bluuebunny/crossref_metadata_2025_split huggingface dataset:
Racial Differences in Long‐Term Outcomes after Percutaneous Coronary Intervention with Paclitaxel‐Eluting Coronary Stents
Authors: BATCHELOR WAYNE B. , ELLIS STEPHEN G. , ORMISTON JOHN A. , STONE GREGG W. , JOSHI ANITA A. , WANG HONG , UNDERWOOD PAUL L. 
Published: September 2012

ObjectivesTo assess the influence of race on long‐term outcomes following percutaneous coronary intervention (PCI) with paclitaxel‐eluting stents (PES).BackgroundData on the influence of race on long‐term outcomes following PCI with drug‐eluting stents are limited because of severe underrepresentation of minority populations in randomized trials.MethodsWe compared 5‐year outcomes of 2,301 Whites, 127 Blacks, and 169 Asians treated with PES in the TAXUS IV, V, and ATLAS trials. Outcomes were adjusted using a propensity score logistic regression model with 1:4 matching.ResultsBlacks were more likely than Whites to be female, have a history of hypertension, diabetes mellitus, congestive heart failure, and stroke, but were less likely to have prior coronary artery disease. Compared with Whites, Asians were younger, more likely to be male, have stable angina, and left anterior descending disease, and less likely to have silent ischemia, previous coronary artery bypass surgery, prior coronary artery disease, diabetes mellitus, peripheral vascular disease, and to receive glycoprotein IIb/IIIa inhibitors. Despite higher antiplatelet compliance, the adjusted 5‐year rates of myocardial infarction (15.4% vs. 5.4%, P < 0.001) and stent thrombosis (5.6% vs. 1.1%, P = 0.002) were higher in Blacks than Whites. Despite lower antiplatelet compliance, Asians had no differences in myocardial infarction and stent thrombosis compared with Whites. Mortality and revascularization rates were similar between the three groups.ConclusionsThe long‐term risk of major thrombotic events after PCI with PES was higher in Blacks, but not Asians, compared with Whites. The mechanisms underlying these racial differences warrant further investigation. (J Interven Cardiol 2013;26:49–57)
Nurse practice environment, workload, burnout, job outcomes, and quality of care in psychiatric hospitals: a structural equation model approach
Authors: Van Bogaert Peter , Clarke Sean , Willems Riet , Mondelaers Mieke 
Published: September 2012

AbstractAimTo study the relationships between nurse practice environment, workload, burnout, job outcomes and nurse‐reported quality of care in psychiatric hospital staff.BackgroundNurses' practice environments in general hospitals have been extensively investigated. Potential variations across practice settings, for instance in psychiatric hospitals, have been much less studied.DesignA cross‐sectional design with a survey.MethodA structural equation model previously tested in acute hospitals was evaluated using survey data from a sample of 357 registered nurses, licensed practical nurses, and non‐registered caregivers from two psychiatric hospitals in Belgium between December 2010–April 2011. The model included paths between practice environment dimensions and outcome variables, with burnout in a mediating position. A workload measure was also tested as a potential mediator between the practice environment and outcome variables.ResultsAn improved model, slightly modified from the one validated earlier in samples of acute care nurses, was confirmed. This model explained 50% and 38% of the variance in job outcomes and nurse‐reported quality of care respectively. In addition, workload was found to play a mediating role in accounting for job outcomes and significantly improved a model that ultimately explained 60% of the variance in these variables.ConclusionIn psychiatric hospitals as in general hospitals, nurse–physician relationship and other organizational dimensions such as nursing and hospital management were closely associated with perceptions of workload and with burnout and job satisfaction, turnover intentions, and nurse‐reported quality of care. Mechanisms linking key variables and differences across settings in these relationships merit attention by managers and researchers.
Crystal structure of the MrkD1P receptor binding domain of Klebsiella pneumoniae and identification of the human collagen V binding interface
Authors: Rêgo Ana Toste , Johnson Jeremiah G. , Geibel Sebastian , Enguita Francisco J. , Clegg Steven , Waksman Gabriel 
Published: September 2012

