bluuebunny/crossref_metadata_2025_split huggingface dataset:
Variety in Fruit and Vegetable Consumption and the Risk of Lung Cancer in the European Prospective Investigation into Cancer and Nutrition
Authors: Büchner Frederike L. , Bueno-de-Mesquita H. Bas , Ros Martine M. , Overvad Kim , Dahm Christina C. , Hansen Louise , Tjønneland Anne , Clavel-Chapelon Françoise , Boutron-Ruault Marie-Christine , Touillaud Marina , Kaaks Rudolf , Rohrmann Sabine , Boeing Heiner , Nöthlings Ute , Trichopoulou Antonia , Zylis Dimosthenis , Dilis Vardis , Palli Domenico , Sieri Sabina , Vineis Paolo , Tumino Rosario , Panico Salvatore , Peeters Petra H.M. , van Gils Carla H. , Lund Eiliv , Gram Inger T. , Braaten Tonje , Sánchez María-José , Agudo Antonio , Larrañaga Nerea , Ardanaz Eva , Navarro Carmen , Argüelles Marcial V. , Manjer Jonas , Wirfält Elisabet , Hallmans Göran , Rasmuson Torgny , Key Tim J. , Khaw Kay-Tee , Wareham Nick , Slimani Nadia , Vergnaud Anne-Claire , Xun Wei W. , Kiemeney Lambertus A.L.M. , Riboli Elio 
Published: September 2010

Abstract
Background: We investigated whether a varied consumption of vegetables and fruits is associated with lower lung cancer risk in the European Prospective Investigation into Cancer and Nutrition study.
Methods: After a mean follow-up of 8.7 years, 1,613 of 452,187 participants with complete information were diagnosed with lung cancer. Diet diversity scores (DDS) were used to quantify the variety in fruit and vegetable consumption. Multivariable proportional hazards models were used to assess the associations between DDS and lung cancer risk. All models were adjusted for smoking behavior and the total consumption of fruit and vegetables.
Results: With increasing variety in vegetable subgroups, risk of lung cancer decreases [hazard ratios (HR), 0.77; 95% confidence interval (CI), 0.64-0.94 highest versus lowest quartile; P trend = 0.02]. This inverse association is restricted to current smokers (HR, 0.73; 95% CI, 0.57-0.93 highest versus lowest quartile; P trend = 0.03). In continuous analyses, in current smokers, lower risks were observed for squamous cell carcinomas with more variety in fruit and vegetable products combined (HR/two products, 0.88; 95% CI, 0.82-0.95), vegetable subgroups (HR/subgroup, 0.88; 95% CI, 0.79-0.97), vegetable products (HR/two products, 0.87; 95% CI, 0.79-0.96), and fruit products (HR/two products, 0.84; 95% CI, 0.72-0.97).
Conclusion: Variety in vegetable consumption was inversely associated with lung cancer risk among current smokers. Risk of squamous cell carcinomas was reduced with increasing variety in fruit and/or vegetable consumption, which was mainly driven by the effect in current smokers.
Impact: Independent from quantity of consumption, variety in fruit and vegetable consumption may decrease lung cancer risk. Cancer Epidemiol Biomarkers Prev; 19(9); 2278–86. ©2010 AACR.
Rising Melanoma Incidence Rates of the Trunk among Younger Women in the United States
Authors: Bradford Porcia T. , Anderson William F. , Purdue Mark P. , Goldstein Alisa M. , Tucker Margaret A. 
Published: September 2010

