bluuebunny/crossref_metadata_2025_split huggingface dataset:
The molecular epidemiology of equine influenza in Ireland from 2007–2010 and its international significance
Authors: GILDEA S. , QUINLIVAN M. , ARKINS S. , CULLINANE A. 
Published: October 2011

SummaryReasons for performing the study: Antigenic and genetic drift of equine influenza (EI) virus is monitored annually by the Expert Surveillance Panel (ESP), which make recommendations on the need to update vaccines. Surveillance programmes are essential for this process to operate effectively and to decrease the risk of disease spread through the international movement of subclinically infected vaccinated horses. Not only is surveillance necessary to inform vaccine companies which strains are in circulation, but it serves as an early warning system for horse owners, trainers and veterinary clinicians, facilitating the implementation of appropriate prophylactic and control measures.Objective: To summarise the genetic analysis of EI viruses detected in Ireland from June 2007 to January 2010.Methods: The HA1 gene of 18 viruses was sequenced and phylogenetic analysis undertaken.Results: All viruses belonged to the Florida sublineage of the American lineage. Clade 2 viruses predominated up to 2009. The viruses identified on 4 premises in 2007 displayed 100% nucleotide identity to A/eq/Richmond/1/07, the current clade 2 prototype. The first clade 1 virus was identified in November 2009 and, thereafter, clade 1 viruses were responsible for all the outbreaks identified. The Irish clade 1 viruses differ from the clade 1 virus responsible for the EI outbreaks in Japan and Australia in 2007. No virus of the Eurasian lineage was isolated during this surveillance period.Conclusions: In 2010 the ESP recommended that the vaccines should not include a H7N7 virus or a H3N8 virus of the Eurasian lineage but that they should contain both a clade 1 and clade 2 virus of the Florida sublineage. The surveillance data presented here support these recommendations and indicate that they are epidemiologically relevant.Potential relevance: These data also serve as a scientific basis for investigating the source of epizootics and outbreaks both nationally and internationally.
A grounded theory approach to understand the cancer‐coping process
Authors: Knott Vikki , Turnbull Deborah , Olver Ian , Winefield Anthony 
Published: October 2011

Objectives. A focus on individualistic coping strategies such as positivity and fighting spirit has done little to inform the development of interventions for people affected by cancer. The aim of this study was to conduct an inquiry, which focused on the ‘lived experience’ and the social context within which communication about cancer occurs.Design. A semi‐structured interview schedule was used. These interviews were complemented by the Mini‐International Neuropsychiatric Interview (M.I.N.I., Sheehan et al., 1998).Methods. Twenty participants with mixed diagnoses (13 female and seven male), ranging in age from 44 to 73 (Mean = 58.35, SD= 8.20) were interviewed. Consistent with Glaser's (1992) constant comparative method, research data were open coded, selectively coded, and then theoretically coded so that initial codes were collapsed into models and compared against existing literature for completeness.Results. Fifty percent of participants met criteria for an Axis 1 diagnosis. Three models emerged from the research interview; the first provides a description of the way in which patients evaluate the quality of care they receive across the cancer pathway. Other models refer to the cancer‐coping process in which participants describe successful and unsuccessful attempts at coping via communication and whereby coping with cancer is characterized by a series of losses accompanied by increased distress.Conclusions. A research focus on the social environment in which cancer is experienced provides considerable insight into the cancer‐coping process. As such, interventions focused on understanding the social context in which patients experience cancer, and attempt to cope, may facilitate improved adjustment for those directly, and potentially indirectly, affected by cancer. Further research is required to develop interventions to address the unique needs of survivors.
Recalled peer relationship experiences and current levels of self‐criticism and self‐reassurance
Authors: Kopala‐Sibley Daniel C. , Zuroff David C. , Leybman Michelle J. , Hope Nora 
Published: October 2011

