bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B82: Metabolic risk factors and colorectal adenoma risk in Korean population
Authors: Kim Byung Chang , Shin Aesun , Hong Chang Won , Sohn Dae Kyung , Han Kyung Su , Chang Hee Jin , Kim Jeongseon , Oh Jae Hwan 
Published: January 2011

Abstract
Recent epidemiologic studies reported that diabetes mellitus and metabolic syndrome increase the risk of colorectal neoplasms. Although the exact mechanism is not clearly explained, it might be mediated by several process including insulin resistance, dysregulation of insulin-like growth factor axis, oxidative stress, DNA damage, and adipokine production. The objective of the current study was to assess the associations between metabolic risk factors and the risk for developing colorectal adenomatous polyp according to detailed clinical information on polyps in a large colonoscopy-based study. The study participants visited the National Cancer Center, Korea for cancer screening between April 2007 and April 2009. A total of 1,771 newly diagnosed colorectal adenoma patients and 4,967 polyp-free controls were included in the analysis. Metabolic syndrome was defined based on the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) criteria with a modified waist circumference for Asian population.
In men, high body mass index, waist circumference, blood pressure, and triglyceride were associated with an increased risk for colorectal adenoma. Possessing three and more metabolic risk factors was associated with an increased risk for adenoma (OR = 1.49, 95% CI = 1.23-1.81). The association between metabolic syndrome and colorectal adenoma was observed for the risk for right colon adenoma (OR = 1.64, 95% CI 1.27-2.10) or adenomas in multiple anatomical locations (OR = 1.55, 95% CI = 1.12-2.15). In women, high waist circumference and triglyceride were associated with an increased risk for adenoma, and metabolic syndrome was associated with a high risk for adenoma (OR = 1.45, 95% CI 1.09-1.94), especially that for adenoma of left colon (OR = 1.62, 95% CI = 1.02-2.59). In conclusion, metabolic risk factors and metabolic syndrome were risk factors for colorectal adenoma, and the increased risks were more prominent for right colon adenoma in men and left colon adenoma in women.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):B82.
Abstract CN05-04: Early molecular changes in prostate carcinogenesis
Authors: Nelson William G. , Haffner Michael C. , Aryee Martin J. , Esopi David M. , Isaacs William B. , Bova G. Steven , Meeker Alan K. , Netto George , Marzo Angelo M. De , Yegnasubramanian Srinivasan 
Published: January 2011

Abstract
After castration was shown by Charles Huggins in 1941 to be an effective treatment for advanced prostate cancer, androgenic hormones were assumed to be responsible in some way for disease development.
Nonetheless, the manner in which androgens might contribute to prostatic carcinogenesis has remained elusive over the subsequent seven decades. Androgen levels decline steadily throughout adulthood in men, just as prostate cancers begin to appear (Rohrmann S et al. J Clin Endocrinol Metabol 92:2519-25, 2007). In addition, the action of testosterone, and its metabolite dihydrotestosterone, on prostate epithelial cells in adult men tends to be the promotion of terminal differentiation by activating transcription of target genes, such as PSA and TMPRSS2, which form the secretion elaborated by the prostate for the ejaculate. By driving terminal differentiation of normal prostate cells, androgens seem unlikely to cause neoplastic transformation. However, new insights into the generation of somatic genome rearrangements that create fusion oncogenes in prostate cells have revealed a new mechanism of androgen receptor-associated cancer pathogenesis. The fusion oncogene TMPRSS2-ERG, present in at least half of all prostate cancer cases, may be the most common somatic gene fusion event in all of human cancer (Tomlins SA et al. Science 310:644-8, 2005). We have found that androgen receptor-triggered transcription in prostate cells leads to the recruitment of topoisomerase II-beta (TOP2B) by the receptor to sites of TMPRSS2-ERG genomic breakpoints, promoting TOP2B-mediated DNA double strand breaks and de novo TMPRSS2-ERG fusion transcripts. The results implicate androgens in the creation of TMPRSS2-ERG rearrangements, via a mechanism involving the androgen receptor and TOP2B, and provide new hints as to how prostate cancers might be better prevented.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN05-04.
Abstract CN08-02: Implications of the cancer stem cell hypothesis for breast cancer prevention
Authors: Kakarala Madhuri , Sun Duxin , Wicha Max S. 
Published: January 2011

