<?xml version="1.0" encoding="UTF-8"?>
<rss xmlns:dc="http://purl.org/dc/elements/1.1/" version="2.0">
<channel>
<title>Office of Public Health Studies Faculty &amp;  Researcher Works</title>
<link>http://hdl.handle.net/10125/24276</link>
<description/>
<pubDate>Wed, 19 Jun 2013 09:46:01 GMT</pubDate>
<dc:date>2013-06-19T09:46:01Z</dc:date>
<item>
<title>Inhibition of colonic aberrant crypt formation by the dietary flavonoids (+)-catechin and hesperidin.</title>
<link>http://hdl.handle.net/10125/26043</link>
<pubDate>Tue, 01 Jan 2002 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26043</guid>
<dc:date>2002-01-01T00:00:00Z</dc:date>
<dc:creator>Franke, Adrian A; Custer, Laurie J; Cooney, Robert V; Tanaka, Yuichiro; Xu, Meirong; Dashwood, Roderick H</dc:creator>
</item>
<item>
<title>The nitration product 5-nitro-gamma-tocopherol is increased in the Alzheimer brain.</title>
<link>http://hdl.handle.net/10125/26042</link>
<description>Oxidative stress and quasi-inflammatory processes recently have been recognized as contributing factors in the pathogenesis of Alzheimer's disease (AD). Reactive nitrating species have specifically been implicated in AD based on immunochemical and instrumental detection of nitrotyrosine in AD brain protein. The significance of lipid-phase nitration has not been investigated in AD. This study documents a significant two- to threefold increase in the lipid nitration product 5-nitro-gamma-tocopherol in affected regions of the AD brain as determined by high-performance liquid chromatography with electrochemical detection. In a bioassay to compare the relative potency of alpha-tocopherol and gamma-tocopherol against nitrative stress, rat brain mitochondria were exposed to the peroxynitrite-generating compound SIN-1. The oxidation-sensitive Kreb's cycle enzyme alpha-ketoglutarate dehydrogenase was inactivated by SIN-1, in a manner that could be significantly attenuated by gamma-tocopherol (at &lt;10 microM) but not by alpha-tocopherol. These data indicate that nitric oxide-derived species are significant contributors to lipid oxidation in the AD brain. The findings are discussed in reference to the neuroinflammatory hypothesis of AD and the possible role of gamma-tocopherol as a major lipid-phase scavenger of reactive nitrogen species.
</description>
<pubDate>Fri, 01 Mar 2002 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26042</guid>
<dc:date>2002-03-01T00:00:00Z</dc:date>
<dc:creator>Williamson, Kelly S; Gabbita, S Prasad; Mou, Shenyun; West, Melinda; Pye, Quentin N; Markesbery, William R; Cooney, Robert V; Grammas, Paula; Reimann-Philipp, Ulrich; Floyd, Robert A; Hensley, Kenneth</dc:creator>
</item>
<item>
<title>Bioavailability and antioxidant effects of orange juice components in humans.</title>
<link>http://hdl.handle.net/10125/26041</link>
<description>Seven healthy females and six males consumed daily 256 mg of vitamin C, 271 mg of flavanones (mainly as glycosides), 6 mg of carotenoids (mainly xanthophylls and cryptoxanthins), and 0.16 mg of folate by incorporation of daily three times 236 mL of not from concentrate orange juice (OJ) into their habitual diet. At the end of 3 weeks, mean vitamin C, folate, carotenoid, and flavanone plasma concentrations increased significantly relative to baseline by 59% (p &lt; 0.001), 46% (p = 0.018), and 22% (p &lt; 0.001), and 8-fold (p = 0.045), respectively. Flavanones were excreted in urine 9-fold more at the end of the intervention (p = 0.01) but returned to baseline 2 days after study completion. After the 3 week intervention, plasma concentrations of vitamins A and E did not change. 8-Hydroxydeoxyguanosine in white blood cells declined by 16% (p = 0.38; n = 11), and in individuals with high baseline concentrations by 29% (p = 0.36; n = 7), respectively. Low-density lipoprotein (LDL)-/high-density lipoprotein (HDL)-cholesterol ratios decreased but cholesterol (HDL, LDL, total) and thiobarbituric acid reactive substance plasma concentrations did not change significantly. We conclude from this pilot study that OJ is an excellent food source to enhance circulating concentrations of valuable hydrophilic as well as lipophilic phytochemicals.
