bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cancer Risk Assessment by Rural and Appalachian Family Medicine Physicians
Authors: Kelly Kimberly M. , Love Margaret M. , Pearce Kevin A. , Porter Kyle , Barron Mary A. , Andrykowski Michael 
Published: September 2009

ABSTRACT:
Context:

Challenges to the identification of hereditary cancer in primary care may be more pronounced in rural Appalachia, a medically underserved region. Purpose: To examine primary care physicians’ identification of hereditary cancers. Methods: A cross‐sectional survey was mailed to family physicians in the midwestern and southeastern United States, stratified by rural/non‐rural and Appalachian/non‐Appalachian practice location (n = 176). Identification of hereditary breast‐ovarian cancer (BRCA1/2), hereditary non‐polyposis colon cancer (HNPCC), and other hereditary cancers was assessed. Findings: Less than half of physicians (45%) reported having patients with cancer genetic testing. Most (70%) correctly identified the BRCA1/2‐relevant scenario; 49% correctly identified the HNPCC‐relevant scenario. Factor analysis of psychosocial variables revealed 2 factors: Confidence (knowledge, comfort, confidence) and importance (responsible, important, effective, need) of identifying hereditary cancer. Greater confidence was associated with use of 3 generation pedigree in taking family history. Greater knowledge and access to genetic services were associated with use of genetic testing. More recent graduation year, greater knowledge, and greater confidence were associated with identifying the BRCA1/2‐relevant scenario. Greater knowledge and confidence were associated with identifying the HNPCC‐relevant scenario. Conclusions: Though rural Appalachian physicians do not differ in ability to identify high risk individuals, access barriers may exist for genetic testing. Interventions are needed to boost physician confidence in identifying hereditary cancer and to improve availability and awareness of availability of genetic services.
A comparative study of nursing staff, care recipients’ and their relatives’ perceptions of quality of older people care
Authors: Hasson Henna , Arnetz Judith E. 
Published: September 2009

hasson h. & arnetz j.e. (2009) A comparative study of nursing staff, care recipients’ and their relatives’ perceptions of quality of older people care. International Journal of Older People Nursing 5, 5–15 doi: 10.1111/j.1748‐3743.2009.00186.xBackground.  Comparisons of different stakeholders’ ratings of the quality of older people care can help to drive quality improvement.Aim.  The aim was to compare staff, older care recipients’ and their relatives’ quality of care ratings.Design.  Cross‐sectional questionnaire surveys in 2003 and 2004, using a repeated measures design on an organizational level.Methods.  Nursing staff, care recipients and relatives in two older people care organizations were included. The ratings of an overall quality grade, information, activities, general care and staff skills were compared between the respondent groups.Results.  Care recipients in both organizations rated the overall quality grade significantly higher than nursing staff and relatives. Staff ratings of the information given to care recipients were significantly more positive than care recipients’ and relatives’ ratings. All three groups gave lowest ratings to the quality of activities offered to care recipients, with lowest ratings from nursing staff.Conclusions.  Concurrent measurements of staff, care recipients and relatives’ care quality perceptions can provide a broad evaluation of an organization’s strength and limitations.Relevance to clinical practice.  Staff, care recipients’ and relatives’ perceptions can be useful for older people care organizations and decision makers in developing care processes and outcomes of care.
How can We Reduce the Distress Associated with Health Screening? From Psychological Theory to Clinical Practice
Authors: Bennett Paul 
Published: September 2009

AbstractHealth screening involves the early identification of risk factors for disease or early‐stage disease. There is clear evidence of a health benefit following many screening programs. However, these programs may also contribute to significant psychological distress in a significant minority of vulnerable individuals. This paper considers the impact of screening in relation to breast cancer, focusing on assessment of genetic risk for breast cancer and mammography. It then reviews how these programs presently try to minimize any distress among participants before examining how health and clinical psychological theory can contribute to the development of new interventions, focusing on the use of cognitive challenge and teaching appropriate emotion‐focused coping strategies such as mindfulness and distraction. Future research developments are then addressed.
Getting Emotional About Explanations: Social Explanations and Social Explanatory Styles as Bases of Prosocial Emotions and Intergroup Attitudes
Authors: Gill Michael J. , Andreychik Michael R. 
Published: September 2009

