bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunoglobulin Enhancer HS1,2 polymorphism: a new powerful anthropogenetic marker
Authors: Giambra V. , Martínez‐Labarga C. , Giufre' M. , Modiano D. , Simpore' J. , Gisladottir B. K. , Francavilla R. , Zhelezova G. , Kilic S. S. , Crawford M. , Biondi G. , Rickards O. , Frezza D. 
Published: October 2006

SummaryThe human HS1,2 enhancer of the immunoglobulin (Ig) heavy chain 3′ enhancer complex plays a central role in the regulation of Ig maturation and production. Four common alleles HS1,2‐A*1, *2, *3, *4 are directly implicated with the transcription level and at least one of them, HS1, 2‐A*2, seems to be related to immune disorders, such as coeliac disease, herpetiform dermatitis and Berger syndrome. Given their clinical significance it is of interest to know the distribution of HS1,2‐A variants in populations from different continents, as well as to determine whether the polymorphism is associated to specific evolutionary factors. In this paper we report the distribution of the HS1,2‐A polymorphism in 1098 individuals from various African, Asian and European populations. HS1,2‐A*3 and HS1,2‐A*4 alleles are at their highest frequencies among Africans, and HS1,2‐A*2 is significantly lower in Africans in comparison with both Europeans and, to a lesser extent, Asians. Analysis of molecular variance of the allele frequencies indicates that the HS1,2‐A polymorphism can be considered as a reliable anthropogenetic marker.
Estimating the Effects of Prescription Drug Coverage for Medicare Beneficiaries
Authors: Shea Dennis G. , Terza Joseph V. , Stuart Bruce C. , Briesacher Becky 
Published: October 2006

Objective. To identify the effect of insurance coverage on prescription utilization by Medicare beneficiaries.Data Sources/Study Setting. Secondary data from the 1999 Medicare Current Beneficiary Survey (MCBS) Cost and Use files, a nationally representative survey of Medicare enrollees.Study Design. The paper uses a cross‐sectional design with (1) a standard regression framework to estimate the impact of prescription coverage on utilization controlling for potential selection bias with covariate control based on the Diagnostic Cost Group/Hierarchical Condition Category (DCG/HCC) risk adjuster, and (2) a multistage residual inclusion method using instrumental variables to control for selection bias and identify the insurance coverage effect.Data Collection/Extraction Methods. Data were extracted from the 1999 MCBS. Study inclusion criteria are community‐dwelling MCBS respondents with full‐year Medicare enrollment and supplemental medical insurance with or without full‐year drug benefits. The final sample totaled 5,270 Medicare beneficiaries.Principal Findings. Both the model using the DCG/HCC risk adjuster and the model using the residual inclusion method produced similar results. The estimated price elasticity of demand for prescription drugs for the Medicare beneficiaries in our sample was −0.54.Conclusions. Our results confirm that selection into prescription coverage is predictable based on observable health. Our results further confirm prior estimates of price sensitivity of prescription drug demand for Medicare beneficiaries, though our estimate is slightly above prior results.
Identification of Ethanol Responsive Domains of Adenylyl Cyclase
Authors: Yoshimura Masami , Pearson Susan , Kadota Yoichi , Gonzalez Cristina E. 
Published: October 2006

Background: The activity of adenylyl cyclase (AC) is enhanced by pharmacologically relevant concentrations of ethanol. The enhancing effect of ethanol on AC activity is AC isoform‐specific. Therefore, we hypothesized that within a cyclic AMP–generating system, AC is the target of ethanol's action and that ethanol‐sensitive AC molecules contain structural elements modulated by ethanol. The structural elements are designated as “ethanol responsive domains.”Methods: By using a series of chimeric mutants, we searched regions of the AC molecule that are important for the ethanol effect. These chimeric mutants were derived from 3 isoforms of AC: AC7 (type 7), the most ethanol responsive isoform; AC3 (type 3), an isoform that is far less responsive to ethanol; and AC2 (type 2), an isoform that is homologous to AC7 but less responsive to ethanol.Results: We identified 2 discrete regions of the AC molecule that are important for the enhancement of AC activity by ethanol. The first is the N‐terminal 28‐amino‐acid (aa) region of the C1a domain. The second is the C‐terminal region (∼140 aa) of the AC molecule. Sequence differences in the N‐terminal tail, 2 putative transmembrane domains, and the C1b domain are not important for ethanol's effect.Conclusions: The current study with mammalian ACs provides a new class of alcohol‐responsive protein and possibly a new mechanism of alcohol action on cellular function. The identification of ethanol responsive domains will facilitate the elucidation of the mechanisms by which ethanol enhances the activity of AC.
Ontogeny of Acute Tolerance to Ethanol‐Induced Social Inhibition in Sprague–Dawley Rats
Authors: Varlinskaya Elena I. , Spear Linda P. 
Published: October 2006

