Biomedical subjects

L Hoffman-Goetz

Publications and source records attributed to L Hoffman-Goetz.

At least 19 recordsLinked to original sources

PubMed2006

Health literacy and the World Wide Web: comparing the readability of leading incident cancers on the Internet.

PRIMARY OBJECTIVE: to assess the readability level of Web-based information on leading incident cancers. RESEARCH DESIGN: websites on breast, prostate, and colorectal cancers were selected for analysis by comparing the first 100 hits across 10 popular search engines. A total of 100 websites on breast (n=33), prostate (n=34), and colorectal (n=33) cancers were included in the final analysis. METHODS: readability was assessed using SMOG, Flesch-Kincaid (F - K), and Flesch Reading Ease (FRE) measures. SMOG was hand-calculated on 10 - 30 lines of continuous text. Identical text was entered into Microsoft Word 2002 where F - K and FRE scores were determined automatically by the word processor. RESULTS: the mean readability score of the cancer websites was Grade 12.9 using SMOG and Grade 10.7 according to F - K. The mean FRE score was 45.3, a score considered 'difficult'. Colorectal cancer websites were most difficult to read compared to breast and prostate cancer websites. All measures indicated that prostate cancer websites were written at the lowest readability. Significantly higher reading levels were required for concluding paragraphs of Web articles compared to introduction paragraphs. CONCLUSIONS: findings suggest the need for readable cancer information on the Web. Health promoters, health informaticians, medical journalists, and web page editors must collaborate to ensure the use of plain language to match the literacy skills of consumers.

Adult↗

PubMed2006

Long-duration freewheel running and submandibular lymphocyte response to forced exercise in older mice.

Submandibular lymph nodes (SLN) are crucial for immune surveillance of the anterior ocular chamber and upper respiratory tract; little is known about how training and exercise affect SLN lymphocytes. The intent of this study was to describe the impact of long term freewheel running followed by acute strenuous exercise on SLN lymphocytes in mice. Female C57BL/6 mice were assigned to running wheels or remained sedentary for 8 months, and further randomized to treadmill exercise and sacrifice immediately, treadmill exercise and sacrifice 24 h after exercise cessation, or no treadmill exposure. SLN lymphocytes were isolated and analyzed for CD3, CD4, CD8, and CD19 cell surface markers, phosphatidylserine externalization as a marker of apoptosis, and intracellular glutathione as a marker of oxidative stress. Compared with running wheel mice, older sedentary mice had a lower percent of T cells and higher percent of B cells (p < 0.05). Although intracellular glutathione did not differ between groups, running mice had a lower percent of Annexin V(+) SLN lymphocytes 24 h after treadmill exercise. Further research will be needed to determine if voluntary exercise translates into improved anterior ocular and upper respiratory tract health.

Animals↗

PubMed2005

Freewheel running selectively prevents mouse CD4+ intestinal lymphocyte death produced after a bout of acute strenuous exercise.

Aerobic exercise increases oxidant stress and leads to apoptosis of mouse intestinal lymphocytes (IL). The purpose of this study was to determine whether freewheel running prevents IL loss 24 h after a bout of strenuous exercise. Mice were randomly assigned to in-cage running wheels with 24 h access (WR) or individual cages without running wheels (NR) for 4 months. WR mice accumulated 364 km over 4 months and had higher cytochrome oxidase activity in the plantaris (p < .05), indicative of training. Total intestinal, CD3alphabeta, CD3gammadelta, CD8alpha, and CD8beta lymphocytes and intracellular glutathione were significantly lower in WR and NR mice 24 h post-exercise. The number of CD4 IL decreased 24 h after exercise in NR (p < .01) but not in WR mice relative to their respective no exercise controls. Thus, freewheel running in mice for 4 months prevented CD4 IL loss after acute exercise.

Analysis of Variance↗

PubMed2005

Intravenous catecholamine administration affects mouse intestinal lymphocyte number and apoptosis.

The purposes of this study were to determine plasma and intestinal epinephrine (E) and norepinephrine (NE) concentrations in mice after exercise stress and, the effect of intravenous injection of E and NE (at concentrations during exercise) on viability of intestinal lymphocytes (IL). Exhaustive exercise significantly elevated plasma E and NE, and intestinal E, compared with sedentary animals. Twenty-four hours after intravenous NE administration, IL counts were higher (p<0.001) and % apoptotic IL were lower (p<0.001) than saline conditions. E resulted in fewer apoptotic IL at 24 h compared to saline controls. E and NE differentially influence IL numbers at 24 h after injection although both result in fewer % apoptotic IL relative to mice given saline only.