SummaryKlebsiella species are members of the family enterobacteriaceae, opportunistic pathogens that are among the eight most prevalent infectious agents in hospitals. Among other virulence factors in Klebsiella, type 3 pili exhibit a unique binding pattern in the human kidney via interaction of two MrkD adhesion variants 1C1 and 1P to type IV and/or V collagen. However, very little is known about the nature of this recognition. Here we present the crystal structure of the plasmid born MrkD1P receptor domain (MrkDrd). The structure reveals a jelly‐roll β‐barrel fold comprising 17 β‐strands very similar to the receptor domain of GafD, the tip adhesin from the F17 pilus that recognizes n‐acetyl‐d‐glucosamine (GlcNAc). Analysis of collagen V binding of different MrkD1P mutants revealed that two regions were responsible for its binding: a pocket, that aligns approximately with the GlcNAc binding pocket of GafD involving residues R105 and Y155, and a transversally oriented patch that spans strands β2a, β9b and β6 including residues V49, T52, V91, R102 and I136. Taken together, these data provide structural and functional insights on MrkD1P recognition of host cells, providing a tool for future development of rationally designed drugs with the prospect of blocking Klebsiella adhesion to collagen V.
A Multicenter Blinded Analysis Indicates No Association between Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and either Xenotropic Murine Leukemia Virus-Related Virus or Polytropic Murine Leukemia Virus
Authors: Alter Harvey J. , Mikovits Judy A. , Switzer William M. , Ruscetti Francis W. , Lo Shyh-Ching , Klimas Nancy , Komaroff Anthony L. , Montoya Jose G. , Bateman Lucinda , Levine Susan , Peterson Daniel , Levin Bruce , Hanson Maureen R. , Genfi Afia , Bhat Meera , Zheng HaoQiang , Wang Richard , Li Bingjie , Hung Guo-Chiuan , Lee Li Ling , Sameroff Stephen , Heneine Walid , Coffin John , Hornig Mady , Lipkin W. Ian 
Published: September 2012

ABSTRACT
The disabling disorder known as chronic fatigue syndrome or myalgic encephalomyelitis (CFS/ME) has been linked in two independent studies to infection with xenotropic murine leukemia virus-related virus (XMRV) and polytropic murine leukemia virus (pMLV). Although the associations were not confirmed in subsequent studies by other investigators, patients continue to question the consensus of the scientific community in rejecting the validity of the association. Here we report blinded analysis of peripheral blood from a rigorously characterized, geographically diverse population of 147 patients with CFS/ME and 146 healthy subjects by the investigators describing the original association. This analysis reveals no evidence of either XMRV or pMLV infection.

IMPORTANCE
Chronic fatigue syndrome/myalgic encephalomyelitis has an estimated prevalence of 42/10,000 in the United States, with annual direct medical costs of $7 billion. Here, the original investigators who found XMRV and pMLV (polytropic murine leukemia virus) in blood of subjects with this disorder report that this association is not confirmed in a blinded analysis of samples from rigorously characterized subjects. The increasing frequency with which molecular methods are used for pathogen discovery poses new challenges to public health and support of science. It is imperative that strategies be developed to rapidly and coherently address discoveries so that they can be carried forward for translation to clinical medicine or abandoned to focus resource investment more productively. Our study provides a paradigm for pathogen dediscovery that may be helpful to others working in this field.
Rab25 Is a Tumor Suppressor Gene with Antiangiogenic and Anti-Invasive Activities in Esophageal Squamous Cell Carcinoma
Authors: Tong Man , Chan Kwok Wah , Bao Jessie Y.J. , Wong Kai Yau , Chen Jin-Na , Kwan Pak Shing , Tang Kwan Ho , Fu Li , Qin Yan-Ru , Lok Si , Guan Xin-Yuan , Ma Stephanie 
Published: September 2012

