bluuebunny/crossref_metadata_2025_split huggingface dataset:
CYP17Genotypes Differ in Salivary 17-β Estradiol Levels: A Study Based on Hormonal Profiles from Entire Menstrual Cycles
Authors: Jasienska Grazyna , Kapiszewska Maria , Ellison Peter T. , Kalemba-Drozdz Malgorzata , Nenko Ilona , Thune Inger , Ziomkiewicz Anna 
Published: November 2006

AbstractVariation in the levels of sex-steroid hormones results from differences in developmental conditions, adult lifestyle, and genetic polymorphism. Genes involved in sex-steroid biosynthesis have been implicated to influence levels of hormones in premenopausal women, but the results were inconclusive. We tested variation among women in levels of salivary estradiol (E2) corresponding to CYP17 genotypes. CYP17 encodes cytochrome P450c17α, which mediates two enzymes important in E2 synthesis. In contrast to the earlier studies that relied on one or a few samples for assessing the E2 levels of an individual woman, our study is based on daily collected saliva samples for one entire menstrual cycle. Sixty Polish women, ages 24 to 36 years, with regular menstrual cycles and no reported fertility problems participated in the study. Women with A2/A2 genotype had 54% higher mean E2 levels than women with A1/A1 genotype (P = 0.0001) and 37% higher than women with A1/A2 genotype (P = 0.0008). Heterozygous A1/A2 women had 13 % higher E2 levels than homozygous A1/A1 women (but this difference was significant only in a nonparametric test). Levels of E2 during the day with highest E2 (day −1) were 72% higher in A2/A2 compared with A1/A1 (P = 0.01) and 52 % higher compared with A1/A2 (P = 0.03). Our results suggest that CYP17 genotype may serve as a biomarker of endocrine function in women of reproductive age. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2131–5)
Genes Involved in DNA Repair and Nitrosamine Metabolism and Those Located on Chromosome 14q32 Are Dysregulated in Nasopharyngeal Carcinoma
Authors: Dodd Lori E. , Sengupta Srikumar , Chen I-How , den Boon Johan A. , Cheng Yu-Juen , Westra William , Newton Michael A. , Mittl Beth F. , McShane Lisa , Chen Chien-Jen , Ahlquist Paul , Hildesheim Allan 
Published: November 2006

Abstract
Polymorphisms in nitrosamine metabolism, DNA repair, and immune response genes have been associated with nasopharyngeal carcinoma (NPC). Studies have suggested chromosomal regions involved in NPC. To shed light on NPC etiology, we evaluated host gene expression patterns in 31 NPC and 10 normal nasopharyngeal tissue specimens using the Affymetrix Human Genome U133 Plus 2.0 Array. We focused on genes in five a priori biological pathways and chromosomal locations. Rates of differential expression within these prespecified lists and overall were tested using a bootstrap method. Differential expression was observed for 7.6% of probe sets overall. Elevations in rate of differential expression were observed within the DNA repair (13.7%; P = 0.01) and nitrosamine metabolism (17.5%; P = 0.04) pathways. Differentially expressed probe sets within the DNA repair pathway were consistently overexpressed (93%), with strong effects observed for PRKDC, PCNA, and CHEK1. Differentially expressed probe sets within the nitrosamine metabolism pathway were consistently underexpressed (100%), with strong effects observed for NQ01, CYP2B6, and CYP2E1. No significant evidence of increases in rate of differential expression was seen within the immune/inflammatory pathway. A significant elevation in rate of differential expression was noted for chromosome 4p15.1-4q12 (13.0%; P = 0.04); both overexpression and underexpression were evident (38% and 62%, respectively). An elevation in the rate of differential expression on chromosome 14q32 was observed (11.3%; P = 0.06) with a consistent pattern of gene underexpression (100%; P &lt; 0.0001). These effects were similar when excluding late-stage tumors. Our results suggest that nitrosamine activation and DNA repair are important in NPC. The consistent down-regulation of expression on chromosome 14q32 suggests loss of heterozygosity in this region. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2216–25)
A Prospective Investigation of Height and Prostate Cancer Risk
Authors: Sequoia Jacqueline S.P. , Wright Margaret E. , McCarron Peter , Pietinen Pirjo , Taylor Philip R. , Virtamo Jarmo , Albanes Demetrius 
Published: November 2006