</description>
<pubDate>Wed, 01 Jun 2005 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26041</guid>
<dc:date>2005-06-01T00:00:00Z</dc:date>
<dc:creator>Franke, Adrian A; Cooney, Robert V; Henning, Susanne M; Custer, Laurie J</dc:creator>
</item>
<item>
<title>Tocopherols and prostate cancer.</title>
<link>http://hdl.handle.net/10125/26040</link>
<pubDate>Fri, 01 Sep 2006 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26040</guid>
<dc:date>2006-09-01T00:00:00Z</dc:date>
<dc:creator>Cooney, Robert V</dc:creator>
</item>
<item>
<title>Enhancement of intracellular gamma-tocopherol levels in cytokine-stimulated C3H 10T1/2 fibroblasts: relation to NO synthesis, isoprostane formation, and tocopherol oxidation.</title>
<link>http://hdl.handle.net/10125/26039</link>
<description>Stimulation of C3H 10T1/2 murine fibroblasts with interferon-gamma(IFN) and bacterial lipopolysaccharide (LPS) generates reactive oxygen and nitrogen species leading to DNA damage, lipid oxidation, and tocopherol oxidation. The tocopherols possess unique chemical and biological properties that suggest they have important roles related to intracellular defense against radical-mediated damage.; Despite increased levels of reactive oxidants and decreased media tocopherol, cellular levels of gamma-tocopherol, but not alpha-tocopherol, were observed to increase significantly when cells were treated with IFN/LPS. Inhibition of nitric oxide (NO) synthesis by a specific inhibitor of inducible NO synthase (iNOS) increased both intracellular alpha-tocopherol and gamma-tocopherol concentrations, but did not significantly alter the reduction in media tocopherol levels caused by IFN/LPS treatment. Both exposure to exogenous NO and cellular synthesis of NO in cell culture increased media levels of 8-epi-prostaglandin F2alpha, a marker of oxidative lipid damage, whereas inhibition of endogenous NO synthesis reduced media 8-epi-prostaglandin F2alpha formation to control levels.; Elevated intracellular levels of gamma-tocopherol in response to the cellular inflammatory state may indicate that it serves a unique role in minimizing cellular damage resulting from endogenous NO synthesis. Results of the current study suggest that NO is an important mediator of damage within the cell, as well as in the oxidation of both alpha- and gamma-tocopherols. The paradoxical increase in cellular tocopherol associated with the induction of NO synthesis may indicate either enhanced cellular transport/decreased export for tocopherols or recruitment of free tocopherol from tocopherol storage molecules.
</description>
<pubDate>Mon, 01 Jan 2007 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26039</guid>
<dc:date>2007-01-01T00:00:00Z</dc:date>
<dc:creator>Tanaka, Yuichiro; Wood, Leslie A Lesoon; Cooney, Robert V</dc:creator>
</item>
<item>
<title>Association of leptin, 25-hydroxyvitamin D, and parathyroid hormone in women.</title>
<link>http://hdl.handle.net/10125/26038</link>
<description>Vitamin D deficiency and adipocytokines have been implicated in the etiology of aging-related diseases such as cancer, osteoporosis, and diseases of the cardiovascular system. The association between elevated parathyroid hormone (PTH) and low 25-hydroxyvitamin D (25-OH-VitD) in plasma is used to define vitamin D deficiency, yet their associated mechanistic pathways are unclear. Utilizing plasma samples from women in a previous intervention study, we measured plasma 25-OH-VitD, leptin, adiponectin, PTH, and lipid levels. We observed strong positive associations for leptin with PTH, gamma -tocopherol, and body mass index (BMI) and inverse associations with 25-OH-VitD and adiponectin. Although commonly accepted that vitamin D deficiency causes hyperparathyroidism, we observed this association primarily in individuals with elevated leptin levels, suggesting that leptin may be an important modifier of this effect consistent with 25-OH-VitD-mediated inhibition of leptin. Leptin was highly correlated with the BMI/25-OH-VitD ratio (r = 0.80; P &lt; 0.0001), consistent with a model in which BMI (adiposity) and 25-OH-VitD are the primary determinants of circulating leptin and PTH levels. This model may explain the failure of some studies to observe elevated PTH in vitamin D deficient adolescents and provides important insight into epidemiological studies exploring the associations of these individual biomarkers with chronic disease risk and mortality.