AbstractWe are interested in the bases of social emotions such as compassion and hostility. Our analysis centers on social explanations, or people’s answers to the question: Why does the target behave that way or experience those outcomes? Below, we review classic approaches to social explanation and then review work linking explanations to emotions. Finally, we focus on work from our lab that connects explanations to prosocial emotions and intergroup attitudes, including compassion for the disadvantaged and reduced vengefulness toward the violent. A crucial contribution of our work is to illuminate complex connections between explanations and emotions: A given explanation has different socio‐emotional implications depending on the explainer’s motives. Finally, we review our work suggesting that individuals have social explanatory styles, and that particular styles are predictive of dispositional compassion. A key implication of our work is that social explanations are another basis of prosociality, in addition to factors such as empathy and moral principles.
On the Relationship between Social Capital and Individualism–Collectivism
Authors: Realo Anu , Allik Jüri 
Published: September 2009

AbstractBoth social capital and individualism–collectivism (IC) have been, and still are, popular and well‐researched constructs in social sciences. Many theorists have argued that individualism poses a threat to social cohesion and communal association. Other researchers believe that growth of individuality, autonomy, and self‐sufficiency are necessary conditions for the development of social solidarity and cooperation. The present article reviews the studies on the relationship between social capital and IC, using different data and different measures. We conclude that countries with higher level of social capital (where people believe that most people can be trusted) are also more individualistic, emphasizing the importance of independence, personal accomplishments, and freedom to choose one’s own goals. In societies where trust is limited to the nuclear family or kinship alone, people have lower levels of social capital. Social capital increases as the radius of trust widens to encompass a larger number of people and social networks, bridging the ‘gap’ between the family and state.
The effect of deep sclerectomy on intraocular pressure of normal‐tension glaucoma patients: 1‐year results
Authors: Suominen Sakari , Harju Mika , Ihanamäki Tapio , Vesti Eija 
Published: September 2009

Abstract.Purpose:  To study the intraocular pressure (IOP)‐reducing effect of deep sclerectomy on normal‐tension glaucoma (NTG) patients.Methods:  We retrospectively analysed 21 eyes of 18 consecutive NTG patients who had undergone deep sclerectomy with mitomycin‐C and a collagen implant.Results:  Median (range) preoperative IOP was 15.1 mmHg (9.3–20.8) and median follow‐up time 13 months (12–18). At the 1‐year follow‐up visit, median IOP was significantly (P < 0.001) reduced to 10.5 mmHg (4–15) with median IOP reduction from preoperative values of 37% (12–78). Laser goniopuncture was performed in 10 eyes (48%) 1–16 months postoperatively. After 13 months’ follow‐up, a complete success at 20%, 25% and 30% IOP reduction levels was achieved in 67%, 62% and 52% of eyes, respectively. Few complications were encountered, but these included reduced visual acuity, problems with conjunctiva, microperforation, hyphaema, Dellen formation and encapsulated bleb. We encountered no complications related to postoperative hypotony.Conclusion:  Deep sclerectomy with a collagen implant and mitomycin‐C was a safe and effective method for reducing IOP in NTG patients during 1‐year follow‐up.
Occupational exposure to polycyclic aromatic hydrocarbons and lung cancer risk: a multicenter study in Europe
Authors: Olsson Ann C , Fevotte Joelle , Fletcher Tony , Cassidy Adrian , 't Mannetje Andrea , Zaridze David , Szeszenia-Dabrowska Neonila , Rudnai Peter , Lissowska Jolanta , Fabianova Eleonora , Mates Dana , Bencko Vladimir , Foretova Lenka , Janout Vladimir , Brennan Paul , Boffetta Paolo 
Published: September 2009

BackgroundLung cancer incidence in Central and Eastern Europe (CEE) is among the highest in the world, and the role of occupational exposures has not been adequately studied in these countries.ObjectivesTo investigate the contribution of occupational exposure to polycyclic aromatic hydrocarbons (PAH) to lung cancer in CEE.MethodsA case–control study was conducted in the Czech Republic, Hungary, Poland, Romania, Russia and Slovakia, as well as the United Kingdom (UK) between 1998 and 2002. Occupational and socio-demographic information was collected through interviews from 2861 newly diagnosed lung cancer cases and 2936 population or hospital controls. Industrial hygiene experts in each country evaluated exposure to 70 occupational agents, whereof 15 mixtures containing PAH. ORs of lung cancer were calculated after adjusting for other occupational exposures and tobacco smoking.ResultsThe OR for ever exposure to PAH in the CEE countries was 0.93 (95% CI 0.77 to 1.14). The ORs for the highest category of cumulative exposure, duration of exposure and intensity of exposure were 1.13 (95% CI 0.80 to 1.58), 1.02 (95% CI 0.66 to 1.57) and 1.11 (95% CI 0.60 to 2.05), respectively. The OR for ever PAH exposure in the UK was 1.97 (95% CI 1.16 to 3.35).ConclusionOccupational PAH exposure does not appear to substantially contribute to the burden of lung cancer in CEE. The apparently stronger effect observed in the UK may be due to high exposure levels and a joint effect with asbestos.
Respiratory health effects of ultrafine and fine particle exposure in cyclists
Authors: Strak Maciej , Boogaard Hanna , Meliefste Kees , Oldenwening Marieke , Zuurbier Moniek , Brunekreef Bert , Hoek Gerard 
Published: September 2009