Abstract
The cancer stem cell hypothesis proposes that cancers arise in cell populations that either dysregulate or acquire the stem cell property of self-renewal. Resulting cancers are hierarchically organized and driven by a subpopulation that retains stem cell properties. This suggests that dysregulation of self-renewal plays an important role in early stages of carcinogenesis and that an understanding of the pathways which regulate self-renewal may lead to new strategies for cancer prevention. Our laboratory has identified markers including CD44+/CD24- and Aldehyde dehydrogenase which have proven useful in identifying populations of normal and transformed breast epithelial cells. Furthermore, we have developed in vitro and animal models to elucidate pathways which regulate self-renewal in these cells. These studies, and others, suggest that stem cell self-renewal is regulated by an interaction of intrinsic and extrinsic pathways. Intrinsic regulation occurs through interacting developmental pathways including Notch, hedgehog, Wnt and Akt. Cytokine networks in the stem cell niche including IL-8 and IL6 also play important roles in stem cell regulation. These pathways may also contribute to the well-known links between inflammation and cancer. Inflammatory cytokines may contribute to clonal expansion of stem cell populations which can then acquire secondary genetic changes resulting in expression of the fully malignant phenotype. We have demonstrated that dietary components including curcumin and sulforaphane which have been shown to have chemopreventive properties are able to target Wnt signaling in stem cell populations. These and other studies support the approach of targeting stem cell self-renewal pathways for cancer prevention.
References:
1. Liu S, Wicha MS. Targeting breast cancer stem cells. J Clin Oncol 28:4006-12, 2010.
2. Kakarala M, Brenner DE, Korkaya H, et al: Targeting breast stem cells with the cancer preventive compounds curcumin and piperine. Breast Cancer Res Treat, 2009.
3. Li Y, Zhang T, Korkaya H, et al. Sulforaphane, a dietary component of broccoli/broccoli sprouts, inhibits breast cancer stem cells. Clin Cancer Res 16:2580-90, 2010.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN08-02.
Abstract ED01-02: Untargeted plasma metabolite profiling: Strategies and approaches for comprehensive characterization of gene mutations and drug actions
Authors: Gross Steven S. , Chen Qiuying 
Published: January 2011

Abstract
The small molecule metabolome (&lt; 1000 Da) defines a cell's phenotype on a moment-to-moment basis. Notably, the composition of the metabolome remains a biomedical frontier, since it is not predicted by other “omic” information (neither the genome, transcriptome nor proteome) and is only partially defined at present. Accordingly, tools for defining molecular structures, NMR and mass spectrometry (MS), have provided the essential platforms for current metabolomic studies. This presentation will describe the use of MS-based workflows for broad untargeted metabolite profiling. A proof-of-principal study will be described, showing that thousands of plasma metabolites can be effectively surveyed in a mouse model and metabolic consequences of a gene deletion or drug treatment can be specified. Additionally, the potential of untargeted metabolite profiling to screen neonatal plasma for rare inborn errors of metabolism will be considered and preliminary findings will be described.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):ED01-02.
Abstract ED01-03: Metabolomics of disease progression
Authors: Beecher Christopher , Rajendiran Thekkelnaycke , Chinnaiyan Arul 
Published: January 2011