Abstract
Greater adult height, which reflects a combination of early nutrition, exposure to androgens, growth hormones, and other factors during growth and development, as well as heredity, has been associated with increased prostate cancer risk in several observational studies, but findings have been inconsistent. We examined this relationship in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort. At baseline, 29,119 Finnish male smokers 50 to 69 years old had height and weight measured by trained personnel, provided information on demographic, smoking, medical, and other characteristics, and completed an extensive diet history questionnaire. A total of 1,346 incident prostate cancer cases were identified during a follow-up period of up to 17.4 years (median, 14.1 years). In age-adjusted Cox proportional hazards models, the hazard ratios and 95% confidence intervals for prostate cancer according to increasing quintiles of height [≤168, 169-171, 172-175, 176-178, and &gt;178 cm] were 1.00 (reference), 1.11 (0.93-1.32), 1.11 (0.95-1.31), 1.30 (1.01-1.55), and 1.14 (0.96-1.35); Ptrend = 0.04. In analyses stratified by disease stage (available for 916 cases), a strong dose-response relationship was observed between greater height and advanced, but not earlier-stage, disease [tumor-node-metastasis stage III-IV, hazard ratio and 95% confidence interval for increasing quintiles of height: 1.77 (1.18-2.65), 1.82 (1.25-2.65), 1.93 (1.29-2.90), and 2.02 (1.37-2.97); Ptrend = 0.0008, Pinteraction = 0.002]. Our study provides additional evidence that increased height is a risk factor for prostate cancer and suggests that taller men are particularly susceptible to advanced disease. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2174–8)
Effects of Parity on Pregnancy Hormonal Profiles Across Ethnic Groups with a Diverse Incidence of Breast Cancer
Authors: Arslan Alan A. , Zeleniuch-Jacquotte Anne , Lukanova Annekatrin , Afanasyeva Yelena , Katz Joseph , Levitz Mortimer , Del Priore Giuseppe , Toniolo Paolo 
Published: November 2006

Abstract
Epidemiologic evidence suggests that a full-term pregnancy may affect maternal risk of breast cancer later in life. The objective of this cross-sectional study was to compare circulating levels of maternal hormones affecting breast differentiation (human chorionic gonadotropin and prolactin) and proliferation [α-fetoprotein, insulin-like growth factor I (IGF-I), and estradiol] between women at a low to moderate risk (Asians and Hispanics), as compared with women at a high risk for breast cancer (Caucasians and African-Americans). Between May 2002 and December 2004, a total of 586 pregnant women were approached during a routine prenatal visit. Among them, 450 women (206 Caucasian, 126 Asian, 88 Hispanic, and 30 African-American) met the inclusion criteria and signed the informed consent. Only singleton pregnancies were considered. Blood samples were drawn during the second trimester of pregnancy. Laboratory analyses were done using the IMMULITE 2000 immunoassay system. Gestational age standardized mean levels of estradiol, IGF-I, and prolactin were significantly higher in Hispanic women compared with Caucasian women. Mean concentration of IGF-I was significantly higher in African-American women compared with Caucasian and Asian women. No significant differences in pregnancy hormone levels were observed between Caucasian and Asian (predominantly second-generation Chinese) women in this study. Irrespective of ethnicity, women who had their first pregnancy had substantially higher mean levels of α-fetoprotein, human chorionic gonadotropin, estradiol, and prolactin compared with women who previously had at least one full-term pregnancy. These data suggest that circulating pregnancy hormone levels may explain some of the ethnic differences in breast cancer risk. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2123–30)
Reproductive Factors, Oral Contraceptive Use, and Human Papillomavirus Infection: Pooled Analysis of the IARC HPV Prevalence Surveys
Authors: Vaccarella Salvatore , Herrero Rolando , Dai Min , Snijders Peter J.F. , Meijer Chris J.L.M. , Thomas Jaiye O. , Hoang Anh Pham Thi , Ferreccio Catterina , Matos Elena , Posso Hector , de Sanjosé Silvia , Shin Hai-Rim , Sukvirach Sukhon , Lazcano-Ponce Eduardo , Ronco Guglielmo , Rajkumar Raj , Qiao You-Lin , Muñoz Nubia , Franceschi Silvia ,   and IARC HPV Prevalence Surveys Study Group
Published: November 2006