Background:Adolescent rats are less sensitive than adults to a number of acute effects of ethanol, including ethanol‐induced social inhibition. Adolescent insensitivity to the suppressing effects of ethanol on social interactions could be related in part to age differences in compensatory responses, including acute tolerance, that serve to counteract these inhibitory effects of ethanol. The present study explored ontogenetic development of acute tolerance within 30 minutes after administration of a relatively low ethanol dose, using ethanol‐induced social impairment as the target response measure.Methods:Overall social activity was examined following challenge with 1 g/kg ethanol (intraperitoneally) at 2 postinjection intervals (5 or 30 minutes) in early [postnatal day (P) 28], mid (P35), or late (P42) adolescent or adult (P70) group‐housed male and female Sprague–Dawley rats (Experiment 1). Blood and brain ethanol concentrations (BECs and BrECs) were assessed in separate groups of animals 5 or 30 minutes after ethanol administration (Experiment 2). Expression of acute tolerance was examined by assessing the relationship between BrECs and the degree of social impairment in individual animals at P28, P35, P42, and P70 during early recovery period (up to 30 minutes) following acute ethanol challenge (Experiment 3).Results:Effects of ethanol on overall social activity were age‐dependent and time‐dependent. Whereas all age groups showed equivalent ethanol‐induced social inhibition 5 minutes after injection, testing at 30 minutes revealed marked age differences. Social inhibition was still pronounced at this time in adults, but was diminished in an age‐related manner at younger ages (Experiment 1). In contrast to the ontogenetic differences in rates of decline in social impairment across time, decreases in brain and blood ethanol levels over time were similar across age (Experiment 2). Only P28 and P35 adolescents showed acute tolerance to ethanol‐induced social inhibition, as indexed by an increasing time‐dependent dissociation between BrECs and ethanol‐induced social impairment, with social impairment declining faster than BrECs (Experiment 3).Conclusions:This is the first study to document enhanced acute tolerance in adolescent rats relative to adult animals at nonhypnotic doses of ethanol. The greater expression of acute tolerance in young animals may reflect an enhanced predisposition of their nervous systems to respond rapidly to even modest doses of ethanol with compensatory adaptations. A greater propensity of early adolescents to develop acute tolerance may contribute to their resistance to adverse effects of ethanol, thereby permitting heavy drinking at this age and placing early adolescents at higher risk for extensive alcohol use.
Sexual Function in Women with Urinary Incontinence Treated by Pelvic Floor Transvaginal Electrical Stimulation
Authors: Giuseppe Paradiso Galatioto , Pace Gianna , Vicentini Carlo 
Published: October 2006

ABSTRACT

Introduction
Women’s sexual dysfunctions (WSD) have been commonly associated with urinary incontinence (UI). Women with UI and who scored low on the Female Sexual Function Index (FSFI) showed an improvement in urinary leakage and also in their sexual life following treatment by transvaginal electrical stimulation (TES).

Aims
To determine the effects of TES in 37 women complaining of UI, of whom 23 also had WSD, and to compare the FSFI scores of women with UI and 43 women not affected by UI who underwent routine urologic evaluation.

Methods
Thirty-seven women complaining of UI were evaluated by voiding diary and with FSFI before and after 3 months of TES. All had a urogynecologic evaluation and urodynamic study.

Main Outcome Measures
In the voiding diary the women reported the types of liquid they ingested, urinary frequency, and episodes of urgency and urine leakage. The domain scores of the FSFI, including desire, arousal, lubrication, orgasm, satisfaction, and pain, were calculated. TES was conducted for 15–30 minutes, twice a week for 3 months, using biphasic intermittent current with a frequency of 50 Hz for stress UI (SUI) and 20 Hz for urge UI (UUI), and the most tolerable intensity of stimulation.