Abstract
While the total potential of a biological systems response is defined by their genes, and the organism's desired response (to its current status) may be embodied in their transcripts, the metabolome embodies what an organism is actually of doing at a biochemical level. For this reason the metabolomic data may be quite diagnostic of a given disease state, that may or may not be dictated by either the genetic or transcriptomic levels. In this presentation we will discuss an application of metabolomics to define a series of biomarkers. The subsequent explorations of the details of this biomarker have revealed mechanisms that are likely to be significant to the progression of cancer.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):ED01-03.
Abstract ED06-02: Understanding the structure and function of the gut microbiota
Authors: Young Vincent B. 
Published: January 2011

Abstract
Until recently, the study of complex microbial communities was limited by the culture-based methodologies that only captured a subset of the diversity present. The advent of molecular methods for the study of microbial consortia has allowed us to greatly increase our understanding of the structure, function and dynamics of the indigenous human microbiota. In this opening lecture of the session I will introduce the techniques and strategies for studying the structure and function of complex consortia of microbes, with a focus on the community that inhabits the gastrointestinal tract. Using the example of Clostridium difficile infection following antibiotic administration as an example, I will demonstrate how changes in the community structure of the gut microbiota can be monitored over time. The associated functional changes associated with changes in microbial community structure will be discussed. We have recently applied culture-independent molecular methods, largely based on retrieval of 16S rRNA-encoding gene sequences, to investigate the role of the indigenous microbiota in C. difficile infection (CDI). Through studies of human patients with CDI we have demonstrated that recurrent disease is associated with an overall decrease in the diversity of the fecal microbiota. We have leveraged a recently described murine model of CDI to conduct more detailed studies of the role of the microbiota in C. difficile infection. Data from this model system indicates that a subset of the indigenous microbiota is important in mediating colonization resistance against C. difficile and possibly in modulating the effects of C. difficile toxin. This example will allow the audience to understand and appreciate the growing number of studies that are examining associations between the community structure of the gut microbiota and a variety of disease states including colorectal cancer.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):ED06-02.
Abstract PL05-03: Global trends in cancer: The imperative for prevention
Authors: Thun Michael J. , Jemal Ahmedin , Carter Brian D. , Ward Elizabeth M. 
Published: January 2011

Abstract
Despite the encouraging decrease in the incidence and death rates from all cancers combined in the United States, and the decrease in death rates from selected cancers in many industrialized countries, the number of people affected by cancer continues to increase rapidly worldwide. More than 12 million new cases and 7.5 million cancer deaths are estimated to have occurred globally in 2008. The number of deaths from cancer has increased by 25% since 1990 and is projected to nearly double (to 13.1 million) by 2030. Moreover, the global increase in the disease burden from cancer disproportionately affects low- and medium-resource countries, which currently account for nearly two-thirds of all cancer deaths, and are projected to contribute over 70% by 2030.
Underlying this global increase in the cancer burden and its disproportionate impact on economically developing countries is a combination of both demographic changes and the shifting distribution of major risk factors. Three particularly important factors are the growth and aging of populations (especially longer life expectancy for massive numbers of young adults in developing countries), the entrenchment of modifiable risk factors (particularly cigarette smoking, Western diet, and physical inactivity), and the slower decline in cancers related to infectious etiologies in low-resource countries than in high-resource countries.
Given these trends, the success of future efforts in global cancer control will require considerably greater emphasis on the development and implementation of effective population-level approaches to cancer prevention and early detection than exist currently in most countries. This talk will describe several successful models of tobacco control and interventions against chronic infections caused by hepatitis B and human papillomavirus that have been developed and implemented in high-risk developing countries. Other talks in the session will describe promising examples of population-level prevention in the U.S., Australia, and Canada.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):PL05-03.
Abstract PR-07: A new resource to accelerate research into the cause and prevention of breast cancer: The Love/Avon Army of Women
Authors: Love Susan M. 
Published: January 2011

