Validation of dietary patterns assessed with a food-frequency questionnaire.
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Biomedical subjects
Publications and source records attributed to M Tseng.
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Gallbladder disease is a common source of morbidity in the Mexican American population. Genetic heritage has been proposed as a possible contributor, but evidence for this is limited. Because gallbladder disease has been associated with Native American heritage, genetic admixture may serve as a useful proxy for genetic susceptibility to the disease in epidemiologic studies. The objective of our study was to examine the possibility that gallbladder disease is associated with greater Native American admixture in Mexican Americans. This study used data from the Hispanic Health and Nutrition Examination Survey and was based on 1,145 Mexican Americans who underwent gallbladder ultrasonography and provided usable phenotypic information. We used the GM and KM immunoglobulin antigen system to generate estimates of admixture proportions and compared these for individuals with and without gallbladder disease. Overall, the proportionate genetic contributions from European, Native American, and African ancestries in our sample were 0.575, 0.390, and 0.035, respectively. Admixture proportions did not differ between cases and noncases: Estimates of Native American admixture for the two groups were 0.359 and 0.396, respectively, but confidence intervals for estimates overlapped. This study found no evidence for the hypothesis that greater Native American admixture proportion is associated with higher prevalence of gallbladder disease in Mexican Americans. Reasons for the finding that Native American admixture proportions did not differ between cases and noncases are discussed. Improving our understanding of the measurement, use, and limitations of genetic admixture may increase its usefulness as an epidemiologic tool as well as its potential for contributing to our understanding of disease distributions across populations.
Many women take supplemental estrogens after menopause, a practice called hormone replacement therapy (HRT). Moderate alcohol consumption may increase estrogen levels in women receiving HRT, potentially affecting their risk for various adverse health effects. Two recent studies, however, provide no strong evidence for an effect of alcohol on hormones in postmenopausal women. The possible association between alcohol consumption and risk of cancer of the breast does not appear to be mediated by estrogens. Both estrogens and moderate alcohol consumption have been associated with a decreased risk for cardiovascular disease; however, alcohol's beneficial effect on heart disease does not appear to involve hormonal mechanisms. Additional research is needed to define the consequences of moderate drinking on hormone levels after menopause.
The expression of intercellular adhesion molecule-1 (ICAM-1) on pulmonary endothelial cells after stimulus and subsequent binding of neutrophils is a first step leading to lung injury. A similar process may dictate the binding of tumor cells to the pulmonary endothelium during metastasis. We report the development of a new technique that allowed us to monitor the location and relative expression of ICAM-1 levels on the luminal surface of the pulmonary microvasculature in vivo. This technique uses intravital microscopy together with a two-step labeling procedure involving fluorescent microspheres. Constitutive expression of ICAM-1 was not detectable to a significant level by our model, but expression was observed after upregulation by the systemic administration of TNF alpha. Sprague-Dawley rats were injected with 0-5.0 micrograms/kg TNF alpha and ICAM-1 expression was monitored through 24 hr. ICAM-1 expression was related to both the dose of TNF alpha administered and the time elapsed between injection of TNF alpha and observation. Injection of 5 micrograms/kg TNF alpha caused upregulation of ICAM-1 protein expression from 0.30 +/- 2.76 binding events/175,000 microns2 to 62.6 +/- 5.48 through 4 hr observation, after which levels returned to near baseline within 24 hr. The delay required for maximal expression is likely related to the time required for the cell to respond to the stimulus and generate ICAM-1 protein. Reductions in the relative numbers of ICAM-1 protein expressed between 4 and 24 hr in vivo are likely a result of protein turnover after the initial stimulus.
Although determining iron intakes is essential in assessing adequacy of iron in the diet, estimating iron availability may be more useful for evaluating whether iron requirements are met. Our objectives were to describe the dietary information, analytical steps, and computer algorithms needed for iron bioavailability adjustments and to demonstrate the effects of various dietary factors on calculated iron absorption. Our study was based on 9890 women and children participating in the Russian Longitudinal Monitoring Survey. Between August 1992 and February 1993, two 24-h recalls were collected from each participant, and total, heme and nonheme iron intakes were calculated. Nonheme iron availability was adjusted for meat, fish and poultry and vitamin C consumed in the same meal and then further adjusted for tea and phytates. We found mean total iron intakes to be comparable to those of women of reproductive age in the United States and lower than those of United States children. When these intakes were adjusted for enhancers and inhibitors of absorption, the iron bioavailability in these vulnerable Russian groups was extremely low. Mean bioavailable iron as well as the 25th-75th percentile ranges of intake were below the bottom of the range of requirements, indicating that iron adequacy in this population may be considerably less than expected based on total iron intakes alone. Furthermore, rural and urban food availability had a significant effect on iron bioavailability. Future research on dietary iron adequacy should be based on estimates of available iron by collecting meal-level dietary data and using detailed information on mixed dishes and phytates.