Results
After TES, only two of the 10 women with UUI experienced a few leakage incidents; patients with SUI were completely dry during TES; and only three reported a few episodes of UI during intense activities. The five patients with mixed UI improved mainly as regards urgency. The FSFI scores of patients complaining of UI showed significantly lower desire and sexual satisfaction, and higher sexual pain than controls. After 3 months, the 23 women affected by WSD, of the 37 participants with UI, reported a remarkable improvement in their sexual life.

Conclusion
TES was found to be a safe and effective therapy for selected patients affected by mild to moderate UI. Because women with UI also complain of WSD compared with the general female population, an investigation of female sexuality is suggested for these patients.
Risk of Colorectal Cancer Is Linked to Erythrocyte Compositions of Fatty Acids as Biomarkers for Dietary Intakes of Fish, Fat, and Fatty Acids
Authors: Kuriki Kiyonori , Wakai Kenji , Hirose Kaoru , Matsuo Keitaro , Ito Hidemi , Suzuki Takeshi , Saito Toshiko , Kanemitsu Yukihide , Hirai Takashi , Kato Tomoyuki , Tatematsu Masae , Tajima Kazuo 
Published: October 2006

Abstract
Consumption of fish rich in n-3 polyunsaturated fatty acids (PUFAs), such as docosahexaenoic acid, is suggested to reduce colorectal cancer risk through inhibition of the arachidonic acid (AA) cascade related to tumorigenesis and cell proliferation. High intake of saturated fatty acids (SFAs) may increase the risk. To examine associations between colorectal cancer risk and fatty acid compositions in erythrocyte membranes, as biomarkers for dietary intakes of fish, fat, and fatty acids, we conducted a case-control study with 74 incident cases and 221 noncancer controls (matched by age, sex, and season of sample collection). Erythrocyte fatty acids were measured using an accelerated solvent extraction and a gas-liquid chromatography. Colorectal cancer had no association with dietary intakes of meat, fish, fat, and fatty acids. However, the risk was inversely associated with erythrocyte compositions of docosahexaenoic acid, AA, and PUFAs [the highest to the lowest tertile, odds ratios, 0.36, 0.42, and 0.15; 95% confidence intervals, 0.14-0.93, 0.18-0.95, and 0.05-0.46; Ptrend &lt; 0.05, respectively] and positively with those of palmitic acid, SFAs, and the ratio of SFAs/PUFAs (odds ratios, 6.46, 8.20, and 9.45; 95% confidence intervals, 2.41-17.26, 2.86-23.52, and 2.84-31.43; Ptrend &lt; 0.005, respectively). In conclusion, we could clearly show decreased and increased risks for colorectal cancer related to PUFAs and SFAs compositions in erythrocyte membranes, respectively, but further research is needed to investigate the discrepancy between our findings and the generally accepted role of the AA cascade. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1791–8)
Effect of Staining Procedures on the Results of Micronucleus Assays with Exfoliated Oral Mucosa Cells
Authors: Nersesyan Armen , Kundi Michael , Atefie Kambis , Schulte-Hermann Rolf , Knasmüller Siegfried 
Published: October 2006