Objectives. Numerous studies have shown that personality factors may increase or decrease individuals’ vulnerability to depression, but little research has examined the role of peer relationships in the development of these factors. Accordingly, this study examined the role of recalled parenting and peer experiences in the development of self‐criticism and self‐reassurance. It was hypothesized that, controlling for recalled parenting behaviours, specific recalled experiences of peer relationships would be related to current levels of specific forms of self‐criticism and self‐reassurance.Design. Hypotheses were tested using a retrospective design in which participants were asked to recall experiences of parenting and peer relationships during early adolescence. This age was chosen as early adolescence has been shown to be a critical time for the development of vulnerability to depression.Methods. A total of 103 female and 97 male young adults completed measures of recalled parenting, overt and relational victimization and prosocial behaviour by peers, and current levels of self‐criticism and self‐reassurance.Results. Hierarchical regression analyses showed that parents and peers independently contributed to the development of self‐criticism and self‐reassurance. Specifically, controlling for parental care and control, overt victimization predicted self‐hating self‐criticism, relational victimization predicted inadequacy self‐criticism, and prosocial behaviour predicted self‐reassurance. As well, prosocial behaviour buffered the effect of overt victimization on self‐reassurance.Conclusions. Findings highlight the importance of peers in the development of personality risk and resiliency factors for depression, and suggest avenues for interventions to prevent the development of depressive vulnerabilities in youth.Practitioner points

The nature of a patient's personality vulnerability to depression may be better understood through a consideration of the patient's relationships with their peers as well as with parents during adolescence.

An understanding of adult patients’ past peer relationships may further the therapist's understanding of the client's core schemas and dysfunctional attitudes, as well as potential transference reactions during therapy.

Identifying and helping youth to better cope with peer victimization may help prevent the development of a vulnerable personality style in adulthood.

Fostering positive peer relationships in adolescence may buffer the effects of other more negative relationships with peers.
Complete Genome Sequence of a Chinese Virulent Porcine Epidemic Diarrhea Virus Strain
Authors: Chen Jianfei , Wang Chengbao , Shi Hongyan , Qiu Hua-Ji , Liu Shengwang , Shi Da , Zhang Xin , Feng Li 
Published: October 2011

ABSTRACT
CH/S is a virulent porcine epidemic diarrhea virus (PEDV) strain and is used as the virulent strain to evaluate the protection rates of vaccines against PEDV infection in China. Here, we report the complete genome sequence of strain CH/S, which may aid in understanding the molecular characteristics of this strain.
Evaluation of a new model of short-term palliative care for people severely affected with multiple sclerosis: a randomised fast-track trial to test timing of referral and how long the effect is maintained
Authors: Higginson Irene J , Costantini Massimo , Silber Eli , Burman Rachel , Edmonds Polly 
Published: October 2011

ABSTRACT

Aims
In this randomised fast-track phase II trial, the authors examined (1) whether the timing of referral to short-term palliative care (PC) affected selected outcomes, and (2) the potential staff-modifying effect of the short-term PC intervention (whether the effects were sustained over time after PC was withdrawn).

Methods
PC comprised a multiprofessional PC team that provided, on average, three visits, with all care completed by 6 weeks. Recruitment commenced in August 2004 and continued for 1 year. Follow-up was performed for 6 months in both groups. Outcomes were a composite measure of five key symptoms (pain, nausea, vomiting, mouth problems and sleeping difficulty) using the Palliative care Outcome Scale–MS Symptom Scale, and care giver burden was measured using the Zarit (Care Giver) Burden Interview (ZBI).

Results
52 patients severely affected by multiple sclerosis were randomised to receive PC either immediately (fast-track group) or after 12 weeks (control group). Patients had a high level of disability (mean Expanded Disability Status Scale: 7.7; median: 8; SD: 1). Following PC, there was an improvement in Palliative care Outcome Scale–MS Symptom Scale score and ZBI score. A higher rate of improvement in ZBI score was seen in the fast-track group. After withdrawal of PC, effects were maintained at 12 weeks, but not at 24 weeks.

Conclusions
Receiving PC earlier has a similar effect on reducing symptoms but greater effects on reducing care giver burden, compared to later referral. In this phase II trial, the authors lacked the power to detect small differences. The effect of PC is maintained for 6 weeks after withdrawal but then appears to wane.

