bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B50: Differential influence of vitamin D on the tumor promoting eicosanoid PGE2 in women at increased breast cancer risk
Authors: Qin Wenyi , Walker Charles , Sauter Edward 
Published: October 2015

Abstract
Numerous lines of evidence point to the tumor promoting properties of prostaglandin (PG)E2. Preclinical studies have demonstrated the ability of both vitamin D (vitD) and celecoxib to downregulate the eicosanoid. We previously reported that vitD, but not the combination, significantly downregulated PGE2 in normal risk women. We hypothesized that there would be a similar or greater benefit of vitD alone, or in combination with celecoxib, in women at increased breast cancer risk. 40 women at increased breast cancer risk were prospectively enrolled and randomized in double blind fashion for one month (postmenopausal) or one menstrual cycle (premenopausal) to one of four daily treatment regimens: placebo, 400 IU vitD, 2000 IU vitD, or 2000 IU vitD + 400 mg celecoxib. Breast nipple aspirate fluid (NAF) and serum were collected. Both breast specific and systemic levels of PGE2 were measured. There was a significant increase (p=.02) in circulating levels of vitD after treatment in women receiving 2000 IU vitD with or without celecoxib, but not in women receiving placebo or 400 IU vitD. Celecoxib levels increased in those treated with celecoxib but not in the other groups. In the breast, as reflected in NAF, there was a 20% increase (p=.07) in PGE2 after treatment with 2000 IU vitD, with little change after treatment in the other groups. No treatment significantly changed circulating levels of PGE2. These findings suggest that, unlike in normal risk women, 2000 IU vitD may increase levels of a key cancer promoting enzyme in women of increased breast cancer risk. Supported in part with funds from the Komen Foundation and the Department of Defense.
Citation Format: Wenyi Qin, Charles Walker, Edward Sauter. Differential influence of vitamin D on the tumor promoting eicosanoid PGE2 in women at increased breast cancer risk. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr B50.
Abstract CN02-01: Is it too late or too little? Prevention through physical activity
Authors: Wolin Kate Y. 
Published: October 2015

Abstract
Physical activity is one of the leading ways to prevent cancer with estimates concluding 30% of cancers in the US could be improved through improvements to diet, obesity and exercise behaviors. Despite the cancer and other chronic disease benefits from physical activity, the majority of the US population remains inactive. Efforts to implement cancer prevention through physical activity are met with questions about the specifics of the relation between physical activity and cancer: Everyone? How much? How hard?
Evidence is accumulating that physical activity across the lifecourse is important for cancer prevention. In addition to reducing risk of colon cancer by more than 20%, physical activity also reduces risk of colon polyps. Lifetime physical activity levels are consistently related to several cancers. Adolescent physical activity is associated with a reduced risk of colon cancer. This epidemiologic evidence has important policy implications as school physical education classes and class time are being reduced.
Research has also suggested that physical activity may have less effect on cancer risk among population subgroups including obese individuals for some cancers.
While the physical activity guidelines recommend 30 minutes of moderate activity each day, they also suggest more is better. However, health promotion and behavioral science research has had only modest success at achieving sustained physical activity levels through intervention. We will review data on whether some benefit can be achieved at lower levels or how much greater the risk reduction may be at higher levels.
This is particularly important in light of research indicating that sedentary time is, independent of physical activity level, associated with an elevated risk of several cancers. Together, this data has pushed prevention messaging in the direction of “do something” instead of “do more.” While the risks of sedentary behavior are important, such messages may detract from research suggesting that for some cancers, such as prostate, participation in vigorous physical activity may be necessary to see a reduction in risk.
The benefits of physical activity for cancer prevention are well known. However, the message may need more refinement in light of emerging evidence on the timing, intensity and duration of activity necessary to reduce risk of specific cancers.
Citation Format: Kate Y. Wolin. Is it too late or too little? Prevention through physical activity. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr CN02-01.
Abstract CN12-02: Dietary HDAC inhibitors: Prevention or therapy?
Authors: Dashwood Roderick H. 
Published: October 2015

