bluuebunny/crossref_metadata_2025_split huggingface dataset:
Population Differences in Breast Cancer: Survey in Indigenous African Women Reveals Over-Representation of Triple-Negative Breast Cancer
Authors: Huo Dezheng , Ikpatt Francis , Khramtsov Andrey , Dangou Jean-Marie , Nanda Rita , Dignam James , Zhang Bifeng , Grushko Tatyana , Zhang Chunling , Oluwasola Olayiwola , Malaka David , Malami Sani , Odetunde Abayomi , Adeoye Adewumi O. , Iyare Festus , Falusi Adeyinka , Perou Charles M. , Olopade Olufunmilayo I. 
Published: August 2009

Purpose Compared with white women, black women experience a disproportionate burden of aggressive breast cancer for reasons that remain unknown and understudied. In the first study of its kind, we determined the distribution of molecular subtypes of invasive breast tumors in indigenous black women in West Africa. Patients and Methods The study comprised 507 patients diagnosed with breast cancer between 1996 and 2007 at six geographic regions in Nigeria and Senegal. Formalin-fixed and paraffin-embedded sections were constructed into tissue microarrays and immunostained with 15 antibodies. Five molecular subtypes were determined, and hierarchical cluster analysis was conducted to explore subgroups for unclassified cases. Results The mean (± standard deviation) age of 378 patients in the first cohort was 44.8 ± 11.8 years, with the majority of women presenting with large (4.4 ± 2.0 cm) high-grade tumors (83%) in advanced stages (72% node positive). The proportions of estrogen receptor (ER) –positive, progesterone receptor–positive, and human epidermal growth factor receptor 2 (HER2) –positive tumors were 24%, 20%, and 17%, respectively. Triple negativity for these markers was predominant, including basal-like (27%) and unclassified subtype (28%). Other subtypes were luminal A (27%), luminal B (2%), and HER2 positive/ER negative (15%). The findings were replicated in the second cohort of 129 patients. The unclassified cases could be grouped into a bad prognosis branch, with expression of vascular endothelial growth factor, B-cell lymphoma extra-large protein, and Cyclin E, and a good prognosis branch, with expression of B-cell lymphoma protein 2 and Cyclin D1. Conclusion These findings underscore the urgent need for research into the etiology and treatment of the aggressive molecular subtypes that disproportionately affect young women in the African diaspora.
Determinants of Aggressive End-of-Life Care for Taiwanese Cancer Decedents, 2001 to 2006
Authors: Tang Siew Tzuh , Wu Shiao-Chi , Hung Yen-Ni , Chen Jen-Shi , Huang Ean-Wen , Liu Tsang-Wu 
Published: August 2009

Purpose To assess the association between aggressiveness of end-of-life (EOL) care and patient demographics, disease characteristics, primary physician's specialty, hospital characteristics, and availability of health care resources at the hospital and regional levels in Taiwan for a cohort of 210,976 cancer decedents in 2001 to 2006. Methods This retrospective cohort study examined administrative data. Aggressiveness of EOL care was examined by a composite measure adapted from Earle et al. Scores range from 0 to 6, with higher scores indicating more aggressive EOL care. Results The mean composite score for aggressiveness of EOL care was 2.04 (mean) ± 1.26 (standard deviation), increasing from 1.96 ± 1.26 in 2001 to 2.10 ± 1.26 in 2006. Each successive year of death significantly increased the composite score. Cancer decedents received more aggressive EOL care if they were male, younger, single, had a higher level of comorbidity, had more malignant and extensive diseases or hematologic malignancies, were cared for by oncologists, and received care in a hospital with a greater density of beds. Conclusion Controlling for patient demographics and cormorbidity burden, EOL care in Taiwan was more aggressive for patients with cancer with highly malignant and extensive diseases, for patients with oncologists as primary care providers, or in hospitals with abundant health care resources. Health policies should aim to ensure that all patients receive treatments that best meet their individual needs and interests and that resources are devoted to care that produces the greatest health benefits.
Phase I Study of C-TPF in Patients With Locally Advanced Squamous Cell Carcinoma of the Head and Neck
Authors: Haddad Robert I. , Tishler Roy B. , Norris Charles , Goguen Laura , Balboni Tracy A. , Costello Rosemary , Wirth Lori , Lorch Jochen , Andreozzi Britta , Annino Donald , Posner Marshall R. 
Published: August 2009