</description>
<pubDate>Thu, 01 Jan 2009 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26038</guid>
<dc:date>2009-01-01T00:00:00Z</dc:date>
<dc:creator>Maetani, Micah; Maskarinec, Gertraud; Franke, Adrian A; Cooney, Robert V</dc:creator>
</item>
<item>
<title>Plasma carotenoids, retinol, and tocopherols and postmenopausal breast cancer risk in the Multiethnic Cohort Study: a nested case-control study.</title>
<link>http://hdl.handle.net/10125/26037</link>
<description>Assessments by the handful of prospective studies of the association of serum antioxidants and breast cancer risk have yielded inconsistent results. This multiethnic nested case-control study sought to examine the association of plasma carotenoids, retinol, and tocopherols with postmenopausal breast cancer risk.; From the biospecimen subcohort of the Multiethnic Cohort Study, 286 incident postmenopausal breast cancer cases were matched to 535 controls on age, sex, ethnicity, study location (Hawaii or California), smoking status, date/time of collection and hours of fasting. We measured prediagnostic circulating levels of individual carotenoids, retinol, and tocopherols. Conditional logistic regression was used to compute odds ratios and 95% confidence intervals.; Women with breast cancer tended to have lower levels of plasma carotenoids and tocopherols than matched controls, but the differences were not large or statistically significant and the trends were not monotonic. No association was seen with retinol. A sensitivity analysis excluding cases diagnosed within 1 year after blood draw did not alter the findings.; The lack of significant associations in this multiethnic population is consistent with previously observed results from less racially-diverse cohorts and serves as further evidence against a causal link between plasma micronutrient concentrations and postmenopausal breast cancer risk.
</description>
<pubDate>Thu, 01 Jan 2009 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26037</guid>
<dc:date>2009-01-01T00:00:00Z</dc:date>
<dc:creator>Epplein, Meira; Shvetsov, Yurii B; Wilkens, Lynne R; Franke, Adrian A; Cooney, Robert V; Le Marchand, Loïc; Henderson, Brian E; Kolonel, Laurence N; Goodman, Marc T</dc:creator>
</item>
<item>
<title>Inflammatory markers in a 2-year soy intervention among premenopausal women.</title>
<link>http://hdl.handle.net/10125/26036</link>
<description>Epidemiologic evidence supports a role of soy foods in breast cancer etiology. Because chronic inflammation appears to be a critical component in carcinogenesis, we examined the potential anti-inflammatory effects of soy foods.; The original 2-year dietary intervention randomized 220 premenopausal women of whom 183 women (90 in the intervention group and 93 in the control group) were included in the current investigation; 40% were of Asian ancestry. The intervention group consumed two daily soy servings containing 50 mg of isoflavones (aglycone equivalents), whereas the controls maintained their regular diet. Five serum samples obtained at month 0, 3, 6, 12, and 24 were analyzed for interleukin (IL)-6, C-reactive protein (CRP), leptin, and adiponectin by ELISA. For statistical analysis, mixed models were applied to incorporate the repeated measurements.Results:The levels of all analytes were lower in Asian than Caucasian women. Overweight women had significantly higher levels of CRP, IL-6, and leptin and lower levels of adiponectin than normal weight women. We did not observe a significant effect of soy foods on the four markers, but leptin increased in the control and not in the intervention group (p = 0.20 for group-time effect); this difference was significant for Asian (p = 0.01) and obese women (p = 0.005).; During this 2-year intervention, soy foods did not modify serum levels of CRP, IL-6, leptin, and adiponectin in premenopausal women although leptin levels remained stable among women in the intervention group who were obese or of Asian ancestry. Further studies with diverse markers of inflammation are necessary to clarify the specific effect of soy on immune responses.