ObjectivesMonitoring studies have shown that commuters are exposed to high air pollution concentrations, but there is limited evidence of associated health effects. We carried out a study to investigate the acute respiratory health effects of air pollution related to commuting by bicycle.MethodsTwelve healthy adults cycled a low- and a high-traffic intensity route during morning rush hour in Utrecht, The Netherlands. Exposure to traffic-related air pollution was characterised by measurements of PM10, soot and particle number. Before, directly after and 6 h after cycling we measured lung function (FEV1, FVC, PEF), exhaled NO (FENO) and respiratory symptoms. The association between post- minus pre-exposure difference in health effects and exposure during cycling was evaluated with linear regression models.ResultsThe average particle number concentration was 59% higher, while the average soot concentration was 39% higher on the high-traffic route than on the low-traffic route. There was no difference for PM10. Contrary to our hypothesis, associations between air pollution during cycling and lung function changes immediately after cycling were mostly positive. Six hours after cycling, associations between air pollution exposure and health were mostly negative for lung function changes and positive for changes in exhaled NO, although non-significant.ConclusionsWe found substantial differences in ultrafine particle number and soot exposure between two urban cycling routes. Exposure to ultrafine particles and soot during cycling was weakly associated with increased exhaled NO, indicative of airway inflammation, and decrements in lung function 6 h after exposure. A limitation of the study was the relatively small sample size.
HIGH-FREQUENCY RESPONSE AND VOLTAGE NOISE IN MAGNETIC NANOCOMPOSITES
Authors: BUZNIKOV N. A. , IAKUBOV I. T. , RAKHMANOV A. L. , KUGEL K. I. , SBOYCHAKOV A. O. 
Published: September 2009

We study the noise spectra and high-frequency permeability of inhomogeneous magnetic materials consisting of single-domain magnetic nanoparticles embedded into an insulating matrix. Possible mechanisms of 1/f voltage noise in phase-separated manganites is analyzed. The material is modelled by a system of small ferromagnetic metallic droplets (magnetic polarons or ferrons) in insulating antiferromagnetic or paramagnetic matrix. The electron transport is related to tunnelling of charge carriers between droplets. One of the sources of the 1/f noise in such a system stems from fluctuations of the number of droplets with extra electron. In the case of strong magnetic anisotropy, the 1/f noise can arise also due to the fluctuations of the magnetic moments of ferrons. The high frequency magnetic permeability of nanocomposite film with magnetic particles in insulating non-magnetic matrix is studied in detail. The case of strong magnetic dipole interaction and strong magnetic anisotropy of ferromagnetic granules is considered. The composite is modelled by a cubic regular array of ferromagnetic particles. The high-frequency permeability tensor components are found as a functions of frequency, temperature, ferromagnetic phase content, and magnetic anisotropy. The results demonstrate that magnetic dipole interaction leads to a shift of the resonance frequencies towards higher values, and nanocomposite film could have rather high value of magnetic permeability in the microwave range.
TrkBT1 Induces Liver Metastasis of Pancreatic Cancer Cells by Sequestering Rho GDP Dissociation Inhibitor and Promoting RhoA Activation
Authors: Li Zhongkui , Chang Zhe , Chiao Lucia J. , Kang Ya'an , Xia Qianghua , Zhu Cihui , Fleming Jason B. , Evans Douglas B. , Chiao Paul J. 
Published: September 2009