Purpose Phase I study to determine the maximum tolerated dose (MTD) of fluorouracil (FU) in the docetaxel/cisplatin/FU (TPF) regimen when combined with cetuximab (C) for induction treatment of locally advanced squamous cell carcinoma of the head and neck (SCCHN). Patients and Methods Patients with previously untreated SCCHN were enrolled. FU cohorts were 700, 850, and 1,000 mg/m2/d for 4 days via continuous infusion. TPF given every 3 weeks for three cycles and C was given weekly for a total of 9 weeks, starting on day 1 of TPF. All patients received chemoradiotherapy after C-TPF. Results A total of 30 patients were enrolled and 28 were assessable. The median age was 57 years, 92% had stage 4 disease, 71% were oropharynx, and 100% had a performance status of 0. No dose-limiting toxicity (DLT) was encountered on dose levels 1 and 2. At dose level 3 of 1000 mg/m2, one DLT was encountered and three more patients were enrolled with no DLTs. In the expansion cohort at the MTD, three DLT's were encountered. The decision was made to decrease the FU from 1,000 mg/m2 to dose level 2 of 850 mg/m2. A total of 13 patients were enrolled at the MTD of 850 mg/m2. The number of average weeks that C was delivered was seven of nine planned. Conclusion C-TPF appears to be safe and feasible as given in this study. GI toxicity (mucositis, enteritis, and diarrhea) appears to be the major combined DLT. Reducing the FU in TPF to 850 mg/m2 reduces GI toxicity and is the recommended phase II dose.
Prognostic Significance and Molecular Associations of 18q Loss of Heterozygosity: A Cohort Study of Microsatellite Stable Colorectal Cancers
Authors: Ogino Shuji , Nosho Katsuhiko , Irahara Natsumi , Shima Kaori , Baba Yoshifumi , Kirkner Gregory J. , Meyerhardt Jeffrey A. , Fuchs Charles S. 
Published: August 2009

Purpose Loss of heterozygosity (LOH) at chromosome 18q frequently occurs late during colon cancer development and is inversely associated with microsatellite instability (MSI). 18q LOH has been reported to predict shorter survival in patients with colorectal cancer, whereas MSI-high status has been associated with superior prognosis. However, it is unclear whether 18q LOH in colorectal cancer has any prognostic implication independent of MSI status and other potential predictors of clinical outcome. Patients and Methods Among 555 non–MSI-high colorectal cancers (stage I to IV) in two independent prospective cohort studies, we examined 18q LOH in relation to other molecular events and patient survival. Cox proportional hazard models computed hazard ratio of death, adjusted for clinical and tumoral characteristics, including KRAS, BRAF, PIK3CA, β-catenin, p53, CpG island methylator phenotype, LINE-1 methylation, and John Cunningham (JC) virus T antigen. Results In multivariate logistic regression, 18q LOH was independently associated with JC virus T antigen (odds ratio [OR] = 1.93; P = .0077), body mass index ≥ 30 kg/m2 (obesity; OR = 2.01; P = .014), high tumor grade (OR = 0.40; P = .018), KRAS mutation (OR = 0.66; P = .40), and LINE-1 hypomethylation (for a 30% decrease; OR = 1.92; P = .045). Five-year colorectal cancer–specific survival was 75% among patients with 18q LOH-positive tumors and 74% among those with 18q LOH-negative tumors (log-rank P = .80). Five-year overall survival was 70% among patients with 18q LOH-positive tumors and 68% among those with 18q LOH-negative tumors (log-rank P = .54). Multivariate analysis did not show prognostic significance of 18q LOH. Conclusion In our large prospective study of patients with non–MSI-high colorectal cancer, 18q LOH or allelic imbalance was not associated with patient survival.
Remediation of Harbor Sediments Contaminated by Polycyclic Aromatic Hydrocarbon and Metals
Authors: Nosari Valeriano Pastore Nicola , Geddo Gianluigi 
Published: August 2009

Abstract
The Taranto harbor area is included in the Italian National Priority List of contaminated sites. For the enlargement works of the fourth quay in the Taranto harbor, the remediation of contaminated sediments shall be carried out. The existing jetty was devoted to unloading of iron ore for the nearby ILVA steel mill. The sea depth in the intervention area ranges between 2 and 10 m and contaminated sediments (up to 3 m thick) are deposited on a layer of overconsolidated hard clay. The characterization activity of the area was carried out by ICRAM (a public sea research institute) indicating the presence of both organic (polycyclic aromatic hydrocarbon) and inorganic (metals) contaminants in the sediments. The remediation project consists of the two following phases: Mechanical dredging of highly contaminated sediments (15.500 m3) using low-turbidity tools and hydraulic excavation of sediments with a lower level of contamination (360.000 m3). Abiding by national regulations, the highly contaminated sediments will be treated in a dedicated plant while the sediments with a low level of contamination will be deposited in large ponds. The impact of dredging activities shall be mitigated by specific precautions. The possibility of beneficial reuse of dredged material was also studied, especially for low contamination sediments, as well as compatibility with national regulations. A specific monitoring plan will be enacted for the entire duration of remediation works, which are expected to start in 2010.
A Comprehensive Review of Lubricant Chemistry, Technology, Selection, and Design
Authors: Rizvi Syed Q. A. 
Published: August 2009

