bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diversity of VacA Intermediate Region amongHelicobacter pyloriStrains from Several Regions of the World
Authors: Chung Christine , Olivares Asalia , Torres Eugenia , Yilmaz Ozlem , Cohen Henry , Perez-Perez Guillermo 
Published: January 2010

ABSTRACTHelicobacter pyloriis known to be a major cause of gastric carcinoma and peptic ulceration.cagApositivity andvacA's signal regions and mid-regions are well-characterized markers ofH. pylori's virulence. Recently, an intermediate region has been identified as another strong marker ofH. pylori-associated disease, and its i1 allele has been linked with severe diseases in colonized hosts. The goal of this study was to determine the prevalence of the intermediate alleles inH. pyloriisolates from China, Turkey, and Uruguay and from U.S. Africans and to compare their distribution with other well-characterized virulence factors. Originally, 123H. pyloristrains were studied, but 3 were excluded due to the failure to amplify the intermediate region in these samples. Therefore, a total of 120 strains were analyzed: 30 Chinese isolates, 35 Turkish isolates, 30 Uruguayan isolates, and 25 U.S. African isolates. The s type and the m type were determined by PCR amplification. The i type was identified by PCR amplification and DNA sequencing. CagA status was determined by PCR methodology. There was a strong correlation among CagA positivity, s1, and i1 in Chinese, U.S. African, and Uruguayan isolates, but less correlation among these markers in Turkish isolates. A new intermediate variant (i3) was identified in 25.7% of Turkish strains and 3.3% of the Chinese strains. In summary, the distribution of CagA positivity and s1 correlated with the i1 in the three populations, except in the Turkish population, which showed a disproportionate representation of the i3 allele. Phylogenetic mapping confirmed the i-typing method previously defined and adopted for this study. The phylogenetic tree showed country-specific correlation with the intermediate region. Our results showed that the i1 allele is strongly associated with CagA positivity and thevacAs1 allele, suggesting its role as a virulence marker and potential predictor for clinical outcome.
Performance of Fusidic Acid (CEM-102) Susceptibility Testing Reagents: Broth Microdilution, Disk Diffusion, and Etest Methods as Applied to
Staphylococcus aureus
Authors: Jones Ronald N. , Castanheira Mariana , Rhomberg Paul R. , Woosley Leah N. , Pfaller Michael A. 
Published: January 2010

ABSTRACT

Fusidic acid (CEM-102) is an established antistaphylococcal agent that has been used in clinical practice for more than 4 decades. The activity of fusidic acid against 778 isolates of
Staphylococcus aureus
collected from U.S. (53.8% were methicillin-resistant
S. aureus
[MRSA]) and Canadian (46.5% were MRSA) medical centers was assessed to determine the intermethod accuracy of the Clinical and Laboratory Standards Institute (CLSI) and Etest methods. Broth microdilution MIC results were compared by scattergram analysis to zone diameters around commercially available 5- and 10-μg disks. Acceptable correlation (
r
= 0.74 to 0.76) was observed for the two disk concentrations, and applying breakpoints of ≤1 μg/ml (≥22 mm) for susceptibility (S) and ≥4 μg/ml (≤19 mm) for resistance (R) provided 99.9% absolute intermethod categorical agreement. Reference CLSI MIC versus Etest MIC results (
r
= 0.77; 728 strains) showed 55.4% identical results and agreement of 99.7% ± one log
2
dilution. The diagnostic susceptibility testing reagents (including Etest) for fusidic acid (CEM-102) performed at an excellent level of intermethod agreement for the proposed breakpoint criteria.
Highly Pathogenic H5N1 Avian Influenza Virus Induces Extracellular Ca
2+
Influx, Leading to Apoptosis in Avian Cells
Authors: Ueda Mayo , Daidoji Tomo , Du Anariwa , Yang Cheng-Song , Ibrahim Madiha S. , Ikuta Kazuyoshi , Nakaya Takaaki 
Published: January 2010