AbstractBackground: Melanoma rates are rising among young women, possibly due to increasing UV radiation to previously protected body sites. Therefore, we examined melanoma incidence trends by age, gender, and body site. Descriptive methods were complemented with the age-period-cohort parameters net drift and longitudinal age trend.Methods: Case and population data were obtained from the Surveillance, Epidemiology, and End Results (SEER) 9 Registries Database (1975-2006). Net drift summarized the average annual percentage change in log-linear rates per year of calendar-time (or year of diagnosis). Longitudinal age trend summarized the average annual percentage change by attained age at diagnosis. Early- and late-onset melanomas have low and high longitudinal age trends, respectively.Results: There were 105,829 melanomas diagnosed in the SEER 9 Registries. The overall age-adjusted incidence rate (IR) for melanoma was 17.7/100,000 person-years. Age-specific IRs were greater among women than men prior to age 40 years. Among women, IRs decreased for all anatomic sites relative to the trunk. The highest net drift occurred in truncal lesions among women (net drift, 3.8%/year of calendar time; 95% confidence interval, 3.5-4.0%). The lowest longitudinal age trends also were observed for truncal lesions among women (longitudinal age trend, 5.4%/year of attained age; 95% confidence interval, 5.1-5.7).Conclusions: Although melanoma IRs overall have risen for decades, the combination of high net drift and low longitudinal age trend show that melanomas are rising preferentially on the trunk among young women.Impact: Future surveillance and analytic studies should consider melanoma effect modification by age, gender, and body site. Cancer Epidemiol Biomarkers Prev; 19(9); 2401–6. ©2010 AACR.
Histone γH2AX and Poly(ADP-Ribose) as Clinical Pharmacodynamic Biomarkers
Authors: Redon Christophe E. , Nakamura Asako J. , Zhang Yong-Wei , Ji Jiuping (Jay) , Bonner William M. , Kinders Robert J. , Parchment Ralph E. , Doroshow James H. , Pommier Yves 
Published: September 2010

Abstract
Tumor cells are often deficient in DNA damage response (DDR) pathways, and anticancer therapies are commonly based on genotoxic treatments using radiation and/or drugs that damage DNA directly or interfere with DNA metabolism, leading to the formation of DNA double-strand breaks (DSB), and ultimately to cell death. Because DSBs induce the phosphorylation of histone H2AX (γH2AX) in the chromatin flanking the break site, an antibody directed against γH2AX can be employed to measure DNA damage levels before and after patient treatment. Poly(ADP-ribose) polymerases (PARP1 and PARP2) are also activated by DNA damage, and PARP inhibitors show promising activity in cancers with defective homologous recombination (HR) pathways for DSB repair. Ongoing clinical trials are testing combinations of PARP inhibitors with DNA damaging agents. Poly(ADP-ribosylation), abbreviated as PAR, can be measured in clinical samples and used to determine the efficiency of PARP inhibitors. This review summarizes the roles of γH2AX and PAR in the DDR, and their use as biomarkers to monitor drug response and guide clinical trials, especially phase 0 clinical trials. We also discuss the choices of relevant samples for γH2AX and PAR analyses. Clin Cancer Res; 16(18); 4532–42. ©2010 AACR.
Poly (ADP-Ribose) Polymerase as a Novel Therapeutic Target in Cancer
Authors: Annunziata Christina M. , O'Shaughnessy Joyce 
Published: September 2010

Abstract
Cancer chemotherapy exploits limitations in repairing DNA damage in order to kill proliferating malignant cells. Recent evidence suggests that cancers within and across tissue types have specific defects in DNA repair pathways, and that these defects may predispose for sensitivity and resistance to various classes of cytotoxic agents. Poly (ADP-ribose) polymerase (PARP) and BRCA proteins are central to the repair of DNA strand breaks and, when defective, lead to the accumulation of mutations introduced by error-prone DNA repair. Breast, ovarian, and other cancers develop in the setting of BRCA deficiency, and these cancers may be more sensitive to cytotoxic agents that induce DNA strand breaks, as well as inhibitors of PARP activity. A series of recent clinical trials has tested whether PARP inhibitors can achieve synthetic lethality in BRCA-pathway-deficient tumors. Future studies must seek to identify sporadic cancers that harbor genomic instability, rendering susceptibility to agents that induce additional and lethal DNA damage. Clin Cancer Res; 16(18); 4517–26. ©2010 AACR.
DNA Damage and Repair in Translational Oncology: An Overview
Authors: Reed Eddie 
Published: September 2010

Abstract
Unknown to early investigators, DNA damage and repair has been a major focus of anticancer therapy from the beginning of clinical oncology. From the early days of using x-irradiation, to the development of nitrogen mustard analogs, to today's more sophisticated approaches, DNA damage and repair has strongly impacted our ability to successfully treat human malignancy. This area of basic, translational, and clinical science is very broad. The traditional focus of DNA damage and repair has been on diseases such as Xeroderma pigmentosum, and attempting to understand the basic molecular mechanisms of DNA repair processes. It is only recently that we have begun to appreciate how we might modulate these processes to improve our ability to advance cancer care. No fewer than 10 separate DNA repair processes are operative in higher organisms, and the total number of separable processes could be substantially higher. Some of our most useful clinical agents depend on causing DNA damage that is repaired by nucleotide excision repair. X-irradiation induces damage that is mostly repaired by base excision repair and double-strand break repair. We are now learning how to modulate select DNA repair pathways to benefit patients with breast cancer and other malignancies. Clin Cancer Res; 16(18); 4511–6. ©2010 AACR.
Regulation of Excision Repair Cross-Complementation Group 1 by Snail Contributes to Cisplatin Resistance in Head and Neck Cancer
Authors: Hsu Dennis Shin-Shian , Lan Hsin-Yi , Huang Chi-Hung , Tai Shyh-Kuan , Chang Shyue-Yih , Tsai Tung-Lung , Chang Cheng-Chi , Tzeng Cheng-Hwai , Wu Kou-Juey , Kao Jung-Yie , Yang Muh-Hwa 
Published: September 2010