</description>
<pubDate>Thu, 01 Jan 2009 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26036</guid>
<dc:date>2009-01-01T00:00:00Z</dc:date>
<dc:creator>Maskarinec, Gertraud; Steude, Jana S; Franke, Adrian A; Cooney, Robert V</dc:creator>
</item>
<item>
<title>Association of plasma micronutrient levels and urinary isoprostane with risk of lung cancer: the multiethnic cohort study.</title>
<link>http://hdl.handle.net/10125/26035</link>
<description>Although smoking is the primary risk factor for lung cancer, there is evidence to suggest that fruit and vegetable intake are important cofactors. The present case-control study, nested within the Multiethnic Cohort Study, examined the associations of biomarkers of fruit and vegetable intake (individual plasma micronutrient levels), serum selenium, and a urinary biomarker for total lipid peroxidation with lung cancer risk. Two hundred seven incident cases were matched to 414 controls on age, sex, ethnicity, study location (Hawaii or California), smoking status, date/time of collection, and hours of fasting. We measured prediagnositic circulating levels of individual tocopherols and carotenoids, retinol, and serum selenium, and urinary 15-isoprostane F(2t). Conditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI). For men, strong reductions in risk were seen with increasing tertiles of each plasma carotenoid, with the ORs for the third tertile, compared with the first tertile, ranging from 0.24 to 0.45 (P(trends), 0.002-0.04). No associations were found among women for carotenoids or among either sex for tocopherols, selenium, and retinol. A doubling in risk was seen for men in the second and third tertiles, compared with the first tertile of urinary 15-isoprostane F(2t) (OR, 2.31; 95% CI, 1.02-5.25; and OR, 2.16; 95% CI, 0.98-4.78). This study supports the previously observed association between circulating carotenoids and lung cancer risk in men, and adds to the limited literature regarding urinary 15-isoprostane F(2t) as a marker of cancer risk. Future research examining the possible relationship between isoprostanes and lung cancer is warranted.
</description>
<pubDate>Wed, 01 Jul 2009 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26035</guid>
<dc:date>2009-07-01T00:00:00Z</dc:date>
<dc:creator>Epplein, Meira; Franke, Adrian A; Cooney, Robert V; Morris, J Steven; Wilkens, Lynne R; Goodman, Marc T; Murphy, Suzanne P; Henderson, Brian E; Kolonel, Laurence N; Le Marchand, Loïc</dc:creator>
</item>
<item>
<title>Association of selenium, tocopherols, carotenoids, retinol, and 15-isoprostane F(2t) in serum or urine with prostate cancer risk: the multiethnic cohort.</title>
<link>http://hdl.handle.net/10125/26034</link>
<description>We examine the association of antioxidants and 15-isoprostane F(2t) with risk of prostate cancer.; We conducted a nested case-control study of serum antioxidant biomarkers (selenium, tocopherols, carotenoids, and retinol) and a urinary oxidation biomarker (15-isoprostane F(2t)) with risk of prostate cancer within the Multiethnic Cohort. Demographic, dietary, and other exposure information was collected by self-administered questionnaire in 1993-1996. We compared prediagnostic biomarker levels from 467 prostate cancer cases and 936 cancer free controls that were matched on several variables. Multivariate conditional logistic regression models were used to compute adjusted odds ratios (ORs) and 95% confidence intervals (CIs).; We observed that there was no overall association of serum concentrations of antioxidants and urinary concentrations of 15-isoprostane F(2t) with risk of prostate cancer or risk of advanced prostate cancer. However, we did observe an inverse association for serum selenium only among African-American men (p trend = 0.02); men in the third tertile of selenium concentrations had a 41% lower risk (95% CI: 0.38-0.93) of prostate cancer when compared to men in the first tertile.; Overall, our study found no association of serum antioxidants or 15-isoprostane F(2t) with the risk of prostate cancer. The observed inverse association of selenium with prostate cancer in African-Americans needs to be validated in other studies.
</description>
<pubDate>Tue, 01 Sep 2009 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26034</guid>
<dc:date>2009-09-01T00:00:00Z</dc:date>
<dc:creator>Gill, Jasmeet K; Franke, Adrian A; Steven Morris, J; Cooney, Robert V; Wilkens, Lynne R; Le Marchand, Loic; Goodman, Marc T; Henderson, Brian E; Kolonel, Laurence N</dc:creator>
</item>
<item>
<title>The relation of leptin and adiponectin with breast density among premenopausal women.</title>
<link>http://hdl.handle.net/10125/26033</link>
<description>The adipocytokine leptin may increase breast cancer risk, while adiponectin may be protective. We examined the association of the two circulating markers with mammographic density, a strong predictor of breast cancer risk. For 183 premenopausal participants of a nutritional trial, mammograms performed at baseline, year 1 and year 2 were assessed for density using a computer-assisted method. Serum samples obtained at the same time were analyzed for leptin and adiponectin by enzyme-linked immunosorbent assay. We applied mixed models to incorporate the repeated measurements while adjusting for confounders including body mass index (BMI). At baseline, the mean age of the participants was 42.6+/-2.9 years; 40% were of Asian ancestry. Leptin was lower and adiponectin higher in normal weight than overweight women. Neither marker was related to absolute breast density. The significant inverse association of leptin with percent density disappeared when BMI was added to the model. After stratification by weight, percent density decreased with higher leptin levels in normal weight women, whereas it increased among overweight participants. After adjustment for BMI, the positive association between percent density and adiponectin was greatly reduced and no longer significant. These results do not support a strong association of leptin or adiponectin with breast cancer risk as assessed by mammographic density. In contrast, the findings suggest the possibility that the inverse association of BMI with breast cancer risk in premenopausal women is mediated by adipocytokines.