Animals↗

PubMed2005

In vivo corticosterone administration at levels occurring with intense exercise does not induce intestinal lymphocyte apoptosis in mice.

Intestinal lymphocyte apoptosis can occur following physiological and pathophysiological stress as well as exhaustive exercise. In this study we investigated whether corticosterone (CORT) administration at physiological concentrations observed following strenuous exercise induces intestinal lymphocyte apoptosis and cell loss in mice. CORT injection (14 mg/kg; i.p.) caused a four-fold increase in plasma CORT concentrations, but did not affect intestinal lymphocyte cell loss or alter baseline intestinal lymphocyte apoptosis, as measured by phosphatidylserine externalization, cell viability, mitochondrial membrane depolarization, caspase 3, Bcl-2 and cytosolic cytochrome c protein levels. These findings indicate that CORT at levels observed following strenuous exercise is not involved in intestinal lymphocyte apoptosis and cell loss.

Acetylcysteine↗

PubMed2005

Ethnicity, genetics, and breast cancer: media portrayal of disease identities.

OBJECTIVE: To describe, compare, and analyze how the risk of breast cancer is framed in newspapers directed towards an ethnic minority population (Jewish) with higher risk of inherited breast cancer compared with newspaper coverage for the general population (Anglo-Canadian) without this risk. DESIGN: This investigation utilized a mixed methods (quantitative and qualitative) approach. The design emphasized a content analysis conducted on ethnically specific and non-ethnic newspaper articles. RESULTS: It is noteworthy that the 'Jewish' newspapers devote a substantially larger proportion of articles on breast cancer to genetic risk as the key risk factor for this disease. Articles in the Jewish newspapers tend to link being a Jewish woman with being at risk for a diagnosis of breast cancer. This ethnic 'identity' is reinforced through the repeated association of Jewish heritage and genetic breast cancer risk at the exclusion of other known risk factors. This isolated genetic link to breast cancer is not a message that is replicated within the provincial newsprint articles. CONCLUSIONS: These findings assist in the facilitation of prevention and treatment of those with or at risk of breast cancer. The health policy implications of this portrayal as well as suggestions for change are considered.

Breast Neoplasms↗

PubMed2005

Polyethylene glycol but not mifepristone prevents intestinal lymphocyte loss following treadmill exercise in mice.

UNLABELLED: Circulating lymphocyte numbers decrease following intense physical activity, possibly due to exercise-induced apoptosis. Increased reactive oxygen species (ROS) and glucocorticoids (GC) following exercise contribute to lymphocyte apoptosis. Intestinal lymphocyte (IL) numbers also decrease following exercise. AIM: The purpose of this study was to determine the contribution of GC to exercise-induced IL loss. METHODS: Female C57BL/6 mice (n = 178) were randomized to five drug conditions: (1) single injection of the glucocorticoid receptor antagonist mifepristone (MIF) solubilized in polyethylene glycol (PEG); (2) three injections of MIF (repeated MIF) PEG; (3) single injection of PEG (PEG); (4) three injections of PEG (repeated PEG); or (5) repeated injections of saline (SAL). Within each drug group mice were further randomized to exercise conditions: (1) control condition (non-exercised); (2) treadmill running with sacrifice immediately following the exercise; or (3) treadmill running with sacrifice 24 h after completion of the exercise. RESULTS: There was a significant exercise effect, across all T lymphocyte subsets, in SAL (P < 0.01), PEG (P < 0.01) and MIF (P < 0.01) treated mice but not in mice given repeated PEG or repeated MIF exposure. The exercise effect was due to reduced IL numbers 24 h post-exercise compared with non-exercised controls. CONCLUSION: These results suggest that GC are not directly responsible for IL cell loss following exercise. Repeated exposure to PEG may confer protection in the gastrointestinal tract from exercise-induced lymphocyte depletion. Because PEG inhibits ROS generation in experimental cell injury, the mechanisms for IL loss after exercise may involve oxidative stress.

Animals↗

PubMed2004

N-Acetyl-L-cysteine prevents exercise-induced intestinal lymphocyte apoptosis by maintaining intracellular glutathione levels and reducing mitochondrial membrane depolarization.