Trial Registration Number
National Institutes of Health, USA, http://www.Clinicaltrials.gov, NCT00364936.
Host Response to Short-term, Single-Agent Chemotherapy Induces Matrix Metalloproteinase-9 Expression and Accelerates Metastasis in Mice
Authors: Gingis-Velitski Svetlana , Loven David , Benayoun Liat , Munster Michal , Bril Rotem , Voloshin Tali , Alishekevitz Dror , Bertolini Francesco , Shaked Yuval 
Published: October 2011

Abstract
Mounting evidence suggests that bone marrow–derived cells (BMDC) contribute to tumor growth, angiogenesis, and metastasis. In acute reactions to cancer therapy, several types of BMDCs are rapidly mobilized to home tumors. Although this host reaction to therapy can promote tumor regrowth, its contribution to metastasis has not been explored. To focus only on the effects of chemotherapy on the host, we studied non–tumor-bearing mice. Plasma from animals treated with the chemotherapy paclitaxel induced angiogenesis, migration, and invasion of tumor cells along with host cell colonization. Lesser effects were seen with the chemotherapy gemcitabine. Conditioned medium from BMDCs and plasma from chemotherapy-treated mice each promoted metastatic properties in tumor cells by inducing matrix metalloproteinase-9 (MMP9) and epithelial-to-mesenchymal transition. In mice in which Lewis lung carcinoma cells were injected intravenously, treatment with paclitaxel, but not gemcitabine or vehicle, accelerated metastases in a manner that could be blocked by an MMP9 inhibitor. Moreover, chimeric mice reconstituted with BMDC where MMP9 activity was attenuated did not support accelerated metastasis by carcinoma cells that were pretreated with chemotherapy before their introduction to host animals. Taken together, our findings illustrate how some chemotherapies can exert prometastatic effects that may confound treatment outcomes. Cancer Res; 71(22); 6986–96. ©2011 AACR.
Cooperative Phosphorylation of FADD by Aur-A and Plk1 in Response to Taxol Triggers Both Apoptotic and Necrotic Cell Death
Authors: Jang Moon-Sun , Lee Su-Jin , Kang Nam Sook , Kim Eunhee 
Published: October 2011

Abstract
Administration of the antimitotic chemotherapeutic taxol is known to cause accumulation of the mitotic kinase Aurora-A (Aur-A). Here, we report that Aur-A phosphorylates S203 of the Fas associated with death domain protein (FADD) in response to taxol treatment. In addition, polo-like kinase 1 (Plk1) failed to phosphorylate the Aur-A–unphosphorylatable FADD substitution mutant S203A, indicating that phosphorylation of S203 by Aur-A serves to prime FADD for Plk1-mediated phosphorylation at S194. The double-phosphorylation-mimicking mutant form of FADD, FADD-S194D/S203D (FADD-DD), recruited caspase-8, activating the caspase-dependent cell death pathway. FADD-DD also dissociated the cell death protein RIP1 from FADD, resulting in activation of RIP1 and triggering of caspase-independent cell death. Consistent with its death-promoting potential, FADD-DD showed robust tumor suppressor activity. However, single-phosphorylation-mimicking mutant forms of FADD, FADD-S194D/S203A (FADD-DA) and FADD-S194A/S203D (FADD-AD), were incapable of carrying out such functions, indicating that double phosphorylation of FADD is critical for the execution of cell death and tumor suppression. Collectively, our data show the existence of cooperative actions between Aur-A and Plk1 mitotic kinases in response to taxol, providing a molecular explanation for the action mechanism of taxol. Cancer Res; 71(23); 7207–15. ©2011 AACR.
Epigenetic Alteration of PRKCDBP in Colorectal Cancers and Its Implication in Tumor Cell Resistance to TNFα-Induced Apoptosis
Authors: Lee Jin-Hee , Kang Min-Ju , Han Hye-Yeon , Lee Min-Goo , Jeong Seong-In , Ryu Byung-Kyu , Ha Tae-Kyu , Her Nam-Goo , Han Jikhyon , Park Sun Jin , Lee Kil Yeon , Kim Hyo-Jong , Chi Sung-Gil 
Published: October 2011