</description>
<pubDate>Fri, 01 Jan 2010 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26033</guid>
<dc:date>2010-01-01T00:00:00Z</dc:date>
<dc:creator>Maskarinec, Gertraud; Woolcott, Christy; Steude, Jana S; Franke, Adrian A; Cooney, Robert V</dc:creator>
</item>
<item>
<title>Plasma 25-hydroxyvitamin D and prostate cancer risk: the multiethnic cohort.</title>
<link>http://hdl.handle.net/10125/26032</link>
<description>The purpose of this study was to examine the relationship of plasma 25-hydroxyvitamin D (25(OH)D) concentrations to prostate cancer within a large multiethnic cohort in Hawaii and California using a nested case-control design. The study included 329 incidents of prostate cancer of African American, Native Hawaiian, Japanese, Latino and White ancestry, and 656 controls matched on age, race/ethnicity, date/time of blood collection and fasting status. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CI). No association with prostate cancer risk was found in an analysis based on quartiles of 25(OH)D. When clinically defined cutpoints were used, there was no increased risk for the lowest 25(OH)D concentration (OR for &lt;20 versus 30-&lt;50ng/ml=1.10, 95% CI=0.68-1.78), while there was a suggestive increased risk for higher concentrations (OR for 50ng/ml=1.52, 95% CI=0.92-2.51). The findings from this prospective study of men in the Multiethnic Cohort do not support the hypothesis that vitamin D lowers the risk of prostate cancer. Further follow-up is warranted to determine whether the findings are consistent across ethnic groups.
</description>
<pubDate>Mon, 01 Mar 2010 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26032</guid>
<dc:date>2010-03-01T00:00:00Z</dc:date>
<dc:creator>Park, Song-Yi; Cooney, Robert V; Wilkens, Lynne R; Murphy, Suzanne P; Henderson, Brian E; Kolonel, Laurence N</dc:creator>
</item>
<item>
<title>Associations between obesity and serum lipid-soluble micronutrients among premenopausal women.</title>
<link>http://hdl.handle.net/10125/26031</link>
<description>Elucidating potential pathways that micronutrients may reduce/promote chronic disease may contribute to our understanding of the underlying etiology of disease and their utility as markers of risk. In the current study, we examined associations of serum lipid-soluble micronutrients with body mass index (BMI). We hypothesized that obesity may differentially influence serum micronutrient levels, thereby affecting risk for chronic disease incidence and mortality. Baseline serum samples from 180 premenopausal women from a nutritional trial were analyzed for leptin, C-reactive protein, 25-hydroxyvitamin D, carotenoids, and tocopherols. Participants were stratified into normal-weight (18.5-24.9), overweight (25-29.9), and obese (&gt;or=30) subgroups by BMI (in kilograms per square meter). Differences in serum biomarkers among BMI subgroups were adjusted for Asian ethnicity and smoking status. As expected, obese individuals had significantly higher serum levels of leptin and C-reactive protein (Ps &lt; .05) compared with normal-weight women. gamma-Tocopherol levels were significantly higher in obese individuals (P &lt; .05), whereas alpha-tocopherol levels did not differ among BMI subgroups. Serum levels of 25-hydroxyvitamin D and carotenoids (except lycopene) were significantly lower in obese than in normal-weight women (Ps &lt; .05). The associations between BMI and carotenoids were independent of dietary intake. The obesity-associated reduction for total provitamin A carotenoids (45%) was approximately 3-fold greater than that observed for non-provitamin A carotenoids (16%). Our results indicate potential influences of obesity on serum levels of lipid-soluble micronutrients and suggest that metabolism of provitamin A carotenoids may contribute to the differences observed.