Intense exercise leads to post-exercise lymphocytopenia and immunosuppression, possibly by triggering lymphocyte apoptosis. To test the role of oxidative stress on exercise-induced lymphocyte apoptosis, we administered the antioxidant N-acetyl--cysteine (NAC) and measured apoptosis in intestinal lymphocytes (IL) from exhaustively exercised animals. Eighty-seven female C57BL/6 mice were randomly assigned to receive NAC (1 g/kg) or saline 30 min prior to treadmill exercise for 90 min at 2degrees slope (30 min at 22 m min(-1), 30 min at 25 m min(-1), and 30 min at 28 m min(-1)) and sacrificed immediately (Imm) or 24 hours (24 h) after cessation of exercise. Control mice (nonexercised) were exposed to treadmill noise and vibration without running. Exercise increased IL phosphatidylserine externalization (p<0.001), mitochondrial membrane depolarization (p<0.05), and decreased intracellular glutathione concentrations (p<0.05) immediately following exercise in saline relative to nonexercised mice. At 24 h post-exercise, saline injected mice had fewer total (p<0.001) and CD3+ (p<0.005) IL compared to nonexercised animals. NAC injection in mice maintained intracellular glutathione levels, prevented phosphatidylserine externalization, mitochondrial membrane depolarization, and loss of IL immediately and 24 h after exercise. These data suggest that lymphocyte apoptosis precedes post-exercise lymphocytopenia and may be due to oxidative stress.

Acetylcysteine↗

PubMed2004

Beta-adrenergic receptor blockade during exercise decreases intestinal lymphocyte apoptosis but not cell loss in mice.

Catecholamines induce apoptosis in various lymphoid populations. This process can occur with both alpha- and beta-adrenoreceptors. Heavy exercise increases plasma catecholamine concentrations, and is also a cause of lymphocyte apoptosis, a possible explanation for postexercise lymphocytopenia. The purpose of this study was to examine the effects of adrenoreceptor antagonism on exercise-induced decreases and apoptosis of intestinal lymphocytes. Mice received an intraperitoneal injection of phentolamine (a nonselective alpha-blocker), nadolol (a nonselective beta-blocker), or saline (vehicle) prior to an exhaustive bout of exercise. Total intestinal lymphocyte numbers, percent and number of CD3+ lymphocytes, and cell viability were assessed. Neither alpha- nor beta-antagonism prevented exercise-induced cell loss in the intestine; however, pretreatment with nadolol significantly reduced the number of apoptotic and necrotic cells. Phentolamine administration appeared to increase the incidence of cell death among intestinal lymphocytes. Both drugs decreased the percentage of CD3+ intestinal lymphocytes. Our study suggests that catecholamines are not responsible for postexercise lymphocytopenia, but beta-adrenoceptor blockade may confer protection against exercise-induced apoptosis of intestinal lymphocytes.

Adrenergic Antagonists↗

PubMed2004

Adrenalectomy in mice does not prevent loss of intestinal lymphocytes after exercise.

Exhaustive exercise is associated with an increase in circulating glucocorticoids (GCs), lymphocyte apoptosis, and a reduction in intestinal lymphocyte number. The present study examined the role of GCs on the numerical changes seen in intestinal lymphocytes after exercise. Female C57BL/6 mice were bilaterally adrenalectomized (ADX; n = 18) or given sham surgery (Sham; n = 18) and assigned to one of three exercise conditions: treadmill running (28 m/min, 90 min, 2 degrees slope) and killed immediately or after 24 h recovery, or not exercised and killed immediately after 90-min exposure to the treadmill environment. Lymphocytes were isolated from the intestines with CD45(+) cells collected by positive selection using magnetic bead separation columns, and lymphocyte subpopulations were analyzed by flow cytometry for CD45(+), CD3alphabeta(+), CD3gammadelta(+), CD8beta(+), CD8alpha(+), CD4(+), and NK(+) phenotypic markers. ADX mice had significantly more intestinal CD45(+) leukocytes (P < 0.05) and CD3alphabeta(+) (P < 0.05), CD3gammadelta(+) (P < 0.01), CD8alpha(+) (P < 0.001), and NK(+) (P < 0.05) intestinal lymphocytes than Sham mice. There was a significant effect of exercise condition on total intestinal CD45(+) leukocytes (P < 0.01) and CD3alphabeta(+) (P < 0.05), CD8alpha(+) (P < 0.001), and CD4(+) (P < 0.05) intestinal lymphocytes, with fewer cells at 24 h postexercise compared with the other treatment conditions. There were no surgical x exercise interaction effects on the CD3 and CD8 phenotype numbers. Plasma corticosterone was virtually nil in ADX mice regardless of exercise condition but was significantly elevated in Sham mice immediately postexercise (P < 0.001). The data indicate that ADX does not prevent the loss of lymphocytes from the intestinal mucosa 24 h after strenuous exercise and GCs are not directly causal in the leukopenia of exercise.

