Animals↗

Occupational physical activity and non-Hodgkin's lymphoma.

PURPOSE: The purpose of this study was to evaluate the role of physical activity in the development of non-Hodgkin's lymphoma (NHL). METHODS: Incident NHL cases and population-based controls were identified from three case-control studies conducted in four midwestern states: Iowa, Kansas, Minnesota, and Nebraska. A total of 1177 cases (993 men, 184 women) and 3625 controls (2918 men, 707 women) were interviewed. Usual occupation (all states) and lifetime occupational histories (Iowa and Minnesota only), obtained from interviews, were classified for energy expenditure (EE) and sitting time. Odds ratios (OR) and 95% confidence intervals were calculated comparing moderate and high activity levels with sedentary levels. RESULTS: There was no evidence of an association between NHL and occupational physical activity measured either by EE or sitting time. Among men, the OR associated with usual occupation moderate and high EE were 1.1 and 1.0, respectively. For sitting time, the OR were also 1.1 and 1.0 for moderate and high activity, respectively. Among women, slight nonsignificant elevations in risk of NHL were observed among the high energy level and high activity sitting categories. The trends were not significant. There was no evidence of confounding or effect modification by vital status, hair dye use, or solvent exposure. Among subjects with lifetime occupational histories, there were no significant increases or trends for cumulative or average EE or sitting time. There was no association between occupational physical activity and NHL. CONCLUSION: Research on nonoccupational physical activity, which in the U.S. is likely the more important component of daily activity than occupational activity, may still be warranted given the laboratory evidence linking physical activity and immune function, an important factor in the etiology of NHL.

Adult↗

Intrathymic and intrasplenic oxidative stress mediates thymocyte and splenocyte damage in acutely exercised mice.

Reactive oxygen species may contribute to apoptosis in lymphoid tissues observed after exercise. Thymic and splenic tissues excised from control mice (C) or mice immediately after (t0) or 24 h after (t24) a run to exhaustion (RTE) were assayed for biochemical indexes of oxidative stress [thymic and splenic membrane lipid peroxides, superoxide dismutase, catalase, plasma uric acid (UA), and ascorbic acid (AA)]. There were significant increases in membrane lipid peroxides in thymus (P < 0.001) and spleen (P < 0.001) in acutely exercised mice relative to controls (thymus: C = 2.74 +/- 0.80 microM; t0 = 7.45 +/- 0.48 microM; t24 = 9.44 +/-1.41 microM; spleen: C = 0.48 +/- 0.22 microM; t0 = 1.78 +/- 0.28 microM; t24 = 2. 81 +/- 0.34 microM). The thymic and splenic tissue antioxidant enzymes concentrations of superoxide dismutase and catalase were significantly lower in samples collected at t0 relative to C and t24 mice (P < 0.001). Plasma UA and AA levels were used to assess the impact of the RTE on the peripheral antioxidant pool. There was no significant change in UA levels and a significant reduction in plasma AA concentrations (P < 0.001); the reduction in plasma AA occurred at t24 (6.53 +/- 1.64 microM) relative to t0 (13.11 +/- 0. 71 microM) and C (13.26 +/- 1.2 microM). These results suggest that oxidative damage occurs in lymphoid tissues after RTE exercise and that such damage may contribute to lymphocyte damage observed after acute exercise.

Animals↗

In vitro apoptosis of lymphocytes after exposure to levels of corticosterone observed following submaximal exercise.

BACKGROUND: To evaluate the in vitro effects of corticosterone, equivalent to blood levels measured after a single submaximal treadmill exercise, on apoptosis and necrosis of mouse thymic and peripheral lymphocytes. METHODS EXPERIMENTAL DESIGN: analysis of variance with independent factors of time (0, 90, 210 minutes of incubation) and concentration of corticosterone (0, 150, 250, 450, 850 ng/ml). MEASURES: percentage of apoptotic, necrotic, and viable thymocytes and splenocytes determined by flow cytometry using Annexin V-FITC antibody and propidium iodide. RESULTS: There was a significantly higher % of apoptotic thymocytes at 210 min at the higher corticosterone concentrations but not in % of apoptotic splenocytes at the same time point. For both lymphoid populations, corticosterone incubation was associated with a higher % of necrotic cells at 210 minutes but not at 0 or 90 minutes. For thymocytes, the interaction (time x concentration) was significant, with greater % necrosis observed at the lower (150 and 250 ng/ml) concentrations of corticosterone. CONCLUSIONS: The data suggest that in vitro exposure to corticosterone, at physiological concentrations (< or = 450 ng/ml) observed after a moderate exercise stress, induces apoptosis in thymocytes and necrosis in both thymocytes and splenocytes. The implications for exercise-mediated glucocorticoid regulation of immune function remain to be investigated.