Abstract
Purpose: We investigated the mechanism and clinical significance of the epithelial-mesenchymal transition (EMT)-induced chemoresistance in head and neck squamous cell carcinoma (HNSCC).
Experimental Design: The correlation between the expression of different EMT regulators and chemoresistance genes, such as excision repair cross complementation group 1 (ERCC1), was evaluated in cancer cell lines from the NCI-60 database and four human HNSCC cell lines. Ectopic expression of Snail or short-interference RNA-mediated repression of Snail or ERCC1 was done in HNSCC cell lines. Cell viability was examined for cells after cisplatin treatment. A luciferase reporter assay and chromatin immunoprecipitation were used to identify the transcriptional regulation of ERCC1 by Snail. Immunohistochemical analysis of Snail, Twist1, ERCC1, hypoxia inducible factor-1 α (HIF-1α), and NBS1 were done in samples from 72 HNSCC patients receiving cisplatin-based chemotherapy.
Results: The correlation between the expression of Snail and ERCC1 was confirmed in different cell lines, including HNSCC cells. In HNSCC cell lines, overexpression of Snail in the low endogenous Snail/ERCC1 cell lines FaDu or CAL-27 increased ERCC1 expression, and hypoxia or overexpression of NBS1 also upregulated ERCC1. Knockdown of Snail in the high endogenous Snail/ERCC1 cell line OECM-1 downregulated ERCC1 expression and attenuated cisplatin resistance. Furthermore, suppression of ERCC1 in Snail- or NBS1-overexpressing HNSCC cells enhanced sensitivity to cisplatin. Snail directly regulated ERCC1 transcription. In patients with HNSCC, coexpression of Snail and ERCC1 correlated with cisplatin resistance and a poor prognosis.
Conclusions: Activation of ERCC1 by Snail is critical in the generation of cisplatin resistance of HNSCC cells. Clin Cancer Res; 16(18); 4561–71. ©2010 AACR.
Therapeutic Targeting of the DNA Mismatch Repair Pathway
Authors: Martin Sarah A. , Lord Christopher J. , Ashworth Alan 
Published: September 2010

Abstract
The mismatch repair (MMR) pathway is involved in the removal of DNA base mismatches that arise either during DNA replication or are caused by DNA damage. Mutations in four genes involved in MMR, MSH2, MLH1, PMS2 and MSH6, predispose to a range of tumorigenic conditions, including hereditary nonpolyposis colon cancer, also known as Lynch syndrome. Here we discuss the canonical MMR pathway and the burgeoning evidence for noncanonical roles for the MMR genes, and highlight the therapeutic implications of MMR. In particular, we discuss how the DNA repair defect in MMR-deficient cancers could be exploited by the development of novel therapeutic strategies based on synthetic lethal approaches. Clin Cancer Res; 16(21); 5107–13. ©2010 AACR.
Spectrum and Outcome of Reoperations After the Ross Procedure
Authors: Stulak John M. , Burkhart Harold M. , Sundt Thoralf M. , Connolly Heidi M. , Suri Rakesh M. , Schaff Hartzell V. , Dearani Joseph A. 
Published: September 2010

Background—
Proposed advantages to the Ross procedure included presumed increased freedom from reoperation and simpler reoperation for pulmonary conduit replacement if needed. It is increasingly apparent, however, that reoperations are frequent after the Ross procedure and that when required, they may be more complex than previously thought.