AbstractEsophageal squamous cell carcinoma (ESCC), the major histologic subtype of esophageal cancer, is a devastating disease characterized by distinctly high incidences and mortality rates. However, there remains limited understanding of molecular events leading to development and progression of the disease, which are of paramount importance to defining biomarkers for diagnosis, prognosis, and personalized treatment. By high-throughout transcriptome sequence profiling of nontumor and ESCC clinical samples, we identified a subset of significantly differentially expressed genes involved in integrin signaling. The Rab25 gene implicated in endocytic recycling of integrins was the only gene in this group significantly downregulated, and its downregulation was confirmed as a frequent event in a second larger cohort of ESCC tumor specimens by quantitative real-time PCR and immunohistochemical analyses. Reduced expression of Rab25 correlated with decreased overall survival and was also documented in ESCC cell lines compared with pooled normal tissues. Demethylation treatment and bisulfite genomic sequencing analyses revealed that downregulation of Rab25 expression in both ESCC cell lines and clinical samples was associated with promoter hypermethylation. Functional studies using lentiviral-based overexpression and suppression systems lent direct support of Rab25 to function as an important tumor suppressor with both anti-invasive and -angiogenic abilities, through a deregulated FAK–Raf–MEK1/2–ERK signaling pathway. Further characterization of Rab25 may provide a prognostic biomarker for ESCC outcome prediction and a novel therapeutic target in ESCC treatment. Cancer Res; 72(22); 6024–35. ©2012 AACR.
Clinical Significance of the Genetic Landscape of Pancreatic Cancer and Implications for Identification of Potential Long-term Survivors
Authors: Yachida Shinichi , White Catherine M. , Naito Yoshiki , Zhong Yi , Brosnan Jacqueline A. , Macgregor-Das Anne M. , Morgan Richard A. , Saunders Tyler , Laheru Daniel A. , Herman Joseph M. , Hruban Ralph H. , Klein Alison P. , Jones Siân , Velculescu Victor , Wolfgang Christopher L. , Iacobuzio-Donahue Christine A. 
Published: September 2012

Abstract
Purpose: Genetic alterations of KRAS, CDKN2A, TP53, and SMAD4 are the most frequent events in pancreatic cancer. We determined the extent to which these 4 alterations are coexistent in the same carcinoma, and their impact on patient outcome.
Experimental Design: Pancreatic cancer patients who underwent an autopsy were studied (n = 79). Matched primary and metastasis tissues were evaluated for intragenic mutations in KRAS, CDKN2A, and TP53 and immunolabeled for CDKN2A, TP53, and SMAD4 protein products. The number of altered driver genes in each carcinoma was correlated to clinicopathologic features. Kaplan–Meier estimates were used to determine median disease free and overall survival, and a Cox proportional hazards model used to compare risk factors.
Results: The number of genetically altered driver genes in a carcinoma was variable, with only 29 patients (37%) having an alteration in all 4 genes analyzed. The number of altered driver genes was significantly correlated with disease free survival (P = 0.008), overall survival (P = 0.041), and metastatic burden at autopsy (P = 0.002). On multivariate analysis, the number of driver gene alterations in a pancreatic carcinoma remained independently associated with overall survival (P = 0.046). Carcinomas with only 1 to 2 driver alterations were enriched for those patients with the longest survival (median 23 months, range 1 to 53).
Conclusions: Determinations of the status of the 4 major driver genes in pancreatic cancer, and specifically the extent to which they are coexistent in an individual patients cancer, provides distinct information regarding disease progression and survival that is independent of clinical stage and treatment status. Clin Cancer Res; 18(22); 6339–47. ©2012 AACR.
Targeting Protein Tyrosine Kinase 6 Enhances Apoptosis of Colon Cancer Cells following DNA Damage
Authors: Gierut Jessica J. , Mathur Priya S. , Bie Wenjun , Han Jin , Tyner Angela L. 
Published: September 2012