Previous research suggests that iron acts as a prooxidant to increase the risk of colorectal neoplasia. This study examined effects of dietary intake of iron on colorectal adenoma recurrence using data from an antioxidant clinical trial. All subjects were free of polyps at study entry but had at least one adenoma removed within the 3 months before enrollment. Follow-up colonoscopies were conducted after 1 and 4 years. Patients who developed one or more adenomatous polyps between years 1 and 4 were classified as cases; all others were controls. Dietary iron intake at baseline and at the end of the study was estimated from self-administered food frequency questionnaires and averaged together for each subject, energy-adjusted, and categorized into quartiles. Odds ratios were adjusted for age, center, sex, calories, treatment group, and alcohol, fiber, folate, and fat intakes in unconditional logistic regression analysis. Dietary iron was inversely associated with adenoma risk, although risk did not decrease monotonically with increasing intake. Odds ratios comparing second, third, and fourth quartiles to the lowest quartile were 0.61 [95% confidence interval (CI), 0.37-1.02], 0.80 (95% CI, 0.45-1.44), and 0.37 (95% CI, 0.19-0.73), respectively. A limited examination showed no clear evidence that use of iron supplements affected risk of recurrence in this study population. This study provides evidence against the hypothesis that recent dietary intake of iron increases risk for colorectal adenomas. However, these results may reflect the presence of other dietary factors found in combination with iron.
Recent studies suggest that micronutrients, especially folate, calcium, iron, and antioxidant vitamins, affect the risk of colorectal neoplasia. The objective of this case-control study was to examine the association between these micronutrients and the risk of colorectal adenomas. The study was based on 236 cases with adenomatous polyps or cancer and 409 controls, all colonoscopy patients at University of North Carolina Hospitals between July 1988 and March 1991. After colonoscopy, subjects were interviewed using a semi-quantitative food frequency questionnaire, and average daily nutrient intakes were calculated. Sex-specific odds ratios relative to the lowest quartile of intake for each micronutrient were determined using unconditional logistic regression while adjusting for a number of potential confounders. In women, folate, iron, and vitamin C were inversely related to the risk of adenomas. Folate appeared to be most protective, with women in the highest quartile only 40% as likely to develop adenomas compared with women in the lowest (odds ratio = 0.39, 95% confidence interval 0.15-1.01). In men, greater vitamin E and calcium intakes were associated with reduced risk of adenomas, with vitamin E showing the strongest inverse association. Men in the highest vitamin E quartile had a risk of 0.35 (95% confidence interval 0.14-0.92) relative to those in the lowest. These study results support previous research findings that selected micronutrients protect against colorectal neoplasia.
Transient global ischemia was used to produce a rat model of generalized tonic-clonic epilepsy. Controlled chest compression in ketamine-anesthesized Long-Evans rats produced transient global ischemia by mechanically preventing the heart from pumping blood. Circulation was restored by standard cardiopulmonary resuscitation techniques. With a temporal muscle (skull) temperature of 35 +/- 0.4 degrees C, 75% (76/102) of the rats survived 7 min of chest compression. Generalized seizures could be evoked in 78% (59/76) of the surviving rats by a 60 s exposure to a loud sound (bell, 110 dB) beginning 24 h after the ischemic episode. The seizure patterns seen resembled those described by Maresceaux (1987) for genetically seizure-prone Wistar rats. Susceptibility to sound-induced seizures declined with time, with wide variations in recovery rate between individuals; one rat showed a daily sound-induced seizure for over 5 months. Seizures were attenuated or blocked by treatment with carbamazepine or sodium valproate. This model is similar to the great vessel occlusion model used by Kawai et al. (1995), but is less invasive. We believe it will be useful in the evaluation of therapies for acquired generalized (grand mal) seizures.
Isolated abdominal wall recurrence, following resection of a primary large bowel adenocarcinoma, is an infrequent finding. Over a ten year period, 22 patients were submitted to en bloc resection of such localized neoplastic foci. In 13 cases, recurrent tumor was located in a previous midline or para median incision. Nine patients underwent palliative radiotherapy and/or chemotherapy once the recurrent disease was identified, and were operated on when uncontrolled progression was clinically evident. In all cases, 4-5 cm disease-free margins were obtained. In eight patients it was possible to close the defect primarily and 14 patients required marlex mesh. Twelve patients were alive at two years and ten patients at five-years follow-up mark. Mucin-producing or poorly differentiated adenocarcinoma had the worse prognosis. Synthetic prosthesis allowed for adequate resections with little morbidity and acceptable cosmesis. Symptomatic relief and long-term palliation can be achieved with aggressive surgery. The role of adjuvant chemotherapy and radiation therapy still needs to be evaluated. The aggressiveness of poorly differentiated and the mucin producing adenocarcinoma should temper radical surgical exercises.
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A medium composed of blood agar base (40 g/liter), yeast extract (5 g/liter), and cysteine hydrochloride (0.05 g/liter), completely filling screw-cap tubes (13 by 100 mm), can keep Bacteroides species alive for at least 10 months without refrigeration.