Abstract
Lysine deacetylase inhibitors, which include inhibitors of histone deacetylase (HDAC) enzymes, are undergoing clinical trials as anticancer agents. Some exhibit resistance mechanisms linked to anti-apoptotic Bcl-2 functions, such as BH3-only protein silencing. HDAC inhibitors that reactivate BH3-only family members might offer an improved therapeutic approach. We show here that a novel seleno-α-keto metabolite of the dietary compound methylselenocysteine triggers global histone acetylation in human colon cancer cells and activates apoptosis in a p21-independent manner. Profiling of multiple survival factors identified a critical role for the BH3-only member Bcl-2 modifying factor (Bmf). On the corresponding BMF gene promoter, loss of HDAC8 was associated with STAT3/Sp3 transcription factor exchange and recruitment of p300. Treatment with a p300 inhibitor, or transient overexpression of exogenous HDAC8 interfered with BMF induction, whereas RNAi-mediated silencing of STAT3 activated the target gene. This is the first study to identify a direct target gene of HDAC8 repression, namely BMF. Interestingly, the repressive role of HDAC8 could be uncoupled from HDAC1 to trigger Bmf-mediated apoptosis. These findings have implications for the development of HDAC8-selective inhibitors and their roles as chemopreventive vs. therapeutic agents. Supported by NIH P01 grant CA090890.
Citation Format: Roderick H. Dashwood. Dietary HDAC inhibitors: Prevention or therapy? [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr CN12-02.
Abstract PL01-02: Influence of the microbiota on cellular proliferation and survival
Authors: Neish Andrew Scott 
Published: October 2015

Abstract
The resident prokaryotic microbiota of the mammalian intestine influences diverse homeostatic functions of the gut, including maintenance of barrier function, modulation of immune responses, as well as energy and nutrient extraction. Additionally, through studies of germ free mice, it has become apparent that commensal prokaryotic organisms are involved in the regulation of growth and survival in the intestinal epithelia, and thus may play fundamental roles in the pathogenesis of colon cancers. However, the molecular mechanisms of growth control by prokaryotes in the gut are largely unknown. It is increasingly recognized that physiologically generated reactive oxygen species (ROS) function as signaling secondary messengers that influence cellular proliferation and differentiation in a variety of biological systems. We have shown that commensal bacteria, particularly members of the genus Lactobacillus, can activate NADPH oxidase 1 (Nox1)-dependent ROS generation and modulate multiple cellular pathways, including NF-kB, ERK-MAPK and focal adhesion kinase, that are involved in control of epithelial cellular survival, proliferation, and migration. ROS inducing commensal bacteria can rapidly stimulate consequent cellular proliferation in intestinal stem cells upon initial ingestion into the murine or Drosophila intestine, illustrating the highly conserved nature of this host microbe interaction. Additionally, a well-studied and evolutionarily highly conserved system for transducing exogenous stimuli into eukaryotic host tissues is Nrf2 signaling. Nrf2 pathway activation upregulates a regulon of genes including those involved in xenobiotic and ROS detoxification, as well as pro-restitutive function. This pathway has attracted considerable attention because small molecule inducers of Nrf2 have cytoprotective and growth modulatory effects. We show cellular ROS generated in response to contact with lactobacilli have cytoprotective effects in the intestinal epithelium through the activation of Nrf2 responsive cytoprotective genes. These data suggest that the Nrf2 pathway, and perhaps other highly conserved pathways that respond to environmental alterations, have been adapted as signaling conduits between eukaryotic host and prokaryotic symbiont, and highlight the role the microbiota plays in eukaryotic cytoprotective pathways. Characterization of these pathways may have significant implications in the delineation of a eubiotic microbiota, and in the identification of probiotic microbes with potential to influence epithelial growth and survival.
Citation Format: Andrew Scott Neish. Influence of the microbiota on cellular proliferation and survival. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL01-02.
Abstract PL02-01: Nutrition, epigenetics, and cancer
Authors: Waterland Robert A. 
Published: October 2015

Abstract
Transient nutritional exposures during critical ontogenic periods can cause persistent changes in gene expression, metabolism, and risk of various diseases including cancer. We have been investigating whether such ‘developmental programming’ occurs via nutritional influences on developmental epigenetics. Our studies in agouti viable yellow and axin fused mice showed that developmental establishment of DNA methylation at ‘metastable epialleles’ is especially sensitive to maternal nutritional status around the time of conception. Lately, using a multiple-tissue screen for interindividual variation in DNA methylation, we have identified human genomic regions that appear to be metastable epialleles. Stochastic establishment of DNA methylation at these loci is affected by maternal nutrition around the time of conception, consistent across multiple tissues, and stable for many years. Most recently, our studies using genome-wide bisulfite sequencing have identified candidate metastable epialleles that are associated with genes implicated in human cancer, potentially providing opportunities for cancer risk assessment and prevention.
Citation Format: Robert A. Waterland. Nutrition, epigenetics, and cancer. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL02-01.
Abstract PL02-03: Diet, nutrition, and cancer: Past, present, and future
Authors: Mayne Susan T. 
Published: October 2015