Adrenalectomy↗

PubMed2004

Portrayal of genetic risk for breast cancer in ethnic and non-ethnic newspapers.

There has been enormous attention paid to the genetics of breast cancer in this era of genomic medicine. A great deal of the interest has been generated through discourse in the public mass media. However, genetic risk is a probabilistic concept and one that requires adequate numeracy skills. The purpose of this qualitative content analysis was to describe and evaluate the portrayal of genetic risk for breast cancer in mass print media. Mass print newspapers targeting high (Ashkenazi Jews) and low (general Canadian population) genetic risk audiences and published at least monthly, available in English and accessible through public archives at the National Library of Canada, were identified and hand searched for articles on breast cancer. Approximately 47% of breast cancer articles in 6 Jewish newspapers and published between 1996-2000 identified genetics in the title, first or last paragraph compared with 17% of 145 articles in 6 provincial newspapers published in 2000. The description of breast cancer risk was equally problematic in print media targeting high and low risk audiences. Statistics were presented in complex and contradictory ways, with, for example, the confounding of individual and population based risk estimates. Inconsistent messages about the value of genetic screening for breast cancer characterized articles in both ethnic and non-ethnic newspapers. Deciphering the information into a comprehensible form is likely challenging, particularly in light of widespread numeric-literacy limitations. The publication of discrepant research findings and the perplexing statistical information consequently brought into question the credibility of the scientific process and the recommendations of health care professionals.

Bibliometrics↗

PubMed2004

The effect of chronic and acute exercise on thymocyte apoptosis and necrosis in ovariectomized mice given dietary genistein.

AIM: At menopause, many women consume phytoestrogens instead of beginning hormone replacement therapy. Many also start exercise programs for health benefits. Genistein, a soy isoflavone with estrogen-like properties, induces lymphocyte apoptosis in vitro. Aerobic exercise also induces apoptosis in lymphoid cells. The present study was designed to determine the effect of chronic (wheel running, WR) and acute (treadmill) exercise on in vivo apoptosis of thymocytes using an animal model of menopause with supplementation from dietary genistein. METHODS: Using a randomized design, 99 ovariectomized B6D2F1 mice were fed 250 (GEN) or 0 (C) ppm genistein and given concurrent exercise (voluntary wheel running-WR; or WR followed by a bout of high intensity treadmill running-WR+TREAD) or remained sedentary (SED). After 21 days, mice were sacrificed for measurements of body weights, tissue weights, thymocyte apoptosis and necrosis by annexin-V FITC and propidium iodide staining and flow cytometry, DNA fragmentation by ELISA, and plasma estrogen concentrations by RIA. RESULTS: WR+TREAD mice had lower percentages of viable and higher percentages of apoptotic and necrotic cells from thymus compared with SED or WR conditions (p<0.001). WR resulted in greater DNA fragmentation in thymus cell lysates than in samples from SED mice (p<0.005). There were no differences in thymocyte apoptosis or DNA fragmentation between GEN and C mice, either independently or interactively with exercise. GEN mice tended to have greater wheel running activity than C mice (0.05<p<0.09, depending on day). CONCLUSIONS: These findings suggest that 1) intense aerobic exercise increases the percentage of early apoptotic cells in the thymus and 2) dietary genistein is associated with a small increase in voluntary wheel running activity in ovariectomized mice.

Animals↗

PubMed2003

Treadmill exercise in mice increases intestinal lymphocyte loss via apoptosis.