Abstract
Micronuclei in exfoliated epithelial cells are widely used as biomarkers of cancer risk in humans. To elucidate the effect of different staining procedures on the outcome of such investigation, we conducted a study in which the micronuclei frequencies in oral mucosa cells of heavy smokers (n = 20) and nonsmokers (n = 10) were evaluated with nonspecific (Giemsa, May-Grünwald-Giemsa) and DNA-specific (4′,6-diamidino-2-phenylindole, Feulgen, acridine orange) stains, whereas with Giemsa-based stains, the frequencies of micronuclei in smokers were significantly (4- to 5-fold) higher in the smokers group, no significant increase was observed with any of the DNA-specific stains. Furthermore, the evaluation of cells of the two study groups with Feulgen stain showed that oral mucosa cells from smokers had significantly increased levels of nuclear anomalies other than micronuclei. These anomalies are consequences of cell injury found in epithelial cells and are paralleled by formation of keratin bodies in the cytoplasm that resemble micronuclei. Correlation analyses showed that micronuclei frequencies scored in Giemsa-stained slides correlated significantly with karyorrhexis, karyolysis, condensed chromatin, and binucleates, whereas no such correlations were found with DNA-specific stains. These findings indicate that nuclear anomalies (and possibly keratin bodies) may be misinterpreted as micronuclei with nonspecific DNA stains and lead to false-positive results in studies with cells of epithelial origin. Furthermore, our results show that exposure of oral mucosa cells to genotoxic carcinogens contained in tobacco smoke does not lead to induction of micronuclei in these cells. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1835–40)
BRCA1 and BRCA2 Mutation Carriers, Oral Contraceptive Use, and Breast Cancer Before Age 50
Authors: Haile Robert W. , Thomas Duncan C. , McGuire Valerie , Felberg Anna , John Esther M. , Milne Roger L. , Hopper John L. , Jenkins Mark A. , Levine A. Joan , Daly Mary M. , Buys Saundra S. , Senie Ruby T. , Andrulis Irene L. , Knight Julia A. , Godwin Andrew K. , Southey Melissa , McCredie Margaret R.E. , Giles Graham G. , Andrews Lesley , Tucker Katherine , Miron Alexander , Apicella Carmel , Tesoriero Andrea , Bane Anita , Pike Malcolm C. , Whittemore Alice S. ,   kConFab Investigators Ontario Cancer Genetics Network Investigators
Published: October 2006

Abstract
Background: Understanding the effect of oral contraceptives on risk of breast cancer in BRCA1 or BRCA2 mutation carriers is important because oral contraceptive use is a common, modifiable practice.
Methods: We studied 497 BRCA1 and 307 BRCA2 mutation carriers, of whom 195 and 128, respectively, had been diagnosed with breast cancer. Case-control analyses were conducted using unconditional logistic regression with adjustments for family history and familial relationships and were restricted to subjects with a reference age under 50 years.
Results: For BRCA1 mutation carriers, there was no significant association between risk of breast cancer and use of oral contraceptives for at least 1 year [odds ratio (OR), 0.77; 95% confidence interval (95% CI), 0.53-1.12] or duration of oral contraceptive use (Ptrend = 0.62). For BRCA2 mutation carriers, there was no association with use of oral contraceptives for at least 1 year (OR, 1.62; 95% CI, 0.90-2.92); however, there was an association of elevated risk with oral contraceptive use for at least 5 years (OR, 2.06; 95% CI, 1.08-3.94) and with duration of use (ORtrend per year of use, 1.08; P = 0.008). Similar results were obtained when we considered only use of oral contraceptives that first started in 1975 or later.
Conclusions: We found no evidence overall that use of oral contraceptives for at least 1 year is associated with breast cancer risk for BRCA1 and BRCA2 mutation carriers before age 50. For BRCA2 mutation carriers, use of oral contraceptives may be associated with an increased risk of breast cancer among women who use them for at least 5 years. Further studies reporting results separately for BRCA1 and BRCA2 mutation carriers are needed to resolve this important issue. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1863–70)
Interleukin-1B Polymorphisms and Gastric Cancer Risk—A Meta-analysis
Authors: Kamangar Farin , Cheng Cindy , Abnet Christian C. , Rabkin Charles S. 
Published: October 2006