ABSTRACT

In this study, we show that the highly pathogenic H5N1 avian influenza virus (AIV) (A/crow/Kyoto/53/04 and A/chicken/Egypt/CL6/07) induced apoptosis in duck embryonic fibroblasts (DEF). In contrast, apoptosis was reduced among cells infected with low-pathogenic AIVs (A/duck/HK/342/78 [H5N2], A/duck/HK/820/80 [H5N3], A/wigeon/Osaka/1/01 [H7N7], and A/turkey/Wisconsin/1/66 [H9N2]). Thus, we investigated the molecular mechanisms of apoptosis induced by H5N1-AIV infection. Caspase-dependent and -independent pathways contributed to the cytopathic effects. We further showed that, in the induction of apoptosis, the hemagglutinin of H5N1-AIV played a major role and its cleavage sequence was not critical. We also observed outer membrane permeabilization and loss of the transmembrane potential of the mitochondria of infected DEF, indicating that mitochondrial dysfunction was caused by the H5N1-AIV infection. We then analyzed Ca
2+
dynamics in the infected cells and demonstrated an increase in the concentration of Ca
2+
in the cytosol ([Ca
2+
]
i
) and mitochondria ([Ca
2+
]
m
) after H5N1-AIV infection. Regardless, gene expression important for regulating Ca
2+
efflux from the endoplasmic reticulum did not significantly change after H5N1-AIV infection. These results suggest that extracellular Ca
2+
may enter H5N1-AIV-infected cells. Indeed, EGTA, which chelates extracellular free Ca
2+
, significantly reduced the [Ca
2+
]
i
, [Ca
2+
]
m
, and apoptosis induced by H5N1-AIV infection. In conclusion, we identified a novel mechanism for influenza A virus-mediated cell death, which involved the acceleration of extracellular Ca
2+
influx, leading to mitochondrial dysfunction and apoptosis. These findings may be useful for understanding the pathogenesis of H5N1-AIV in avian species as well as the impact of Ca
2+
homeostasis on influenza A virus infection.
Biochemical and Structural Characterization of Cathepsin L-Processed Ebola Virus Glycoprotein: Implications for Viral Entry and Immunogenicity
Authors: Hood Chantelle L. , Abraham Jonathan , Boyington Jeffrey C. , Leung Kwanyee , Kwong Peter D. , Nabel Gary J. 
Published: January 2010

ABSTRACT
Ebola virus (EBOV) cellular attachment and entry is initiated by the envelope glycoprotein (GP) on the virion surface. Entry of this virus is pH dependent and associated with the cleavage of GP by proteases, including cathepsin L (CatL) and/or CatB, in the endosome or cell membrane. Here, we characterize the product of CatL cleavage of Zaire EBOV GP (ZEBOV-GP) and evaluate its relevance to entry. A stabilized recombinant form of the EBOV GP trimer was generated using a trimerization domain linked to a cleavable histidine tag. This trimer was purified to homogeneity and cleaved with CatL. Characterization of the trimeric product by N-terminal sequencing and mass spectrometry revealed three cleavage fragments, with masses of 23, 19, and 4 kDa. Structure-assisted modeling of the cathepsin L-cleaved ZEBOV-GP revealed that cleavage removes a glycosylated glycan cap and mucin-like domain (MUC domain) and exposes the conserved core residues implicated in receptor binding. The CatL-cleaved ZEBOV-GP intermediate bound with high affinity to a neutralizing antibody, KZ52, and also elicited neutralizing antibodies, supporting the notion that the processed intermediate is required for viral entry. Together, these data suggest that CatL cleavage of EBOV GP exposes its receptor-binding domain, thereby facilitating access to a putative cellular receptor in steps that lead to membrane fusion.
GUARDING RECTANGULAR PARTITIONS
Authors: DINITZ YEFIM , KATZ MATTHEW J. , KRAKOVSKI ROI 
Published: January 2010