UNLABELLED: Strenuous exercise is associated with a transient decline in circulating lymphocytes, possibly through increased apoptosis. Intestinal lymphocytes are important effector cells of intestinal immune function but have not been studied in relation to exercise. AIM: The purpose of the present study was to examine the effect of exercise on intestinal lymphocyte phenotypes and apoptosis. METHODS: Female C57BL/6 mice (n = 112) were randomized to: (1) treadmill running (90 min, 32 m min-1, 8 degrees grade) and killed immediately after exercise, (2) treadmill running and killed 2 h after exercise, (3) treadmill running and killed 24 h after exercise or (4) a non-exercised control condition with exposure to treadmill noise and vibration without running. RESULTS: Flow cytometry indicated that the total intestinal CD3+T (P < 0.01), CD4+T (P < 0.005), CD8+T (P < 0.05), pan-NK (P < 0.005) and CD19+B (P < 0.05) lymphocytes were significantly lower 24 h after exercise compared with non-exercised controls. Significantly more CD3+T (P < 0.05) and CD8+T (P < 0.05) intestinal lymphocytes stained positive for annexin V, a marker of apoptosis, at 24 h after exercise compared with intestinal lymphocytes from non-exercised controls. Plasma corticosterone and 8-isoprostane concentrations were also significantly higher immediately after exercise compared with other exercise conditions. CONCLUSION: Acute strenuous exercise increases intestinal T (CD3+ and CD8+) lymphocyte loss and apoptosis. The extent to which the exercise-induced apoptosis in intestinal lymphocytes is mediated by increased glucocorticoid concentrations in the gastrointestinal tract will require further studies.

Animals↗

PubMed2003

Lymphocyte distribution in mouse submandibular lymph nodes in response to acute treadmill exercise.

The submandibular lymph nodes (LN), part of the nasal-associated lymphoid tissue (NALT), are involved in local immune responses in the eye, upper respiratory tract (URT), and oral mucosa. Although athletes have been reported to be at increased risk for URT and ocular infections, little is known about the impact of exercise on LN included in the NALT. The purpose of this study was to examine the impact of intense acute exercise on submandibular lymphocyte distribution. Female C57BL/6 mice were randomly assigned to a nonexercised control condition or a single session of treadmill exercise (32 m.min-1, 8 degrees grade for 90 min) and sacrificed immediately, 2, and 24 h after exercise. Running resulted in a significant increase in plasma corticosterone immediately following exercise compared with other times (p < 0.001). Percentages and total numbers of CD3+ and CD4+CD8- T lymphocytes in submandibular LN were significantly lower 24 h after exercise compared with controls. The percentage of pan-NK and CD19+ B cells increased immediately and 24 h after exercise, respectively, but the total numbers were not affected. The results suggest that decreased percentages and absolute numbers of T cells in submandibular LN following a single session of intense exercise may be partially mediated by increased corticosterone concentrations and may have consequences for ocular health among athletes.

Animals↗

PubMed2003

Physical activity and colon cancer. A systematic review of potential mechanisms.

Colorectal cancer is a multifactorial disease, with complex interactions between genetic and environmental factors. Physical activity has been shown to have a significant inverse relationship with colon cancer risk. Studies in experimental animals suggest that physical activity is protective in chemical carcinogenesis in the colon. Various mechanisms for this protective effect have been extensively cited throughout the literature, although few have been empirically tested. The purpose of this review was to review the published evidence on physical activity and the hypothesized mechanisms. A systematic review of the literature was conducted using the Medline database from 1970-2002, using the terms "colorectal cancer, colon cancer, neoplasm, carcinoma, exercise, fitness, and physical activity". This yielded 330 articles of which 23 review articles were searched for proposed mechanisms of this association. Following identification of possible mechanisms, additional searches were conducted to identify empirical studies in the exercise literature examining these mechanisms. These mechanisms include changes in gastrointestinal transit time, altered immune function and prostaglandin levels as well as changes in insulin levels, insulin-like growth factors, bile acid secretion, serum cholesterol and gastrointestinal and pancreatic hormone profiles. There is currently little empirical data to support any of the hypothesized biological mechanisms for the protective effect of exercise on colon cancer. Moreover, it is likely that no one mechanism is responsible for the risk reduction observed in epidemiological and animal studies and, therefore, the observed benefits of physical activity in colon cancer may be a combination of these and other factors. A greater understanding of the biological mechanisms involved will be an important step in developing exercise prescriptions targeted to reduce the burden of colon cancer across different populations.

Animals↗

PubMed2002

Effects of oestrogen and exercise on caspase-3 activity in primary and secondary lymphoid compartments in ovariectomized mice.

