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H W Lane

Publications and source records attributed to H W Lane.

At least 55 records · Page 3Linked to original sources

Factors influencing duration of breast feeding among low-income women.

Forty low-income breast feeding primiparous women were interviewed to determine whether family member and peer attitudes toward breast feeding and available postpartum support were associated with continued or early termination of breast feeding. Mean breast feeding duration equalled 20.5 weeks (range, 1 to 52 weeks). When an outside source of assistance (a doula) was available during the first 2 weeks postpartum, mean duration was 23.4 weeks compared with 12.3 weeks when a doula was unavailable (p less than .05). Breast feeding duration was independent of the doula's attitude regarding breast feeding. Duration of breast feeding was significantly longer for breast feeding women who participated in the USDA Special Supplemental Program for Women, Infants, and Children (WIC) than for those who did not participate. All of the women claimed to like breast feeding; 93% of the husbands or boyfriends, 83% of the women's mothers, and 81% of the women's best friends had positive attitudes toward breast feeding. The more breast feeding friends the woman had, the longer she breast fed (r = .32, p less than .05). Termination of breast feeding was not due to perceived negative attitudes of family members and peers regarding breast feeding.

Adolescent↗

Breast cancer: incidence, nutritional concerns, and treatment approaches.

Breast cancer is the leading cause of cancer death in women in the United States. Western cultural factors, such as high socioeconomic status, early age of menarche, and late age at first pregnancy, may be risk factors in the development of breast cancer. A strong positive correlation exists worldwide between fat consumption and breast cancer. Case-controlled studies also support an association of a high-fat diet and breast cancer. Animal studies using rats or mice have verified that fat is a promoter of breast cancer after exposure to a known chemical carcinogen. A high-fat diet resulted in a higher incidence of breast tumors than a low-fat diet. Recent rodent studies further suggest that a reduction in calories alone reduces breast cancer incidence. Furthermore, studies reveal that the 5-year survival is about 80% after appropriate therapy (surgery, radiation, and/or chemotherapy) for breast cancer, with early detection by self-examination as the first step to improve outcomes. Excision of the breast tumor (segmental mastectomy) and some surrounding normal tissue followed by radiation therapy can be as effective therapy for most small breast cancers as total or radical mastectomy. The authors strongly recommend obtaining medical evaluation for any lump or thickening in the breast and following good dietary practices.

Animals↗

The role of high levels of dietary fat in 7,12-dimethylbenzanthracene-induced mouse mammary tumorigenesis: lack of an effect on lipid peroxidation.

The effects of dietary fat on 7,12-dimethylbenzanthracene (DMBA)-induced mammary tumorigenesis were examined in BALB/c female mice. In the first experiment, BALB/c mice were treated with a total dose of 1, 3, or 6 mg DMBA to induce mammary tumors. One week after the last dose of DMBA, the mice were placed on a 5% (LF) or 20% (HF) corn oil semi-purified diet. The 20% corn oil diet resulted in a significantly decreased mean tumor latency period in each of the three groups of mice (p less than 0.05). However, the mammary tumor incidences at 11 months after DMBA treatment were the following: 6 mg DMBA (LF-14/32, HF-17/32); 3 mg DMBA (LF-13/50, HF-14/50); 1 mg (LF-2/50, HF-6/50). In the second experiment, prolonged hormonal stimulation by pituitary isografts, but not a HF diet, enhanced the incidence of mammary tumors in BALB/c mice given a threshold dose of DMBA (0.5 mg). In a further attempt to examine the mechanism of the enhancing effects of dietary fat, lipid peroxidation was measured in the microsomal-mitochondrial fractions of the mammary glands by two assays; measurements of conjugated dienes and TBA reactants (malonyldialdehyde). The high fat diet had no effect on the levels of conjugated dienes in mammary cell membrane preparations and decreased the levels of TBA reactants (malonyldialdehyde). The results indicated that a high fat diet did not lead to enhanced levels of lipid peroxidation in preparations of microsomal mitochondrial membranes from mouse mammary glands. The implications of these results are discussed with respect to the role of dietary fat as a promoter of mouse mammary tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗

Mode of action of selenium inhibition of 7,12-dimethylbenz[a]anthracene-induced mouse mammary tumorigenesis.