A rectangular partition is a partition of a rectangle into non-overlapping rectangles, such that no four rectangles meet at a common point. A vertex guard is a guard located at a vertex of the partition (i.e., at a corner of a rectangle); it guards the rectangles that meet at this vertex. An edge guard is a guard that patrols along an edge of the partition, and is thus equivalent to two adjacent vertex guards. We consider the problem of finding a minimum-cardinality guarding set for the rectangles of the partition. For vertex guards, we prove that guarding a given subset of the rectangles is NP-hard. For edge guards, we prove that guarding all rectangles, where guards are restricted to a given subset of the edges, is NP-hard. For both results we show a reduction from vertex cover in non-bipartite 3-connected cubic planar graphs of girth greater than three. For the second NP-hardness result, we obtain a graph-theoretic result which establishes a connection between the set of faces of a plane graph of vertex degree at most three and a vertex cover for this graph. More precisely, we prove that one can assign to each internal face a distinct vertex of the cover, which lies on the face's boundary. We show that the vertices of a rectangular partition can be colored red, green, or black, such that each rectangle has all three colors on its boundary. We conjecture that the above is also true for four colors. Finally, we obtain a worst-case upper bound on the number of edge guards that are sufficient for guarding rectangular partitions with some restrictions on their structure.
New age constraints on the evolution of the Mt Carmel structure and its implications on a Late Miocene extensional phase of the Levant continental margin
Authors: Steinberg Josh , Gvirtzman Zohar , Folkman Yehoshua 
Published: January 2010

Abstract:
The Mt Carmel structure is one of the most prominent topographical elements along the Levant continental margin and is the surface expression of a deep tectonic structure. The use of 3D seismic data allows us to set new constraints on the uplift of the Carmel structure and define the Or Akiva fault as its southern boundary. The Or Akiva fault was created during a Late Miocene extensional phase that had also created the Carmel fault at the northern edges of Mt Carmel. The different topographic expression across these two boundary faults reflects a change in the post-Miocene activity, where activity along the Or Akiva fault ceased and its southern side began subsiding, whereas its northern side bordered by the Carmel fault continued to rise. We conclude that the Late Miocene north–south extension, previously recognized only along branches of the Dead Sea Transform in northern Israel and Lebanon, affected larger areas than previously thought and can be related to regional kinematic changes during the breakup of Arabia from Africa and its collision with Eurasia.
TD-GC-MS Analysis of Volatile Metabolites of Human Lung Cancer and Normal Cells In vitro
Authors: Filipiak Wojciech , Sponring Andreas , Filipiak Anna , Ager Clemens , Schubert Jochen , Miekisch Wolfram , Amann Anton , Troppmair Jakob 
Published: January 2010

Abstract
The aim of this study was to confirm the existence of volatile organic compounds (VOC) specifically released or consumed by the lung cancer cell line A549, which could be used in future screens as biomarkers for the early detection of lung cancer. For comparison, primary human bronchial epithelial cells (HBEpC) and human fibroblasts (hFB) were included. VOCs were detected in the headspace of cell cultures or medium controls following adsorption on solid sorbents, thermodesorption, and analysis by gas chromatography mass spectrometry. Using this approach, we identified VOCs that behaved similarly in normal and transformed cells. Thus, concentrations of 2-pentanone and 2,4-dimethyl-1-heptene were found to increase in the headspace of A549, HBEpC, and hFB cell cultures. In addition, the ethers methyl tert-butyl ether and ethyl tert-butyl ether could be detected at elevated levels in the case of A549 cells and one of the untransformed cell lines. However, especially branched hydrocarbons and alcohols were seen increased more frequently in untransformed than A549 cells. A big variety of predominantly aldehydes and the ester n-butyl acetate were found at decreased concentrations in the headspace of all cell lines tested compared with medium controls. Again, more different aldehydes were found to be decreased in hFB and HBEpC cells compared with A549 cells and 2-butenal was metabolized exclusively by both control cell lines. These data suggest that certain groups of VOCs may be preferentially associated with the transformed phenotype. Cancer Epidemiol Biomarkers Prev; 19(1); 182–95
Arsenic in Drinking Water and Risk of Urinary Tract Cancer: A Follow-up Study from Northeastern Taiwan
Authors: Chen Chi-Ling , Chiou Hung-Yi , Hsu Ling-I , Hsueh Yu-Mei , Wu Meei-Maan , Wang Yuan-Hung , Chen Chien-Jen 
Published: January 2010