Methods and Results—
Between September 1991 and August 2008, 56 patients underwent reoperation at our institution after a Ross procedure performed by ourselves (n=13) or elsewhere (n=43). Median age at first reoperation at our institution was 26 years (range 1 to 69 years). The 4 most common indications for reoperation were isolated autograft (neoaortic) regurgitation in 11 cases (20), isolated pulmonary conduit regurgitation/stenosis in 9 (16), combined autograft regurgitation/dilatation in 8 (14), and combined autograft regurgitation and pulmonary conduit regurgitation/stenosis in 6 (11). A total of 144 procedures were performed in these 56 patients during first reoperation at our institution. The autograft valve required replacement in 21 cases (38) and aortic root replacement in 21 (38), with ascending aortic/arch reconstruction in 13 (23) and mitral valve surgery in 5 (9). The pulmonary valve was replaced in 33 cases (59) and the tricuspid valve was repaired/replaced in 10 (18). Early mortality was 1.8 (1 of 56 patients), and morbidity included 6 patients with respiratory failure and 3 who required postcardiotomy extracorporeal membrane oxygenation. There were 4 late deaths during the median follow-up of 8 months (range 1 to 179 months).

Conclusions—
A broad spectrum of complex reoperations may be required after the Ross procedure. Patients and family members considering the procedure should be informed of the potential for associated morbidity should reoperation be necessary.
Association of Colony-Forming Units With Coronary Artery and Abdominal Aortic Calcification
Authors: Cheng Susan , Cohen Kenneth S. , Shaw Stanley Y. , Larson Martin G. , Hwang Shih-Jen , McCabe Elizabeth L. , Martin Roderick P. , Klein Rachael J. , Hashmi Basma , Hoffmann Udo , Fox Caroline S. , Vasan Ramachandran S. , O'Donnell Christopher J. , Wang Thomas J. 
Published: September 2010

Background—
Certain bone marrow–derived cell populations, called endothelial progenitor cells, have been reported to possess angiogenic activity. Experimental data suggest that depletion of these angiogenic cell populations may promote atherogenesis, but limited data are available on their relation to subclinical atherosclerotic cardiovascular disease in humans.

Methods and Results—

We studied 889 participants of the Framingham Heart Study who were free of clinically apparent cardiovascular disease (mean age, 65 years; 55% women). Participants underwent endothelial progenitor cell phenotyping with an early-outgrowth colony-forming unit assay and cell surface markers. Participants also underwent noncontrast multidetector computed tomography to assess the presence of subclinical atherosclerosis, as reflected by the burden of coronary artery calcification and abdominal aortic calcification. Across decreasing tertiles of colony-forming units, there was a progressive increase in median coronary artery calcification and abdominal aortic calcification scores. In multivariable analyses adjusting for traditional cardiovascular risk factors, each 1-SD increase in colony-forming units was associated with a ≈16% decrease in coronary artery calcification (
P
=0.02) and 17% decrease in abdominal aortic calcification (
P
=0.03). In contrast, neither CD34
+
/KDR
+
nor CD34
+
variation was associated with significant differences in coronary or aortic calcification.

Conclusions—
In this large, community-based sample of men and women, lower colony-forming unit number was associated with a higher burden of subclinical atherosclerosis in the coronary arteries and aorta. Decreased angiogenic potential could contribute to the development of atherosclerosis in humans.
Preeclampsia and Gestational Hypertension Are Associated With Childhood Blood Pressure Independently of Family Adiposity Measures
Authors: Geelhoed J.J. Miranda , Fraser Abigail , Tilling Kate , Benfield Li , Davey Smith George , Sattar Naveed , Nelson Scott M. , Lawlor Debbie A. 
Published: September 2010

Background—
Offspring of women with hypertensive disorders of pregnancy are at increased risk of cardiovascular complications later in life, but the mechanisms underlying these associations are unclear. Our aim was to examine whether adjusting for birth weight and familial adiposity changed the association of hypertensive disorders of pregnancy with offspring blood pressure.

Methods and Results—
Using data from 6343 nine-year-old participants in the Avon Longitudinal Study of Parents and Children, we examined the association between hypertensive disorders of pregnancy (preeclampsia and gestational hypertension) and offspring blood pressure. Both preeclampsia and gestational hypertension were associated with systolic and diastolic blood pressures in the 9-year-old offspring; after adjustment for parental and own adiposity and for other potential confounders, the mean difference in systolic blood pressure was 2.05 mm Hg (95 confidence interval, 0.72 to 3.38) and 2.04 mm Hg (95 confidence interval, 1.42 to 2.67) for preeclampsia and gestational hypertension, respectively, compared with those with no hypertensive disorders of pregnancy. Equivalent results for diastolic blood pressure were 1.00 mm Hg (95 confidence interval, −0.01 to 2.10) and 1.07 mm Hg (95 confidence interval, 0.60 to 1.54). The association of preeclampsia with offspring systolic and diastolic blood pressures attenuated toward the null with further adjustment for birth weight and gestational age, whereas these adjustments did not attenuate the association of gestational hypertension with offspring blood pressure.