AbstractMany genetic and molecular alterations, such as K-ras mutation and NF-κB activation, have been identified in pancreatic cancer. However, the mechanisms by which pancreatic cancer metastasizes still remain to be determined. Although we previously showed that the tropomyosin-related kinase B (TrkB) was significantly correlated with the development of liver metastasis, its function in pancreatic cancer metastasis remained unresolved. In the present study, we showed that overexpressed TrkB is an alternatively spliced transcript variant of TrkB (TrkBT1) with a unique COOH-terminal 12–amino acid sequence and is mainly localized in the cytoplasm. Our results showed that overexpression of Flag-tagged TrkBT1 but not a Flag-tagged TrkBT1 COOH-terminal deletion mutant (Flag-TrkBT1ΔC) in nonmetastatic pancreatic cancer cells enhanced cell proliferation, promoted formation of colonies in soft agar, stimulated tumor cell invasion, and induced liver metastasis in an orthotopic xenograft mouse model of pancreatic cancer. TrkBT1 interacted with Rho GDP dissociation inhibitor (GDI) in vivo, but Flag-TrkBT1ΔC did not. Furthermore, overexpression of Flag-TrkBT1 and knockdown of RhoGDI expression by RhoGDI short hairpin RNAs promoted RhoA activation, but Flag-TrkBT1ΔC overexpression did not. Therefore, our results showed that TrkBT1 overexpression induces liver metastasis of pancreatic cancer and uncovered a unique signaling mechanism by which TrkBT1 sequesters GDI and activates RhoA signaling. [Cancer Res 2009;69(19):7851–9]
Acting Locally and Globally: Myc's Ever-Expanding Roles on Chromatin
Authors: Varlakhanova Natalia V. , Knoepfler Paul S. 
Published: September 2009

Abstract
Myc regulates key cellular processes including cell cycle, differentiation, and apoptosis. It has long been thought to direct these functions by acting solely as a classic transcription factor regulating expression of a small number of key target genes through discrete chromatin events in their promoters. A recent wave of genomics studies together directly challenge the narrowness of this model. For example, Myc binds to tens of thousands of sites in the human genome. It also regulates histone acetylation at and transcription of a remarkable number of genes, far beyond that expected of a classical transcription factor. The influence of Myc on chromatin also surprisingly extends to both genic and expansive intergenic regions. These studies support an evolving model in which Myc activity on chromatin is far more complex than previously imagined. The ability of Myc to act both locally and globally on chromatin may be responsible for its wide-ranging effects on the biology of stem and tumor cells. [Cancer Res 2009;69(19):7487–90]
Molecular Distinctions between Stasis and Telomere Attrition Senescence Barriers Shown by Long-term Culture of Normal Human Mammary Epithelial Cells
Authors: Garbe James C. , Bhattacharya Sanchita , Merchant Batul , Bassett Ekaterina , Swisshelm Karen , Feiler Heidi S. , Wyrobek Andrew J. , Stampfer Martha R. 
Published: September 2009

Abstract
Normal human epithelial cells in culture have generally shown a limited proliferative potential of ∼10 to 40 population doublings before encountering a stress-associated senescence barrier (stasis) associated with elevated levels of cyclin-dependent kinase inhibitors p16 and/or p21. We now show that simple changes in medium composition can expand the proliferative potential of human mammary epithelial cells (HMEC) initiated as primary cultures to 50 to 60 population doublings followed by p16-positive, senescence-associated β-galactosidase–positive stasis. We compared the properties of growing and senescent pre-stasis HMEC with growing and senescent post-selection HMEC, that is, cells grown in a serum-free medium that overcame stasis via silencing of p16 expression and that display senescence associated with telomere dysfunction. Cultured pre-stasis populations contained cells expressing markers associated with luminal and myoepithelial HMEC lineages in vivo in contrast to the basal-like phenotype of the post-selection HMEC. Gene transcript and protein expression, DNA damage–associated markers, mean telomere restriction fragment length, and genomic stability differed significantly between HMEC populations at the stasis versus telomere dysfunction senescence barriers. Senescent isogenic fibroblasts showed greater similarity to HMEC at stasis than at telomere dysfunction, although their gene transcript profile was distinct from HMEC at both senescence barriers. These studies support our model of the senescence barriers encountered by cultured HMEC in which the first barrier, stasis, is retinoblastoma-mediated and independent of telomere length, whereas a second barrier (agonescence or crisis) results from telomere attrition leading to telomere dysfunction. Additionally, the ability to maintain long-term growth of genomically stable multilineage pre-stasis HMEC populations can greatly enhance experimentation with normal HMEC. [Cancer Res 2009;69(19):7557–68]
Nitrosative Stress–Induced S-Glutathionylation of Protein Disulfide Isomerase Leads to Activation of the Unfolded Protein Response
Authors: Townsend Danyelle M. , Manevich Yefim , He Lin , Xiong Ying , Bowers Robert R. , Hutchens Steven , Tew Kenneth D. 
Published: September 2009