UNLABELLED: This study investigated the effect of oestrogen exposure and exercise on caspase-3 activity, a measure of apoptosis, in lymphocytes from the thymus, spleen, and lymph nodes in ovariectomized mice. Fifty-nine female B6D2F1 mice were randomized to hormone and exercise conditions. Hormone treatment consisted of implantation with oestradiol pellets (0.72 mg oestradiol) or placebo pellets (0 mg) for 21 days following bilateral ovariectomy (OVX). Exercise consisted of a single treadmill exercise bout (26 m min(-1), 6 degrees slope, 90-min) or sedentary condition. Mice were killed and the thymus, spleen and lymph nodes were removed for the determination of caspase-3 expression by enzyme-linked immunosorbent assay (ELISA), serum oestrogen levels by RIA, and tissue weights. Body weights were monitored throughout the study. In the thymus, oestrogen exposure, exercise and both treatments together were associated with higher caspase-3 activity (P < 0.05) and lower thymus weights (P < 0.05). In contrast, oestrogen exposure and exercise treatment were not associated with greater caspase-3 activity or change in tissue weight in secondary lymphoid tissues (spleen, lymph nodes). Oestrogen-replaced OVX mice had a higher concentration of plasma oestradiol than placebo OVX mice (P < 0.05). CONCLUSION: The results suggest that oestrogen and treadmill exercise are associated with greater apoptosis, as measured by caspase-3 activity, in the thymus but not in the spleen or lymph nodes. Clinical studies will be necessary to determine if women who take oestrogen have higher rates of apoptosis in primary lymphoid tissues and the significance of thymocyte apoptosis for maintenance of cellular immune function during the post-menopausal years.

Animals↗

PubMed2002

Lymphocyte apoptosis in ovariectomized mice given progesterone and voluntary exercise.

BACKGROUND: At menopause, many women begin both exercise programs and hormone replacement therapy (HRT). Although the effects of estrogen on exercise behavior and immune functions have been well characterized, less is known about the behavioral and immunological consequences of progesterone (P) administration. The purpose of the present study was to describe the effect of P on running behavior and on lymphoid tissue cell viability and apoptosis in ovariectomized female mice. METHODS: Adult female B6D2F1 mice were ovariectomized, allowed to recover for 1 week and implanted subcutaneously with 25 mg progesterone (n=42) or placebo pellet (n=42). Within hormone treatment, mice were randomized to running wheels or no running wheel conditions. After 21 days of wheel running and hormone exposure, mice were sacrificed for measurements of body weight, tissue weights, and thymocyte and splenocyte apoptosis, necrosis and viability with annexin-V FITC and propidium iodide by flow cytometry. RESULTS: P treated mice were heavier than placebo controls at sacrifice (p<0.001). Irrespective of hormone condition, mice increased the volume of spontaneous activity over time (p<0.001). Within the thymus, there were no differences by hormone or running condition on percent apoptosis, necrosis and viability. In the spleen, P marginally increased percent apoptosis (p<0.05) and reduced percent viability (p<0.001). Serum levels of P were higher in the hormone replaced mice compared with placebo mice (p<0.001) and in running compared with sedentary mice (p<0.01). CONCLUSIONS: P replacement in ovariectomized mice does not alter running volume relative to placebo animals. P alone was associated with a small increase in splenocyte apoptosis. The clinical relevance for postmenopausal women of lymphocyte viability changes needs to be determined.

Animals↗

PubMed2001

17 beta-estradiol increases Ca(2+) influx and down regulates interleukin-2 receptor in mouse thymocytes.

The influx of Ca(2+) across the T lymphocyte membrane is an essential triggering signal for activation and proliferation by an antigen. The aim of this study was to determine if Ca(2+) influx through estradiol receptor (ER) operated channels of Ca(2+) entry induced activation of lymphoid cells. Mouse thymocytes were incubated with 17 beta-estradiol (E) and in the presence or absence of the mitogen, phytohemagglutinin (PHA). Despite evidence of an enhanced binding of E to ER on thymocyte membranes, and an E dose-related influx of Ca(2+), there was a consistent down regulation of IL-2 receptor expression (P < 0.001). Incubation of thymocytes with PHA enhanced IL-2 receptor expression although the down regulatory effect of E was still evident. The results suggest that the Ca(2+) channel activated by E may have a down regulatory effect on the IL-2 receptor in thymus cells leading to the dampening of cell activation process.

Animals↗