Abstract
Purpose: PRKCDBP is a putative tumor suppressor in which alteration has been observed in several human cancers. We investigated expression and function of PRKCDBP in colorectal cells and tissues to explore its candidacy as a suppressor in colorectal tumorigenesis.
Experimental Design: Expression and methylation status of PRKCDBP and its effect on tumor growth were evaluated. Transcriptional regulation by NF-κB signaling was defined by luciferase reporter and chromatin immunoprecipitation assays.
Results: PRKCDBP expression was hardly detectable in 29 of 80 (36%) primary tumors and 11 of 19 (58%) cell lines, and its alteration correlated with tumor stage and grade. Promoter hypermethylation was commonly found in cancers. PRKCDBP expression induced the G1 cell-cycle arrest and increased cellular sensitivity to various apoptotic stresses. PRKCDBP was induced by TNFα, and its level correlated with tumor cell sensitivity to TNFα-induced apoptosis. PRKCDBP induction by TNFα was disrupted by blocking NF-κB signaling while it was enhanced by RelA transfection. The PRKCDBP promoter activity was increased in response to TNFα, and this response was abolished by disruption of a κB site in the promoter. PRKCDBP delayed the formation and growth of xenograft tumors and improved tumor response to TNFα-induced apoptosis.
Conclusions: PRKCDBP is a proapoptotic tumor suppressor which is commonly altered in colorectal cancer by promoter hypermethylation, and its gene transcription is directly activated by NF-κB in response to TNFα. This suggests that PRKCDBP inactivation may contribute to tumor progression by reducing cellular sensitivity to TNFα and other stresses, particularly under chronic inflammatory microenvironment. Clin Cancer Res; 17(24); 7551–62. ©2011 AACR.
Cytoplasmic Estrogen Receptor in Breast Cancer
Authors: Welsh Allison W. , Lannin Donald R. , Young Gregory S. , Sherman Mark E. , Figueroa Jonine D. , Henry N. Lynn , Ryden Lisa , Kim Chungyeul , Love Richard R. , Schiff Rachel , Rimm David L. 
Published: October 2011

Abstract
Purpose: In addition to genomic signaling, it is accepted that estrogen receptor-α (ERα) has nonnuclear signaling functions, which correlate with tamoxifen resistance in preclinical models. However, evidence for cytoplasmic ER localization in human breast tumors is less established. We sought to determine the presence and implications of nonnuclear ER in clinical specimens.
Experimental Design: A panel of ERα-specific antibodies (SP1, MC20, F10, 60c, and 1D5) was validated by Western blot and quantitative immunofluorescent (QIF) analysis of cell lines and patient controls. Then eight retrospective cohorts collected on tissue microarrays were assessed for cytoplasmic ER. Four cohorts were from Yale (YTMA 49, 107, 130, and 128) and four others (NCI YTMA 99, South Swedish Breast Cancer Group SBII, NSABP B14, and a Vietnamese Cohort) from other sites around the world.
Results: Four of the antibodies specifically recognized ER by Western and QIF analysis, showed linear increases in amounts of ER in cell line series with progressively increasing ER, and the antibodies were reproducible on YTMA 49 with Pearson correlations (r2 values) ranging from 0.87 to 0.94. One antibody with striking cytoplasmic staining (MC20) failed validation. We found evidence for specific cytoplasmic staining with the other four antibodies across eight cohorts. The average incidence was 1.5%, ranging from 0 to 3.2%.
Conclusions: Our data show ERα is present in the cytoplasm in a number of cases using multiple antibodies while reinforcing the importance of antibody validation. In nearly 3,200 cases, cytoplasmic ER is present at very low incidence, suggesting its measurement is unlikely to be of routine clinical value. Clin Cancer Res; 18(1); 118–26. ©2011 AACR.
Lysosomal Sequestration of Sunitinib: A Novel Mechanism of Drug Resistance
Authors: Gotink Kristy J. , Broxterman Henk J. , Labots Mariette , de Haas Richard R. , Dekker Henk , Honeywell Richard J. , Rudek Michelle A. , Beerepoot Laurens V. , Musters René J. , Jansen Gerrit , Griffioen Arjan W. , Assaraf Yehuda G. , Pili Roberto , Peters Godefridus J. , Verheul Henk M.W. 
Published: October 2011