Animals↗

Possible mechanisms mediating an association between physical activity and breast cancer.

The epidemiologic, methodologic, and biologic evidence that physical activity may be related inversely to breast cancer risk was the focus of a recent workshop. This article presents the workshop summary on biologic mechanisms that may mediate this association between physical activity and breast cancer. There is some evidence that physical activity may reduce breast cancer risk, although the exact biologic pathways have not been determined. Among the potential mechanisms discussed at the workshop were reductions in endogenous steroid exposure, alterations in menstrual cycle patterns, delay of age at menarche, increased energy expenditure and reduction in body weight, changes in insulin-like and other growth factors, and enhancement of natural immune mechanisms. Although physical activity may prove to be a modifiable risk factor for breast cancer, further mechanistically oriented research is necessary to both verify whether this is the case and to clarify the details of this association so that public health recommendations can be developed.

Breast Neoplasms↗

Teaching public health practitioners about health communication: the MPH curriculum experience.

The dissemination of health information to the public often occurs through the mass media. Media strategies as a component of behavior change assume knowledge of communication theories and methods by public health practitioners. We surveyed the curricula of 52 accredited graduate programs leading to the Master's in Public Health (MPH) degree to assess their communication component. Graduate bulletins for admission year 1996 were examined for public health mission statement, goals and objectives of the MPH training program, and for course titles. Courses were identified as having a communication focus if the terms communication, information, marketing or media were used in the title. There were a total of 82 communication courses offered, with 65 courses in 26 Schools of Public Health (SPH), 13 courses in 18 Community Health and Preventive Medicine departments (CHPM), and 4 courses in 8 Community Health Education departments (CHE). The difference in mean number of health communication courses was significant by type of MPH program (p < 0.003) with SPH offering an average of 3 courses, CHPM departments offering an average of 1 course, and CHE offering an average of 0.5 course. The distribution of communication courses ranged from 10 courses to 0 courses per program. Seven SPH offered 3 or more communication courses, whereas 5 SPH offered no health communication courses in the MPH curriculum. These data point to a shortcoming in the training of MPH students in health communication theory and skills as ascertained by course titles in graduate bulletins.

Communication↗

The impact of social class on the use of cancer screening within three racial/ethnic groups in the United States.

Despite the consistent and strong association of social class with health status, the extent to which racial/ethnic disparities in cancer screening reflect social class is rarely addressed. We hypothesized that the use of cancer screening is positively correlated with social class for black, white and Hispanic Americans. Data from the 1987 and 1992 National Health Interview Survey Cancer Control Supplements were compared for each racial/ethnic group by income, education, age, and gender. For each racial/ethnic group, individuals with less education or income are less likely to be screened. Although specific subgroups increased their use of screening modalities between 1987 and 1992, older black Americans who were poor or had less education reported less screening than similar older white Americans. Although social class is a powerful explanatory variable for younger Americans, racial disparities in cancer screening persist among older black Americans.

Black or African American↗

Cancer coverage and tobacco advertising in African-American women's popular magazines.

Mass circulating magazines offer an opportunity to inform large segments of the population about preventive health behaviors relevant for cancer control. We collected information about the number and type of cancer articles from January 1987 through December 1994 in Jet, Ebony and Essence magazines. These magazines each have a principal readership of African-American women and a paid circulation of 1,000,000 or more annually. Cancer articles were counted if the content was gender neutral or specifically targeted for women. There were 84 articles on cancer including 6 on lung cancer and 3 on other tobacco-related cancers. Nine additional references to lung cancer were mentioned under the general cancer category, but lung cancer was not the primary focus of the articles. There were 24 articles on breast cancer and 9 on cervical cancer over the 8 year period. Most of the articles (> 70%) were short fillers of less than one page in length. A prevention focus was included in 42.2%, 75.0%, and 71.0% of the cancer articles in Jet, Ebony, and Essence respectively. Of the 649 health articles, 116 were on cardiovascular disease. In contrast, there were 1,477 tobacco advertisements over the 8 years. The number of cancer articles was not significantly associated with the number of tobacco advertisements. Because tobacco-related cancers are entirely preventable and contribute to the significant cancer burden, the lack of coverage of tobacco-related cancers is a missed opportunity for health promotion among African-American females.