Possible mechanisms for the inhibitory effect of selenium on mouse mammary gland tumorigenesis were evaluated in two different mouse models, in 7,12-dimethylbenz[a]anthracene [(DMBA) CAS:57-97-6]treated and hormonally stimulated mammary glands with two dietary levels of Se (0.2 and 2.0 ppm). In (C57BL X DBA/2f)F1 (BD2F1) and BALB/c strains of female mice, Se at 2.0 ppm decreased mammary tumor incidences by 36 and 68%, respectively. Selenium-dependent glutathione peroxidase (GSH-Px) activity in the mammary glands of BD2F1 female mice decreased at 6 months of age and then increased to the highest levels at 9 months of age. Mammary glands from DMBA-treated mice had lower GSH-Px activity than those from control mice. The increase of dietary Se to 2.0 ppm did not overcome this DMBA effect. These results indicate that GSH-Px activity does not correlate with the tumorigenic inhibitory effects of Se. In the hormonally stimulated mammary gland, increasing dietary Se to 2.0 ppm increased GSH-Px activity threefold and decreased mammary-gland-membrane-localized lipid peroxidation by 16%. In vitro peroxidation of hormonally stimulated mammary glands was inversely proportional to the level of GSH present in the incubation mixture. The marginal decrease in lipid peroxidation found in the mammary glands exposed to 2.0 ppm Se could not explain the inhibitory effect of Se on tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗

Growth, reproduction rates and mammary gland selenium concentration and glutathione-peroxidase activity of BALB/c female mice fed two dietary levels of selenium.

This research was designed to determine the effect of various levels of dietary selenium on growth of BALB/c female mice. The selenium concentration and glutathione peroxidase (GSH-Px) activity in different developmental stages of the mammary gland was determined in the female mice fed 0.03 and 1.5 ppm Se. The development stages studied were: virgin (at 20 and 26 weeks of age), pregnant, lactating and involuted mammary gland. Also, the effect of the two levels of dietary selenium (0.03 and 1.5 ppm Se) on second generation reproductive rates were determined. There was no effect of dietary selenium (0.03, 0.20 or 2.00 ppm Se) on the growth rate of the mice except during pregnancy. The pregnant mice fed the 1.5 ppm Se diet had a greater growth rate than the mice fed the 0.03 ppm diet. Selenium levels in the mammary glands were higher in mice fed the 1.5 ppm Se diet than those fed the 0.03 p]pm Se diet. However, only in the mice with the highest growth rate, 10-week-old virgins, pregnant and lactating mice, was there an effect of dietary selenium on mammary gland GSH-Px activity. The reproductive rates for the second generation mice fed the two diets were similar to rates of mice fed stock diet. When both mating pairs (male and female) consumed the 0.03 ppm Se diet, the reproductive rates were lower than all other mating pairs. Thus, two conclusions can be made from these studies. First, as measured by growth and reproductive capabilities there were no signs of toxicity in mice fed the 1.5-2.0 ppm Se diet. Secondly, the differentiative states of the mammary gland influenced the selenium requirement for GSH-Px activity

Aging↗

Selenium and glutathione peroxidase levels in patients with epidermoid carcinoma of the oral cavity and oropharynx.

Selenium ingestion may inhibit carcinogenesis. Epidemiologic studies have shown that age-adjusted death rates for cancer at most head and neck sites are lower in states where the soil and forage crops contain higher levels of selenium. The mode of action is incompletely understood, but may be mediated through an increase in the activity of the selenium dependent, antioxidant enzyme glutathione peroxidase (GSH-Px). The authors studied blood selenium levels and blood and tissue GSH-Px activities in 50 patients with untreated cancer of the oral cavity and oropharynx. Mean erythrocyte selenium and glutathione peroxidase were significantly depressed when compared to age-matched controls. Mean plasma selenium, on the other hand, was significantly elevated in the cancer patient group. Data from subsets within the cancer patient group were also discussed. GSH-Px activity did not differ in tumor and adjacent normal tissue. The concept of chemoprevention of carcinogenesis with inhibitory chemical compounds is particularly apropos to head and neck cancer control. Further work is indicated to determine if ingestion of supplemental selenium corrects the abnormalities identified here, and what affect, if any, this would have on the development and behavior of squamous cell cancers in the upper aerodigestive tract.

Aged↗

Effect of dietary selenium levels on 7,12-dimethylbenzanthracene-induced mouse mammary tumorigenesis.