Abstract
The evidence linking arsenic in drinking water with increased urinary cancer risk comes from populations in relatively high exposure areas (&gt;100 μg/L), whereas studies from lower exposure areas (&lt;100 μg/L) reported inconsistent results. A previous study conducted in northeastern Taiwan, where residents were exposed to relatively lower concentrations, reported increased risk of urinary cancer in a dose-response way. Using the same cohort with longer follow-up, we conducted analysis to elucidate the relationship between ingested arsenic and urinary cancer in lower exposure groups and assessed the influence of duration, recency, and latency of drinking arsenic-containing well water. A total of 8,086 residents from northeastern Taiwan were followed for 12 years. Incident urinary cancer was ascertained through linkage with the national cancer registry. All analysis was done by Cox proportional hazards regression models. There were 45 incidences of urinary cancer and a monotonic increased risk of urinary cancer was found with increasing arsenic concentration (P &lt; 0.001). For the highly exposed (&gt;100 μg/L), the relative risks (RR) were &gt;5-fold, whereas the risk was elevated but not significant for low exposure (&lt;100 μg/L). Relative to the arsenic concentration &lt;10 μg/L, those who drank well water with higher concentration from birth [RR, 3.69; 95% confidence interval (95% CI), 1.31-10.4], still drank at enrollment (RR, 3.50; 95% CI, 1.33-9.22), and drank for &gt;50 years (RR, 4.12; 95% CI, 1.48-11.5) had a significantly increased risk of urinary cancer. When restricted to urothelial carcinoma, all risk estimates including concentration and characteristics of well water consumption were higher. Cancer Epidemiol Biomarkers Prev; 19(1); 101–10
Gene Methylation in Breast Ductal Fluid from BRCA1 and BRCA2 Mutation Carriers
Authors: Antill Yoland C. , Mitchell Gillian , Johnson Sandra A. , Devereux Lisa , Milner Alvin , Di Iulio Juliana , Lindeman Geoffrey J. , Kirk Judy , Phillips Kelly Anne , Campbell Ian G. 
Published: January 2010

Abstract
Purpose: Genomic alterations (including gene hypermethylation) are likely to precede the phenotypic changes associated with breast tumorigenesis. From a prospective collection of ductal lavage (DL) samples from women with a known mutation in BRCA1 or BRCA2, we have assessed promoter methylation with a comparison of results with several variables, including breast cancer (BC) outcome.
Experimental Design: Hypermethylation of p16, RASSF1A, twist, and RARβ was assessed using a qualitative, real-time, nested PCR assay. Associations between methylation status and variables were tested using Fisher's exact test or logistic regression. Analyses were done at three levels: a single breast, a single duct (both over time), and each DL sample in isolation.
Results: A total of 168 samples from 93 ducts in 54 breasts have been analyzed in 34 women (16 BRCA1 and 18 BRCA2 mutation carriers). A median of 2 DL was done (range, 1–5), with 7 women developing BC on study, 1 bilateral. Methylation of p16 was associated with a known BRCA1 mutation (P = 0.001, P &lt; 0.001, and P &lt; 0.001 for breast, duct, and sample levels, respectively) and women with a history of contralateral BC (P = 0.001 and P &lt; 0.001 for duct and sample levels, respectively). An association was seen for women who developed BC on study and RASSF1A methylation (P = 0.001 for sample level).
Conclusions: Genetic methylation patterns could potentially be used to predict future BC risk. In addition, p16 methylation may be a predictor of BRCA1 mutation status. Further research is required to corroborate these findings. Cancer Epidemiol Biomarkers Prev; 19(1); 265–74
Influence of High-Dose Estrogen Exposure during Adolescence on Mammographic Density for Age in Adulthood
Authors: Jordan Helen L. , Hopper John L. , Thomson Russell J. , Kavanagh Anne M. , Gertig Dorota M. , Stone Jennifer , Venn Alison J. 
Published: January 2010