AbstractHigh parity, early age at first full-term pregnancy (FTP), and long-term oral contraceptive (OC) use increase cervical cancer risk, but it is unclear whether these variables are also associated with increased risk of acquisition and persistence of human papillomavirus (HPV) infection, the main cause of cervical cancer. Information on reproductive and menstrual characteristics and OC use were collected from 14 areas worldwide, among population-based, age-stratified random samples of women aged 15 years or older. HPV testing was done using PCR-based enzyme immunoassay. Unconditional logistic regression was used to estimate the odds ratios (OR) of being HPV-positive according to reproductive and menstrual factors and corresponding 95% confidence intervals (CI). When more than two groups were compared, floating CIs (FCI) were estimated. A total of 15,145 women (mean age, 40.9 years) were analyzed. Women with ≥5 FTPs (OR, 0.90; 95% FCI, 0.76-1.06) showed a similar risk of being HPV-positive compared with women with only one FTP (OR, 1.00; 95% FCI, 0.86-1.16). However, nulliparous women showed an OR of 1.40 (95% CI, 1.16-1.69) compared with parous women. Early age at first FTP was not significantly related to HPV positivity. HPV positivity was similar for women who reported ≥10 years of use of OCs (OR, 1.16; 95% FCI, 0.85-1.58) and never users of OCs (OR, 1.00; 95% FCI, 0.90-1.12). Our study suggests, therefore, that high parity, early age at first FTP, and long-term OC use are not associated with HPV prevalence, but rather these factors might be involved in the transition from HPV infection to neoplastic cervical lesions. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2148–53)
Alleviating the Burden of Cancer: A Perspective on Advances, Challenges, and Future Directions
Authors: Schottenfeld David , Beebe-Dimmer Jennifer 
Published: November 2006

AbstractThe control of the burden of cancer would be achievable by promoting health-maintaining lifestyle behavioral practices in conjunction with facilitated access to affordable and effective periodic screening and early detection examinations combined with comprehensive treatment services. In a global population exceeding six billion in the year 2002, there were ∼10.9 million new cancer cases, 6.7 million cancer deaths, and 22.4 million persons surviving from cancer diagnosed in the previous 5 years. In 2020, the world's population is projected to increase to 7.5 billion and will experience 15 million new cancer cases and 12 million cancer deaths. This perspective on advances, challenges, and future directions in cancer epidemiology and prevention reviews the conceptual foundation for multistep carcinogenesis, causal mechanisms associated with chronic inflammation and the microenvironment of the cancer cell, and obesity, energy expenditure, and insulin resistance. Strategic priorities in global cancer control initiatives should embrace these fundamental concepts by targeting tobacco and alcohol consumption, the increasing prevalence of obesity and metabolic sequelae, and persistent microbial infections. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2049–55)
In the Shadow of the Khmer Rouge Tribunal: The Domestic Trials of Nuon Paet, Chhouk Rin and Sam Bith, and the Search for Judicial Legitimacy in Cambodia
Authors: Hall John 
Published: November 2006

AbstractIn 1994, Khmer Rouge guerrillas attacked a train in Kampot province, Cambodia, taking hostage three young Western backpackers. Two months later, after negotiations for their release collapsed, the three were murdered. Australian, British, and French government representatives exerted considerable diplomatic pressure on the Cambodian government, demanding that those responsible for the kidnapping and murders be brought to justice. In response, three former Khmer Rouge commanders, Chhouk Rin, Nuon Paet and Sam Bith, were arrested, and in a series of trials that lasted from 1999 until 2006, were convicted and sentenced to life imprisonment by Cambodian domestic courts.Crucially, these trials took place in the middle of difficult negotiations between Cambodia and the United Nations over the scope and nature of the proposed Khmer Rouge tribunal. A key point of disagreement was over the proper role in the tribunal for Cambodia's notoriously inefficient, corrupt and government-dominated judiciary. For that reason, the trials became a closely watched test of the Cambodian legal system, and took on a symbolic weight unusual for domestic trials. Dismissed by some observers as mere show trials aimed at legitimizing Prime Minister Hun Sen on the international stage, the trials nevertheless marked a significant step forward in the development of a functioning – albeit seriously flawed – judiciary.This article is the first to examine these highly significant cases. The Paet, Bith and Rin trials demonstrate the ability of Cambodian judges to convict Khmer Rouge members brought before them; what remains less clear is whether the Cambodian judicial appointees to the tribunal will be capable of meeting internationally recognized standards of justice. Perhaps, if permitted by their government to do so, they will grow to meet this historic challenge. If they do not, then the trials of Paet, Bith and Rin, may prove to be the high watermark in the search for judicial legitimacy in Cambodia.
Water Mass Distribution and Ventilation Time Scales in a Cost-Efficient, Three-Dimensional Ocean Model
Authors: Müller S. A. , Joos F. , Edwards N. R. , Stocker T. F. 
Published: November 2006