Abstract
The rapid proliferation of cancer cells mandates a high protein turnover. The endoplasmic reticulum (ER) is intimately involved in protein processing. An accumulation of unfolded or misfolded proteins in the ER leads to a cascade of transcriptional and translational events collectively called the unfolded protein response (UPR). Protein disulfide isomerase (PDI) is one of the most abundant ER proteins and maintains a sentinel function in organizing accurate protein folding. Treatment of cells with O2-[2,4-dinitro-5-(N-methyl-N-4-carboxyphenylamino)phenyl]1-(N,N-dimethylamino)diazen-1-ium-1,2-diolate (PABA/NO) resulted in a dose-dependent increase in intracellular nitric oxide that caused S-glutathionylation of various proteins. Within 4 h, PABA/NO activated the UPR and led to translational attenuation as measured by the phosphorylation and activation of the ER transmembrane kinase, pancreatic ER kinase, and its downstream effector eukaryotic initiation factor 2 in human leukemia (HL60) and ovarian cancer cells (SKOV3). Cleavage of the transcription factor X-box protein 1 and transcriptional activation of the ER resident proteins BiP, PDI, GRP94, and ERO1 (5- to 10-fold induction) also occurred. Immunoprecipitation of PDI showed that whereas nitrosylation was undetectable, PABA/NO treatment caused S-glutathionylation of PDI. Mass spectroscopy analysis showed that single cysteine residues within each of the catalytic sites of PDI had a mass increase [+305.3 Da] consistent with S-glutathionylation. Circular dichroism confirmed that S-glutathionylation of PDI results in alterations in the α-helix content of PDI and is concurrent with inhibition of its isomerase activity. Thus, it appears that S-glutathionylation of PDI is an upstream signaling event in the UPR and may be linked with the cytotoxic potential of PABA/NO. [Cancer Res 2009;69(19):7626–34]
MicroRNA-34a Inhibits Glioblastoma Growth by Targeting Multiple Oncogenes
Authors: Li Yunqing , Guessous Fadila , Zhang Ying , DiPierro Charles , Kefas Benjamin , Johnson Elizabeth , Marcinkiewicz Lukasz , Jiang Jinmai , Yang Yanzhi , Schmittgen Thomas D. , Lopes Beatriz , Schiff David , Purow Benjamin , Abounader Roger 
Published: September 2009

AbstractMicroRNA-34a (miR-34a) is a transcriptional target of p53 that is down-regulated in some cancer cell lines. We studied the expression, targets, and functional effects of miR-34a in brain tumor cells and human gliomas. Transfection of miR-34a down-regulated c-Met in human glioma and medulloblastoma cells and Notch-1, Notch-2, and CDK6 protein expressions in glioma cells. miR-34a expression inhibited c-Met reporter activities in glioma and medulloblastoma cells and Notch-1 and Notch-2 3′-untranslated region reporter activities in glioma cells and stem cells. Analysis of human specimens showed that miR-34a expression is down-regulated in glioblastoma tissues as compared with normal brain and in mutant p53 gliomas as compared with wild-type p53 gliomas. miR-34a levels in human gliomas inversely correlated to c-Met levels measured in the same tumors. Transient transfection of miR-34a into glioma and medulloblastoma cell lines strongly inhibited cell proliferation, cell cycle progression, cell survival, and cell invasion, but transfection of miR-34a into human astrocytes did not affect cell survival and cell cycle status. Forced expression of c-Met or Notch-1/Notch-2 transcripts lacking the 3′-untranslated region sequences partially reversed the effects of miR-34a on cell cycle arrest and cell death in glioma cells and stem cells, respectively. Also, transient expression of miR-34a in glioblastoma cells strongly inhibited in vivo glioma xenograft growth. Together, these findings represent the first comprehensive analysis of the role of miR-34a in gliomas. They show that miR-34a suppresses brain tumor growth by targeting c-Met and Notch. The results also suggest that miR-34a could serve as a potential therapeutic agent for brain tumors. [Cancer Res 2009;69(19):7569–76]