</description>
<pubDate>Thu, 01 Apr 2010 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26031</guid>
<dc:date>2010-04-01T00:00:00Z</dc:date>
<dc:creator>Chai, Weiwen; Conroy, Shannon M; Maskarinec, Gertraud; Franke, Adrian A; Pagano, Ian S; Cooney, Robert V</dc:creator>
</item>
<item>
<title>Coenzyme Q10 in human blood: native levels and determinants of oxidation during processing and storage.</title>
<link>http://hdl.handle.net/10125/26030</link>
<description>Coenzyme Q10 (Q10) is present in the circulation mainly in its reduced form (ubiquinol-10; UL10), but oxidizes quickly ex vivo to ubiquinone-10 (UN10). Therefore, native UL10:UN10 ratios, used as markers of redox status and disease risk, are difficult to measure. We established an RP-(U)HPLC method with coulometric detection to measure natively circulating UL10 and UN10 concentrations by adding a ubiquinol/ubiquinone mixture as an internal standard immediately after plasma preparation. This allowed adjustment for unavoidable artificial UL10 oxidation as well as for total losses (or gains) of analytes during sample storage, processing, and analysis because the internal standards exactly paralleled the chemical behavior of Q10. This technique applied to blood (n = 13) revealed Q10 levels of 680-3300 nM with a mean UL10:UN10 ratio of 95:5, which was inversely associated with total Q10 (r=-0.69; p=0.004). The oxidation of UL10 to UN10 was equimolar, increased by O(2), and decreased by lower temperatures or various degassing methods. Although UL10 was stable in blood or when pure in organic solvents at 22 degrees C, its oxidation was catalyzed dose dependently by alpha-tocopherol and butylated hydroxytoluene, particularly when present in combination. Key structural features for the catalytic pro-oxidant properties of phenolic antioxidants included two substituents vicinal to the phenolic hydroxyl group.
</description>
<pubDate>Tue, 01 Jun 2010 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26030</guid>
<dc:date>2010-06-01T00:00:00Z</dc:date>
<dc:creator>Franke, Adrian A; Morrison, Cynthia M; Bakke, Jesse L; Custer, Laurie J; Li, Xingnan; Cooney, Robert V</dc:creator>
</item>
<item>
<title>Plasma coenzyme Q10 levels and postmenopausal breast cancer risk: the multiethnic cohort study.</title>
<link>http://hdl.handle.net/10125/26029</link>
<description>Coenzyme Q10 (CoQ10) is a component of the mitochondrial electron transport chain and is considered an important cellular antioxidant. Decreased circulating CoQ10 levels have been reported in women with breast cancer, but evidence is limited. We examined the association of plasma CoQ10 levels with postmenopausal breast cancer risk using prospectively collected blood samples.; Prediagnostic plasma levels of total CoQ10 were measured among 160 incident postmenopausal breast cancer cases and 289 controls in the Multiethnic Cohort Study. Cases and controls were individually matched on age, sex, ethnicity, study location (Hawaii or California), hormone replacement therapy use, date and time of specimen collection, and hours of fasting. Logistic regression was used to compute odds ratios and 95% confidence intervals.; Plasma CoQ10 levels were positively associated with breast cancer risk, overall (P = 0.04). The association was stronger after women diagnosed within 1 year of blood draw were excluded to eliminate possible preclinical cases (odds ratio for the highest versus the lowest tertile, 2.26; 95% confidence interval, 1.22-4.19; P for trend = 0.01).; Higher CoQ10 levels in postmenopausal women may be associated with increased breast cancer risk.; A potential role for CoQ10 in the development and progression of breast cancer has been postulated, but epidemiologic evidence is lacking. Findings from this prospective cohort study add to the limited literature, indicating the potential positive association of circulating CoQ10 with postmenopausal breast cancer risk.