Abstract
For many years, Dr. John Milner was a champion for research on diet, nutrition and cancer. As part of his memorial symposium, this presentation will review the state of science on this topic, including a consideration of where the field has been, where it is today, and opportunities for future progress. The 1980s focused research on this topic, with the publication of several landmark reports, including the 1982 publication on “Diet, Nutrition and Cancer” by the U.S. National Academy of Sciences, which was followed by a Surgeon General's Report on Nutrition and Health in 1988 and several other landmark publications. The conclusions of these reports reflected a cautious optimism that diet might provide a strategy for cancer prevention, at least for selected cancers, and noted new directions for research to propel the field forward. Nearly a decade later (in 1997), another landmark report on nutrition and cancer was released, the World Cancer Research Fund/American Institute for Cancer Research report on “Food, Nutrition and the Prevention of Cancer: A Global Perspective,” which was updated in 2007 and continuously thereafter. The decades of research described in these reports demonstrate a substantial evolution in the scientific evidence base linking diet, nutrition and cancer prevention. As will be discussed, advances in dietary assessment and analysis, interpretation of dietary/nutrient data in relation to cancer risk, recognition of tumor heterogeneity, and consideration of hierarchy of research evidence have provided greater clarity to early findings in the field. Similarly, a new wave of technological advances, largely based in genetics/genomics, is now enabling exciting new lines of investigation into diet, nutrition and cancer. Dr. Milner was a passionate advocate for the incorporation of genetic and genomic technologies into nutrition research, and emphasized the value of mechanistically-based research for a more comprehensive understanding of the role of nutrition in carcinogenesis. The impact of his vision and leadership on emerging topics in diet, nutrition and cancer is evident as will be presented.
Citation Format: Susan T. Mayne. Diet, nutrition, and cancer: Past, present, and future. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL02-03.
Abstract PL05-01: Obesity, IGF-1 and cancer prevention: Mechanistic insights from transdisciplinary studies
Authors: Hursting Stephen D. 
Published: October 2015

Abstract
The prevalence of obesity, an established risk and progression factor for many cancers, has more than doubled over the past three decades in the US, with ~36% of adults currently obese. The mechanisms underlying the obesity and cancer connection are becoming increasingly clear and reveal several potential targets and strategies for breaking the obesity-cancer link. We have established in multiple genetically engineered mouse models (GEMMs) of mammary, pancreatic and other epithelial cancers that diet-induced obesity (DIO) increases serum levels of bioavailable insulin-like growth factor (IGF)-1, induces insulin resistance, and enhances tumor development and progression. In contrast the maintenance of a lean phenotype via a calorie restriction (CR) regimen decreases IGF-1 levels, improves insulin sensitivity, and inhibits cancer development and progression in these same models. Furthermore, biochemical, genetic and pharmacologic studies in GEMMS further suggest components of the mammalian target of rapamycin (mTOR) pathway, downstream of insulin and IGF-1 receptors, interact with inflammatory signals and provide important targets for disrupting the obesity-cancer link. Translational studies involving weight loss interventions in obese women at high risk for breast cancer show good concordance between mouse and human serum markers of energy balance-related hormones (including bioavailable IGF-1) and cytokines, as well as tissue mTOR signaling. We conclude from these transdisciplinary findings that several promising molecular targets (such as mTOR) are emerging for offsetting the procancer effects of obesity. Moreover, preclinical studies of several CR-mimetic agents (such as rapamycin, metformin, and several bioactive food components) provide further proof of the principle that mechanism-based approaches to break the obesity-cancer link by targeting mTOR and/or inflammation are plausible.
Citation Format: Stephen D. Hursting. Obesity, IGF-1 and cancer prevention: Mechanistic insights from transdisciplinary studies. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr PL05-01.
Antral mucosal diaphragm as a misdiagnosed cause of gastric outlet obstruction: case report and review of the literature
Authors: Bernardi Marcela Del Carlo , Imakuma Ernesto Sasaki , Dantas Anna Carolina Bastista , Freiberg Alyne Korukian , Lopasso Fabio Pinatel , Zilberstein Bruno , Cecconello Ivan 
Published: October 2015

The antral web is a thin septum with an aperture varying from 2 to 30 mm usually discovered in middle or late life because of associated gastric outlet obstruction or peptic ulcer. It is commonly mistaken for a pyloric obstruction. Since surgical excision of the antral diaphragm can cure patient’s symptoms, a correct diagnosis is important for not delaying treatment. However, the diagnosis is difficult even after adequate investigation with barium upper gastrointestinal x-ray series or endoscopy. Therefore, the present study seek to notify this pathology as a possible cause of gastric outlet obstruction providing an illustrative case report and review the pertinent literature. Case Report: A 56 years old man presented complaint of pyrosis, epigastric fullness after eating and loss of weight for over three years. His past clinical history revealed a perforated peptic ulcer surgery three years ago. Investigation was initially performed with barium upper gastrointestinal x-ray which suggested pyloric stenosis secondary to the previous surgery. Gastric endoscopy identified a mucous tunnel formation with a 10 mm diameter aperture in the pre-pyloric region. The patient was also submitted to a computerized tomography (CT) of the abdomen and pelvis for surgical planning for correction of pyloric stenosis and demonstrated an apparently thickening of the gastric wall and reduction of the diameter of the antropyloric region. The patient was then submitted to lapartomy with resection of the antral web. After 6 months, the patient is asymptomatic.
Solar Theology and Civil Religion in Plato’s Laws
Authors: Abolafia Jacob 
Published: October 2015