Abstract
Background: It is well-established that there is a need for more research into the cause and prevention of breast cancer. While many studies are done in cell lines and laboratory animals, translation of findings to women often falters due to perceived difficulty in recruiting women for research. The Dr. Susan Love Research Foundation received a grant from the Avon Foundation to form the Love/Avon Army of Women (AOW): an online recruitment resource designed to partner women with the research community in an effort to accelerate breast cancer research.
Methods: The AOW was launched in 2008 with the goal of recruiting 1 million women interested in participating in breast cancer research. Researchers interested in having the AOW recruit for their studies submit a proposal to be reviewed by the AOW Scientific Advisory Committee, comprised of nominees from AACR and NBCC. If a study is accepted, a mass e-mail describing the study procedures and inclusion/exclusion criteria is sent to the entire AOW database. Women sign up at www.armyofwomen.org to join the AOW. Women aren't committing to participating in a particular study, but agree to receive AOW e-mails about breast cancer research studies. If the individual is interested and qualifies for a study, she undergoes a secondary online screening and then her contact information is passed on to the principal investigator.
Results: Over 336,500 women have signed up, including survivors and healthy women, ranging from age 18 to 100, representing all 50 U.S. states and 49 countries. To date, the AOW has recruited for 34 studies, both regional and national, that vary from biomarker and circadian rhythm research to psychosocial and quality-of-life studies. With over 44,000 AOW members having participated in the research process, this method of recruitment has been found to be effective and efficient. The diversity of the AOW members has proved beneficial for many studies such as those needing to enroll African American women, women of varying sexual orientations, or young survivors.
Many studies were closed to enrollment within the first 48 hours after accruing all subjects while others were very quickly overenrolled by 5% to 10%. This overwhelming response has led many researchers to seek additional funding to increase their statistical significance and accommodate all eligible subjects.
Conclusions: The Love/Avon Army of Women is a novel resource for scientists to accelerate accrual, expand the number and diversity of their subject population and to obtain exactly the type of specimens they need when they need it. This new partnership between women and scientists can revolutionize research and accelerate efforts to eradicate breast cancer.
This talk is also presented as Poster A62.
Citation Information: Cancer Prev Res 2010;3(12 Suppl):PR-07.
Object-Based Analysis and Verification of WRF Model Precipitation in the Low- and Midlatitude Pacific Ocean
Authors: Skok Gregor , Tribbia Joe , Rakovec Jože 
Published: January 2011

Abstract
An extended version of the Method for Object-based Diagnostic Evaluation (MODE) was used to perform a verification of precipitation provided by the Weather Research and Forecasting (WRF) model Tropical Channel Simulation (performed by NCAR). Model 3-hourly precipitation accumulations were compared to the Tropical Rainfall Measuring Mission (TRMM) 3B42 satellite-derived precipitation in the low- and midlatitude Pacific Ocean during 1998–2000. Overall, the spatial distribution of annual mean precipitation (i.e., the clear shape of the ITCZ with two maxima—one located in the east and one in the west) was reproduced well by the WRF model; however, there was considerably more precipitation in the WRF simulation than in the TRMM dataset. Object-based analysis identified more precipitation objects with life spans less than 30 h and fewer objects with life spans longer than 60 h in the TRMM dataset compared to the WRF simulation. Objects with the longest life span (&gt;90 h) tended to occur in similar regions in both the modeled and satellite-derived datasets. Two of these regions were in the western part of the domain and one was in the eastern portion of the ITCZ, although these regions did not necessarily coincide with the regions of maximum precipitation accumulations. Both datasets had mostly eastward movement in the midlatitudes. The datasets, however, diverged around the central part of the ITCZ where the TRMM dataset displayed both eastward and westward movement, while westward movement was dominant in the WRF simulation. The analysis also showed that precipitation object trajectories were smoother in the model than in the TRMM dataset.
Book Reviews
Authors: Wellisz Stanislaw 
Published: January 2011