</description>
<pubDate>Wed, 01 Sep 2010 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26029</guid>
<dc:date>2010-09-01T00:00:00Z</dc:date>
<dc:creator>Chai, Weiwen; Cooney, Robert V; Franke, Adrian A; Shvetsov, Yurii B; Caberto, Christian P; Wilkens, Lynne R; Le Marchand, Loïc; Henderson, Brian E; Kolonel, Laurence N; Goodman, Marc T</dc:creator>
</item>
<item>
<title>Leptin, adiponectin, and obesity among Caucasian and Asian women.</title>
<link>http://hdl.handle.net/10125/26028</link>
<description>Ethnic differences in adipose tissue distribution may contribute to different chronic disease risks across ethnic groups, and adipokines may mediate the risk. In a cross-sectional study, we examined ethnic differences in adipokines and inflammatory markers as related to body mass index (BMI) among 183 premenopausal women with Caucasian and Asian ancestry. General linear models were used to estimate adjusted mean levels of leptin, adiponectin, interleukin-6, and C-reactive protein (CRP). Asian women had significantly lower serum levels of leptin, adiponectin, and CRP than Caucasian participants (P≤.01) across all levels of BMI. Among overweight and obese women, Asians showed a stronger association of CRP with leptin (β=1.34 versus β=0.64) and with adiponectin (β=-0.95 versus β=-0.75) than Caucasians. Compared to Caucasians of similar BMI, Asians may experience a higher chronic disease risk due to lower levels of adiponectin despite their lower levels of leptin.
</description>
<pubDate>Sat, 01 Jan 2011 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26028</guid>
<dc:date>2011-01-01T00:00:00Z</dc:date>
<dc:creator>Conroy, Shannon M; Chai, Weiwen; Lim, Unhee; Franke, Adrian A; Cooney, Robert V; Maskarinec, Gertraud</dc:creator>
</item>
<item>
<title>Plasma coenzyme Q10 levels and prostate cancer risk: the multiethnic cohort study.</title>
<link>http://hdl.handle.net/10125/26027</link>
<description>Coenzyme Q10 (CoQ10) is considered to be a potential anticancer agent, but epidemiologic evidence regarding CoQ10 and prostate cancer risk is lacking. We examined the association of circulating CoQ10 levels with prostate cancer risk, using prediagnostic blood samples.; Each of the 307 cases was individually matched to approximately 2 controls, for a total of 596 controls, on age, ethnicity, geographic location, date/time of specimen collection, and hours of fasting. Logistic regression was used to compute ORs and 95% CIs.; There was no overall statistically significant association of plasma CoQ10 levels with prostate cancer risk (P(trend) = 0.50). However, after matched sets in which controls who had possible undiagnosed prostate cancer (prostate specific antigen value &gt;4.0) were excluded, the ORs for quintiles 2 to 5 were all less than 1.0.; The results suggest the possibility that moderate levels of circulating CoQ10 may be optimal for the reduction of prostate cancer risk; however, the findings were weak and not statistically significant. Because this is the first epidemiologic study of the association between CoQ10 and prostate cancer, further research on this topic is needed.; If a nutritional factor such as CoQ10 were determined to reduce prostate cancer risk, it would have considerable public health significance because of the very high incidence of this cancer.
</description>
<pubDate>Fri, 01 Apr 2011 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26027</guid>
<dc:date>2011-04-01T00:00:00Z</dc:date>
<dc:creator>Chai, Weiwen; Cooney, Robert V; Franke, Adrian A; Caberto, Christian P; Wilkens, Lynne R; Le Marchand, Loïc; Goodman, Marc T; Henderson, Brian E; Kolonel, Laurence N</dc:creator>
</item>
<item>
<title>Low plasma coenzyme Q(10) levels and breast cancer risk in Chinese women.</title>
<link>http://hdl.handle.net/10125/26026</link>
<description>Low circulating levels of coenzyme Q(10) (CoQ(10)) have been associated with increased cancer incidence and poor prognosis for a number of cancer types, while a recent prospective study observed a positive association for CoQ(10) with breast cancer risk.; We prospectively examined the association of plasma CoQ(10) with breast cancer risk in a nested case-control study of Chinese women within the Shanghai Women's Health Study (SWHS). Prediagnostic plasma samples were obtained from 340 cases and 653 age-matched controls and analyzed for total CoQ(10).; A borderline significant inverse association for breast cancer incidence with plasma CoQ(10) level was observed by a conditional logistic regression model adjusted for age and age at first live birth, which became significant after elimination of cases diagnosed within 1 year of blood draw (P(trend) = 0.03). This association was independent of menopausal status. Plasma CoQ(10) levels were also observed to be significantly associated with circulating γ-tocopherol (r = 0.50; P &lt; 0.0001) and α-tocopherol (r = 0.38; P &lt; 0.0001) levels.; Circulating levels of CoQ(10) were generally low in this population and the observed association with breast cancer risk may be limited to those women with exceptionally low values.; This study reports an inverse relationship between circulating CoQ(10) and breast cancer risk, while the only other prospective study of CoQ(10) and breast cancer to date found a positive association. Lower levels of CoQ(10) in the SWHS population suggest that the 2 studies may not be contradictory and indicate a possible nonlinear (U-shaped) association of CoQ(10) with risk.