Abstract
Protein tyrosine kinase 6 (PTK6) is an intracellular tyrosine kinase that has distinct functions in normal epithelia and cancer. It is expressed primarily in nondividing epithelial cells in the normal intestine, where it promotes differentiation. However, after DNA damage, PTK6 is induced in proliferating progenitor cells, where it contributes to apoptosis. We examined links between PTK6 and the tumor suppressor p53 in the isogenic p53+/+ and p53−/− HCT116 colon tumor cell lines. We found that p53 promotes expression of PTK6 in HCT116 cells, and short hairpin RNA-mediated knockdown of PTK6 leads to reduced induction of the cyclin-dependent kinase inhibitor p21. Knockdown of PTK6 enhances apoptosis in HCT116 cells with wild-type p53, following treatment of cells with γ-radiation, doxorubicin, or 5-fluorouracil. No differences in the activation of AKT, ERK1/2, or ERK5, known PTK6-regulated prosurvival signaling proteins, were detected. However, activity of STAT3, a PTK6 substrate, was impaired in cells with knockdown of PTK6 following DNA damage. In contrast to its role in the normal epithelium following DNA damage, PTK6 promotes survival of cancer cells with wild-type p53 by promoting p21 expression and STAT3 activation. Targeting PTK6 in combination with use of chemotherapeutic drugs or radiation may enhance death of colon tumor cells with wild-type p53. Mol Cancer Ther; 11(11); 2311–20. ©2012 AACR.
Dll4-Fc, an Inhibitor of Dll4-Notch Signaling, Suppresses Liver Metastasis of Small Cell Lung Cancer Cells through the Downregulation of the NF-κB Activity
Authors: Kuramoto Takuya , Goto Hisatsugu , Mitsuhashi Atsushi , Tabata Sho , Ogawa Hirohisa , Uehara Hisanori , Saijo Atsuro , Kakiuchi Soji , Maekawa Yoichi , Yasutomo Koji , Hanibuchi Masaki , Akiyama Shin-ichi , Sone Saburo , Nishioka Yasuhiko 
Published: September 2012

Abstract
Notch signaling regulates cell-fate decisions during development and postnatal life. Little is known, however, about the role of Delta-like-4 (Dll4)-Notch signaling between cancer cells, or how this signaling affects cancer metastasis. We, therefore, assessed the role of Dll4-Notch signaling in cancer metastasis. We generated a soluble Dll4 fused to the IgG1 constant region (Dll4-Fc) that acts as a blocker of Dll4-Notch signaling and introduced it into human small cell lung cancer (SCLC) cell lines expressing either high levels (SBC-3 and H1048) or low levels (SBC-5) of Dll4. The effects of Dll4-Fc on metastasis of SCLC were evaluated using a mouse model. Although Dll4-Fc had no effect on the liver metastasis of SBC-5, the number of liver metastasis inoculated with SBC-3 and H1048 cells expressing Dll4-Fc was significantly lower than that injected with control cells. To study the molecular mechanisms of the effects of Dll4-Fc on liver metastasis, a PCR array analysis was conducted. Because the expression of NF-κB target genes was affected by Dll4-Fc, we conducted an electrophoretic mobility shift assay and observed that NF-κB activities, both with and without stimulation by TNF-α, were downregulated in Dll4-Fc–overexpressing SBC-3 and H1048 cells compared with control cells. Moreover, Dll4-Fc attenuates, at least in part, the classical and alternative NF-κB activation pathway by reducing Notch1 signaling. These results suggest that Dll4-Notch signaling in cancer cells plays a critical role in liver metastasis of SCLC by regulating NF-κB signaling. Mol Cancer Ther; 11(12); 2578–87. ©2012 AACR.
Decoupled Response of Ocean Acidification to Variations in Climate Sensitivity
Authors: Matsumoto Katsumi , McNeil Ben 
Published: September 2012

Abstract
It is now well understood that the global surface ocean, whose pH has been reduced by ~0.1 in response to rising atmospheric CO2 since industrialization, will continue to become more acidic as fossil fuel CO2 emissions escalate. However, it is unclear how uncertainties in climate sensitivity to future CO2 emissions will alter the manifestation of ocean acidification. Using an earth system model of intermediate complexity, this study performs a set of simulations that varies equilibrium climate sensitivity by 1.0°–4.5°C for a given CO2 emissions scenario and finds two unexpected and decoupled responses. First, the greater the climate sensitivity, the larger the surface mixed layer acidification signal but the smaller the subsurface acidification. However, taken throughout the ocean, the highest climate sensitivity will paradoxically cause greater global warming while buffering whole-ocean pH by up to 24% on centennial time scales. Second, this study finds a large decoupling between pH and carbonate ion concentration in surface waters whereby these chemical properties show opposite effects under variable climate sensitivity. For every 1°C increase in climate sensitivity, the surface ocean pH reduction grows by 4%, while surface ocean carbonate ion reduction shrinks by 2%. The chemical and spatial decoupling found here highlights the importance of distinguishing the biological impacts of pH and aragonite saturation and understanding the spatial extent of important calcifying biomes so as to truly understand the long-term impacts of ocean acidification.
Small nucleolar RNA expression profiling identifies potential prognostic markers in peripheral T-cell lymphoma
Authors: Valleron Wilfried , Ysebaert Loic , Berquet Laure , Fataccioli Virginie , Quelen Cathy , Martin Antoine , Parrens Marie , Lamant Laurence , de Leval Laurence , Gisselbrecht Christian , Gaulard Philippe , Brousset Pierre 
Published: September 2012