The effect of dietary selenium levels on 7,12-dimethylbenzanthracene (DMBA)-induced mammary tumors was examined in mice fed a semi-purified diet (20% casein, 50% sucrose, 5% corn oil). (C57BLxDBA/2f)F1 (BD2F1) female mice were fed diets containing 0.2, 0.5, 1.0 and 2.0 p.p.m. selenium starting at 7 weeks of age. The mammary tumor incidence was 56, 30, 25 and 16%, respectively, after the mice were on the diet for 9 months. In a second experiment, BALB/cV female mice were fed diets containing 0.2 and 2.0 p.p.m. selenium. After 9 months on the diet, the mammary tumor incidence was 39 and 7%, respectively. Both strains of mice grew equally well on the 0.2 and 2.0 p.p.m. selenium diets indicating that the highest dietary selenium level was compatible with normal growth. The selenium concentration and selenium dependent-glutathione peroxidase (GSH-Px) activity of mammary glands from control BD2F1 mice fed 0.2, 1.0 and 2.0 p.p.m. dietary selenium was examined at 8, 9 and 10 months of age. As in previous experiments in adult BALB/c mice, the concentration of mammary gland selenium, but not GSH-Px activity, increased with increasing levels of dietary selenium. These results document that nutritional levels of dietary selenium (0.5 p.p.m. Se) as well as non-toxic higher levels (2.0 p.p.m. Se) inhibit DMBA-induced mammary tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗

Blood selenium and glutathione peroxidase levels and dietary selenium of free-living and institutionalized elderly subjects.

The purpose of this study was to evaluate the selenium status of healthy free-living and institutionalized elderly people. For the 36 free-living elderly dietary selenium intake averaged 94 +/- 44 micrograms Se/day and a positive correlation coefficient was found between dietary selenium and dietary calories (r = 0.46; P less than 0.05), dietary protein (r = 0.60; P less than 0.01), and dietary fat (r = 0.43; P less than 0.05). Diet histories from the institutionalized subjects revealed a strong correlation coefficient between selenium and carbohydrate (r = 0.51; P less than 0.005) and selenium and calories (r = 0.44; P less than 0.05). Mean erythrocyte and plasma selenium levels for the free-living subjects were 0.20 +/- 0.06 micrograms/ml and 0.10 +/- 0.03 micrograms/ml, respectively, while mean erythrocyte glutathione peroxidase (GSH-Px) activity was 27.5 +/- 5.0 units/g protein. For the free-living subjects positive correlation was found between dietary selenium and erythrocyte selenium levels (r = 0.38; P less than 0.05) but no correlation existed between dietary selenium and plasma selenium (r = 0.13; P greater than 0.05) and RBC GSH-Px (r = -0.15; P greater than 0.05). The dietary selenium levels and blood selenium and GSH-Px levels were above the levels found in populations proposed to be at risk for selenium deficiency. Thus, these elderly appear to have adequate selenium status.

Aged↗

Selenium and mouse mammary tumorigenesis: an investigation of possible mechanisms.

The effects of selenium on 7,12-dimethylbenzanthracene-induced mammary tumorigenesis were examined in C57BL X DBA/2f F1 mice fed a semipurified diet. Mice fed 0.2 ppm selenium developed 56% mammary tumors; in contrast, mice fed 2.0 ppm selenium developed only 16% mammary tumors at 11 months of age. Mice fed the 2.0-ppm selenium diet grew as well as did their counterparts fed the 0.2-ppm selenium diet. In a separate experiment, the level of selenium-dependent glutathione peroxidase was measured in the mammary glands of control and 7,12-dimethylbenzanthracene-treated BALB/c mice fed basal and selenium-supplemented diets. 7,12-Dimethylbenzanthracene treatment resulted in decreased glutathione peroxidase activity n mice fed both low (0.03 ppm)- and high (1.50 ppm)-selenium diets. Thus, the chemopreventive effects of selenium could not be attributed to maintaining high levels of glutathione peroxidase. In a second series of experiments, the effects of selenium were further examined on the growth of mammary cell line YN-4 in monolayer cell culture. The mitochondrial inclusions seen in cells exposed to 5 X 10(-6) M selenium could not be correlated with changes in the activity of the mitochondrial enzymes, cytochrome c oxidase and succinate dehydrogenase, thus implying that there was no demonstratable impairment of mitochondria. The examination of selenium-treated cells with flow cytofluorometry indicated that cells were blocked in S-G2 phases of the cell cycle. This latter result illustrates one feasible approach towards identifying specific mechanisms for the chemopreventive effects of selenium.