</description>
<pubDate>Wed, 01 Jun 2011 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26026</guid>
<dc:date>2011-06-01T00:00:00Z</dc:date>
<dc:creator>Cooney, Robert V; Dai, Qi; Gao, Yu-Tang; Chow, Wong-Ho; Franke, Adrian A; Shu, Xiao-Ou; Li, Honglan; Ji, Butian; Cai, Qiuyin; Chai, Weiwen; Zheng, Wei</dc:creator>
</item>
<item>
<title>Predicting total, abdominal, visceral and hepatic adiposity with circulating biomarkers in Caucasian and Japanese American women.</title>
<link>http://hdl.handle.net/10125/26025</link>
<description>Characterization of abdominal and intra-abdominal fat requires imaging, and thus is not feasible in large epidemiologic studies.; We investigated whether biomarkers may complement anthropometry (body mass index [BMI], waist circumference [WC], and waist-hip ratio [WHR]) in predicting the size of the body fat compartments by analyzing blood biomarkers, including adipocytokines, insulin resistance markers, sex steroid hormones, lipids, liver enzymes and gastro-neuropeptides.; Fasting levels of 58 blood markers were analyzed in 60 healthy, Caucasian or Japanese American postmenopausal women who underwent anthropometric measurements, dual energy X-ray absorptiometry (DXA), and abdominal magnetic resonance imaging. Total, abdominal, visceral and hepatic adiposity were predicted based on anthropometry and the biomarkers using Random Forest models.; Total body fat was well predicted by anthropometry alone (R(2) = 0.85), by the 5 best predictors from the biomarker model alone (leptin, leptin-adiponectin ratio [LAR], free estradiol, plasminogen activator inhibitor-1 [PAI1], alanine transaminase [ALT]; R(2) = 0.69), or by combining these 5 biomarkers with anthropometry (R(2) = 0.91). Abdominal adiposity (DXA trunk-to-periphery fat ratio) was better predicted by combining the two types of predictors (R(2) = 0.58) than by anthropometry alone (R(2) = 0.53) or the 5 best biomarkers alone (25(OH)-vitamin D(3), insulin-like growth factor binding protein-1 [IGFBP1], uric acid, soluble leptin receptor [sLEPR], Coenzyme Q10; R(2) = 0.35). Similarly, visceral fat was slightly better predicted by combining the predictors (R(2) = 0.68) than by anthropometry alone (R(2) = 0.65) or the 5 best biomarker predictors alone (leptin, C-reactive protein [CRP], LAR, lycopene, vitamin D(3); R(2) = 0.58). Percent liver fat was predicted better by the 5 best biomarker predictors (insulin, sex hormone binding globulin [SHBG], LAR, alpha-tocopherol, PAI1; R(2) = 0.42) or by combining the predictors (R(2) = 0.44) than by anthropometry alone (R(2) = 0.29).; The predictive ability of anthropometry for body fat distribution may be enhanced by measuring a small number of biomarkers. Studies to replicate these data in men and other ethnic groups are warranted.
</description>
<pubDate>Sun, 01 Jan 2012 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26025</guid>
<dc:date>2012-01-01T00:00:00Z</dc:date>
<dc:creator>Lim, Unhee; Turner, Stephen D; Franke, Adrian A; Cooney, Robert V; Wilkens, Lynne R; Ernst, Thomas; Albright, Cheryl L; Novotny, Rachel; Chang, Linda; Kolonel, Laurence N; Murphy, Suzanne P; Le Marchand, Loïc</dc:creator>
</item>
<item>
<title>UH Cancer Center hotline: modern medicine and the road to prevention: a long and tortuous path.</title>
<link>http://hdl.handle.net/10125/26023</link>
<pubDate>Wed, 01 Feb 2012 00:00:00 GMT</pubDate>
<guid isPermaLink="false">http://hdl.handle.net/10125/26023</guid>
<dc:date>2012-02-01T00:00:00Z</dc:date>
<dc:creator>Cooney, Robert V</dc:creator>
</item>
</channel>
</rss>