How is a legislator to harness the positive cohesive power of religion without falling prey to a charge of hypocrisy? As with so many theoretical puzzles, it was Plato who first recognized this paradox of civil religion. Consequently, the multi-tiered religion he proposes in the Laws should be understood as western thought’s first attempt to solve this problem.
At the centre of the Laws stands a single icon – the sun – that fits within both the Olympian schema of polis-religion and a naturalistic, rationalist account persuasive to the more philosophically minded. Using the language and imagery of solar worship, Plato designed a shared ‘civil religion’ (to use an anachronistic term), that can reasonably claim to link the social forms of political life to the higher truths of reason, even if not all the city’s citizens will mean the same thing when they speak of the god and his rites.
Numerical Investigation of Wind Waves in the Persian Gulf: Bathymetry Effects
Authors: Liao Ying-Po , Kaihatu James M. 
Published: October 2015

AbstractThe effects of bathymetry on the process of wind-wave generation in the Persian Gulf have been investigated using a long-term hindcasting analysis. A 5-yr (2004–08) hindcasting procedure is first performed (denoted asorigin) by using the Simulating Waves Nearshore (SWAN) model and COAMPS wind field data. Two alternative scenarios, in which wave breaking (noBrek) and depth-induced refraction (noRefc) are deactivated, are also generated. By comparing the results from alternative cases with those from the ordinary cases, a 5-yr total energy deviation (TED) is calculated and presented as seasonal contour maps depicting the sensitivity to bathymetry. The results show only ±2% TED found innoBrek, but up to ±20% TED found in noRefc, an order of magnitude larger than depth-induced breaking. Similarly, the seasonal effects of refraction on the nearshore wave-propagating directions can be investigated by comparison betweenoriginandnoRefc. The seasonal histograms of mean wave angleare plotted and discussed for three selected nearshore sites around Qatar, located at the western, northern, and eastern sides of the peninsula. The largest relative occurrence percentageand the largest peak shift ranging in 10°–20° can be found at the northern side, while the eastern side results in a weaker and more randomdistribution in the winter (the strong shamal season) due to the leeside location. The effect of fetch-limited wind-wave generation is also present at the eastern site, as remotely generated waves propagating eastward over a long fetch toward this site offset southward-propagating waves generated by dominant winds from the north over a limited fetch.
Building a Dashboard for the Punjab Health Department
Authors: Rana M. Ahsan 
Published: October 2015

This case is about monitoring and evaluation (M&E) challenges in the Punjab Department of Health (DOH). Despite his substantial experience of working in senior managerial positions, Arif Nadeem, the department secretary, finds himself somewhat lost in the numerous department related reports and data sheets that keep on coming from various quarters. He feels under-informed and over-informed at the same time. DOH regularly collects data on a range of indicators and there are multiple systems in place to collect the data from various health facilities. The following four systems are important. First, the District Health Information System (DHIS) collects data on around eighty indicators covering treatment and spread of communicable and non-communicable diseases, human resources, facility utilization, etc. Second, the M&E assistants (MEAs) inspect primary health care facilities and report on fourteen indicators covering the number of patients attended, staff presence, medicine availability, public opinion, etc. Third, the DOH field operatives visit health facilities and report on various aspects of functioning in monthly meetings of officials at the district level. Since 2011, they have been using simple smartphone based applications to enter data on site and transmit it to the points of analyses instantaneously. Fourth, progress on development projects is reported every month on prescribed pro forma covering physical progress as well as the amount spent. In addition, tertiary care hospitals report on various aspects of their functioning on need basis and receipt/expense statements are regularly prepared by the budget and accounts section in the department. Often there is too much information to absorb. There is no effective system of filtering and processing information according to the needs of various managerial tiers. Arif realizes that he needs a dashboard that can provide just enough detail to various users. Arif and his team deliberate on the choice of indicators for the dashboard. There is substantial disagreement on what to include and what to leave. The disagreement partly emanates from a lack of clarity on the mandate of the department and its senior management. Farasat, a key team member, proposes eight key areas for the dashboard. He suggests displaying these eight areas on the main screen and creating links to detailed district, tehsil and facility-wise data on selected indicators.