Adult↗

Cancer coverage in women's magazines: what information are women receiving?

BACKGROUND: Women use magazines as sources of health-related information, including information about cancer. Given this reliance on magazines for cancer-related information, it may interest cancer educators to know which cancers are reported on in women's magazines and what types of information are being presented. METHODS: Four widely circulated monthly women's magazines were analyzed for their coverage of cancers during the years 1987-1995. The types of cancers discussed and the frequencies of coverage were noted for each issue of every magazine. Additionally, the content of every cancer-related article was assessed for issues in cancer prevention (primary and secondary), risks, treatment, and genetics. RESULTS: All four magazines in this study reported on breast cancer more often than any other cancer. Lung and colon cancers received very little coverage. The percentages of articles devoted to the six most-discussed cancers (breast, cervical, colon, lung, ovarian, and skin) did not reflect either the mortality rates or the incidence rates of these cancers. CONCLUSIONS: The discussions of cancers in these four women's magazines focused mostly on breast and skin cancers and neglected two very important cancers--lung and colon. If women are indeed receiving much of their cancer information from such media coverage, these findings should alert cancer educators to the possible need to work with these media to help in the dissemination of additional information about cancers to women.

Adolescent↗

Lack of colon cancer coverage in seven women's magazines.

Women's magazines are an important source of health information. To evaluate the relevancy of articles in these publications to known disease risks, seven women's magazines were reviewed to assess their coverage of colon cancer, the third leading cause of cancer mortality in U.S. women. Specifically, the amount of coverage devoted to colon cancer as well as the presentation of issues in the prevention, risks, treatment, diagnosis and genetics of colon cancer were recorded. Twenty articles were published on colon cancer in these magazines during the years 1987-1995. Compared to five other cancers that also affect women, colon cancer was the focus of the fewest articles in the seven magazines analyzed.

Colonic Neoplasms↗

Exercise and in vivo natural cytotoxicity against tumour cells of varying metastatic capacity.

Identification of modifiable risk factors which contribute to tumour metastasis is an important goal of cancer prevention research. This study was designed to evaluate the role of moderate exercise conditioning on the in vivo retention of radiolabelled H-ras-transformed fibroblasts (CIRAS 1 and CIRAS 3 cell lines) in mice with (C3H/He-bg2J/+) and without (C3H/HeJ) the beige (bg) mutation which produces impaired natural killer (NK) cell function. Mice were randomly assigned to treadmill training (20 m/min, 30 min/day, 5 times/week) or remained sedentary for 9 weeks. C3H beige mice had significantly higher retention in the lungs of CIRAS 1 tumour cells (P < 0.0001) than genotypically normal C3H/HeJ mice. There was a significant main effect of exercise conditioning (P < 0.05) with trained mice (irrespective of genotype) having lower tumour retention (44 +/- 3%) than sedentary controls (53 +/- 3%). Comparing the in vivo retention of CIRAS 1 and CIRAS 3 in the lungs of genotypically normal mice, we observed higher retention of CIRAS 1 (48 +/- 2%, compared with 18 +/- 2% for CIRAS 3; P < 0.0001). There was a significant interaction effect of exercise and tumour type (P < 0.05); trained mice had a lower retention for CIRAS 1 than sedentary controls (43 +/- 3%, compared with 53 +/- 3%), while training status had no effect on CIRAS 3 retention. There were no significant differences in final tumour multiplicity in the lung as a function of exercise condition. The data suggest that exercise conditioning reduces some measures of in vivo burden but only for the less aggressive tumour variant (CIRAS 1); further, innate immune mechanisms other than NK cells are likely to be involved in this modest protective effect.

Animals↗