Description
Get a comprehensive overview of lubricant technology and its use in formulating new lubricants.
This unique, new ASTM manual is written from the perspectives of both chemists and lubrication engineers, and therefore places equal emphasis on the chemistry and the formulation of lubricants. In addition it includes additive technology that is used in petroleum exploration, refining, and fuels.
Manual 59 complements ASTM's Fuels and Lubricants Handbook (Manual 37) in that it integrates the information in the Handbook in a manner that will be especially useful to practicing lubrication engineers.
Adaptive Divergence in Experimental Populations ofPseudomonas fluorescens. IV. Genetic Constraints Guide Evolutionary Trajectories in a Parallel Adaptive Radiation
Authors: McDonald Michael J , Gehrig Stefanie M , Meintjes Peter L , Zhang Xue-Xian , Rainey Paul B 
Published: August 2009

AbstractThe capacity for phenotypic evolution is dependent upon complex webs of functional interactions that connect genotype and phenotype. Wrinkly spreader (WS) genotypes arise repeatedly during the course of a model Pseudomonas adaptive radiation. Previous work showed that the evolution of WS variation was explained in part by spontaneous mutations in wspF, a component of the Wsp-signaling module, but also drew attention to the existence of unknown mutational causes. Here, we identify two new mutational pathways (Aws and Mws) that allow realization of the WS phenotype: in common with the Wsp module these pathways contain a di-guanylate cyclase-encoding gene subject to negative regulation. Together, mutations in the Wsp, Aws, and Mws regulatory modules account for the spectrum of WS phenotype-generating mutations found among a collection of 26 spontaneously arising WS genotypes obtained from independent adaptive radiations. Despite a large number of potential mutational pathways, the repeated discovery of mutations in a small number of loci (parallel evolution) prompted the construction of an ancestral genotype devoid of known (Wsp, Aws, and Mws) regulatory modules to see whether the types derived from this genotype could converge upon the WS phenotype via a novel route. Such types—with equivalent fitness effects—did emerge, although they took significantly longer to do so. Together our data provide an explanation for why WS evolution follows a limited number of mutational pathways and show how genetic architecture can bias the molecular variation presented to selection.
Imprinting of the Y Chromosome Influences Dosage Compensation inroX1 roX2 Drosophila melanogaster
Authors: Menon Debashish U , Meller Victoria H 
Published: August 2009

AbstractDrosophila melanogaster males have a well-characterized regulatory system that increases X-linked gene expression. This essential process restores the balance between X-linked and autosomal gene products in males. A complex composed of the male-specific lethal (MSL) proteins and RNA is recruited to the body of transcribed X-linked genes where it modifies chromatin to increase expression. The RNA components of this complex, roX1 and roX2 (RNA on the X1, RNA on the X2), are functionally redundant. Males mutated for both roX genes have dramatically reduced survival. We show that reversal of sex chromosome inheritance suppresses lethality in roX1 roX2 males. Genetic tests indicate that the effect on male survival depends upon the presence and source of the Y chromosome, revealing a germ line imprint that influences dosage compensation. Conventional paternal transmission of the Y chromosome enhances roX1 roX2 lethality, while maternal transmission of the Y chromosome suppresses lethality. roX1 roX2 males with both maternal and paternal Y chromosomes have very low survival, indicating dominance of the paternal imprint. In an otherwise wild-type male, the Y chromosome does not appreciably affect dosage compensation. The influence of the Y chromosome, clearly apparent in roX1 roX2 mutants, thus requires a sensitized genetic background. We believe that the Y chromosome is likely to act through modulation of a process that is defective in roX1 roX2 mutants: X chromosome recognition or chromatin modification by the MSL complex.
Telomerase Is Essential to Alleviate Pif1-Induced Replication Stress at Telomeres
Authors: Chang Michael , Luke Brian , Kraft Claudine , Li Zhijian , Peter Matthias , Lingner Joachim , Rothstein Rodney 
Published: August 2009