The World Bank: Its First Half Century. Volume 1: History. Volume 2, Perspecitves. Edited by Devesh Kapur, John P. Lewis, and Richard Webb. Washington, D.C.: Brookings Institution Press. 1997. Pp. xviii, 1275, vol. 1; xviii, 766, vol. 2. $79.95, vol. 1; ‘.95, vol. 2. ISBN 0–8157–5236–9, vol. 1; 0–8157–5234–2, vol. 2. JEL 98–0690 JEL 98–0691
Book Reviews
Authors: Furubotn Eirik G 
Published: January 2011

Neoclassical Microeconomic Theory: The Founding Austrian Version. By A. M. Endres. Foundations of the Market Economy series. London and New York: Routledge. 1997. Pp. xiii, 271. £45.00. ISBN 0–415–15209–7. JEL 97–0800
A Novel Component of the Disulfide-Reducing Pathway Required for Cytochrome c Assembly in Plastids
Authors: Gabilly Stéphane T , Kropat Janette , Karamoko Mohamed , Page M Dudley , Nakamoto Stacie S , Merchant Sabeeha S , Hamel Patrice P 
Published: January 2011

Abstract
In plastids, the conversion of energy in the form of light to ATP requires key electron shuttles, the c-type cytochromes, which are defined by the covalent attachment of heme to a CXXCH motif. Plastid c-type cytochrome biogenesis occurs in the thylakoid lumen and requires a system for transmembrane transfer of reductants. Previously, CCDA and CCS5/HCF164, found in all plastid-containing organisms, have been proposed as two components of the disulfide-reducing pathway. In this work, we identify a small novel protein, CCS4, as a third component in this pathway. CCS4 was genetically identified in the green alga Chlamydomonas reinhardtii on the basis of the rescue of the ccs4 mutant, which is blocked in the synthesis of holoforms of plastid c-type cytochromes, namely cytochromes f and c6. Although CCS4 does not display sequence motifs suggestive of redox or heme-binding function, biochemical and genetic complementation experiments suggest a role in the disulfide-reducing pathway required for heme attachment to apoforms of cytochromes c. Exogenous thiols partially rescue the growth phenotype of the ccs4 mutant concomitant with recovery of holocytochrome f accumulation, as does expression of an ectopic copy of the CCDA gene, encoding a trans-thylakoid transporter of reducing equivalents. We suggest that CCS4 might function to stabilize CCDA or regulate its activity.
Metronidazole Population Pharmacokinetics in Preterm Neonates Using Dried Blood-Spot Sampling
Authors: Suyagh Maysa , Collier Paul S. , Millership Jeffrey S. , Iheagwaram Godwill , Millar Muriel , Halliday Henry L. , McElnay James C. 
Published: January 2011

OBJECTIVES:
To characterize the population pharmacokinetics of metronidazole in preterm neonates.

PATIENTS AND METHODS:
Data were collected prospectively from 32 preterm neonates who received intravenous metronidazole for the treatment of or prophylaxis against necrotizing enterocolitis. Dried blood spots (n = 203) on filter paper were analyzed by high-performance liquid chromatography, and the data were subjected to pharmacokinetic analysis performed by using nonlinear mixed-effect modeling.

RESULTS:
A 1-compartment model best described the data. Significant covariates were weight (WT) and postmenstrual age (PMA). The final population models for metronidazole clearance (CL) and volume of distribution (V) were: CL = 0.0247 × (WT/1.00)0.75 × (1 + 0.107 × [PMA − 30]) and V = 0.726 × WT, where CL is in liters per hour, WT is in kilograms, PMA is in weeks, and V is in liters. This model predicts that the half-life of metronidazole decreases rapidly from ∼40 hours at 25 weeks' PMA to 19 hours at 32 weeks' PMA, after which it starts to plateau. This decrease in half-life is the result of a 5-fold increase in CL compared with only a 2.5-fold increase in V during the same period.

CONCLUSIONS:
Currently, there are no specific dose recommendations for metronidazole in preterm neonates. However, a dosing scheme for preterm neonates that takes into consideration both the weight and PMA has been suggested and should avoid administration of doses that are excessive or more frequent than necessary.