AbstractHigh-dose estrogen exposure during adolescence has been hypothesized to increase a woman's breast cancer risk, possibly mediated through an increase in mammographic density, a well-established breast cancer risk factor. In 2006 to 2007, we conducted a retrospective study of women assessed for tall stature as an adolescent between 1959 and 1993. Eligible participants were ages ≥40 years and treated during adolescence with 3 mg diethylstilbestrol or 150 μg ethinyl estradiol daily or untreated. Mammograms from 167 treated and 142 untreated women were digitized. Total breast area, dense area, nondense area, and percent density were measured using a computer thresholding technique. Data on potential determinants were collected from medical records and telephone interview. Treated women had, on average, 17% lower dense area (P = 0.032). Means (95% confidence intervals) adjusted for age and body mass index for treated and untreated women were 24.5 cm2 (21.8-27.2) and 29.1 cm2 (26.0-32.4), respectively. There was no difference in adjusted means (95% confidence intervals) between treated and untreated women for nondense area [71.7 cm2 (66.2-77.7) versus 70.5 cm2 (64.7-76.9); P = 0.78], percent dense area [24.8% (22.4-27.4) versus 27.7% (24.8-30.7); P = 0.16], or total area [105.6 cm2 (100.1-111.4) versus 109.3 cm2 (103.1-115.8); P = 0.41], respectively. High-dose estrogen exposure during adolescence appears to curtail growth of mammographically dense tissue and therefore is unlikely to increase breast cancer risk through mechanisms related to mammographic density. Cancer Epidemiol Biomarkers Prev; 19(1); 121–9
Plasma 25-Hydroxyvitamin D Levels and the Risk of Colorectal Cancer: The Multiethnic Cohort Study
Authors: Woolcott Christy G. , Wilkens Lynne R. , Nomura Abraham M.Y. , Horst Ronald L. , Goodman Marc T. , Murphy Suzanne P. , Henderson Brian E. , Kolonel Laurence N. , Le Marchand Loïc 
Published: January 2010

AbstractVitamin D is obtained from the diet and synthesized in skin exposed to sunlight. Vitamin D status, assessed by circulating 25-hydroxyvitamin D [25(OH)D], has been associated with a reduced risk of colorectal cancer in previous studies. To complement existing evidence, we conducted a case-control study nested within the Multiethnic Cohort including men and women of Japanese, Latino, African-American, White, and Native Hawaiian ancestry. Using a direct competitive chemiluminescence immunoassay, 25(OH)D level was determined in plasma drawn before diagnosis from 229 cases and 434 controls matched to cases by area (Hawaii, Los Angeles), sex, ethnicity, birth year, blood draw date and time, and hours fasting. Odds ratios (OR) were estimated with conditional logistic regression. An inverse trend was observed (OR per doubling of 25(OH)D, 0.68; 95% confidence interval, 0.51-0.92; P = 0.01), but when examined in categories, relative to the first quintile (&lt;16.8 ng/mL), the ORs in all other quintiles were quite similarly reduced between 37% and 46%. The association was not significantly heterogeneous among the four largest ethnic groups (Pheterogeneity = 0.46). In summary, this study provides evidence of an association between vitamin D status and reduced risk of colorectal cancer in an ethnically diverse population. Cancer Epidemiol Biomarkers Prev; 19(1); 130–4
Randomized Trial of a Lay Health Advisor and Computer Intervention to Increase Mammography Screening in African American Women
Authors: Russell Kathleen M. , Champion Victoria L. , Monahan Patrick O. , Millon-Underwood Sandra , Zhao Qianqian , Spacey Nicole , Rush Nathan L. , Paskett Electra D. 
Published: January 2010