Abstract
Purpose: Resistance to antiangiogenic tyrosine kinase inhibitors such as sunitinib is an important clinical problem, but its underlying mechanisms are largely unknown. We analyzed tumor sunitinib levels in mice and patients and studied sensitivity and resistance mechanisms to sunitinib.
Experimental Design: Intratumoral and plasma sunitinib concentrations in mice and patients were determined. Sunitinib exposure on tumor cell proliferation was examined. Resistant tumor cells were derived by continuous exposure and studied for alterations in intracellular sunitinib accumulation and activity.
Results: Intratumoral concentrations of sunitinib in mice and patients were 10.9 ± 0.5 and 9.5 ± 2.4 μmol/L, respectively, whereas plasma concentrations were 10-fold lower, 1.0 ± 0.1 and 0.3 ± 0.1 μmol/L, respectively. Sunitinib inhibited tumor cell growth at clinically relevant concentrations in vitro, with IC50 values of 1.4 to 2.3 μmol/L. Continuous exposure to sunitinib resulted in resistance of 786-O renal and HT-29 colon cancer cells. Fluorescent microscopy revealed intracellular sunitinib distribution to acidic lysosomes, which were significantly higher expressed in resistant cells. A 1.7- to 2.5-fold higher sunitinib concentration in resistant cells was measured because of increased lysosomal sequestration. Despite the higher intracellular sunitinib accumulation, levels of the key signaling p-Akt and p-ERK 1/2 were unaffected and comparable with untreated parental cells, indicating reduced effectiveness of sunitinib.
Conclusion: We report that sunitinib inhibits tumor cell proliferation at clinically relevant concentrations and found lysosomal sequestration to be a novel mechanism of sunitinib resistance. This finding warrants clinical evaluation whether targeting lysosomal function will overcome sunitinib resistance. Clin Cancer Res; 17(23); 7337–46. ©2011 AACR.
Direct Role of Adiponectin and Adiponectin Receptors in Endometrial Cancer: In Vitro and Ex Vivo Studies in Humans
Authors: Moon Hyun-Seuk , Chamberland John P. , Aronis Konstantinos , Tseleni-Balafouta Sofia , Mantzoros Christos S. 
Published: October 2011

Abstract
Low adiponectin levels are an independent risk factor for and mediate the effect of obesity on endometrial cancer in epidemiology studies. The direct or indirect mechanisms underlying these findings remain to be elucidated. We first examined the expression of adiponectin receptor 1 (AdipoR1) and 2 (AdipoR2) in normal human endometrium and in endometrial cancer tissues ex vivo. We then used KLE and RL95-2 human endometrial cancer cell lines in vitro to study relative expression of AdipoRs, to investigate the effect of adiponectin on activating intracellular signaling pathways, and to assess its potential to alter malignant properties. We report for the first time that the relative expression level of AdipoR1 is higher than AdipoR2 in human endometrial cancer tissue, but the expression of AdipoRs is not statistically different from nonneoplastic tissues. We also show for the first time in endometrial cancer cell lines in vitro that adiponectin suppresses endometrial cancer proliferation acting through AdipoRs. Adiponectin also increases the expression of the adaptor molecule LKB1, which is required for adiponectin-mediated activation of AMPK/S6 axis and modulation of cell proliferation, colony formation, adhesion, and invasion of KLE and RL95-2 cell lines. These novel mechanistic studies provide for the first time in vitro and ex vivo evidence for a causal role of adiponectin in endometrial cancer. Mol Cancer Ther; 10(12); 2234–43. ©2011 AACR.
Spatial Distribution and Mechanical Function of Elastin in Resistance Arteries
Authors: Clifford Philip S. , Ella Srikanth R. , Stupica Aaron J. , Nourian Zahra , Li Min , Martinez-Lemus Luis A. , Dora Kim A. , Yang Yan , Davis Michael J. , Pohl Ulrich , Meininger Gerald A. , Hill Michael A. 
Published: October 2011

Objective—
Despite the role that extracellular matrix (ECM) plays in vascular signaling, little is known of the complex structural arrangement between specific ECM proteins and vascular smooth muscle cells. Our objective was to examine the hypothesis that adventitial elastin fibers are dominant in vessels subject to longitudinal stretch.

Methods and Results—
Cremaster muscle arterioles were isolated, allowed to develop spontaneous tone, and compared with small cerebral arteries. 3D confocal microscopy was used to visualize ECM within the vessel wall. Pressurized arterioles were fixed and stained with Alexa 633 hydrazide (as a nonselective ECM marker), anti-elastin, or anti-type 1 collagen antibody and a fluorescent nuclear stain. Exposure of cremaster muscle arterioles to elastase for 5 minutes caused an irreversible lengthening of the vessel segment that was not observed in cerebral arteries. Longitudinal elastin fibers were demonstrated on cremaster muscle arterioles using 3D imaging but were confirmed to be absent in cerebral vessels. The fibers were also distinct from type I collagen fibers and were degraded by elastase treatment.

Conclusion—
These results indicate the importance of elastin in bearing longitudinal stress in the arteriolar wall and that these fibers constrain vascular smooth muscle cells. Differences between skeletal muscle and cerebral small arteries may reflect differences in the local mechanical environment, such as exposure to longitudinal stretch.