Abstract
A cost-efficient, seasonally forced three-dimensional frictional geostrophic balance ocean model (Bern3D) has been developed that features isopycnal diffusion and Gent–McWilliams transport parameterization, 32 depth layers, and an implicit numerical scheme for the vertical diffusion. It has been tuned toward observed chlorofluorocarbon (CFC-11) inventories and deep ocean radiocarbon signatures to reproduce the ventilation time scales of the thermocline and the deep ocean. Model results are consistent with the observed large-scale distributions of temperature, salinity, natural and bomb-produced radiocarbon, CFC-11, anthropogenic carbon, 39Ar/Ar, and estimates of the meridional heat transport. Root-mean-square errors for the temperature and salinity fields are 1 K and 0.2 psu, comparable to results from the Ocean Carbon-Cycle Model Intercomparison Project. Global inventories of CFC-11 and anthropogenic carbon agree closely with observation-based estimates. Model weaknesses include a too-weak formation and propagation of Antarctic Intermediate Water and of North Atlantic Deep Water. The model has been applied to quantify the recent carbon balance, surface-to-deep transport mechanisms, and the importance of vertical resolution for deep equatorial upwelling. Advection is a dominant surface-to-deep transport mechanism, whereas explicit diapycnal mixing is of little importance for passive tracers and contributes less than 3% to the modeled CFC-11 inventory in the Indo-Pacific. Decreasing the vertical resolution from 32 to 8 layers causes deep equatorial upwelling to increase by more than a factor of 4. Modeled ocean uptake of anthropogenic carbon is 19.7 GtonC over the decade from 1993 to 2003, comparable to an estimate from atmospheric oxygen data of 22.4 ± 6.1 GtonC.
Variability of the Winter Wind Waves and Swell in the North Atlantic and North Pacific as Revealed by the Voluntary Observing Ship Data
Authors: Gulev Sergey K. , Grigorieva Vika 
Published: November 2006

Abstract
This paper analyses secular changes and interannual variability in the wind wave, swell, and significant wave height (SWH) characteristics over the North Atlantic and North Pacific on the basis of wind wave climatology derived from the visual wave observations of voluntary observing ship (VOS) officers. These data are available from the International Comprehensive Ocean–Atmosphere Data Set (ICOADS) collection of surface meteorological observations for 1958–2002, but require much more complicated preprocessing than standard meteorological variables such as sea level pressure, temperature, and wind. Visual VOS data allow for separate analysis of changes in wind sea and swell, as well as in significant wave height, which has been derived from wind sea and swell estimates. In both North Atlantic and North Pacific midlatitudes winter significant wave height shows a secular increase from 10 to 40 cm decade−1 during the last 45 yr. However, in the North Atlantic the patterns of trend changes for wind sea and swell are quite different from each other, showing opposite signs of changes in the northeast Atlantic. Trend patterns of wind sea, swell, and SWH in the North Pacific are more consistent with each other. Qualitatively the same conclusions hold for the analysis of interannual variability whose leading modes demonstrate noticeable differences for wind sea and swell. Statistical analysis shows that variability in wind sea is closely associated with the local wind speed, while swell changes can be driven by the variations in the cyclone counts, implying the importance of forcing frequency for the resulting changes in significant wave height. This mechanism of differences in variability patterns of wind sea and swell is likely more realistic than the northeastward propagation of swells from the regions from which the wind sea signal originates.
von Willebrand factor and factor VIII are independently required to form stable occlusive thrombi in injured veins
Authors: Chauhan Anil K. , Kisucka Janka , Lamb Colin B. , Bergmeier Wolfgang , Wagner Denisa D. 
Published: November 2006