Abstract
Pif1, an evolutionarily conserved helicase, negatively regulates telomere length by removing telomerase from chromosome ends. Pif1 has also been implicated in DNA replication processes such as Okazaki fragment maturation and replication fork pausing. We find that overexpression of Saccharomyces cervisiae PIF1 results in dose-dependent growth inhibition. Strong overexpression causes relocalization of the DNA damage response factors Rfa1 and Mre11 into nuclear foci and activation of the Rad53 DNA damage checkpoint kinase, indicating that the toxicity is caused by accumulation of DNA damage. We screened the complete set of ∼4800 haploid gene deletion mutants and found that moderate overexpression of PIF1, which is only mildly toxic on its own, causes growth defects in strains with mutations in genes involved in DNA replication and the DNA damage response. Interestingly, we find that telomerase-deficient strains are also sensitive to PIF1 overexpression. Our data are consistent with a model whereby increased levels of Pif1 interfere with DNA replication, causing collapsed replication forks. At chromosome ends, collapsed forks result in truncated telomeres that must be rapidly elongated by telomerase to maintain viability.
Outcome of Extreme Prematurity: A Prospective Comparison of 2 Regional Cohorts Born 20 Years Apart
Authors: Bode Michelle M. , D'Eugenio Diane B. , Forsyth Nancy , Coleman Janice , Gross Caroline R. , Gross Steven J. 
Published: August 2009

OBJECTIVE: To determine changes that have occurred over the past 20 years in perinatal characteristics, neonatal treatments, morbidities, and early neurodevelopmental outcomes of infants born at ≤30 weeks' gestation.METHODS: This was a prospective regional study including all live-born infants ≤30 weeks' gestation born between July 1985 and June 1986 (cohort 1) and July 2005 and June 2006 (cohort 2). Sociodemographically matched term controls were recruited for each cohort. Perinatal characteristics, mortality rates, and survival with and without impairments at 24 months' corrected age were compared.RESULTS: There was a 35% increase in the number of live-born preterm births (138 in cohort 1 and 187 in cohort 2) despite a &gt;10% decline in total births in the region (P &lt; .001). Assisted fertility (rarely available for mothers in cohort 1) was responsible for 20% of pregnancies in cohort 2. Survival to hospital discharge increased over 20 years from 82% to 93% (P = .002), primarily because of higher survival for infants born at &lt;27 weeks' gestation (63% vs 88%; P = .004). Changes in management in cohort 2 included the use of surfactant (62% of infants) and increased use of postnatal steroids (39% vs 9%; P &lt; .001), that were associated with a shorter median duration of mechanical ventilation (13 vs 21 days; P &lt; .001); however, the incidence of bronchopulmonary dysplasia was higher in cohort 2 (56% vs 35%; P &lt; .001). There was a significant decrease in incidence of severe ultrasound abnormalities from 17% in cohort 1 to 7% in cohort 2 (P = .008). At 24 months of age, 7% of cohort 1 and 5% of cohort 2 had an abnormal neurologic exam. Bayley cognitive scores were improved in cohort 2 (significantly closer to the mean of their controls). As a result, survival without severe neurodevelopmental impairment increased from 62% in cohort 1 to 81% in cohort 2 (P &lt; .001).CONCLUSION: Over 20 years, there has been a significant increase in live births at ≤30 weeks' gestational age, with a greater percentage of these neonates surviving without severe neurodevelopmental impairment at 24 months.
Glucose Metabolism in Overweight Hispanic Adolescents With and Without Polycystic Ovary Syndrome
Authors: Nur Marcela M. , Newman Ilana M. , Siqueira Lorena M. 
Published: August 2009