9,10-Dimethyl-1,2-benzanthracene↗

Selenium concentration and glutathione peroxidase activity in normal and neoplastic development of the mouse mammary gland.

This study was divided into three experiments. (a) The levels of selenium and glutathione peroxidase (GSH-PX) activity were determined for various developmental states of the mammary gland: normal (virgin, pregnant, and lactating); preneoplastic hyperplastic outgrowth lines; and neoplastic mammary tissues. Tissues from the pregnant and lactating mice had higher selenium concentrations and GSH-PX activities than did tissues from virgin mice, but the levels were similar to levels found in preneoplastic and neoplastic mammary tissues of lines C4 and D2. This suggests that the appropriate comparisons for studies determining the effect of selenium on preneoplastic mammary tissues are glands from pregnant and lactating mice. In addition, these results suggest that the refractory state of mammary tumors to selenium-mediated growth inhibition is not due to the absence of GSH-PX or the inability to incorporate selenium. (b) For the second experiment, the effect of feeding various levels of selenium on selenium and GSH-PX levels was determined in mammary and hepatic tissues of virgin mice. GSH-PX activity increased when dietary selenium increased from less than 0.02 to 0.1 ppm selenium but was not further increased when dietary selenium was above 0.1 ppm. (c) Finally, the mammary GSH-PX activity was evaluated at different concentrations of the substrates in order to document the biochemical characteristics of the mammary gland GSH-PX.

Aging↗

Glutathione peroxidase acitvity in intestinal and liver tissues of rats fed various levels of selenium, sulfur and alpha-tocopherol.

The effects of various levels of selenium, alpha-tocopherol and sulfur on glutathione peroxidase (GSH-Px) activity in intestinal and liver tissues were determined in male rats fed corn-soybean or Torula yeast diets. Rats fed corn-soybean diets had greater GSH-Px activity in the small intestine, colon and liver tissues, catalase activity and selenium in the liver, and body weight gains than those fed Torula yeast diets. GSH-Px activity in the small intestine, colon, and liver tissues as well as concentration of selenium in the liver increased with increasing levels of selenium in Torula yeast diets but not with corn-soybean diets. Tocopherol supplementation had no significant effect on GSH-Px activity in rats fed Torula yeast or corn-soybean diets supplemented with selenium. Supplemental sulfur decreased GSH-Px activity in the small intestine tissues and increased activity in colon tissues.

Animal Feed↗

Effect of physical activity on human potassium metabolism in a hot and humid environment.

Previous investigations have suggested that there are high potassium losses during heavy physical activities in hot climates. In order to determine if high levels of potassium losses could be offset by potassium loading, this study was conducted with five long-distance track runners who had trained in hot and humid environments. The liquid supplements containing 4.3, 98.0, and 0.0 mEq/liter of potassium were given 1 to 2 hr before physical activity. The daily diet contained 2.6 g of potassium. A sodium and potassium balance study was conducted in which stool, urine, and dermal losses were measured. In order to determine if there was a change in the distribution of body potassium during physical exercise, seven subjects total body potassium was estimated before and after exercise. This measurement was performed by counting 40K in a whole body counter. Although the subjects with potassium supplementation and higher urinary sodium and potassium losses, the 98 mEq/liter of potassium supplement resulted in a positive potassium balance. The subjects' potassium requirements exceeded the National Research Council suggested dietary intake. The total body potassium measurements indicated that the counting efficiency of 40K increases significantly immediately after the period of vigorous exercise.

Adult↗

Nutrition in space.

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Adaptation, Physiological↗

Folic acid content in thermostabilized and freeze-dried space shuttle foods.

This study was designed to determine whether freeze-dried and thermostabilized foods on a space shuttle contain adequate folate and to investigate any effects of freeze-drying on folacin. Frozen vegetables were analyzed after three states of processing: thawed; cooked; and rehydrated. Thermostabilized items were analyzed as supplied with no further processing. Measurable folate decreased in some freeze-dried vegetables and increased in others. Folacin content of thermostabilized food items was comparable with published values. We concluded that although the folacin content of some freeze-dried foods was low, adequate folate is available from the shuttle menu to meet RDA guidelines.

Folic Acid↗