AbstractBackground: Low-income African American women face numerous barriers to mammography screening. We tested the efficacy of a combined interactive computer program and lay health advisor intervention to increase mammography screening.Methods: In this randomized, single blind study, participants were 181 African American female health center patients of ages 41 to 75 years, at ≤250% of poverty level, with no breast cancer history, and with no screening mammogram in the past 15 months. They were assigned to either (a) a low-dose comparison group consisting of a culturally appropriate mammography screening pamphlet or (b) interactive, tailored computer instruction at baseline and four monthly lay health advisor counseling sessions. Self-reported screening data were collected at baseline and 6 months and verified by medical record.Results: For intent-to-treat analysis of primary outcome (medical record–verified mammography screening, available on all but two participants), the intervention group had increased screening to 51% (45 of 89) compared with 18% (16 of 90) for the comparison group at 6 months. When adjusted for employment status, disability, first-degree relatives with breast cancer, health insurance, and previous breast biopsies, the intervention group was three times more likely (adjusted relative risk, 2.7; 95% confidence interval, 1.8-3.7; P &lt; 0.0001) to get screened than the low-dose comparison group. Similar results were found for self-reported mammography stage of screening adoption.Conclusions: The combined intervention was efficacious in improving mammography screening in low-income African American women, with an unadjusted effect size (relative risk, 2.84) significantly higher (P &lt; 0.05) than that in previous studies of each intervention alone. Cancer Epidemiol Biomarkers Prev; 19(1); 201–10
Cytoplasmic Localization of β-Catenin is a Marker of Poor Outcome in Breast Cancer Patients
Authors: López-Knowles Elena , Zardawi Sarah J. , McNeil Catriona M. , Millar Ewan K.A. , Crea Paul , Musgrove Elizabeth A. , Sutherland Robert L. , O'Toole Sandra A. 
Published: January 2010

Abstract
β-catenin is involved in cell adhesion through catenin-cadherin complexes and as a transcriptional regulator in the Wnt signaling pathway. Its deregulation is important in the genesis of a number of human malignancies, particularly colorectal cancer. A range of studies has been undertaken in breast cancer, with contradictory associations reported among β-catenin expression, clinicopathologic variables, and disease outcome. We undertook an immunohistochemical study measuring the levels and subcellular localization of β-catenin in 292 invasive ductal breast cancers with known treatment and outcome. No association with breast cancer–specific death was observed for cytoplasmic or membrane expression alone; however, a continuous score representing both locations (membrane minus cytoplasmic expression: MTC score) was associated with a worse outcome in univariate analysis (P = 0.004), and approached significance in a multivariate analysis model that included lymph node, progesterone receptor (PR), and HER2 status (P = 0.054). Therefore, the MTC score was used for further statistical analyses due to the importance of both the subcellular location and the levels of expression of β-catenin. An association was identified between high cytoplasmic expression (low MTC score), and high tumor grade (P = 0.004), positive Ki67 (P = 0.005), negative estrogen receptor (ER) (P = 0.005), positive HER2 (P = 0.04) status, and an active phosphoinositide 3-kinase pathway (P = 0.005), measured as PIK3CA mutations (P = 0.05) or PTEN loss (P = 0.05). Low cytoplasmic expression (high MTC score) was associated with the luminal A subtype (P = 0.004). In conclusion, a low β-catenin MTC score is associated with an adverse outcome in breast cancer, which may be of mechanistic significance in the disease process. Cancer Epidemiol Biomakers Prev; 19(1); 301–9