OBJECTIVES: About one third of overweight women with polycystic ovary syndrome (PCOS) have either impaired glucose tolerance (IGT) or type 2 diabetes mellitus (DM) by the age of 30. We sought to determine if overweight Hispanic adolescents with PCOS are more likely to be insulin resistant and glucose intolerant than those without PCOS.
METHODS: A retrospective chart review of 101 subjects with PCOS and 40 without PCOS was conducted. Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), Quantitative Insulin Sensitivity Check Index (QUICKI), and fasting glucose/insulin ratio (FGIR) values were calculated by using fasting glucose and insulin levels. Insulin resistance (IR) was defined as a fasting insulin level of &gt;15 μU/mL, a 2-hour insulin level of &gt;75 μU/mL, a HOMA-IR value of &gt;3.16, a QUICKI value of &lt;0.357, and/or a FGIR value of &lt;7.
RESULTS: Of the 101 overweight subjects with PCOS (BMI: 33.2 ± 5.9 kg/m2), 4 had IGT and 2 had DM versus none of the 40 subjects without PCOS (BMI: 32.4 ± 5.3 kg/m2). IR was more frequent in the overweight PCOS than in the overweight non-PCOS group (QUICKI: 68.4% vs 14.3%, P = .014) and FGIR (47.4% vs 0%, P = .024). Of the 6 subjects with glucose intolerance, only the QUICKI value was abnormal in all.
CONCLUSIONS: This retrospective study demonstrated that overweight Hispanic adolescents with PCOS had more IR, IGT and DM than their non-PCOS counterparts. As the QUICKI Index was abnormal in all subjects with IGT and DM, we suggest its use as the first step in deciding which overweight Hispanic adolescents with PCOS should be further tested with an OGTT.
Parents' Interest in Predictive Genetic Testing for Their Children When a Disease Has No Treatment
Authors: Tarini Beth A. , Singer Dianne , Clark Sarah J. , Davis Matthew M. 
Published: August 2009

OBJECTIVE: The goal was to measure parents' interest in obtaining predictive genetic testing for their children for a disease that has no treatment.METHODS: We conducted a nationally representative, Internet-based survey of parents. Parents received 2 vignettes describing hypothetical diseases without treatments. The first vignette described a disease in which symptoms were severe and timing of symptom onset was uncertain. The second vignette described a disease in which both symptom severity and timing of symptom onset were uncertain. Parents reported their interest in predictive genetic testing for their youngest child in each vignette by using a 5-point Likert scale. We collected information on parents' demographic features and parents' general opinions about genetic testing. We conducted logistic regression analyses to evaluate the independent associations between these factors and parents' interest in testing for both vignettes.RESULTS: The response rate was 71%. For the first vignette, 35% of parents were definitely or probably interested in predictive genetic testing for their youngest child, 35% were unsure, and 31% were definitely or probably not interested. Responses were similar for the second vignette. More than one fourth of parents consistently expressed interest in testing in both vignettes.CONCLUSIONS: Approximately one third of parents are interested in predictive genetic testing for their children, even for disorders with no treatment. Uncertainty about the severity of symptoms was not related to parents' testing preferences.
Cerebral Arteriopathy in Children With Neurofibromatosis Type 1
Authors: Rea David , Brandsema John F. , Armstrong Derek , Parkin Patricia C. , deVeber Gabrielle , MacGregor Daune , Logan William J. , Askalan Rand 
Published: August 2009

OBJECTIVE: Cerebrovascular abnormalities are serious but underrecognized complications of neurofibromatosis type 1 (NF1). The aim of this study was to investigate the prevalence, clinical presentation, imaging findings, and prognosis of cerebral arteriopathies in childhood NF1.
METHODS: Patients followed at the NF1 clinic at the Hospital for Sick Children, Toronto, Ontario, Canada, between 1990 and 2007 were studied. Patients with confirmed NF1 diagnosis and neuroimaging results were included. All neuroimaging studies were reviewed for the presence of arteriopathy by 2 study pediatric neuroradiologists blinded to clinical information. Clinical records of children with cerebral arteriopathy were reviewed.
RESULTS: Among 419 children with confirmed NF1, 266 (63%) received neuroimaging. Among children with neuroimaging results, 17 had cerebral arteriopathy (minimum prevalence rate of 6%). Among the 35 patients who received magnetic resonance angiography (MRA), arteriopathy was more common in patients with NF1 with optic gliomas (11 of 21) compared with those without optic glioma (4 of 14). Forty-seven percent of children developed focal deficits months to years after the diagnosis of the arteriopathy. Follow-up at a mean of 7 years after diagnosis of arteriopathy showed that 35% (6 of 17) had progressive arteriopathy requiring revascularization surgery. Seven patients received aspirin for primary stroke prevention. On retrospective review of imaging studies, a mean delay of 51 months to clinical radiographic reporting of these findings was observed.
CONCLUSIONS: The prevalence of cerebral arteriopathy in children with NF1 in this study was at least 6% and was associated with young age and optic glioma. Arteriopathy causes stroke with resultant neurologic deficits. Medical and/or surgical interventions may prevent these complications. Therefore, the addition of vascular imaging (MRA/conventional angiography) to brain imaging studies for early detection of arteriopathy should be considered for children with NF1, particularly young patients with optic glioma.