Abstract
von Willebrand factor (VWF) protects factor VIII (FVIII) from proteolysis and mediates the initial contact of platelets with the injured vessel wall, thus playing an important role in hemostasis and thrombosis. VWF is crucial for the formation of occlusive thrombi at arterial shear rates. However, with only a few conflicting studies published, the role of VWF in venous thrombosis is still unclear. Using gene-targeted mice, we show that in ferric chloride–injured veins platelet adhesion to subendothelium is decreased and thrombus growth is impaired in VWF−/− mice when compared with wild type (WT). We also observed increased embolization in the VWF−/− mice, which was due to lower FVIII levels in these mice as recombinant factor VIII (r-FVIII) restored thrombus stability. Despite normalization of blood clotting time and thrombus stability after r-FVIII infusion, the VWF−/− venules did not occlude. Transgenic platelets lacking the VWF receptor GPIbα extracellular domain showed decreased adhesion to injured veins. But, after a delay, all the injured venules occluded in these transgenic mice. Thus, VWF likely uses other adhesion receptors besides GPIbα in thrombus growth under venous shear conditions. Our studies document crucial roles for VWF and FVIII in experimental thrombosis under venous flow conditions in vivo.
Late cardiotoxicity after treatment for Hodgkin lymphoma
Authors: Aleman Berthe M. P. , van den Belt-Dusebout Alexandra W. , De Bruin Marie L. , van 't Veer Mars B. , Baaijens Margreet H. A. , Boer Jan Paul de , Hart Augustinus A. M. , Klokman Willem J. , Kuenen Marianne A. , Ouwens Gabey M. , Bartelink Harry , van Leeuwen Flora E. 
Published: November 2006

Abstract
We assessed cardiovascular disease (CVD) incidence in 1474 survivors of Hodgkin lymphoma (HL) younger than 41 years at treatment (1965-1995). Multivariable Cox regression and competing risk analyses were used to quantify treatment effects on CVD risk. After a median follow-up of 18.7 years, risks of myocardial infarction (MI) and congestive heart failure (CHF) were strongly increased compared with the general population (standardized incidence ratios [SIRs] = 3.6 and 4.9, respectively), resulting in 35.7 excess cases of MI and 25.6 excess cases of CHF per 10 000 patients/year. SIRs of all CVDs combined remained increased for at least 25 years and were more strongly elevated in younger patients. Mediastinal radiotherapy significantly increased the risks of MI, angina pectoris, CHF, and valvular disorders (2- to 7-fold). Anthracyclines significantly added to the elevated risks of CHF and valvular disorders from mediastinal RT (hazard ratios [HRs] were 2.81 and 2.10, respectively). The 25-year cumulative incidence of CHF after mediastinal radiotherapy and anthracyclines in competing risk analyses was 7.9%. In conclusion, risks of several CVDs are 3- to 5-fold increased in survivors of HL compared with the general population, even after prolonged follow-up, leading to increasing absolute excess risks over time. Anthracyclines further increase the elevated risks of CHF and valvular disorders from mediastinal radiotherapy.
Ultrastructural analysis of development of myocardium in calreticulin-deficient mice
Authors: Lozyk Mira D , Papp Sylvia , Zhang Xiaochu , Nakamura Kimitoshi , Michalak Marek , Opas Michal 
Published: November 2006

AbstractBackgroundCalreticulin is a Ca2+binding chaperone of the endoplasmic reticulum which influences gene expression and cell adhesion. The levels of both vinculin and N-cadherin are induced by calreticulin expression, which play important roles in cell adhesiveness. Cardiac development is strictly dependent upon the ability of cells to adhere to their substratum and to communicate with their neighbours.ResultsWe show here that the levels of N-cadherin are downregulated in calreticulin-deficient mouse embryonic hearts, which may lead to the disarray and wavy appearance of myofibrils in these mice, which we detected at all investigated stages of cardiac development. Calreticulin wild type mice exhibited straight, thick and abundant myofibrils, which were in stark contrast to the thin, less numerous, disorganized myofibrils of the calreticulin-deficient hearts. Interestingly, these major differences were only detected in the developing ventricles while the atria of both calreticulin phenotypes were similar in appearance at all developmental stages. Glycogen also accumulated in the ventricles of calreticulin-deficient mice, indicating an abnormality in cardiomyocyte metabolism.ConclusionCalreticulin is temporarily expressed during heart development where it is required for proper myofibrillogenesis. We postulate that calreticulin be considered as a novel cardiac fetal gene.