Abstract
Peripheral T-cell lymphoma (PTCL) is a rare, heterogeneous type of non-Hodgkin lymphoma (NHL) that, in general, is associated with a poor clinical outcome. Therefore, a current major challenge is the discovery of new prognostic tools for this disease. In the present study, a cohort of 122 patients with PTCL was collected from a multicentric T-cell lymphoma consortium (TENOMIC). We analyzed the expression of 80 small nucleolar RNAs (snoRNAs) using high-throughput quantitative PCR. We demonstrate that snoRNA expression analysis may be useful in both the diagnosis of some subtypes of PTCL and the prognostication of both PTCL-not otherwise specified (PTCL-NOS; n = 26) and angio-immunoblastic T-cell lymphoma (AITL; n = 46) patients treated with chemotherapy. Like miRNAs, snoRNAs are globally down-regulated in tumor cells compared with their normal counterparts. In the present study, the snoRNA signature was robust enough to differentiate anaplastic large cell lymphoma (n = 32) from other PTCLs. For PTCL-NOS and AITL, we obtained 2 distinct prognostic signatures with a reduced set of 3 genes. Of particular interest was the prognostic value of HBII-239 snoRNA, which was significantly over-expressed in cases of AITL and PTCL-NOS that had favorable outcomes. Our results suggest that snoRNA expression profiles may have a diagnostic and prognostic significance for PTCL, offering new tools for patient care and follow-up.
Depression, suicidal ideation, and associated factors: a cross-sectional study in rural Haiti
Authors: Wagenaar Bradley H , Hagaman Ashley K , Kaiser Bonnie N , McLean Kristen E , Kohrt Brandon A 
Published: September 2012

Abstract

Background
Since the 2010 earthquake in Haiti, there has been increased international attention to mental health needs throughout the country. The present study represents one of the first epidemiologic studies of depression symptomatology, suicidal ideation, and associated factors in Haiti’s Central Plateau.

Methods
We conducted a cross-sectional, zone-stratified household survey of 408 adults in Haiti’s Central Plateau. Depression symptomatology was assessed with a culturally-adapted Kreyòl version of the Beck Depression Inventory (BDI). Multivariable linear and logistic regression models were built using backward elimination, with the outcomes being continuous BDI scores and endorsing suicidal ideation, respectively.

Results
The mean BDI score was 20.4 (95% confidence interval [CI]: 19.3-21.5), and 6.13% (N = 25) of participants endorsed current suicidal ideation. Factors associated with BDI scores were: continuous age (adjusted beta [aβ]: 0.14, CI: 0.06-0.22), female gender (aβ: 2.1, CI: 0.18-4.0), suicidal ideation (aβ: 11.1, CI: 7.3-14.9), death in family (aβ: 2.7, CI: 0.57-4.9), and prior life-threatening illness (aβ: 2.6, CI: 0.77-4.5). Education was a risk factor for depression among women but not among men, and employment was a risk factor for both genders. Factors associated with endorsing suicidal ideation were: BDI score (ten point change) (adjusted odds ratio [aOR]: 2.5, CI: 1.7-3.6), lack of care if sick (aOR: 5.5, CI: 1.1-28.6), alcohol use (aOR: 3.3, CI: 1.3-8.2), and ever having been to a Vodou priest (aOR: 3.2, CI: 1.1-9.5).

Conclusions
A large proportion of Haiti’s Central Plateau may be experiencing high levels of depression symptomatology and/or current suicidal ideation. Screening could be conducted in biomedical, religious, and Vodou healing contexts. For prevention, poverty reduction and improved healthcare access are key elements. For treatment, general psychiatric services, psychosocial services for the medically ill and their families, and substance abuse interventions should be explored. Paradoxical associations related to education and employment require further exploration.