Conclusions—
The associations of hypertensive disorders of pregnancy with higher offspring blood pressure are not explained by familial adiposity. The mechanisms linking preeclampsia and gestational hypertension with offspring blood pressure may differ, with the former mediated at least in part by the effect of preeclampsia on intrauterine growth restriction.
Culture, Institutions, and Disability Policy in Japan: The Translation of Culture into Policy
Authors: Meyer Heinz-Dieter , Murakami Yui 
Published: September 2010

AbstractWhy is the Japanese rate of students with disability a fraction of that of the United States? Barring genetic differences between Americans and Japanese, the difference in disability rates must be what Durkheim called a “social fact,” a phenomenon explained by social differences between the two countries. In this paper we focus on the institutional and cultural factors that enter into the Japanese construction of disability of school-aged students. We argue that the lower incidence of disability in Japan is a result of Japan’s strong collectivist and paternalistic orientation and the requisite institutions promulgating those beliefs. The latter play a key role in the translation of general cultural dispositions into concrete policies and behavior on the ground.
Framing Disability: Comparing Individualist and Collectivist Societies
Authors: Meyer Heinz-Dieter 
Published: September 2010

AbstractIn this paper I use international differences in disability rates as a window to address the question how national culture influences a nation’s understanding and practice of disability. I apply the well-established distinction between individualistic and collectivistic cultures to explore the relationship between culture and disability rates. I argue and find support for the hypothesis that individualistic cultures exhibit higher rates of disability. In the second part I add cultural and institutional detail to the account. While individualistic and collectivist cultures both value assistance to the disabled, only the Western individualist tradition produces a rights-based approach to disability.
Relationship between Meniscal Extrusion and various Clinical Findings after Meniscus Allograft Transplantation
Authors: Ha Jeong Ku , Shim Jae Chan , Kim Deok Won , Lee Yong Seuk , Ra Ho Jong , Kim Jin Goo 
Published: September 2010

Background Meniscus allograft transplantation (MAT) is useful for meniscus-deficient knees. Although meniscal extrusion is common after MAT, there is no consensus regarding the criteria for normal meniscal extrusion or the relationship between clinical and radiologic results. Hypothesis Meniscal extrusion after MAT results in poor clinical, radiologic, and arthroscopic outcomes. Study Design Case series; Level of evidence, 4. Methods Thirty-six of 60 patients undergoing MAT from September 2002 to June 2007 who were available for follow-up evaluation for more than 2 years were evaluated. The study population (31 men, 5 women) consisted of 15 and 21 cases of medial and lateral meniscus transplant, respectively. Knee status was evaluated by Lysholm score, plain radiography, and magnetic resonance imaging preoperatively and postoperatively. Second-look examinations were performed in 18 cases. Results Mean follow-up was 31.4 months (range, 24-36). Lysholm knee score increased significantly (mean, 88.2; range, 70-100) on final visit versus the preoperative value (mean, 61.2; range, 26-83; P < .001). Joint-space narrowing was 0.08 mm (range, —2.58 to 1.92) in extension AP and —0.09 mm (range, —2.3 to 1.8) in Rosenberg view. Kellgren-Lawrence arthrosis grade did not change in 28 knees (77.8%) and progressed by 1 grade in 8 knees. Meniscal extrusion extent was 3.87 ± 1.94 mm and relative percentage extrusion was 42.1% ± 17.7%. Seven cases (19.4%) showed minor extrusion (<3 mm), 27 (75%) showed major extrusion (>3 mm), and 2 (5.6%) showed no extrusion. Further degeneration was absent in 28 knees (77.8%) on magnetic resonance imaging. In second-look arthroscopic examinations at an average of 26.3 months, 11 of 18 (63.6%) cases showed no progression of cartilage degeneration. There was no significant correlation between meniscal extrusion and other parameters. Conclusion This study indicated that MAT can improve the clinical status of the meniscectomized knee. Although meniscal extrusion occurred after surgery in most cases, there was no significant correlation with various clinical, radiologic, or arthroscopic outcomes. Further studies are required to evaluate long-term effects of meniscal extrusion.