Abstract
Some studies have reported that proinflammatory polymorphisms in interleukin-1B (IL-1B) and IL-1 receptor antagonist (IL-1RN) genes are associated with increased gastric cancer risk. However, other studies have shown null or inverse associations. This meta-analysis reviews and summarizes published evidence for these associations. Searching the PubMed Database yielded 35 studies that reported on the association between IL-1B −511 C&gt;T, IL-1B −31 T&gt;C, or IL-1RN variable number tandem repeat polymorphisms and gastric cancer risk. Q-statistics and I2 statistics were calculated to examine heterogeneity. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated in the random-effects model using the DerSimonian-Laird method. For all gastric cancers, the overall ORs (95% CIs) for IL-1B −511 CT versus CC and TT versus CC genotypes were 1.07 (0.91-1.25) and 1.16 (0.95-1.42), respectively. ORs (95% CIs) for the association between IL-1B −31 CT versus TT and CC versus TT genotypes were 0.99 (0.83-1.19) and 0.98 (0.78-1.21), respectively. For the associations between IL-1RN and gastric cancer, ORs (95% CIs) for *2/L versus LL and *2/*2 versus L/L were 1.15 (0.96-1.38) and 1.23 (0.79-1.92). For each of the examined associations, there was significant heterogeneity among studies; Pheterogeneity ≤ 0.001 and I2 ranged from 0.54 to 0.71. Noncardia cancers showed stronger associations with IL-1B −511 CT or TT and IL1-RN *2/*2 genotypes, but limiting the analysis to intestinal-type cancers, studies conducted in Western countries, or studies in which polymorphisms were in Hardy-Weinberg equilibrium, made no material difference in the results. The overall associations between IL-1B or IL-1RN proinflammatory polymorphisms and gastric cancer were null but several studies showed an association. The sources of this variation are unclear. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1920–8)
Perinatal Factors and Mortality from Breast Cancer
Authors: Sanderson Maureen , Daling Janet R. , Doody David R. , Malone Kathleen E. 
Published: October 2006

AbstractInverse associations have been reported between birthweight and subsequent mortality from circulatory disease and diabetes among women. In the current study, we assessed whether perinatal factors were associated with mortality from breast cancer. This follow-up study consists of breast cancer cases who participated in two population-based case-control studies of breast cancer in women under age 45 years conducted between 1983 and 1992 in three western Washington counties. This analysis is restricted to the 1,024 cases or their proxies who completed a supplementary questionnaire on perinatal factors from 1994 to 1996. The mean and median length of follow-up among living cohort members were 153 and 148 months, respectively. Relative to women who were firstborn, women who were born second or higher in the birth order seemed to have lower mortality from breast cancer [hazard ratio (HR), 0.2; 95% confidence interval (95% CI), 0.2-0.3]. In contrast, maternal age of ≥35 years (HR, 1.7; 95% CI, 1.1-2.8) was associated with higher breast cancer mortality relative to a maternal age of &lt;25 years. Birth order modified the effect of maternal age on mortality from breast cancer (P = 0.03). There was evidence of increased breast cancer mortality for birthweight of ≥4,000 g (HR, 1.8; 95% CI, 1.0-3.1) and twin membership (HR, 2.5; 95% CI, 1.0-6.2). The protective effect of being born second or higher in the birth order against breast cancer mortality regardless of maternal age is striking and needs to be confirmed in future studies. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1984–7)
General and Abdominal Obesity and Survival among Young Women with Breast Cancer
Authors: Abrahamson Page E. , Gammon Marilie D. , Lund Mary Jo , Flagg Elaine W. , Porter Peggy L. , Stevens June , Swanson Christine A. , Brinton Louise A. , Eley J. William , Coates Ralph J. 
Published: October 2006

Abstract
Among postmenopausal women, obesity is linked to increased risk of breast cancer and poorer subsequent survival. For premenopausal women, obesity may reduce incidence, but less is known about its effect on prognosis, particularly for abdominal obesity. This study investigated whether general or abdominal obesity at diagnosis influenced survival in a cohort of young women with breast cancer. A population-based follow-up study was conducted among 1,254 women ages 20 to 54 who were diagnosed with invasive breast cancer between 1990 and 1992 in Atlanta or New Jersey. Women were interviewed within several months of diagnosis and asked about their weight and height at age 20 and in the year before diagnosis. Study personnel did anthropometric measures at the interview. With 8 to 10 years of follow-up, all-cause mortality status was determined using the National Death Index (n = 290 deaths). Increased mortality was observed for women who were obese [body mass index (BMI), ≥30] at the time of interview compared with women of ideal weight [BMI, 18.5-24.9; stage- and income-adjusted hazard ratio (HR), 1.48; 95% confidence interval (95% CI), 1.09-2.01]. A similar result was seen for the highest versus lowest quartile of waist-to-hip ratio (HR, 1.52; 95% CI, 1.05-2.19). Strong associations with mortality were found for women who were obese at age 20 (HR, 2.49; 95% CI, 1.15-5.37) or who were overweight/obese (BMI, ≥25) at both age 20 and the time of interview (HR, 2.22; 95% CI, 1.45-3.40). This study provides evidence that breast cancer survival is reduced among younger women with general or abdominal obesity. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1871–7)